PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
6628714-10	1983	The effect of hCG on plasma estradiol levels was virtually eliminated in hyperandrogenic baboons.	Estradiol	28-37	hypertrichosis 2 (generalised, congenital)	Homo sapiens	14-17
6671461-5	1983	Replacement with progesterone 1 h after the simultaneous injection of hCG and anti-progesterone partly reversed the reduced incidence of meiosis.	Progesterone	17-29	hypertrichosis 2 (generalised, congenital)	Homo sapiens	70-73
6671461-6	1983	An injection of rabbit antiserum to estrone, in addition to the replacement with progesterone 1 h after the simultaneous injections of hCG and anti-progesterone, restored the incidence of meiosis to a value comparable to the values found for control rats treated sequentially with PMS and hCG.	pms	281-284	hypertrichosis 2 (generalised, congenital)	Homo sapiens	135-138
6195275-1	1983	A radioimmunoassay (CTP-RIA) for urinary human chorionic gonadotropin (hCG) with the use of an antiserum to be carboxyl-terminal peptide of hCG beta subunit was employed to detect hCG production in patients with gestational trophoblastic disease.	Cytidine Triphosphate	20-23	hypertrichosis 2 (generalised, congenital)	Homo sapiens	71-74
6195275-1	1983	A radioimmunoassay (CTP-RIA) for urinary human chorionic gonadotropin (hCG) with the use of an antiserum to be carboxyl-terminal peptide of hCG beta subunit was employed to detect hCG production in patients with gestational trophoblastic disease.	Cytidine Triphosphate	20-23	hypertrichosis 2 (generalised, congenital)	Homo sapiens	140-143
6195275-1	1983	A radioimmunoassay (CTP-RIA) for urinary human chorionic gonadotropin (hCG) with the use of an antiserum to be carboxyl-terminal peptide of hCG beta subunit was employed to detect hCG production in patients with gestational trophoblastic disease.	Cytidine Triphosphate	20-23	hypertrichosis 2 (generalised, congenital)	Homo sapiens	140-143
6195275-10	1983	This specific and sensitive CTP-RIA method for the detection of hCG production was found to improve the ability to diagnose persistent or recurrent trophoblastic disease.	Cytidine Triphosphate	28-31	hypertrichosis 2 (generalised, congenital)	Homo sapiens	64-67
6630052-2	1983	Testosterone production was assessed in both control nd gossypol treated groups after 0 to 4 hours incubation in the presence of hCG.	Testosterone	0-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	129-132
6863482-1	1983	In normal men a single dose of hCG induces an increase in plasma testosterone (T) and 17 alpha-hydroxyprogesterone (17 alpha-OHP) 2-4 h after the injection; after 24-36 h a maximum increase in plasma 17 beta-estradiol (E2) and 17 alpha-OHP occurs followed by a second surge in T after 48-96 h. The present investigation focuses on the effect of a single dose of hCG (3500 IU/m2 body surface) on testicular steroid production in 12 boys aged 13 months to 12 yr.	Testosterone	65-77	hypertrichosis 2 (generalised, congenital)	Homo sapiens	31-34
6863482-1	1983	In normal men a single dose of hCG induces an increase in plasma testosterone (T) and 17 alpha-hydroxyprogesterone (17 alpha-OHP) 2-4 h after the injection; after 24-36 h a maximum increase in plasma 17 beta-estradiol (E2) and 17 alpha-OHP occurs followed by a second surge in T after 48-96 h. The present investigation focuses on the effect of a single dose of hCG (3500 IU/m2 body surface) on testicular steroid production in 12 boys aged 13 months to 12 yr.	17-alpha-Hydroxyprogesterone	86-114	hypertrichosis 2 (generalised, congenital)	Homo sapiens	31-34
6863482-1	1983	In normal men a single dose of hCG induces an increase in plasma testosterone (T) and 17 alpha-hydroxyprogesterone (17 alpha-OHP) 2-4 h after the injection; after 24-36 h a maximum increase in plasma 17 beta-estradiol (E2) and 17 alpha-OHP occurs followed by a second surge in T after 48-96 h. The present investigation focuses on the effect of a single dose of hCG (3500 IU/m2 body surface) on testicular steroid production in 12 boys aged 13 months to 12 yr.	alpha-ohp	119-128	hypertrichosis 2 (generalised, congenital)	Homo sapiens	31-34
6863482-1	1983	In normal men a single dose of hCG induces an increase in plasma testosterone (T) and 17 alpha-hydroxyprogesterone (17 alpha-OHP) 2-4 h after the injection; after 24-36 h a maximum increase in plasma 17 beta-estradiol (E2) and 17 alpha-OHP occurs followed by a second surge in T after 48-96 h. The present investigation focuses on the effect of a single dose of hCG (3500 IU/m2 body surface) on testicular steroid production in 12 boys aged 13 months to 12 yr.	Estradiol	203-217	hypertrichosis 2 (generalised, congenital)	Homo sapiens	31-34
6863482-1	1983	In normal men a single dose of hCG induces an increase in plasma testosterone (T) and 17 alpha-hydroxyprogesterone (17 alpha-OHP) 2-4 h after the injection; after 24-36 h a maximum increase in plasma 17 beta-estradiol (E2) and 17 alpha-OHP occurs followed by a second surge in T after 48-96 h. The present investigation focuses on the effect of a single dose of hCG (3500 IU/m2 body surface) on testicular steroid production in 12 boys aged 13 months to 12 yr.	2-hydroxyphenylacetic acid	124-128	hypertrichosis 2 (generalised, congenital)	Homo sapiens	31-34
6863482-1	1983	In normal men a single dose of hCG induces an increase in plasma testosterone (T) and 17 alpha-hydroxyprogesterone (17 alpha-OHP) 2-4 h after the injection; after 24-36 h a maximum increase in plasma 17 beta-estradiol (E2) and 17 alpha-OHP occurs followed by a second surge in T after 48-96 h. The present investigation focuses on the effect of a single dose of hCG (3500 IU/m2 body surface) on testicular steroid production in 12 boys aged 13 months to 12 yr.	Steroids	406-413	hypertrichosis 2 (generalised, congenital)	Homo sapiens	31-34
6863482-4	1983	The results show that hCG peaked 2 h after administration of the hormone and high levels persisted for up until 72 h. Plasma T and dihydrotestosterone increased after 48 h and remained significantly high for another 48 h; 17 alpha-OHP, A, and E2 did not change.	alpha-ohp	225-234	hypertrichosis 2 (generalised, congenital)	Homo sapiens	22-25
6224978-0	1983	Comparison of serum steroid responses to a single injection of hCG in man and rat.	Steroids	20-27	hypertrichosis 2 (generalised, congenital)	Homo sapiens	63-66
6224978-1	1983	The responses of peripheral serum steroids to a single injection of hCG (80 IU/kg b wt) were compared in adult male rats and humans.	Steroids	34-42	hypertrichosis 2 (generalised, congenital)	Homo sapiens	68-71
6224978-3	1983	One hour after hCG the concentrations of testosterone and all its precursors measured except for pregnenolone were significantly elevated in the rat serum, whereas a clear rapid response was not observed in the men.	Testosterone	41-53	hypertrichosis 2 (generalised, congenital)	Homo sapiens	15-18
6224978-4	1983	Transient blockade of C21 steroid side-chain cleavage was seen in both species at about 24-36 h after hCG, which occurred at the same time as the maximum concentration of estradiol in the men.	Steroids	26-33	hypertrichosis 2 (generalised, congenital)	Homo sapiens	102-105
6224978-7	1983	Our findings are compatible with the concept that the main difference in the gonadotropin-stimulated steroidogenesis in man and rat is the magnitude of the rapid steroidogenic response to hCG, which is very small in man and indicates smaller supply or lesser metabolism of mitochondrial cholesterol in human testis.	Cholesterol	287-298	hypertrichosis 2 (generalised, congenital)	Homo sapiens	188-191
6861718-8	1983	In animals treated with the antiestrogen tamoxifen, stimulation of RNA polymerase activity by hCG was completely inhibited.	Tamoxifen	41-50	hypertrichosis 2 (generalised, congenital)	Homo sapiens	94-97
6861718-11	1983	These studies have indicated that the hCG-induced RNA polymerase activation in the Leydig cell is mediated through nuclear actions of estradiol, since stimulation of the enzymes was prevented by tamoxifen and inhibition of steroid biosynthesis, and was induced by estradiol administration.	Estradiol	134-143	hypertrichosis 2 (generalised, congenital)	Homo sapiens	38-41
6861718-11	1983	These studies have indicated that the hCG-induced RNA polymerase activation in the Leydig cell is mediated through nuclear actions of estradiol, since stimulation of the enzymes was prevented by tamoxifen and inhibition of steroid biosynthesis, and was induced by estradiol administration.	Tamoxifen	195-204	hypertrichosis 2 (generalised, congenital)	Homo sapiens	38-41
6861718-11	1983	These studies have indicated that the hCG-induced RNA polymerase activation in the Leydig cell is mediated through nuclear actions of estradiol, since stimulation of the enzymes was prevented by tamoxifen and inhibition of steroid biosynthesis, and was induced by estradiol administration.	Steroids	223-230	hypertrichosis 2 (generalised, congenital)	Homo sapiens	38-41
6861718-11	1983	These studies have indicated that the hCG-induced RNA polymerase activation in the Leydig cell is mediated through nuclear actions of estradiol, since stimulation of the enzymes was prevented by tamoxifen and inhibition of steroid biosynthesis, and was induced by estradiol administration.	Estradiol	264-273	hypertrichosis 2 (generalised, congenital)	Homo sapiens	38-41
6408218-3	1983	Testicular blood flow per testis followed testis weight closely, and as a result the production of testosterone by the smaller testes (calculated as the product of plasma flow and the veno-arterial difference in testosterone concentration) was markedly reduced especially when the rats had been stimulated with human chorionic gonadotrophin (hCG).	Testosterone	99-111	hypertrichosis 2 (generalised, congenital)	Homo sapiens	342-345
6864645-0	1983	Effect of oestradiol and tamoxifen on the testosterone response in male rats to a single injection of hCG.	Estradiol	10-20	hypertrichosis 2 (generalised, congenital)	Homo sapiens	102-105
6864645-0	1983	Effect of oestradiol and tamoxifen on the testosterone response in male rats to a single injection of hCG.	Tamoxifen	25-34	hypertrichosis 2 (generalised, congenital)	Homo sapiens	102-105
6864645-0	1983	Effect of oestradiol and tamoxifen on the testosterone response in male rats to a single injection of hCG.	Testosterone	42-54	hypertrichosis 2 (generalised, congenital)	Homo sapiens	102-105
6864645-6	1983	The basal in-vitro testosterone production by decapsulated testes from animals injected with hCG was enhanced at 2 h. Stimulation by hCG increased the amount of testosterone produced (X 1.5 that in controls).	Testosterone	19-31	hypertrichosis 2 (generalised, congenital)	Homo sapiens	93-96
6864645-6	1983	The basal in-vitro testosterone production by decapsulated testes from animals injected with hCG was enhanced at 2 h. Stimulation by hCG increased the amount of testosterone produced (X 1.5 that in controls).	Testosterone	19-31	hypertrichosis 2 (generalised, congenital)	Homo sapiens	133-136
6864645-6	1983	The basal in-vitro testosterone production by decapsulated testes from animals injected with hCG was enhanced at 2 h. Stimulation by hCG increased the amount of testosterone produced (X 1.5 that in controls).	Testosterone	161-173	hypertrichosis 2 (generalised, congenital)	Homo sapiens	93-96
6864645-6	1983	The basal in-vitro testosterone production by decapsulated testes from animals injected with hCG was enhanced at 2 h. Stimulation by hCG increased the amount of testosterone produced (X 1.5 that in controls).	Testosterone	161-173	hypertrichosis 2 (generalised, congenital)	Homo sapiens	133-136
6305195-1	1983	The results of the present investigation support the conclusion that low-density lipoprotein (LDL)-cholesterol facilitates androgen synthesis in human chorionic gonadotropin (hCG)-treated human fetal testicular tissue in vitro.	Cholesterol	99-110	hypertrichosis 2 (generalised, congenital)	Homo sapiens	175-178
6305195-2	1983	Moreover, the number of LDL receptors and the rate of de novo synthesis of cholesterol are high during the period of active fetal testicular steroidogenesis and fall with advancing gestational age, suggestive of regulation by hCG.	Cholesterol	75-86	hypertrichosis 2 (generalised, congenital)	Homo sapiens	226-229
6299707-8	1983	The incorporation of tritium into progesterone was increased by hCG and inhibited by an excess of unlabeled LDL in the incubation medium.	Tritium	21-28	hypertrichosis 2 (generalised, congenital)	Homo sapiens	64-67
6299707-8	1983	The incorporation of tritium into progesterone was increased by hCG and inhibited by an excess of unlabeled LDL in the incubation medium.	Progesterone	34-46	hypertrichosis 2 (generalised, congenital)	Homo sapiens	64-67
6832068-6	1983	In contrast, estradiol and testosterone levels in the ovarian vein increased from 0.7 +/- 0.1 and 0.6 +/- 3.4 ng/ml, respectively, in vehicle-treated rats to 12.5 +/- 3.5 and 4.8 +/- 1.4 ng/ml in hCG-treated animals.	Estradiol	13-22	hypertrichosis 2 (generalised, congenital)	Homo sapiens	196-199
6832068-6	1983	In contrast, estradiol and testosterone levels in the ovarian vein increased from 0.7 +/- 0.1 and 0.6 +/- 3.4 ng/ml, respectively, in vehicle-treated rats to 12.5 +/- 3.5 and 4.8 +/- 1.4 ng/ml in hCG-treated animals.	Testosterone	27-39	hypertrichosis 2 (generalised, congenital)	Homo sapiens	196-199
6832068-7	1983	In vivo treatment with hCG dramatically increased the in vitro capacity of luteal cells to synthesize de novo both testosterone and estradiol but had no stimulatory effect on progesterone synthesis.	Testosterone	115-127	hypertrichosis 2 (generalised, congenital)	Homo sapiens	23-26
6832068-7	1983	In vivo treatment with hCG dramatically increased the in vitro capacity of luteal cells to synthesize de novo both testosterone and estradiol but had no stimulatory effect on progesterone synthesis.	Estradiol	132-141	hypertrichosis 2 (generalised, congenital)	Homo sapiens	23-26
6832068-9	1983	hCG also increased follicular synthesis of both estradiol and testosterone.	Estradiol	48-57	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
6832068-9	1983	hCG also increased follicular synthesis of both estradiol and testosterone.	Testosterone	62-74	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
6832068-10	1983	The interstitium responded to the hCG challenge with a 50-fold increase in testosterone synthesis but with no change in estradiol production.	Testosterone	75-87	hypertrichosis 2 (generalised, congenital)	Homo sapiens	34-37
6832068-11	1983	To determine whether hCG rapidly stimulates ovarian production of testosterone, both in vivo and in vitro approaches were used.	Testosterone	66-78	hypertrichosis 2 (generalised, congenital)	Homo sapiens	21-24
6832068-15	1983	In summary, this study demonstrates that in the pregnant rat a sustained increase in serum hCG activity stimulates ovarian secretion of both testosterone and estradiol.	Testosterone	141-153	hypertrichosis 2 (generalised, congenital)	Homo sapiens	91-94
6832068-15	1983	In summary, this study demonstrates that in the pregnant rat a sustained increase in serum hCG activity stimulates ovarian secretion of both testosterone and estradiol.	Estradiol	158-167	hypertrichosis 2 (generalised, congenital)	Homo sapiens	91-94
6884026-1	1983	Chemically deglycosylated preparations of hCG (DG-hCG) which have been shown to have hormonal antagonistic activity in vitro were able to compete with 125I-labeled hCG for binding sites in the ovary in pseudo-pregnant rats.	Iodine-125	151-155	hypertrichosis 2 (generalised, congenital)	Homo sapiens	42-45
6884026-1	1983	Chemically deglycosylated preparations of hCG (DG-hCG) which have been shown to have hormonal antagonistic activity in vitro were able to compete with 125I-labeled hCG for binding sites in the ovary in pseudo-pregnant rats.	Iodine-125	151-155	hypertrichosis 2 (generalised, congenital)	Homo sapiens	50-53
6884026-1	1983	Chemically deglycosylated preparations of hCG (DG-hCG) which have been shown to have hormonal antagonistic activity in vitro were able to compete with 125I-labeled hCG for binding sites in the ovary in pseudo-pregnant rats.	Iodine-125	151-155	hypertrichosis 2 (generalised, congenital)	Homo sapiens	50-53
6307847-1	1983	HCG receptors of porcine ovarian plasma membranes were loaded with 125I-hCG and covalently crosslinked with glutaraldehyde.	Glutaral	108-122	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
6307847-7	1983	Analysis of the Biogel P 300 purified 125I-hCG receptor complex by polyacrylamide gel electrophoresis in sodium dodecyl sulfate resulted in two radioactivity peaks.	polyacrylamide	67-81	hypertrichosis 2 (generalised, congenital)	Homo sapiens	43-46
6307847-7	1983	Analysis of the Biogel P 300 purified 125I-hCG receptor complex by polyacrylamide gel electrophoresis in sodium dodecyl sulfate resulted in two radioactivity peaks.	Sodium Dodecyl Sulfate	105-127	hypertrichosis 2 (generalised, congenital)	Homo sapiens	43-46
6321335-0	1983	Presence of low molecular weight LH/hCG & FSH binding inhibitors in human & sheep ovaries.	Adenosine Monophosphate	41-44	hypertrichosis 2 (generalised, congenital)	Homo sapiens	36-39
6321335-0	1983	Presence of low molecular weight LH/hCG & FSH binding inhibitors in human & sheep ovaries.	Adenosine Monophosphate	79-82	hypertrichosis 2 (generalised, congenital)	Homo sapiens	36-39
6288829-5	1982	Administration of hCG 65h after PMSG caused a rapid rise in the concentration of cyclic AMP but the concentration of cyclic GMP tended to fall.	Cyclic AMP	81-91	hypertrichosis 2 (generalised, congenital)	Homo sapiens	18-21
6422686-0	1983	Monitoring of Clomid-hMG-hCG controlled ovulation by ultrasound and a rapid (15 minutes) total urinary estrogen assay.	clomid-hmg	14-24	hypertrichosis 2 (generalised, congenital)	Homo sapiens	25-28
6295747-4	1983	Cell viability was also monitored by: 1) trypan blue dye exclusion, 2) the ability of the cells to synthesize protein, and 3) basal and hCG-stimulated secretion of progesterone.	Progesterone	164-176	hypertrichosis 2 (generalised, congenital)	Homo sapiens	136-139
6295747-8	1983	Treatment with CHX increased the amounts of membrane-bound and internalized [125I]iodo-hCG and decreased the amounts of [125I]iodo-hCG that were degraded.	Cycloheximide	15-18	hypertrichosis 2 (generalised, congenital)	Homo sapiens	87-90
6295747-8	1983	Treatment with CHX increased the amounts of membrane-bound and internalized [125I]iodo-hCG and decreased the amounts of [125I]iodo-hCG that were degraded.	Cycloheximide	15-18	hypertrichosis 2 (generalised, congenital)	Homo sapiens	131-134
6833935-3	1983	However, in two out of five corpora lutea, higher concentrations of prolactin (100 and 1000 ng/ml) significantly reduced the oestradiol-17 beta production induced by human chorionic gonadotrophin (hCG; 10 i.u./ml); lower doses of prolactin had little effect.	Estradiol	125-143	hypertrichosis 2 (generalised, congenital)	Homo sapiens	197-200
6403699-0	1983	Plasma testosterone response to hCG stimulation in the male marmoset monkey (Callithrix jacchus jacchus).	Testosterone	7-19	hypertrichosis 2 (generalised, congenital)	Homo sapiens	32-35
6403699-1	1983	In adult animals the intramuscular injection of hCG was followed by a rapid rise in plasma testosterone levels within 2-3 h and at doses of 40 and 80 i.u.	Testosterone	91-103	hypertrichosis 2 (generalised, congenital)	Homo sapiens	48-51
6403699-2	1983	hCG this primary response was followed by a second peak of testosterone at 48 h. Prepubertal marmosets also responded to hCG stimulation with a rapid increase in plasma testosterone levels within 3 h, but the magnitude of this peak was lower than that observed in adult animals and no biphasic pattern was observed.	Testosterone	59-71	hypertrichosis 2 (generalised, congenital)	Homo sapiens	121-124
6403699-2	1983	hCG this primary response was followed by a second peak of testosterone at 48 h. Prepubertal marmosets also responded to hCG stimulation with a rapid increase in plasma testosterone levels within 3 h, but the magnitude of this peak was lower than that observed in adult animals and no biphasic pattern was observed.	Testosterone	169-181	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
6403699-2	1983	hCG this primary response was followed by a second peak of testosterone at 48 h. Prepubertal marmosets also responded to hCG stimulation with a rapid increase in plasma testosterone levels within 3 h, but the magnitude of this peak was lower than that observed in adult animals and no biphasic pattern was observed.	Testosterone	169-181	hypertrichosis 2 (generalised, congenital)	Homo sapiens	121-124
6404842-4	1983	The hCG test was performed at least 2 weeks (0.5-12 months) after the last injection of depot testosterone in the treated patients.	Testosterone	94-106	hypertrichosis 2 (generalised, congenital)	Homo sapiens	4-7
6296184-5	1983	Adenosine also amplified cAMP accumulation in response to increasing hCG concentrations by 2- to 3-fold in human luteal cells.	Adenosine	0-9	hypertrichosis 2 (generalised, congenital)	Homo sapiens	69-72
6296184-5	1983	Adenosine also amplified cAMP accumulation in response to increasing hCG concentrations by 2- to 3-fold in human luteal cells.	Cyclic AMP	25-29	hypertrichosis 2 (generalised, congenital)	Homo sapiens	69-72
6296184-6	1983	The ability of the human luteal cell to respond to hCG with cAMP accumulation and the ability of adenosine to amplify this cAMP response appeared to be inversely related to human luteal cell age.	Cyclic AMP	60-64	hypertrichosis 2 (generalised, congenital)	Homo sapiens	51-54
6651640-4	1983	Consequently testosterone production (defined as the product of plasma flow and the veno-arterial concentration difference for testosterone) was markedly reduced during aspermatogenesis, both before and after stimulation with hCG.	Testosterone	13-25	hypertrichosis 2 (generalised, congenital)	Homo sapiens	226-229
6324939-1	1983	Lutropin (LH) and human choriogonadotropin (hCG) share the same receptor and stimulate testosterone production in porcine Leydig cells in primary culture.	Testosterone	87-99	hypertrichosis 2 (generalised, congenital)	Homo sapiens	44-47
6406633-5	1983	Challenging the animals with hCG provoked an increase in serum testosterone, but the magnitude of the rise was greater by far in the control rats.	Testosterone	63-75	hypertrichosis 2 (generalised, congenital)	Homo sapiens	29-32
6682882-4	1983	In contrast, PA activity of animals given hCG alone increased after the treatment, reaching a peak value of 0.112 +/- 0.071 mumol/l X 6 mg tissue per 30 min 12h later, before decreasing to 0.023 +/- 0.014 mumol/l X 6 mg tissue per 30 min at 32 h. Contrary to expectations, a dose of indomethacin which completely blocked ovulation had no effect on either the magnitude or the time-course of PA synthesis after hCG administration (P greater than 0.05).	Indomethacin	283-295	hypertrichosis 2 (generalised, congenital)	Homo sapiens	42-45
6221767-7	1983	Stimulation by hCG led to an increase in apparent steroid production for all steroids, including estrogens, with the greatest quantities seen with DHAS (greater than 200 ng/1 X 10(6) cells/3 h).	Steroids	50-57	hypertrichosis 2 (generalised, congenital)	Homo sapiens	15-18
6221767-7	1983	Stimulation by hCG led to an increase in apparent steroid production for all steroids, including estrogens, with the greatest quantities seen with DHAS (greater than 200 ng/1 X 10(6) cells/3 h).	Steroids	77-85	hypertrichosis 2 (generalised, congenital)	Homo sapiens	15-18
6221767-7	1983	Stimulation by hCG led to an increase in apparent steroid production for all steroids, including estrogens, with the greatest quantities seen with DHAS (greater than 200 ng/1 X 10(6) cells/3 h).	Dehydroepiandrosterone Sulfate	147-151	hypertrichosis 2 (generalised, congenital)	Homo sapiens	15-18
6135519-8	1983	The responses of serum oestradiol and 17-hydroxyprogesterone to hCG appeared later during the boys" development than the response of serum testosterone.	Estradiol	23-33	hypertrichosis 2 (generalised, congenital)	Homo sapiens	64-67
6135519-8	1983	The responses of serum oestradiol and 17-hydroxyprogesterone to hCG appeared later during the boys" development than the response of serum testosterone.	17-alpha-Hydroxyprogesterone	38-60	hypertrichosis 2 (generalised, congenital)	Homo sapiens	64-67
6135519-10	1983	It is suggested that testicular oestradiol production in response to LH/hCG appears in the course of puberty and results in intratesticular short-loop feed-back inhibition of androgen production.	Estradiol	32-42	hypertrichosis 2 (generalised, congenital)	Homo sapiens	72-75
6135519-10	1983	It is suggested that testicular oestradiol production in response to LH/hCG appears in the course of puberty and results in intratesticular short-loop feed-back inhibition of androgen production.	Luteinizing Hormone	69-71	hypertrichosis 2 (generalised, congenital)	Homo sapiens	72-75
6832045-5	1983	Monkeys receiving hCG on day 14 had 4-fold elevations in serum progesterone, but concentrations did not exceed 6 ng/ml.	Progesterone	63-75	hypertrichosis 2 (generalised, congenital)	Homo sapiens	18-21
6832045-6	1983	Serum estradiol increased significantly after hCG to concentrations between 200-300 pg/ml in all treatment groups; peak values were seen at the time of or in the days immediately after the last hCG injection.	Estradiol	6-15	hypertrichosis 2 (generalised, congenital)	Homo sapiens	46-49
6832045-6	1983	Serum estradiol increased significantly after hCG to concentrations between 200-300 pg/ml in all treatment groups; peak values were seen at the time of or in the days immediately after the last hCG injection.	Estradiol	6-15	hypertrichosis 2 (generalised, congenital)	Homo sapiens	194-197
6832045-9	1983	A 10-day regimen of increasing hCG doses beginning on day 10 of the luteal phase mimicked the steroid hormone secretion patterns observed in control monkeys during early pregnancy.	Steroids	94-109	hypertrichosis 2 (generalised, congenital)	Homo sapiens	31-34
6353025-0	1983	[Clinical evaluation of serum LH/hCG level determined by hCG enzyme immunoassay--fundamental and clinical studies].	Luteinizing Hormone	30-32	hypertrichosis 2 (generalised, congenital)	Homo sapiens	57-60
6300050-3	1983	Heated solutions (100 degrees C) of hCG and A-hCG quickly lost their ability to enhance the fluorescence of the probe 1-anilino-8-naphthalenesulfonate (1,8-ANS) indicating dissociation into subunits.	1-anilino-8-naphthalenesulfonate	118-150	hypertrichosis 2 (generalised, congenital)	Homo sapiens	36-39
6300050-3	1983	Heated solutions (100 degrees C) of hCG and A-hCG quickly lost their ability to enhance the fluorescence of the probe 1-anilino-8-naphthalenesulfonate (1,8-ANS) indicating dissociation into subunits.	1-anilino-8-naphthalenesulfonate	118-150	hypertrichosis 2 (generalised, congenital)	Homo sapiens	46-49
6300050-3	1983	Heated solutions (100 degrees C) of hCG and A-hCG quickly lost their ability to enhance the fluorescence of the probe 1-anilino-8-naphthalenesulfonate (1,8-ANS) indicating dissociation into subunits.	1-anilino-8-naphthalenesulfonate	152-159	hypertrichosis 2 (generalised, congenital)	Homo sapiens	36-39
6300050-3	1983	Heated solutions (100 degrees C) of hCG and A-hCG quickly lost their ability to enhance the fluorescence of the probe 1-anilino-8-naphthalenesulfonate (1,8-ANS) indicating dissociation into subunits.	1-anilino-8-naphthalenesulfonate	152-159	hypertrichosis 2 (generalised, congenital)	Homo sapiens	46-49
6300050-4	1983	DG-hCG solutions were more stable in this respect suggesting significant preservation of conformational features required for the interaction with 1,8-ANS.	1-anilino-8-naphthalenesulfonate	147-154	hypertrichosis 2 (generalised, congenital)	Homo sapiens	3-6
6300050-5	1983	Solutions of hCG and A-hCG which had been thermally denatured (100 degrees C, 10 min) required almost 48 h at 37 degrees C to regain complete ANS binding ability as well as receptor binding activity.	1-anilino-8-naphthalenesulfonate	142-145	hypertrichosis 2 (generalised, congenital)	Homo sapiens	13-16
6300050-5	1983	Solutions of hCG and A-hCG which had been thermally denatured (100 degrees C, 10 min) required almost 48 h at 37 degrees C to regain complete ANS binding ability as well as receptor binding activity.	1-anilino-8-naphthalenesulfonate	142-145	hypertrichosis 2 (generalised, congenital)	Homo sapiens	23-26
6300050-8	1983	Thus, removal of carbohydrate residues (approximately 75% loss) from hCG renders the hormone more resistant to thermal denaturation.	Carbohydrates	17-29	hypertrichosis 2 (generalised, congenital)	Homo sapiens	69-72
6315561-4	1983	cAMP and T production by enriched preparations of dispersed interstitial cells from control testes was increased by hCG in all groups.	Cyclic AMP	0-4	hypertrichosis 2 (generalised, congenital)	Homo sapiens	116-119
6141498-3	1983	Ethylketocyclazocine stimulate K+-induced hCG release.	Ethylketocyclazocine	0-20	hypertrichosis 2 (generalised, congenital)	Homo sapiens	42-45
6681829-4	1983	However, in BeWo cells, an inverse relationship between the incorporation of 3H-thymidine and secretion of hCG was not clearly observed.	3h-thymidine	77-89	hypertrichosis 2 (generalised, congenital)	Homo sapiens	107-110
6413269-5	1983	In spite of the similarities in t 1/2 values between the two preparations, serum progesterone levels were significantly increased 48 to 96 hours after the administration of Desialo hCG, and only 8 to 10 hours after the administration of the hCG hybrid.	Progesterone	81-93	hypertrichosis 2 (generalised, congenital)	Homo sapiens	181-184
6297629-3	1982	Highly purified human chorionic gonadotropin (hCG) increased testosterone production relative to controls.	Testosterone	61-73	hypertrichosis 2 (generalised, congenital)	Homo sapiens	46-49
6297629-4	1982	Concomitant administration of either natural (cortisone greater than deoxycorticosterone = aldosterone) or synthetic (dexamethasone greater than or equal to prednisolone) corticosteroids inhibited hCG-stimulated testosterone production in a dose-dependent manner.	Cortisone	46-55	hypertrichosis 2 (generalised, congenital)	Homo sapiens	197-200
6297629-4	1982	Concomitant administration of either natural (cortisone greater than deoxycorticosterone = aldosterone) or synthetic (dexamethasone greater than or equal to prednisolone) corticosteroids inhibited hCG-stimulated testosterone production in a dose-dependent manner.	Desoxycorticosterone	69-88	hypertrichosis 2 (generalised, congenital)	Homo sapiens	197-200
6297629-4	1982	Concomitant administration of either natural (cortisone greater than deoxycorticosterone = aldosterone) or synthetic (dexamethasone greater than or equal to prednisolone) corticosteroids inhibited hCG-stimulated testosterone production in a dose-dependent manner.	Aldosterone	91-102	hypertrichosis 2 (generalised, congenital)	Homo sapiens	197-200
6297629-4	1982	Concomitant administration of either natural (cortisone greater than deoxycorticosterone = aldosterone) or synthetic (dexamethasone greater than or equal to prednisolone) corticosteroids inhibited hCG-stimulated testosterone production in a dose-dependent manner.	Dexamethasone	118-131	hypertrichosis 2 (generalised, congenital)	Homo sapiens	197-200
6297629-4	1982	Concomitant administration of either natural (cortisone greater than deoxycorticosterone = aldosterone) or synthetic (dexamethasone greater than or equal to prednisolone) corticosteroids inhibited hCG-stimulated testosterone production in a dose-dependent manner.	Prednisolone	157-169	hypertrichosis 2 (generalised, congenital)	Homo sapiens	197-200
6297629-4	1982	Concomitant administration of either natural (cortisone greater than deoxycorticosterone = aldosterone) or synthetic (dexamethasone greater than or equal to prednisolone) corticosteroids inhibited hCG-stimulated testosterone production in a dose-dependent manner.	Testosterone	212-224	hypertrichosis 2 (generalised, congenital)	Homo sapiens	197-200
6297629-6	1982	In the presence or absence of a phosphodiesterase inhibitor, dexamethasone decreased hCG-stimulated cAMP production by approximately 60%.	Dexamethasone	61-74	hypertrichosis 2 (generalised, congenital)	Homo sapiens	85-88
6297629-6	1982	In the presence or absence of a phosphodiesterase inhibitor, dexamethasone decreased hCG-stimulated cAMP production by approximately 60%.	Cyclic AMP	100-104	hypertrichosis 2 (generalised, congenital)	Homo sapiens	85-88
6297629-9	1982	Exogenous progesterone and 17 alpha-hydroxyprogesterone augmented hCG-stimulated testosterone production.	Progesterone	10-22	hypertrichosis 2 (generalised, congenital)	Homo sapiens	66-69
6297629-9	1982	Exogenous progesterone and 17 alpha-hydroxyprogesterone augmented hCG-stimulated testosterone production.	17-alpha-Hydroxyprogesterone	27-55	hypertrichosis 2 (generalised, congenital)	Homo sapiens	66-69
6297629-9	1982	Exogenous progesterone and 17 alpha-hydroxyprogesterone augmented hCG-stimulated testosterone production.	Testosterone	81-93	hypertrichosis 2 (generalised, congenital)	Homo sapiens	66-69
7160092-0	1982	[Rapid radioimmunoassay method for hCG using protein A-sepharose CL-4 B].	sepharose cl-4	55-69	hypertrichosis 2 (generalised, congenital)	Homo sapiens	35-38
7174742-6	1982	Hydroxyurea (HU) at a concentration of 1 mM mediated a small, statistically significant increase in hCG production (p less than 0.01) in all constitutive strains, but had no effect on non-hCG-producing fibroblast strains.	Hydroxyurea	0-11	hypertrichosis 2 (generalised, congenital)	Homo sapiens	100-103
7174742-6	1982	Hydroxyurea (HU) at a concentration of 1 mM mediated a small, statistically significant increase in hCG production (p less than 0.01) in all constitutive strains, but had no effect on non-hCG-producing fibroblast strains.	Hydroxyurea	13-15	hypertrichosis 2 (generalised, congenital)	Homo sapiens	100-103
7174742-7	1982	Sodium butyrate (Bu) was effective in increasing hCG synthesis in only one constitutive strain, derived from a newborn foreskin.	Butyric Acid	0-15	hypertrichosis 2 (generalised, congenital)	Homo sapiens	49-52
7174742-7	1982	Sodium butyrate (Bu) was effective in increasing hCG synthesis in only one constitutive strain, derived from a newborn foreskin.	Butyrates	17-19	hypertrichosis 2 (generalised, congenital)	Homo sapiens	49-52
7174742-9	1982	All Bu-treated strains, both those producing hCG and the nonproducers, showed morphological alterations; cells were flattened and they contained ordered arrays of refractile granules.	Butyrates	4-6	hypertrichosis 2 (generalised, congenital)	Homo sapiens	45-48
6296852-2	1982	Exposure of the cells to hCG, but not to mEGF, also resulted in a decrease in steroidogenic responses to cholera toxin and cAMP.	Cyclic AMP	123-127	hypertrichosis 2 (generalised, congenital)	Homo sapiens	25-28
6296852-3	1982	The results presented herein show that the hCG-induced loss of steroidogenic response to cAMP is due to the depletion of intracellular cholesterol and that this depletion can be prevented by the addition of low density lipoprotein.	Cyclic AMP	89-93	hypertrichosis 2 (generalised, congenital)	Homo sapiens	43-46
6296852-3	1982	The results presented herein show that the hCG-induced loss of steroidogenic response to cAMP is due to the depletion of intracellular cholesterol and that this depletion can be prevented by the addition of low density lipoprotein.	Cholesterol	135-146	hypertrichosis 2 (generalised, congenital)	Homo sapiens	43-46
7181949-2	1982	Treatment of rats with human chorionic gonadotropin (hCG) resulted in elevated levels of microsomal heme and cytochrome P-450 and increased activity of delta-aminolevulinic acid (ALA) synthase (EC 2.3.1.37).	Heme	100-104	hypertrichosis 2 (generalised, congenital)	Homo sapiens	53-56
7181949-3	1982	However, the hCG-mediated elevations of testicular microsomal heme and cytochrome P-450 content failed to occur in animals treated with EB.	Heme	62-66	hypertrichosis 2 (generalised, congenital)	Homo sapiens	13-16
7181949-5	1982	The increased microsomal heme and cytochrome P-450 content mediated by hCG in hypophysectomized animals was again prevented by administration of EB.	Heme	25-29	hypertrichosis 2 (generalised, congenital)	Homo sapiens	71-74
7181949-5	1982	The increased microsomal heme and cytochrome P-450 content mediated by hCG in hypophysectomized animals was again prevented by administration of EB.	estradiol 3-benzoate	145-147	hypertrichosis 2 (generalised, congenital)	Homo sapiens	71-74
7124285-2	1982	For this purpose, hCG stimulation of steroid testicular production was performed in 12 boars and fat androstenone concentration subsequently measured.	Steroids	37-44	hypertrichosis 2 (generalised, congenital)	Homo sapiens	18-21
7124285-4	1982	The results show that: 1) although plasma testosterone response to hCG stimulation was similar in all boars, fat and plasma androstenone responses were very variable between boars, 2) weight of fatty tissue appeared to have little influence, if any, on androstenone exchanges between plasma and fatty tissue and 3) plasma androstenone/testosterone ratio appeared to be less variable within boars than between boars.	Testosterone	42-54	hypertrichosis 2 (generalised, congenital)	Homo sapiens	67-70
7106051-11	1982	When PMSG-hCG-primed animals received iv injections of hCG on day 8 post-hCG, ovarian sterol ester stores were markedly depleted within 2 h. The ovarian ACAT activity of hCG-treated rats measured without cholesterol was significantly lower than that of controls.	sterol ester	86-98	hypertrichosis 2 (generalised, congenital)	Homo sapiens	10-13
7106051-11	1982	When PMSG-hCG-primed animals received iv injections of hCG on day 8 post-hCG, ovarian sterol ester stores were markedly depleted within 2 h. The ovarian ACAT activity of hCG-treated rats measured without cholesterol was significantly lower than that of controls.	sterol ester	86-98	hypertrichosis 2 (generalised, congenital)	Homo sapiens	55-58
7106051-11	1982	When PMSG-hCG-primed animals received iv injections of hCG on day 8 post-hCG, ovarian sterol ester stores were markedly depleted within 2 h. The ovarian ACAT activity of hCG-treated rats measured without cholesterol was significantly lower than that of controls.	sterol ester	86-98	hypertrichosis 2 (generalised, congenital)	Homo sapiens	55-58
7106051-11	1982	When PMSG-hCG-primed animals received iv injections of hCG on day 8 post-hCG, ovarian sterol ester stores were markedly depleted within 2 h. The ovarian ACAT activity of hCG-treated rats measured without cholesterol was significantly lower than that of controls.	sterol ester	86-98	hypertrichosis 2 (generalised, congenital)	Homo sapiens	55-58
7106051-11	1982	When PMSG-hCG-primed animals received iv injections of hCG on day 8 post-hCG, ovarian sterol ester stores were markedly depleted within 2 h. The ovarian ACAT activity of hCG-treated rats measured without cholesterol was significantly lower than that of controls.	Cholesterol	204-215	hypertrichosis 2 (generalised, congenital)	Homo sapiens	10-13
7106051-11	1982	When PMSG-hCG-primed animals received iv injections of hCG on day 8 post-hCG, ovarian sterol ester stores were markedly depleted within 2 h. The ovarian ACAT activity of hCG-treated rats measured without cholesterol was significantly lower than that of controls.	Cholesterol	204-215	hypertrichosis 2 (generalised, congenital)	Homo sapiens	55-58
7106051-11	1982	When PMSG-hCG-primed animals received iv injections of hCG on day 8 post-hCG, ovarian sterol ester stores were markedly depleted within 2 h. The ovarian ACAT activity of hCG-treated rats measured without cholesterol was significantly lower than that of controls.	Cholesterol	204-215	hypertrichosis 2 (generalised, congenital)	Homo sapiens	55-58
7106051-11	1982	When PMSG-hCG-primed animals received iv injections of hCG on day 8 post-hCG, ovarian sterol ester stores were markedly depleted within 2 h. The ovarian ACAT activity of hCG-treated rats measured without cholesterol was significantly lower than that of controls.	Cholesterol	204-215	hypertrichosis 2 (generalised, congenital)	Homo sapiens	55-58
7106051-12	1982	With cholesterol, ACAT activities of hCG-treated rats were similar to those in controls.	Cholesterol	5-16	hypertrichosis 2 (generalised, congenital)	Homo sapiens	37-40
6811736-6	1982	Pituitary homogenate and hCG injected on Day 16 shortened the PGF-2 alpha treatment cycle by 2 days, but stimulated ovulation in only 42% of the animals.	Dinoprost	62-67	hypertrichosis 2 (generalised, congenital)	Homo sapiens	25-28
6956731-0	1982	Inhibitory effect of PGF-2 alpha on hCG-stimulated progesterone production in vitro by luteal cells from guinea-pigs at different stages of the oestrous cycle.	Dinoprost	21-26	hypertrichosis 2 (generalised, congenital)	Homo sapiens	36-39
6956731-0	1982	Inhibitory effect of PGF-2 alpha on hCG-stimulated progesterone production in vitro by luteal cells from guinea-pigs at different stages of the oestrous cycle.	Progesterone	51-63	hypertrichosis 2 (generalised, congenital)	Homo sapiens	36-39
6956731-2	1982	Luteal cells incubated with hCG produced increased amounts of progesterone.	Progesterone	62-74	hypertrichosis 2 (generalised, congenital)	Homo sapiens	28-31
6956731-4	1982	PGF-2 alpha (1 mumol/l), had no effect on basal production of progesterone but significantly inhibited hCG-stimulated progesterone production by luteal cells isolated on Days 7, 9, 10, 12 and 13 of the cycle.	Dinoprost	0-5	hypertrichosis 2 (generalised, congenital)	Homo sapiens	103-106
6294398-5	1982	Similarly, plasma estradiol concentrations in response to submaximal hCG stimulation were diminished.	Estradiol	18-27	hypertrichosis 2 (generalised, congenital)	Homo sapiens	69-72
6294398-13	1982	The diminished response of ovarian cAMP content to submaximal doses of hCG was not corrected by bromocriptine (1 mg/kg) despite normalization of hyperprolactinemia.	Cyclic AMP	35-39	hypertrichosis 2 (generalised, congenital)	Homo sapiens	71-74
6288829-5	1982	Administration of hCG 65h after PMSG caused a rapid rise in the concentration of cyclic AMP but the concentration of cyclic GMP tended to fall.	Cyclic GMP	117-127	hypertrichosis 2 (generalised, congenital)	Homo sapiens	18-21
7130927-6	1982	Large dosages of cyproterone and cyproterone acetate (100 mg/kg body weight) generally decreased the ovulation number in gonadotrophin-injected mice, suggesting a role for androgen in preovulatory events that occur within the ripened follicle after the ovulatory stimulus (hCG) has been received.	Cyproterone	17-28	hypertrichosis 2 (generalised, congenital)	Homo sapiens	273-276
7130927-6	1982	Large dosages of cyproterone and cyproterone acetate (100 mg/kg body weight) generally decreased the ovulation number in gonadotrophin-injected mice, suggesting a role for androgen in preovulatory events that occur within the ripened follicle after the ovulatory stimulus (hCG) has been received.	Cyproterone Acetate	33-52	hypertrichosis 2 (generalised, congenital)	Homo sapiens	273-276
7130927-9	1982	Experiments in which the time of administration of hCG +/- cyproterone was varied after PMSG priming suggested that cyproterone at a dosage of 25 mg/kg had a "rescuing" effect on follicles destined to become atretic for up to 96 hr after PMSG priming.	Cyproterone	116-127	hypertrichosis 2 (generalised, congenital)	Homo sapiens	51-54
7130927-11	1982	Experiments in which the time of administration of cyproterone (100 mg/kg) was varied after hCG suggested that whatever the important androgen-mediated events preceding ovulation, these events occur within 2 to 3 hr after the hCG signal.	Cyproterone	51-62	hypertrichosis 2 (generalised, congenital)	Homo sapiens	92-95
7130927-11	1982	Experiments in which the time of administration of cyproterone (100 mg/kg) was varied after hCG suggested that whatever the important androgen-mediated events preceding ovulation, these events occur within 2 to 3 hr after the hCG signal.	Cyproterone	51-62	hypertrichosis 2 (generalised, congenital)	Homo sapiens	226-229
6282920-6	1982	LRH increased hCG output in Dulbecco"s Modified Eagle"s Medium with penicillin, streptomycin, insulin, and glucose alone, but not in the presence of added LDL or DHEAS, while dbcAMP (1, 2, and 4 mM) increased the output of hCG in all three media and decreased 17 beta-estradiol output in medium supplemented with DHEAS.	modified	39-47	hypertrichosis 2 (generalised, congenital)	Homo sapiens	14-17
7130777-5	1982	When hCG was administered, P and 17-OHP showed a trend to elevate in Group A, but they showed a trend to decline in Group B.	17-alpha-Hydroxyprogesterone	33-39	hypertrichosis 2 (generalised, congenital)	Homo sapiens	5-8
6282920-6	1982	LRH increased hCG output in Dulbecco"s Modified Eagle"s Medium with penicillin, streptomycin, insulin, and glucose alone, but not in the presence of added LDL or DHEAS, while dbcAMP (1, 2, and 4 mM) increased the output of hCG in all three media and decreased 17 beta-estradiol output in medium supplemented with DHEAS.	dulbecco	28-36	hypertrichosis 2 (generalised, congenital)	Homo sapiens	14-17
6282920-6	1982	LRH increased hCG output in Dulbecco"s Modified Eagle"s Medium with penicillin, streptomycin, insulin, and glucose alone, but not in the presence of added LDL or DHEAS, while dbcAMP (1, 2, and 4 mM) increased the output of hCG in all three media and decreased 17 beta-estradiol output in medium supplemented with DHEAS.	Penicillins	68-78	hypertrichosis 2 (generalised, congenital)	Homo sapiens	14-17
6282920-6	1982	LRH increased hCG output in Dulbecco"s Modified Eagle"s Medium with penicillin, streptomycin, insulin, and glucose alone, but not in the presence of added LDL or DHEAS, while dbcAMP (1, 2, and 4 mM) increased the output of hCG in all three media and decreased 17 beta-estradiol output in medium supplemented with DHEAS.	Streptomycin	80-92	hypertrichosis 2 (generalised, congenital)	Homo sapiens	14-17
6282920-8	1982	Basal progesterone, basal hCG, and dbcAMP-stimulated hCG outputs were unaffected by the addition of LDL or DHEAS.	Bucladesine	35-41	hypertrichosis 2 (generalised, congenital)	Homo sapiens	53-56
6282920-9	1982	Both LDL and DHEAS inhibited the stimulatory effect of LRH on the output of hCG.	Dehydroepiandrosterone Sulfate	13-18	hypertrichosis 2 (generalised, congenital)	Homo sapiens	76-79
7050537-0	1982	Effects of age and 1,4,6-androstatriene-3,17-dione on activities of hCG-induced 19-hydroxylase and aromatase of rat testes.	androsta-1,4,6-triene-3,17-dione	19-50	hypertrichosis 2 (generalised, congenital)	Homo sapiens	68-71
6288487-0	1982	[Calcium ions in the steroidogenic action of HCG].	Calcium	1-8	hypertrichosis 2 (generalised, congenital)	Homo sapiens	45-48
6210708-2	1982	During hCG treatment, testosterone (T), which was in the prepuberal range under basal conditions, rose considerably to the upper end of the normal range and remained at that level during the 23 months of observation.	Testosterone	22-34	hypertrichosis 2 (generalised, congenital)	Homo sapiens	7-10
6210708-3	1982	A 2.5-fold increase was observed in serum levels of 17 beta-estradiol (E2) an increment less than seen with T. The increment in 17 alpha-hydroxyprogesterone was also lower than that in T throughout the study; thus, the 17 alpha-hydroxyprogesterone to T ratio, despite continuous hCG administration, remained low.	Estradiol	52-69	hypertrichosis 2 (generalised, congenital)	Homo sapiens	279-282
6210708-4	1982	Serum androstenedione was slightly increased during hCG therapy.	Androstenedione	6-21	hypertrichosis 2 (generalised, congenital)	Homo sapiens	52-55
6282830-1	1982	A chemical method of deglycosylation of human choriogonadotropin (hCG) was used to assess the role of carbohydrate moiety in the maintenance of quaternary structure and functional parameters such as receptor binding, immunological activity, and in vitro biological response.	Carbohydrates	102-114	hypertrichosis 2 (generalised, congenital)	Homo sapiens	66-69
6282830-2	1982	Treatment of purified hCG with anhydrous HF at 0 degrees C for 60 min was effective in removing more than 75% of the carbohydrate moiety.	Carbohydrates	117-129	hypertrichosis 2 (generalised, congenital)	Homo sapiens	22-25
6282830-5	1982	The deglycosylated hCG was stable in the lyophilized form and retained its quaternary structure as revealed by the fluorescence probe 8-anilino 1-naphthalene sulfonic acid, receptor binding, and immunological activities.	8-anilino-1-naphthalenesulfonic acid	134-171	hypertrichosis 2 (generalised, congenital)	Homo sapiens	19-22
6288487-7	1982	(2) Production rates of both C-AMP and progesterone in the presence of HCG were maximum at 10(-7) g/ml HCG.	Progesterone	39-51	hypertrichosis 2 (generalised, congenital)	Homo sapiens	71-74
6288487-7	1982	(2) Production rates of both C-AMP and progesterone in the presence of HCG were maximum at 10(-7) g/ml HCG.	Progesterone	39-51	hypertrichosis 2 (generalised, congenital)	Homo sapiens	103-106
6288487-13	1982	This acceleration by HCG is affected by Ca and is remarkably inhibited by verapamil.	Verapamil	74-83	hypertrichosis 2 (generalised, congenital)	Homo sapiens	21-24
7047657-0	1982	[Use of Biotin-Avidin system and monoclonal antibody for highly sensitive quantitative assay of hCG].	Biotin	8-14	hypertrichosis 2 (generalised, congenital)	Homo sapiens	96-99
7113599-1	1982	A single injection of 1500 IU of human chorionic gonadotrophin (hCG) in normal men, induced a block in the conversion of 17-hydroxyprogesterone (17-OHP) to testosterone (T) which reached its maximum 24 h after hCG loading.	17-alpha-Hydroxyprogesterone	121-143	hypertrichosis 2 (generalised, congenital)	Homo sapiens	64-67
7113599-1	1982	A single injection of 1500 IU of human chorionic gonadotrophin (hCG) in normal men, induced a block in the conversion of 17-hydroxyprogesterone (17-OHP) to testosterone (T) which reached its maximum 24 h after hCG loading.	17-alpha-Hydroxyprogesterone	145-151	hypertrichosis 2 (generalised, congenital)	Homo sapiens	64-67
7113599-1	1982	A single injection of 1500 IU of human chorionic gonadotrophin (hCG) in normal men, induced a block in the conversion of 17-hydroxyprogesterone (17-OHP) to testosterone (T) which reached its maximum 24 h after hCG loading.	Testosterone	156-168	hypertrichosis 2 (generalised, congenital)	Homo sapiens	64-67
7113599-1	1982	A single injection of 1500 IU of human chorionic gonadotrophin (hCG) in normal men, induced a block in the conversion of 17-hydroxyprogesterone (17-OHP) to testosterone (T) which reached its maximum 24 h after hCG loading.	Testosterone	156-168	hypertrichosis 2 (generalised, congenital)	Homo sapiens	210-213
7113599-4	1982	hCG administration one week after the priming dose elicited an increase in the ratio 17-OHP to T, which was about twice as high as after the first hCG injection.	17-alpha-Hydroxyprogesterone	85-91	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
7113599-4	1982	hCG administration one week after the priming dose elicited an increase in the ratio 17-OHP to T, which was about twice as high as after the first hCG injection.	17-alpha-Hydroxyprogesterone	85-91	hypertrichosis 2 (generalised, congenital)	Homo sapiens	147-150
6890895-5	1982	Administration of exogenous hCG causes a significant rise in the serum testosterone level in cycling monkeys.	Testosterone	71-83	hypertrichosis 2 (generalised, congenital)	Homo sapiens	28-31
6896179-5	1982	Whether mitochondria were prepared from the ovaries of rats acutely treated with cycloheximide, hCG, or vehicle, cardiolipin stimulated steroid production to the same absolute value.	Steroids	136-143	hypertrichosis 2 (generalised, congenital)	Homo sapiens	96-99
7100493-4	1982	The optimum time to give indomethacin was at 7-8 h after hCG (i.e., 2-3 h before expected rupture of the follicle) at which time the minimum effective dose was 2.5 mg/kg.	Indomethacin	25-37	hypertrichosis 2 (generalised, congenital)	Homo sapiens	57-60
6286378-2	1982	Ovarian hCG receptors in immature rats induced by PMS-hCG priming maintained a binding activity for about 20 days after hCG injection.	Promethium	50-53	hypertrichosis 2 (generalised, congenital)	Homo sapiens	8-11
6286378-2	1982	Ovarian hCG receptors in immature rats induced by PMS-hCG priming maintained a binding activity for about 20 days after hCG injection.	Promethium	50-53	hypertrichosis 2 (generalised, congenital)	Homo sapiens	54-57
6286378-2	1982	Ovarian hCG receptors in immature rats induced by PMS-hCG priming maintained a binding activity for about 20 days after hCG injection.	Promethium	50-53	hypertrichosis 2 (generalised, congenital)	Homo sapiens	54-57
6286378-3	1982	The administration of hCG to pseudopregnant rats caused time and dose related changes in ovarian 125I-hCG binding percentage and the concentration of serum progesterone.	Progesterone	156-168	hypertrichosis 2 (generalised, congenital)	Homo sapiens	22-25
6286378-9	1982	After the injection of hCG into pregnant rats, the binding percentage rapidly decreased and the serum concentration of progesterone increased.	Progesterone	119-131	hypertrichosis 2 (generalised, congenital)	Homo sapiens	23-26
6286378-13	1982	In the treatment of hCG-antibody in pregnant rats, the binding percentage did not change but the serum concentration of progesterone showed a tendency to decrease to the control level.	Progesterone	120-132	hypertrichosis 2 (generalised, congenital)	Homo sapiens	20-23
6806421-2	1982	After intravenous injection of hypogonadal females with 125I-labelled human chorionic gonadotrophin (hCG), followed by autoradiography of semi-thin (1 micrometer) slices of the ovary, labelled hCG was found to be associated with interstitial cells and thecal cells with little or no labelling of granulosa cells.	Iodine-125	56-60	hypertrichosis 2 (generalised, congenital)	Homo sapiens	101-104
6806421-7	1982	In the male, after injection of 125-I-labelled hCG, silver grains were associated with the interstitial cells alone in both hypogonadal and normal mice.	Iodine-125	32-37	hypertrichosis 2 (generalised, congenital)	Homo sapiens	47-50
16725700-8	1982	Plasma testosterone was elevated (P<.05) by 30 min (4.7 +/- .5 ng/ml; X +/- SEM) and 15 min (5.5 +/- 1.1 ng/ml) post-treatment in boars administered hCG and ACTH, respectively, when compared with the S (1.0 +/- .3 ng/ml) group.	Testosterone	7-19	hypertrichosis 2 (generalised, congenital)	Homo sapiens	152-155
16725700-9	1982	Testosterone in hCG treated boars peaked by 90 min (21.8 +/- 1.8 ng/ml) post-treatment, declined slightly until 210 min (18.8 +/- 1.8 ng/ml) post-treatment and increased thereafter.	Testosterone	0-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	16-19
6313366-1	1983	In vivo and in vitro HCG-stimulated testosterone production.	Testosterone	36-48	hypertrichosis 2 (generalised, congenital)	Homo sapiens	21-24
6279190-1	1982	The direct effects of insulin on basal and human chorionic gonadotropin (hCG)-stimulated accumulation of testosterone were investigated in vitro using a primary culture system of rat testicular cells from adult hypophysectomized male rats.	Testosterone	105-117	hypertrichosis 2 (generalised, congenital)	Homo sapiens	73-76
6279190-3	1982	Treatment of testicular cells with insulin (10 micrograms/ml) by itself was without effect on the basal accumulation of testosterone, while treatment with increasing concentrations (0.1--10 ng/ml) of hCG resulted in dose-dependent increases in the accumulation of testosterone.	Testosterone	120-132	hypertrichosis 2 (generalised, congenital)	Homo sapiens	200-203
6279190-3	1982	Treatment of testicular cells with insulin (10 micrograms/ml) by itself was without effect on the basal accumulation of testosterone, while treatment with increasing concentrations (0.1--10 ng/ml) of hCG resulted in dose-dependent increases in the accumulation of testosterone.	Testosterone	264-276	hypertrichosis 2 (generalised, congenital)	Homo sapiens	200-203
6279190-4	1982	Furthermore, concomitant treatment with increasing concentrations (0.01--10 micrograms/ml) of insulin led to a dose-dependent augmentation (up to 116% on Day 10) in the hCG-stimulated accumulation of testosterone, as well as a 1.6-fold increase in the testicular responsiveness to hCG.	Testosterone	200-212	hypertrichosis 2 (generalised, congenital)	Homo sapiens	169-172
6279190-6	1982	Increasing duration (12--72 h) of treatment with insulin resulted in time-dependent increases in the hCG-stimulated accumulation of testosterone achieving statistical significance (P less than 0.05) by 36 h. In addition, pretreatment with insulin (10 micrograms/ml) brought about significant (P less than 0.01) increases in the choleragen and Bt2cAMP-stimulated accumulation of testosterone.	Testosterone	132-144	hypertrichosis 2 (generalised, congenital)	Homo sapiens	101-104
6279190-6	1982	Increasing duration (12--72 h) of treatment with insulin resulted in time-dependent increases in the hCG-stimulated accumulation of testosterone achieving statistical significance (P less than 0.05) by 36 h. In addition, pretreatment with insulin (10 micrograms/ml) brought about significant (P less than 0.01) increases in the choleragen and Bt2cAMP-stimulated accumulation of testosterone.	Bucladesine	343-350	hypertrichosis 2 (generalised, congenital)	Homo sapiens	101-104
6279190-6	1982	Increasing duration (12--72 h) of treatment with insulin resulted in time-dependent increases in the hCG-stimulated accumulation of testosterone achieving statistical significance (P less than 0.05) by 36 h. In addition, pretreatment with insulin (10 micrograms/ml) brought about significant (P less than 0.01) increases in the choleragen and Bt2cAMP-stimulated accumulation of testosterone.	Testosterone	378-390	hypertrichosis 2 (generalised, congenital)	Homo sapiens	101-104
7100493-5	1982	Since a significant elevation in prostaglandin synthesis occurs as early as 3-5 h after hCG stimulation of rabbit follicles (1), these results reveal that nonsteroidal antiinflammatory agents can interrupt the ovulatory process even after the follicle has begun producing substantial amounts of prostaglandins.	Prostaglandins	33-46	hypertrichosis 2 (generalised, congenital)	Homo sapiens	88-91
7061899-5	1982	Progesterone restored" the antiserum blocked ovulation completely or incompletely when administered intravenously within 6 h of treatment with hCG.	Progesterone	0-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	143-146
7040256-0	1982	Serum Testosterone response to single injection of hCG ovine-LH and LHRH in male rats.	Testosterone	6-18	hypertrichosis 2 (generalised, congenital)	Homo sapiens	51-54
7040256-1	1982	A biphasic pattern of testosterone secretion in response to a single injection of 100 IU hCG has been observed in the rat.	Testosterone	22-34	hypertrichosis 2 (generalised, congenital)	Homo sapiens	89-92
7040256-2	1982	Serum testosterone increased from basal levels of 8.7 +/- 3.1 ng/ml (mean +/- SEM) to 23.0 +/- 1.4 ng/ml within 2 h of hCG-stimulation and returned to control levels by 2 days.	Testosterone	6-18	hypertrichosis 2 (generalised, congenital)	Homo sapiens	119-122
7040256-5	1982	Administration of 10 IU hCG produced a single peak of testosterone, which did not occur until 24 h. Differences in the serum testosterone response were related to the concentration of hCG measured in the serum after injection, as injection of 1 IU, which failed to increase serum hCG levels above detection, was also inadequate to increase serum testosterone.	Testosterone	54-66	hypertrichosis 2 (generalised, congenital)	Homo sapiens	24-27
7040256-5	1982	Administration of 10 IU hCG produced a single peak of testosterone, which did not occur until 24 h. Differences in the serum testosterone response were related to the concentration of hCG measured in the serum after injection, as injection of 1 IU, which failed to increase serum hCG levels above detection, was also inadequate to increase serum testosterone.	Testosterone	54-66	hypertrichosis 2 (generalised, congenital)	Homo sapiens	184-187
7040256-5	1982	Administration of 10 IU hCG produced a single peak of testosterone, which did not occur until 24 h. Differences in the serum testosterone response were related to the concentration of hCG measured in the serum after injection, as injection of 1 IU, which failed to increase serum hCG levels above detection, was also inadequate to increase serum testosterone.	Testosterone	54-66	hypertrichosis 2 (generalised, congenital)	Homo sapiens	184-187
7040256-5	1982	Administration of 10 IU hCG produced a single peak of testosterone, which did not occur until 24 h. Differences in the serum testosterone response were related to the concentration of hCG measured in the serum after injection, as injection of 1 IU, which failed to increase serum hCG levels above detection, was also inadequate to increase serum testosterone.	Testosterone	125-137	hypertrichosis 2 (generalised, congenital)	Homo sapiens	24-27
7040256-5	1982	Administration of 10 IU hCG produced a single peak of testosterone, which did not occur until 24 h. Differences in the serum testosterone response were related to the concentration of hCG measured in the serum after injection, as injection of 1 IU, which failed to increase serum hCG levels above detection, was also inadequate to increase serum testosterone.	Testosterone	125-137	hypertrichosis 2 (generalised, congenital)	Homo sapiens	184-187
7040256-5	1982	Administration of 10 IU hCG produced a single peak of testosterone, which did not occur until 24 h. Differences in the serum testosterone response were related to the concentration of hCG measured in the serum after injection, as injection of 1 IU, which failed to increase serum hCG levels above detection, was also inadequate to increase serum testosterone.	Testosterone	125-137	hypertrichosis 2 (generalised, congenital)	Homo sapiens	184-187
7040256-5	1982	Administration of 10 IU hCG produced a single peak of testosterone, which did not occur until 24 h. Differences in the serum testosterone response were related to the concentration of hCG measured in the serum after injection, as injection of 1 IU, which failed to increase serum hCG levels above detection, was also inadequate to increase serum testosterone.	Testosterone	125-137	hypertrichosis 2 (generalised, congenital)	Homo sapiens	24-27
7040256-5	1982	Administration of 10 IU hCG produced a single peak of testosterone, which did not occur until 24 h. Differences in the serum testosterone response were related to the concentration of hCG measured in the serum after injection, as injection of 1 IU, which failed to increase serum hCG levels above detection, was also inadequate to increase serum testosterone.	Testosterone	125-137	hypertrichosis 2 (generalised, congenital)	Homo sapiens	184-187
7040256-5	1982	Administration of 10 IU hCG produced a single peak of testosterone, which did not occur until 24 h. Differences in the serum testosterone response were related to the concentration of hCG measured in the serum after injection, as injection of 1 IU, which failed to increase serum hCG levels above detection, was also inadequate to increase serum testosterone.	Testosterone	125-137	hypertrichosis 2 (generalised, congenital)	Homo sapiens	184-187
6274906-3	1982	Testosterone secretion could be stimulated by hCG, suppressed by dexamethasone, and was not affected by ACTH.	Testosterone	0-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	46-49
6811376-10	1982	A detailed analysis of the treatment cycles is given for the four groups: the number of ampoules of hMG/hCG increased from 21.4 ampoules in patients with corpus luteum insufficiency to 47.7 ampoules in patients with hypogonadotropic amenorrhea.	Menotropins	100-103	hypertrichosis 2 (generalised, congenital)	Homo sapiens	104-107
6300388-8	1982	The concentration of testosterone in spermatic venous blood rose from 6-20 ng/ml to 160-270 ng/ml within about 30 min after hCG.	Testosterone	21-33	hypertrichosis 2 (generalised, congenital)	Homo sapiens	124-127
6122657-1	1982	Some biochemical and biophysical variables of human follicular fluid have been studied both in normal women after the LH peak (preovulatory follicles) and in women treated with clomiphene and hCG (clomiphene treated follicles).	Clomiphene	197-207	hypertrichosis 2 (generalised, congenital)	Homo sapiens	192-195
6271776-10	1981	These data suggest that the physiological intracellular mediator of acute cAMP-regulated, hCG-triggered functions in rabbit ovarian follicles is the type II isozyme of cAMP-dependent protein kinase while in CL of 4-day pseudopregnant rabbits, it is the type I enzyme form.	Cyclic AMP	74-78	hypertrichosis 2 (generalised, congenital)	Homo sapiens	90-93
6279742-3	1981	2) When dbcAMP was added to chorionic villi, there was a significant increase estradiol production in chorionic villi and hCG secretion in media.	Bucladesine	8-14	hypertrichosis 2 (generalised, congenital)	Homo sapiens	122-125
6279742-5	1981	4) When dbcAMP or synthetic LH-RH was added to BeWo cells, increased secretion of hCG and estradiol into media was seen.	Bucladesine	8-14	hypertrichosis 2 (generalised, congenital)	Homo sapiens	82-85
6797954-0	1981	Effect of clomiphene treatment on the human testicular response to a single dose of hCG.	Clomiphene	10-20	hypertrichosis 2 (generalised, congenital)	Homo sapiens	84-87
6797954-8	1981	When compared with these elevated values, the response of serum 17-hydroxyprogesterone, dehydroepiandrosterone, androstenedione and testosterone to hCG were diminished.	17-alpha-Hydroxyprogesterone	64-86	hypertrichosis 2 (generalised, congenital)	Homo sapiens	148-151
6797954-8	1981	When compared with these elevated values, the response of serum 17-hydroxyprogesterone, dehydroepiandrosterone, androstenedione and testosterone to hCG were diminished.	Dehydroepiandrosterone	88-110	hypertrichosis 2 (generalised, congenital)	Homo sapiens	148-151
6797954-8	1981	When compared with these elevated values, the response of serum 17-hydroxyprogesterone, dehydroepiandrosterone, androstenedione and testosterone to hCG were diminished.	Androstenedione	112-127	hypertrichosis 2 (generalised, congenital)	Homo sapiens	148-151
6797954-8	1981	When compared with these elevated values, the response of serum 17-hydroxyprogesterone, dehydroepiandrosterone, androstenedione and testosterone to hCG were diminished.	Testosterone	132-144	hypertrichosis 2 (generalised, congenital)	Homo sapiens	148-151
6797954-9	1981	The ratios of the steroid concentrations support previous reports that hCG-induced inhibition of 17-hydroxylase, 17--20 desmolase and 3 beta-hydroxysteroid dehydrogenase-delta 4-5 isomerase is decreased during antioestrogen administration.	Steroids	18-25	hypertrichosis 2 (generalised, congenital)	Homo sapiens	71-74
6797954-10	1981	This further substantiates the idea of a central role for endogenous testicular oestradiol in the mediation of steroidogenic lesions following acute large doses of hCG.	Estradiol	80-90	hypertrichosis 2 (generalised, congenital)	Homo sapiens	164-167
6795552-3	1981	Women with serum hCG levels of less than 200 mIU/ml exhibited a normal increase in serum E2 levels in response to hMG, whereas women with serum hCG levels of 2000 mIU/ml or more did not show any change after hMG administration.	Estradiol	89-91	hypertrichosis 2 (generalised, congenital)	Homo sapiens	17-20
7320597-2	1981	Possible role of progesterone on the resumption of meiosis was studied by examining the effects of neutralization of endogenous progesterone induced by an ovulatory dose of hCG with rabbit antiserum to progesterone (anti-P) on oocyte maturation in rats.	Progesterone	128-140	hypertrichosis 2 (generalised, congenital)	Homo sapiens	173-176
6271964-2	1981	Cyclic AMP and hCG stimulated progesterone and oestradiol production during at least the mid- and late luteal phases, but FSH stimulated only oestradiol production during the early and mid-luteal phases and had no effect on progesterone production.	Estradiol	47-57	hypertrichosis 2 (generalised, congenital)	Homo sapiens	15-18
6271964-2	1981	Cyclic AMP and hCG stimulated progesterone and oestradiol production during at least the mid- and late luteal phases, but FSH stimulated only oestradiol production during the early and mid-luteal phases and had no effect on progesterone production.	Progesterone	30-42	hypertrichosis 2 (generalised, congenital)	Homo sapiens	15-18
6795552-3	1981	Women with serum hCG levels of less than 200 mIU/ml exhibited a normal increase in serum E2 levels in response to hMG, whereas women with serum hCG levels of 2000 mIU/ml or more did not show any change after hMG administration.	Menotropins	114-117	hypertrichosis 2 (generalised, congenital)	Homo sapiens	17-20
6268505-3	1981	Testosterone treatment reduced the binding sites for hCG in testis of young rats but did not correct the already low values observed in the old animals.	Testosterone	0-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	53-56
6276245-5	1981	Divalent metal ions influenced hormone binding in 2 ways: (i) Specific bonding of hCG was greatest in the absence of metal ions and in the presence of low levels of chelating agents.	Metals	9-14	hypertrichosis 2 (generalised, congenital)	Homo sapiens	82-85
6276245-5	1981	Divalent metal ions influenced hormone binding in 2 ways: (i) Specific bonding of hCG was greatest in the absence of metal ions and in the presence of low levels of chelating agents.	Metals	117-122	hypertrichosis 2 (generalised, congenital)	Homo sapiens	82-85
6276247-0	1981	hCG-induced inhibition of testicular steroidogenesis: an oestradiol-mediated process?	Estradiol	57-67	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
6276247-2	1981	injections of hCG (10 U) in adult male rats resulted, within 24 h, in a 2-fold decrease in the maximal LH-stimulated testosterone production in vitro, while pregnenolone production was not changed.	Luteinizing Hormone	103-105	hypertrichosis 2 (generalised, congenital)	Homo sapiens	14-17
6276247-2	1981	injections of hCG (10 U) in adult male rats resulted, within 24 h, in a 2-fold decrease in the maximal LH-stimulated testosterone production in vitro, while pregnenolone production was not changed.	Testosterone	117-129	hypertrichosis 2 (generalised, congenital)	Homo sapiens	14-17
6276247-2	1981	injections of hCG (10 U) in adult male rats resulted, within 24 h, in a 2-fold decrease in the maximal LH-stimulated testosterone production in vitro, while pregnenolone production was not changed.	Pregnenolone	157-169	hypertrichosis 2 (generalised, congenital)	Homo sapiens	14-17
6271226-2	1981	Incubation of luteal cells with human, horse and rat sera, but not bovine sera resulted in enhanced basal and hCG-stimulated progesterone accumulation.	Progesterone	125-137	hypertrichosis 2 (generalised, congenital)	Homo sapiens	110-113
6271226-3	1981	The stimulatory effect of human or rat sera on basal, hCG- or 8 Br-cyclic AMP-induced progesterone synthesis in luteal cells was evident within 15-30 min after incubation, reaching a maximum after 3-4 h. The stimulatory effects of hCG and/or sera were blocked by inhibitors of RNA and protein synthesis.	Cyclic AMP	67-77	hypertrichosis 2 (generalised, congenital)	Homo sapiens	231-234
6271226-3	1981	The stimulatory effect of human or rat sera on basal, hCG- or 8 Br-cyclic AMP-induced progesterone synthesis in luteal cells was evident within 15-30 min after incubation, reaching a maximum after 3-4 h. The stimulatory effects of hCG and/or sera were blocked by inhibitors of RNA and protein synthesis.	Progesterone	86-98	hypertrichosis 2 (generalised, congenital)	Homo sapiens	54-57
6271226-3	1981	The stimulatory effect of human or rat sera on basal, hCG- or 8 Br-cyclic AMP-induced progesterone synthesis in luteal cells was evident within 15-30 min after incubation, reaching a maximum after 3-4 h. The stimulatory effects of hCG and/or sera were blocked by inhibitors of RNA and protein synthesis.	Progesterone	86-98	hypertrichosis 2 (generalised, congenital)	Homo sapiens	231-234
6271226-4	1981	Similarly, lysosomotropic agents, chloroquine (100 microM) and ammonium chloride (10 mM), partly blocked the steroidogenic response of luteal cells to hCG and/or human or rat sera.	Chloroquine	34-45	hypertrichosis 2 (generalised, congenital)	Homo sapiens	151-154
6271226-4	1981	Similarly, lysosomotropic agents, chloroquine (100 microM) and ammonium chloride (10 mM), partly blocked the steroidogenic response of luteal cells to hCG and/or human or rat sera.	Ammonium Chloride	63-80	hypertrichosis 2 (generalised, congenital)	Homo sapiens	151-154
6271226-5	1981	Incubation of cells in the presence of 2-deoxyglucose, sodium azide and phenylmethylsulfonyl fluoride resulted in partial inhibition of progesterone secretion in response to hCG or sera.	Deoxyglucose	39-53	hypertrichosis 2 (generalised, congenital)	Homo sapiens	174-177
6271226-5	1981	Incubation of cells in the presence of 2-deoxyglucose, sodium azide and phenylmethylsulfonyl fluoride resulted in partial inhibition of progesterone secretion in response to hCG or sera.	Sodium Azide	55-67	hypertrichosis 2 (generalised, congenital)	Homo sapiens	174-177
6271226-5	1981	Incubation of cells in the presence of 2-deoxyglucose, sodium azide and phenylmethylsulfonyl fluoride resulted in partial inhibition of progesterone secretion in response to hCG or sera.	Phenylmethylsulfonyl Fluoride	72-101	hypertrichosis 2 (generalised, congenital)	Homo sapiens	174-177
6271226-9	1981	Further, [3H]cholesterol from [3H]cholesteryl linoleate-LDL was incorporated into luteal cell progesterone and the extent of this incorporation was enhanced by hCG.	Tritium	10-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	160-163
6271226-9	1981	Further, [3H]cholesterol from [3H]cholesteryl linoleate-LDL was incorporated into luteal cell progesterone and the extent of this incorporation was enhanced by hCG.	Cholesterol	13-24	hypertrichosis 2 (generalised, congenital)	Homo sapiens	160-163
6271226-9	1981	Further, [3H]cholesterol from [3H]cholesteryl linoleate-LDL was incorporated into luteal cell progesterone and the extent of this incorporation was enhanced by hCG.	Tritium	9-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	160-163
6271226-9	1981	Further, [3H]cholesterol from [3H]cholesteryl linoleate-LDL was incorporated into luteal cell progesterone and the extent of this incorporation was enhanced by hCG.	cholesteryl linoleate	34-55	hypertrichosis 2 (generalised, congenital)	Homo sapiens	160-163
6263934-4	1981	In addition, LH-hCG saturation analyses performed on membrane preparations from the testicular tissue revealed no binding.	Luteinizing Hormone	13-15	hypertrichosis 2 (generalised, congenital)	Homo sapiens	16-19
6781872-1	1981	Hyperprolactinemia induced in immature female rats by treatment with sulpiride, a dopaminergic receptor blocker, increased the in vitro release of ovarian progesterone (P) in response to different doses of both highly purified hCG and human FSH.	Sulpiride	69-78	hypertrichosis 2 (generalised, congenital)	Homo sapiens	227-230
7228992-3	1981	Maximal secretion of progesterone was dependent on the presence of both low density lipoprotein (LDL) and hCG in the culture medium, whereas high density lipoprotein (HDL) was ineffective in supporting progesterone biosynthesis.	Progesterone	21-33	hypertrichosis 2 (generalised, congenital)	Homo sapiens	106-109
7228992-4	1981	Human corpus luteum tissue degraded [125I]iodo-LDL by a mechanism which was saturable, and degradation of [125I]iodo-LDL was stimulated by hCG.	iodo-ldl	112-120	hypertrichosis 2 (generalised, congenital)	Homo sapiens	139-142
7228997-5	1981	The binding substance appeared to be a gamma-globulin of the immunoglobulin G class, which bound labeled hCG and human LH (hLH) more avidly than it bound hFSH and interfered with the biological response to hCG therapy.	Luteinizing Hormone	119-121	hypertrichosis 2 (generalised, congenital)	Homo sapiens	206-209
7228997-5	1981	The binding substance appeared to be a gamma-globulin of the immunoglobulin G class, which bound labeled hCG and human LH (hLH) more avidly than it bound hFSH and interfered with the biological response to hCG therapy.	MY 12-62c	123-126	hypertrichosis 2 (generalised, congenital)	Homo sapiens	105-108
7228997-5	1981	The binding substance appeared to be a gamma-globulin of the immunoglobulin G class, which bound labeled hCG and human LH (hLH) more avidly than it bound hFSH and interfered with the biological response to hCG therapy.	MY 12-62c	123-126	hypertrichosis 2 (generalised, congenital)	Homo sapiens	206-209
7228997-8	1981	Despite the apparent infrequency of the development of clinically observable interference with the biological activity of hLH/hCG in hCG-treated patients, this report indicates that a potential hazard exists.	MY 12-62c	122-125	hypertrichosis 2 (generalised, congenital)	Homo sapiens	126-129
7228997-8	1981	Despite the apparent infrequency of the development of clinically observable interference with the biological activity of hLH/hCG in hCG-treated patients, this report indicates that a potential hazard exists.	MY 12-62c	122-125	hypertrichosis 2 (generalised, congenital)	Homo sapiens	133-136
7215574-2	1981	In the presence of a low dose of human chorionic gonadotropin (hCG), bromocriptine produced a further increase in T production, whereas in the presence of a high concentration of hCG it was ineffective.	Bromocriptine	69-82	hypertrichosis 2 (generalised, congenital)	Homo sapiens	63-66
6781872-1	1981	Hyperprolactinemia induced in immature female rats by treatment with sulpiride, a dopaminergic receptor blocker, increased the in vitro release of ovarian progesterone (P) in response to different doses of both highly purified hCG and human FSH.	Progesterone	155-167	hypertrichosis 2 (generalised, congenital)	Homo sapiens	227-230
6788718-7	1981	In order to obtain some indication whether melatonin may affect testicular function directly, we have examined the influenced of melatonin on the production of testosterone by hamster testes in response to hCG in vitro.	Melatonin	129-138	hypertrichosis 2 (generalised, congenital)	Homo sapiens	206-209
7472271-2	1981	Twenty-four hours after the injection of ovulatory dosages of hCG (10-100 IU), a dose-related loss of luteal estrogen receptor and in vitro progesterone production was observed.	Progesterone	140-152	hypertrichosis 2 (generalised, congenital)	Homo sapiens	62-65
7472271-4	1981	The loss of steroidogenesis induced by hCG was not permanent and could be reversed by estradiol treatment started within 24 h of hCG injection.	Estradiol	86-95	hypertrichosis 2 (generalised, congenital)	Homo sapiens	39-42
7472271-4	1981	The loss of steroidogenesis induced by hCG was not permanent and could be reversed by estradiol treatment started within 24 h of hCG injection.	Estradiol	86-95	hypertrichosis 2 (generalised, congenital)	Homo sapiens	129-132
6788718-7	1981	In order to obtain some indication whether melatonin may affect testicular function directly, we have examined the influenced of melatonin on the production of testosterone by hamster testes in response to hCG in vitro.	Testosterone	160-172	hypertrichosis 2 (generalised, congenital)	Homo sapiens	206-209
7251206-4	1981	More 5 alpha-DHT was released into the medium from the testes mince in the presence of hCG, while the addition of 10 or 50 micrometers of Colprone inhibited 5 alpha-DHT release as compared to hCG controls.	alpha-dht	7-16	hypertrichosis 2 (generalised, congenital)	Homo sapiens	87-90
7243104-0	1981	Effects of hCG on prostaglandin synthesis and function of corpus luteum.	Prostaglandins	18-31	hypertrichosis 2 (generalised, congenital)	Homo sapiens	11-14
6259190-2	1981	Five minutes after hCG administration, spermatic cAMP increased to 5 times the pretreated level, and after 30 min, it increased to 20 times the pretreated level.	Cyclic AMP	49-53	hypertrichosis 2 (generalised, congenital)	Homo sapiens	19-22
6259190-3	1981	Testosterone increased gradually after hCG injection, and the 2-fold increase was demonstrated at 50 min.	Testosterone	0-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	39-42
6259190-6	1981	These results are consistent with the view that cAMP may participate in the action of hCG upon steroidogenesis in the testis of human beings in vivo, as has previously been observed with rat and human testes in vitro.	Cyclic AMP	48-52	hypertrichosis 2 (generalised, congenital)	Homo sapiens	86-89
7243104-1	1981	The effect of intramuscular injections of human chorionic gonadotropin (hCG) on subsequent in vitro prostaglandin (PG) production by the corpus luteum was studied in the rhesus monkey.	Prostaglandins	100-113	hypertrichosis 2 (generalised, congenital)	Homo sapiens	72-75
7243104-1	1981	The effect of intramuscular injections of human chorionic gonadotropin (hCG) on subsequent in vitro prostaglandin (PG) production by the corpus luteum was studied in the rhesus monkey.	Prostaglandins	115-117	hypertrichosis 2 (generalised, congenital)	Homo sapiens	72-75
7243104-5	1981	The production of prostaglandins F (PGF) and E (PGE) by the corpus luteum of the animals treated wit hCG was significantly lower than that of the controls (P less than .01).	Prostaglandins F	18-34	hypertrichosis 2 (generalised, congenital)	Homo sapiens	101-104
7243104-5	1981	The production of prostaglandins F (PGF) and E (PGE) by the corpus luteum of the animals treated wit hCG was significantly lower than that of the controls (P less than .01).	Prostaglandins F	36-39	hypertrichosis 2 (generalised, congenital)	Homo sapiens	101-104
7243104-5	1981	The production of prostaglandins F (PGF) and E (PGE) by the corpus luteum of the animals treated wit hCG was significantly lower than that of the controls (P less than .01).	Prostaglandins E	48-51	hypertrichosis 2 (generalised, congenital)	Homo sapiens	101-104
7243104-6	1981	After hCG treatment, the decrease in PGF production was greater than that of PGE, resulting in a lower ratio of PGF:PGE production than in the controls (P less than .01).	Prostaglandins F	37-40	hypertrichosis 2 (generalised, congenital)	Homo sapiens	6-9
7243104-6	1981	After hCG treatment, the decrease in PGF production was greater than that of PGE, resulting in a lower ratio of PGF:PGE production than in the controls (P less than .01).	Prostaglandins E	77-80	hypertrichosis 2 (generalised, congenital)	Homo sapiens	6-9
7243104-6	1981	After hCG treatment, the decrease in PGF production was greater than that of PGE, resulting in a lower ratio of PGF:PGE production than in the controls (P less than .01).	Prostaglandins F	112-115	hypertrichosis 2 (generalised, congenital)	Homo sapiens	6-9
7243104-6	1981	After hCG treatment, the decrease in PGF production was greater than that of PGE, resulting in a lower ratio of PGF:PGE production than in the controls (P less than .01).	Prostaglandins E	116-119	hypertrichosis 2 (generalised, congenital)	Homo sapiens	6-9
6450776-3	1981	Increasing doses of hCG administered from days 6-10 post ovulation prevented the luteolytic effect of D-Trp6-LRH.	d-trp6-lrh	102-112	hypertrichosis 2 (generalised, congenital)	Homo sapiens	20-23
6264875-0	1981	Temporal relationship between hCG induced desensitization of LH/hCG responsive adenylyl cyclase and downregulation of LH/hCG receptors in the rat testis.	Luteinizing Hormone	61-63	hypertrichosis 2 (generalised, congenital)	Homo sapiens	30-33
6264875-2	1981	Two hours after the injection of hCG, LH/hCG responsive AC was reduced by 40%, whereas LH binding was still normal.	Luteinizing Hormone	38-40	hypertrichosis 2 (generalised, congenital)	Homo sapiens	33-36
6264875-2	1981	Two hours after the injection of hCG, LH/hCG responsive AC was reduced by 40%, whereas LH binding was still normal.	Luteinizing Hormone	38-40	hypertrichosis 2 (generalised, congenital)	Homo sapiens	41-44
7460836-8	1981	Administration of bromocriptine (1 mg/day) concurrent with hCG during the last 20 days of Thio-feeding significantly suppressed ovarian weight gain and PCO formation.	Thiouracil	90-94	hypertrichosis 2 (generalised, congenital)	Homo sapiens	59-62
7343084-0	1981	Effect in vitro of high doses of hCG in the progesterone synthesis from pregnenolone in human term placenta.	Progesterone	44-56	hypertrichosis 2 (generalised, congenital)	Homo sapiens	33-36
6261996-2	1981	Testosterone response to hCG was normal in all subjects.	Testosterone	0-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	25-28
7343084-0	1981	Effect in vitro of high doses of hCG in the progesterone synthesis from pregnenolone in human term placenta.	Pregnenolone	72-84	hypertrichosis 2 (generalised, congenital)	Homo sapiens	33-36
7460824-6	1981	Thus, sialic acid alone and/or differences in subunit assembly seem to be responsible for the electrophoretic heterogeneity of highly purified hCG.	N-Acetylneuraminic Acid	6-17	hypertrichosis 2 (generalised, congenital)	Homo sapiens	143-146
7460824-1	1981	A highly purified urinary hCG preparation was subjected to electrofocusing on polyacrylamide gel.	polyacrylamide	78-92	hypertrichosis 2 (generalised, congenital)	Homo sapiens	26-29
6461588-5	1981	Plasma testosterone (T) increments (delta) after hCG were lower in 1-day-old animals than in other age groups.	Testosterone	7-19	hypertrichosis 2 (generalised, congenital)	Homo sapiens	49-52
6113211-4	1981	The oviduct obtained from animals sacrificed 24 h after human chorionic gonadotropin (hCG) administration was more responsive to acetylcholine as compared to the oviduct obtained 72 h after hCG and from animals without ovulation induction.	Acetylcholine	129-142	hypertrichosis 2 (generalised, congenital)	Homo sapiens	86-89
6132006-9	1981	Autoradiographic localization techniques were used to show the existence of LH/hCG binding sites in cryptorchid testes.	Luteinizing Hormone	76-78	hypertrichosis 2 (generalised, congenital)	Homo sapiens	79-82
6820054-7	1981	Treatment of hypophysectomized rams with PMSG, hCG or testosterone shows that spermatogonial divisions are sensitive to the hormonal milieu with specific stages being controlled by the LH-like activity of hCG (A1 spermatogonia), and the FSH-like activity of PMSG (transition from intermediate spermatogonia to leptotene spermatocytes).	Testosterone	54-66	hypertrichosis 2 (generalised, congenital)	Homo sapiens	205-208
6820054-7	1981	Treatment of hypophysectomized rams with PMSG, hCG or testosterone shows that spermatogonial divisions are sensitive to the hormonal milieu with specific stages being controlled by the LH-like activity of hCG (A1 spermatogonia), and the FSH-like activity of PMSG (transition from intermediate spermatogonia to leptotene spermatocytes).	Luteinizing Hormone	185-187	hypertrichosis 2 (generalised, congenital)	Homo sapiens	47-50
6820054-7	1981	Treatment of hypophysectomized rams with PMSG, hCG or testosterone shows that spermatogonial divisions are sensitive to the hormonal milieu with specific stages being controlled by the LH-like activity of hCG (A1 spermatogonia), and the FSH-like activity of PMSG (transition from intermediate spermatogonia to leptotene spermatocytes).	Luteinizing Hormone	185-187	hypertrichosis 2 (generalised, congenital)	Homo sapiens	205-208
6820054-7	1981	Treatment of hypophysectomized rams with PMSG, hCG or testosterone shows that spermatogonial divisions are sensitive to the hormonal milieu with specific stages being controlled by the LH-like activity of hCG (A1 spermatogonia), and the FSH-like activity of PMSG (transition from intermediate spermatogonia to leptotene spermatocytes).	leptotene	310-319	hypertrichosis 2 (generalised, congenital)	Homo sapiens	205-208
7452615-0	1981	Stimulation by hCG in vivo of oxygen consumption by rabbit oocytes in vitro.	Oxygen	30-36	hypertrichosis 2 (generalised, congenital)	Homo sapiens	15-18
7203686-3	1980	The presence of an LH/hCG responsive adenylyl cyclase in the testis of tfm rats and mice shows that the greatly elevated LH levels present in males having this syndrome, giving 80-90% reduction in LH/hCG receptors, do not cause an uncoupling of the remaining receptors from the adenylyl cyclase.	Luteinizing Hormone	19-21	hypertrichosis 2 (generalised, congenital)	Homo sapiens	200-203
7203686-6	1980	Desensitization of the LH responsive adenylyl cyclase by hCG in normal rats, confirms previous studies showing lack of hCG stimulated cyclic-AMP secretion after a comparable dose of hCG in vivo.	Luteinizing Hormone	23-25	hypertrichosis 2 (generalised, congenital)	Homo sapiens	57-60
6254312-5	1980	Morphological observations, after injection of trypan blue to a small number of the rats, showed that follicular growth, ovulation and formation of new corpora lutea could occur after both hCG and LH.	Trypan Blue	47-58	hypertrichosis 2 (generalised, congenital)	Homo sapiens	189-192
6254312-6	1980	The possibility that the corpora lutea which started to respond to LH stimulation 5-7 days after the hCG injection were not the ones originally desensitized by hCG but new corpora lutea, is discussed.	Luteinizing Hormone	67-69	hypertrichosis 2 (generalised, congenital)	Homo sapiens	101-104
7419679-1	1980	Intramuscular administration of 1500 IU hCG daily for 3 days induced a transient accumulation of 17 alpha-hydroxyprogesterone (17 OHP) relative to testosterone (T) in normal men, reaching its maximum 24 h after the first injection (17 OHP to T ratio, 1.7 +/- 0.3 times baseline; P < 0.01).	17-alpha-Hydroxyprogesterone	97-125	hypertrichosis 2 (generalised, congenital)	Homo sapiens	40-43
7419679-1	1980	Intramuscular administration of 1500 IU hCG daily for 3 days induced a transient accumulation of 17 alpha-hydroxyprogesterone (17 OHP) relative to testosterone (T) in normal men, reaching its maximum 24 h after the first injection (17 OHP to T ratio, 1.7 +/- 0.3 times baseline; P < 0.01).	17-alpha-Hydroxyprogesterone	127-133	hypertrichosis 2 (generalised, congenital)	Homo sapiens	40-43
7419679-1	1980	Intramuscular administration of 1500 IU hCG daily for 3 days induced a transient accumulation of 17 alpha-hydroxyprogesterone (17 OHP) relative to testosterone (T) in normal men, reaching its maximum 24 h after the first injection (17 OHP to T ratio, 1.7 +/- 0.3 times baseline; P < 0.01).	Testosterone	147-159	hypertrichosis 2 (generalised, congenital)	Homo sapiens	40-43
7419679-1	1980	Intramuscular administration of 1500 IU hCG daily for 3 days induced a transient accumulation of 17 alpha-hydroxyprogesterone (17 OHP) relative to testosterone (T) in normal men, reaching its maximum 24 h after the first injection (17 OHP to T ratio, 1.7 +/- 0.3 times baseline; P < 0.01).	17-alpha-Hydroxyprogesterone	232-238	hypertrichosis 2 (generalised, congenital)	Homo sapiens	40-43
7419679-2	1980	Simultaneous administration of hCG and the estrogen antagonist tamoxifen (20 mg twice daily) almost completely abolished the hCG-induced steroidogenic block localized between 17 OHP and T (17 OHP to T ratio at 24 h, 1.1 +/- 0.1 times baseline; P < 0.01 vs. hCG alone).	Tamoxifen	63-72	hypertrichosis 2 (generalised, congenital)	Homo sapiens	125-128
7419679-2	1980	Simultaneous administration of hCG and the estrogen antagonist tamoxifen (20 mg twice daily) almost completely abolished the hCG-induced steroidogenic block localized between 17 OHP and T (17 OHP to T ratio at 24 h, 1.1 +/- 0.1 times baseline; P < 0.01 vs. hCG alone).	Tamoxifen	63-72	hypertrichosis 2 (generalised, congenital)	Homo sapiens	125-128
7419679-2	1980	Simultaneous administration of hCG and the estrogen antagonist tamoxifen (20 mg twice daily) almost completely abolished the hCG-induced steroidogenic block localized between 17 OHP and T (17 OHP to T ratio at 24 h, 1.1 +/- 0.1 times baseline; P < 0.01 vs. hCG alone).	17-alpha-Hydroxyprogesterone	175-181	hypertrichosis 2 (generalised, congenital)	Homo sapiens	31-34
7419679-2	1980	Simultaneous administration of hCG and the estrogen antagonist tamoxifen (20 mg twice daily) almost completely abolished the hCG-induced steroidogenic block localized between 17 OHP and T (17 OHP to T ratio at 24 h, 1.1 +/- 0.1 times baseline; P < 0.01 vs. hCG alone).	17-alpha-Hydroxyprogesterone	175-181	hypertrichosis 2 (generalised, congenital)	Homo sapiens	125-128
7419679-2	1980	Simultaneous administration of hCG and the estrogen antagonist tamoxifen (20 mg twice daily) almost completely abolished the hCG-induced steroidogenic block localized between 17 OHP and T (17 OHP to T ratio at 24 h, 1.1 +/- 0.1 times baseline; P < 0.01 vs. hCG alone).	17-alpha-Hydroxyprogesterone	175-181	hypertrichosis 2 (generalised, congenital)	Homo sapiens	125-128
7419679-2	1980	Simultaneous administration of hCG and the estrogen antagonist tamoxifen (20 mg twice daily) almost completely abolished the hCG-induced steroidogenic block localized between 17 OHP and T (17 OHP to T ratio at 24 h, 1.1 +/- 0.1 times baseline; P < 0.01 vs. hCG alone).	2-hydroxyphenylacetic acid	178-181	hypertrichosis 2 (generalised, congenital)	Homo sapiens	31-34
7419679-2	1980	Simultaneous administration of hCG and the estrogen antagonist tamoxifen (20 mg twice daily) almost completely abolished the hCG-induced steroidogenic block localized between 17 OHP and T (17 OHP to T ratio at 24 h, 1.1 +/- 0.1 times baseline; P < 0.01 vs. hCG alone).	2-hydroxyphenylacetic acid	178-181	hypertrichosis 2 (generalised, congenital)	Homo sapiens	125-128
7419679-2	1980	Simultaneous administration of hCG and the estrogen antagonist tamoxifen (20 mg twice daily) almost completely abolished the hCG-induced steroidogenic block localized between 17 OHP and T (17 OHP to T ratio at 24 h, 1.1 +/- 0.1 times baseline; P < 0.01 vs. hCG alone).	2-hydroxyphenylacetic acid	178-181	hypertrichosis 2 (generalised, congenital)	Homo sapiens	125-128
7192265-2	1980	Raised LH levels, due to a cross reaction with hCG in the radioimmunoassay, were observed in 20 out of 29 patients with active disease and were mainly caused by gonadotrophin production in the tumour tissue.	Luteinizing Hormone	7-9	hypertrichosis 2 (generalised, congenital)	Homo sapiens	47-50
7192265-7	1980	These data strongly suggest that the tumour hCG has a biological activity, stimulating the remaining testis to increased testosterone secretion in these patients.	Testosterone	121-133	hypertrichosis 2 (generalised, congenital)	Homo sapiens	44-47
7240828-1	1980	HCG of chorionic tissues of hydatidiform mole was purified using ammonium sulfate fractionation, ion exchange chromatography and gel filtration.	Ammonium Sulfate	65-81	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
6264790-7	1981	FSH increased acute human chorionic gonadotropin (hCG)-responsive progesterone secretion in short-term incubations of cultured granulosa cells.	Progesterone	66-78	hypertrichosis 2 (generalised, congenital)	Homo sapiens	50-53
6773818-3	1980	Serum testosterone and dihydrotestosterone (DHT) levels were reliably increased by one intramuscular injection of hCG (P < 0.05).	Testosterone	6-18	hypertrichosis 2 (generalised, congenital)	Homo sapiens	114-117
7192190-0	1980	Response of peripheral serum sex steroids and some of their precursors to a single injection of hCG in adult men.	Steroids	33-41	hypertrichosis 2 (generalised, congenital)	Homo sapiens	96-99
6773818-3	1980	Serum testosterone and dihydrotestosterone (DHT) levels were reliably increased by one intramuscular injection of hCG (P < 0.05).	Dihydrotestosterone	23-42	hypertrichosis 2 (generalised, congenital)	Homo sapiens	114-117
6773818-3	1980	Serum testosterone and dihydrotestosterone (DHT) levels were reliably increased by one intramuscular injection of hCG (P < 0.05).	Dihydrotestosterone	44-47	hypertrichosis 2 (generalised, congenital)	Homo sapiens	114-117
6773818-4	1980	Although testosterone responses to hCG were not significantly different in normal PRL and suppressed PRL cycles (P > 0.05), the DHT response was significantly increased in the suppressed cycle (P < 0.05), suggesting a physiologic 5 alpha-reductase blockage by PRL in men.	Testosterone	9-21	hypertrichosis 2 (generalised, congenital)	Homo sapiens	35-38
6994038-0	1980	[Determination of steroids in the human spermatic vein in the basic state and after stimulation by hCG].	Steroids	18-26	hypertrichosis 2 (generalised, congenital)	Homo sapiens	99-102
6251689-2	1980	Blocking of the hypophyseal prolactin secretion by twice daily injections of 2 microgram/g body weight bromocriptine into rats from the first day of pregnancy onwards prevents the increase in ovarian hCG-binding and progesterone production.	Bromocriptine	103-116	hypertrichosis 2 (generalised, congenital)	Homo sapiens	200-203
7409912-6	1980	Intravenous injection of hCG increased the levels of oestradiol-17 beta in all tissues and markedly in the cauda epididymidis and vas deferens.	Estradiol	53-71	hypertrichosis 2 (generalised, congenital)	Homo sapiens	25-28
6776276-5	1980	In-vivo studies with oestrogen-primed hypophysectomized immature rats indicate that androgens secreted by LH/hCG-stimulated thecal and/or interstitial cells may act directly on the preantral follicle to promote atresia.	Luteinizing Hormone	106-108	hypertrichosis 2 (generalised, congenital)	Homo sapiens	109-112
7240855-0	1980	[Dual action of prostaglandins in the regulation of HCG-induced ovulation in immature rats (author"s transl)].	Prostaglandins	16-30	hypertrichosis 2 (generalised, congenital)	Homo sapiens	52-55
7240855-2	1980	Mean number of ova shed following treatment of immature rats sequentially with PMS and hCG was reduced in a dose-dependent manner by simultaneous injection with increasing doses of indomethacin.	Indomethacin	181-193	hypertrichosis 2 (generalised, congenital)	Homo sapiens	87-90
7240855-5	1980	Another dose-dependent relationship was found 10 h after hCG injection, the closest time prior to the onset of ovulation, the minimum effective dose necessary to prevent ovulation was 8 times higher than at 0 h, suggesting that prostaglandins acted differently on ovulation in the later stage of the preovulatory process.	Prostaglandins	228-242	hypertrichosis 2 (generalised, congenital)	Homo sapiens	57-60
7240855-6	1980	It is concluded that prostaglandins may mediate the action of hCG on ovulation at least through two mechanisms.	Prostaglandins	21-35	hypertrichosis 2 (generalised, congenital)	Homo sapiens	62-65
6245577-6	1980	The addition of hCG elicited a significant increase in cyclic AMP formation in specimens from ovaries with stromal hyperplasia, indicating a preserved responsiveness to gonadotropin in this type of ovaries.	Cyclic AMP	55-65	hypertrichosis 2 (generalised, congenital)	Homo sapiens	16-19
6250254-2	1980	Plasma testosterone levels before and after a single injection of hCG were significantly lower in 24-month old rats than 60--90 day old animals (p less than 0.001).	Testosterone	7-19	hypertrichosis 2 (generalised, congenital)	Homo sapiens	66-69
6250254-3	1980	Even with repeated hCG administration for three weeks, plasma testosterone levels of old rats could not be restored to levels present in unstimulated young rats.	Testosterone	62-74	hypertrichosis 2 (generalised, congenital)	Homo sapiens	19-22
6771092-0	1980	Levels of HCG in subjects using the Progestasert(TM) intrauterine progesterone systems.	Progesterone	66-78	hypertrichosis 2 (generalised, congenital)	Homo sapiens	10-13
6263999-2	1980	1) Twenty out of 178 cases of hydatidiform mole developed into cases of invasive mole or choriocarcinoma after D & C. There was a decrease in hCG value to the LH level in the remaining 158 cases.	Luteinizing Hormone	163-165	hypertrichosis 2 (generalised, congenital)	Homo sapiens	146-149
6263999-3	1980	2) The hCG level fell to the LH level in 59 cases of invasive mole and choriocarcinoma after treatment, with a subsequent reoccurrence of recurrence in 3 cases in which there was no additional chemotherapy.	Luteinizing Hormone	29-31	hypertrichosis 2 (generalised, congenital)	Homo sapiens	7-10
6263999-6	1980	4) A cellular effect was observed in 5.6% where hCG values decrease in LH levels.	Luteinizing Hormone	71-73	hypertrichosis 2 (generalised, congenital)	Homo sapiens	48-51
6263999-7	1980	Remission is determined in hydatidiform mole when the hCG value persists at the LH level, and remission in invasive mole and choriocarcinoma when no cellular effect is detected after two courses of chemotherapy following decrease of hCG value to the LH level.	Luteinizing Hormone	80-82	hypertrichosis 2 (generalised, congenital)	Homo sapiens	54-57
6245583-5	1980	Removal of sialic acid from hCG increased this rate; removal of other carbohydrate residues decreased it.	N-Acetylneuraminic Acid	11-22	hypertrichosis 2 (generalised, congenital)	Homo sapiens	28-31
6245583-11	1980	The threshold was inversely proportional to the efficacy of the hCG derivative used and was reduced by the presence of isobutylmethylxanthine.	1-Methyl-3-isobutylxanthine	119-141	hypertrichosis 2 (generalised, congenital)	Homo sapiens	64-67
6766948-1	1980	Estradiol has been previously reported to be a potent inhibitor of hCG-stimulated progesterone accumulation in isolated cells from human corpora lutea of the menstrual cycle.	Estradiol	0-9	hypertrichosis 2 (generalised, congenital)	Homo sapiens	67-70
6766948-1	1980	Estradiol has been previously reported to be a potent inhibitor of hCG-stimulated progesterone accumulation in isolated cells from human corpora lutea of the menstrual cycle.	Progesterone	82-94	hypertrichosis 2 (generalised, congenital)	Homo sapiens	67-70
6766948-3	1980	The inhibition by estradiol of hCG-stimulated progesterone accumulation occurred without any increase in PGF accumulation in the incubations.	Estradiol	18-27	hypertrichosis 2 (generalised, congenital)	Homo sapiens	31-34
6766948-3	1980	The inhibition by estradiol of hCG-stimulated progesterone accumulation occurred without any increase in PGF accumulation in the incubations.	Progesterone	46-58	hypertrichosis 2 (generalised, congenital)	Homo sapiens	31-34
6766948-4	1980	Furthermore, PGF accumulation was markedly reduced (P less than 0.05) at all concentrations of indomethacin testes (0.1, 1, and 10 microgram/ml), but the inhibitory effect of estradiol on hCG-stimulated progesterone accumulation was not prevented.	Estradiol	175-184	hypertrichosis 2 (generalised, congenital)	Homo sapiens	188-191
7189630-3	1980	Response to hCG was assessed by measurement of steroids in serum collected before and for 5 days after im administration of 10 000 IU hCG.	Steroids	47-55	hypertrichosis 2 (generalised, congenital)	Homo sapiens	12-15
7376988-0	1980	Inhibition of PG biosynthesis as the maintenance mechanism of pregnancy of hCG.	pg	14-16	hypertrichosis 2 (generalised, congenital)	Homo sapiens	75-78
7376988-1	1980	In general, when the hCG values in the serum and urine reached their first peak, the PGF2 alpha and PGF2 alpha-MUM levels dropped.	Dinoprost	85-89	hypertrichosis 2 (generalised, congenital)	Homo sapiens	21-24
7376988-1	1980	In general, when the hCG values in the serum and urine reached their first peak, the PGF2 alpha and PGF2 alpha-MUM levels dropped.	Dinoprost	100-104	hypertrichosis 2 (generalised, congenital)	Homo sapiens	21-24
7376988-2	1980	The hCG fell rapidly in inverse proportion to PGF2 alpha.	Dinoprost	46-50	hypertrichosis 2 (generalised, congenital)	Homo sapiens	4-7
7350181-1	1980	After both single (1500 IU) and daily repeated (1500 IU daily for 3 days) im administration of hCG, peak values of 17-hydroxyprogesterone (17OHP) were achieved 24 h after the single or first injection, whereas plasma testosterone (T) levels reached their maximum 48 h later.	17-alpha-Hydroxyprogesterone	115-137	hypertrichosis 2 (generalised, congenital)	Homo sapiens	95-98
6446358-4	1980	The releasing kinetic of the 3 steroids under hCG influence was studied; after 12 days of culture, the medium was analysed during 96 hours (8 periods of 12 hours); the steroid production started immediately and showed a progressive increase then slightly slowed down at the end of the 4 days.	Steroids	31-39	hypertrichosis 2 (generalised, congenital)	Homo sapiens	46-49
6446358-4	1980	The releasing kinetic of the 3 steroids under hCG influence was studied; after 12 days of culture, the medium was analysed during 96 hours (8 periods of 12 hours); the steroid production started immediately and showed a progressive increase then slightly slowed down at the end of the 4 days.	Steroids	31-38	hypertrichosis 2 (generalised, congenital)	Homo sapiens	46-49
6446359-0	1980	[Effect of hCG on the production of androstenedione, testosterone and dihydrotestosterone by long term organ culture testicular tissue from hypophysectomized boars].	Androstenedione	36-51	hypertrichosis 2 (generalised, congenital)	Homo sapiens	11-14
6446359-0	1980	[Effect of hCG on the production of androstenedione, testosterone and dihydrotestosterone by long term organ culture testicular tissue from hypophysectomized boars].	Testosterone	53-65	hypertrichosis 2 (generalised, congenital)	Homo sapiens	11-14
6446359-0	1980	[Effect of hCG on the production of androstenedione, testosterone and dihydrotestosterone by long term organ culture testicular tissue from hypophysectomized boars].	Dihydrotestosterone	70-89	hypertrichosis 2 (generalised, congenital)	Homo sapiens	11-14
6114047-13	1980	The increased dosage of hCG used in this series is considered to be a decisive factor in the induction of ovulation and the maintenance of pregnancies through the abundant steroid production it induced.	Steroids	172-179	hypertrichosis 2 (generalised, congenital)	Homo sapiens	24-27
7350181-1	1980	After both single (1500 IU) and daily repeated (1500 IU daily for 3 days) im administration of hCG, peak values of 17-hydroxyprogesterone (17OHP) were achieved 24 h after the single or first injection, whereas plasma testosterone (T) levels reached their maximum 48 h later.	17-alpha-Hydroxyprogesterone	139-144	hypertrichosis 2 (generalised, congenital)	Homo sapiens	95-98
7350181-1	1980	After both single (1500 IU) and daily repeated (1500 IU daily for 3 days) im administration of hCG, peak values of 17-hydroxyprogesterone (17OHP) were achieved 24 h after the single or first injection, whereas plasma testosterone (T) levels reached their maximum 48 h later.	Testosterone	217-229	hypertrichosis 2 (generalised, congenital)	Homo sapiens	95-98
7350181-3	1980	In both the single and repeated hCG experiments, the initial rise of 17-OHP was more pronounced than that of T, leading to a steep temporary increase of the 17-OHP to T ratio in the first 24 h. Repeated hCG administration for 3 days to the same subjects elicited T responses at 48 and 72 h quantitatively similar to those produced by single hCG loading, although the 17-OHP response appeared slightly higher in the multiple dose experiment.	17-alpha-Hydroxyprogesterone	69-75	hypertrichosis 2 (generalised, congenital)	Homo sapiens	32-35
7350181-3	1980	In both the single and repeated hCG experiments, the initial rise of 17-OHP was more pronounced than that of T, leading to a steep temporary increase of the 17-OHP to T ratio in the first 24 h. Repeated hCG administration for 3 days to the same subjects elicited T responses at 48 and 72 h quantitatively similar to those produced by single hCG loading, although the 17-OHP response appeared slightly higher in the multiple dose experiment.	17-alpha-Hydroxyprogesterone	69-75	hypertrichosis 2 (generalised, congenital)	Homo sapiens	203-206
7350181-3	1980	In both the single and repeated hCG experiments, the initial rise of 17-OHP was more pronounced than that of T, leading to a steep temporary increase of the 17-OHP to T ratio in the first 24 h. Repeated hCG administration for 3 days to the same subjects elicited T responses at 48 and 72 h quantitatively similar to those produced by single hCG loading, although the 17-OHP response appeared slightly higher in the multiple dose experiment.	17-alpha-Hydroxyprogesterone	69-75	hypertrichosis 2 (generalised, congenital)	Homo sapiens	203-206
7350181-3	1980	In both the single and repeated hCG experiments, the initial rise of 17-OHP was more pronounced than that of T, leading to a steep temporary increase of the 17-OHP to T ratio in the first 24 h. Repeated hCG administration for 3 days to the same subjects elicited T responses at 48 and 72 h quantitatively similar to those produced by single hCG loading, although the 17-OHP response appeared slightly higher in the multiple dose experiment.	17-alpha-Hydroxyprogesterone	157-163	hypertrichosis 2 (generalised, congenital)	Homo sapiens	203-206
7350181-3	1980	In both the single and repeated hCG experiments, the initial rise of 17-OHP was more pronounced than that of T, leading to a steep temporary increase of the 17-OHP to T ratio in the first 24 h. Repeated hCG administration for 3 days to the same subjects elicited T responses at 48 and 72 h quantitatively similar to those produced by single hCG loading, although the 17-OHP response appeared slightly higher in the multiple dose experiment.	17-alpha-Hydroxyprogesterone	157-163	hypertrichosis 2 (generalised, congenital)	Homo sapiens	203-206
7350181-3	1980	In both the single and repeated hCG experiments, the initial rise of 17-OHP was more pronounced than that of T, leading to a steep temporary increase of the 17-OHP to T ratio in the first 24 h. Repeated hCG administration for 3 days to the same subjects elicited T responses at 48 and 72 h quantitatively similar to those produced by single hCG loading, although the 17-OHP response appeared slightly higher in the multiple dose experiment.	17-alpha-Hydroxyprogesterone	157-163	hypertrichosis 2 (generalised, congenital)	Homo sapiens	203-206
7350181-3	1980	In both the single and repeated hCG experiments, the initial rise of 17-OHP was more pronounced than that of T, leading to a steep temporary increase of the 17-OHP to T ratio in the first 24 h. Repeated hCG administration for 3 days to the same subjects elicited T responses at 48 and 72 h quantitatively similar to those produced by single hCG loading, although the 17-OHP response appeared slightly higher in the multiple dose experiment.	17-alpha-Hydroxyprogesterone	157-163	hypertrichosis 2 (generalised, congenital)	Homo sapiens	203-206
227212-9	1979	Repeated injection of hCG results in equally elevated testosterone concentrations in young and old rats.	Testosterone	54-66	hypertrichosis 2 (generalised, congenital)	Homo sapiens	22-25
229781-3	1979	Treatment of intact rats with CB-154 reduced the quantity of androgen produced by the Leydig cells in vitro after exposure to hCG and decreased LH binding to the same cells by 50%.	Bromocriptine	30-36	hypertrichosis 2 (generalised, congenital)	Homo sapiens	126-129
36274-4	1979	Testicular stimulation in vitro with a high dose of hCG (360 pM) resulted in significantly greater production of testosterone, pregnenolone, and estradiol by cryptorchid than by control rat tissue.	Testosterone	113-125	hypertrichosis 2 (generalised, congenital)	Homo sapiens	52-55
512993-0	1979	Influence of hCG injection and steroid treatment on prostaglandin metabolism by rabbit uterus and oviduct.	Prostaglandins	52-65	hypertrichosis 2 (generalised, congenital)	Homo sapiens	13-16
512993-3	1979	After an ovulating injection of hCG metabolism of both PGE-2 and PGF-2 alpha by lung and uterus declined linearly up to 72 h (during the time of ovum transport).	Dinoprostone	55-60	hypertrichosis 2 (generalised, congenital)	Homo sapiens	32-35
512993-3	1979	After an ovulating injection of hCG metabolism of both PGE-2 and PGF-2 alpha by lung and uterus declined linearly up to 72 h (during the time of ovum transport).	Dinoprost	65-70	hypertrichosis 2 (generalised, congenital)	Homo sapiens	32-35
36274-4	1979	Testicular stimulation in vitro with a high dose of hCG (360 pM) resulted in significantly greater production of testosterone, pregnenolone, and estradiol by cryptorchid than by control rat tissue.	Pregnenolone	127-139	hypertrichosis 2 (generalised, congenital)	Homo sapiens	52-55
36274-4	1979	Testicular stimulation in vitro with a high dose of hCG (360 pM) resulted in significantly greater production of testosterone, pregnenolone, and estradiol by cryptorchid than by control rat tissue.	Estradiol	145-154	hypertrichosis 2 (generalised, congenital)	Homo sapiens	52-55
36274-5	1979	The in vitro binding of [125I]hCG per testis was decreased in the cryptorchid state to 40% of control values, probably as a result of down-regulation of LH receptors due to the 4-fold elevation of serum LH levels in the cryptorchid rats.	Luteinizing Hormone	153-155	hypertrichosis 2 (generalised, congenital)	Homo sapiens	30-33
231005-2	1979	Nutrient medium, oxygen tension and Gelfoam support matrix influence the synthesis of hCG by these cultures.	Oxygen	17-23	hypertrichosis 2 (generalised, congenital)	Homo sapiens	86-89
231005-6	1979	The functional responsiveness of these placental cultures was demonstrated by modulation of hCG synthesis with theophylline and 3"5" dibutyryl cyclic AMP.	Theophylline	111-123	hypertrichosis 2 (generalised, congenital)	Homo sapiens	92-95
231005-6	1979	The functional responsiveness of these placental cultures was demonstrated by modulation of hCG synthesis with theophylline and 3"5" dibutyryl cyclic AMP.	3"5" dibutyryl cyclic amp	128-153	hypertrichosis 2 (generalised, congenital)	Homo sapiens	92-95
483947-6	1979	Such repair disturbances may cause reduced H3-thymidine incorporation in PHA-stimulated and hCG-treated lymphocytes.	h3-thymidine	43-55	hypertrichosis 2 (generalised, congenital)	Homo sapiens	92-95
455255-4	1979	The development of a hypermetabolic syndrome in patients with choriocarcinoma may be due to secondary thyrotoxicosis from either the TSH-like activity of hCG or from the concomitant production of molar thyrotropin by the tumor.	Thyrotropin	133-136	hypertrichosis 2 (generalised, congenital)	Homo sapiens	154-157
445343-4	1979	The ascitic fluid and tumor cell lysate, but not serum, contained hCG by specific assay, and the immunoreactive hCG had characteristics similar to purified hCG in filtration on Sephadex G-100.	sephadex	177-191	hypertrichosis 2 (generalised, congenital)	Homo sapiens	112-115
222100-4	1979	A normal response of LH to conjugated oestrogens was observed at a serum hCG level of 20 mIU/ml or less.	Luteinizing Hormone	21-23	hypertrichosis 2 (generalised, congenital)	Homo sapiens	73-76
429524-9	1979	We propose that hCG, as a weak thyroid stimulator, causes a modest rise in free thyroid hormone levels early in pregnancy which in turn causes a modest reduction in pituitary TSH secretion.	Thyrotropin	175-178	hypertrichosis 2 (generalised, congenital)	Homo sapiens	16-19
445343-4	1979	The ascitic fluid and tumor cell lysate, but not serum, contained hCG by specific assay, and the immunoreactive hCG had characteristics similar to purified hCG in filtration on Sephadex G-100.	sephadex	177-191	hypertrichosis 2 (generalised, congenital)	Homo sapiens	112-115
510226-4	1979	When testes from CdCl2 treated males were incubated in vitro with hCG, a dose and time dependent stimulation of steroidogenesis was evident.	Cadmium Chloride	17-22	hypertrichosis 2 (generalised, congenital)	Homo sapiens	66-69
572336-3	1979	Similarly, cytochalasin B, an agent that interferes with microfilament function, doubled both basal hCG secretion, and secretion of hCG stimulated by 1 mM dibutyryl cyclic AMP plus 1 mM theophylline (dbT).	Cytochalasin B	11-25	hypertrichosis 2 (generalised, congenital)	Homo sapiens	100-103
572336-3	1979	Similarly, cytochalasin B, an agent that interferes with microfilament function, doubled both basal hCG secretion, and secretion of hCG stimulated by 1 mM dibutyryl cyclic AMP plus 1 mM theophylline (dbT).	Cytochalasin B	11-25	hypertrichosis 2 (generalised, congenital)	Homo sapiens	132-135
572336-3	1979	Similarly, cytochalasin B, an agent that interferes with microfilament function, doubled both basal hCG secretion, and secretion of hCG stimulated by 1 mM dibutyryl cyclic AMP plus 1 mM theophylline (dbT).	Cyclic AMP	165-175	hypertrichosis 2 (generalised, congenital)	Homo sapiens	132-135
572336-3	1979	Similarly, cytochalasin B, an agent that interferes with microfilament function, doubled both basal hCG secretion, and secretion of hCG stimulated by 1 mM dibutyryl cyclic AMP plus 1 mM theophylline (dbT).	Theophylline	186-198	hypertrichosis 2 (generalised, congenital)	Homo sapiens	132-135
572336-3	1979	Similarly, cytochalasin B, an agent that interferes with microfilament function, doubled both basal hCG secretion, and secretion of hCG stimulated by 1 mM dibutyryl cyclic AMP plus 1 mM theophylline (dbT).	di-n-butyltin	200-203	hypertrichosis 2 (generalised, congenital)	Homo sapiens	132-135
222777-2	1979	Maximum accumulation of cyclic AMP is noted 30 minutes after addition of either human chorionic gonadotropin (hCG) or follicle stimulating hormone (FSH).	Cyclic AMP	24-34	hypertrichosis 2 (generalised, congenital)	Homo sapiens	110-113
222777-4	1979	The enhancement of intracellular cyclic AMP levels by hCG is hormone concentration dependent, with maximal stimulation observed at 10 micrograms/ml hCG.	Cyclic AMP	33-43	hypertrichosis 2 (generalised, congenital)	Homo sapiens	54-57
222777-4	1979	The enhancement of intracellular cyclic AMP levels by hCG is hormone concentration dependent, with maximal stimulation observed at 10 micrograms/ml hCG.	Cyclic AMP	33-43	hypertrichosis 2 (generalised, congenital)	Homo sapiens	148-151
218993-3	1979	Estradiol markedly inhibited (P less than 0.001) this hCG effect in luteal cells of the menstrual cycle, and this inhibition was dose dependent.	Estradiol	0-9	hypertrichosis 2 (generalised, congenital)	Homo sapiens	54-57
439071-4	1979	In immature rats this effect of hCG was dose-dependent and time-related and the accumulated fluid contained high levels of potassium and phosphate; levels of sodium, calcium and protein were similar to those in serum.	Potassium	123-132	hypertrichosis 2 (generalised, congenital)	Homo sapiens	32-35
439071-4	1979	In immature rats this effect of hCG was dose-dependent and time-related and the accumulated fluid contained high levels of potassium and phosphate; levels of sodium, calcium and protein were similar to those in serum.	Phosphates	137-146	hypertrichosis 2 (generalised, congenital)	Homo sapiens	32-35
439071-4	1979	In immature rats this effect of hCG was dose-dependent and time-related and the accumulated fluid contained high levels of potassium and phosphate; levels of sodium, calcium and protein were similar to those in serum.	Sodium	158-164	hypertrichosis 2 (generalised, congenital)	Homo sapiens	32-35
439071-4	1979	In immature rats this effect of hCG was dose-dependent and time-related and the accumulated fluid contained high levels of potassium and phosphate; levels of sodium, calcium and protein were similar to those in serum.	Calcium	166-173	hypertrichosis 2 (generalised, congenital)	Homo sapiens	32-35
221290-1	1979	This study examines the effect of preincubation of sheep ovarian follicles with hCG or FSH on the ability of isolated theca and granulosa to increase cAMP levels in response to a second incubation with hCG or FSH.	Cyclic AMP	150-154	hypertrichosis 2 (generalised, congenital)	Homo sapiens	80-83
221290-1	1979	This study examines the effect of preincubation of sheep ovarian follicles with hCG or FSH on the ability of isolated theca and granulosa to increase cAMP levels in response to a second incubation with hCG or FSH.	Cyclic AMP	150-154	hypertrichosis 2 (generalised, congenital)	Homo sapiens	202-205
221290-2	1979	Secondly, the effect of preincubation of small follicles with hCG on androstenedione and testosterone production is examined in intact follicles.	Androstenedione	69-84	hypertrichosis 2 (generalised, congenital)	Homo sapiens	62-65
221290-2	1979	Secondly, the effect of preincubation of small follicles with hCG on androstenedione and testosterone production is examined in intact follicles.	Testosterone	89-101	hypertrichosis 2 (generalised, congenital)	Homo sapiens	62-65
221290-3	1979	Preincubation with hCG resulted in a decrease in the ability of theca from large (4--6 mm in diameter) and small (1--3 mm) follicles and granulosa from large follicles to increase cAMP levels in response to a second exposure to hCG.	Cyclic AMP	180-184	hypertrichosis 2 (generalised, congenital)	Homo sapiens	19-22
221290-3	1979	Preincubation with hCG resulted in a decrease in the ability of theca from large (4--6 mm in diameter) and small (1--3 mm) follicles and granulosa from large follicles to increase cAMP levels in response to a second exposure to hCG.	Cyclic AMP	180-184	hypertrichosis 2 (generalised, congenital)	Homo sapiens	228-231
419922-5	1979	The increase in plasma testosterone levels after hCG was (median and range) 204 (83-393) ng/100 ml in the control group, whereas in the hypospadiac group a median increase of only 90 (33-272) ng/100 ml was found.	Testosterone	23-35	hypertrichosis 2 (generalised, congenital)	Homo sapiens	49-52
419922-6	1979	The difference between the median testosterone levels after hCG stimulation in the two groups investigated is statistically highly significant (P less than 0.0001).	Testosterone	34-46	hypertrichosis 2 (generalised, congenital)	Homo sapiens	60-63
571793-3	1979	hCG, but not FSH or vehicle, stimulated serum testosterone levels more than 100-fold.	Testosterone	46-58	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
122429-5	1978	Maximum testosterone levels of 2060 ng/dl (basal, 784 ng/dl) were seen 96 h after hCG administration.	Testosterone	8-20	hypertrichosis 2 (generalised, congenital)	Homo sapiens	82-85
223390-9	1979	The second phase of desensitization, which occurs after the first hour following hCG-LH-receptor interaction, is characterized by a loss of responsiveness to FSH as well as to LH and can be promoted by dibutryl cAMP (in the absence of LH).	Luteinizing Hormone	85-87	hypertrichosis 2 (generalised, congenital)	Homo sapiens	81-84
223390-9	1979	The second phase of desensitization, which occurs after the first hour following hCG-LH-receptor interaction, is characterized by a loss of responsiveness to FSH as well as to LH and can be promoted by dibutryl cAMP (in the absence of LH).	dibutryl camp	202-215	hypertrichosis 2 (generalised, congenital)	Homo sapiens	81-84
122429-7	1978	The testosterone response to hCG could be attenuated by preceding hCG administration with an injection of 17 beta-estradiol.	Testosterone	4-16	hypertrichosis 2 (generalised, congenital)	Homo sapiens	29-32
122429-7	1978	The testosterone response to hCG could be attenuated by preceding hCG administration with an injection of 17 beta-estradiol.	Testosterone	4-16	hypertrichosis 2 (generalised, congenital)	Homo sapiens	66-69
122429-7	1978	The testosterone response to hCG could be attenuated by preceding hCG administration with an injection of 17 beta-estradiol.	Estradiol	106-123	hypertrichosis 2 (generalised, congenital)	Homo sapiens	29-32
122429-7	1978	The testosterone response to hCG could be attenuated by preceding hCG administration with an injection of 17 beta-estradiol.	Estradiol	106-123	hypertrichosis 2 (generalised, congenital)	Homo sapiens	66-69
34508-12	1978	At pH 7.4, the cross-reactivity of normal human gamma-globulin, bovine thyroglobulin, and pure hCG with bTSH binding to both lymphocytes and thyroid cells was below 1%.	btsh	104-108	hypertrichosis 2 (generalised, congenital)	Homo sapiens	95-98
719103-0	1978	Effects of oxytocin antiserum and of indomethacin on hCG-induced ovulation in the rabbit.	Indomethacin	37-49	hypertrichosis 2 (generalised, congenital)	Homo sapiens	53-56
722669-3	1978	Addition of hCG to the culture medium stimulated progesterone production in a biphasic manner.	Progesterone	49-61	hypertrichosis 2 (generalised, congenital)	Homo sapiens	12-15
712699-3	1978	The assays are sensitive, reproducible and precise and should be both economical and convenient for studies on the relationship between the molecular structure and the biological activity of hCG and LH.	Luteinizing Hormone	199-201	hypertrichosis 2 (generalised, congenital)	Homo sapiens	191-194
217642-1	1978	Removal of the sugar residues internal to sialic acid from the hCG molecule markedly diminished the ability of hCG to stimulate cAMP accumulation by porcine granulosa cells during a 30-min incubation period.	Sugars	15-20	hypertrichosis 2 (generalised, congenital)	Homo sapiens	63-66
217642-1	1978	Removal of the sugar residues internal to sialic acid from the hCG molecule markedly diminished the ability of hCG to stimulate cAMP accumulation by porcine granulosa cells during a 30-min incubation period.	Sugars	15-20	hypertrichosis 2 (generalised, congenital)	Homo sapiens	111-114
217642-1	1978	Removal of the sugar residues internal to sialic acid from the hCG molecule markedly diminished the ability of hCG to stimulate cAMP accumulation by porcine granulosa cells during a 30-min incubation period.	N-Acetylneuraminic Acid	42-53	hypertrichosis 2 (generalised, congenital)	Homo sapiens	63-66
217642-1	1978	Removal of the sugar residues internal to sialic acid from the hCG molecule markedly diminished the ability of hCG to stimulate cAMP accumulation by porcine granulosa cells during a 30-min incubation period.	N-Acetylneuraminic Acid	42-53	hypertrichosis 2 (generalised, congenital)	Homo sapiens	111-114
217642-1	1978	Removal of the sugar residues internal to sialic acid from the hCG molecule markedly diminished the ability of hCG to stimulate cAMP accumulation by porcine granulosa cells during a 30-min incubation period.	Cyclic AMP	128-132	hypertrichosis 2 (generalised, congenital)	Homo sapiens	63-66
217642-1	1978	Removal of the sugar residues internal to sialic acid from the hCG molecule markedly diminished the ability of hCG to stimulate cAMP accumulation by porcine granulosa cells during a 30-min incubation period.	Cyclic AMP	128-132	hypertrichosis 2 (generalised, congenital)	Homo sapiens	111-114
217642-2	1978	At the same time, removal of sugars internal to sialic acid enabled the resulting hCG derivatives to become competitive inhibitors of hCG stimulation of cAMP accumulation.	Sugars	29-35	hypertrichosis 2 (generalised, congenital)	Homo sapiens	82-85
217642-2	1978	At the same time, removal of sugars internal to sialic acid enabled the resulting hCG derivatives to become competitive inhibitors of hCG stimulation of cAMP accumulation.	Sugars	29-35	hypertrichosis 2 (generalised, congenital)	Homo sapiens	134-137
217642-2	1978	At the same time, removal of sugars internal to sialic acid enabled the resulting hCG derivatives to become competitive inhibitors of hCG stimulation of cAMP accumulation.	N-Acetylneuraminic Acid	48-59	hypertrichosis 2 (generalised, congenital)	Homo sapiens	82-85
217642-2	1978	At the same time, removal of sugars internal to sialic acid enabled the resulting hCG derivatives to become competitive inhibitors of hCG stimulation of cAMP accumulation.	N-Acetylneuraminic Acid	48-59	hypertrichosis 2 (generalised, congenital)	Homo sapiens	134-137
217642-2	1978	At the same time, removal of sugars internal to sialic acid enabled the resulting hCG derivatives to become competitive inhibitors of hCG stimulation of cAMP accumulation.	Cyclic AMP	153-157	hypertrichosis 2 (generalised, congenital)	Homo sapiens	82-85
217642-2	1978	At the same time, removal of sugars internal to sialic acid enabled the resulting hCG derivatives to become competitive inhibitors of hCG stimulation of cAMP accumulation.	Cyclic AMP	153-157	hypertrichosis 2 (generalised, congenital)	Homo sapiens	134-137
217642-4	1978	It would, therefore, seem that hCG with sugars internal to sialic acid removed is able to bind to the receptor, but that, once bound, it is unable to activate adenylate cyclase.	Sugars	40-46	hypertrichosis 2 (generalised, congenital)	Homo sapiens	31-34
217642-4	1978	It would, therefore, seem that hCG with sugars internal to sialic acid removed is able to bind to the receptor, but that, once bound, it is unable to activate adenylate cyclase.	N-Acetylneuraminic Acid	59-70	hypertrichosis 2 (generalised, congenital)	Homo sapiens	31-34
217642-5	1978	Under these conditions, it can also act as a competitive inhibitor of hCG stimulation of cAMP accumulation.	Cyclic AMP	89-93	hypertrichosis 2 (generalised, congenital)	Homo sapiens	70-73
217640-5	1978	Testicular and thyroid TSH-binding sites also appeared to demonstrate a similar degree of cross-reactivity with a crude preparation of hCG.	Thyrotropin	23-26	hypertrichosis 2 (generalised, congenital)	Homo sapiens	135-138
217636-1	1978	Previously, we have shown that preparations of hCG bind to bovine thyroid membranes, as judged from their ability both to inhibit the binding of 125I-labeled bovine TSH (bTSH) and to activate adenylate cyclase (Amir, S.M., H. Uchimura, and S.H.	Iodine-125	145-149	hypertrichosis 2 (generalised, congenital)	Homo sapiens	47-50
217640-7	1978	Furthermore, the ability of hCG to inhibit the binding of TSH to thyroid membranes provides a possible mechanism for the known thyroid-stimulating properties of hCG.	Thyrotropin	58-61	hypertrichosis 2 (generalised, congenital)	Homo sapiens	28-31
217636-1	1978	Previously, we have shown that preparations of hCG bind to bovine thyroid membranes, as judged from their ability both to inhibit the binding of 125I-labeled bovine TSH (bTSH) and to activate adenylate cyclase (Amir, S.M., H. Uchimura, and S.H.	Thyrotropin	165-168	hypertrichosis 2 (generalised, congenital)	Homo sapiens	47-50
217640-7	1978	Furthermore, the ability of hCG to inhibit the binding of TSH to thyroid membranes provides a possible mechanism for the known thyroid-stimulating properties of hCG.	Thyrotropin	58-61	hypertrichosis 2 (generalised, congenital)	Homo sapiens	161-164
217636-12	1978	Purified bTSH inhibited the binding of [125I]hCG to testis particulate fraction but contained only about 2% of the activity of purified hCG.	btsh	9-13	hypertrichosis 2 (generalised, congenital)	Homo sapiens	45-48
217636-13	1978	Lineweaver-Burk analysis suggested that inhibition of [125I]hCG binding by bTSH was competitive in nature.	btsh	75-79	hypertrichosis 2 (generalised, congenital)	Homo sapiens	60-63
357717-3	1978	Ovulation was restored by injection of hCG and the inhibition was associated with reduced cyclic and tonic LH secretion while hypophysial LH levels were generally unaffected.	Luteinizing Hormone	107-109	hypertrichosis 2 (generalised, congenital)	Homo sapiens	39-42
217636-16	1978	bTSH, like hCG, is capable of stimulating the production of cAMP in rat Leydig cells, but is much less potent than hCG in this regard.	Cyclic AMP	60-64	hypertrichosis 2 (generalised, congenital)	Homo sapiens	11-14
162472-4	1978	A significant increase in DHAS production was observed in the presence of hCG.	Dehydroepiandrosterone Sulfate	26-30	hypertrichosis 2 (generalised, congenital)	Homo sapiens	74-77
573768-3	1978	No significant differences were found between baseline levels of 17-OHP, delta, DHEA, DHEAS, A-diol, and F. After hCG stimulation between T, DHT, E2 and 17-OHP levels showed a significant increase in the two groups of subjects.	Dehydroepiandrosterone	80-84	hypertrichosis 2 (generalised, congenital)	Homo sapiens	114-117
573768-3	1978	No significant differences were found between baseline levels of 17-OHP, delta, DHEA, DHEAS, A-diol, and F. After hCG stimulation between T, DHT, E2 and 17-OHP levels showed a significant increase in the two groups of subjects.	diol	95-99	hypertrichosis 2 (generalised, congenital)	Homo sapiens	114-117
573768-3	1978	No significant differences were found between baseline levels of 17-OHP, delta, DHEA, DHEAS, A-diol, and F. After hCG stimulation between T, DHT, E2 and 17-OHP levels showed a significant increase in the two groups of subjects.	Dihydrotestosterone	141-144	hypertrichosis 2 (generalised, congenital)	Homo sapiens	114-117
573768-3	1978	No significant differences were found between baseline levels of 17-OHP, delta, DHEA, DHEAS, A-diol, and F. After hCG stimulation between T, DHT, E2 and 17-OHP levels showed a significant increase in the two groups of subjects.	17-alpha-Hydroxyprogesterone	153-159	hypertrichosis 2 (generalised, congenital)	Homo sapiens	114-117
162472-6	1978	In the presence of hCG (250 ng/ml), DHAS secretion increased significantly (P less than 0.01) over the controls to 116 +/- 12.0 at 120 min, and remained above the controls thereafter.	Dehydroepiandrosterone Sulfate	36-40	hypertrichosis 2 (generalised, congenital)	Homo sapiens	19-22
162472-7	1978	These results support the hypothesis that hCG is one of the regulators of DHAS production by the human fetal adrenal gland early in gestation.	Dehydroepiandrosterone Sulfate	74-78	hypertrichosis 2 (generalised, congenital)	Homo sapiens	42-45
628528-4	1978	From the response patterns of steroidogenesis, four functional stages of follicular development can be distinguished, each subsequent stage being characterized by an increasing spontaneous estradiol production and a decreasing capacity to produce extra estradiol in response to stimulation with additional hCG.	Estradiol	253-262	hypertrichosis 2 (generalised, congenital)	Homo sapiens	306-309
259039-4	1978	In primates at least, neutralization of the biological effects of CG during this critical period results in a reduction of blood progesterone levels and the interruption of pregnancy.	Progesterone	129-141	hypertrichosis 2 (generalised, congenital)	Homo sapiens	66-68
202706-3	1978	The LH/hCG binding "sites" may be related to the initiation of steroidogenesis in the embryo.	Luteinizing Hormone	4-6	hypertrichosis 2 (generalised, congenital)	Homo sapiens	7-10
663870-0	1978	Ovulation induction stimulated with HCG in functional sterility patients treated with clomiphene.	Clomiphene	86-96	hypertrichosis 2 (generalised, congenital)	Homo sapiens	36-39
201452-0	1977	Potent inhibitory activity of [D-Leu6, Des-Gly-NH2(10)]LHRH ethylamide on LH/hCG and PRL testicular receptor levels in the rat.	[d-leu6	30-37	hypertrichosis 2 (generalised, congenital)	Homo sapiens	77-108
201452-0	1977	Potent inhibitory activity of [D-Leu6, Des-Gly-NH2(10)]LHRH ethylamide on LH/hCG and PRL testicular receptor levels in the rat.	des-gly-nh2(10)]lhrh ethylamide	39-70	hypertrichosis 2 (generalised, congenital)	Homo sapiens	77-108
201969-6	1977	Administration of hCG in vivo or incubation with LH in vitro did not elevate endogenous ovarian free arachidonate, while PGE production was enhanced.	Prostaglandins E	121-124	hypertrichosis 2 (generalised, congenital)	Homo sapiens	18-21
201969-7	1977	Dexamethasone prevented this stimulatory effect of hCG.	Dexamethasone	0-13	hypertrichosis 2 (generalised, congenital)	Homo sapiens	51-54
593833-6	1977	The specific assay of hCG with an anti beta-hCG antiserum enables the resolution of diagnostic problems raised by the cross-reaction of hypopituitary LH when using the classic antiserum and particularly the differential diagnosis between the retention of trophoblastic tissue and a beginning pregnancy immediately following a mole, or a high level of LH after castration.	Luteinizing Hormone	150-152	hypertrichosis 2 (generalised, congenital)	Homo sapiens	22-25
593833-6	1977	The specific assay of hCG with an anti beta-hCG antiserum enables the resolution of diagnostic problems raised by the cross-reaction of hypopituitary LH when using the classic antiserum and particularly the differential diagnosis between the retention of trophoblastic tissue and a beginning pregnancy immediately following a mole, or a high level of LH after castration.	Luteinizing Hormone	150-152	hypertrichosis 2 (generalised, congenital)	Homo sapiens	44-47
593833-6	1977	The specific assay of hCG with an anti beta-hCG antiserum enables the resolution of diagnostic problems raised by the cross-reaction of hypopituitary LH when using the classic antiserum and particularly the differential diagnosis between the retention of trophoblastic tissue and a beginning pregnancy immediately following a mole, or a high level of LH after castration.	Luteinizing Hormone	351-353	hypertrichosis 2 (generalised, congenital)	Homo sapiens	22-25
199069-1	1977	Ovarian follicles removed from immature rats (preantral follicles) and immature rats treated in vivo with follicle stimulating hormone (FSH) (antral follicles) released progesterone in vitro in response to either human chorionic gonadotropin (hCG), hFSH, or DBcAMP in a time- and concentration-dependent fashion.	Progesterone	169-181	hypertrichosis 2 (generalised, congenital)	Homo sapiens	243-246
410075-2	1977	Animals treated with either PG after pretreatment with human chorionic gonadotropin (hCG) had peripheral plasma progesterone concentrations that were not statistically different from those in animals treated with hCG and vehicle.	pg	28-30	hypertrichosis 2 (generalised, congenital)	Homo sapiens	85-88
410075-2	1977	Animals treated with either PG after pretreatment with human chorionic gonadotropin (hCG) had peripheral plasma progesterone concentrations that were not statistically different from those in animals treated with hCG and vehicle.	Progesterone	112-124	hypertrichosis 2 (generalised, congenital)	Homo sapiens	85-88
195801-5	1977	During incubation with hCG, cyclic AMP and testosterone responses of purified Leydig cells were considerably increased, and hCG concentrations as low as 0.2 pM caused activation of cAMP-dependent protein kinase.	Cyclic AMP	28-38	hypertrichosis 2 (generalised, congenital)	Homo sapiens	23-26
195801-5	1977	During incubation with hCG, cyclic AMP and testosterone responses of purified Leydig cells were considerably increased, and hCG concentrations as low as 0.2 pM caused activation of cAMP-dependent protein kinase.	Testosterone	43-55	hypertrichosis 2 (generalised, congenital)	Homo sapiens	23-26
885121-3	1977	Ten microgram of testosterone or 5alpha-dihydrotestosterone dissolved in NRS administered iv 1 h after simultaneous injection of hCG and antiserum to progesterone (anti-P) restored ovulation that would otherwise have been blocked by anti-P, with a comparable number of ova to control animals not given anti-P.	Testosterone	17-29	hypertrichosis 2 (generalised, congenital)	Homo sapiens	129-132
885121-3	1977	Ten microgram of testosterone or 5alpha-dihydrotestosterone dissolved in NRS administered iv 1 h after simultaneous injection of hCG and antiserum to progesterone (anti-P) restored ovulation that would otherwise have been blocked by anti-P, with a comparable number of ova to control animals not given anti-P.	Dihydrotestosterone	33-59	hypertrichosis 2 (generalised, congenital)	Homo sapiens	129-132
876553-1	1977	It is assumed that one function of hCG is to preserve the developing corpus luteum and maintain pregnancy by producing progesterone and thus preventing menstrual shedding.	Progesterone	119-131	hypertrichosis 2 (generalised, congenital)	Homo sapiens	35-38
6246660-2	1980	In the first experiment, cells were pre-incubated in TR, then incubated at 37 degrees C for 3h with human chorionic gonadotropin (hCG) after the addition of soybean-trypsin inhibitor (STI).	Tritium	92-94	hypertrichosis 2 (generalised, congenital)	Homo sapiens	130-133
6246660-4	1980	Cells that were preincubated with TR responded to hCG stimulation with increased progesterone secretion (P less than 0.01) in a fashion similar to untreated cells.	Progesterone	81-93	hypertrichosis 2 (generalised, congenital)	Homo sapiens	50-53
6246660-6	1980	However, continuous exposure (3h) of cells to TR significantly depressed (P less than 0.01) basal P secretion and inhibited the response to hCG.	Tritium	30-32	hypertrichosis 2 (generalised, congenital)	Homo sapiens	140-143
325991-4	1977	While basal testosterone was similar in the two groups of children, after hCG testosterone was significantly (p less than 0.001) lower in the obese boys, In the normal children a significant positive correlation between bone age and basal and after hCG testosterone was demonstrated; this correlation was not found in the obese boys.	Testosterone	78-90	hypertrichosis 2 (generalised, congenital)	Homo sapiens	74-77
325991-4	1977	While basal testosterone was similar in the two groups of children, after hCG testosterone was significantly (p less than 0.001) lower in the obese boys, In the normal children a significant positive correlation between bone age and basal and after hCG testosterone was demonstrated; this correlation was not found in the obese boys.	Testosterone	78-90	hypertrichosis 2 (generalised, congenital)	Homo sapiens	74-77
849732-6	1977	Addition of 200 IU of human chorionic gonadotropin (hCG) in vitro to normal basal zone placentae sharply increased the production of progesterone, 17alpha-hydroxyprogesterone, androstenedione and 5alpha-pregnane-3,20-dione.	Progesterone	133-145	hypertrichosis 2 (generalised, congenital)	Homo sapiens	52-55
849732-6	1977	Addition of 200 IU of human chorionic gonadotropin (hCG) in vitro to normal basal zone placentae sharply increased the production of progesterone, 17alpha-hydroxyprogesterone, androstenedione and 5alpha-pregnane-3,20-dione.	17-alpha-Hydroxyprogesterone	147-174	hypertrichosis 2 (generalised, congenital)	Homo sapiens	52-55
849732-6	1977	Addition of 200 IU of human chorionic gonadotropin (hCG) in vitro to normal basal zone placentae sharply increased the production of progesterone, 17alpha-hydroxyprogesterone, androstenedione and 5alpha-pregnane-3,20-dione.	Androstenedione	176-191	hypertrichosis 2 (generalised, congenital)	Homo sapiens	52-55
849732-6	1977	Addition of 200 IU of human chorionic gonadotropin (hCG) in vitro to normal basal zone placentae sharply increased the production of progesterone, 17alpha-hydroxyprogesterone, androstenedione and 5alpha-pregnane-3,20-dione.	5-alpha-Dihydroprogesterone	196-222	hypertrichosis 2 (generalised, congenital)	Homo sapiens	52-55
192755-1	1977	The role of hCG in the regulation of testicular steroid production in human fetuses from 14 to 20 weeks gestational age was studied.	Steroids	48-55	hypertrichosis 2 (generalised, congenital)	Homo sapiens	12-15
192755-2	1977	Saturable binding of 125I-hCG to testicular homogenates was demonstrated, and physiologic concentrations of hCG were able to stimulate testosterone formation in testicular minces without the addition of exogenous precursors.	Testosterone	135-147	hypertrichosis 2 (generalised, congenital)	Homo sapiens	108-111
192755-7	1977	The greatest increase in testosterone production occurred when the hCG concentration was increased from 0.5 to 5 ng/ml.	Testosterone	25-37	hypertrichosis 2 (generalised, congenital)	Homo sapiens	67-70
192755-10	1977	It is concluded that human fetal testes bind hCG, and that physiologic levels of hCG stimulate fetal testicular testosterone formation in vitro at this stage of gestation.	Testosterone	112-124	hypertrichosis 2 (generalised, congenital)	Homo sapiens	81-84
122597-8	1977	Testosterone levels in the perfusate rose for 90 min in response to hCG.	Testosterone	0-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	68-71
122597-9	1977	There was a dose-response relationship between hCG (20-1000 mIU/ml of medium) and testosterone levels at 90 min.	Testosterone	82-94	hypertrichosis 2 (generalised, congenital)	Homo sapiens	47-50
20414-7	1977	Gonadotropin treatment was successful in 20 patients, clomiphene-hCG in two, tamoxifen in two, bromocriptine in two, and combined bromocriptine and clomiphene in one.	Clomiphene	54-64	hypertrichosis 2 (generalised, congenital)	Homo sapiens	65-68
188702-3	1977	However, it was demonstrated that (a) the hCGs used were biologically active since they stimulated cAMP and testosterone production by rat Leydig cells, and (b) there are receptor sites on the rat ovary that bind [125I]hCG and recognize rat luteinizing hormone (LH).	Cyclic AMP	99-103	hypertrichosis 2 (generalised, congenital)	Homo sapiens	42-45
188702-3	1977	However, it was demonstrated that (a) the hCGs used were biologically active since they stimulated cAMP and testosterone production by rat Leydig cells, and (b) there are receptor sites on the rat ovary that bind [125I]hCG and recognize rat luteinizing hormone (LH).	Testosterone	108-120	hypertrichosis 2 (generalised, congenital)	Homo sapiens	42-45
63368-2	1976	The results indicate that this cross-reaction is incomplete and that the anti-oLH sera used have the ability to distinguish between LH and hCG.	Luteinizing Hormone	79-81	hypertrichosis 2 (generalised, congenital)	Homo sapiens	139-142
1001265-0	1976	FSH and testosterone levels in the plasma of juvenile male rats after application of ovine FSH, HCG and PMS at different ages.	Testosterone	8-20	hypertrichosis 2 (generalised, congenital)	Homo sapiens	96-99
1001265-3	1976	Plasma testosterone increases after application of hCG and PMS, not ovine FSH.	Testosterone	7-19	hypertrichosis 2 (generalised, congenital)	Homo sapiens	51-54
939193-7	1976	hCG-induced desensitization was rapid (50% loss of LH-stimulated activity was obtained within 5 min of injection), was dose-dependent, requiring an ovulatory dose; was selective for LH- and FSH-stimulated activity, being without effect on basal and PGE1 as well as NaF-stimulated activities; and was induced specifically by LH (mating) and hCG-FSH and PRL being without effect.	Luteinizing Hormone	51-53	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
939193-7	1976	hCG-induced desensitization was rapid (50% loss of LH-stimulated activity was obtained within 5 min of injection), was dose-dependent, requiring an ovulatory dose; was selective for LH- and FSH-stimulated activity, being without effect on basal and PGE1 as well as NaF-stimulated activities; and was induced specifically by LH (mating) and hCG-FSH and PRL being without effect.	Luteinizing Hormone	51-53	hypertrichosis 2 (generalised, congenital)	Homo sapiens	340-343
939193-7	1976	hCG-induced desensitization was rapid (50% loss of LH-stimulated activity was obtained within 5 min of injection), was dose-dependent, requiring an ovulatory dose; was selective for LH- and FSH-stimulated activity, being without effect on basal and PGE1 as well as NaF-stimulated activities; and was induced specifically by LH (mating) and hCG-FSH and PRL being without effect.	Luteinizing Hormone	182-184	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
939193-7	1976	hCG-induced desensitization was rapid (50% loss of LH-stimulated activity was obtained within 5 min of injection), was dose-dependent, requiring an ovulatory dose; was selective for LH- and FSH-stimulated activity, being without effect on basal and PGE1 as well as NaF-stimulated activities; and was induced specifically by LH (mating) and hCG-FSH and PRL being without effect.	Alprostadil	249-253	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
939193-7	1976	hCG-induced desensitization was rapid (50% loss of LH-stimulated activity was obtained within 5 min of injection), was dose-dependent, requiring an ovulatory dose; was selective for LH- and FSH-stimulated activity, being without effect on basal and PGE1 as well as NaF-stimulated activities; and was induced specifically by LH (mating) and hCG-FSH and PRL being without effect.	Sodium Fluoride	265-268	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
939193-7	1976	hCG-induced desensitization was rapid (50% loss of LH-stimulated activity was obtained within 5 min of injection), was dose-dependent, requiring an ovulatory dose; was selective for LH- and FSH-stimulated activity, being without effect on basal and PGE1 as well as NaF-stimulated activities; and was induced specifically by LH (mating) and hCG-FSH and PRL being without effect.	Luteinizing Hormone	182-184	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
939193-13	1976	The injection of ovulatory doses of hCG into 6-day PSP rabbits produced, within 2 h, a 50% desensitization of the luteal AC systems to LH stimulation.	Luteinizing Hormone	135-137	hypertrichosis 2 (generalised, congenital)	Homo sapiens	36-39
939195-5	1976	At least a 50% decline in the LH-stimulated AC system was demonstrable 2 h after the hCG injection in CL obtained during PSP and the first 18 days of pregnancy.	Luteinizing Hormone	30-32	hypertrichosis 2 (generalised, congenital)	Homo sapiens	85-88
939195-9	1976	hCG-induced desensitization of CL adenylyl cyclase in rabbits was prevented neither by cauterization of tertiary follicles not by the continued administration of estradiol-17beta (1.5 mug SC twice daily), suggesting that this effect of hCG is due to a direct interaction with the CL, and not due to interruption of the follicular estrogen supply.	Estradiol	162-178	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
1264402-2	1976	Phenol in quantities comparable to its concentration in commercial lyophilized APL hCG also completely inhibited all three mitogenic responses.	Phenol	0-6	hypertrichosis 2 (generalised, congenital)	Homo sapiens	83-86
1264403-12	1976	4)The levels of 17-P were elevated in both patients, did not suppress on Dex, and increased markedly following hCG, suggesting the ovary as the source of excess 17-P.	17-p	16-20	hypertrichosis 2 (generalised, congenital)	Homo sapiens	111-114
954680-7	1976	3H-proline was almost exclusively incorporated into the large immunologic forms of hCG, hCGalpha and hCGbeta within the chrionic tissue during the 5-hour exposure.	3h-proline	0-10	hypertrichosis 2 (generalised, congenital)	Homo sapiens	83-86
954680-9	1976	After a 15-minute pulse, the 3H-radioactivity peak within the chorionic tissue appeared in the void volume, conicidental with hCG immunoreactivity.	Tritium	29-31	hypertrichosis 2 (generalised, congenital)	Homo sapiens	126-129
954680-10	1976	During the chase period, there was shift of the 3H-radioactivity peak associated with hCG immunoreactivity from the void volume to the more retarded area.	Tritium	48-50	hypertrichosis 2 (generalised, congenital)	Homo sapiens	86-89
954680-12	1976	Within the media after 3-hour chase, no labeled hCG peak associated with 3H-radioactivity was more retarded on Sephadex G-100 than that within the tissue extract after the 15-MINUTE pulse.	sephadex	111-125	hypertrichosis 2 (generalised, congenital)	Homo sapiens	48-51
954680-14	1976	In the culture of molar trophoblastic tissues after a 15-minute pulse, considerable amounts of hCG and its subunits accompanied by high 3H-radioactively had already been secreted into the media.	Tritium	136-138	hypertrichosis 2 (generalised, congenital)	Homo sapiens	95-98
986960-7	1976	A peak in the overall incorporation of 14C- acetate into the ten steroids at the 3rd hour after hCG injection, followed by gradual decrease up to the 9th hour was observed.	14c- acetate	39-51	hypertrichosis 2 (generalised, congenital)	Homo sapiens	96-99
986960-7	1976	A peak in the overall incorporation of 14C- acetate into the ten steroids at the 3rd hour after hCG injection, followed by gradual decrease up to the 9th hour was observed.	Steroids	65-73	hypertrichosis 2 (generalised, congenital)	Homo sapiens	96-99
986960-9	1976	Comparable quantitative fluctuations were found with the fractionated incorporation of 14C-acetate into the C21 and C18 steroids in the time sequence following hCG injection.	14c-acetate	87-98	hypertrichosis 2 (generalised, congenital)	Homo sapiens	160-163
986960-9	1976	Comparable quantitative fluctuations were found with the fractionated incorporation of 14C-acetate into the C21 and C18 steroids in the time sequence following hCG injection.	Steroids	120-128	hypertrichosis 2 (generalised, congenital)	Homo sapiens	160-163
986960-10	1976	However, the fractionated incorporation into C19 steroids reached to a maximum at the 6th hour after hCG injection.	Steroids	49-57	hypertrichosis 2 (generalised, congenital)	Homo sapiens	101-104
986960-13	1976	Divergent steroids were formed from radioactive acetate at the 3rd hour after hCG injection.	Steroids	10-18	hypertrichosis 2 (generalised, congenital)	Homo sapiens	78-81
986960-16	1976	The three androgens were the major steroids formed at the 12th hour after hCG injection.	Steroids	35-43	hypertrichosis 2 (generalised, congenital)	Homo sapiens	74-77
823055-5	1975	T-hCG-C was poorer in aspartic acid and glycine, and richer in serine, threonine and tyrosin to which carbohydrates bind than hCFSH from normal pregnancy.	Carbohydrates	102-115	hypertrichosis 2 (generalised, congenital)	Homo sapiens	2-5
1008504-3	1976	Administration of h CG at pharmacological doses for three days to male rat during puberty increases plasma testosterone levels and 3H-thymidine incorporation into testicular DNA.	Testosterone	107-119	hypertrichosis 2 (generalised, congenital)	Homo sapiens	20-22
1008504-3	1976	Administration of h CG at pharmacological doses for three days to male rat during puberty increases plasma testosterone levels and 3H-thymidine incorporation into testicular DNA.	3h-thymidine	131-143	hypertrichosis 2 (generalised, congenital)	Homo sapiens	20-22
1008504-4	1976	Simultaneous administration of dexamethasone partially blocks both effects of hCG.	Dexamethasone	31-44	hypertrichosis 2 (generalised, congenital)	Homo sapiens	78-81
823055-5	1975	T-hCG-C was poorer in aspartic acid and glycine, and richer in serine, threonine and tyrosin to which carbohydrates bind than hCFSH from normal pregnancy.	Aspartic Acid	22-35	hypertrichosis 2 (generalised, congenital)	Homo sapiens	2-5
1122878-1	1975	Inhibition by antiestradiol serum of ovarian weight gain and follicular growth in hypophysectomized immature rats given FSH and hCG suggested that gonadotrophin induced endogenous estrogen secretion plays a role in the ovarian augmentation reaction.	antiestradiol	14-27	hypertrichosis 2 (generalised, congenital)	Homo sapiens	128-131
1168129-2	1975	At all ages studied, testosterone production was significantly elevated in the presence of hCG.	Testosterone	21-33	hypertrichosis 2 (generalised, congenital)	Homo sapiens	91-94
1132164-5	1975	Administration of hCG produced qualitatively normal acute responses of testosterone and estrogens.	Testosterone	71-83	hypertrichosis 2 (generalised, congenital)	Homo sapiens	18-21
1091731-8	1975	After HCG treatment, the level of testosterone rose threefold within 30 min and did not decline during the experiment, but there was no effect on the LH level.	Testosterone	34-46	hypertrichosis 2 (generalised, congenital)	Homo sapiens	6-9
1091731-11	1975	Treatment with Gn-RH results in a rise in both the testosterone and LH levels, but only testosterone is affected by HCG.	Testosterone	88-100	hypertrichosis 2 (generalised, congenital)	Homo sapiens	116-119
4153231-0	1974	[Plasma levels of testosterone and estradiol in prepuberal children with cryptorchism and anorchia before and after administration of HCG].	Testosterone	18-30	hypertrichosis 2 (generalised, congenital)	Homo sapiens	134-137
4344363-0	1973	Stimulation of cyclic AMP production by the rat testis during incubation with hCG in vitro.	Cyclic AMP	15-25	hypertrichosis 2 (generalised, congenital)	Homo sapiens	78-81
5063546-0	1972	Biological properties of hCG after removal of terminal sialic acid and galactose residues.	N-Acetylneuraminic Acid	55-66	hypertrichosis 2 (generalised, congenital)	Homo sapiens	25-28
5063546-0	1972	Biological properties of hCG after removal of terminal sialic acid and galactose residues.	Galactose	71-80	hypertrichosis 2 (generalised, congenital)	Homo sapiens	25-28
33688893-3	2021	Herein, double-carbon confined cobalt germanium hydroxide (CGH@C/rGO) composites has been facilely synthesized with the supportion of l-ascorbic acid and graphene oxide (GO) as anode materials for sodium-ion storage.	Carbon	15-21	hypertrichosis 2 (generalised, congenital)	Homo sapiens	59-62
33688893-3	2021	Herein, double-carbon confined cobalt germanium hydroxide (CGH@C/rGO) composites has been facilely synthesized with the supportion of l-ascorbic acid and graphene oxide (GO) as anode materials for sodium-ion storage.	cobalt germanium hydroxide	31-57	hypertrichosis 2 (generalised, congenital)	Homo sapiens	59-62
33688893-3	2021	Herein, double-carbon confined cobalt germanium hydroxide (CGH@C/rGO) composites has been facilely synthesized with the supportion of l-ascorbic acid and graphene oxide (GO) as anode materials for sodium-ion storage.	Ascorbic Acid	134-149	hypertrichosis 2 (generalised, congenital)	Homo sapiens	59-62
33688893-3	2021	Herein, double-carbon confined cobalt germanium hydroxide (CGH@C/rGO) composites has been facilely synthesized with the supportion of l-ascorbic acid and graphene oxide (GO) as anode materials for sodium-ion storage.	graphene oxide	154-168	hypertrichosis 2 (generalised, congenital)	Homo sapiens	59-62
33688893-3	2021	Herein, double-carbon confined cobalt germanium hydroxide (CGH@C/rGO) composites has been facilely synthesized with the supportion of l-ascorbic acid and graphene oxide (GO) as anode materials for sodium-ion storage.	graphene oxide	66-68	hypertrichosis 2 (generalised, congenital)	Homo sapiens	59-62
33688893-3	2021	Herein, double-carbon confined cobalt germanium hydroxide (CGH@C/rGO) composites has been facilely synthesized with the supportion of l-ascorbic acid and graphene oxide (GO) as anode materials for sodium-ion storage.	Sodium	197-203	hypertrichosis 2 (generalised, congenital)	Homo sapiens	59-62
33688893-6	2021	Such outstanding electrochemical performance could be accredited to a strong interaction between CGH, carbon, and graphene, which increases the electronic conductivity, relieves the volume expansion aroused by sodiation/desodiation, shortens the pathway of electron/ion transportation that further improving the reaction kinetics and endowing the material with remarkable cycling capability.	Carbon	102-108	hypertrichosis 2 (generalised, congenital)	Homo sapiens	97-100
33688893-6	2021	Such outstanding electrochemical performance could be accredited to a strong interaction between CGH, carbon, and graphene, which increases the electronic conductivity, relieves the volume expansion aroused by sodiation/desodiation, shortens the pathway of electron/ion transportation that further improving the reaction kinetics and endowing the material with remarkable cycling capability.	Graphite	114-122	hypertrichosis 2 (generalised, congenital)	Homo sapiens	97-100
32696218-10	2020	However, the association of nanoprogesterone with hCG causes the cellular death of initial follicles but shows efficacy in IVM.	nanoprogesterone	28-44	hypertrichosis 2 (generalised, congenital)	Homo sapiens	50-53
32603965-9	2020	As synthesized user friendly microcleaner (HTC-2) exhibits maximum adsorption capacity (qmax) of 564.97 mg g-1 for EBT dye at pH 4.	Eriochrome Black T	115-118	hypertrichosis 2 (generalised, congenital)	Homo sapiens	43-48
32581156-5	2020	hCG treatment significantly increased CL diameter on day 7 and plasma P4 concentration on days 7 and 14 in the contralateral group, but not the ipsilateral group.	propiverine	70-72	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
32141676-9	2020	Level of hCG pre-dactinomycin remained a significant risk-factor in multivariate analysis (OR 2.93(95% CI 1.02 - 8.40) p=0.045.	Dactinomycin	17-29	hypertrichosis 2 (generalised, congenital)	Homo sapiens	9-12
32500221-1	2020	PURPOSE: In a low-risk gestational trophoblastic neoplasia (GTN) treated with methotrexate (MTX), the modeled hCG (human chorionic gonadotropin) residual concentration (hCGres), calculated with NONMEM program  (NM) during the first 50 treatment days, is a predictor of MTX-resistance risk.	Methotrexate	78-90	hypertrichosis 2 (generalised, congenital)	Homo sapiens	110-113
32500221-1	2020	PURPOSE: In a low-risk gestational trophoblastic neoplasia (GTN) treated with methotrexate (MTX), the modeled hCG (human chorionic gonadotropin) residual concentration (hCGres), calculated with NONMEM program  (NM) during the first 50 treatment days, is a predictor of MTX-resistance risk.	Methotrexate	92-95	hypertrichosis 2 (generalised, congenital)	Homo sapiens	110-113
32500221-1	2020	PURPOSE: In a low-risk gestational trophoblastic neoplasia (GTN) treated with methotrexate (MTX), the modeled hCG (human chorionic gonadotropin) residual concentration (hCGres), calculated with NONMEM program  (NM) during the first 50 treatment days, is a predictor of MTX-resistance risk.	Methotrexate	269-272	hypertrichosis 2 (generalised, congenital)	Homo sapiens	110-113
32500221-10	2020	The website is meant to help clinicians in the interpretation of hCG decline curves of MTX-treated GTN patients.	Methotrexate	87-90	hypertrichosis 2 (generalised, congenital)	Homo sapiens	65-68
32472447-0	2020	Is the probability of pregnancy after ovarian stimulation for IVF associated with serum estradiol levels on the day of triggering final oocyte maturation with hCG?	Estradiol	88-97	hypertrichosis 2 (generalised, congenital)	Homo sapiens	159-162
32472447-2	2020	PURPOSE: The objective of this systematic review and metaanalysis was to examine if the probability of pregnancy after ovarian stimulation for in vitro fertilization (IVF), using GnRH analogues and gonadotrophins is associated with serum estradiol level (Epsilon2) on the day of triggering final oocyte maturation with human chorionic gonadotrophin (hCG).	Estradiol	238-247	hypertrichosis 2 (generalised, congenital)	Homo sapiens	350-353
32581156-6	2020	In contrast, hCG treatment decreased plasma E2 concentration on days 7 and 14 in both groups.	Estradiol	44-46	hypertrichosis 2 (generalised, congenital)	Homo sapiens	13-16
32581156-7	2020	In summary, our results indicate that the hCG treatment more significantly promoted CL development and increased plasma P4 concentration in the contralateral than in the ipsilateral group.	propiverine	120-122	hypertrichosis 2 (generalised, congenital)	Homo sapiens	42-45
32544009-4	2020	Paired urine and serum hCG measurements differed quite widely but were well correlated and the degree of correlation improved after creatinine correction.	Creatinine	132-142	hypertrichosis 2 (generalised, congenital)	Homo sapiens	23-26
32126410-7	2020	CONCLUSION: In patients with tubal EP carefully selected for and treated with MTX, it may be reasonable to eliminate the D4 hCG in the follow-up algorithm.	Methotrexate	78-81	hypertrichosis 2 (generalised, congenital)	Homo sapiens	124-127
31953167-1	2020	Production of testosterone is under tight control by human chorion gonadotropin (hCG) during fetal life and luteinizing hormone (LH) in adulthood.	Testosterone	14-26	hypertrichosis 2 (generalised, congenital)	Homo sapiens	81-84
31953167-7	2020	Interestingly, men with impaired Leydig cell function and vitamin D deficiency had a significantly lower hCG-mediated increase in total and free testosterone compared with vitamin D sufficient men (p < 0.05).	Vitamin D	58-67	hypertrichosis 2 (generalised, congenital)	Homo sapiens	105-108
31953167-7	2020	Interestingly, men with impaired Leydig cell function and vitamin D deficiency had a significantly lower hCG-mediated increase in total and free testosterone compared with vitamin D sufficient men (p < 0.05).	Testosterone	145-157	hypertrichosis 2 (generalised, congenital)	Homo sapiens	105-108
31953167-7	2020	Interestingly, men with impaired Leydig cell function and vitamin D deficiency had a significantly lower hCG-mediated increase in total and free testosterone compared with vitamin D sufficient men (p < 0.05).	Vitamin D	172-181	hypertrichosis 2 (generalised, congenital)	Homo sapiens	105-108
31953167-9	2020	In conclusion, vitamin D deficiency is associated with lower testosterone/estradiol ratio in young men and lower Leydig cell sensitivity after hCG-stimulation in men with impaired gonadal function.	Vitamin D	15-24	hypertrichosis 2 (generalised, congenital)	Homo sapiens	143-146
32483804-5	2020	RESULTS:  In both groups, the prevalence of persistent L&P serum hCG levels was < 5%.	l&p	55-58	hypertrichosis 2 (generalised, congenital)	Homo sapiens	65-68
32483804-10	2020	CONCLUSION:  The limited use of HD Vit-A seems to have a safe and significant effect on the treatment of postmolar patients with L&P serum hCG levels and may decrease the development of postmolar GTN in this population.	Vitamin A	35-40	hypertrichosis 2 (generalised, congenital)	Homo sapiens	139-142
32483804-10	2020	CONCLUSION:  The limited use of HD Vit-A seems to have a safe and significant effect on the treatment of postmolar patients with L&P serum hCG levels and may decrease the development of postmolar GTN in this population.	l&p	129-132	hypertrichosis 2 (generalised, congenital)	Homo sapiens	139-142
32141676-14	2020	Chance of curative treatment with dactinomycin is strongly related to the hCG level.	Dactinomycin	34-46	hypertrichosis 2 (generalised, congenital)	Homo sapiens	74-77
32223011-0	2020	A switch to dactinomycin: What is the cutoff value for hCG?	Dactinomycin	12-24	hypertrichosis 2 (generalised, congenital)	Homo sapiens	55-58
31963729-7	2020	In xenografts exposed continuously to hCG, we demonstrate the maintenance of Leydig cell steroidogenesis, the acquisition of features of Sertoli cell maturation (androgen receptor, lumen development), and the formation of the blood-testis barrier (connexin 43), none of which were present prior to the transplantation or in xenografts in which hCG was withdrawn after 7 months.	Androgens	162-170	hypertrichosis 2 (generalised, congenital)	Homo sapiens	38-41
31669651-10	2020	The expression of npr and ar induced by LH/hCG was also blocked, which further suppressed the signaling of progestin and androgen.	Androgens	121-129	hypertrichosis 2 (generalised, congenital)	Homo sapiens	43-46
31864498-3	2020	There was greater ovarian follicular growth in the groups treated with gonadotropins, compared to the control, and there were greater progesterone concentrations in the eCG + hCG group on D9 (P &lt; 0.05).	Progesterone	134-146	hypertrichosis 2 (generalised, congenital)	Homo sapiens	175-178
31886877-24	2020	Persistent hCG levels were resolved after methotrexate in three cases and four cases received both curettage and methotrexate.	Methotrexate	42-54	hypertrichosis 2 (generalised, congenital)	Homo sapiens	11-14
31967304-2	2020	SUMMARY ANSWER: The peak concentration of progesterone occurred 4 days after oocyte pick-up (OPU + 4), with an average 35% fall from OPU + 4 to OPU + 6, and progesterone levels before and 12 h after hCG administration predicted levels during the early luteal phase.	Progesterone	42-54	hypertrichosis 2 (generalised, congenital)	Homo sapiens	199-202
31967304-18	2020	The best correlations between the number of follicles >=11 mm and serum progesterone level were seen at 24 and 36 h after hCG and OPU + 1.	Progesterone	72-84	hypertrichosis 2 (generalised, congenital)	Homo sapiens	122-125
30225585-7	2019	By activating the cAMP/PKA pathway, hCG not only alters the modification of histones but also increases the expression of Sp1 which activates the transcription of HSD11B2.	Cyclic AMP	18-22	hypertrichosis 2 (generalised, congenital)	Homo sapiens	36-39
31640230-0	2019	Increased Progesterone on the Day of Administration of hCG in Controlled Ovarian Hyperstimulation Affects the Expression of HOXA10 in Primates" Endometrial Receptivity.	Progesterone	10-22	hypertrichosis 2 (generalised, congenital)	Homo sapiens	55-58
31640230-1	2019	The increase in progesterone (P4) levels on the day of human chorionic gonadotropin (hCG) administration have a negative effect on endometrial receptivity.	Progesterone	16-28	hypertrichosis 2 (generalised, congenital)	Homo sapiens	85-88
31422280-8	2019	Upon examining the results from the various conformational studies, we identified that CGH had an enhanced binding affinity and inhibitory activity against the aggregated mutant SOD1 protein than other tripeptides and hexapeptide.	tripeptides	202-213	hypertrichosis 2 (generalised, congenital)	Homo sapiens	87-90
31150065-7	2019	Finally, the effect of atorvastatin on human chorionic gonadotropin (hCG)-stimulated progesterone production and the expression of key steroidogenic enzymes was also examined.	Progesterone	85-97	hypertrichosis 2 (generalised, congenital)	Homo sapiens	69-72
31150065-10	2019	The granulosa-lutein cells pretreated with atorvastatin also showed decreased responsiveness to hCG by decreasing the mRNA and protein expression of steroidogenic enzymes.	Atorvastatin	43-55	hypertrichosis 2 (generalised, congenital)	Homo sapiens	96-99
31150065-11	2019	Atorvastatin also attenuated LH/hCG-induced progesterone production.	Atorvastatin	0-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	32-35
31150065-11	2019	Atorvastatin also attenuated LH/hCG-induced progesterone production.	Progesterone	44-56	hypertrichosis 2 (generalised, congenital)	Homo sapiens	32-35
30689188-4	2019	Induced expression of Stau1 and Gemin 5 in the uterine tissue post hCG treatment at 12 h and 24 h-the duration between ovulation and post-ovulation-suggests their regulation by hCG and/or ovarian steroids, which are required for pregnancy establishment and maintenance.	Steroids	196-204	hypertrichosis 2 (generalised, congenital)	Homo sapiens	67-70
30915128-0	2019	Melatonin receptor depletion suppressed hCG-induced testosterone expression in mouse Leydig cells.	Testosterone	52-64	hypertrichosis 2 (generalised, congenital)	Homo sapiens	40-43
30915128-3	2019	To understand the biological function of melatonin receptors in hCG-induced testosterone synthesis, we generated melatonin receptor knockdown cells using specific siRNA and performed testosterone detection after hCG treatment.	Testosterone	76-88	hypertrichosis 2 (generalised, congenital)	Homo sapiens	64-67
30266436-5	2019	The lowest effective concentration of genistein that inhibited hCG-induced GVBD was 30 muM, while endosulfan inhibited it at 0.03 muM concentration.	Genistein	38-47	hypertrichosis 2 (generalised, congenital)	Homo sapiens	63-66
30266436-6	2019	In addition, malathion inhibited hCG-induced GVBD at the lowest concentration of 60 muM.	Malathion	13-22	hypertrichosis 2 (generalised, congenital)	Homo sapiens	33-36
30266436-8	2019	Fungicide iprodione, possibly acting as a progestin mimic, promoted hCG-induced GVBD at the lowest concentration of 20 muM, while the weed killer glyphosate inhibited hCG-induced GVBD starting at the 50 muM concentration.	iprodione	10-19	hypertrichosis 2 (generalised, congenital)	Homo sapiens	68-71
30266436-8	2019	Fungicide iprodione, possibly acting as a progestin mimic, promoted hCG-induced GVBD at the lowest concentration of 20 muM, while the weed killer glyphosate inhibited hCG-induced GVBD starting at the 50 muM concentration.	glyphosate	146-156	hypertrichosis 2 (generalised, congenital)	Homo sapiens	167-170
31586455-5	2020	This effect of hCG was via Lhcgr and its associated cAMP and PKC signaling pathways.	Cyclic AMP	52-56	hypertrichosis 2 (generalised, congenital)	Homo sapiens	15-18
31337386-3	2019	We herein report a rare case of Q-GTD in which the hCG level spontaneously returned to normal after a successful pregnancy.	q-gtd	32-37	hypertrichosis 2 (generalised, congenital)	Homo sapiens	51-54
31308661-0	2019	High-affinity carboxyl-graphene oxide-based SPR aptasensor for the detection of hCG protein in clinical serum samples.	carboxyl-graphene oxide	14-37	hypertrichosis 2 (generalised, congenital)	Homo sapiens	80-83
31308661-2	2019	Methods: In this study, we developed an ultra-sensitive carboxyl-graphene oxide (carboxyl-GO)-based surface plasmon resonance (SPR) aptasensor using peptides to detect human chorionic gonadotropin (hCG) in clinical serum samples.	carboxyl-graphene oxide	56-79	hypertrichosis 2 (generalised, congenital)	Homo sapiens	198-201
31308661-2	2019	Methods: In this study, we developed an ultra-sensitive carboxyl-graphene oxide (carboxyl-GO)-based surface plasmon resonance (SPR) aptasensor using peptides to detect human chorionic gonadotropin (hCG) in clinical serum samples.	carboxyl-go	81-92	hypertrichosis 2 (generalised, congenital)	Homo sapiens	198-201
31151753-8	2019	Either forskolin or phorbol 12 myristate 13-acetate can mimic hCG induction of Kctd11 expression.	Colforsin	7-16	hypertrichosis 2 (generalised, congenital)	Homo sapiens	62-65
31151753-8	2019	Either forskolin or phorbol 12 myristate 13-acetate can mimic hCG induction of Kctd11 expression.	Tetradecanoylphorbol Acetate	20-51	hypertrichosis 2 (generalised, congenital)	Homo sapiens	62-65
25905272-1	2000	This is postulated to be secondary to human chorionic gonadotropin (hCG) stimulation of the thyroid due to the structural homology between the TSH and hCG molecules and their receptors.	Thyrotropin	143-146	hypertrichosis 2 (generalised, congenital)	Homo sapiens	68-71
25905272-3	2000	A negative correlation was later demonstrated between hCG and TSH in women undergoing elective abortion.	Thyrotropin	62-65	hypertrichosis 2 (generalised, congenital)	Homo sapiens	54-57
31466074-10	2019	AMH, hCG-stimulated testosterone, and dihydrotestosterone levels contributed to determining etiology, whilst basal testosterone and basal dihydrotestosterone did not.	Testosterone	20-32	hypertrichosis 2 (generalised, congenital)	Homo sapiens	5-8
30428978-0	2018	Ultrasensitive ELISA for the detection of hCG based on assembled gold nanoparticles induced by functional polyamidoamine dendrimers.	Poly(amidoamine)	106-120	hypertrichosis 2 (generalised, congenital)	Homo sapiens	42-45
30428978-2	2018	Herein we report an ultrasensitive ELISA applying for the detection of hCG based on the assemble of AuNPs induced by functional PAMAM.	pamam	128-133	hypertrichosis 2 (generalised, congenital)	Homo sapiens	71-74
30300333-10	2018	In the oxygen-induced retinopathy model, number of preretinal nuclei (representing pathologic retinal neovascularization) significantly increases by 57% (P&lt;0.05) in hCG-treated mice.	Oxygen	7-13	hypertrichosis 2 (generalised, congenital)	Homo sapiens	168-171
30692298-10	2018	Chemotherapy containing cisplatin(CDDP)and irinotecan(CPT-11)was initiated; although the blood hCG level was temporally lowered, the patient died of liver failure 8 months after the surgery.	Cisplatin	24-33	hypertrichosis 2 (generalised, congenital)	Homo sapiens	95-98
30194850-3	2018	Previously virilised men with adult-onset HH and normal testicular volume respond well to monotherapy in which human chorionic gonadotrophin (hCG) acts as a long-acting LH-analogue stimulating spermatogenesis.	Luteinizing Hormone	169-171	hypertrichosis 2 (generalised, congenital)	Homo sapiens	142-145
30692298-10	2018	Chemotherapy containing cisplatin(CDDP)and irinotecan(CPT-11)was initiated; although the blood hCG level was temporally lowered, the patient died of liver failure 8 months after the surgery.	Cisplatin	34-38	hypertrichosis 2 (generalised, congenital)	Homo sapiens	95-98
30692298-10	2018	Chemotherapy containing cisplatin(CDDP)and irinotecan(CPT-11)was initiated; although the blood hCG level was temporally lowered, the patient died of liver failure 8 months after the surgery.	Irinotecan	43-53	hypertrichosis 2 (generalised, congenital)	Homo sapiens	95-98
30692298-10	2018	Chemotherapy containing cisplatin(CDDP)and irinotecan(CPT-11)was initiated; although the blood hCG level was temporally lowered, the patient died of liver failure 8 months after the surgery.	Irinotecan	54-60	hypertrichosis 2 (generalised, congenital)	Homo sapiens	95-98
30688925-12	2018	The cutoff hCG value, which determined the failure of methotrexate treatment, was found to be 1362 mIU/mL.	Methotrexate	54-66	hypertrichosis 2 (generalised, congenital)	Homo sapiens	11-14
30342668-3	2018	To avoid emergent oocyte retrieval in the midnight, indomethacin was given (150 mg/day, there times a day) from 2 h after incorrect hCG and GnRHa injection to the night before ovum pickup.	Indomethacin	52-64	hypertrichosis 2 (generalised, congenital)	Homo sapiens	132-135
30342668-6	2018	CONCLUSION: The presented case demonstrates that indomethacin can be used safely and effectively as an emergent prescription to prevent and postpone ovulation till up to 45 h after hCG and GnRHa triggering.	Indomethacin	49-61	hypertrichosis 2 (generalised, congenital)	Homo sapiens	181-184
29366778-4	2018	Human chorionic gonadotropin (hCG) prevents luteolysis and stimulates progesterone synthesis via protein kinase A (PKA).	Progesterone	70-82	hypertrichosis 2 (generalised, congenital)	Homo sapiens	30-33
29366778-6	2018	Basal and hCG-stimulated progesterone secretion was significantly decreased by the combined actions of the LXR agonist T0901317 and the SREBP inhibitor fatostatin, which was associated with reduced intracellular cholesterol storage.	T0901317	119-127	hypertrichosis 2 (generalised, congenital)	Homo sapiens	10-13
29366778-6	2018	Basal and hCG-stimulated progesterone secretion was significantly decreased by the combined actions of the LXR agonist T0901317 and the SREBP inhibitor fatostatin, which was associated with reduced intracellular cholesterol storage.	fatostatin	152-162	hypertrichosis 2 (generalised, congenital)	Homo sapiens	10-13
29366778-6	2018	Basal and hCG-stimulated progesterone secretion was significantly decreased by the combined actions of the LXR agonist T0901317 and the SREBP inhibitor fatostatin, which was associated with reduced intracellular cholesterol storage.	Cholesterol	212-223	hypertrichosis 2 (generalised, congenital)	Homo sapiens	10-13
30125945-0	2018	The predictive role of serum hCG 0-4 days after methotrexate treatment for ectopic pregnancy is yet to be determined-Authors" response.	Methotrexate	48-60	hypertrichosis 2 (generalised, congenital)	Homo sapiens	29-32
30124866-13	2018	A selective FOS inhibitor blocked hCG-induced increases in PGE2 and the expression of prostaglandin (PG) synthases and transporters (PTGES, SLCO2A1, and ABCC1).	Dinoprostone	59-63	hypertrichosis 2 (generalised, congenital)	Homo sapiens	34-37
30124866-13	2018	A selective FOS inhibitor blocked hCG-induced increases in PGE2 and the expression of prostaglandin (PG) synthases and transporters (PTGES, SLCO2A1, and ABCC1).	Prostaglandins	86-99	hypertrichosis 2 (generalised, congenital)	Homo sapiens	34-37
30415744-12	2018	RESULTS: and Discussion: RA-induced iPSCs exhibited these syncytiotrophoblast-like features and hCG secretion was maintained for at least 28 days after treatment with RA (500 nM) without BMP4.	Tretinoin	25-27	hypertrichosis 2 (generalised, congenital)	Homo sapiens	96-99
30415744-12	2018	RESULTS: and Discussion: RA-induced iPSCs exhibited these syncytiotrophoblast-like features and hCG secretion was maintained for at least 28 days after treatment with RA (500 nM) without BMP4.	Tretinoin	167-169	hypertrichosis 2 (generalised, congenital)	Homo sapiens	96-99
32212468-9	2018	Testosterone was observed in the culture medium, its concentration gradually increasing and reaching the peak on d 3, and its secretion stimulated by hCG.	Testosterone	0-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	150-153
29905829-10	2018	Leydig cell in vitro exposure to hCG results in qualitatively similar cAMP/PKA and pERK1/2 activation compared with LH and testosterone.	Cyclic AMP	70-74	hypertrichosis 2 (generalised, congenital)	Homo sapiens	33-36
29905829-10	2018	Leydig cell in vitro exposure to hCG results in qualitatively similar cAMP/PKA and pERK1/2 activation compared with LH and testosterone.	Luteinizing Hormone	116-118	hypertrichosis 2 (generalised, congenital)	Homo sapiens	33-36
29905829-10	2018	Leydig cell in vitro exposure to hCG results in qualitatively similar cAMP/PKA and pERK1/2 activation compared with LH and testosterone.	Testosterone	123-135	hypertrichosis 2 (generalised, congenital)	Homo sapiens	33-36
30688925-13	2018	CONCLUSION: In present study, patients with hCG value &lt;1362 mIU/mL were found to be good candidates for methotrexate treatment.	Methotrexate	107-119	hypertrichosis 2 (generalised, congenital)	Homo sapiens	44-47
30688925-14	2018	Although not strictly decisional, this hCG threshold level can be used to decide on the likelihood of methotrexate success or failure.	Methotrexate	102-114	hypertrichosis 2 (generalised, congenital)	Homo sapiens	39-42
30251729-2	2018	OBJECTIVES: To compare immunohistochemical detection of Human chorionic gonadotropin (hCG) expression in paraffin embedded tissue of squamous cell carcinomas (SCC) and high grade squamous intraepithelial lesions (HSIL).	Paraffin	105-113	hypertrichosis 2 (generalised, congenital)	Homo sapiens	86-89
29223051-0	2018	Ultrasensitive colorimetric immunoassay for hCG detection based on dual catalysis of Au@Pt core-shell nanoparticle functionalized by horseradish peroxidase.	Gold	85-87	hypertrichosis 2 (generalised, congenital)	Homo sapiens	44-47
30038945-0	2018	Post-operative use of human chorionic gonadotrophin (u-hCG) inpatients treated for intrabdominal unilateral undescended testes.	Uranium	15-16	hypertrichosis 2 (generalised, congenital)	Homo sapiens	55-58
29429918-3	2018	This concept was borrowed from historical pharmacological studies, when discrepancies between ligand-receptor binding and dose-response curves of cAMP were evaluated by treating mouse or rat Leydig cells with hCG in vitro.	Cyclic AMP	146-150	hypertrichosis 2 (generalised, congenital)	Homo sapiens	209-212
29582418-6	2018	The mean estimated beta hCG clearance duration was 29.2 days longer in patients with local methotrexate compared with systemic methotrexate (64.7 vs. 31.5 days, respectively; p = 0.026).	Methotrexate	91-103	hypertrichosis 2 (generalised, congenital)	Homo sapiens	24-27
29582418-10	2018	CONCLUSIONS: In patients with uterine ectopic pregnancies, the mean estimated beta hCG clearance duration was 29.2 days longer when applying local methotrexate compared with systemic methotrexate.	Methotrexate	147-159	hypertrichosis 2 (generalised, congenital)	Homo sapiens	83-86
30338234-9	2018	Serum level of estradiol (E2) level at the time of hCG administration was significantly higher in those who were treated with CC when compared to control (1153.5 +- 326.4 vs. 943.2 +- 215.3; P &lt; 0.001).	Estradiol	15-24	hypertrichosis 2 (generalised, congenital)	Homo sapiens	51-54
29626608-9	2018	Knockdown of RUNX1 and RUNX2 significantly decreased progesterone productions and the mRNA abundance of key steroidogenic enzymes (StAR, CYP11A1 and HSD3B) after hCG treatment.	Progesterone	53-65	hypertrichosis 2 (generalised, congenital)	Homo sapiens	162-165
29223051-1	2018	In this paper, an ultrasensitive colorimetric biosensor for human chorionic gonadotrophin (hCG) detection was designed from bottom-up method based on the dual catalysis of the horseradish peroxidase (HRP) and Au@Pt nanoparticles (NPs) relative to H2O2-TEM system.	Hydrogen Peroxide	247-251	hypertrichosis 2 (generalised, congenital)	Homo sapiens	91-94
29223051-2	2018	HRP and monoclonal mouse anti-hCG antibody (beta-submit, mAb1) were co-immobilized onto the Au@Pt NP surface to improve catalytic efficiency and specificity, which formed a dual functionalized Au@Pt-HRP probe with the mean size of 42.8nm (D50).	Gold	92-94	hypertrichosis 2 (generalised, congenital)	Homo sapiens	30-33
29223051-2	2018	HRP and monoclonal mouse anti-hCG antibody (beta-submit, mAb1) were co-immobilized onto the Au@Pt NP surface to improve catalytic efficiency and specificity, which formed a dual functionalized Au@Pt-HRP probe with the mean size of 42.8nm (D50).	Gold	193-195	hypertrichosis 2 (generalised, congenital)	Homo sapiens	30-33
29223051-5	2018	The dual functionalized Au@Pt-HRP probe as a type of signal amplified method was firstly applied in the colorimetric immunoassay for the hCG detection.	Gold	24-26	hypertrichosis 2 (generalised, congenital)	Homo sapiens	137-140
29334310-0	2018	Dendritic polyglycerol nanoparticles show charge dependent bio-distribution in early human placental explants and reduce hCG secretion.	polyglycerol	10-22	hypertrichosis 2 (generalised, congenital)	Homo sapiens	121-124
29147846-7	2018	RESULTS: Among patients who received hCG for ovulation induction, the hCG-positive test and clinical pregnancy rates in modified-NC were significantly lower in cycles with LH &gt;= 13 mIU/ml in respect to those with LH &lt; 13 mIU/ml (45.4 vs 73.3 and 36.4 vs 65.9%, in LH &gt;= 13 and LH &lt; 13 groups, respectively).	Luteinizing Hormone	172-174	hypertrichosis 2 (generalised, congenital)	Homo sapiens	37-40
29147846-7	2018	RESULTS: Among patients who received hCG for ovulation induction, the hCG-positive test and clinical pregnancy rates in modified-NC were significantly lower in cycles with LH &gt;= 13 mIU/ml in respect to those with LH &lt; 13 mIU/ml (45.4 vs 73.3 and 36.4 vs 65.9%, in LH &gt;= 13 and LH &lt; 13 groups, respectively).	Luteinizing Hormone	172-174	hypertrichosis 2 (generalised, congenital)	Homo sapiens	70-73
29147846-7	2018	RESULTS: Among patients who received hCG for ovulation induction, the hCG-positive test and clinical pregnancy rates in modified-NC were significantly lower in cycles with LH &gt;= 13 mIU/ml in respect to those with LH &lt; 13 mIU/ml (45.4 vs 73.3 and 36.4 vs 65.9%, in LH &gt;= 13 and LH &lt; 13 groups, respectively).	Luteinizing Hormone	216-218	hypertrichosis 2 (generalised, congenital)	Homo sapiens	37-40
29147846-7	2018	RESULTS: Among patients who received hCG for ovulation induction, the hCG-positive test and clinical pregnancy rates in modified-NC were significantly lower in cycles with LH &gt;= 13 mIU/ml in respect to those with LH &lt; 13 mIU/ml (45.4 vs 73.3 and 36.4 vs 65.9%, in LH &gt;= 13 and LH &lt; 13 groups, respectively).	Luteinizing Hormone	216-218	hypertrichosis 2 (generalised, congenital)	Homo sapiens	70-73
29147846-7	2018	RESULTS: Among patients who received hCG for ovulation induction, the hCG-positive test and clinical pregnancy rates in modified-NC were significantly lower in cycles with LH &gt;= 13 mIU/ml in respect to those with LH &lt; 13 mIU/ml (45.4 vs 73.3 and 36.4 vs 65.9%, in LH &gt;= 13 and LH &lt; 13 groups, respectively).	Luteinizing Hormone	216-218	hypertrichosis 2 (generalised, congenital)	Homo sapiens	37-40
29147846-7	2018	RESULTS: Among patients who received hCG for ovulation induction, the hCG-positive test and clinical pregnancy rates in modified-NC were significantly lower in cycles with LH &gt;= 13 mIU/ml in respect to those with LH &lt; 13 mIU/ml (45.4 vs 73.3 and 36.4 vs 65.9%, in LH &gt;= 13 and LH &lt; 13 groups, respectively).	Luteinizing Hormone	216-218	hypertrichosis 2 (generalised, congenital)	Homo sapiens	70-73
29147846-7	2018	RESULTS: Among patients who received hCG for ovulation induction, the hCG-positive test and clinical pregnancy rates in modified-NC were significantly lower in cycles with LH &gt;= 13 mIU/ml in respect to those with LH &lt; 13 mIU/ml (45.4 vs 73.3 and 36.4 vs 65.9%, in LH &gt;= 13 and LH &lt; 13 groups, respectively).	Luteinizing Hormone	216-218	hypertrichosis 2 (generalised, congenital)	Homo sapiens	37-40
29147846-7	2018	RESULTS: Among patients who received hCG for ovulation induction, the hCG-positive test and clinical pregnancy rates in modified-NC were significantly lower in cycles with LH &gt;= 13 mIU/ml in respect to those with LH &lt; 13 mIU/ml (45.4 vs 73.3 and 36.4 vs 65.9%, in LH &gt;= 13 and LH &lt; 13 groups, respectively).	Luteinizing Hormone	216-218	hypertrichosis 2 (generalised, congenital)	Homo sapiens	70-73
29147846-12	2018	In the presence of LH level &gt;= 13 mIU/ml, hCG administration should be avoided, and the embryo transfer should be planned only after spontaneous follicular rupture.	Luteinizing Hormone	19-21	hypertrichosis 2 (generalised, congenital)	Homo sapiens	45-48
28987889-11	2018	The formation of 1.0 +- 0.4 and 1.1 +- 0.3 acc-CL was observed in the GnRH and hCG groups, respectively (P   0.05), but was not observed in the Control group (P &lt; 0.05).	acc-cl	43-49	hypertrichosis 2 (generalised, congenital)	Homo sapiens	79-82
28295471-3	2018	Testosterone production by Leydig cells significantly increased when cultured with hCG by feeding the maca extract to maturing rats for 27 weeks (35 weeks of age) and when cultured with 22R-hydroxycholesterol by feeding it to mature rats for 30 weeks (48 weeks of age).	Testosterone	0-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	83-86
28933569-7	2018	We conclude that bolus of 1500 IU hCG, administered 2 days after retrieval, can provide excellent support, without the need to further supplement with progesterone.	Progesterone	151-163	hypertrichosis 2 (generalised, congenital)	Homo sapiens	34-37
28987889-15	2018	In conclusion, administration of hCG or GnRH on day 4 post FTAI induced the formation of one acc-CL from follicles of 3, 4 or 5 mm, indistinctly.	acc-cl	93-99	hypertrichosis 2 (generalised, congenital)	Homo sapiens	33-36
27872196-9	2017	The hCG-stimulated expression of Enpp3 mRNA was blocked by a protein kinase C inhibitor (GF109203) instead of the protein kinase A inhibitor (H89).	gf109203	89-97	hypertrichosis 2 (generalised, congenital)	Homo sapiens	4-7
27943496-9	2017	All 15 patients were treated successfully, without the need for blood transfusion or surgical procedures; however, three patients required an additional local MTX injection due to a poor decline in serum hCG level following the initial injection, while one patient required uterine artery embolization due to persistent vaginal bleeding and an enlarging gestational sac with blood vessels visible on contrast-enhanced MRI.	Methotrexate	159-162	hypertrichosis 2 (generalised, congenital)	Homo sapiens	204-207
27943496-10	2017	The mean time following initial MTX injection for hCG normalization was 43.8 (95% CI, 33.3-54.3) days and for resumption of menses was 68.4 (95% CI, 51.9-84.9) days.	Methotrexate	32-35	hypertrichosis 2 (generalised, congenital)	Homo sapiens	50-53
28815566-4	2017	Our data suggest that hCG surge increased cyclic nucleotides level in encircling granulosa cells but decreased their level in oocyte.	Nucleotides, Cyclic	42-60	hypertrichosis 2 (generalised, congenital)	Homo sapiens	22-25
29726663-9	2017	CONCLUSIONS: Trigger treatment by injection of hMG and hCG combined with adjunctive oral medication has a certain effect on unexplainable NOA.	noa	138-141	hypertrichosis 2 (generalised, congenital)	Homo sapiens	55-58
28325095-3	2017	Lower mean total doses of FSH administered and higher mean oestradiol level and mature oocyte rates were observed in the low-dose hCG group.	Estradiol	59-69	hypertrichosis 2 (generalised, congenital)	Homo sapiens	130-133
29120657-6	2017	The users mainly well informed from internet use for amelioration of the symptoms injections of human choriogonadotropin (hCG), selective estrogen receptor modulators (SERM) or aromatase inhibitors.Key words: anabolic steroids - doping - hypogonadotropic hypogonadism - side effects.	Steroids	218-226	hypertrichosis 2 (generalised, congenital)	Homo sapiens	122-125
28708540-6	2017	A significant increase in LH concentrations was first detected (P &lt; 0.05) at 24 hours after treatment in hCG group, while no changes (P &gt; 0.1) on LH levels were found during H0-H30 and between OV-6 and OV-1 in the Saline group.	Luteinizing Hormone	26-28	hypertrichosis 2 (generalised, congenital)	Homo sapiens	108-111
28708540-8	2017	A weak correlation between the preovulatory follicle vascularity and the plasma LH concentration was found in GnRH, hCG and Saline groups (r = +0.29, +0.29 and -0.23, respectively; P   0.0001).	Luteinizing Hormone	80-82	hypertrichosis 2 (generalised, congenital)	Homo sapiens	116-119
28333280-2	2017	SUMMARY ANSWER: hCG signaling in ESCs activates the extracellular signal-regulated protein kinases 1 and 2 (Erk1/2) pathway through exchange protein activated by cyclic AMP (cAMP) (Epac) and transiently increases progesterone receptor (PR) transcript and protein expression and its transcriptional function.	Cyclic AMP	162-172	hypertrichosis 2 (generalised, congenital)	Homo sapiens	16-19
28323945-11	2017	Inhibitors for P4/PGR and EGF-signaling pathways reduced hCG-induced increases in PTG production and the expression of EGF-like factors.	Prostaglandins	82-85	hypertrichosis 2 (generalised, congenital)	Homo sapiens	57-60
28323945-14	2017	In vitro studies indicated that collaborative actions of P4/PGR and EGF signaling are required for hCG-induced increases in PTG production and potentiation of EGF signaling in human periovulatory granulosa cells.	Prostaglandins	124-127	hypertrichosis 2 (generalised, congenital)	Homo sapiens	99-102
28333280-2	2017	SUMMARY ANSWER: hCG signaling in ESCs activates the extracellular signal-regulated protein kinases 1 and 2 (Erk1/2) pathway through exchange protein activated by cyclic AMP (cAMP) (Epac) and transiently increases progesterone receptor (PR) transcript and protein expression and its transcriptional function.	Cyclic AMP	174-178	hypertrichosis 2 (generalised, congenital)	Homo sapiens	16-19
28333280-4	2017	hCG signals through cAMP/protein kinase A (PKA) in gonadal cells, but in endometrial epithelial cells, hCG induces Erk1/2 activation independent of the cAMP/PKA pathway.	Cyclic AMP	20-24	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
28333280-16	2017	MAIN RESULTS AND THE ROLE OF CHANCE: Addition of hCG to ESCs in vitro induced the phosphorylation of Erk1/2 through cAMP accumulation.	Cyclic AMP	116-120	hypertrichosis 2 (generalised, congenital)	Homo sapiens	49-52
29259465-5	2017	Thus, this study evaluated whether hCG supplementation can be beneficial for cryopreserved-thawed embryo transfer in estrogen/progesterone replacement cycles.	Progesterone	126-138	hypertrichosis 2 (generalised, congenital)	Homo sapiens	35-38
28333280-19	2017	ESCs stimulated with hCG for up to 72 h showed a significant increase in PR mRNA and immunofluorescent label at 48 h only; an effect that was abrogated with the mitogen-activated protein kinase kinase inhibitor UO126.	U 0126	211-216	hypertrichosis 2 (generalised, congenital)	Homo sapiens	21-24
28333280-22	2017	HOXA10 mRNA up-regulation by hCG was not enhanced by co-stimulation with progesterone; however, it was completely abolished in the presence of RU486 (P = 0.036 hCG versus hCG + RU486).	Mifepristone	143-148	hypertrichosis 2 (generalised, congenital)	Homo sapiens	29-32
28333280-22	2017	HOXA10 mRNA up-regulation by hCG was not enhanced by co-stimulation with progesterone; however, it was completely abolished in the presence of RU486 (P = 0.036 hCG versus hCG + RU486).	Mifepristone	143-148	hypertrichosis 2 (generalised, congenital)	Homo sapiens	160-163
28333280-22	2017	HOXA10 mRNA up-regulation by hCG was not enhanced by co-stimulation with progesterone; however, it was completely abolished in the presence of RU486 (P = 0.036 hCG versus hCG + RU486).	Mifepristone	143-148	hypertrichosis 2 (generalised, congenital)	Homo sapiens	160-163
28333280-27	2017	WIDER IMPLICATIONS OF THE FINDINGS: We have determined that hCG induces the PR through the Erk1/2 pathway in ESCs which may render them more sensitive to progesterone, increasing our understanding about the effects of hCG at the embryo-maternal interface.	Progesterone	154-166	hypertrichosis 2 (generalised, congenital)	Homo sapiens	60-63
28266530-6	2017	In PLCs, 17beta-estradiol and the ESR1-selective agonist propylpyrazoletriol suppressed human chorionic gonadotropin (hCG)-induced progesterone production and steroidogenic gene expression.	Estradiol	9-25	hypertrichosis 2 (generalised, congenital)	Homo sapiens	118-121
28214759-0	2017	The role of HCG increment in the 48h prior to methotrexate treatment as a predictor for treatment success.	Methotrexate	46-58	hypertrichosis 2 (generalised, congenital)	Homo sapiens	12-15
28214759-1	2017	OBJECTIVE: To evaluate the role HCG change in the 48h prior to methotrexate treatment as a predictor for treatment success.	Methotrexate	63-75	hypertrichosis 2 (generalised, congenital)	Homo sapiens	32-35
28214759-5	2017	HCG levels in days 1, 4 and 7 were used to evaluate methotrexate treatment success.	Methotrexate	52-64	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
28214759-6	2017	The percentage of HCG change in the 48h prior to methotrexate treatment was compared between patients who were successfully treated and those who failed treatment with methotrexate.	Methotrexate	49-61	hypertrichosis 2 (generalised, congenital)	Homo sapiens	18-21
28214759-8	2017	The medians of HCG change in the 48h prior to methotrexate administration were significantly higher in the "failure group" (21% vs. 4%, p&lt;0.01).	Methotrexate	46-58	hypertrichosis 2 (generalised, congenital)	Homo sapiens	15-18
28214759-9	2017	In a logistic regression analysis, the of HCG percent increment prior to methotrexate administration was shown to be an independent predictor for treatment outcome.	Methotrexate	73-85	hypertrichosis 2 (generalised, congenital)	Homo sapiens	42-45
28214759-11	2017	CONCLUSIONS: Percentage of HCG increment in the 48h prior to methotrexate administration is an independent predictor for methotrexate treatment success.	Methotrexate	61-73	hypertrichosis 2 (generalised, congenital)	Homo sapiens	27-30
28214759-11	2017	CONCLUSIONS: Percentage of HCG increment in the 48h prior to methotrexate administration is an independent predictor for methotrexate treatment success.	Methotrexate	121-133	hypertrichosis 2 (generalised, congenital)	Homo sapiens	27-30
28214759-12	2017	HCG increment &lt;12% prior to methotrexate treatment is a good predictor for treatment success.	Methotrexate	31-43	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
28266530-6	2017	In PLCs, 17beta-estradiol and the ESR1-selective agonist propylpyrazoletriol suppressed human chorionic gonadotropin (hCG)-induced progesterone production and steroidogenic gene expression.	4,4',4''-(4-propyl-((1)H)-pyrazole-1,3,5-triyl) tris-phenol	57-76	hypertrichosis 2 (generalised, congenital)	Homo sapiens	118-121
28266530-6	2017	In PLCs, 17beta-estradiol and the ESR1-selective agonist propylpyrazoletriol suppressed human chorionic gonadotropin (hCG)-induced progesterone production and steroidogenic gene expression.	Progesterone	131-143	hypertrichosis 2 (generalised, congenital)	Homo sapiens	118-121
28266530-10	2017	In cultured PLCs, 17beta-estradiol, propylpyrazoletriol, and diarylpropionitrile reduced hCG-stimulated Ki67 and Pcna mRNA expression and the number of KI67-positive PLCs, suggesting that oestrogen inhibits PLC proliferation via both ESR1 and ESR2.	Estradiol	18-34	hypertrichosis 2 (generalised, congenital)	Homo sapiens	89-92
28266530-10	2017	In cultured PLCs, 17beta-estradiol, propylpyrazoletriol, and diarylpropionitrile reduced hCG-stimulated Ki67 and Pcna mRNA expression and the number of KI67-positive PLCs, suggesting that oestrogen inhibits PLC proliferation via both ESR1 and ESR2.	4,4',4''-(4-propyl-((1)H)-pyrazole-1,3,5-triyl) tris-phenol	36-55	hypertrichosis 2 (generalised, congenital)	Homo sapiens	89-92
28266530-10	2017	In cultured PLCs, 17beta-estradiol, propylpyrazoletriol, and diarylpropionitrile reduced hCG-stimulated Ki67 and Pcna mRNA expression and the number of KI67-positive PLCs, suggesting that oestrogen inhibits PLC proliferation via both ESR1 and ESR2.	diarylpropionitrile	61-80	hypertrichosis 2 (generalised, congenital)	Homo sapiens	89-92
28100869-10	2017	Taken together, the current knowledge from human studies indicating that testosterone optimization by clomiphene, hCG and/or aromatase inhibitors and high dose hCG/FSH treatment can, at least in part, improve spermatogenesis in NOA.	Testosterone	73-85	hypertrichosis 2 (generalised, congenital)	Homo sapiens	114-117
28400828-2	2017	This study was designed to assess the effects of intrauterine injection of hCG before the embryo transfer in an in vitro fertilization (IVF) or intracytoplasmic sperm injection (ICSI) cycle on pregnancy rate in infertile patients.	intrauterine	49-61	hypertrichosis 2 (generalised, congenital)	Homo sapiens	75-78
27467188-5	2017	DESIGN/SETTING: A prospective case study was conducted in 26 paediatric endocrine centres PATIENTS/INTERVENTIONS: HCG and rFSH were administered until cessation of testicular growth and plateauing of spermatogenesis to (1) prepubertal HH boys with absent or early arrested puberty (group A) and to (2) HH adolescents who had previously received full testosterone replacement (group B).	Testosterone	350-362	hypertrichosis 2 (generalised, congenital)	Homo sapiens	114-117
28056997-0	2017	Human LH and hCG stimulate differently the early signalling pathways but result in equal testosterone synthesis in mouse Leydig cells in vitro.	Testosterone	89-101	hypertrichosis 2 (generalised, congenital)	Homo sapiens	13-16
28056997-5	2017	RESULTS: We found that hCG is about 10-fold more potent than LH in cAMP recruitment, and slightly but significantly more potent on cAMP-dependent Erk1/2 phosphorylation.	Cyclic AMP	67-71	hypertrichosis 2 (generalised, congenital)	Homo sapiens	23-26
28056997-5	2017	RESULTS: We found that hCG is about 10-fold more potent than LH in cAMP recruitment, and slightly but significantly more potent on cAMP-dependent Erk1/2 phosphorylation.	Cyclic AMP	131-135	hypertrichosis 2 (generalised, congenital)	Homo sapiens	23-26
28056997-7	2017	CONCLUSIONS: These data demonstrate that the responses to human LH/hCG are only quantitatively and not qualitatively different in murine cells, at least in terms of cAMP and Erk1/2 activation, and equal in activating downstream steroidogenic events.	Cyclic AMP	165-169	hypertrichosis 2 (generalised, congenital)	Homo sapiens	64-70
27467188-13	2017	CONCLUSIONS: HCG/rFSH replacement during adolescence successfully induces testicular growth and spermatogenesis, irrespective of previous testosterone replacement, and enhances QoL.	Testosterone	138-150	hypertrichosis 2 (generalised, congenital)	Homo sapiens	13-16
27888702-14	2017	CONCLUSION: In this study, we showed that an initial hCG value &lt;1000IU/l and favorable early HCG kinetics were predictive factors for the successful medical treatment of ectopic pregnancy by methotrexate, and hematosalpinx and pretherapeutic blood progesterone &gt;5ng/ml at diagnosis were predictive of its failure.	Methotrexate	194-206	hypertrichosis 2 (generalised, congenital)	Homo sapiens	53-56
27888702-14	2017	CONCLUSION: In this study, we showed that an initial hCG value &lt;1000IU/l and favorable early HCG kinetics were predictive factors for the successful medical treatment of ectopic pregnancy by methotrexate, and hematosalpinx and pretherapeutic blood progesterone &gt;5ng/ml at diagnosis were predictive of its failure.	Methotrexate	194-206	hypertrichosis 2 (generalised, congenital)	Homo sapiens	96-99
29509368-4	2017	Paracine properties-of hCG comprise control of fusing of trophoblasts into syncytiotrophoblasts, angiogenesis, immunity regulation and endometrium predisposition to implantation.	paracine	0-8	hypertrichosis 2 (generalised, congenital)	Homo sapiens	23-26
28473891-4	2017	In experiment 2, testosterone production was assessed in testicular cells cultured on ECM or plastic (control) and exposed to different concentrations of hCG.	Testosterone	17-29	hypertrichosis 2 (generalised, congenital)	Homo sapiens	154-157
27888702-11	2017	Methotrexate treatment was successful in 90% of women who had D0 hCG &lt;1000IU/l.	Methotrexate	0-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	65-68
28473891-7	2017	In experiment 2, testosterone concentration was increased in response to hCG in both groups but cells cultured on ECM were more responsive to hCG than those cultured on plastic (p &lt; 0.05).	Testosterone	17-29	hypertrichosis 2 (generalised, congenital)	Homo sapiens	73-76
27756557-3	2016	The selection of chemotherapy regimen following methotrexate-resistance depended on the volume of residual disease as indicated by the serum hCG value at the time, with patients switching to either single-agent dactinomycin at an hCG level&lt;150IU/L from 2001-2010 and &lt;300IU/L since 2010, or to combination treatment with etoposide/dactinomycin (EA) above these thresholds.	Methotrexate	48-60	hypertrichosis 2 (generalised, congenital)	Homo sapiens	141-144
27865941-14	2016	Additional systematic methotrexate administration was required in one case because of remaining villi at the implantation site with persistence of serum hCG levels after the procedure.	Methotrexate	22-34	hypertrichosis 2 (generalised, congenital)	Homo sapiens	153-156
27756557-8	2016	With carboplatin, 17/21 (81%) achieved an overall complete hCG response rate, with 4 patients requiring third-line EA.	Carboplatin	5-16	hypertrichosis 2 (generalised, congenital)	Homo sapiens	59-62
27718294-6	2016	RESULTS: The results from the levonorgestrel and hCG group were closer to those displayed by human PCOS patients than the sodium prasterone sulfate and hCG group.	sodium prasterone sulfate	122-147	hypertrichosis 2 (generalised, congenital)	Homo sapiens	49-52
27208477-2	2016	When hCG was present in the peptide probe solution, the AgNPs did not aggregate and it had strong catalytic effect on the gold nanoparticle reaction with a strong resonance Rayleigh scattering (RRS) peak at 370nm and a strong surface enhanced Raman scattering (SERS) peak at 1615cm(-1) in the presence of molecular probe of Victoria blue 4R (VB4R).	sers	261-265	hypertrichosis 2 (generalised, congenital)	Homo sapiens	5-8
27208477-5	2016	And the SERS intensity at 1615cm(-1) increased linearly with the hCG concentration in the range of 0.05-20ng/mL, with a linear regression equation of DeltaI1615cm-1=142C+134.	sers	8-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	65-68
27208477-6	2016	Based on this, two new methods of nanocatalytic SERS and RRS were proposed for the determination of trace hCG.	sers	48-52	hypertrichosis 2 (generalised, congenital)	Homo sapiens	106-109
27177022-2	2016	In the current study, we observed that the extremely high level of expression of MT1 in mice granulosa cells was rapidly induced by hCG (equivalent LH) within 2 hours and this was referred as MT1 surge.	Luteinizing Hormone	148-150	hypertrichosis 2 (generalised, congenital)	Homo sapiens	132-135
27230625-5	2016	In GT derivatized testis tissues of mice treated with human chorionic gonadotropin (hCG), testosterone was broadly observed both inside and outside the seminiferous tubules by using an iMScope.	Testosterone	90-102	hypertrichosis 2 (generalised, congenital)	Homo sapiens	84-87
27230625-6	2016	To evaluate our imaging results, we performed quantification experiments of underivatized testosterone extracted from hCG-treated testes and control testes using LC-MS/MS.	Testosterone	90-102	hypertrichosis 2 (generalised, congenital)	Homo sapiens	118-121
27572300-9	2016	MTX is an alternative to conservative treatment such as laparoscopic salpingotomy for uncomplicated tubal pregnancy (Grade A) with pretreatment hCG levels&lt;=5000IU/l (Grade B).	Methotrexate	0-3	hypertrichosis 2 (generalised, congenital)	Homo sapiens	144-147
27572300-14	2016	In pregnancies of unknown location persisting more than 10days in an asymptomatic woman who has an hCG level&gt;2000IU/l, routine MTX treatment is an option.	Methotrexate	130-133	hypertrichosis 2 (generalised, congenital)	Homo sapiens	99-102
27397793-3	2016	We hypothesised that injection of the LH analogue human chorionic gonadotropin (hCG) would induce growth of estrogenic follicles and, by mimicking the signal for MRP and stimulating progesterone secretion, increase primiparous sow fertility.	Progesterone	182-194	hypertrichosis 2 (generalised, congenital)	Homo sapiens	80-83
26108912-4	2016	Rats treated with insulin + hCG had heavier bodyweight and ovarian weight, higher circulating concentrations of luteinising hormone (LH) and testosterone (T), and greater homeostatic model assessment of insulin resistance (HOMA-IR) values compared with control rats (P&lt;0.05).	Testosterone	141-153	hypertrichosis 2 (generalised, congenital)	Homo sapiens	28-31
27397793-9	2016	In Experiment 1, injection of hCG increased (P&lt;0.001) follicle diameter and serum concentrations of estradiol (P&lt;0.01) and progesterone (P&lt;0.05).	Estradiol	103-112	hypertrichosis 2 (generalised, congenital)	Homo sapiens	30-33
27397793-9	2016	In Experiment 1, injection of hCG increased (P&lt;0.001) follicle diameter and serum concentrations of estradiol (P&lt;0.01) and progesterone (P&lt;0.05).	Progesterone	129-141	hypertrichosis 2 (generalised, congenital)	Homo sapiens	30-33
26895433-10	2016	In addition, p,p"-DDT increased the sensitivity of FSHR to hCG and to a low molecular weight agonist of the FSHR, 3-((5methyl)-2-(4-benzyloxy-phenyl)-5-{[2-[3-ethoxy-4-methoxy-phenyl)-ethylcarbamoyl]-methyl}-4-oxo-thiazolidin-3-yl)-benzamide (16a).	DDT	13-21	hypertrichosis 2 (generalised, congenital)	Homo sapiens	59-62
27475410-6	2016	Stimulation of spermatogenesis by gonadotrophins rFSH and/or hCG is the most used but others treatments, like pulsatile GnRH therapy or clomifene citrate can be used.	Clomiphene	136-153	hypertrichosis 2 (generalised, congenital)	Homo sapiens	61-64
27301360-2	2016	SUMMARY ANSWER: Basal (Day 2 of the menstrual cycle) serum progesterone concentration and history of PE are baseline variables that can predict the occurrence of PE on the day of hCG independently of the intensity of ovarian stimulation.	Progesterone	59-71	hypertrichosis 2 (generalised, congenital)	Homo sapiens	179-182
27539669-0	2016	hCG-induced Sprouty2 mediates amphiregulin-stimulated COX-2/PGE2 up-regulation in human granulosa cells: a potential mechanism for the OHSS.	Dinoprostone	60-64	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
27539669-3	2016	Our previous study has shown that human chorionic gonadotropin (hCG)/luteinizing hormone (LH) up-regulates the expression levels of EGF-like growth factor, amphiregulin (AREG), which subsequently contributes to the hCG/LH-induced COX-2 expression and PGE2 production.	Dinoprostone	251-255	hypertrichosis 2 (generalised, congenital)	Homo sapiens	64-67
27539669-3	2016	Our previous study has shown that human chorionic gonadotropin (hCG)/luteinizing hormone (LH) up-regulates the expression levels of EGF-like growth factor, amphiregulin (AREG), which subsequently contributes to the hCG/LH-induced COX-2 expression and PGE2 production.	Dinoprostone	251-255	hypertrichosis 2 (generalised, congenital)	Homo sapiens	215-218
27539669-4	2016	The aim of the present study was to investigate the effect of hCG on SPRY2 expression and the role of hCG-induced SPRY2 in AREG-stimulated COX-2 expression and PGE2 production in human granulosa cells.	Dinoprostone	160-164	hypertrichosis 2 (generalised, congenital)	Homo sapiens	102-105
27554787-0	2016	Atrazine activates multiple signaling pathways enhancing the rapid hCG-induced androgenesis in rat Leydig cells.	Atrazine	0-8	hypertrichosis 2 (generalised, congenital)	Homo sapiens	67-70
27554787-4	2016	Low hCG concentration (0.25ng/mL) caused cAMP-independent, but ERK1/2-dependent increase in androgen production after 60min of incubation.	Cyclic AMP	41-45	hypertrichosis 2 (generalised, congenital)	Homo sapiens	4-7
27554787-5	2016	Co-treatment with ATR for 60min enhanced the cAMP production in hCG-stimulated cells.	Cyclic AMP	45-49	hypertrichosis 2 (generalised, congenital)	Homo sapiens	64-67
27554787-8	2016	After 120min, hCG further increased androgenesis in Leydig cells that was sensitive to inhibition of the cAMP/PKA, ERK1/2 and ROS signaling pathways.	Cyclic AMP	105-109	hypertrichosis 2 (generalised, congenital)	Homo sapiens	14-17
27554787-8	2016	After 120min, hCG further increased androgenesis in Leydig cells that was sensitive to inhibition of the cAMP/PKA, ERK1/2 and ROS signaling pathways.	ros	126-129	hypertrichosis 2 (generalised, congenital)	Homo sapiens	14-17
27554787-9	2016	Co-treatment with ATR for 120min further enhanced the hCG-induced androgen production, which was prevented by inhibition of the calcium, PKC and EGFR signaling cascades.	Atrazine	18-21	hypertrichosis 2 (generalised, congenital)	Homo sapiens	54-57
27554787-9	2016	Co-treatment with ATR for 120min further enhanced the hCG-induced androgen production, which was prevented by inhibition of the calcium, PKC and EGFR signaling cascades.	Calcium	128-135	hypertrichosis 2 (generalised, congenital)	Homo sapiens	54-57
27547681-9	2016	Intrauterine insemination can be done successfully at either 24 or 36 h after hCG in clomiphene citrate stimulated cycles.	Clomiphene	85-103	hypertrichosis 2 (generalised, congenital)	Homo sapiens	78-81
27188454-8	2016	RESULTS: Progesterone (P), 17-hydroxyprogesterone (17OHP), TS, and estradiol (E2) showed a significant increase (P&lt;0.001) after hCG stimulation in both groups.	Progesterone	9-21	hypertrichosis 2 (generalised, congenital)	Homo sapiens	131-134
27177499-16	2016	In conclusion, hCG is the major pregnancy glycoprotein hormone, whose maternal concentration and glycan structure change all along pregnancy.	Polysaccharides	97-103	hypertrichosis 2 (generalised, congenital)	Homo sapiens	15-18
27188454-8	2016	RESULTS: Progesterone (P), 17-hydroxyprogesterone (17OHP), TS, and estradiol (E2) showed a significant increase (P&lt;0.001) after hCG stimulation in both groups.	17-alpha-Hydroxyprogesterone	27-49	hypertrichosis 2 (generalised, congenital)	Homo sapiens	131-134
27188454-8	2016	RESULTS: Progesterone (P), 17-hydroxyprogesterone (17OHP), TS, and estradiol (E2) showed a significant increase (P&lt;0.001) after hCG stimulation in both groups.	17-alpha-Hydroxyprogesterone	51-56	hypertrichosis 2 (generalised, congenital)	Homo sapiens	131-134
27188454-8	2016	RESULTS: Progesterone (P), 17-hydroxyprogesterone (17OHP), TS, and estradiol (E2) showed a significant increase (P&lt;0.001) after hCG stimulation in both groups.	Estradiol	67-76	hypertrichosis 2 (generalised, congenital)	Homo sapiens	131-134
27050251-10	2016	hCG and LHRH can effectively increase TCDR and there was no significant difference between them.	tcdr	38-42	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
27288338-11	2016	LH, however, was more beneficial to early embryonic development than hCG.	Luteinizing Hormone	0-2	hypertrichosis 2 (generalised, congenital)	Homo sapiens	69-72
26896825-7	2016	Although there was no difference in survival between groups, increased resistance to first-line methotrexate chemotherapy was significantly associated with a diagnosis of postmolar CCA (OR 2.67, p=0.007)), pretreatment hCG level at &gt;10,000mIU/mL (OR 2.62, p=0.002), and higher FIGO score (3-4: OR 2.02, p=0.027; 5-6: OR 5.56, p&lt;0.001) on multivariate analysis.	Methotrexate	96-108	hypertrichosis 2 (generalised, congenital)	Homo sapiens	219-222
27679137-0	2015	The Role of beta hCG Increment in the 48 Hours Prior to Methotrexate Treatment as a Predictor for Treatment Success.	Methotrexate	56-68	hypertrichosis 2 (generalised, congenital)	Homo sapiens	17-20
27088205-6	2016	Human chorionic gonadotropin (hCG) and selective estrogens receptor modulators (SERM) are efficacy in treatment of clinical signs and symptoms of hypoigonadism, has been shown to reverse spermatogenesis disturbances and can to maintain elevated intratesticular testosterone levels necessary to optimal spermatogenesis.	Testosterone	261-273	hypertrichosis 2 (generalised, congenital)	Homo sapiens	30-33
26893072-7	2016	BMP4 inhibition attenuated the induction effects of hCG and DHT on estrogen and progesterone secretion in CMKLR1 KO mice, but not in WT mice, implicating the BMP4 signaling pathway in the CMKLR1-dependent response to DHT.	Progesterone	80-92	hypertrichosis 2 (generalised, congenital)	Homo sapiens	52-55
26690776-4	2016	We show that in the presence of FSH, hCG biopotency is about 5-fold increased, in the presence of FSH, in terms of cAMP activation.	Cyclic AMP	115-119	hypertrichosis 2 (generalised, congenital)	Homo sapiens	37-40
26690776-5	2016	Accordingly, CREB phosphorylation and steroid production is increased under hCG and FSH co-treatment.	Steroids	38-45	hypertrichosis 2 (generalised, congenital)	Homo sapiens	76-79
26690776-7	2016	The different modulatory activity of FSH on LH and hCG action in vitro corresponds to their different physiological functions, reflecting proliferative effects exerted by LH during the follicular phase and before trophoblast development, and the high steroidogenic potential of hCG requested to sustain pregnancy from the luteal phase onwards.	Luteinizing Hormone	44-46	hypertrichosis 2 (generalised, congenital)	Homo sapiens	278-281
26690776-7	2016	The different modulatory activity of FSH on LH and hCG action in vitro corresponds to their different physiological functions, reflecting proliferative effects exerted by LH during the follicular phase and before trophoblast development, and the high steroidogenic potential of hCG requested to sustain pregnancy from the luteal phase onwards.	Luteinizing Hormone	171-173	hypertrichosis 2 (generalised, congenital)	Homo sapiens	51-54
26122485-3	2016	METHODS: MA-10 cells were stimulated with different concentrations of d-Asp, in presence or absence of hCG.	D-Aspartic Acid	70-75	hypertrichosis 2 (generalised, congenital)	Homo sapiens	103-106
26122485-10	2016	Finally, d-Asp attenuated displacement of LHR staining, from cell membrane to cytoplasm, subsequent to hCG stimulation.	D-Aspartic Acid	9-14	hypertrichosis 2 (generalised, congenital)	Homo sapiens	103-106
25370006-6	2015	The epithelium height in the AMP and AIJ was increased in the eCG/hCG group when compared to the control and P4 groups.	Adenosine Monophosphate	29-32	hypertrichosis 2 (generalised, congenital)	Homo sapiens	66-69
25370006-6	2015	The epithelium height in the AMP and AIJ was increased in the eCG/hCG group when compared to the control and P4 groups.	(2S,3R)-3-(4-HYDROXYPHENYL)-2-(4-{[(2S)-2-PYRROLIDIN-1-YLPROPYL]OXY}PHENYL)-2,3-DIHYDRO-1,4-BENZOXATHIIN-6-OL	37-40	hypertrichosis 2 (generalised, congenital)	Homo sapiens	66-69
25370006-12	2015	Moreover, eCG/hCG treatment increased the height of the epithelium in the AMP and AIJ, while in this last region, the P4 treatment decreased the epithelium height.	Adenosine Monophosphate	74-77	hypertrichosis 2 (generalised, congenital)	Homo sapiens	14-17
26698678-13	2016	CONCLUSION(S): The decline in serum hCG is slower in EPs than in SAB and can be used to aid clinicians in the frequency and duration of follow-up.	exophthalmos producing substance	53-56	hypertrichosis 2 (generalised, congenital)	Homo sapiens	36-39
26893072-7	2016	BMP4 inhibition attenuated the induction effects of hCG and DHT on estrogen and progesterone secretion in CMKLR1 KO mice, but not in WT mice, implicating the BMP4 signaling pathway in the CMKLR1-dependent response to DHT.	Dihydrotestosterone	217-220	hypertrichosis 2 (generalised, congenital)	Homo sapiens	52-55
26745711-3	2016	The results showed that the TQE rate significantly correlated with progesterone levels on the day of human chorionic gonadotropin (hCG) trigger (P = 0.009).	Progesterone	67-79	hypertrichosis 2 (generalised, congenital)	Homo sapiens	131-134
26745711-4	2016	Multivariate linear regression analysis of factors related to the TQE rate, in conventional IVF cycles, showed that the TQE rate was negatively associated with progesterone concentration on the day of hCG (OR was -1.658, 95% CI: -2.806 to -0.510, P = 0.005).	Progesterone	160-172	hypertrichosis 2 (generalised, congenital)	Homo sapiens	201-204
26745711-8	2016	In conclusion, the results of this study clearly demonstrated a negative effect of elevated progesterone levels on the day of hCG trigger, on TQE rate, regardless of the basal FSH, the total gonadotropin, the age of the woman, or the time of ovarian stimulation.	Progesterone	92-104	hypertrichosis 2 (generalised, congenital)	Homo sapiens	126-129
26569059-2	2016	Mathematical modeling of hCG kinetics may allow prediction of methotrexate (MTX) resistance, with production parameter "hCGres."	Methotrexate	62-74	hypertrichosis 2 (generalised, congenital)	Homo sapiens	25-28
26569059-2	2016	Mathematical modeling of hCG kinetics may allow prediction of methotrexate (MTX) resistance, with production parameter "hCGres."	Methotrexate	76-79	hypertrichosis 2 (generalised, congenital)	Homo sapiens	25-28
26324114-10	2015	The results of 20-oxo-pregnane measurements indicated that hCG can be applied to induce ovulation.	20-oxo-pregnane	15-30	hypertrichosis 2 (generalised, congenital)	Homo sapiens	59-62
26116232-5	2015	Pretreatment with GC7, a specific inhibitor of eIF5A hypusination significantly abolished hCG-induced LRBP mRNA and protein expression.	2-(7-aminoheptyl)guanidine	18-21	hypertrichosis 2 (generalised, congenital)	Homo sapiens	90-93
26025242-8	2015	The use of combinations of GnRH, eCG, and hCG in progesterone-based protocols can improve results.	Progesterone	49-61	hypertrichosis 2 (generalised, congenital)	Homo sapiens	42-45
26422433-2	2015	Systemic Methotrexate (MTX) was effective in 56 out of 65 patients (failure rate 13.8%), in whom hCG level was significantly lower when compared to the failure group (p&amp;lt;0,05); we performed 299 salpingectomies, 297 of whom through laparoscopic approach.	Methotrexate	9-21	hypertrichosis 2 (generalised, congenital)	Homo sapiens	97-100
26422433-2	2015	Systemic Methotrexate (MTX) was effective in 56 out of 65 patients (failure rate 13.8%), in whom hCG level was significantly lower when compared to the failure group (p&amp;lt;0,05); we performed 299 salpingectomies, 297 of whom through laparoscopic approach.	Methotrexate	23-26	hypertrichosis 2 (generalised, congenital)	Homo sapiens	97-100
26109617-2	2015	SUMMARY ANSWER: During the luteal phase of letrozole-associated COS cycles (triggered with human chorionic gonadotrophin (hCG)) progesterone levels are similarly elevated to those obtained after standard COS without letrozole.	Letrozole	43-52	hypertrichosis 2 (generalised, congenital)	Homo sapiens	122-125
26109617-2	2015	SUMMARY ANSWER: During the luteal phase of letrozole-associated COS cycles (triggered with human chorionic gonadotrophin (hCG)) progesterone levels are similarly elevated to those obtained after standard COS without letrozole.	carbonyl sulfide	64-67	hypertrichosis 2 (generalised, congenital)	Homo sapiens	122-125
26116232-8	2015	Taken together, these results suggest that hCG-induced LHR mRNA downregulation is mediated by cAMP-PKA-ERK1/2 signaling leading to activation of eIF5A hypusination.	Cyclic AMP	94-98	hypertrichosis 2 (generalised, congenital)	Homo sapiens	43-46
25656291-8	2015	Leydig cells in hCG treated grafts produced significantly more testosterone than nonhCG treated grafts.	Testosterone	63-75	hypertrichosis 2 (generalised, congenital)	Homo sapiens	16-19
25337850-5	2015	Treatment with human chorionic gonadotropin (hCG) has shown the ability not only to reverse azoospermia brought on by testosterone supplementation therapy but also to help maintain elevated intratesticular testosterone levels.	Testosterone	118-130	hypertrichosis 2 (generalised, congenital)	Homo sapiens	45-48
25236690-0	2015	[The influence of exogenous LH/hCG activity on serum progesterone levels on the day of hCG administration in in vitro fertilization].	Progesterone	53-65	hypertrichosis 2 (generalised, congenital)	Homo sapiens	31-34
25236690-0	2015	[The influence of exogenous LH/hCG activity on serum progesterone levels on the day of hCG administration in in vitro fertilization].	Progesterone	53-65	hypertrichosis 2 (generalised, congenital)	Homo sapiens	87-90
25236690-1	2015	OBJECTIVES: Clarifying whether the addition of recombinant LH (rLH) to recombinant FSH (rFSH) leads to progesterone (P4) levels on dhCG comparable to those obtained with stimulation with FSH and hCG (HP-hMG) MATERIALS AND METHODS: Pituitary-desensitized patients, matched for age and follicle reserve, received rFSH+LH (n=729) or HP-hMG (n=729).	Luteinizing Hormone	59-61	hypertrichosis 2 (generalised, congenital)	Homo sapiens	132-135
25236690-5	2015	CONCLUSIONS: HP-hMG led to lower P4 levels on day hCG than rFSH+rLH irrespective of the intensity of the ovarian response and the adjunction of rLH (75 IU/day from day 6 onward).	hp-hmg	13-19	hypertrichosis 2 (generalised, congenital)	Homo sapiens	50-53
25784278-5	2015	BPA also augmented aromatase, glucose transporter-1, CRH, and hCG mRNA levels while reducing the level of leptin mRNA.	bisphenol A	0-3	hypertrichosis 2 (generalised, congenital)	Homo sapiens	62-65
25707740-17	2015	In conclusion, hCG is the major pregnancy glycoprotein hormone, whose maternal concentration and glycan structure change all along pregnancy.	Polysaccharides	97-103	hypertrichosis 2 (generalised, congenital)	Homo sapiens	15-18
26116232-4	2015	Pretreatment with H89, a specific inhibitor of PKA, and U0126, a specific inhibitor of ERK1/2 significantly inhibited both hCG-induced eIF5A mRNA expression and hypusination of eIF5A protein.	N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide	18-21	hypertrichosis 2 (generalised, congenital)	Homo sapiens	123-126
26116232-4	2015	Pretreatment with H89, a specific inhibitor of PKA, and U0126, a specific inhibitor of ERK1/2 significantly inhibited both hCG-induced eIF5A mRNA expression and hypusination of eIF5A protein.	U 0126	56-61	hypertrichosis 2 (generalised, congenital)	Homo sapiens	123-126
26051455-6	2015	However, hCG levels &gt;= 4000 mIU/mL and ADAM-12 levels &gt;= 2500 pg/mL were independently associated with complete uterine expulsion after one dose of misoprostol in our population.	Misoprostol	154-165	hypertrichosis 2 (generalised, congenital)	Homo sapiens	9-12
26137037-10	2015	The lesion disappeared following five cycles of methotrexate+ etoposide+actinomycin D therapy, which was performed as postoperative chemotherapy, and the patient"s serum hCG level decreased to below the detection limit.	Methotrexate	48-60	hypertrichosis 2 (generalised, congenital)	Homo sapiens	170-173
26137037-10	2015	The lesion disappeared following five cycles of methotrexate+ etoposide+actinomycin D therapy, which was performed as postoperative chemotherapy, and the patient"s serum hCG level decreased to below the detection limit.	Etoposide	62-71	hypertrichosis 2 (generalised, congenital)	Homo sapiens	170-173
26137037-10	2015	The lesion disappeared following five cycles of methotrexate+ etoposide+actinomycin D therapy, which was performed as postoperative chemotherapy, and the patient"s serum hCG level decreased to below the detection limit.	Dactinomycin	72-85	hypertrichosis 2 (generalised, congenital)	Homo sapiens	170-173
25748801-0	2015	Reduction of progesterone, estradiol and hCG secretion by perfluorooctane sulfonate via induction of apoptosis in human placental syncytiotrophoblasts.	perfluorooctane sulfonic acid	58-83	hypertrichosis 2 (generalised, congenital)	Homo sapiens	41-44
25748801-9	2015	DISCUSSION: These results indicate that PFOS may disrupt the secretion of hCG, progesterone and estradiol by human placental syncytiotrophoblasts via induction of apoptosis.	perfluorooctane sulfonic acid	40-44	hypertrichosis 2 (generalised, congenital)	Homo sapiens	74-77
25337850-5	2015	Treatment with human chorionic gonadotropin (hCG) has shown the ability not only to reverse azoospermia brought on by testosterone supplementation therapy but also to help maintain elevated intratesticular testosterone levels.	Testosterone	206-218	hypertrichosis 2 (generalised, congenital)	Homo sapiens	45-48
25337850-6	2015	In addition, selective estrogen receptor modulators, often used with hCG have been shown both to elevate total testosterone levels and to maintain spermatogenesis in hypogonadal men.	Testosterone	111-123	hypertrichosis 2 (generalised, congenital)	Homo sapiens	69-72
25661494-4	2015	RESULTS: Methotrexate can be used as a treatment of tubal ectopic pregnancy with hCG&lt;5000 UI/L and expectative is an option if hCG level is lower than 1500 UI/L.	Methotrexate	9-21	hypertrichosis 2 (generalised, congenital)	Homo sapiens	81-84
25661494-4	2015	RESULTS: Methotrexate can be used as a treatment of tubal ectopic pregnancy with hCG&lt;5000 UI/L and expectative is an option if hCG level is lower than 1500 UI/L.	Methotrexate	9-21	hypertrichosis 2 (generalised, congenital)	Homo sapiens	130-133
25385007-2	2015	Recently, the co-administration of GnRH agonist and hCG for final oocyte maturation - 40 and 34 h prior to OPU, respectively (double trigger) was suggested to improve IVF outcome in patient with genuine empty follicle syndrome.	opu	107-110	hypertrichosis 2 (generalised, congenital)	Homo sapiens	52-55
26151993-1	2015	PURPOSE: To determine the effect of a drop in serum estradiol the day after injection of human chorionic gonadotropin (hCG) in in vitro fertilization-embryo transfer (IVF-ET) cycles in women aged 40-42 with diminished oocyte reserve.	Estradiol	52-61	hypertrichosis 2 (generalised, congenital)	Homo sapiens	119-122
25271059-7	2014	We identified a mechanism in which galactosyltransferase 4 isoform regulated N-glycan branching on the nascent protein, subsequently controlling biological activity in an in vivo model of hCG activity.	n-glycan	77-85	hypertrichosis 2 (generalised, congenital)	Homo sapiens	188-191
25447361-7	2014	Human chorionic gonadotropin (hCG) and progesterone are useful for pregnancy of unknown location (i.e. no gestational sac at transvaginal sonography): hCG ratio&lt;15% between two-day serum samples when first hCG is&lt;2000UI/mL (LE2) or low serum progesterone level (&lt;3.2ng/mL) (LE2) exclude viable intrauterine pregnancy.	Progesterone	39-51	hypertrichosis 2 (generalised, congenital)	Homo sapiens	151-154
25192259-6	2014	From the fifth day after hCG treatment, the level of vascular endothelial growth factor (VEGF) increased in the control, but decreased in the letrozole groups in a dose-dependent manner.	Letrozole	142-151	hypertrichosis 2 (generalised, congenital)	Homo sapiens	25-28
25430541-0	2014	In high responding patients undergoing an initial IVF cycle, elevated estradiol on the day of hCG has no effect on live birth rate.	Estradiol	70-79	hypertrichosis 2 (generalised, congenital)	Homo sapiens	94-97
25430541-1	2014	BACKGROUND: The impact of elevated estradiol on the day of human chorionic gonadotropin (hCG) administration on in vitro fertilization (IVF) outcomes has been debated for over 25 years.	Estradiol	35-44	hypertrichosis 2 (generalised, congenital)	Homo sapiens	89-92
25430541-11	2014	RESULTS: We found that estradiol was significantly related to + hCG, clinical pregnancy rate, age, and most other IVF cycle response variables.	Estradiol	23-32	hypertrichosis 2 (generalised, congenital)	Homo sapiens	64-67
25430541-15	2014	LB rates and AEQS were also not different in a subgroup of patients having an elevated level of estradiol (&gt;4200 pg/ml) on the day of hCG in patients having embryo transfer on day 3 or day 5.	Estradiol	96-105	hypertrichosis 2 (generalised, congenital)	Homo sapiens	137-140
25447361-7	2014	Human chorionic gonadotropin (hCG) and progesterone are useful for pregnancy of unknown location (i.e. no gestational sac at transvaginal sonography): hCG ratio&lt;15% between two-day serum samples when first hCG is&lt;2000UI/mL (LE2) or low serum progesterone level (&lt;3.2ng/mL) (LE2) exclude viable intrauterine pregnancy.	Progesterone	39-51	hypertrichosis 2 (generalised, congenital)	Homo sapiens	151-154
25275660-1	2014	INTRODUCTION: Hyperglycosylated human chorionic gonadotropin (hCG) is a variant of hCG with large oligosaccharide side chains.	Oligosaccharides	98-113	hypertrichosis 2 (generalised, congenital)	Homo sapiens	62-65
25275660-1	2014	INTRODUCTION: Hyperglycosylated human chorionic gonadotropin (hCG) is a variant of hCG with large oligosaccharide side chains.	Oligosaccharides	98-113	hypertrichosis 2 (generalised, congenital)	Homo sapiens	83-86
25229504-6	2014	Inhibition of p38 MAPK with SB203580 not only reduced the basal HSD11B2 mRNA and protein levels but also attenuated HSD11B2 levels induced by either hCG or dbcAMP.	SB 203580	28-36	hypertrichosis 2 (generalised, congenital)	Homo sapiens	149-152
25296696-1	2014	BACKGROUND: Recently, the co-administration of GnRH agonist and hCG for final oocyte maturation- 40 and 34 hours prior to OPU, respectively (double trigger) was suggested as the treatment of genuine empty follicle syndrome.	opu	122-125	hypertrichosis 2 (generalised, congenital)	Homo sapiens	64-67
25096723-2	2014	In cattle, treatment with human chorionic gonadotrophin (hCG) during the early postovulatory phase stimulates endogenous progesterone synthesis, which is an important factor for maintenance of early pregnancy via stimulation of endometrial function and conceptus development.	Progesterone	121-133	hypertrichosis 2 (generalised, congenital)	Homo sapiens	57-60
25229504-0	2014	Cross-talk between cAMP and MAPK pathways in HSD11B2 induction by hCG in placental trophoblasts.	Cyclic AMP	19-23	hypertrichosis 2 (generalised, congenital)	Homo sapiens	66-69
25229504-3	2014	Human chorionic gonadotropin (hCG) plays an important role in maintaining placental HSD11B2 expression via activation of the cAMP pathway.	Cyclic AMP	125-129	hypertrichosis 2 (generalised, congenital)	Homo sapiens	30-33
25229504-4	2014	In this study, we investigated the relationship between the activation of the cAMP pathway by hCG and subsequent phosphorylation of extracellular signal-regulated kinase1/2 (ERK1/2) or p38 mitogen-activated protein kinase (MAPK) pathways in the regulation of placental HSD11B2 expression in human placental syncytiotrophoblasts.	Cyclic AMP	78-82	hypertrichosis 2 (generalised, congenital)	Homo sapiens	94-97
24650341-4	2014	hCG (1,000 mIU/mL) increased progesterone (P4) synthesis after 24 H (P&lt;0.05).	Progesterone	29-41	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
25324873-0	2014	Adverse effects of 4-tert-octylphenol on the production of oxytocin and hCG in pregnant rats.	4-tert-octylphenol	19-37	hypertrichosis 2 (generalised, congenital)	Homo sapiens	72-75
24721478-5	2014	Native hCG is weakly thyrotropic but is produced in prodigious quantities and suppresses the production of thyroid stimulating hormone (TSH) but not curiously when TSH levels are in the higher deciles.	Thyrotropin	107-134	hypertrichosis 2 (generalised, congenital)	Homo sapiens	7-10
24721478-5	2014	Native hCG is weakly thyrotropic but is produced in prodigious quantities and suppresses the production of thyroid stimulating hormone (TSH) but not curiously when TSH levels are in the higher deciles.	Thyrotropin	136-139	hypertrichosis 2 (generalised, congenital)	Homo sapiens	7-10
24721478-5	2014	Native hCG is weakly thyrotropic but is produced in prodigious quantities and suppresses the production of thyroid stimulating hormone (TSH) but not curiously when TSH levels are in the higher deciles.	Thyrotropin	164-167	hypertrichosis 2 (generalised, congenital)	Homo sapiens	7-10
24721478-6	2014	Higher levels of hCG induce higher maternal production of thyroxine (T4).	Thyroxine	58-67	hypertrichosis 2 (generalised, congenital)	Homo sapiens	17-20
24721478-8	2014	This has lead to the suggestion that hCG serves as a backup system, albeit incomplete, for the production of essential thyroid hormone during pregnancy.	essential thyroid hormone	109-134	hypertrichosis 2 (generalised, congenital)	Homo sapiens	37-40
25229504-8	2014	These data suggest that p38 MAPK is involved in both basal and hCG/cAMP-induced expression of HSD11B2, and ERK1/2 may play a role opposite to p38 MAPK at least in the basal expression of HSD11B2 in human placental syncytiotrophoblasts and that there is complicated cross-talk between hCG/cAMP and MAPK cascades in the regulation of placental HSD11B2 expression.	Cyclic AMP	67-71	hypertrichosis 2 (generalised, congenital)	Homo sapiens	63-66
25229504-8	2014	These data suggest that p38 MAPK is involved in both basal and hCG/cAMP-induced expression of HSD11B2, and ERK1/2 may play a role opposite to p38 MAPK at least in the basal expression of HSD11B2 in human placental syncytiotrophoblasts and that there is complicated cross-talk between hCG/cAMP and MAPK cascades in the regulation of placental HSD11B2 expression.	Cyclic AMP	67-71	hypertrichosis 2 (generalised, congenital)	Homo sapiens	284-287
25229504-8	2014	These data suggest that p38 MAPK is involved in both basal and hCG/cAMP-induced expression of HSD11B2, and ERK1/2 may play a role opposite to p38 MAPK at least in the basal expression of HSD11B2 in human placental syncytiotrophoblasts and that there is complicated cross-talk between hCG/cAMP and MAPK cascades in the regulation of placental HSD11B2 expression.	Cyclic AMP	288-292	hypertrichosis 2 (generalised, congenital)	Homo sapiens	63-66
24793994-1	2014	During the first two trimesters of intrauterine life, fetal sex steroid production is driven by maternal human chorionic gonadotropin (hCG).	Steroids	64-71	hypertrichosis 2 (generalised, congenital)	Homo sapiens	135-138
24939956-1	2014	STUDY QUESTION: Are low serum progesterone levels on the day of human chorionic gonadotrophin (hCG) administration detrimental for live birth delivery rates during in vitro fertilization (IVF)?	Progesterone	30-42	hypertrichosis 2 (generalised, congenital)	Homo sapiens	95-98
24939956-18	2014	WIDER IMPLICATIONS OF THE FINDINGS: This study comprehensively assessed the relationship between live birth delivery rates and progesterone levels on the day of hCG administration during ovarian stimulation for IVF.	Progesterone	127-139	hypertrichosis 2 (generalised, congenital)	Homo sapiens	161-164
24438591-3	2014	We utilized a specific hLHR variant that lacks exon 10 (hLHR-delExon10), which maintains full cAMP signaling by hCG, but decreases hLH-induced receptor signaling, resulting in a pathogenic phenotype.	Cyclic AMP	94-98	hypertrichosis 2 (generalised, congenital)	Homo sapiens	112-115
23458081-0	2014	Effect of hCG administration during corpus luteum establishment on subsequent corpus luteum development and circulating progesterone concentrations in beef heifers.	Progesterone	120-132	hypertrichosis 2 (generalised, congenital)	Homo sapiens	10-13
24607250-3	2014	Human chorionic gonadotropin (hCG) is a glycoprotein hormone normally secreted by the human placenta, and structurally and functionally it is related to pituitary LH.	Luteinizing Hormone	163-165	hypertrichosis 2 (generalised, congenital)	Homo sapiens	30-33
24607250-5	2014	There are many physiological and pathological conditions where LH/hCG levels and actions are elevated.	Luteinizing Hormone	63-65	hypertrichosis 2 (generalised, congenital)	Homo sapiens	66-69
24607250-8	2014	This article summarizes recent findings on the mechanisms involved in pituitary gland tumorigenesis and hyperprolactinemia in the female mice hypersecreting hCG, in particular the relationship of progesterone with the hyperprolactinemic condition of the model.	Progesterone	196-208	hypertrichosis 2 (generalised, congenital)	Homo sapiens	157-160
23925891-5	2014	DHP and testosterone productions were increased with the increase of incubation time from 9 h through 15 h. E2 production was not further increased beyond 12 h. DHP production was highest by hCG compared to other effectors.	dhp	0-3	hypertrichosis 2 (generalised, congenital)	Homo sapiens	191-194
24161589-4	2014	GH promoter activation induced by hCG occurred with concurrent rise in cAMP production, CREB phosphorylation, and could be inhibited by inactivation of adenylate cyclase (AC), PKA, MEK1/2, P(38) MAPK, PI3K and mTOR.	Cyclic AMP	71-75	hypertrichosis 2 (generalised, congenital)	Homo sapiens	34-37
24161589-5	2014	AC activation, presumably via cAMP production, could mimic hCG-induced CREB phosphorylation and GH promoter activity, and these stimulatory effects were also sensitive to the blockade of PKA-, MAPK- and PI3K- dependent cascades.	Cyclic AMP	30-34	hypertrichosis 2 (generalised, congenital)	Homo sapiens	59-62
24297796-1	2014	CONTEXT: The role of human chorionic gonadotropin (hCG) supplementation on the intrafollicular steroid milieu has been studied.	Steroids	95-102	hypertrichosis 2 (generalised, congenital)	Homo sapiens	51-54
24297796-7	2014	RESULTS: In large follicles, hCG supplementation induced a nearly 3-fold increase of estradiol (nanomoles per liter) [D0: 1496; D50: 3138; D100: 4338; D150: 4009 (P &lt; .001)], a significant 3-fold increase of androstenedione, and a 5-fold increase of T (nanomoles per liter) [D0: 15; D50: 38; D100: 72; D150: 56 (P &lt; .001)].	Estradiol	85-94	hypertrichosis 2 (generalised, congenital)	Homo sapiens	29-32
24297796-7	2014	RESULTS: In large follicles, hCG supplementation induced a nearly 3-fold increase of estradiol (nanomoles per liter) [D0: 1496; D50: 3138; D100: 4338; D150: 4009 (P &lt; .001)], a significant 3-fold increase of androstenedione, and a 5-fold increase of T (nanomoles per liter) [D0: 15; D50: 38; D100: 72; D150: 56 (P &lt; .001)].	Androstenedione	211-226	hypertrichosis 2 (generalised, congenital)	Homo sapiens	29-32
24482059-13	2014	This review includes two RCTs with low risk of bias that compared urinary human chorionic gonadotrophin (hCG) versus no treatment in anovulatory women receiving clomiphene citrate.	Clomiphene	161-179	hypertrichosis 2 (generalised, congenital)	Homo sapiens	105-108
23925891-9	2014	hCG, like DHP, is equally potent and induces oocyte maturation via DHP production in vitro.	dhp	10-13	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
23925891-9	2014	hCG, like DHP, is equally potent and induces oocyte maturation via DHP production in vitro.	dhp	67-70	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
23925891-10	2014	hCG with DHP has synergistic action on oocyte maturation in mullet ovary.	dhp	9-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
23925891-5	2014	DHP and testosterone productions were increased with the increase of incubation time from 9 h through 15 h. E2 production was not further increased beyond 12 h. DHP production was highest by hCG compared to other effectors.	Testosterone	8-20	hypertrichosis 2 (generalised, congenital)	Homo sapiens	191-194
23925891-5	2014	DHP and testosterone productions were increased with the increase of incubation time from 9 h through 15 h. E2 production was not further increased beyond 12 h. DHP production was highest by hCG compared to other effectors.	dhp	161-164	hypertrichosis 2 (generalised, congenital)	Homo sapiens	191-194
23925891-6	2014	The hCG of all the test compounds was most effective in both the induction of GVBD% and steroid production.	Steroids	88-95	hypertrichosis 2 (generalised, congenital)	Homo sapiens	4-7
25387978-3	2014	Also, through its LH-mimicking effect, hCG can induce high oestradiol levels, resulting in stormy pubertal development.	Luteinizing Hormone	18-20	hypertrichosis 2 (generalised, congenital)	Homo sapiens	39-42
25387978-3	2014	Also, through its LH-mimicking effect, hCG can induce high oestradiol levels, resulting in stormy pubertal development.	Estradiol	59-69	hypertrichosis 2 (generalised, congenital)	Homo sapiens	39-42
24783055-9	2013	CONCLUSIONS: Pregnancy-associated hormones, particularly oxytocin and hCG, have a role in promoting placental iodide uptake which may protect the fetus against iodine deficiency.	Iodides	110-116	hypertrichosis 2 (generalised, congenital)	Homo sapiens	70-73
24783055-9	2013	CONCLUSIONS: Pregnancy-associated hormones, particularly oxytocin and hCG, have a role in promoting placental iodide uptake which may protect the fetus against iodine deficiency.	Iodine	160-166	hypertrichosis 2 (generalised, congenital)	Homo sapiens	70-73
24012150-1	2013	OBJECTIVE: During in vitro fertilization (IVF) treatment, elevated progesterone on the day of human chorionic gonadotrophin (hCG) administration has been reported to be associated with a reduced chance of live birth.	Progesterone	67-79	hypertrichosis 2 (generalised, congenital)	Homo sapiens	125-128
23448396-4	2013	RESULTS: A significant hCG dose-dependent incremental increase was found for progesterone (49-160%), 17-OH-progesterone (223-614%), androstenedione (91-340%) and testosterone (95-338%) from Dose 0 to Dose 150, respectively.	Progesterone	77-89	hypertrichosis 2 (generalised, congenital)	Homo sapiens	23-26
23448396-4	2013	RESULTS: A significant hCG dose-dependent incremental increase was found for progesterone (49-160%), 17-OH-progesterone (223-614%), androstenedione (91-340%) and testosterone (95-338%) from Dose 0 to Dose 150, respectively.	17-alpha-Hydroxyprogesterone	101-119	hypertrichosis 2 (generalised, congenital)	Homo sapiens	23-26
23448396-4	2013	RESULTS: A significant hCG dose-dependent incremental increase was found for progesterone (49-160%), 17-OH-progesterone (223-614%), androstenedione (91-340%) and testosterone (95-338%) from Dose 0 to Dose 150, respectively.	Androstenedione	132-147	hypertrichosis 2 (generalised, congenital)	Homo sapiens	23-26
23448396-4	2013	RESULTS: A significant hCG dose-dependent incremental increase was found for progesterone (49-160%), 17-OH-progesterone (223-614%), androstenedione (91-340%) and testosterone (95-338%) from Dose 0 to Dose 150, respectively.	Testosterone	162-174	hypertrichosis 2 (generalised, congenital)	Homo sapiens	23-26
23448396-9	2013	CONCLUSION: Supplementation with hCG resulted in a clear dose-related response for androgens, progesterone and 17-OH-progesterone.	Progesterone	94-106	hypertrichosis 2 (generalised, congenital)	Homo sapiens	33-36
23448396-9	2013	CONCLUSION: Supplementation with hCG resulted in a clear dose-related response for androgens, progesterone and 17-OH-progesterone.	17-alpha-Hydroxyprogesterone	111-129	hypertrichosis 2 (generalised, congenital)	Homo sapiens	33-36
23448396-10	2013	Oestradiol concentration reached maximum levels with an hCG dose of 100 IU/day, suggesting saturation of aromatase function.	Estradiol	0-10	hypertrichosis 2 (generalised, congenital)	Homo sapiens	56-59
24012150-8	2013	RESULTS: After adjusting for age, oestradiol level on the day of hCG administration and number of oocytes retrieved, the proportion of women with elevated progesterone on the day of hCG administration remained significantly different between the three groups: Group I, 16.8%; Group II, 31.7%; and Group III, 39.7% (p &lt; 0.001).	Progesterone	155-167	hypertrichosis 2 (generalised, congenital)	Homo sapiens	182-185
24012150-10	2013	Women with two or more IVF failures are twice as likely to have elevated progesterone on the day of hCG administration as women undergoing their first IVF cycle.	Progesterone	73-85	hypertrichosis 2 (generalised, congenital)	Homo sapiens	100-103
24012449-8	2013	The CPR was significantly higher in women with progesterone levels &lt;1.5 ng/ml at hCG (50%) compared with women with progesterone concentration &gt;= 1.5 ng/ml (33.3%) (odds ratio = 2.00, 95% confidence interval 1.07-3.75).	Progesterone	47-59	hypertrichosis 2 (generalised, congenital)	Homo sapiens	84-87
23932375-1	2013	OBJECTIVE: To investigate the relationship of the progesterone-to-estradiol (P/E2) ratio on the day of hCG administration with ongoing pregnancy rates in patients with normal ovarian reserve undergoing GnRH antagonist cycles.	Estradiol	66-75	hypertrichosis 2 (generalised, congenital)	Homo sapiens	103-106
23340513-2	2013	In recent years, CGH method using custom-designed high-density oligonucleotide-based arrays allowed the development of a powerful tool for detection of alterations at the level of exons and made it possible to provide flexibility through the possibility of modeling chips.	density oligonucleotide	55-78	hypertrichosis 2 (generalised, congenital)	Homo sapiens	17-20
23872290-2	2013	tEPs with pretreatment serum human chorionic gonadotrophin (hCG) levels &lt;1000 IU/L respond well to outpatient medical treatment with intramuscular methotrexate (MTX).	Methotrexate	150-162	hypertrichosis 2 (generalised, congenital)	Homo sapiens	60-63
23788572-9	2013	In CEC, hCG induced the phosphorylation of endothelial NO synthase through cAMP/PKA signaling and ERK1/2, Akt, p38 MAPK involvement, which were activated as downstream effectors of beta2-adrenoceptor stimulation.	Cyclic AMP	75-79	hypertrichosis 2 (generalised, congenital)	Homo sapiens	8-11
23506998-12	2013	Treatment with hCG plus carprofen at ET induced formation of secondary CL in 90% of heifers but decreased the luteotrophic effect of hCG, resulting in no effect on embryo survival.	carprofen	24-33	hypertrichosis 2 (generalised, congenital)	Homo sapiens	133-136
23427180-8	2013	In the endometrial explant model, the progesterone receptor antagonist RU486 inhibited the increases in the levels of C3 and DAF in response to hCG.	Mifepristone	71-76	hypertrichosis 2 (generalised, congenital)	Homo sapiens	144-147
23824416-14	2013	As a causative mechanism, we propose that gestational hyperandrogenism and hypoestrogenism reduced inhibition of placental GnRH and hCG secretion by progesterone, resulting in persistently elevated hCG.	Progesterone	149-161	hypertrichosis 2 (generalised, congenital)	Homo sapiens	132-135
23824416-14	2013	As a causative mechanism, we propose that gestational hyperandrogenism and hypoestrogenism reduced inhibition of placental GnRH and hCG secretion by progesterone, resulting in persistently elevated hCG.	Progesterone	149-161	hypertrichosis 2 (generalised, congenital)	Homo sapiens	198-201
23872290-2	2013	tEPs with pretreatment serum human chorionic gonadotrophin (hCG) levels &lt;1000 IU/L respond well to outpatient medical treatment with intramuscular methotrexate (MTX).	Methotrexate	164-167	hypertrichosis 2 (generalised, congenital)	Homo sapiens	60-63
23872290-3	2013	TEPs with hCG &gt;1000 IU/L take a significant time to resolve with MTX and require multiple outpatient monitoring visits.	Methotrexate	68-71	hypertrichosis 2 (generalised, congenital)	Homo sapiens	10-13
23872290-9	2013	We now describe the protocol of a larger single arm trial to estimate the efficacy and side effects of combination gefitinib and MTX to treat stable tEPs with hCG 1000-10 000 IU/L METHODS AND ANALYSIS: We propose to undertake a single-arm multicentre open label trial (in Edinburgh and Melbourne) and recruit 28 women with tEPs (pretreatment serum hCG 1000-10 000 IU/L).	Gefitinib	115-124	hypertrichosis 2 (generalised, congenital)	Homo sapiens	159-162
23872290-9	2013	We now describe the protocol of a larger single arm trial to estimate the efficacy and side effects of combination gefitinib and MTX to treat stable tEPs with hCG 1000-10 000 IU/L METHODS AND ANALYSIS: We propose to undertake a single-arm multicentre open label trial (in Edinburgh and Melbourne) and recruit 28 women with tEPs (pretreatment serum hCG 1000-10 000 IU/L).	Gefitinib	115-124	hypertrichosis 2 (generalised, congenital)	Homo sapiens	348-351
23872290-9	2013	We now describe the protocol of a larger single arm trial to estimate the efficacy and side effects of combination gefitinib and MTX to treat stable tEPs with hCG 1000-10 000 IU/L METHODS AND ANALYSIS: We propose to undertake a single-arm multicentre open label trial (in Edinburgh and Melbourne) and recruit 28 women with tEPs (pretreatment serum hCG 1000-10 000 IU/L).	Methotrexate	129-132	hypertrichosis 2 (generalised, congenital)	Homo sapiens	159-162
23875165-6	2013	The serum LH levels (mIU/mL) on hCG day were significantly higher in group B and C than in group A (22.7+-14.9 vs. 30.3+-15.9 vs. 3.2+-2.9, respectively; p&gt;0.001).	Luteinizing Hormone	10-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	32-35
23278834-7	2013	In the hCG-treated group, triglyceride level decreased, and luteinizing hormone level, TS and TV increased significantly.	Triglycerides	26-38	hypertrichosis 2 (generalised, congenital)	Homo sapiens	7-10
24032271-8	2013	CONCLUSIONS: 250 microg of r-hCG is sufficient and safe to trigger ovulation in women with BMI &gt; or = 30.	bmi &gt	91-98	hypertrichosis 2 (generalised, congenital)	Homo sapiens	29-32
23941020-2	2013	The syndrome has been previously reported in rare instances of increased production of human chorionic gonadotrophin (hCG) such as multiple pregnancies, hydatiforme mole, polycystic ovary disease and elevated concentrations of thyroid-stimulating hormone (TSH) in hypothyreoidism.	Thyrotropin	256-259	hypertrichosis 2 (generalised, congenital)	Homo sapiens	118-121
23510856-5	2013	The co-incubation of the follicles with both hCG (20IU/ml) and VT (100nM) increased significantly PGF2alpha level at 8h, higher than that elicited by each when incubated alone.	Dinoprost	98-107	hypertrichosis 2 (generalised, congenital)	Homo sapiens	45-48
23197744-12	2013	of lorglumide, a selective CCK(1) receptor antagonist, attenuated the hCG-induced inhibition of gastric emptying in Ovx rats, whereas central administration via the i.c.v.	lorglumide	3-13	hypertrichosis 2 (generalised, congenital)	Homo sapiens	70-73
23672306-10	2013	In contrast, thyroid stimulating hormone, fT3 and fT4 levels (thyroid hormones) either trended towards a correlation, or were significantly correlated with serum hCG levels in the two groups.	Thyrotropin	13-40	hypertrichosis 2 (generalised, congenital)	Homo sapiens	162-165
23408242-0	2013	Adverse placental effect of formic acid on hCG secretion is mitigated by folic acid.	formic acid	28-39	hypertrichosis 2 (generalised, congenital)	Homo sapiens	43-46
23408242-0	2013	Adverse placental effect of formic acid on hCG secretion is mitigated by folic acid.	Folic Acid	73-83	hypertrichosis 2 (generalised, congenital)	Homo sapiens	43-46
23408242-7	2013	Compared with the control period, there was a significant decrease in hCG secretion (P = 0.03) after addition of formic acid.	formic acid	113-124	hypertrichosis 2 (generalised, congenital)	Homo sapiens	70-73
23408242-8	2013	The addition of folic acid to the perfusate mitigated the decrease in hCG.	Folic Acid	16-26	hypertrichosis 2 (generalised, congenital)	Homo sapiens	70-73
23408242-10	2013	Formic acid decreases hCG secretion in the placenta, which may alter steroidogenesis and differentiation of the cytotrophoblasts, and this adverse effect can be mitigated by folate.	formic acid	0-11	hypertrichosis 2 (generalised, congenital)	Homo sapiens	22-25
23408242-10	2013	Formic acid decreases hCG secretion in the placenta, which may alter steroidogenesis and differentiation of the cytotrophoblasts, and this adverse effect can be mitigated by folate.	Folic Acid	174-180	hypertrichosis 2 (generalised, congenital)	Homo sapiens	22-25
23180308-11	2013	When we reviewed first trimester screening results, free-Beta-HCG was found to be lower for the group of IUFD after 34 weeks" gestation than in the group of live births (p &lt; 0.05).	free	52-56	hypertrichosis 2 (generalised, congenital)	Homo sapiens	62-65
23543584-23	2013	AUTHORS" CONCLUSIONS: We are very uncertain of the effect on live birth, OHSS and miscarriage of using low-dose hCG to replace FSH during the late follicular phase of COH in women undergoing ART, compared to the use of conventional COH.	coh	167-170	hypertrichosis 2 (generalised, congenital)	Homo sapiens	112-115
23583632-8	2013	ERK1/2 inactivation restores the ability of hCG to induce expression of the ovulatory genes in atrazine-exposed granulosa cells.	Atrazine	95-103	hypertrichosis 2 (generalised, congenital)	Homo sapiens	44-47
23587111-10	2013	RESULTS: We show that cAMP has an inductive effect on syncytialisation, as evidenced by induction of hCG secretion, by ERVW-1 mRNA expression and by formation of multinuclear cells.	Cyclic AMP	22-26	hypertrichosis 2 (generalised, congenital)	Homo sapiens	101-104
22872102-6	2013	The CNVs were detected by an exon-targeted array CGH with dense oligonucleotide coverage in exons of genes known or hypothesized to be causative of multiple human phenotypes.	Oligonucleotides	64-79	hypertrichosis 2 (generalised, congenital)	Homo sapiens	49-52
23256993-2	2013	It has been reported that Leydig cells, which produce testosterone in response to human chorionic gonadotropin (hCG), express key steroidogenic enzymes for the regulation of testosterone synthesis.	Testosterone	54-66	hypertrichosis 2 (generalised, congenital)	Homo sapiens	112-115
23369098-0	2013	Using a decline in serum hCG between days 0-4 to predict ectopic pregnancy treatment success after single-dose methotrexate: a retrospective cohort study.	Methotrexate	111-123	hypertrichosis 2 (generalised, congenital)	Homo sapiens	25-28
23369098-1	2013	BACKGROUND: The current measure of treatment efficacy of single-dose methotrexate for ectopic pregnancy, is a fall in serum hCG of &gt;=15% between days 4-7 of treatment, which has a positive predictive value of 93% for treatment success.	Methotrexate	69-81	hypertrichosis 2 (generalised, congenital)	Homo sapiens	124-127
23369098-4	2013	METHODS: We conducted a retrospective study of women (n=206) treated with single-dose methotrexate for ectopic pregnancy (pre-treatment serum hCG levels &lt;=3000 IU/L) at Scottish hospitals between 2006-2011.	Methotrexate	86-98	hypertrichosis 2 (generalised, congenital)	Homo sapiens	142-145
23369098-11	2013	CONCLUSIONS: We have verified that a decline in serum hCG between days 0-4 after methotrexate treatment for ectopic pregnancies, with pre-treatment serum hCG levels &lt;=3000 IU/L, provides an early indication of likelihood of treatment success, and performs just as well as the existing measure, which only provides prognostic information on day 7.	Methotrexate	81-93	hypertrichosis 2 (generalised, congenital)	Homo sapiens	54-57
23369098-11	2013	CONCLUSIONS: We have verified that a decline in serum hCG between days 0-4 after methotrexate treatment for ectopic pregnancies, with pre-treatment serum hCG levels &lt;=3000 IU/L, provides an early indication of likelihood of treatment success, and performs just as well as the existing measure, which only provides prognostic information on day 7.	Methotrexate	81-93	hypertrichosis 2 (generalised, congenital)	Homo sapiens	154-157
23256993-2	2013	It has been reported that Leydig cells, which produce testosterone in response to human chorionic gonadotropin (hCG), express key steroidogenic enzymes for the regulation of testosterone synthesis.	Testosterone	174-186	hypertrichosis 2 (generalised, congenital)	Homo sapiens	112-115
23256993-9	2013	Based on transmission electron microscopy and H&amp;E staining of the testis, it was shown that abnormal ER morphology and destruction of testicular histology induced by high-level hCG treatment were reversed by the addition of TUDCA.	Adenosine Monophosphate	48-51	hypertrichosis 2 (generalised, congenital)	Homo sapiens	181-184
23256993-9	2013	Based on transmission electron microscopy and H&amp;E staining of the testis, it was shown that abnormal ER morphology and destruction of testicular histology induced by high-level hCG treatment were reversed by the addition of TUDCA.	ursodoxicoltaurine	228-233	hypertrichosis 2 (generalised, congenital)	Homo sapiens	181-184
23555083-2	2013	In this study, array CGH was applied in 64 prenatal samples with whole genome oligonucleotide arrays (BlueGnome, Ltd.) on DNA extracted from chorionic villi, amniotic fluid, foetal blood, and skin samples.	Oligonucleotides	78-93	hypertrichosis 2 (generalised, congenital)	Homo sapiens	21-24
23081873-0	2013	Methotrexate or expectant management in women with an ectopic pregnancy or pregnancy of unknown location and low serum hCG concentrations?	Methotrexate	0-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	119-122
24383016-4	2013	Testosterone to DHT ratio (T/DHT) was elevated before (15.72) and further increased after hCG stimulation (32.46).	Testosterone	0-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	90-93
22967399-1	2013	OBJECTIVE: To evaluate the efficacy of estradiol supplementation starting on the day of human chorionic gonadotrophin (hCG) in patients with thin endometrium in intracytoplasmic sperm injection (ICSI) cycles.	Estradiol	39-48	hypertrichosis 2 (generalised, congenital)	Homo sapiens	119-122
22967399-4	2013	Estradiol supplemented (ES) group received estradiol hemihydrate 4 mg/day started on the day of hCG.	Estradiol	0-9	hypertrichosis 2 (generalised, congenital)	Homo sapiens	96-99
23081873-4	2013	WHAT IS KNOWN AND WHAT THIS PAPER ADDS: MTX is often used in asymptomatic women with an ectopic pregnancy or a PUL with low and plateauing serum hCG concentrations.	Methotrexate	40-43	hypertrichosis 2 (generalised, congenital)	Homo sapiens	145-148
23081873-19	2013	WIDER IMPLICATIONS OF THE FINDINGS: Sixty percent of women after expectant management had an uneventful clinical course with steadily declining serum hCG levels without any intervention, which means that MTX, a potentially harmful drug, can be withheld in these women.	Methotrexate	204-207	hypertrichosis 2 (generalised, congenital)	Homo sapiens	150-153
22791754-4	2012	A ceiling level of estradiol (E(2)) was reached with hCG doses above 100 IU/day.	Estradiol	19-28	hypertrichosis 2 (generalised, congenital)	Homo sapiens	53-56
23540161-2	2012	The study evaluated MTX treatment efficacy in 35 women with ectopic pregnancies in relation to the initial levels of human chorionic gonadotropin (hCG) and progesterone.	Methotrexate	20-23	hypertrichosis 2 (generalised, congenital)	Homo sapiens	147-150
23540161-5	2012	The mean initial hCG level was 393.10 +/- 305.9 IU/L in patients successfully treated with a single dose of MTX and 973.5 +/- 722.40 IU/L in those with an additional dose of MTX (p &lt; 0.002).	Methotrexate	108-111	hypertrichosis 2 (generalised, congenital)	Homo sapiens	17-20
23540161-8	2012	It is concluded that pretreatment values of hCG and progesterone are inversely related to medicamentous treatment success in selected cases ofhemodynamically stable patients, thus they may be used as an important predictor in the management of ectopic pregnancy treated with MTX.	Methotrexate	275-278	hypertrichosis 2 (generalised, congenital)	Homo sapiens	44-47
22713854-3	2012	hCG or forskolin+PMA induced the transient increase in Runx1, Ptgs2, and Tnfaip6 expression, while the expression of Runx2 continued to increase until 48 h. The knockdown of the agonist-stimulated Runx2 expression increased Runx1, Ptgs2, and Tnfaip6 expression and PGE(2) levels in luteinizing granulosa cells.	Prostaglandins E	265-268	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
22867812-6	2012	Our results showed that BDE-47 could reduce progesterone production and decrease the intracellular cAMP level induced by hCG or forskolin.	2,2',4,4'-tetrabromodiphenyl ether	24-30	hypertrichosis 2 (generalised, congenital)	Homo sapiens	121-124
22867812-6	2012	Our results showed that BDE-47 could reduce progesterone production and decrease the intracellular cAMP level induced by hCG or forskolin.	Cyclic AMP	99-103	hypertrichosis 2 (generalised, congenital)	Homo sapiens	121-124
21988613-1	2012	The influence of sexual stimulation and human chorionic gonadotrophin (hCG) administration on plasma testosterone concentrations was assessed in five male Beagles.	Testosterone	101-113	hypertrichosis 2 (generalised, congenital)	Homo sapiens	71-74
22878993-7	2012	She was given a second dose of methotrexate after 1&amp;emsp14;week, since her beta hCG levels did not demonstrate a satisfactory fall.	Methotrexate	31-43	hypertrichosis 2 (generalised, congenital)	Homo sapiens	84-87
22818453-11	2012	Pregnancy per AI at d 32 or 60 after first AI was less in hCG- than saline-treated cows because pregnancy outcome for hCG cows that had only 1 pretreatment CL and failed to respond to hCG was only 55 to 61% of that observed in controls.	Sodium Chloride	68-74	hypertrichosis 2 (generalised, congenital)	Homo sapiens	118-121
22818453-11	2012	Pregnancy per AI at d 32 or 60 after first AI was less in hCG- than saline-treated cows because pregnancy outcome for hCG cows that had only 1 pretreatment CL and failed to respond to hCG was only 55 to 61% of that observed in controls.	Sodium Chloride	68-74	hypertrichosis 2 (generalised, congenital)	Homo sapiens	118-121
22540910-5	2012	The aim of this study is to verify if MTX is more effective than the placebo in women with tubal EP and rising/plateauing serum human chorionic gonadotrophin (hCG) levels.	Methotrexate	38-41	hypertrichosis 2 (generalised, congenital)	Homo sapiens	159-162
22540910-14	2012	If any increase in serum hCG &gt; 15% between days 4 - 7 or at any subsequent follow-up, women will be treated with MTX.	Methotrexate	116-119	hypertrichosis 2 (generalised, congenital)	Homo sapiens	25-28
22540910-17	2012	DISCUSSION: This trial will clarify the actual effectiveness of MTX in haemodynamically stable women with an early tubal EPs and rising or plateauing hCG.	Methotrexate	64-67	hypertrichosis 2 (generalised, congenital)	Homo sapiens	150-153
22455390-3	2012	hCG is the most acidic glycoprotein containing the highest proportion of sugars.	Sugars	73-79	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
22619348-6	2012	The brother"s low testosterone (1.87 nmol/l) responded to combined hCG and human menopausal gonadotropin (hCG) and HMG therapies, but the testes remained small (1-2 ml).	Testosterone	18-30	hypertrichosis 2 (generalised, congenital)	Homo sapiens	67-70
22619348-6	2012	The brother"s low testosterone (1.87 nmol/l) responded to combined hCG and human menopausal gonadotropin (hCG) and HMG therapies, but the testes remained small (1-2 ml).	Testosterone	18-30	hypertrichosis 2 (generalised, congenital)	Homo sapiens	106-109
22427666-4	2012	Human chorionic gonadotropin (hCG) induces de novo synthesis of STAR, a process shown to parallel maximal steroid production.	Steroids	106-113	hypertrichosis 2 (generalised, congenital)	Homo sapiens	30-33
22427666-11	2012	The binding site of 14-3-3gamma on STAR was identified to be Ser-194 in the STAR-related sterol binding lipid transfer (START) domain, the site phosphorylated in response to hCG.	Serine	61-64	hypertrichosis 2 (generalised, congenital)	Homo sapiens	174-177
22427666-11	2012	The binding site of 14-3-3gamma on STAR was identified to be Ser-194 in the STAR-related sterol binding lipid transfer (START) domain, the site phosphorylated in response to hCG.	Sterols	89-95	hypertrichosis 2 (generalised, congenital)	Homo sapiens	174-177
22138749-7	2012	Our results show that (i) LHCGR, the hCG receptor, is expressed both in cyto- and syncytiotrophoblasts, (ii) hCG increases EG-VEGF, PROKR1 and PROKR2 mRNA and protein expression in a dose- and time-dependent manner, (iii) hCG increases the release of EG-VEGF from PEX conditioned media, (iv) hCG effects are transcriptional and post-transcriptional and (v) the hCG effects are mediated by cAMP via cAMP response elements present in the EG-VEGF promoter region.	Cyclic AMP	389-393	hypertrichosis 2 (generalised, congenital)	Homo sapiens	37-40
22138749-7	2012	Our results show that (i) LHCGR, the hCG receptor, is expressed both in cyto- and syncytiotrophoblasts, (ii) hCG increases EG-VEGF, PROKR1 and PROKR2 mRNA and protein expression in a dose- and time-dependent manner, (iii) hCG increases the release of EG-VEGF from PEX conditioned media, (iv) hCG effects are transcriptional and post-transcriptional and (v) the hCG effects are mediated by cAMP via cAMP response elements present in the EG-VEGF promoter region.	Cyclic AMP	389-393	hypertrichosis 2 (generalised, congenital)	Homo sapiens	109-112
22138749-7	2012	Our results show that (i) LHCGR, the hCG receptor, is expressed both in cyto- and syncytiotrophoblasts, (ii) hCG increases EG-VEGF, PROKR1 and PROKR2 mRNA and protein expression in a dose- and time-dependent manner, (iii) hCG increases the release of EG-VEGF from PEX conditioned media, (iv) hCG effects are transcriptional and post-transcriptional and (v) the hCG effects are mediated by cAMP via cAMP response elements present in the EG-VEGF promoter region.	Cyclic AMP	389-393	hypertrichosis 2 (generalised, congenital)	Homo sapiens	109-112
22138749-7	2012	Our results show that (i) LHCGR, the hCG receptor, is expressed both in cyto- and syncytiotrophoblasts, (ii) hCG increases EG-VEGF, PROKR1 and PROKR2 mRNA and protein expression in a dose- and time-dependent manner, (iii) hCG increases the release of EG-VEGF from PEX conditioned media, (iv) hCG effects are transcriptional and post-transcriptional and (v) the hCG effects are mediated by cAMP via cAMP response elements present in the EG-VEGF promoter region.	Cyclic AMP	389-393	hypertrichosis 2 (generalised, congenital)	Homo sapiens	109-112
22138749-7	2012	Our results show that (i) LHCGR, the hCG receptor, is expressed both in cyto- and syncytiotrophoblasts, (ii) hCG increases EG-VEGF, PROKR1 and PROKR2 mRNA and protein expression in a dose- and time-dependent manner, (iii) hCG increases the release of EG-VEGF from PEX conditioned media, (iv) hCG effects are transcriptional and post-transcriptional and (v) the hCG effects are mediated by cAMP via cAMP response elements present in the EG-VEGF promoter region.	Cyclic AMP	389-393	hypertrichosis 2 (generalised, congenital)	Homo sapiens	109-112
22138749-7	2012	Our results show that (i) LHCGR, the hCG receptor, is expressed both in cyto- and syncytiotrophoblasts, (ii) hCG increases EG-VEGF, PROKR1 and PROKR2 mRNA and protein expression in a dose- and time-dependent manner, (iii) hCG increases the release of EG-VEGF from PEX conditioned media, (iv) hCG effects are transcriptional and post-transcriptional and (v) the hCG effects are mediated by cAMP via cAMP response elements present in the EG-VEGF promoter region.	Cyclic AMP	398-402	hypertrichosis 2 (generalised, congenital)	Homo sapiens	37-40
22138749-7	2012	Our results show that (i) LHCGR, the hCG receptor, is expressed both in cyto- and syncytiotrophoblasts, (ii) hCG increases EG-VEGF, PROKR1 and PROKR2 mRNA and protein expression in a dose- and time-dependent manner, (iii) hCG increases the release of EG-VEGF from PEX conditioned media, (iv) hCG effects are transcriptional and post-transcriptional and (v) the hCG effects are mediated by cAMP via cAMP response elements present in the EG-VEGF promoter region.	Cyclic AMP	398-402	hypertrichosis 2 (generalised, congenital)	Homo sapiens	109-112
22138749-7	2012	Our results show that (i) LHCGR, the hCG receptor, is expressed both in cyto- and syncytiotrophoblasts, (ii) hCG increases EG-VEGF, PROKR1 and PROKR2 mRNA and protein expression in a dose- and time-dependent manner, (iii) hCG increases the release of EG-VEGF from PEX conditioned media, (iv) hCG effects are transcriptional and post-transcriptional and (v) the hCG effects are mediated by cAMP via cAMP response elements present in the EG-VEGF promoter region.	Cyclic AMP	398-402	hypertrichosis 2 (generalised, congenital)	Homo sapiens	109-112
22138749-7	2012	Our results show that (i) LHCGR, the hCG receptor, is expressed both in cyto- and syncytiotrophoblasts, (ii) hCG increases EG-VEGF, PROKR1 and PROKR2 mRNA and protein expression in a dose- and time-dependent manner, (iii) hCG increases the release of EG-VEGF from PEX conditioned media, (iv) hCG effects are transcriptional and post-transcriptional and (v) the hCG effects are mediated by cAMP via cAMP response elements present in the EG-VEGF promoter region.	Cyclic AMP	398-402	hypertrichosis 2 (generalised, congenital)	Homo sapiens	109-112
22138749-7	2012	Our results show that (i) LHCGR, the hCG receptor, is expressed both in cyto- and syncytiotrophoblasts, (ii) hCG increases EG-VEGF, PROKR1 and PROKR2 mRNA and protein expression in a dose- and time-dependent manner, (iii) hCG increases the release of EG-VEGF from PEX conditioned media, (iv) hCG effects are transcriptional and post-transcriptional and (v) the hCG effects are mediated by cAMP via cAMP response elements present in the EG-VEGF promoter region.	Cyclic AMP	398-402	hypertrichosis 2 (generalised, congenital)	Homo sapiens	109-112
22313871-8	2012	In addition, E(2) concentrations are poorly reproducible and a wide range of variation in all serum steroids investigated-including E(2)-after hCG injection was observed.	Estradiol	13-16	hypertrichosis 2 (generalised, congenital)	Homo sapiens	143-146
21988613-6	2012	In the control treatment, the testosterone plasma levels did not show significant changes throughout the tested period (mean values ranging between 2.8 and 4.7 ng/ml); the hCG group presented a significant increase (p &lt; 0.05) in plasma testosterone levels 30 min after hCG administration and had the highest value (8.7 ng/ml) at 120 min post-hCG.	Testosterone	239-251	hypertrichosis 2 (generalised, congenital)	Homo sapiens	172-175
21988613-8	2012	When the groups were compared, the hCG group showed higher plasma testosterone values (p &lt; 0.05) than did the C and SS groups, starting at 30 min and continuing until the end of sampling.	Testosterone	66-78	hypertrichosis 2 (generalised, congenital)	Homo sapiens	35-38
22053093-4	2012	Forskolin induces both hCG secretion and BeWo cell syncytial fusion.	Colforsin	0-9	hypertrichosis 2 (generalised, congenital)	Homo sapiens	23-26
22222192-7	2012	RESULT(S): 1) At a dose of 0.25 IU/mL-2.5 IU/mL LMWH promoted trophoblast proliferation, enhanced their invasion, and increased hCG secretion.	Heparin, Low-Molecular-Weight	48-52	hypertrichosis 2 (generalised, congenital)	Homo sapiens	128-131
22561619-11	2012	RESULTS: Differential effects on cell proliferation were observed in long term cultures, where the untreated and hCG exposed cells showed markedly reduced cell proliferation after second week of exposure while LH treated cells continued to proliferate.	Luteinizing Hormone	210-212	hypertrichosis 2 (generalised, congenital)	Homo sapiens	113-116
22561619-13	2012	On sustained hormonal stimulation, cAMP levels were significantly (P&lt;0.05) higher in hCG treated cultures as compared to controls and LH treated cultures.	Cyclic AMP	35-39	hypertrichosis 2 (generalised, congenital)	Homo sapiens	88-91
22561619-16	2012	Prolonged LH treatment promoted growth and proliferation in caprine ovarian granulosa cells whereas prolonged exposure to hCG led to elevated levels of cAMP and decreased the rate of proliferation.	Cyclic AMP	152-156	hypertrichosis 2 (generalised, congenital)	Homo sapiens	122-125
22740971-6	2012	Following 2 cycles of combinative chemotherapy consisting of fluorouracil (5-FU) and dactinomycin (KSM), hCG concentrations decreased to normal levels.	Fluorouracil	61-73	hypertrichosis 2 (generalised, congenital)	Homo sapiens	105-108
22740971-6	2012	Following 2 cycles of combinative chemotherapy consisting of fluorouracil (5-FU) and dactinomycin (KSM), hCG concentrations decreased to normal levels.	Fluorouracil	75-79	hypertrichosis 2 (generalised, congenital)	Homo sapiens	105-108
22740971-6	2012	Following 2 cycles of combinative chemotherapy consisting of fluorouracil (5-FU) and dactinomycin (KSM), hCG concentrations decreased to normal levels.	Dactinomycin	85-97	hypertrichosis 2 (generalised, congenital)	Homo sapiens	105-108
22740971-6	2012	Following 2 cycles of combinative chemotherapy consisting of fluorouracil (5-FU) and dactinomycin (KSM), hCG concentrations decreased to normal levels.	kasugamycin	99-102	hypertrichosis 2 (generalised, congenital)	Homo sapiens	105-108
22053093-5	2012	Although LIF had no effect on the undifferentiated state of the cells, the cytokine generated a strong reduction in forskolin-induced hCG release.	Colforsin	116-125	hypertrichosis 2 (generalised, congenital)	Homo sapiens	134-137
21856376-0	2012	Differential modulation of apoptotic gene expression by N-acetyl-L-cysteine in Leydig cells stimulated persistently with hCG in vivo.	Acetylcysteine	56-75	hypertrichosis 2 (generalised, congenital)	Homo sapiens	121-124
22289288-12	2012	When follicles cultured with androstenedione were treated with hCG and EGF, the first polar body exclusion, chromosome alignment on metaphase plate, and spindle assembly were inhibited in the oocytes.	Androstenedione	29-44	hypertrichosis 2 (generalised, congenital)	Homo sapiens	63-66
21856376-1	2012	The present study was designed to investigate the molecular mechanisms of NAC (150 mg/kg bw twice/week) action in vivo under repeated hCG (100 IU/rat/day) stimulation to adult rats.	Acetylcysteine	74-77	hypertrichosis 2 (generalised, congenital)	Homo sapiens	134-137
21856376-2	2012	Leydig cell refractoriness led to a significant decline in serum testosterone and intracellular cAMP by day 30 of chronic hCG intervention which improved significantly following NAC co-administration.	Testosterone	65-77	hypertrichosis 2 (generalised, congenital)	Homo sapiens	122-125
21856376-2	2012	Leydig cell refractoriness led to a significant decline in serum testosterone and intracellular cAMP by day 30 of chronic hCG intervention which improved significantly following NAC co-administration.	Cyclic AMP	96-100	hypertrichosis 2 (generalised, congenital)	Homo sapiens	122-125
21856376-2	2012	Leydig cell refractoriness led to a significant decline in serum testosterone and intracellular cAMP by day 30 of chronic hCG intervention which improved significantly following NAC co-administration.	Acetylcysteine	178-181	hypertrichosis 2 (generalised, congenital)	Homo sapiens	122-125
22206043-1	2012	The term human chorionic gonadotropin (hCG) refers to a group of 5 molecules, each sharing the common amino acid sequence but each differing in meric structure and carbohydrate side chain structure.	Carbohydrates	164-176	hypertrichosis 2 (generalised, congenital)	Homo sapiens	39-42
22103973-1	2012	The pregnancy hormone human chorionic gonadotropin (hCG) is essential to sustain early pregnancy and involved in regulation of progesterone production, decidualization, and cytotrophoblast differentiation.	Progesterone	127-139	hypertrichosis 2 (generalised, congenital)	Homo sapiens	52-55
22963487-2	2012	We found that N-(3-dimethyl aminopropyl)-N"-ethylcarbodiimide hydrochloride (EDC) was the best cross-linking reagent to link anti hCG alpha antibody to superparamagnetic particle (SPIO-anti hCG alpha antibody immunomagnetic particle).	n-(3-dimethyl aminopropyl)-n"-ethylcarbodiimide hydrochloride	14-75	hypertrichosis 2 (generalised, congenital)	Homo sapiens	130-133
22963487-2	2012	We found that N-(3-dimethyl aminopropyl)-N"-ethylcarbodiimide hydrochloride (EDC) was the best cross-linking reagent to link anti hCG alpha antibody to superparamagnetic particle (SPIO-anti hCG alpha antibody immunomagnetic particle).	n-(3-dimethyl aminopropyl)-n"-ethylcarbodiimide hydrochloride	14-75	hypertrichosis 2 (generalised, congenital)	Homo sapiens	190-193
22963487-2	2012	We found that N-(3-dimethyl aminopropyl)-N"-ethylcarbodiimide hydrochloride (EDC) was the best cross-linking reagent to link anti hCG alpha antibody to superparamagnetic particle (SPIO-anti hCG alpha antibody immunomagnetic particle).	ethylene dichloride	77-80	hypertrichosis 2 (generalised, congenital)	Homo sapiens	130-133
22963487-2	2012	We found that N-(3-dimethyl aminopropyl)-N"-ethylcarbodiimide hydrochloride (EDC) was the best cross-linking reagent to link anti hCG alpha antibody to superparamagnetic particle (SPIO-anti hCG alpha antibody immunomagnetic particle).	ethylene dichloride	77-80	hypertrichosis 2 (generalised, congenital)	Homo sapiens	190-193
23071612-5	2012	In COS-7/LHCGR cells, hCG is 5-fold more potent than hLH (cAMP ED(50): 107.1+-14.3 pM and 530.0+-51.2 pM, respectively).	Cyclic AMP	58-62	hypertrichosis 2 (generalised, congenital)	Homo sapiens	22-25
22511897-0	2012	Unique Combination of 22q11 and 14qter Microdeletion Syndromes Detected Using Oligonucleotide Array-CGH.	Oligonucleotides	78-93	hypertrichosis 2 (generalised, congenital)	Homo sapiens	100-103
22511897-5	2012	Using comparative genome hybridization on oligonucleotide-based microarray (array-CGH), the deletion at 22q11.21 in the size of ~4.25 Mb was revealed in the proband as well as the deletion of the telomeric area at 14q32.33qter (~3.24 Mb) in the proband and his mother.	Oligonucleotides	42-57	hypertrichosis 2 (generalised, congenital)	Homo sapiens	82-85
23056265-3	2012	We also found that hCG increased cAMP intracellular levels in BeWo cells in a dose-dependent manner, stimulated cAMP response element (CRE) activity and the cotransfection with an expression plasmid of a dominant negative mutant of CREB caused a significant inhibition of hCG stimulation of leptin promoter activity.	Cyclic AMP	33-37	hypertrichosis 2 (generalised, congenital)	Homo sapiens	19-22
23056265-3	2012	We also found that hCG increased cAMP intracellular levels in BeWo cells in a dose-dependent manner, stimulated cAMP response element (CRE) activity and the cotransfection with an expression plasmid of a dominant negative mutant of CREB caused a significant inhibition of hCG stimulation of leptin promoter activity.	Cyclic AMP	112-116	hypertrichosis 2 (generalised, congenital)	Homo sapiens	19-22
23056265-4	2012	These results demonstrate that hCG indeed activates cAMP/PKA pathway, and that this pathway is involved in leptin expression.	Cyclic AMP	52-56	hypertrichosis 2 (generalised, congenital)	Homo sapiens	31-34
23056265-5	2012	Nevertheless, we found leptin induction by hCG is dependent on cAMP levels.	Cyclic AMP	63-67	hypertrichosis 2 (generalised, congenital)	Homo sapiens	43-46
22518314-7	2012	RESULTS: In male-bearing pregnancies, maternal hCG and testosterone serum levels were significantly higher in preeclamptic than normotensive mothers (P &lt; 0.001 and P &lt; 0.001, resp.) in female-bearing pregnancies testosterone levels were significantly higher in preeclamptic than normotensive mothers (P &lt; 0.001).	Testosterone	218-230	hypertrichosis 2 (generalised, congenital)	Homo sapiens	47-50
23071612-6	2012	hLH maximal effect was significantly faster (10 minutes by hLH; 1 hour by hCG).	MY 12-62c	0-3	hypertrichosis 2 (generalised, congenital)	Homo sapiens	74-77
23071612-7	2012	In hGLC continuous exposure to equipotent doses of gonadotropins up to 36 hours revealed that intracellular cAMP production is oscillating and significantly higher by hCG versus hLH.	Cyclic AMP	108-112	hypertrichosis 2 (generalised, congenital)	Homo sapiens	167-170
23071612-10	2012	We conclude that: i) hCG is more potent on cAMP production, while hLH is more potent on ERK and AKT activation; ii) hGLC respond to equipotent, constant hLH or hCG stimulation with a fluctuating cAMP production and progressive progesterone secretion; and iii) the expression of hLH and hCG target genes partly involves the activation of different pathways depending on the ligand.	Cyclic AMP	43-47	hypertrichosis 2 (generalised, congenital)	Homo sapiens	21-24
21562093-0	2011	Cross talk between cAMP and p38 MAPK pathways in the induction of leptin by hCG in human placental syncytiotrophoblasts.	Cyclic AMP	19-23	hypertrichosis 2 (generalised, congenital)	Homo sapiens	76-79
22518314-9	2012	CONCLUSION: According to our results, there is a correlation between maternal serum hCG and testosterone levels and preeclampsia.	Testosterone	92-104	hypertrichosis 2 (generalised, congenital)	Homo sapiens	84-87
21732905-3	2011	HP-hMG provides FSH and exogenous LH activity mainly in the form of human chorionic gonadotrophin (hCG).	hp-hmg	0-6	hypertrichosis 2 (generalised, congenital)	Homo sapiens	99-102
21732905-8	2011	On the other hand, exogenous hCG activity during HP-hMG stimulation is positively associated with treatment outcome.	hp-hmg	49-55	hypertrichosis 2 (generalised, congenital)	Homo sapiens	29-32
23056265-7	2012	We found that specific PKA inhibition by H89 caused a significant increase of hCG leptin induction, suggesting that probably high cAMP levels might inhibit hCG effect.	Cyclic AMP	130-134	hypertrichosis 2 (generalised, congenital)	Homo sapiens	78-81
23056265-7	2012	We found that specific PKA inhibition by H89 caused a significant increase of hCG leptin induction, suggesting that probably high cAMP levels might inhibit hCG effect.	Cyclic AMP	130-134	hypertrichosis 2 (generalised, congenital)	Homo sapiens	156-159
23056265-12	2012	We observed that a cAMP analogue that specifically activates Epac (CPT-OMe) stimulated leptin expression by hCG.	Cyclic AMP	19-23	hypertrichosis 2 (generalised, congenital)	Homo sapiens	108-111
23056265-14	2012	In conclusion, we provide evidence suggesting that hCG induction of leptin gene expression in placenta is mediated not only by activation of the MAPK signaling pathway but also by the alternative cAMP/Epac signaling pathway.	Cyclic AMP	196-200	hypertrichosis 2 (generalised, congenital)	Homo sapiens	51-54
22047664-7	2011	After the interim analysis, the modified study group (n = 107) received intrauterine injection of 500 IU of hCG, and the control group (n = 105) underwent ET without hCG.	intrauterine	72-84	hypertrichosis 2 (generalised, congenital)	Homo sapiens	108-111
21734266-5	2011	Gelatinolytic activity and progesterone were induced in response to hCG; however, there was no difference in progesterone between cells treated with or without the inhibitor.	Progesterone	27-39	hypertrichosis 2 (generalised, congenital)	Homo sapiens	68-71
21512124-10	2011	We conclude that hCG was more effective than GnRH in its ability to cause disappearance of the largest follicle, increase volume of luteal tissue in the subsequent developing luteal structures, and increase concentrations of progesterone in prepubertal heifers.	Progesterone	225-237	hypertrichosis 2 (generalised, congenital)	Homo sapiens	17-20
21600908-2	2011	We evaluated effects of supplementation of exogenous progesterone on human chorionic gonadotropin (hCG)-induced ovulatory response in immature rats.	Progesterone	53-65	hypertrichosis 2 (generalised, congenital)	Homo sapiens	99-102
21600908-3	2011	Equine CG-primed mature follicles responded to hCG with induction of immunoreactive steroidogenic acute regulatory protein (StAR) mainly in thecal layers and a transient enhancement in progesterone synthesis peaking at 6h after hCG (hCG6h).	Progesterone	185-197	hypertrichosis 2 (generalised, congenital)	Homo sapiens	7-9
21600908-3	2011	Equine CG-primed mature follicles responded to hCG with induction of immunoreactive steroidogenic acute regulatory protein (StAR) mainly in thecal layers and a transient enhancement in progesterone synthesis peaking at 6h after hCG (hCG6h).	Progesterone	185-197	hypertrichosis 2 (generalised, congenital)	Homo sapiens	47-50
21061451-5	2011	Those compounds inhibited hCG-stimulated androgen production by Leydig cells at all stages of their development, a process that was associated with the reduced ability of the cells to produce cAMP.	Cyclic AMP	192-196	hypertrichosis 2 (generalised, congenital)	Homo sapiens	26-29
21555360-6	2011	We found that lipoxin A(4) was regulated by human chorionic gonadotrophin (hCG) during early pregnancy, because treatment of human decidua tissue with hCG increased lipoxin A(4) release (P&lt;0.01).	lipoxin A4	14-23	hypertrichosis 2 (generalised, congenital)	Homo sapiens	75-78
21555360-6	2011	We found that lipoxin A(4) was regulated by human chorionic gonadotrophin (hCG) during early pregnancy, because treatment of human decidua tissue with hCG increased lipoxin A(4) release (P&lt;0.01).	lipoxin A4	14-23	hypertrichosis 2 (generalised, congenital)	Homo sapiens	151-154
21555360-6	2011	We found that lipoxin A(4) was regulated by human chorionic gonadotrophin (hCG) during early pregnancy, because treatment of human decidua tissue with hCG increased lipoxin A(4) release (P&lt;0.01).	lipoxin A4	165-174	hypertrichosis 2 (generalised, congenital)	Homo sapiens	75-78
21555360-6	2011	We found that lipoxin A(4) was regulated by human chorionic gonadotrophin (hCG) during early pregnancy, because treatment of human decidua tissue with hCG increased lipoxin A(4) release (P&lt;0.01).	lipoxin A4	165-174	hypertrichosis 2 (generalised, congenital)	Homo sapiens	151-154
21562093-5	2011	Activation of the cAMP pathway with dibutyryl cAMP (db cAMP) or forskolin recapitulated the stimulatory effect of hCG on leptin expression.	Cyclic AMP	18-22	hypertrichosis 2 (generalised, congenital)	Homo sapiens	114-117
21562093-5	2011	Activation of the cAMP pathway with dibutyryl cAMP (db cAMP) or forskolin recapitulated the stimulatory effect of hCG on leptin expression.	Bucladesine	36-50	hypertrichosis 2 (generalised, congenital)	Homo sapiens	114-117
21562093-5	2011	Activation of the cAMP pathway with dibutyryl cAMP (db cAMP) or forskolin recapitulated the stimulatory effect of hCG on leptin expression.	Cyclic AMP	46-50	hypertrichosis 2 (generalised, congenital)	Homo sapiens	114-117
21562093-5	2011	Activation of the cAMP pathway with dibutyryl cAMP (db cAMP) or forskolin recapitulated the stimulatory effect of hCG on leptin expression.	Colforsin	64-73	hypertrichosis 2 (generalised, congenital)	Homo sapiens	114-117
21562093-8	2011	Inhibition of p38 MAPK with SB203580 not only reduced the basal leptin production but also attenuated the leptin-induced production by both hCG and db cAMP.	SB 203580	28-36	hypertrichosis 2 (generalised, congenital)	Homo sapiens	140-143
21562093-9	2011	These data suggest that endogenous hCG plays a significant role in maintaining leptin production in human placental syncytiotrophoblasts, and this effect involves a cross talk between cAMP and p38 MAPK pathways.	Cyclic AMP	184-188	hypertrichosis 2 (generalised, congenital)	Homo sapiens	35-38
21558315-5	2011	In our experiments, human CG (hCG)/cAMP stimulation rapidly and transiently increased MKP-1 mRNA levels by a transcriptional action.	Cyclic AMP	35-39	hypertrichosis 2 (generalised, congenital)	Homo sapiens	26-28
21558315-7	2011	In cells transiently expressing flag-MKP-1 protein, hCG/cAMP promoted the accumulation of the recombinant protein in a time-dependent manner (10-fold at 1 h).	Cyclic AMP	56-60	hypertrichosis 2 (generalised, congenital)	Homo sapiens	52-55
21558315-8	2011	Moreover, hCG/cAMP triggered ERK1/2-dependent MKP-1 phosphorylation.	Cyclic AMP	14-18	hypertrichosis 2 (generalised, congenital)	Homo sapiens	10-13
21832878-4	2011	The patient was diagnosed with negative elevation of testosterone after hCG administration and surgical exploration confirmed the absence of a testicular structure.	Testosterone	53-65	hypertrichosis 2 (generalised, congenital)	Homo sapiens	72-75
21527500-6	2011	cAMP accumulation in response to hCG stimulation in primary cultures of Leydig cells from Mek1(f/f);Mek2(-/-);iCre(+) mice is normal, but basal testosterone and testosterone syntheses provoked by addition of hCG or a cAMP analog, or by addition of substrates such as 22-hydroxycholesterol or pregnenolone, are barely detectable.	Cyclic AMP	0-4	hypertrichosis 2 (generalised, congenital)	Homo sapiens	33-36
21693028-6	2011	LH was lower on the day of hCG administration in the letrozole 2.5 mg/day group vs. the natural group.	Luteinizing Hormone	0-2	hypertrichosis 2 (generalised, congenital)	Homo sapiens	27-30
21693028-6	2011	LH was lower on the day of hCG administration in the letrozole 2.5 mg/day group vs. the natural group.	Letrozole	53-62	hypertrichosis 2 (generalised, congenital)	Homo sapiens	27-30
21406611-8	2011	Expression of NIS and hCG mRNA and protein was low at 1% oxygen but rose significantly at 8 and at 21%.	Oxygen	57-63	hypertrichosis 2 (generalised, congenital)	Homo sapiens	22-25
21406611-10	2011	Desferrioxamine, an iron chelator and hypoxia mimic, decreased NIS and hCG expression and I(125) uptake in BeWo cells.	Deferoxamine	0-15	hypertrichosis 2 (generalised, congenital)	Homo sapiens	71-74
21527500-6	2011	cAMP accumulation in response to hCG stimulation in primary cultures of Leydig cells from Mek1(f/f);Mek2(-/-);iCre(+) mice is normal, but basal testosterone and testosterone syntheses provoked by addition of hCG or a cAMP analog, or by addition of substrates such as 22-hydroxycholesterol or pregnenolone, are barely detectable.	Testosterone	161-173	hypertrichosis 2 (generalised, congenital)	Homo sapiens	33-36
21527500-6	2011	cAMP accumulation in response to hCG stimulation in primary cultures of Leydig cells from Mek1(f/f);Mek2(-/-);iCre(+) mice is normal, but basal testosterone and testosterone syntheses provoked by addition of hCG or a cAMP analog, or by addition of substrates such as 22-hydroxycholesterol or pregnenolone, are barely detectable.	Cyclic AMP	217-221	hypertrichosis 2 (generalised, congenital)	Homo sapiens	33-36
21527500-6	2011	cAMP accumulation in response to hCG stimulation in primary cultures of Leydig cells from Mek1(f/f);Mek2(-/-);iCre(+) mice is normal, but basal testosterone and testosterone syntheses provoked by addition of hCG or a cAMP analog, or by addition of substrates such as 22-hydroxycholesterol or pregnenolone, are barely detectable.	22-hydroxycholesterol	267-288	hypertrichosis 2 (generalised, congenital)	Homo sapiens	33-36
21527500-6	2011	cAMP accumulation in response to hCG stimulation in primary cultures of Leydig cells from Mek1(f/f);Mek2(-/-);iCre(+) mice is normal, but basal testosterone and testosterone syntheses provoked by addition of hCG or a cAMP analog, or by addition of substrates such as 22-hydroxycholesterol or pregnenolone, are barely detectable.	Pregnenolone	292-304	hypertrichosis 2 (generalised, congenital)	Homo sapiens	33-36
21293035-6	2011	Results suggest that the stimulation provided by LH (hCG) is insufficient to induce a maximum oocyte meiotic resumption and that EGFR activation is also required.	Luteinizing Hormone	49-51	hypertrichosis 2 (generalised, congenital)	Homo sapiens	53-56
21457973-7	2011	On the days of the hCG injection, women in the letrozole group had a significantly thicker endometrium than those in the LOD group (P&lt;0.0001).	Letrozole	47-56	hypertrichosis 2 (generalised, congenital)	Homo sapiens	19-22
21704384-9	2011	Finally, a hyperglycosylated form of hCG (hCG-H) only produced by invasive EVCT was shown to promote trophoblast invasion.	evct	75-79	hypertrichosis 2 (generalised, congenital)	Homo sapiens	37-40
21704384-9	2011	Finally, a hyperglycosylated form of hCG (hCG-H) only produced by invasive EVCT was shown to promote trophoblast invasion.	evct	75-79	hypertrichosis 2 (generalised, congenital)	Homo sapiens	42-47
21212137-10	2011	In summary, hCG induction of NFIL3 expression may modulate the process of ovulation and theca-interstitial and granulosa cell differentiation by regulating expression of PTGS2, PGR, AREG, EREG, and HPGD, potentially through interactions with cAMP response element binding protein and CCAAT enhancer binding protein-beta on their target gene promoters.	Cyclic AMP	242-246	hypertrichosis 2 (generalised, congenital)	Homo sapiens	12-15
21292636-10	2011	Women exposed in utero to diethylstilbestrol showed an unusual pattern of slow initial hCG rise followed by a fast increase, a pattern significantly different from that of unexposed women (P= 0.002).	Diethylstilbestrol	26-44	hypertrichosis 2 (generalised, congenital)	Homo sapiens	87-90
21375772-0	2011	MicroRNA array and microarray evaluation of endometrial receptivity in patients with high serum progesterone levels on the day of hCG administration.	Progesterone	96-108	hypertrichosis 2 (generalised, congenital)	Homo sapiens	130-133
22065820-11	2011	Cabergoline inhibits partially the VEGF receptor 2 phosphorylation levels and associated vascular permeability without affecting luteal angiogenesis reduces the "early" (within the first 9 days after hCG) onset of OHSS.	Cabergoline	0-11	hypertrichosis 2 (generalised, congenital)	Homo sapiens	200-203
21289266-2	2011	We hypothesized that serum and IT androstenedione (ADD) and IT dehydroepiandrosterone (DHEA) would be significantly suppressed by the administration of a GnRH antagonist and increased when stimulated by hCG, without a similar suppression of serum DHEA.	Androstenedione	34-49	hypertrichosis 2 (generalised, congenital)	Homo sapiens	203-206
21289266-2	2011	We hypothesized that serum and IT androstenedione (ADD) and IT dehydroepiandrosterone (DHEA) would be significantly suppressed by the administration of a GnRH antagonist and increased when stimulated by hCG, without a similar suppression of serum DHEA.	Dehydroepiandrosterone	63-85	hypertrichosis 2 (generalised, congenital)	Homo sapiens	203-206
21289266-2	2011	We hypothesized that serum and IT androstenedione (ADD) and IT dehydroepiandrosterone (DHEA) would be significantly suppressed by the administration of a GnRH antagonist and increased when stimulated by hCG, without a similar suppression of serum DHEA.	Dehydroepiandrosterone	87-91	hypertrichosis 2 (generalised, congenital)	Homo sapiens	203-206
21289266-2	2011	We hypothesized that serum and IT androstenedione (ADD) and IT dehydroepiandrosterone (DHEA) would be significantly suppressed by the administration of a GnRH antagonist and increased when stimulated by hCG, without a similar suppression of serum DHEA.	Dehydroepiandrosterone	247-251	hypertrichosis 2 (generalised, congenital)	Homo sapiens	203-206
21289266-5	2011	IT ADD and IT DHEA were suppressed by 98 and 82%, respectively, by acyline and significantly increased with hCG administration.	Dehydroepiandrosterone	14-18	hypertrichosis 2 (generalised, congenital)	Homo sapiens	108-111
21289266-8	2011	Serum and IT ADD and IT DHEA are markedly suppressed with GnRH administration and stimulated by hCG, but serum DHEA is not, suggesting that most circulating DHEA is not of testicular origin.	Dehydroepiandrosterone	24-28	hypertrichosis 2 (generalised, congenital)	Homo sapiens	96-99
20969917-5	2011	Intra-follicular glucose increased 3h after hCG, and remained at that level until 12h when levels decline back to pre-hCG concentrations.	Glucose	17-24	hypertrichosis 2 (generalised, congenital)	Homo sapiens	44-47
20969917-5	2011	Intra-follicular glucose increased 3h after hCG, and remained at that level until 12h when levels decline back to pre-hCG concentrations.	Glucose	17-24	hypertrichosis 2 (generalised, congenital)	Homo sapiens	118-121
21268835-2	2010	Effects of a prolonged female exposition on the testicular testosterone output in response to hCG injections were investigated in adult males of two inbred mice strains CBA/Lac and PT.	Testosterone	59-71	hypertrichosis 2 (generalised, congenital)	Homo sapiens	94-97
20969981-1	2011	We describe a 6-year-old boy carrying a de novo 5 Mb interstitial deletion of chromosome 8p23.1 identified by means of oligonucleotide array comparative genomic hybridisation (array CGH), who showed the typical signs of 8p23.1 deletion syndrome, including congenital heart defects, microcephaly, psychomotor delay and behavioural problems.	Oligonucleotides	119-134	hypertrichosis 2 (generalised, congenital)	Homo sapiens	182-185
20850718-2	2011	Despite this finding, the risk of single-dose methotrexate failure increases significantly in patients with initial hCG levels&gt;1,300 IU/L and/or in women who report having ever used combined oral contraception before pregnancy.	Methotrexate	46-58	hypertrichosis 2 (generalised, congenital)	Homo sapiens	116-119
20926582-0	2010	hCG-induced down-regulation of PPARgamma and liver X receptors promotes periovulatory progesterone synthesis by macaque granulosa cells.	Progesterone	86-98	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
20926582-7	2010	A liver X receptor agonist attenuated hCG-induced progesterone synthesis in vitro and increased the expression of ABCA1 and ABCG1, and suppressed STAR, P450 side-chain cleavage A1, hydroxysteroid dehydrogenase 3B, and SCARB1.	Progesterone	50-62	hypertrichosis 2 (generalised, congenital)	Homo sapiens	38-41
20926582-8	2010	These data suggest that an initial action of LH/CG on the primate preovulatory follicle is to rapidly reduce the expression of PPARG, resulting in reduced NR1H3 with the consequence shifting the balance from cholesterol efflux via ABCA1 and ABCG1 to cholesterol uptake (SCARB1) and metabolism (STAR, P450 side-chain cleavage A1, hydroxysteroid dehydrogenase 3B).	Cholesterol	208-219	hypertrichosis 2 (generalised, congenital)	Homo sapiens	48-50
20926582-8	2010	These data suggest that an initial action of LH/CG on the primate preovulatory follicle is to rapidly reduce the expression of PPARG, resulting in reduced NR1H3 with the consequence shifting the balance from cholesterol efflux via ABCA1 and ABCG1 to cholesterol uptake (SCARB1) and metabolism (STAR, P450 side-chain cleavage A1, hydroxysteroid dehydrogenase 3B).	Cholesterol	250-261	hypertrichosis 2 (generalised, congenital)	Homo sapiens	48-50
20805751-2	2010	In humans, aspirin blocks the androgen response to human chorionic gonadotropin (hCG), and, because hCG-stimulated androgen production in utero is crucial for normal testicular descent, exposure to COX inhibitors at vulnerable times during gestation may impair testicular descent.	Aspirin	11-18	hypertrichosis 2 (generalised, congenital)	Homo sapiens	81-84
21046485-3	2010	Current experiments in an in vitro follicle bioassay studied dose-effects of androstenedione and testosterone on FSH and hCG stimulated antral follicle growth and meiotic maturation.	Androstenedione	77-92	hypertrichosis 2 (generalised, congenital)	Homo sapiens	121-124
21046485-3	2010	Current experiments in an in vitro follicle bioassay studied dose-effects of androstenedione and testosterone on FSH and hCG stimulated antral follicle growth and meiotic maturation.	Testosterone	97-109	hypertrichosis 2 (generalised, congenital)	Homo sapiens	121-124
21046485-9	2010	Follicles exposed to a combination of 25 mIU/ml FSH and 3 mIU/ml hCG and elevated aromatizable androgens altered the steroid production profile, affected the follicular development and impaired oocyte meiotic competence.	Steroids	117-124	hypertrichosis 2 (generalised, congenital)	Homo sapiens	65-68
20660042-1	2010	CONTEXT: Human chorionic gonadotropin (hCG) is the major pregnancy glycoprotein hormone whose maternal concentration and glycan structure change all along pregnancy.	Polysaccharides	121-127	hypertrichosis 2 (generalised, congenital)	Homo sapiens	39-42
21485731-4	2011	Metotrexate (50 mg/m2 IM) was used in hemodinamically stable patients (hCG concentrations of patients varied between 450 IU/1 and 3660 IU/1).	metotrexate	0-11	hypertrichosis 2 (generalised, congenital)	Homo sapiens	71-74
21485731-16	2011	DISCUSSION: In selected patients with low serum hCG concentrations systemic methotrexate is a good alternative.	Methotrexate	76-88	hypertrichosis 2 (generalised, congenital)	Homo sapiens	48-51
21552188-3	2011	It has been reported that VPA reduced testosterone secretion stimulated by hCG in isolated rat Leydig cells.	Valproic Acid	26-29	hypertrichosis 2 (generalised, congenital)	Homo sapiens	75-78
21552188-3	2011	It has been reported that VPA reduced testosterone secretion stimulated by hCG in isolated rat Leydig cells.	Testosterone	38-50	hypertrichosis 2 (generalised, congenital)	Homo sapiens	75-78
20800063-4	2010	Ouabain did not induce spermiation in absence of hCG and inhibited hCG-induced spermiation in a dose-dependent manner, reaching 90% inhibition with the higher concentration.	Ouabain	0-7	hypertrichosis 2 (generalised, congenital)	Homo sapiens	67-70
20646984-4	2010	As shown in murine models, the increased receptor levels often seen in tumors, are probably caused by elevated LH/hCG levels.	Luteinizing Hormone	111-113	hypertrichosis 2 (generalised, congenital)	Homo sapiens	114-117
21051988-0	2010	Serum hCG level and rising world health organization score at second-line chemotherapy (pulse dactinomycin): poor prognostic factors for methotrexate-failed low-risk gestational trophoblastic neoplasia.	Methotrexate	137-149	hypertrichosis 2 (generalised, congenital)	Homo sapiens	6-9
21051988-8	2010	The risk of failure with pulse dactinomycin was higher for serum hCG levels 10 or higher when initiating pulse dactinomycin (odds ratio, 8.91; 95% confidence interval, 1.08-73.53) and a rising World Health Organization score of 2 or higher after first-line chemotherapy (odds ratio, 12.59; 95% confidence interval, 1.60-99.25).	Dactinomycin	31-43	hypertrichosis 2 (generalised, congenital)	Homo sapiens	65-68
21051988-8	2010	The risk of failure with pulse dactinomycin was higher for serum hCG levels 10 or higher when initiating pulse dactinomycin (odds ratio, 8.91; 95% confidence interval, 1.08-73.53) and a rising World Health Organization score of 2 or higher after first-line chemotherapy (odds ratio, 12.59; 95% confidence interval, 1.60-99.25).	Dactinomycin	111-123	hypertrichosis 2 (generalised, congenital)	Homo sapiens	65-68
21051988-10	2010	CONCLUSIONS: Serum hCG level and a rising World Health Organization score at the time of initiating pulse dactinomycin are important prognostic factors in patients with methotrexate-failed low-risk GTN receiving pulse actinomycin as second-line chemotherapy.	Methotrexate	169-181	hypertrichosis 2 (generalised, congenital)	Homo sapiens	19-22
21268835-6	2010	It has been shown that the hCG increased the testosterone concentration and its testicular content in control males of both strains, but the testosterone output was expressed more significantly in PT males in comparison with CBA/Lac.	Testosterone	45-57	hypertrichosis 2 (generalised, congenital)	Homo sapiens	27-30
19732888-9	2010	A nonsignificant increase in endometrial thickness on the day of hCG administration was observed in the letrozole group (9.5+/-0.2 mm vs. 9.1+/-0.1 mm).	Letrozole	104-113	hypertrichosis 2 (generalised, congenital)	Homo sapiens	65-68
20591557-3	2010	STUDY DESIGN: The effects of saquinavir and nelfinavir were evaluated on human trophoblast functions and integrity by investigating their effect on human chorionic gonadotropin (hCG) secretion and on P-gp expression and functionality.	Saquinavir	29-39	hypertrichosis 2 (generalised, congenital)	Homo sapiens	178-181
20591557-3	2010	STUDY DESIGN: The effects of saquinavir and nelfinavir were evaluated on human trophoblast functions and integrity by investigating their effect on human chorionic gonadotropin (hCG) secretion and on P-gp expression and functionality.	Nelfinavir	44-54	hypertrichosis 2 (generalised, congenital)	Homo sapiens	178-181
20591557-4	2010	RESULTS: Nelfinavir significantly reduced hCG secretion by 30% after a 48-h treatment but it had no effect on syncytia formation.	Nelfinavir	9-19	hypertrichosis 2 (generalised, congenital)	Homo sapiens	42-45
20154304-0	2010	Predictive values of hCG clearance for risk of methotrexate resistance in low-risk gestational trophoblastic neoplasias.	Methotrexate	47-59	hypertrichosis 2 (generalised, congenital)	Homo sapiens	21-24
20154304-2	2010	We modeled human chorionic gonadotropin (hCG) decline during MTX therapy using a kinetic population approach to calculate individual hCG clearance (CL(hCG)) and assessed the predictive value of CL(hCG) for MTX resistance.	Methotrexate	206-209	hypertrichosis 2 (generalised, congenital)	Homo sapiens	194-201
20154304-10	2010	CONCLUSION: In the second largest cohort of low-risk GTN patients reported to date, choriocarcinoma pathology and CL(hCG) &lt; or =0.37 l/day were major independent predictive factors for MTX resistance risk.	Methotrexate	188-191	hypertrichosis 2 (generalised, congenital)	Homo sapiens	114-121
20444920-12	2010	hCG induced Mcl-1 expression through the LH/hCG receptor, adenylate cyclase, protein kinase A, and cAMP response element-binding protein signal pathway.	Cyclic AMP	99-103	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
20444920-14	2010	CONCLUSIONS: We first demonstrate that hCG prevents apoptosis of granulosa-lutein cells through the induction of Mcl-1 protein via the LH/hCG receptor and a cAMP response element-binding protein-dependent pathway.	Cyclic AMP	157-161	hypertrichosis 2 (generalised, congenital)	Homo sapiens	39-42
20501789-4	2010	The functional states of these follicles were assessed by measuring the FSH- or human chorionic gonadotrophin (hCG)-induced cAMP responses of granulosa cells in vitro.	Cyclic AMP	124-128	hypertrichosis 2 (generalised, congenital)	Homo sapiens	111-114
20619452-1	2010	Hyperglycosylated hCG (hCG-H) is a glycoprotein with the same polypeptide structure as hCG, and much larger N- and O-linked oligosaccharides.	n- and o-linked oligosaccharides	108-140	hypertrichosis 2 (generalised, congenital)	Homo sapiens	18-21
20619452-1	2010	Hyperglycosylated hCG (hCG-H) is a glycoprotein with the same polypeptide structure as hCG, and much larger N- and O-linked oligosaccharides.	n- and o-linked oligosaccharides	108-140	hypertrichosis 2 (generalised, congenital)	Homo sapiens	23-28
20619452-1	2010	Hyperglycosylated hCG (hCG-H) is a glycoprotein with the same polypeptide structure as hCG, and much larger N- and O-linked oligosaccharides.	n- and o-linked oligosaccharides	108-140	hypertrichosis 2 (generalised, congenital)	Homo sapiens	23-26
20619452-2	2010	The oligosaccharides increase the molecular weight of hCG from 36,000 - 37,000 u to 40,000 - 41,000 u, depending on the extent of hyperglycosylation.	Oligosaccharides	4-20	hypertrichosis 2 (generalised, congenital)	Homo sapiens	54-57
20619452-3	2010	hCG-H has triantennary N-linked oligosaccharides and double molecular size O-linked oligosaccharides (hexasaccharide compared with predominantly trisaccharide structures).	n-linked oligosaccharides	23-48	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-5
20619452-3	2010	hCG-H has triantennary N-linked oligosaccharides and double molecular size O-linked oligosaccharides (hexasaccharide compared with predominantly trisaccharide structures).	o-linked oligosaccharides	75-100	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-5
20619452-3	2010	hCG-H has triantennary N-linked oligosaccharides and double molecular size O-linked oligosaccharides (hexasaccharide compared with predominantly trisaccharide structures).	hexasaccharide	102-116	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-5
20619452-3	2010	hCG-H has triantennary N-linked oligosaccharides and double molecular size O-linked oligosaccharides (hexasaccharide compared with predominantly trisaccharide structures).	Trisaccharides	145-158	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-5
20463053-3	2010	In the present study, we address the molecular and cellular mechanisms underlying the effects of MEHP on basal and human chorionic gonadotropin (hCG)-stimulated steroid production by MA-10 Leydig cells, using a systems biology approach.	mono-(2-ethylhexyl)phthalate	97-101	hypertrichosis 2 (generalised, congenital)	Homo sapiens	145-148
20463053-3	2010	In the present study, we address the molecular and cellular mechanisms underlying the effects of MEHP on basal and human chorionic gonadotropin (hCG)-stimulated steroid production by MA-10 Leydig cells, using a systems biology approach.	Steroids	161-168	hypertrichosis 2 (generalised, congenital)	Homo sapiens	145-148
20463053-4	2010	MEHP induced dose-dependent decreases in hCG-stimulated steroid formation.	mono-(2-ethylhexyl)phthalate	0-4	hypertrichosis 2 (generalised, congenital)	Homo sapiens	41-44
20587067-4	2010	Cisplatin based combination chemotherapy produced an initial normalisation of the hCG level, but later in treatment the patient developed new cerebral lesions and a rising serum hCG suggestive of disease progression.	Cisplatin	0-9	hypertrichosis 2 (generalised, congenital)	Homo sapiens	82-85
20587067-4	2010	Cisplatin based combination chemotherapy produced an initial normalisation of the hCG level, but later in treatment the patient developed new cerebral lesions and a rising serum hCG suggestive of disease progression.	Cisplatin	0-9	hypertrichosis 2 (generalised, congenital)	Homo sapiens	178-181
21029591-7	2010	RESULTS: The level of serum LH on the day of hCG administration were (1.59 +- 0.77) U/L in r-hLH group, (0.54 +- 0.25) U/L in non-r-hLH group and (2.39 +- 1.01) U/L in control group, which reached statistical difference between every two groups (P &lt; 0.05).	Luteinizing Hormone	28-30	hypertrichosis 2 (generalised, congenital)	Homo sapiens	45-48
21029591-7	2010	RESULTS: The level of serum LH on the day of hCG administration were (1.59 +- 0.77) U/L in r-hLH group, (0.54 +- 0.25) U/L in non-r-hLH group and (2.39 +- 1.01) U/L in control group, which reached statistical difference between every two groups (P &lt; 0.05).	r-hlh	91-96	hypertrichosis 2 (generalised, congenital)	Homo sapiens	45-48
20668507-0	2010	Effect of ghrelin on proliferation, apoptosis and secretion of progesterone and hCG in the placental JEG-3 cell line.	Ghrelin	10-17	hypertrichosis 2 (generalised, congenital)	Homo sapiens	80-83
20219279-1	2010	OBJECTIVE: The purpose of this study is to assess the effect of luteal phase supplementation (LPS) on pregnancy rates in human chorionic gonadotropin (hCG)-induced natural frozen-thawed (FET) cycles.	lps	94-97	hypertrichosis 2 (generalised, congenital)	Homo sapiens	151-154
20184886-1	2010	In the present investigation, in vitro effects of vasotocin (VT) on oocyte (follicular) hydration during germinal vesicle breakdown (GVBD) and ovulation were demonstrated in hCG-primed and non-primed catfish.	Vasotocin	50-59	hypertrichosis 2 (generalised, congenital)	Homo sapiens	174-177
20184886-3	2010	The priming with hCG resulted in significant increases on percentage GVBD and ovulation, and stimulated follicular hydration, as judged by the increase in diameter, volume, water content, osmolality and Ca(2+) concentration.	Water	173-178	hypertrichosis 2 (generalised, congenital)	Homo sapiens	17-20
20299109-4	2010	HCG with distinct carbohydrate expression is also an effective selectin antagonist, whereas the potency of transferrin is low.	Carbohydrates	18-30	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
20463053-4	2010	MEHP induced dose-dependent decreases in hCG-stimulated steroid formation.	Steroids	56-63	hypertrichosis 2 (generalised, congenital)	Homo sapiens	41-44
20463053-6	2010	Expression profiling indicated that low concentrations of MEHP induced the expression of a number of genes that also were expressed after hCG stimulation.	mono-(2-ethylhexyl)phthalate	58-62	hypertrichosis 2 (generalised, congenital)	Homo sapiens	138-141
20463053-9	2010	The MEHP-induced decreases in hCG-stimulated steroid formation were paralleled by increases in reactive oxygen species generation, with the latter mediated by the Cyp1a1 gene and its network.	mono-(2-ethylhexyl)phthalate	4-8	hypertrichosis 2 (generalised, congenital)	Homo sapiens	30-33
20463053-9	2010	The MEHP-induced decreases in hCG-stimulated steroid formation were paralleled by increases in reactive oxygen species generation, with the latter mediated by the Cyp1a1 gene and its network.	Steroids	45-52	hypertrichosis 2 (generalised, congenital)	Homo sapiens	30-33
20055562-2	2010	To detect pGTN, postmolar surveillance by measurement of maternal human chorionic gonoadotropin (hCG) levels should be performed.	pgtn	10-14	hypertrichosis 2 (generalised, congenital)	Homo sapiens	97-100
20144211-5	2010	Testosterone production was induced either by activators of the cAMP/PKA pathway (hCG and dbcAMP) or substrates of steroidogenesis [22(R)-hydroxy-cholesterol (22(R)-OH-C), which is a substrate for the P450scc enzyme, and pregnenolone, which is the product of the P450scc-catalyzed step].	Testosterone	0-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	82-85
20144211-5	2010	Testosterone production was induced either by activators of the cAMP/PKA pathway (hCG and dbcAMP) or substrates of steroidogenesis [22(R)-hydroxy-cholesterol (22(R)-OH-C), which is a substrate for the P450scc enzyme, and pregnenolone, which is the product of the P450scc-catalyzed step].	Cyclic AMP	64-68	hypertrichosis 2 (generalised, congenital)	Homo sapiens	82-85
20144211-12	2010	CONCLUSION: The results revealed that the Leydig cells from rosiglitazone-treated rats showed significant reduction in testosterone production under basal, hCG/dbcAMP- or 22 (R)-OH-C/pregnenolone-induced conditions, although increased labeling of StAR and P450scc was detected in these cells by immunocytochemistry.	Rosiglitazone	60-73	hypertrichosis 2 (generalised, congenital)	Homo sapiens	156-159
19883722-6	2010	Administration of NP showed a decrease of hCG-induced plasma testosterone.	Testosterone	61-73	hypertrichosis 2 (generalised, congenital)	Homo sapiens	42-45
19883722-8	2010	In contrast, NP inhibited hCG-induced testosterone release in rat Leydig cells.	nonylphenol	13-15	hypertrichosis 2 (generalised, congenital)	Homo sapiens	26-29
19883722-8	2010	In contrast, NP inhibited hCG-induced testosterone release in rat Leydig cells.	Testosterone	38-50	hypertrichosis 2 (generalised, congenital)	Homo sapiens	26-29
19299204-4	2009	Systemic methotrexate in a fixed multiple-dose i/m regimen can be recommended for hemodynamically stable women with an unruptured tubal ectopic pregnancy and no signs of active bleeding presenting with serum hCG concentrations&lt;3,000 IU/l.	Methotrexate	9-21	hypertrichosis 2 (generalised, congenital)	Homo sapiens	208-211
19815440-0	2010	Application of oligonucleotide array CGH to the simultaneous detection of a deletion in the nuclear TK2 gene and mtDNA depletion.	Oligonucleotides	15-30	hypertrichosis 2 (generalised, congenital)	Homo sapiens	37-40
19671625-1	2009	BACKGROUND: The purpose of this prospective observational study was to evaluate the association between estradiol (E(2)) levels on the day of human chorionic gonadotrophin (hCG) administration and pregnancy rates in a recombinant FSH (rec-FSH) antagonist fixed protocol.	Estradiol	104-113	hypertrichosis 2 (generalised, congenital)	Homo sapiens	173-176
19603415-3	2009	Our findings indicate that resveratrol and its analogs structure-dependently attenuated hCG-activated steroidogenesis in Leydig cells through suppression of the expression of steroidogenic acute regulatory protein and cytochrome P450c17.	Resveratrol	27-38	hypertrichosis 2 (generalised, congenital)	Homo sapiens	88-91
18829018-0	2009	Relationship of progesterone/estradiol ratio on day of hCG administration and pregnancy outcomes in high responders undergoing in vitro fertilization.	Estradiol	29-38	hypertrichosis 2 (generalised, congenital)	Homo sapiens	55-58
20677483-3	2009	RESULTS: In patients with uneventful moles and GTN, serum hCG levels recorded using the hCG-CTP and DPC Immulite 2000 tests correlated well (r2 = 0.936 and r2 = 0.958).	dpc	100-103	hypertrichosis 2 (generalised, congenital)	Homo sapiens	58-61
20677483-4	2009	However, the serum hCG titers measured using the DPC Immulite 2000 assay were approximately 2.5- and 2.7-fold higher than those measured with the hCG-CTP test (p &lt; 0.0001) when lower titers of hCG (&lt; 40 mIU/mL) were tested.	dpc	49-52	hypertrichosis 2 (generalised, congenital)	Homo sapiens	19-22
19617207-9	2009	CONCLUSION: In this pilot trial, substitution of rFSH by low-dose hCG in the final days of COS leads to a reduction of FSH consumption whereas ICSI outcome, in terms of oocyte yield and ongoing pregnancy rate, remains comparable to the traditional regimen (ClinicalTrials.gov, trial number: NCT00750100).	carbonyl sulfide	91-94	hypertrichosis 2 (generalised, congenital)	Homo sapiens	66-69
19671625-1	2009	BACKGROUND: The purpose of this prospective observational study was to evaluate the association between estradiol (E(2)) levels on the day of human chorionic gonadotrophin (hCG) administration and pregnancy rates in a recombinant FSH (rec-FSH) antagonist fixed protocol.	Estradiol	115-119	hypertrichosis 2 (generalised, congenital)	Homo sapiens	173-176
19409506-7	2009	During human chorionic gonadotropin (hCG)-induced oocyte maturation, both in vitro and in vivo, StAR mRNA levels were augmented by 2 h and then declined gradually to reach basal levels by 12 h as that of saline-treated controls.	Sodium Chloride	204-210	hypertrichosis 2 (generalised, congenital)	Homo sapiens	37-40
19694686-7	2009	Falling serum hCG levels at 48 h suggest that the ectopic trophoblast is resolving spontaneously and it may be possible to avoid methotrexate administration in this sub-group.	Methotrexate	129-141	hypertrichosis 2 (generalised, congenital)	Homo sapiens	14-17
19694686-8	2009	Women with increasing serum hCG levels at 48 h, indicating the trophoblast is still active, should be targeted for methotrexate.	Methotrexate	115-127	hypertrichosis 2 (generalised, congenital)	Homo sapiens	28-31
19299204-5	2009	In women with serum hCG concentrations&lt;1,500 IU/l, a single-dose methotrexate regimen can be considered.	Methotrexate	68-80	hypertrichosis 2 (generalised, congenital)	Homo sapiens	20-23
19389837-6	2009	To further explore Timp1 and Timp3 regulation, cells were cultured with the progesterone receptor antagonist RU486, which blocked the hCG induction of Timp3 expression, whereas the epidermal growth factor receptor tyrosine kinase inhibitor AG1478 blocked the hCG stimulation of both Timp1 and Timp3 expression.	Mifepristone	109-114	hypertrichosis 2 (generalised, congenital)	Homo sapiens	134-137
19389837-9	2009	Timp3 small interfering RNA resulted in a 20% decrease in hCG-induced progesterone levels and microarray analysis revealed an increase in cytochrome P450 Cyp 17, ubiquitin conjugating enzyme E2T, and heat shock protein 70.	Progesterone	70-82	hypertrichosis 2 (generalised, congenital)	Homo sapiens	58-61
19332066-2	2009	A 100IU/fish of hCG induced ovulation and elicited both periovulatory and post-ovulatory changes in vasotocin concentrations with a significant increase up to 8h in the brain and up to 16h in both plasma and ovary.	Vasotocin	100-109	hypertrichosis 2 (generalised, congenital)	Homo sapiens	16-19
19348805-3	2009	In pre-vitellogenic phase (preparatory phase, GSI-0.48+/-0.03%), both VT and hCG stimulated E(2) significantly, VT in a biphasic manner and hCG in a dose-dependent manner.	Vasotocin	70-72	hypertrichosis 2 (generalised, congenital)	Homo sapiens	140-143
19348805-3	2009	In pre-vitellogenic phase (preparatory phase, GSI-0.48+/-0.03%), both VT and hCG stimulated E(2) significantly, VT in a biphasic manner and hCG in a dose-dependent manner.	Vasotocin	112-114	hypertrichosis 2 (generalised, congenital)	Homo sapiens	77-80
18832102-1	2009	An ovulatory hCG stimulus to rhesus macaques undergoing controlled ovarian stimulation protocols results in a rapid and sustained increase in progesterone synthesis.	Progesterone	142-154	hypertrichosis 2 (generalised, congenital)	Homo sapiens	13-16
19219417-1	2009	An excess of human chorionic gonadotropin (hCG) is a rare differential diagnosis of hyperthyroidism, due to the TSH-like effect of hCG.	Thyrotropin	112-115	hypertrichosis 2 (generalised, congenital)	Homo sapiens	43-46
19219417-1	2009	An excess of human chorionic gonadotropin (hCG) is a rare differential diagnosis of hyperthyroidism, due to the TSH-like effect of hCG.	Thyrotropin	112-115	hypertrichosis 2 (generalised, congenital)	Homo sapiens	131-134
19293810-1	2009	Van Trommel et al have previously shown that serum human chorionic gonadotropin (hCG) cutoff levels can provide early prediction of resistance to first-line methotrexate (MTX) in patients with persistent trophoblastic disease (PTD).	Methotrexate	157-169	hypertrichosis 2 (generalised, congenital)	Homo sapiens	81-84
19293810-1	2009	Van Trommel et al have previously shown that serum human chorionic gonadotropin (hCG) cutoff levels can provide early prediction of resistance to first-line methotrexate (MTX) in patients with persistent trophoblastic disease (PTD).	Methotrexate	171-174	hypertrichosis 2 (generalised, congenital)	Homo sapiens	81-84
19293810-4	2009	Receiver operating characteristics analysis identified an hCG cutoff value of 737 IU l(-1) that enabled us to predict the subsequent development of single-agent chemotherapy resistance in 52% of patients before their fourth MTX course at 97.5% specificity.	Methotrexate	224-227	hypertrichosis 2 (generalised, congenital)	Homo sapiens	58-61
18988674-7	2009	The results indicated changes in expression of genes favorable to PGF(2alpha) action during the late to very late luteal phase, and expressions of many of these genes were regulated in an opposite manner by exogenous hCG treatment.	Prostaglandins F	66-69	hypertrichosis 2 (generalised, congenital)	Homo sapiens	217-220
18988674-8	2009	Collectively, the findings suggest that curtailment of expression of downstream LH-target genes possibly through PGF(2alpha) action on the CL is among the mechanisms underlying cross talk between the luteotropic and luteolytic signaling pathways that result in the cessation of luteal function, but hCG is likely to abrogate the PGF(2alpha)-responsive gene expression changes resulting in luteal rescue crucial for the maintenance of early pregnancy.	Prostaglandins F	113-116	hypertrichosis 2 (generalised, congenital)	Homo sapiens	299-302
19231293-2	2009	Today, serial serum hCG measurements and transvaginal ultrasound examination can provide early detection of most ectopic pregnancies allowing medical treatment with methotrexate.	Methotrexate	165-177	hypertrichosis 2 (generalised, congenital)	Homo sapiens	20-23
18726107-1	2009	INTRODUCTION: The hormone human chorionic gonadotropin (hCG), secreted by molar tissue, is structurally similar to thyroid-stimulating hormone (TSH).	Thyrotropin	115-142	hypertrichosis 2 (generalised, congenital)	Homo sapiens	56-59
18726107-1	2009	INTRODUCTION: The hormone human chorionic gonadotropin (hCG), secreted by molar tissue, is structurally similar to thyroid-stimulating hormone (TSH).	Thyrotropin	144-147	hypertrichosis 2 (generalised, congenital)	Homo sapiens	56-59
19135660-8	2009	The patient"s serum hCG level declined to a normal range after two administrations of dactinomycin.	Dactinomycin	86-98	hypertrichosis 2 (generalised, congenital)	Homo sapiens	20-23
19135660-9	2009	CONCLUSION(S): Dactinomycin could be an alternative in cases for which MTX is not effective and persistently high hCG levels exist.	Dactinomycin	15-27	hypertrichosis 2 (generalised, congenital)	Homo sapiens	114-117
19245075-3	2009	The aim of this study was to determine whether basal inhibin B levels are able to predict testosterone response to hCG in idiopathic hypogonadotropic hypogonadism (IHH) patients and to evaluate the correlation between inhibin B and gonadotropins in these patients and controls.	Testosterone	90-102	hypertrichosis 2 (generalised, congenital)	Homo sapiens	115-118
19245075-7	2009	Inhibin B and the hCG-induced free testosterone and total testosterone increment correlated strongly (r=0.802, P&lt;.001; r=0.793, P&lt;.001, respectively).	Testosterone	35-47	hypertrichosis 2 (generalised, congenital)	Homo sapiens	18-21
19245075-7	2009	Inhibin B and the hCG-induced free testosterone and total testosterone increment correlated strongly (r=0.802, P&lt;.001; r=0.793, P&lt;.001, respectively).	Testosterone	58-70	hypertrichosis 2 (generalised, congenital)	Homo sapiens	18-21
19245075-8	2009	We conclude that basal inhibin B predicts the testosterone response to hCG in IHH patients and therefore gives reliable information about Leydig cell reserve.	Testosterone	46-58	hypertrichosis 2 (generalised, congenital)	Homo sapiens	71-74
18716288-4	2008	Two miRNAs, Mirn132 and Mirn212 (also known as miR-132 and miR-212), were found to be highly upregulated following LH/hCG induction and were further analyzed.	Luteinizing Hormone	115-117	hypertrichosis 2 (generalised, congenital)	Homo sapiens	118-121
18716288-5	2008	In vivo and in vitro temporal expression analysis by quantitative RT-PCR confirmed that LH/hCG and cAMP, respectively, increased transcription of the precursor transcript as well as the mature miRNAs.	Luteinizing Hormone	88-90	hypertrichosis 2 (generalised, congenital)	Homo sapiens	91-94
18522946-16	2008	Systemic MTX is a good alternative in selected patients with low serum hCG concentrations.	Methotrexate	9-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	71-74
19134331-11	2008	Exposure of the granulosa cells to 4-AP reduced the production of progesterone in blank and hCG-induced granulosa cells.	4-Aminopyridine	35-39	hypertrichosis 2 (generalised, congenital)	Homo sapiens	92-95
19134331-12	2008	(3) The flow cytometry analysis and the cellular caspase-3 A(405) showed that 4-AP increased the percentage of early phase apoptosis (P &lt; 0.01): 4-AP treated group vs blank group [(40 +/- 5)% and 0.049 +/- 0.009] vs [(17 +/- 4)% and 0.029 +/- 0.008], hCG + 4-AP co-treated group vs hCG-induced group [(25 +/- 4)% and 0.039 +/- 0.008] vs [(15 +/- 3)% and 0.022 +/- 0.007].	4-Aminopyridine	78-82	hypertrichosis 2 (generalised, congenital)	Homo sapiens	254-257
19134331-12	2008	(3) The flow cytometry analysis and the cellular caspase-3 A(405) showed that 4-AP increased the percentage of early phase apoptosis (P &lt; 0.01): 4-AP treated group vs blank group [(40 +/- 5)% and 0.049 +/- 0.009] vs [(17 +/- 4)% and 0.029 +/- 0.008], hCG + 4-AP co-treated group vs hCG-induced group [(25 +/- 4)% and 0.039 +/- 0.008] vs [(15 +/- 3)% and 0.022 +/- 0.007].	4-Aminopyridine	78-82	hypertrichosis 2 (generalised, congenital)	Homo sapiens	285-288
19134331-13	2008	(4) 24 hours after treated with 4-AP and hCG, the inhibitory rate of cultured granulosa cells of 4-AP treated group was higher than the blank group (19.7% vs 0), and that of hCG + 4-AP co-treated group was obviously higher than hCG-induced group (34.6% vs 0, P &lt; 0.01).	4-Aminopyridine	32-36	hypertrichosis 2 (generalised, congenital)	Homo sapiens	174-177
19134331-13	2008	(4) 24 hours after treated with 4-AP and hCG, the inhibitory rate of cultured granulosa cells of 4-AP treated group was higher than the blank group (19.7% vs 0), and that of hCG + 4-AP co-treated group was obviously higher than hCG-induced group (34.6% vs 0, P &lt; 0.01).	4-Aminopyridine	32-36	hypertrichosis 2 (generalised, congenital)	Homo sapiens	174-177
19134331-13	2008	(4) 24 hours after treated with 4-AP and hCG, the inhibitory rate of cultured granulosa cells of 4-AP treated group was higher than the blank group (19.7% vs 0), and that of hCG + 4-AP co-treated group was obviously higher than hCG-induced group (34.6% vs 0, P &lt; 0.01).	4-Aminopyridine	97-101	hypertrichosis 2 (generalised, congenital)	Homo sapiens	41-44
19134331-13	2008	(4) 24 hours after treated with 4-AP and hCG, the inhibitory rate of cultured granulosa cells of 4-AP treated group was higher than the blank group (19.7% vs 0), and that of hCG + 4-AP co-treated group was obviously higher than hCG-induced group (34.6% vs 0, P &lt; 0.01).	4-Aminopyridine	97-101	hypertrichosis 2 (generalised, congenital)	Homo sapiens	174-177
19134331-13	2008	(4) 24 hours after treated with 4-AP and hCG, the inhibitory rate of cultured granulosa cells of 4-AP treated group was higher than the blank group (19.7% vs 0), and that of hCG + 4-AP co-treated group was obviously higher than hCG-induced group (34.6% vs 0, P &lt; 0.01).	4-Aminopyridine	97-101	hypertrichosis 2 (generalised, congenital)	Homo sapiens	174-177
19134331-13	2008	(4) 24 hours after treated with 4-AP and hCG, the inhibitory rate of cultured granulosa cells of 4-AP treated group was higher than the blank group (19.7% vs 0), and that of hCG + 4-AP co-treated group was obviously higher than hCG-induced group (34.6% vs 0, P &lt; 0.01).	4-Aminopyridine	97-101	hypertrichosis 2 (generalised, congenital)	Homo sapiens	41-44
19134331-13	2008	(4) 24 hours after treated with 4-AP and hCG, the inhibitory rate of cultured granulosa cells of 4-AP treated group was higher than the blank group (19.7% vs 0), and that of hCG + 4-AP co-treated group was obviously higher than hCG-induced group (34.6% vs 0, P &lt; 0.01).	4-Aminopyridine	97-101	hypertrichosis 2 (generalised, congenital)	Homo sapiens	174-177
19134331-13	2008	(4) 24 hours after treated with 4-AP and hCG, the inhibitory rate of cultured granulosa cells of 4-AP treated group was higher than the blank group (19.7% vs 0), and that of hCG + 4-AP co-treated group was obviously higher than hCG-induced group (34.6% vs 0, P &lt; 0.01).	4-Aminopyridine	97-101	hypertrichosis 2 (generalised, congenital)	Homo sapiens	174-177
18554593-9	2008	Five days after triggered ovulation with recombinant hCG, serum progesterone levels rose to 13.8 ng/mL.	Progesterone	64-76	hypertrichosis 2 (generalised, congenital)	Homo sapiens	53-56
18544580-13	2008	CONCLUSIONS: The hCG ratio is significantly higher in those IPUVs which become viable IUPs compared with non-viable IUPs.	ipuvs	60-65	hypertrichosis 2 (generalised, congenital)	Homo sapiens	17-20
18703414-10	2008	1 mM Ba(2+) stimulated cytotrophoblast cell hCG secretion at 66 h compared with control, whereas 5 mM tetraethylammonium (TEA) inhibited hCG secretion by &gt;90%.	Barium	5-7	hypertrichosis 2 (generalised, congenital)	Homo sapiens	44-47
18703414-10	2008	1 mM Ba(2+) stimulated cytotrophoblast cell hCG secretion at 66 h compared with control, whereas 5 mM tetraethylammonium (TEA) inhibited hCG secretion by &gt;90%.	Tetraethylammonium	102-120	hypertrichosis 2 (generalised, congenital)	Homo sapiens	137-140
18703414-10	2008	1 mM Ba(2+) stimulated cytotrophoblast cell hCG secretion at 66 h compared with control, whereas 5 mM tetraethylammonium (TEA) inhibited hCG secretion by &gt;90%.	Tetraethylammonium	122-125	hypertrichosis 2 (generalised, congenital)	Homo sapiens	137-140
18703414-11	2008	0.1-1 mM 4-aminopyridine (4-AP) reduced cytotrophoblast cell hCG secretion and elevated cellular hCG; without altering cellular integrity or syncytialization.	4-Aminopyridine	9-24	hypertrichosis 2 (generalised, congenital)	Homo sapiens	61-64
18703414-11	2008	0.1-1 mM 4-aminopyridine (4-AP) reduced cytotrophoblast cell hCG secretion and elevated cellular hCG; without altering cellular integrity or syncytialization.	4-Aminopyridine	9-24	hypertrichosis 2 (generalised, congenital)	Homo sapiens	97-100
18703414-11	2008	0.1-1 mM 4-aminopyridine (4-AP) reduced cytotrophoblast cell hCG secretion and elevated cellular hCG; without altering cellular integrity or syncytialization.	4-Aminopyridine	26-30	hypertrichosis 2 (generalised, congenital)	Homo sapiens	61-64
18703414-11	2008	0.1-1 mM 4-aminopyridine (4-AP) reduced cytotrophoblast cell hCG secretion and elevated cellular hCG; without altering cellular integrity or syncytialization.	4-Aminopyridine	26-30	hypertrichosis 2 (generalised, congenital)	Homo sapiens	97-100
18703414-12	2008	In villous explants, hCG secretion was not altered by 1 mM Ba(2+) but inhibited by 5 mM 4-AP and 5/10 mM TEA, without affecting LDH release.	4-Aminopyridine	88-92	hypertrichosis 2 (generalised, congenital)	Homo sapiens	21-24
18703414-12	2008	In villous explants, hCG secretion was not altered by 1 mM Ba(2+) but inhibited by 5 mM 4-AP and 5/10 mM TEA, without affecting LDH release.	Tetraethylammonium	105-108	hypertrichosis 2 (generalised, congenital)	Homo sapiens	21-24
18703414-14	2008	In conclusion, 4-AP- and TEA-sensitive K(+) channels (e.g., voltage-gated and Ca(2+)-activated) regulate trophoblast hCG secretion in culture.	4-Aminopyridine	15-19	hypertrichosis 2 (generalised, congenital)	Homo sapiens	117-120
19038077-45	2008	Limited information suggests that, in women with elevated hCG in the second trimester and/or abnormal uterine artery Doppler (at 22-24 weeks), low-dose aspirin (60-81 mg daily) is associated with higher birthweight and lower incidence of gestational hypertension with proteinuria.	Aspirin	152-159	hypertrichosis 2 (generalised, congenital)	Homo sapiens	58-61
18792925-0	2008	Rapid prenatal diagnosis using uncultured amniocytes and oligonucleotide array CGH.	Oligonucleotides	57-72	hypertrichosis 2 (generalised, congenital)	Homo sapiens	79-82
18792925-1	2008	OBJECTIVE: Oligonucleotide-based array comparative genomic hybridization (array CGH) is an established method for detecting chromosomal abnormalities.	Oligonucleotides	11-26	hypertrichosis 2 (generalised, congenital)	Homo sapiens	80-83
18792925-8	2008	CONCLUSION: This study demonstrates the feasibility of prenatal genetic diagnosis using oligonucleotide array CGH analysis for direct analysis of amniocytes without culturing cells.	Oligonucleotides	88-103	hypertrichosis 2 (generalised, congenital)	Homo sapiens	110-113
18544616-7	2008	TSH concentrations at the 25th and fifth centiles become sharply lower at higher hCG levels, whereas 50th centile and above TSH concentrations are only slightly lower.	Thyrotropin	0-3	hypertrichosis 2 (generalised, congenital)	Homo sapiens	81-84
18495695-5	2008	We first evaluated the dose-effect of ehCG on plasma testosterone and estradiol levels, before and after injection of either hCG or vehicle.	Testosterone	53-65	hypertrichosis 2 (generalised, congenital)	Homo sapiens	39-42
18495695-5	2008	We first evaluated the dose-effect of ehCG on plasma testosterone and estradiol levels, before and after injection of either hCG or vehicle.	Estradiol	70-79	hypertrichosis 2 (generalised, congenital)	Homo sapiens	39-42
18565217-1	2008	BACKGROUND: Patients with ectopic pregnancy (EP) and low serum hCG concentrations and women with a pregnancy of unknown location (PUL) and plateauing serum hCG levels are commonly treated with systemic methotrexate (MTX).	Methotrexate	202-214	hypertrichosis 2 (generalised, congenital)	Homo sapiens	63-66
18565217-1	2008	BACKGROUND: Patients with ectopic pregnancy (EP) and low serum hCG concentrations and women with a pregnancy of unknown location (PUL) and plateauing serum hCG levels are commonly treated with systemic methotrexate (MTX).	Methotrexate	202-214	hypertrichosis 2 (generalised, congenital)	Homo sapiens	156-159
18565217-1	2008	BACKGROUND: Patients with ectopic pregnancy (EP) and low serum hCG concentrations and women with a pregnancy of unknown location (PUL) and plateauing serum hCG levels are commonly treated with systemic methotrexate (MTX).	Methotrexate	216-219	hypertrichosis 2 (generalised, congenital)	Homo sapiens	156-159
18565217-17	2008	DISCUSSION: This trial will provide guidance on the present management dilemmas in women with EPs and PULs with low and plateauing serum hCG concentrations.	exophthalmos producing substance	94-97	hypertrichosis 2 (generalised, congenital)	Homo sapiens	137-140
18211694-0	2008	Calcitriol affects hCG gene transcription in cultured human syncytiotrophoblasts.	Calcitriol	0-10	hypertrichosis 2 (generalised, congenital)	Homo sapiens	19-22
18374407-9	2008	Our findings indicate that the use of hCG to induce ovulation in a timed artificial insemination protocol increases plasma progesterone levels and improves fertility in dairy cows during the warmer period of the year.	Progesterone	123-135	hypertrichosis 2 (generalised, congenital)	Homo sapiens	38-41
18343809-4	2008	hCG to normalize testosterone (T) and induce puberty.	Testosterone	17-29	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
18427974-12	2008	A significantly higher endometrial thickness was observed at the time of hCG administration in patients that received letrozole (9.7 +/- 1.6 mm vs. 7.8 +/- 2 mm; P &lt; 0.001).	Letrozole	118-127	hypertrichosis 2 (generalised, congenital)	Homo sapiens	73-76
18379195-0	2008	Human chorionic gonadotropin (hCG) interacts with lovastatin and ionizing radiation to modulate prostate cancer cell viability in vivo.	Lovastatin	50-60	hypertrichosis 2 (generalised, congenital)	Homo sapiens	30-33
18379195-2	2008	Treatment of PC-3 cells in vitro with hCG caused a modest increase in numbers of non-viable cells within 96 h. Treatment of cells with hCG followed by exposure to the HMG CoA reductase inhibitor lovastatin suppressed AKT phosphorylation and enhanced the cytotoxic effects of hCG.	Lovastatin	195-205	hypertrichosis 2 (generalised, congenital)	Homo sapiens	38-41
18379195-2	2008	Treatment of PC-3 cells in vitro with hCG caused a modest increase in numbers of non-viable cells within 96 h. Treatment of cells with hCG followed by exposure to the HMG CoA reductase inhibitor lovastatin suppressed AKT phosphorylation and enhanced the cytotoxic effects of hCG.	Lovastatin	195-205	hypertrichosis 2 (generalised, congenital)	Homo sapiens	135-138
18379195-2	2008	Treatment of PC-3 cells in vitro with hCG caused a modest increase in numbers of non-viable cells within 96 h. Treatment of cells with hCG followed by exposure to the HMG CoA reductase inhibitor lovastatin suppressed AKT phosphorylation and enhanced the cytotoxic effects of hCG.	Lovastatin	195-205	hypertrichosis 2 (generalised, congenital)	Homo sapiens	135-138
18379195-5	2008	In vitro, treatment of PC-3 cells with hCG followed by exposure to ionizing radiation enhanced the cytotoxic effects of hCG, that was further enhanced by lovastatin.	Lovastatin	154-164	hypertrichosis 2 (generalised, congenital)	Homo sapiens	39-42
18379195-5	2008	In vitro, treatment of PC-3 cells with hCG followed by exposure to ionizing radiation enhanced the cytotoxic effects of hCG, that was further enhanced by lovastatin.	Lovastatin	154-164	hypertrichosis 2 (generalised, congenital)	Homo sapiens	120-123
18379195-6	2008	In vivo, hCG radiosensitized PC-3 tumors and significantly enhanced the lethality of hCG and lovastatin treatment.	Lovastatin	93-103	hypertrichosis 2 (generalised, congenital)	Homo sapiens	9-12
18211694-13	2008	The latter, together with findings demonstrating specific effects of calcitriol acting through the VDR and the cAMP/PKA signaling pathway upon hCG expression and secretion, indicate that there is a functional vitamin D endocrine system in the placenta, and recognize calcitriol as an autocrine regulator of hCG.	Calcitriol	69-79	hypertrichosis 2 (generalised, congenital)	Homo sapiens	143-146
18211694-13	2008	The latter, together with findings demonstrating specific effects of calcitriol acting through the VDR and the cAMP/PKA signaling pathway upon hCG expression and secretion, indicate that there is a functional vitamin D endocrine system in the placenta, and recognize calcitriol as an autocrine regulator of hCG.	Cyclic AMP	111-115	hypertrichosis 2 (generalised, congenital)	Homo sapiens	143-146
18211694-13	2008	The latter, together with findings demonstrating specific effects of calcitriol acting through the VDR and the cAMP/PKA signaling pathway upon hCG expression and secretion, indicate that there is a functional vitamin D endocrine system in the placenta, and recognize calcitriol as an autocrine regulator of hCG.	Vitamin D	209-218	hypertrichosis 2 (generalised, congenital)	Homo sapiens	143-146
18211694-13	2008	The latter, together with findings demonstrating specific effects of calcitriol acting through the VDR and the cAMP/PKA signaling pathway upon hCG expression and secretion, indicate that there is a functional vitamin D endocrine system in the placenta, and recognize calcitriol as an autocrine regulator of hCG.	Vitamin D	209-218	hypertrichosis 2 (generalised, congenital)	Homo sapiens	307-310
18211694-13	2008	The latter, together with findings demonstrating specific effects of calcitriol acting through the VDR and the cAMP/PKA signaling pathway upon hCG expression and secretion, indicate that there is a functional vitamin D endocrine system in the placenta, and recognize calcitriol as an autocrine regulator of hCG.	Calcitriol	267-277	hypertrichosis 2 (generalised, congenital)	Homo sapiens	143-146
18604677-7	2008	The use of beta hCG levels in conjunction with serum progesterone is helpful, particularly with serum progesterone levels between 16-80 nmol/l.	Progesterone	102-114	hypertrichosis 2 (generalised, congenital)	Homo sapiens	16-19
18094363-7	2008	Administration of ADM to Leydig cells resulted in an inhibition of hCG- and EDN1-stimulated testosterone production.	Testosterone	92-104	hypertrichosis 2 (generalised, congenital)	Homo sapiens	67-70
17920804-6	2008	Administration of hCG resulted in an increase of plasma cortisol and androstenedione concentrations.	Androstenedione	69-84	hypertrichosis 2 (generalised, congenital)	Homo sapiens	18-21
18325003-4	2008	Activities of both CYP2E1 and CYP2A were lower in hCG-stimulated pigs than control pigs for both Landrace (p = 0.005 for CYP2E1, p = 0.016 for CYP2A) and Duroc breeds (p = 0.003 for CYP2E1, p = 0.001 for CYP2A), and skatole concentrations in fat were higher in the hCG-stimulated pigs of both breeds (p &lt; 0.01).	Skatole	216-223	hypertrichosis 2 (generalised, congenital)	Homo sapiens	50-53
18325003-5	2008	For both control and hCG-stimulated groups, Duroc pigs had lower skatole concentrations than Landrace pigs (p = 0.001 for both groups).	Skatole	65-72	hypertrichosis 2 (generalised, congenital)	Homo sapiens	21-24
18325003-8	2008	Based on these findings, we conclude that hCG stimulation can suppress hepatic CYP2E1 and CYP2A activities, probably through an increase in the levels of testicular steroids.	Steroids	165-173	hypertrichosis 2 (generalised, congenital)	Homo sapiens	42-45
18211694-3	2008	In the present work we studied calcitriol actions upon human chorionic gonadotropin (hCG) secretion and expression in cultured trophoblasts, as well as vitamin D receptor (VDR) and CYP27B1 immunolocalization in placental villi.	Calcitriol	31-41	hypertrichosis 2 (generalised, congenital)	Homo sapiens	85-88
18211694-8	2008	RESULTS: Calcitriol regulated hCG in a time-dependent manner: at 6 h the secosteroid stimulated hCG, whereas longer incubations (24 h) showed opposite effects.	Calcitriol	9-19	hypertrichosis 2 (generalised, congenital)	Homo sapiens	30-33
18211694-8	2008	RESULTS: Calcitriol regulated hCG in a time-dependent manner: at 6 h the secosteroid stimulated hCG, whereas longer incubations (24 h) showed opposite effects.	Calcitriol	9-19	hypertrichosis 2 (generalised, congenital)	Homo sapiens	96-99
18211694-9	2008	Interestingly, calcitriol stimulatory effects on hCG were accompanied by an increase in intracellular cAMP content and were abolished by pre-incubation of the cells with a selective protein kinase A inhibitor.	Calcitriol	15-25	hypertrichosis 2 (generalised, congenital)	Homo sapiens	49-52
18211694-9	2008	Interestingly, calcitriol stimulatory effects on hCG were accompanied by an increase in intracellular cAMP content and were abolished by pre-incubation of the cells with a selective protein kinase A inhibitor.	Cyclic AMP	102-106	hypertrichosis 2 (generalised, congenital)	Homo sapiens	49-52
18053657-4	2008	Fenvalerate treatment inhibited progesterone secretion induced by human chorionic gonadotropin (hCG), cholera toxin (CT) or forskolin and decreased cAMP levels induced by hCG, but not by CT or forskolin, which suggested a repaired site on the upstream components of G protein or G protein per se by fenvalerate in the cAMP-mediated signal pathway.	fenvalerate	0-11	hypertrichosis 2 (generalised, congenital)	Homo sapiens	96-99
18053657-4	2008	Fenvalerate treatment inhibited progesterone secretion induced by human chorionic gonadotropin (hCG), cholera toxin (CT) or forskolin and decreased cAMP levels induced by hCG, but not by CT or forskolin, which suggested a repaired site on the upstream components of G protein or G protein per se by fenvalerate in the cAMP-mediated signal pathway.	fenvalerate	0-11	hypertrichosis 2 (generalised, congenital)	Homo sapiens	171-174
17174489-6	2007	GnRH or hCG treatment increased (P&lt;0.001) mean plasma progesterone concentrations in both age groups, however, post-treatment concentrations were significantly (P&lt;0.05) higher in ewes than in ewe lambs.	Progesterone	57-69	hypertrichosis 2 (generalised, congenital)	Homo sapiens	8-11
18198068-5	2008	The patient returned with signs of a persistent ectopic pregnancy and was subsequently treated with methotrexate with resolution of symptoms and normalization of hCG levels.	Methotrexate	100-112	hypertrichosis 2 (generalised, congenital)	Homo sapiens	162-165
17174489-8	2007	In ewes, but not in ewe lambs, both GnRH and hCG treatments significantly (P&lt;0.05) increased the mean oestradiol concentrations above pre-treatment levels.	Estradiol	105-115	hypertrichosis 2 (generalised, congenital)	Homo sapiens	45-48
17174489-9	2007	Moreover, post-treatment oestradiol concentrations in GnRH- and hCG-treated animals were significantly (P&lt;0.05) higher than those in the saline-treated controls.	Estradiol	25-35	hypertrichosis 2 (generalised, congenital)	Homo sapiens	64-67
17726079-2	2007	NIS is expressed in trophoblast and is regulated by human choriogonadotropin (hCG).	Nickel	0-3	hypertrichosis 2 (generalised, congenital)	Homo sapiens	78-81
17726079-5	2007	OBJECTIVES AND METHODS: The objectives were to examine effects of iodide on expression of NIS and hCG in BeWo choriocarcinoma cells.	Iodides	66-72	hypertrichosis 2 (generalised, congenital)	Homo sapiens	98-101
17726079-16	2007	This may occur through modulation of hCG effects on NIS and hCG gene expression.	Nickel	52-55	hypertrichosis 2 (generalised, congenital)	Homo sapiens	37-40
17290424-7	2007	Furthermore, this study strongly indicates that the different effects of hCG and LH in the maintenance of the CL may be reasoned in different signal transduction pathways triggered by hCG or LH.	Luteinizing Hormone	81-83	hypertrichosis 2 (generalised, congenital)	Homo sapiens	184-187
17290424-7	2007	Furthermore, this study strongly indicates that the different effects of hCG and LH in the maintenance of the CL may be reasoned in different signal transduction pathways triggered by hCG or LH.	Luteinizing Hormone	191-193	hypertrichosis 2 (generalised, congenital)	Homo sapiens	73-76
17716724-9	2007	These results highlight the usefulness of lecirelin for induction and synchronization of ovulation in the jenny, particularly since it would avoid the risk of reduced hCG response in reproductive management programs in which that hormone was repeatedly used.	lecirelin	42-51	hypertrichosis 2 (generalised, congenital)	Homo sapiens	167-170
17011145-16	2007	Shortly, it has been concluded from the study that (1) normal and fertile estrus can be induced more economically in bitches during different stages of anestrus using as a low dose of 0.6 microg/kg of cabergoline formulation marketed for use in women, and that (2) hCG injections on days 1 and 3 of the estrus induced by this method has no positive effects on the ovulation rates, pregnancy rates and the number of offspring per pregnancy.	Cabergoline	201-212	hypertrichosis 2 (generalised, congenital)	Homo sapiens	265-268
17550979-9	2007	To determine the role of Mvk in ligand-mediated down-regulation of LHR mRNA, cells were additionally treated with 25-OHC when treated with hCG.	25-hydroxycholesterol	114-120	hypertrichosis 2 (generalised, congenital)	Homo sapiens	139-142
16820309-5	2007	A human choriongonadotropin (hCG)-stimulation test resulted in an increase in the plasma levels of estrogen sulfate and testosterone, indistinguishable from that of a normal stallion.	estrogen sulfate	99-115	hypertrichosis 2 (generalised, congenital)	Homo sapiens	29-32
19070087-1	2007	The objectives of this study were to determine the effect of administration of exogenous hCG 5 days after Artificial Insemination (AI) on serum progesterone concentration and conception rate in lactating dairy cows.	Progesterone	144-156	hypertrichosis 2 (generalised, congenital)	Homo sapiens	89-92
16820309-5	2007	A human choriongonadotropin (hCG)-stimulation test resulted in an increase in the plasma levels of estrogen sulfate and testosterone, indistinguishable from that of a normal stallion.	Testosterone	120-132	hypertrichosis 2 (generalised, congenital)	Homo sapiens	29-32
17363138-1	2007	Adrenal cortex hyperfunction may occasionally be due to stimulation of steroid hormone production by LH/hCG.	Steroids	71-86	hypertrichosis 2 (generalised, congenital)	Homo sapiens	104-107
17363138-2	2007	The recent demonstration of the LH/hCG receptor in a variety of normal and abnormal human adrenal tissues has provided a novel explanation for these clinical observations and offers the possibility of spontaneous remission (as in pregnancy-related hyperfunction) or effective treatment with GnRH-agonists (to down-regulate LH secretion in menopausal patients).	Luteinizing Hormone	32-34	hypertrichosis 2 (generalised, congenital)	Homo sapiens	35-38
17400803-4	2007	Using MA-10 mouse Leydig tumor cells, we demonstrate that the activation of PKC and PKA signaling, by phorbol-12-myristate-13-acetate (PMA) and dibutyryl cAMP (dbcAMP)/human chorionic gonadotropin (hCG) respectively, was able to phosphorylate ERK1/2, an event markedly decreased by an upstream kinase inhibitor, U0126.	Bucladesine	160-166	hypertrichosis 2 (generalised, congenital)	Homo sapiens	198-201
17400803-6	2007	Inhibition of ERK1/2 activity by U0126 decreased PMA-treated StAR expression but increased dbcAMP/hCG-mediated StAR and P-StAR; however, progesterone levels were attenuated.	U 0126	33-38	hypertrichosis 2 (generalised, congenital)	Homo sapiens	98-101
17400803-8	2007	Further studies demonstrated that the effect of U0126 on PMA- and dbcAMP/hCG-mediated StAR expression and steroid synthesis was tightly correlated with the expression of dosage-sensitive sex reversal, adrenal hypoplasia congenita, critical region on the X chromosome, gene 1 (DAX-1) and scavenger receptor class B type 1 (SR-B1).	U 0126	48-53	hypertrichosis 2 (generalised, congenital)	Homo sapiens	73-76
17382384-10	2007	While hCG alone had no significant effect on endothelial cell apoptosis, the combination of VEGF-A and hCG protected HPMVEC from staurosporine-induced apoptosis.	Staurosporine	129-142	hypertrichosis 2 (generalised, congenital)	Homo sapiens	103-106
17092638-2	2007	This form differs from later pregnancy hCG in carbohydrate moieties.	Carbohydrates	46-58	hypertrichosis 2 (generalised, congenital)	Homo sapiens	39-42
17453685-1	2007	The in vitro effect of extracted fractions of Cordyceps sinensis (CS) mycelium on hCG-treated testosterone production from purified normal mouse Leydig cells was examined.	Testosterone	94-106	hypertrichosis 2 (generalised, congenital)	Homo sapiens	82-85
17453685-3	2007	Testosterone productions stimulated by hCG in mouse Leydig cells were suppressed by F2 at 10 mg/ml and F3 at doses from 3 to 10 mg/ml, respectively.	Testosterone	0-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	39-42
17173905-8	2007	RESULT(S): Five observational studies, including 503 women, were found that reported successes in using single-dose methotrexate stratified by initial hCG concentration.	Methotrexate	116-128	hypertrichosis 2 (generalised, congenital)	Homo sapiens	151-154
17173905-12	2007	CONCLUSION(S): Results support a substantial increase in failure of medical management with single-dose methotrexate when the initial hCG is above 5,000 mIU/mL.	Methotrexate	104-116	hypertrichosis 2 (generalised, congenital)	Homo sapiens	134-137
17173905-13	2007	Methotrexate should be used with caution in patients with ectopic pregnancy who present with hCG levels above this level.	Methotrexate	0-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	93-96
16820309-5	2007	A human choriongonadotropin (hCG)-stimulation test resulted in an increase in the plasma levels of estrogen sulfate and testosterone, indistinguishable from that of a normal stallion.	choriongonadotropin	8-27	hypertrichosis 2 (generalised, congenital)	Homo sapiens	29-32
16476529-9	2007	Injection of hCG resulted in an increase (P&lt;0.01; n=4) in testosterone concentration with a peak (2.9+/-0.3 ng/mL) approximately 4h after injection.	Testosterone	61-73	hypertrichosis 2 (generalised, congenital)	Homo sapiens	13-16
16476529-11	2007	Seasonal changes in testosterone secretion determined after injection of hCG, increased (P=0.03; n=6) from late-autumn, peaked in late-winter, and decreased by early-spring.	Testosterone	20-32	hypertrichosis 2 (generalised, congenital)	Homo sapiens	73-76
18225678-5	2007	Clomiphene citrate or gonadotropins or hCG may be effective but usually only when serum FSH, LH and/or testosterone levels are low or are in the low normal range.	Luteinizing Hormone	93-95	hypertrichosis 2 (generalised, congenital)	Homo sapiens	39-42
17150203-0	2007	Dual action of H2O2 on placental hCG secretion: implications for oxidative stress in preeclampsia.	Hydrogen Peroxide	15-19	hypertrichosis 2 (generalised, congenital)	Homo sapiens	33-36
17150203-4	2007	RESULTS: Stimulation with low concentrations of H(2)O(2) (1-50 microM) enhances cytotrophoblastic hCG secretion, whereas concentrations of H(2)O(2) &gt;50 microM reduce hCG secretion in a dose-dependent manner.	Water	48-53	hypertrichosis 2 (generalised, congenital)	Homo sapiens	98-101
18225678-5	2007	Clomiphene citrate or gonadotropins or hCG may be effective but usually only when serum FSH, LH and/or testosterone levels are low or are in the low normal range.	Testosterone	103-115	hypertrichosis 2 (generalised, congenital)	Homo sapiens	39-42
17951176-0	2007	Rat epididymal epithelial cells and 17beta-estradiol synthesis under hCG stimulation in vitro.	Estradiol	36-52	hypertrichosis 2 (generalised, congenital)	Homo sapiens	69-72
17951176-5	2007	The present studies show the organelles which take part in synthesis of steroids in rat epididymal epithelial cells in vitro and the effect of hCG on E2 synthesis.	Estradiol	150-152	hypertrichosis 2 (generalised, congenital)	Homo sapiens	143-146
17951176-6	2007	The cells were cultured in the medium with/without DHT and without DHT in supplementation with hCG.	Dihydrotestosterone	67-70	hypertrichosis 2 (generalised, congenital)	Homo sapiens	95-98
17951176-7	2007	After hCG stimulation the amount of an active mitochondria were increased when compared to the amount of mitochondria in the epididymal epithelial cells cultured without DHT.	Dihydrotestosterone	170-173	hypertrichosis 2 (generalised, congenital)	Homo sapiens	6-9
17951176-9	2007	The synthesis of 17beta-estradiol was stimulated by hCG, that exerted its effect through LH/hCG receptors, localized in the epididymal epithelial cells.	Estradiol	17-33	hypertrichosis 2 (generalised, congenital)	Homo sapiens	52-55
17951176-9	2007	The synthesis of 17beta-estradiol was stimulated by hCG, that exerted its effect through LH/hCG receptors, localized in the epididymal epithelial cells.	Estradiol	17-33	hypertrichosis 2 (generalised, congenital)	Homo sapiens	92-95
18076825-1	2007	The native form of human chorionic gonadotropin (hCG) is a heterodimer protein with two asparagine (Asn)-linked carbohydrate chains on each subunit.	Asparagine	88-98	hypertrichosis 2 (generalised, congenital)	Homo sapiens	49-52
16928894-3	2007	HDC KO Leydig cells showed lower basal and human choriogonadotropin (hCG)-induced testosterone production compared to WT Leydig cells, presumably due to altered P450scc gene (Cyp11a1) expression levels.	Testosterone	82-94	hypertrichosis 2 (generalised, congenital)	Homo sapiens	69-72
16928894-5	2007	Based on these findings, we propose that prolonged HA deficiency in HDC KO mice affects various aspects of Leydig cell physiology, most importantly the response to hCG, providing definite evidence that HA plays a role as direct modulator of Leydig cell function and steroid synthesis in the testis.	Steroids	266-273	hypertrichosis 2 (generalised, congenital)	Homo sapiens	164-167
17079137-2	2007	In this study, calcitriol rapidly generated intracellular cAMP accumulation in cultured human syncytiotrophoblast cells, which in turn enhanced hCG secretion, a marker of trophoblast endocrine activity.	Calcitriol	15-25	hypertrichosis 2 (generalised, congenital)	Homo sapiens	144-147
17079137-2	2007	In this study, calcitriol rapidly generated intracellular cAMP accumulation in cultured human syncytiotrophoblast cells, which in turn enhanced hCG secretion, a marker of trophoblast endocrine activity.	Cyclic AMP	58-62	hypertrichosis 2 (generalised, congenital)	Homo sapiens	144-147
17079137-5	2007	The use of a selective inhibitor of PKA (H-89) prevented the effects of calcitriol on CYP27B1 gene and hCG secretion, but not on CYP24A1 transcription.	N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide	41-45	hypertrichosis 2 (generalised, congenital)	Homo sapiens	103-106
17079137-5	2007	The use of a selective inhibitor of PKA (H-89) prevented the effects of calcitriol on CYP27B1 gene and hCG secretion, but not on CYP24A1 transcription.	Calcitriol	72-82	hypertrichosis 2 (generalised, congenital)	Homo sapiens	103-106
18076825-1	2007	The native form of human chorionic gonadotropin (hCG) is a heterodimer protein with two asparagine (Asn)-linked carbohydrate chains on each subunit.	Asparagine	100-103	hypertrichosis 2 (generalised, congenital)	Homo sapiens	49-52
18076825-1	2007	The native form of human chorionic gonadotropin (hCG) is a heterodimer protein with two asparagine (Asn)-linked carbohydrate chains on each subunit.	Carbohydrates	112-124	hypertrichosis 2 (generalised, congenital)	Homo sapiens	49-52
18076825-2	2007	Removal of the Asn-linked carbohydrate chains from hCG has resulted in hCG variants with consistent antagonistic properties on isolated murine cells.	Asparagine	15-18	hypertrichosis 2 (generalised, congenital)	Homo sapiens	51-54
16620962-3	2007	Western blot analyses indicated that treatment of trophoblastic SGHPL-5 cells and purified term trophoblasts with potentially EGF-contaminated hCG (hCG-A) resulted in auto-phosphorylation of the EGF receptor at tyrosine 1173 whereas supplementation of another urine-purified hCG preparation (hCG-B), recombinant holo-hCG or recombinant alphahCG had no effects.	Tyrosine	211-219	hypertrichosis 2 (generalised, congenital)	Homo sapiens	143-146
16620962-3	2007	Western blot analyses indicated that treatment of trophoblastic SGHPL-5 cells and purified term trophoblasts with potentially EGF-contaminated hCG (hCG-A) resulted in auto-phosphorylation of the EGF receptor at tyrosine 1173 whereas supplementation of another urine-purified hCG preparation (hCG-B), recombinant holo-hCG or recombinant alphahCG had no effects.	Tyrosine	211-219	hypertrichosis 2 (generalised, congenital)	Homo sapiens	148-151
16620962-3	2007	Western blot analyses indicated that treatment of trophoblastic SGHPL-5 cells and purified term trophoblasts with potentially EGF-contaminated hCG (hCG-A) resulted in auto-phosphorylation of the EGF receptor at tyrosine 1173 whereas supplementation of another urine-purified hCG preparation (hCG-B), recombinant holo-hCG or recombinant alphahCG had no effects.	Tyrosine	211-219	hypertrichosis 2 (generalised, congenital)	Homo sapiens	148-151
16620962-3	2007	Western blot analyses indicated that treatment of trophoblastic SGHPL-5 cells and purified term trophoblasts with potentially EGF-contaminated hCG (hCG-A) resulted in auto-phosphorylation of the EGF receptor at tyrosine 1173 whereas supplementation of another urine-purified hCG preparation (hCG-B), recombinant holo-hCG or recombinant alphahCG had no effects.	alphahcg	336-344	hypertrichosis 2 (generalised, congenital)	Homo sapiens	143-146
16620962-3	2007	Western blot analyses indicated that treatment of trophoblastic SGHPL-5 cells and purified term trophoblasts with potentially EGF-contaminated hCG (hCG-A) resulted in auto-phosphorylation of the EGF receptor at tyrosine 1173 whereas supplementation of another urine-purified hCG preparation (hCG-B), recombinant holo-hCG or recombinant alphahCG had no effects.	alphahcg	336-344	hypertrichosis 2 (generalised, congenital)	Homo sapiens	148-151
16620962-3	2007	Western blot analyses indicated that treatment of trophoblastic SGHPL-5 cells and purified term trophoblasts with potentially EGF-contaminated hCG (hCG-A) resulted in auto-phosphorylation of the EGF receptor at tyrosine 1173 whereas supplementation of another urine-purified hCG preparation (hCG-B), recombinant holo-hCG or recombinant alphahCG had no effects.	alphahcg	336-344	hypertrichosis 2 (generalised, congenital)	Homo sapiens	148-151
16943366-9	2006	PGE2 increased intracellular calcium in granulosa cells obtained 36 h, but not 24 h, after hCG; this effect of PGE2 was blocked by a PTGER1 antagonist.	Dinoprostone	0-4	hypertrichosis 2 (generalised, congenital)	Homo sapiens	91-94
17007849-10	2006	On the day of hCG administration in noncancelled cycles, anastrozole cycles were associated with fewer total follicles (1.6 vs. 3.8, P&lt;.01), fewer mature follicles (1.3 vs. 2.1, P&lt;.01), and an equal endometrial stripe thickness compared with clomiphene citrate cycles.	Anastrozole	57-68	hypertrichosis 2 (generalised, congenital)	Homo sapiens	14-17
17065221-8	2006	By using dibutyryl cAMP, adenylate cyclase, or protein kinase A inhibitors, we demonstrate that hCG-mediated angiogenesis involves adenylyl-cyclase-protein kinase A activation.	Cyclic AMP	19-23	hypertrichosis 2 (generalised, congenital)	Homo sapiens	96-99
16880503-4	2006	These glycoforms, which are called "hyperglycosylated" hCG (hCGh), have been reported to contain more complex glycan moieties.	Polysaccharides	110-116	hypertrichosis 2 (generalised, congenital)	Homo sapiens	55-58
16880503-4	2006	These glycoforms, which are called "hyperglycosylated" hCG (hCGh), have been reported to contain more complex glycan moieties.	Polysaccharides	110-116	hypertrichosis 2 (generalised, congenital)	Homo sapiens	60-64
16880503-12	2006	The glycans of free hCGbeta were larger and had a higher fucose content of Asn-13-linked oligosaccharides than intact hCG.	Polysaccharides	4-11	hypertrichosis 2 (generalised, congenital)	Homo sapiens	20-23
16880503-12	2006	The glycans of free hCGbeta were larger and had a higher fucose content of Asn-13-linked oligosaccharides than intact hCG.	Fucose	57-63	hypertrichosis 2 (generalised, congenital)	Homo sapiens	20-23
16880503-12	2006	The glycans of free hCGbeta were larger and had a higher fucose content of Asn-13-linked oligosaccharides than intact hCG.	asn-13-linked oligosaccharides	75-105	hypertrichosis 2 (generalised, congenital)	Homo sapiens	20-23
16880503-14	2006	Analysis of hCGh affinity purified with antibody B152 confirmed that this antibody recognizes a core-2 glycan on Ser-132.	Polysaccharides	103-109	hypertrichosis 2 (generalised, congenital)	Homo sapiens	12-16
16880503-14	2006	Analysis of hCGh affinity purified with antibody B152 confirmed that this antibody recognizes a core-2 glycan on Ser-132.	Serine	113-116	hypertrichosis 2 (generalised, congenital)	Homo sapiens	12-16
17097894-10	2006	Moreover, while leptin, in various concentrations, did not affect PGE(2) and PGF(2alpha) levels, it inhibited the elevation of PGE(2) and PGF(2alpha) concentrations in response to hCG.	Prostaglandins F	138-141	hypertrichosis 2 (generalised, congenital)	Homo sapiens	180-183
17097894-12	2006	Leptin suppresses hCG-induced PGE(2) formation through the inhibition of COX-2 and mPGES expression.	Prostaglandins E	30-33	hypertrichosis 2 (generalised, congenital)	Homo sapiens	18-21
18076825-2	2007	Removal of the Asn-linked carbohydrate chains from hCG has resulted in hCG variants with consistent antagonistic properties on isolated murine cells.	Asparagine	15-18	hypertrichosis 2 (generalised, congenital)	Homo sapiens	71-74
18076825-2	2007	Removal of the Asn-linked carbohydrate chains from hCG has resulted in hCG variants with consistent antagonistic properties on isolated murine cells.	linked carbohydrate	19-38	hypertrichosis 2 (generalised, congenital)	Homo sapiens	51-54
18076825-2	2007	Removal of the Asn-linked carbohydrate chains from hCG has resulted in hCG variants with consistent antagonistic properties on isolated murine cells.	linked carbohydrate	19-38	hypertrichosis 2 (generalised, congenital)	Homo sapiens	71-74
18076825-3	2007	Specific and direct enzymatic removal of these carbohydrate chains from native hCG with resultant antagonistic properties has not been reported.	Carbohydrates	47-59	hypertrichosis 2 (generalised, congenital)	Homo sapiens	79-82
18076825-5	2007	Therefore, our aim was to use enzymes to specifically remove Asn-linked carbohydrate chains from hCG in the heterodimer form and analyse the resultant bioactivity.	Asparagine	61-64	hypertrichosis 2 (generalised, congenital)	Homo sapiens	97-100
18076825-5	2007	Therefore, our aim was to use enzymes to specifically remove Asn-linked carbohydrate chains from hCG in the heterodimer form and analyse the resultant bioactivity.	linked carbohydrate	65-84	hypertrichosis 2 (generalised, congenital)	Homo sapiens	97-100
18076825-7	2007	Endoglycosidases were able to cleave most of the Asn-linked carbohydrate chains from the native hCG.	Asparagine	49-52	hypertrichosis 2 (generalised, congenital)	Homo sapiens	96-99
18076825-7	2007	Endoglycosidases were able to cleave most of the Asn-linked carbohydrate chains from the native hCG.	linked carbohydrate	53-72	hypertrichosis 2 (generalised, congenital)	Homo sapiens	96-99
18076825-9	2007	These results exemplify a simple and efficient method for creating deglycosylated hCG and provide the most direct evidence for the importance of Asn-linked carbohydrate chains in maintaining hCG bioactivity.	Asparagine	145-148	hypertrichosis 2 (generalised, congenital)	Homo sapiens	191-194
18076825-9	2007	These results exemplify a simple and efficient method for creating deglycosylated hCG and provide the most direct evidence for the importance of Asn-linked carbohydrate chains in maintaining hCG bioactivity.	Carbohydrates	156-168	hypertrichosis 2 (generalised, congenital)	Homo sapiens	191-194
17071778-4	2006	Serum progesterone level, ovulation rate and ovarian prostaglandin E (PGE) content were reduced in rats primed with equine chorionic gonadotrophin (eCG)/hCG and treated with acute doses of leptin (five doses of 5 mug each).	Prostaglandins E	70-73	hypertrichosis 2 (generalised, congenital)	Homo sapiens	153-156
16751622-2	2006	However, it has been shown in several species that an index of the prevailing testosterone biosynthetic capacity of the testes can be obtained by measuring the increase in circulating testosterone after injection of a GnRH agonist or human chorionic gonadotrophin (hCG).	Testosterone	78-90	hypertrichosis 2 (generalised, congenital)	Homo sapiens	265-268
16751622-2	2006	However, it has been shown in several species that an index of the prevailing testosterone biosynthetic capacity of the testes can be obtained by measuring the increase in circulating testosterone after injection of a GnRH agonist or human chorionic gonadotrophin (hCG).	Testosterone	184-196	hypertrichosis 2 (generalised, congenital)	Homo sapiens	265-268
16751622-6	2006	Injection of buserelin and hCG resulted in an increase (P &lt; .05) in blood testosterone concentration.	Testosterone	77-89	hypertrichosis 2 (generalised, congenital)	Homo sapiens	27-30
16751622-9	2006	There were strong positive correlations between the average testosterone concentration over 24 hours and the maximum observed testosterone concentration after stimulation with GnRH and hCG (GnRH, r = .772; P = .07 and hCG, r = 1.0; P &lt; .01).	Testosterone	60-72	hypertrichosis 2 (generalised, congenital)	Homo sapiens	185-188
16751622-9	2006	There were strong positive correlations between the average testosterone concentration over 24 hours and the maximum observed testosterone concentration after stimulation with GnRH and hCG (GnRH, r = .772; P = .07 and hCG, r = 1.0; P &lt; .01).	Testosterone	60-72	hypertrichosis 2 (generalised, congenital)	Homo sapiens	218-221
16751622-9	2006	There were strong positive correlations between the average testosterone concentration over 24 hours and the maximum observed testosterone concentration after stimulation with GnRH and hCG (GnRH, r = .772; P = .07 and hCG, r = 1.0; P &lt; .01).	Testosterone	126-138	hypertrichosis 2 (generalised, congenital)	Homo sapiens	185-188
17165440-1	2006	OBJECTIVE: Hyperglycosylated human chorionic gonadotropin (hCG-H) is a carbohydrate variant of hCG with double-sized oligosaccharide side chains.	Carbohydrates	71-83	hypertrichosis 2 (generalised, congenital)	Homo sapiens	59-64
17165440-1	2006	OBJECTIVE: Hyperglycosylated human chorionic gonadotropin (hCG-H) is a carbohydrate variant of hCG with double-sized oligosaccharide side chains.	Carbohydrates	71-83	hypertrichosis 2 (generalised, congenital)	Homo sapiens	59-62
17165440-1	2006	OBJECTIVE: Hyperglycosylated human chorionic gonadotropin (hCG-H) is a carbohydrate variant of hCG with double-sized oligosaccharide side chains.	Oligosaccharides	117-132	hypertrichosis 2 (generalised, congenital)	Homo sapiens	59-64
17165440-1	2006	OBJECTIVE: Hyperglycosylated human chorionic gonadotropin (hCG-H) is a carbohydrate variant of hCG with double-sized oligosaccharide side chains.	Oligosaccharides	117-132	hypertrichosis 2 (generalised, congenital)	Homo sapiens	59-62
16777379-3	2006	Our findings demonstrate that helenalin inhibits both ACTH- and hCG-activated steroidogenesis in these cells.	helenalin	30-39	hypertrichosis 2 (generalised, congenital)	Homo sapiens	64-67
16777379-6	2006	Indeed, helenalin attenuated StAR protein expression activated by ACTH and hCG in adrenocortical and Leydig cells as assessed by PAGE/Western analyses.	helenalin	8-17	hypertrichosis 2 (generalised, congenital)	Homo sapiens	75-78
16978619-13	2006	A significantly higher endometrial thickness was observed at the time of hCG administration in patients that received letrozole (9.5 +/- 1.5 mm vs. 7.3 +/- 1.1 mm; P=.0001).	Letrozole	118-127	hypertrichosis 2 (generalised, congenital)	Homo sapiens	73-76
16962114-7	2006	RESULT(S): Significant (P&lt;.05) differences were found in the ATP levels; compared with the control (no injection), a dramatic increase was detected after injections of 15 IU of hCG or of 15 IU of PMSG and 15 IU of hCG.	Adenosine Triphosphate	64-67	hypertrichosis 2 (generalised, congenital)	Homo sapiens	180-183
16952382-8	2006	Moreover, hCG increased nitrate uptake into MLTC-1, which suggests the gonadotropin aids nitrite and nitrate ions in their steroidogenesis inhibitory activity.	Nitrates	24-31	hypertrichosis 2 (generalised, congenital)	Homo sapiens	10-13
16952382-8	2006	Moreover, hCG increased nitrate uptake into MLTC-1, which suggests the gonadotropin aids nitrite and nitrate ions in their steroidogenesis inhibitory activity.	Nitrites	89-96	hypertrichosis 2 (generalised, congenital)	Homo sapiens	10-13
16952382-8	2006	Moreover, hCG increased nitrate uptake into MLTC-1, which suggests the gonadotropin aids nitrite and nitrate ions in their steroidogenesis inhibitory activity.	Nitrates	101-108	hypertrichosis 2 (generalised, congenital)	Homo sapiens	10-13
16962114-7	2006	RESULT(S): Significant (P&lt;.05) differences were found in the ATP levels; compared with the control (no injection), a dramatic increase was detected after injections of 15 IU of hCG or of 15 IU of PMSG and 15 IU of hCG.	Adenosine Triphosphate	64-67	hypertrichosis 2 (generalised, congenital)	Homo sapiens	217-220
16962114-9	2006	A significant increase in pyruvate uptake was detected after the injections of 15 IU of PMSG and 15 IU of hCG.	Pyruvic Acid	26-34	hypertrichosis 2 (generalised, congenital)	Homo sapiens	106-109
16962114-11	2006	The injections of 15 IU of hCG, or of 15 IU of PMSG and 15 IU of hCG, dramatically increased the ATP level, the mitochondrial population number, and pyruvate uptake.	Adenosine Triphosphate	97-100	hypertrichosis 2 (generalised, congenital)	Homo sapiens	27-30
16962114-11	2006	The injections of 15 IU of hCG, or of 15 IU of PMSG and 15 IU of hCG, dramatically increased the ATP level, the mitochondrial population number, and pyruvate uptake.	Adenosine Triphosphate	97-100	hypertrichosis 2 (generalised, congenital)	Homo sapiens	65-68
16962114-11	2006	The injections of 15 IU of hCG, or of 15 IU of PMSG and 15 IU of hCG, dramatically increased the ATP level, the mitochondrial population number, and pyruvate uptake.	Pyruvic Acid	149-157	hypertrichosis 2 (generalised, congenital)	Homo sapiens	27-30
16962114-11	2006	The injections of 15 IU of hCG, or of 15 IU of PMSG and 15 IU of hCG, dramatically increased the ATP level, the mitochondrial population number, and pyruvate uptake.	Pyruvic Acid	149-157	hypertrichosis 2 (generalised, congenital)	Homo sapiens	65-68
16930210-6	2006	Testosterone release was studied under basal conditions or in response to human chorionic gonadotropin (hCG).	Testosterone	0-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	104-107
17077584-3	2006	This hCG-induced necrosis was suppressed by an oral treatment (concomitant or delayed by 3 hr) with cyclooxygenase inhibitors (indomethacin, rofecoxib) or prostaglandin (PG) receptor blocker (AA-2414).	Indomethacin	127-139	hypertrichosis 2 (generalised, congenital)	Homo sapiens	5-8
17077584-3	2006	This hCG-induced necrosis was suppressed by an oral treatment (concomitant or delayed by 3 hr) with cyclooxygenase inhibitors (indomethacin, rofecoxib) or prostaglandin (PG) receptor blocker (AA-2414).	rofecoxib	141-150	hypertrichosis 2 (generalised, congenital)	Homo sapiens	5-8
17077584-3	2006	This hCG-induced necrosis was suppressed by an oral treatment (concomitant or delayed by 3 hr) with cyclooxygenase inhibitors (indomethacin, rofecoxib) or prostaglandin (PG) receptor blocker (AA-2414).	Prostaglandins	155-168	hypertrichosis 2 (generalised, congenital)	Homo sapiens	5-8
17077584-3	2006	This hCG-induced necrosis was suppressed by an oral treatment (concomitant or delayed by 3 hr) with cyclooxygenase inhibitors (indomethacin, rofecoxib) or prostaglandin (PG) receptor blocker (AA-2414).	seratrodast	192-199	hypertrichosis 2 (generalised, congenital)	Homo sapiens	5-8
17077584-9	2006	From these results, the mechanism of the hCG-induced necrosis was concluded to be: 1) hCG stimulates Leydig cells to synthesize PGs de novo; 2) PGs induce the intratesticular arteries to contract in the FLPT; and 3) obstruction of blood flow (ischemia) for more than 12 hr induced focal necrosis in the testis.	Phosphatidylglycerols	128-131	hypertrichosis 2 (generalised, congenital)	Homo sapiens	41-44
17077584-9	2006	From these results, the mechanism of the hCG-induced necrosis was concluded to be: 1) hCG stimulates Leydig cells to synthesize PGs de novo; 2) PGs induce the intratesticular arteries to contract in the FLPT; and 3) obstruction of blood flow (ischemia) for more than 12 hr induced focal necrosis in the testis.	Phosphatidylglycerols	128-131	hypertrichosis 2 (generalised, congenital)	Homo sapiens	86-89
16900525-5	2006	CR was defined as an institutional normal serum hCG level sustained for &gt;or=4 consecutive weeks; treatment failure was a &lt;10% fall (3 assays over 4 weeks) or &gt;20% rise (over previous value) in hCG serum level.	Chromium	0-2	hypertrichosis 2 (generalised, congenital)	Homo sapiens	48-51
16930210-15	2006	model, the T response to hCG was blunted for 12 hours following alcohol injection, but showed a rebound at 48 hours.	Alcohols	64-71	hypertrichosis 2 (generalised, congenital)	Homo sapiens	25-28
16768150-12	2006	It is suggested that process of hCG secretion could undergo different endocrine regulations between the artificial sex steroid replacement cycles and spontaneous cycles with corpus luteum function.	Steroids	119-126	hypertrichosis 2 (generalised, congenital)	Homo sapiens	32-35
16552601-1	2006	The present study employs an in vitro system to analyse the role of steroid hormones in hCG-induced spermiation in two species of anuran amphibian: Rana catesbeiana and Leptodactylus ocellatus.	Steroids	68-84	hypertrichosis 2 (generalised, congenital)	Homo sapiens	88-91
16552601-5	2006	Moreover, when combined inhibitors, aminoglutethimide (10(-5)M) plus cyanoketone (10(-5)M), were employed, spermiation evoked by hCG was not modified while hCG-induced androgen secretion significantly decreased.	Aminoglutethimide	36-53	hypertrichosis 2 (generalised, congenital)	Homo sapiens	156-159
16768139-6	2006	After three cycles of combination chemotherapy consisting of ifosfamide, cisplatin, and etoposide, followed by whole brain irradiation with a total dose of 24 Gy, the CSF hCG level fell below the detection limit, but MR imaging demonstrated no significant change.	Ifosfamide	61-71	hypertrichosis 2 (generalised, congenital)	Homo sapiens	171-174
16768139-6	2006	After three cycles of combination chemotherapy consisting of ifosfamide, cisplatin, and etoposide, followed by whole brain irradiation with a total dose of 24 Gy, the CSF hCG level fell below the detection limit, but MR imaging demonstrated no significant change.	Cisplatin	73-82	hypertrichosis 2 (generalised, congenital)	Homo sapiens	171-174
16768139-6	2006	After three cycles of combination chemotherapy consisting of ifosfamide, cisplatin, and etoposide, followed by whole brain irradiation with a total dose of 24 Gy, the CSF hCG level fell below the detection limit, but MR imaging demonstrated no significant change.	Etoposide	88-97	hypertrichosis 2 (generalised, congenital)	Homo sapiens	171-174
17008270-2	2006	Coasting is the practice whereby the gonadotrophins are withheld and the administration of human chorionic gonadotrophin (hCG) is delayed until serum oestradiol (E2) has decreased to what is considered to be a safe level, to prevent the onset of OHSS.	Estradiol	150-160	hypertrichosis 2 (generalised, congenital)	Homo sapiens	122-125
16682403-7	2006	Thus, pronounced hormonal differences exist in follicular fluid, and the collective concentration of all three gonadotropins and the follicular fluid concentration of progesterone were much higher in the group of women receiving hCG for ovulation induction.	Progesterone	167-179	hypertrichosis 2 (generalised, congenital)	Homo sapiens	229-232
22061563-0	2006	Effect of hCG administration on the relationship between testicular steroids and indolic compounds in fat and plasma in entire male pigs.	Steroids	68-76	hypertrichosis 2 (generalised, congenital)	Homo sapiens	10-13
16580403-1	2006	Using saline solution including exuded extract from uterine curettings, hCG tests were performed in 63 women in whom there was a suspicion of ectopic pregnancy, and their results correlated highly with the microscopic existence of chorionic villi and trophoblasts.	Sodium Chloride	6-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	72-75
16352691-10	2006	Pubertal maturation stopped at an average bone age of 13.9 yr. hCG therapy increased testosterone (11 +/- 2 nmol/liter) and reduced FSH (at 16 yr, 1.1 +/- 0.9 U/liter) levels.	Testosterone	85-97	hypertrichosis 2 (generalised, congenital)	Homo sapiens	63-66
16352691-13	2006	hCG therapy stimulates testosterone production and virilization.	Testosterone	23-35	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
16377065-11	2006	We found high normal sex steroid levels in both hCG groups.	Steroids	25-32	hypertrichosis 2 (generalised, congenital)	Homo sapiens	48-51
16569475-9	2006	Caudal membrane extracts could bind human chorionic gonadotropin (hCG), which resulted in the production of cAMP.	Cyclic AMP	108-112	hypertrichosis 2 (generalised, congenital)	Homo sapiens	66-69
22061563-1	2006	Our objective was to evaluate pigs injected with human chorionic gonadotropin (hCG) as a potential model to study the effect of high testicular steroid levels on the variation in indolic compounds.	Steroids	144-151	hypertrichosis 2 (generalised, congenital)	Homo sapiens	79-82
22061563-4	2006	HCG injection increased the levels of testicular steroids (androstenone, testosterone, dehydroepiandrosterone sulphate, oestrone sulphate and oestrone; p&lt;0.001), and indole levels in plasma and fat (p&lt;0.05).	Steroids	49-57	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
22061563-4	2006	HCG injection increased the levels of testicular steroids (androstenone, testosterone, dehydroepiandrosterone sulphate, oestrone sulphate and oestrone; p&lt;0.001), and indole levels in plasma and fat (p&lt;0.05).	androst-16-en-3-one	59-71	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
22061563-4	2006	HCG injection increased the levels of testicular steroids (androstenone, testosterone, dehydroepiandrosterone sulphate, oestrone sulphate and oestrone; p&lt;0.001), and indole levels in plasma and fat (p&lt;0.05).	Testosterone	73-85	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
22061563-4	2006	HCG injection increased the levels of testicular steroids (androstenone, testosterone, dehydroepiandrosterone sulphate, oestrone sulphate and oestrone; p&lt;0.001), and indole levels in plasma and fat (p&lt;0.05).	Dehydroepiandrosterone Sulfate	87-118	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
22061563-4	2006	HCG injection increased the levels of testicular steroids (androstenone, testosterone, dehydroepiandrosterone sulphate, oestrone sulphate and oestrone; p&lt;0.001), and indole levels in plasma and fat (p&lt;0.05).	estrone sulfate	120-137	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
22061563-4	2006	HCG injection increased the levels of testicular steroids (androstenone, testosterone, dehydroepiandrosterone sulphate, oestrone sulphate and oestrone; p&lt;0.001), and indole levels in plasma and fat (p&lt;0.05).	Estrone	120-128	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
22061563-4	2006	HCG injection increased the levels of testicular steroids (androstenone, testosterone, dehydroepiandrosterone sulphate, oestrone sulphate and oestrone; p&lt;0.001), and indole levels in plasma and fat (p&lt;0.05).	indole	169-175	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
22061563-6	2006	The correlation coefficients between androstenone and skatole levels in fat were 0.54 in the hCG-injected group and non-significant in the control group.	androst-16-en-3-one	37-49	hypertrichosis 2 (generalised, congenital)	Homo sapiens	93-96
22061563-6	2006	The correlation coefficients between androstenone and skatole levels in fat were 0.54 in the hCG-injected group and non-significant in the control group.	Skatole	54-61	hypertrichosis 2 (generalised, congenital)	Homo sapiens	93-96
22061563-9	2006	We concluded that hCG-injected pigs might be useful for studying factors responsible for the role of testicular steroids in the occurrence of high indole levels.	Steroids	112-120	hypertrichosis 2 (generalised, congenital)	Homo sapiens	18-21
22061563-9	2006	We concluded that hCG-injected pigs might be useful for studying factors responsible for the role of testicular steroids in the occurrence of high indole levels.	indole	147-153	hypertrichosis 2 (generalised, congenital)	Homo sapiens	18-21
22061563-10	2006	Pre-selection of sires based on plasma skatole levels affected both the levels of indolic compounds and testicular steroids, especially in fat, which might have suppressed the response to hCG.	Steroids	115-123	hypertrichosis 2 (generalised, congenital)	Homo sapiens	188-191
16451718-6	2006	High doses of LHRHa (60 mic.g) with hCG, progesterone, and Pimozide gave the greatest number of toads spawning, however, they resulted in low oocyte numbers, fertilization and neurulation rates.	lhrha	14-19	hypertrichosis 2 (generalised, congenital)	Homo sapiens	36-39
16451718-7	2006	A low dose of LHRHa (4 mic.g) with hCG, or hCG alone as a second administration, and progesterone with Pimozide produced few good quality oocytes.	lhrha	14-19	hypertrichosis 2 (generalised, congenital)	Homo sapiens	35-38
16266371-7	2005	The heat denaturated bacterial extract as well as its low-molecular-weight fraction (&lt;10 kDa) stimulated both the basal and the hCG-stimulated progesterone production; the oestradiol production was slightly inhibited.	Progesterone	146-158	hypertrichosis 2 (generalised, congenital)	Homo sapiens	131-134
16382113-4	2006	A normal serum hCG regression corridor was constructed for 79 patients with low-risk PTD who were cured by single-agent methotrexate (MTX) chemotherapy (control group).	Methotrexate	120-132	hypertrichosis 2 (generalised, congenital)	Homo sapiens	15-18
16382113-4	2006	A normal serum hCG regression corridor was constructed for 79 patients with low-risk PTD who were cured by single-agent methotrexate (MTX) chemotherapy (control group).	Methotrexate	134-137	hypertrichosis 2 (generalised, congenital)	Homo sapiens	15-18
16382113-8	2006	CONCLUSION: In the largest study to date, we describe the regression of serum hCG levels in patients with low-risk PTD successfully treated with MTX.	Methotrexate	145-148	hypertrichosis 2 (generalised, congenital)	Homo sapiens	78-81
16382113-9	2006	At high specificity, hCG levels in the first few courses of MTX can identify half the number of patients who are extremely likely to need alternative chemotherapy to cure their disease and for whom further treatment with single-agent chemotherapy will be ineffective.	Methotrexate	60-63	hypertrichosis 2 (generalised, congenital)	Homo sapiens	21-24
16519621-7	2006	Following systemic MTX therapy, the hCG values normalised within 8 weeks in the singleton pregnancies and in 10 weeks in the twin pregnancy.	Methotrexate	19-22	hypertrichosis 2 (generalised, congenital)	Homo sapiens	36-39
16266371-7	2005	The heat denaturated bacterial extract as well as its low-molecular-weight fraction (&lt;10 kDa) stimulated both the basal and the hCG-stimulated progesterone production; the oestradiol production was slightly inhibited.	Estradiol	175-185	hypertrichosis 2 (generalised, congenital)	Homo sapiens	131-134
16226369-0	2005	Effect of IPs, cAMP, and cGMP on the hPL and hCG secretion from human term placenta.	Cyclic GMP	25-29	hypertrichosis 2 (generalised, congenital)	Homo sapiens	45-48
16257605-5	2005	of 0.05-1.10 ng/ml), injection of hCG resulted in an increase (P &lt; 0.01) of plasma testosterone with peak concentrations at approximately 120 min (4.17, 95% C.I.	Testosterone	86-98	hypertrichosis 2 (generalised, congenital)	Homo sapiens	34-37
16085667-7	2005	Exposure to amitraz 50 microg/ml for 6 h exposure abolished hCG-stimulated progesterone production but not estrogen production.	amitraz	12-19	hypertrichosis 2 (generalised, congenital)	Homo sapiens	60-63
16085667-7	2005	Exposure to amitraz 50 microg/ml for 6 h exposure abolished hCG-stimulated progesterone production but not estrogen production.	Progesterone	75-87	hypertrichosis 2 (generalised, congenital)	Homo sapiens	60-63
16085667-8	2005	CONCLUSIONS: Amitraz inhibited basal and hCG-stimulated progesterone but not estrogen production.	Progesterone	56-68	hypertrichosis 2 (generalised, congenital)	Homo sapiens	41-44
16226369-4	2005	Addition of NaF, forskolin or sodium nitroprusside, activators of the inositol phosphates (IPs), cAMP and cGMP pathways, significantly increased their respective messengers in villous explants but failed to affect the hPL and hCG releases from syncytiotrophoblast.	Colforsin	17-26	hypertrichosis 2 (generalised, congenital)	Homo sapiens	226-229
15961562-7	2005	The effects of hCG were mimicked by forskolin, indicating that they are cAMP dependent.	Colforsin	36-45	hypertrichosis 2 (generalised, congenital)	Homo sapiens	15-18
16226369-4	2005	Addition of NaF, forskolin or sodium nitroprusside, activators of the inositol phosphates (IPs), cAMP and cGMP pathways, significantly increased their respective messengers in villous explants but failed to affect the hPL and hCG releases from syncytiotrophoblast.	Nitroprusside	30-50	hypertrichosis 2 (generalised, congenital)	Homo sapiens	226-229
16230783-10	2005	The selective uptake of HDL-cholesterol was also enhanced by hCG but exposure to Ad A-CREB also abrogated this effect.	Cholesterol	28-39	hypertrichosis 2 (generalised, congenital)	Homo sapiens	61-64
16093648-2	2005	At 3.5 and 4.5 days after hCG injection scanning electron micrographs revealed that the hyperstimulated and progesterone-injected group had well-developed pinopodes while most of the hyperstimulated group without progesterone injection had no pinopodes 3.5 days after stimulation.	Progesterone	108-120	hypertrichosis 2 (generalised, congenital)	Homo sapiens	26-29
16335912-3	2005	In the present study we tested the effects of the phytoestrogens genistein and daidzein on the production of human chorionic gondaotropin (hCG) in isolated trophoblast cells of term placentas in vitro.	Genistein	65-74	hypertrichosis 2 (generalised, congenital)	Homo sapiens	139-142
16335912-3	2005	In the present study we tested the effects of the phytoestrogens genistein and daidzein on the production of human chorionic gondaotropin (hCG) in isolated trophoblast cells of term placentas in vitro.	daidzein	79-87	hypertrichosis 2 (generalised, congenital)	Homo sapiens	139-142
16335912-9	2005	Compared with daidzein, genistein seems to be a more efficient inhibitor of the production of hCG.	daidzein	14-22	hypertrichosis 2 (generalised, congenital)	Homo sapiens	94-97
16335912-9	2005	Compared with daidzein, genistein seems to be a more efficient inhibitor of the production of hCG.	Genistein	24-33	hypertrichosis 2 (generalised, congenital)	Homo sapiens	94-97
16230783-0	2005	LH/hCG-stimulated androgen production and selective HDL-cholesterol transport are inhibited by a dominant-negative CREB construct in primary cultures of rat theca-interstitial cells.	Luteinizing Hormone	0-2	hypertrichosis 2 (generalised, congenital)	Homo sapiens	3-6
16230783-0	2005	LH/hCG-stimulated androgen production and selective HDL-cholesterol transport are inhibited by a dominant-negative CREB construct in primary cultures of rat theca-interstitial cells.	Cholesterol	56-67	hypertrichosis 2 (generalised, congenital)	Homo sapiens	3-6
16230783-4	2005	This process is mediated by an HDL receptor, scavenger receptor class B, type I (SR-BI) and is stimulated by trophic hormone (LH/hCG), which also activates the cAMP cascade.	Cyclic AMP	160-164	hypertrichosis 2 (generalised, congenital)	Homo sapiens	129-132
16230783-5	2005	In this study, we tested whether the adenoviral (Ad)-mediated introduction of a dominant-negative analog of cyclic AMP response element binding protein (A-CREB) inhibits the stimulatory effect of LH/hCG on the selective uptake of high-density lipoprotein (HDL)-cholesterol and androgen production in primary cultures of rat T-I cells.	Cyclic AMP	108-118	hypertrichosis 2 (generalised, congenital)	Homo sapiens	199-202
16230783-6	2005	Androstenedione production by cultured T-I cells was stimulated by hCG and by the adenoviral overexpression of wtCREB.	Androstenedione	0-15	hypertrichosis 2 (generalised, congenital)	Homo sapiens	67-70
15961562-7	2005	The effects of hCG were mimicked by forskolin, indicating that they are cAMP dependent.	Cyclic AMP	72-76	hypertrichosis 2 (generalised, congenital)	Homo sapiens	15-18
15961562-10	2005	These findings indicate that, in JAR cells, hCG activates a cAMP-dependent pathway that can up-regulate WT1 expression through PAX8.	Cyclic AMP	60-64	hypertrichosis 2 (generalised, congenital)	Homo sapiens	44-47
15767042-5	2005	Administration of hCG induced a decline in PPARgamma mRNA, protein, and DNA-binding activity beginning at 4 h. Treatment of preovulatory granulosa cells with the PPARgamma ligand troglitazone (1-10 microM) in vitro decreased cell viability, increased sub-G1 apoptosis, and reduced DNA synthesis.	Troglitazone	179-191	hypertrichosis 2 (generalised, congenital)	Homo sapiens	18-21
15925048-7	2005	Duration of treatment, number of hMG ampoules administered, number of oocytes retrieved, estradiol concentration, and estradiol/progesterone ratio on the day of hCG differed significantly between pregnant and nonpregnant patients.	Progesterone	128-140	hypertrichosis 2 (generalised, congenital)	Homo sapiens	161-164
15821107-7	2005	In pituitary cells pretreated with actinomycin D, the half-life of GH mRNA was not affected by hCG but was enhanced by LH immunoneutralization.	Dactinomycin	35-48	hypertrichosis 2 (generalised, congenital)	Homo sapiens	95-98
15821107-9	2005	hCG increased cAMP synthesis in carp pituitary cells and hCG-induced GH mRNA expression was mimicked by forskolin but suppressed by inhibiting adenylate cyclase and protein kinase A.	Cyclic AMP	14-18	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
15821107-9	2005	hCG increased cAMP synthesis in carp pituitary cells and hCG-induced GH mRNA expression was mimicked by forskolin but suppressed by inhibiting adenylate cyclase and protein kinase A.	Colforsin	104-113	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
15821107-9	2005	hCG increased cAMP synthesis in carp pituitary cells and hCG-induced GH mRNA expression was mimicked by forskolin but suppressed by inhibiting adenylate cyclase and protein kinase A.	Colforsin	104-113	hypertrichosis 2 (generalised, congenital)	Homo sapiens	57-60
15749784-6	2005	Although HCG did not influence the abundance of IGF-II/M6PR mRNA or protein, anti-IGF-II/M6PR antibody decreased HCG-induced migration of EVT, supporting the hypothesis that HCG might stimulate EVT migration by increasing IGF-II binding to the plasma membrane and subsequently by increasing the IGF-II effect probably mediated via the IGF-II/M6PR.	EVT	138-141	hypertrichosis 2 (generalised, congenital)	Homo sapiens	113-116
15749784-6	2005	Although HCG did not influence the abundance of IGF-II/M6PR mRNA or protein, anti-IGF-II/M6PR antibody decreased HCG-induced migration of EVT, supporting the hypothesis that HCG might stimulate EVT migration by increasing IGF-II binding to the plasma membrane and subsequently by increasing the IGF-II effect probably mediated via the IGF-II/M6PR.	EVT	138-141	hypertrichosis 2 (generalised, congenital)	Homo sapiens	113-116
15749784-4	2005	HCG treatment (50-50,000 mU/ml) of the HTR-8/SVneo cells did not alter the expression of either insulin-like growth factor-I or IGF-II mRNA or peptide synthesis, but caused (i) an increase in the (125)I-IGF-II binding to EVT cells, and (ii) an increase in the externalization rate of the IGF-II binding sites without affecting their internalization.	EVT	221-224	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
15749784-6	2005	Although HCG did not influence the abundance of IGF-II/M6PR mRNA or protein, anti-IGF-II/M6PR antibody decreased HCG-induced migration of EVT, supporting the hypothesis that HCG might stimulate EVT migration by increasing IGF-II binding to the plasma membrane and subsequently by increasing the IGF-II effect probably mediated via the IGF-II/M6PR.	EVT	194-197	hypertrichosis 2 (generalised, congenital)	Homo sapiens	113-116
15749784-6	2005	Although HCG did not influence the abundance of IGF-II/M6PR mRNA or protein, anti-IGF-II/M6PR antibody decreased HCG-induced migration of EVT, supporting the hypothesis that HCG might stimulate EVT migration by increasing IGF-II binding to the plasma membrane and subsequently by increasing the IGF-II effect probably mediated via the IGF-II/M6PR.	EVT	194-197	hypertrichosis 2 (generalised, congenital)	Homo sapiens	113-116
15852231-0	2005	[Stimulation of HCG, estrogen and progesterone production in isolated trophoblast cells by glycodelin A or its N-glycans].	n-glycans	111-120	hypertrichosis 2 (generalised, congenital)	Homo sapiens	16-19
15852231-3	2005	The purpose of this study was to investigate the effect of glycodelin A and its N-glycans on hCG, estrogen and progesterone release by cytotrophoblasts in vitro.	n-glycans	80-89	hypertrichosis 2 (generalised, congenital)	Homo sapiens	93-96
15852231-8	2005	The production of hCG, estrogen and progesterone was increased in GdA and glycan-treated cell cultures as compared to untreated trophoblast cell cultures.	Polysaccharides	74-80	hypertrichosis 2 (generalised, congenital)	Homo sapiens	18-21
15683372-7	2005	In contrast, E2, P4, and hCG concentrations continued to increase following mifepristone, followed by rapid declines from day 2 to day 3.	Mifepristone	76-88	hypertrichosis 2 (generalised, congenital)	Homo sapiens	25-28
15331571-7	2004	Levels of pregnenolone and progesterone increased 2- and 4-fold, respectively, within 6 h of hCG treatment, whereas PFT completely blocked this hCG-induced effect.	Pregnenolone	10-22	hypertrichosis 2 (generalised, congenital)	Homo sapiens	93-96
15836959-11	2005	In summary, findings on the knockout model reaffirm that LH and hCG control uterine functions directly as well as indirectly through increasing ovarian synthesis of steroid hormones and both actions are required for normal uterine biology.	Steroids	165-181	hypertrichosis 2 (generalised, congenital)	Homo sapiens	64-67
14551795-4	2004	There were negative correlations between the Th1:Th2 ratio and serum hCG levels (mIU/ml) (Th1:Th2 ratio = 14.5-4.52 x 10(-5)xhCG, r(2)=0.41, p&lt;0.05) and between the Th1:Th2 ratio and serum progesterone levels (ng/dl; Th1:Th2 ratio = 23.0-0.63 x progesterone, r(2)=0.36, p&lt;0.05).	th2	49-52	hypertrichosis 2 (generalised, congenital)	Homo sapiens	69-72
14551795-4	2004	There were negative correlations between the Th1:Th2 ratio and serum hCG levels (mIU/ml) (Th1:Th2 ratio = 14.5-4.52 x 10(-5)xhCG, r(2)=0.41, p&lt;0.05) and between the Th1:Th2 ratio and serum progesterone levels (ng/dl; Th1:Th2 ratio = 23.0-0.63 x progesterone, r(2)=0.36, p&lt;0.05).	xhcg	124-128	hypertrichosis 2 (generalised, congenital)	Homo sapiens	69-72
14551795-4	2004	There were negative correlations between the Th1:Th2 ratio and serum hCG levels (mIU/ml) (Th1:Th2 ratio = 14.5-4.52 x 10(-5)xhCG, r(2)=0.41, p&lt;0.05) and between the Th1:Th2 ratio and serum progesterone levels (ng/dl; Th1:Th2 ratio = 23.0-0.63 x progesterone, r(2)=0.36, p&lt;0.05).	th2	94-97	hypertrichosis 2 (generalised, congenital)	Homo sapiens	69-72
14551795-4	2004	There were negative correlations between the Th1:Th2 ratio and serum hCG levels (mIU/ml) (Th1:Th2 ratio = 14.5-4.52 x 10(-5)xhCG, r(2)=0.41, p&lt;0.05) and between the Th1:Th2 ratio and serum progesterone levels (ng/dl; Th1:Th2 ratio = 23.0-0.63 x progesterone, r(2)=0.36, p&lt;0.05).	Progesterone	192-204	hypertrichosis 2 (generalised, congenital)	Homo sapiens	69-72
14551795-4	2004	There were negative correlations between the Th1:Th2 ratio and serum hCG levels (mIU/ml) (Th1:Th2 ratio = 14.5-4.52 x 10(-5)xhCG, r(2)=0.41, p&lt;0.05) and between the Th1:Th2 ratio and serum progesterone levels (ng/dl; Th1:Th2 ratio = 23.0-0.63 x progesterone, r(2)=0.36, p&lt;0.05).	th2	94-97	hypertrichosis 2 (generalised, congenital)	Homo sapiens	69-72
14551795-4	2004	There were negative correlations between the Th1:Th2 ratio and serum hCG levels (mIU/ml) (Th1:Th2 ratio = 14.5-4.52 x 10(-5)xhCG, r(2)=0.41, p&lt;0.05) and between the Th1:Th2 ratio and serum progesterone levels (ng/dl; Th1:Th2 ratio = 23.0-0.63 x progesterone, r(2)=0.36, p&lt;0.05).	Progesterone	248-260	hypertrichosis 2 (generalised, congenital)	Homo sapiens	69-72
15317690-5	2004	The most likely cause for the poor graft development of marmosets is a deletion of exon 10 in the luteinizing hormone-receptor (LHR) gene, which renders this species insensitive to LH but responsive to chorionic gonadotropin (CG).	Luteinizing Hormone	128-130	hypertrichosis 2 (generalised, congenital)	Homo sapiens	226-228
15331571-8	2004	Estradiol was increased transiently (&gt;10-fold) by hCG plus PFT relative to levels after hCG alone.	Estradiol	0-9	hypertrichosis 2 (generalised, congenital)	Homo sapiens	53-56
15298980-0	2004	Independent regulation of prostaglandins and monocyte chemoattractant protein-1 by interleukin-1beta and hCG in human endometrial cells.	Prostaglandins	26-40	hypertrichosis 2 (generalised, congenital)	Homo sapiens	105-108
15570553-0	2004	[Investigations on regulation of HCG by cortisol (prednisolon) in trophoblast cells in vitro].	Hydrocortisone	40-48	hypertrichosis 2 (generalised, congenital)	Homo sapiens	33-36
15570553-0	2004	[Investigations on regulation of HCG by cortisol (prednisolon) in trophoblast cells in vitro].	Prednisolone	50-61	hypertrichosis 2 (generalised, congenital)	Homo sapiens	33-36
15570553-4	2004	In this study we describe the influence of cortisol (prednisolon) on hCG production of trophoblast cells in vitro.	Hydrocortisone	43-51	hypertrichosis 2 (generalised, congenital)	Homo sapiens	69-72
15570553-4	2004	In this study we describe the influence of cortisol (prednisolon) on hCG production of trophoblast cells in vitro.	Prednisolone	53-64	hypertrichosis 2 (generalised, congenital)	Homo sapiens	69-72
15570553-10	2004	RESULTS: The addition of prednisolon (50 microg/ml) stimulates the concentration of hCG in a time-depending manner.	Prednisolone	25-36	hypertrichosis 2 (generalised, congenital)	Homo sapiens	84-87
15570553-11	2004	CONCLUSIONS: The trophoblast cell shows an increase in the concentration of hCG after stimulation with cortisol.	Hydrocortisone	103-111	hypertrichosis 2 (generalised, congenital)	Homo sapiens	76-79
15570553-12	2004	For the first time an influence of cortisol (prednisolon) on hCG production could be demonstrated in cultured trophoblast cells.	Hydrocortisone	35-43	hypertrichosis 2 (generalised, congenital)	Homo sapiens	61-64
15570553-12	2004	For the first time an influence of cortisol (prednisolon) on hCG production could be demonstrated in cultured trophoblast cells.	Prednisolone	45-56	hypertrichosis 2 (generalised, congenital)	Homo sapiens	61-64
15298980-10	2004	hCG inhibits IL-1beta-induced PG level.	Prostaglandins	30-32	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
15471938-0	2004	Association of estradiol levels on the day of hCG administration and pregnancy achievement in IVF: a systematic review.	Estradiol	15-24	hypertrichosis 2 (generalised, congenital)	Homo sapiens	46-49
15471938-7	2004	Two studies (including 191 patients) suggested that the higher the E2 levels on the day of hCG administration, the higher the probability of pregnancy.	Estradiol	67-69	hypertrichosis 2 (generalised, congenital)	Homo sapiens	91-94
15586646-2	2004	The goal of this study was to elucidate whether hCG administration at 24 or 36 hours after clomiphene citrate stimulation impacts pregnancy rates.	Clomiphene	91-109	hypertrichosis 2 (generalised, congenital)	Homo sapiens	48-51
15641263-0	2004	Plasma testosterone response at 1st and 4th day after short- and long-term hCG stimulation test.	Testosterone	7-19	hypertrichosis 2 (generalised, congenital)	Homo sapiens	75-78
15641263-11	2004	According to our results, while performing hCG test in a patient, if a short-term protocol is planned, it is more convenient to check the 4th day testosterone response.	Testosterone	146-158	hypertrichosis 2 (generalised, congenital)	Homo sapiens	43-46
15224149-0	2004	[Effect of c-myb on hCG-induced testosterone secretion in isolated rat Leydig cells].	Testosterone	32-44	hypertrichosis 2 (generalised, congenital)	Homo sapiens	20-23
15307133-6	2004	Explants under TNFalpha and 17% O2 revealed progressive degeneration of syncytiotrophoblast (ST) followed by restoration of hCG, localized to newly differentiated cytotrophoblasts.	Oxygen	32-34	hypertrichosis 2 (generalised, congenital)	Homo sapiens	124-127
15292303-8	2004	Despite the higher androgen secretion capacity in PCOS, the basal and hCG-stimulated serum estradiol levels were similar to those observed in normal women.	Estradiol	91-100	hypertrichosis 2 (generalised, congenital)	Homo sapiens	70-73
15224149-1	2004	The present study was carried out to investigate the effect of antisense c-myb oligodeoxynucleotides (ODN) on hCG-induced testosterone secretion in isolated rat Leydig cells.	Testosterone	122-134	hypertrichosis 2 (generalised, congenital)	Homo sapiens	110-113
15224149-3	2004	The results showed that antisense c-myb ODN inhibited hCG-induced testosterone secretion of isolated rat Leydig cells in a dose-dependent manner.	Testosterone	66-78	hypertrichosis 2 (generalised, congenital)	Homo sapiens	54-57
15224149-6	2004	Further experiments showed that dbcAMP (100 micromol/L) obviously increased hCG-induced testosterone secretion and integral optical density (IOD) immunostaining of Myb in Leydig cells.	Bucladesine	32-38	hypertrichosis 2 (generalised, congenital)	Homo sapiens	76-79
15224149-6	2004	Further experiments showed that dbcAMP (100 micromol/L) obviously increased hCG-induced testosterone secretion and integral optical density (IOD) immunostaining of Myb in Leydig cells.	Testosterone	88-100	hypertrichosis 2 (generalised, congenital)	Homo sapiens	76-79
15224149-7	2004	Verapamil (10 micromol/L), a Ca(2+) channel blocker, and cycloheximide (50 microg/ml), a protein synthesis inhibitor, reduced the immunostaining of c-Myb, and also lowered hCG-induced testosterone secretion in isolated rat Leydig cells.	Verapamil	0-9	hypertrichosis 2 (generalised, congenital)	Homo sapiens	172-175
15224149-7	2004	Verapamil (10 micromol/L), a Ca(2+) channel blocker, and cycloheximide (50 microg/ml), a protein synthesis inhibitor, reduced the immunostaining of c-Myb, and also lowered hCG-induced testosterone secretion in isolated rat Leydig cells.	Cycloheximide	57-70	hypertrichosis 2 (generalised, congenital)	Homo sapiens	172-175
15224149-8	2004	The results indicate that c-myb closely correlates with hCG-induced testosterone secretion, and that cAMP and Ca(2+)-dependent pathway participates in the expression of protooncogene.	Testosterone	68-80	hypertrichosis 2 (generalised, congenital)	Homo sapiens	56-59
15084906-2	2004	We had reported preliminary evidence that alcohol might stimulate a pituitary-independent, neural pathway between the hypothalamus and the testes whose activation blunts T secretion in response to human chorionic gonadotropin (hCG).	Alcohols	42-49	hypertrichosis 2 (generalised, congenital)	Homo sapiens	227-230
15283048-4	2004	Another 61 Reference Service cases hadfalse positive hCG, and we observed 7 cases with low levels of hCG of pituitary origin (hCG subsequently suppressed by estrogen-progesterone medication).	Progesterone	166-178	hypertrichosis 2 (generalised, congenital)	Homo sapiens	101-104
15283048-4	2004	Another 61 Reference Service cases hadfalse positive hCG, and we observed 7 cases with low levels of hCG of pituitary origin (hCG subsequently suppressed by estrogen-progesterone medication).	Progesterone	166-178	hypertrichosis 2 (generalised, congenital)	Homo sapiens	101-104
15212672-0	2004	Efficacy of a recombinant chimeric anti-hCG antibody to prevent human cytotrophoblasts fusion and block progesterone synthesis.	Progesterone	104-116	hypertrichosis 2 (generalised, congenital)	Homo sapiens	40-43
15212672-7	2004	RESULTS: Recombinant chimeric anti-hCG antibody blocked the synthesis of progesterone by trophoblasts.	Progesterone	73-85	hypertrichosis 2 (generalised, congenital)	Homo sapiens	35-38
15212672-10	2004	CONCLUSION: Recombinant chimeric anti-hCG antibody (cPIPP) was effective to neutralize hCG induced bioactivities in the human derived trophoblast cells.	cpipp	52-57	hypertrichosis 2 (generalised, congenital)	Homo sapiens	38-41
15212672-10	2004	CONCLUSION: Recombinant chimeric anti-hCG antibody (cPIPP) was effective to neutralize hCG induced bioactivities in the human derived trophoblast cells.	cpipp	52-57	hypertrichosis 2 (generalised, congenital)	Homo sapiens	87-90
15126522-7	2004	The total number of follicles at least 11 mm at stimulation d 8 and at the day of hCG administration tended to increase with dose of FSH-CTP, although a significant dose-response relationship was revealed only for the number of follicles at least 15 mm on the day of hCG (P = 0.03).	Cytidine Triphosphate	137-140	hypertrichosis 2 (generalised, congenital)	Homo sapiens	82-85
15126522-7	2004	The total number of follicles at least 11 mm at stimulation d 8 and at the day of hCG administration tended to increase with dose of FSH-CTP, although a significant dose-response relationship was revealed only for the number of follicles at least 15 mm on the day of hCG (P = 0.03).	Cytidine Triphosphate	137-140	hypertrichosis 2 (generalised, congenital)	Homo sapiens	267-270
15190825-0	2004	[Effects of c-jun on hCG-induced testosterone secretion of rat Leydig cells in vitro].	Testosterone	33-45	hypertrichosis 2 (generalised, congenital)	Homo sapiens	21-24
15190825-1	2004	OBJECTIVE: To investigate the effects of c-jun on hCG-induced testosterone secretion in isolated rat Leydig cells by antisense oligodeoxynucleotides(ASODNs).	Testosterone	62-74	hypertrichosis 2 (generalised, congenital)	Homo sapiens	50-53
15190825-1	2004	OBJECTIVE: To investigate the effects of c-jun on hCG-induced testosterone secretion in isolated rat Leydig cells by antisense oligodeoxynucleotides(ASODNs).	Oligodeoxyribonucleotides	127-148	hypertrichosis 2 (generalised, congenital)	Homo sapiens	50-53
15190825-1	2004	OBJECTIVE: To investigate the effects of c-jun on hCG-induced testosterone secretion in isolated rat Leydig cells by antisense oligodeoxynucleotides(ASODNs).	Oligonucleotides, Antisense	149-155	hypertrichosis 2 (generalised, congenital)	Homo sapiens	50-53
15190825-2	2004	METHODS: c-jun ASODNs were used to antagonise the effects of c-jun, hCG was used to induce the testosterone secretion of LC cultured in vitro and testosterone was measured by radioimmunoassay.	Testosterone	95-107	hypertrichosis 2 (generalised, congenital)	Homo sapiens	68-71
15190825-4	2004	c-jun ASODNs decreased the hCG-induced testosterone secretion of LC in a dose-dependent manner(P &lt; 0.05).	Testosterone	39-51	hypertrichosis 2 (generalised, congenital)	Homo sapiens	27-30
15036995-8	2004	Thus, oral melatonin effectively inhibited endogenous ovarian activity and had no adverse impact on embryo quality after AI in the domestic cat; however, this treatment was only marginally effective in minimizing eCG/hCG-induced ovarian hyperstimulation.	Melatonin	11-20	hypertrichosis 2 (generalised, congenital)	Homo sapiens	217-220
15084906-5	2004	injection of alcohol on the T response to hCG, to probe the role of LH and corticotropin-releasing factor (CRF) in both models, and to examine potential changes in levels of the cholesterol transfer protein steroidogenic acute regulatory (StAR) protein.	Alcohols	13-20	hypertrichosis 2 (generalised, congenital)	Homo sapiens	42-45
15084906-13	2004	The ig injection of alcohol, which in contrast induced significant increases in blood alcohol levels, also significantly interfered with the ability of hCG to induce T release.	Alcohols	20-27	hypertrichosis 2 (generalised, congenital)	Homo sapiens	152-155
15117595-5	2004	RESULTS: The geometric mean of hCG levels was established as 17,361.31 mIU/mL in the mild preeclamptic group, 49,817.59 mIU/mL in the severe preeclamptic group, 41,101.09 mIU/mL in the superimposed preeclamptic group, 12,558.57 mIU/mL in the chronic hypertensive group, and 9647.98 mIU/mL in the normotensive group.	N-{(1S)-1-{[4-(3-AMINOPROPYL)PIPERAZIN-1-YL]CARBONYL}-4-[(DIAMINOMETHYLENE)AMINO]BUTYL}-3-(TRIFLUOROMETHYL)BENZENESULFONAMIDE	71-74	hypertrichosis 2 (generalised, congenital)	Homo sapiens	31-34
14766272-10	2004	Although the hCG level decreased for a short period, it soon increased despite treatment with methotrexate.	Methotrexate	94-106	hypertrichosis 2 (generalised, congenital)	Homo sapiens	13-16
15181477-5	2004	Stimulation of mLTC-1 mouse Leydig tumor cells with hCG resulted in the coordinate regulation of StAR mRNA expression and progesterone accumulation in a time-response manner.	Progesterone	122-134	hypertrichosis 2 (generalised, congenital)	Homo sapiens	52-55
14657523-5	2004	Lastly, we attempted to prevent BDCM-induced pregnancy loss using exogenous progesterone or human chorionic gonadotropin (hCG), an LH-agonist.	Luteinizing Hormone	131-133	hypertrichosis 2 (generalised, congenital)	Homo sapiens	122-125
14657523-5	2004	Lastly, we attempted to prevent BDCM-induced pregnancy loss using exogenous progesterone or human chorionic gonadotropin (hCG), an LH-agonist.	bromodichloromethane	32-36	hypertrichosis 2 (generalised, congenital)	Homo sapiens	122-125
14636638-9	2003	The up-regulation of follistatin expression by hCG could be mimicked by all the drugs that increase the intracellular cAMP level including 8-Br-cAMP, db-cAMP, forskolin, and 3-isobutyl-1-methylxanthine (IBMX).	Cyclic AMP	118-122	hypertrichosis 2 (generalised, congenital)	Homo sapiens	47-50
14636638-9	2003	The up-regulation of follistatin expression by hCG could be mimicked by all the drugs that increase the intracellular cAMP level including 8-Br-cAMP, db-cAMP, forskolin, and 3-isobutyl-1-methylxanthine (IBMX).	8-Bromo Cyclic Adenosine Monophosphate	139-148	hypertrichosis 2 (generalised, congenital)	Homo sapiens	47-50
14636638-9	2003	The up-regulation of follistatin expression by hCG could be mimicked by all the drugs that increase the intracellular cAMP level including 8-Br-cAMP, db-cAMP, forskolin, and 3-isobutyl-1-methylxanthine (IBMX).	Bucladesine	150-157	hypertrichosis 2 (generalised, congenital)	Homo sapiens	47-50
14636638-9	2003	The up-regulation of follistatin expression by hCG could be mimicked by all the drugs that increase the intracellular cAMP level including 8-Br-cAMP, db-cAMP, forskolin, and 3-isobutyl-1-methylxanthine (IBMX).	Colforsin	159-168	hypertrichosis 2 (generalised, congenital)	Homo sapiens	47-50
14636638-9	2003	The up-regulation of follistatin expression by hCG could be mimicked by all the drugs that increase the intracellular cAMP level including 8-Br-cAMP, db-cAMP, forskolin, and 3-isobutyl-1-methylxanthine (IBMX).	1-Methyl-3-isobutylxanthine	174-201	hypertrichosis 2 (generalised, congenital)	Homo sapiens	47-50
14636638-9	2003	The up-regulation of follistatin expression by hCG could be mimicked by all the drugs that increase the intracellular cAMP level including 8-Br-cAMP, db-cAMP, forskolin, and 3-isobutyl-1-methylxanthine (IBMX).	1-Methyl-3-isobutylxanthine	203-207	hypertrichosis 2 (generalised, congenital)	Homo sapiens	47-50
14636638-10	2003	The hCG (15IU/ml)- and forskolin (10microM)-induced follistatin expression could be blocked by H89 (10microM), a specific protein kinase A (PKA) inhibitor.	N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide	95-98	hypertrichosis 2 (generalised, congenital)	Homo sapiens	4-7
14657523-11	2004	Both progesterone and hCG prevented BDCM-induced pregnancy loss.	bromodichloromethane	36-40	hypertrichosis 2 (generalised, congenital)	Homo sapiens	22-25
15042852-13	2003	The mitotic index (3-7), proliferation markers (20%), inhibitin alpha, hCG and PLAP with histological picture suggest a specific form of MTT or choriocarcinoma.	monooxyethylene trimethylolpropane tristearate	137-140	hypertrichosis 2 (generalised, congenital)	Homo sapiens	71-74
14636881-1	2003	OBJECTIVES: Hyperglycosylated human chorionic gonadotrophin (hCG) is an hCG variant with extra-large O-linked oligosaccharides, produced by phenotypically invasive cytotrophoblast cells in choriocarcinoma and pregnancy.	o-linked oligosaccharides	101-126	hypertrichosis 2 (generalised, congenital)	Homo sapiens	61-64
14636881-1	2003	OBJECTIVES: Hyperglycosylated human chorionic gonadotrophin (hCG) is an hCG variant with extra-large O-linked oligosaccharides, produced by phenotypically invasive cytotrophoblast cells in choriocarcinoma and pregnancy.	o-linked oligosaccharides	101-126	hypertrichosis 2 (generalised, congenital)	Homo sapiens	72-75
15042852-26	2003	It represents a less differentiated form of MTT, becoming manifest in a low production of hCG.	monooxyethylene trimethylolpropane tristearate	44-47	hypertrichosis 2 (generalised, congenital)	Homo sapiens	90-93
12963106-6	2003	The results show a statistically significant difference for each treatment compared to controls, with the least difference (P&lt;0.05; OR=2.18) for the comparison between hCG treatment group and controls, a significance of P&lt;0.01; OR=3.05 for the comparison between PGF2alpha treatment and controls, and a highly statistically significant difference (P&lt;0.0001; OR=6.37) for the comparison between PGF2alpha plus hCG-treated animals and controls.	Dinoprost	403-412	hypertrichosis 2 (generalised, congenital)	Homo sapiens	171-174
14699320-12	2003	An additional dose of methotrexate is necessary when hCG levels are above the value of the curve on day 2, day 4, day 7 or day 10.	Methotrexate	22-34	hypertrichosis 2 (generalised, congenital)	Homo sapiens	53-56
12871873-10	2003	Serum estradiol level on the day of hCG injection was significantly higher in the FSH-primed group than in the non-FSH-primed group (377.2 pmol/l versus 143.8 pmol/l, P=0.001).	Estradiol	6-15	hypertrichosis 2 (generalised, congenital)	Homo sapiens	36-39
12834759-4	2003	Vanadate doses of 0, 5, 15, and 25mg/kg were administered intraperitoneally immediately after hCG and ovulated oocytes and bone marrow cells were processed for cytogenetic analyses 18h after hCG.	Vanadates	0-8	hypertrichosis 2 (generalised, congenital)	Homo sapiens	94-97
12834759-4	2003	Vanadate doses of 0, 5, 15, and 25mg/kg were administered intraperitoneally immediately after hCG and ovulated oocytes and bone marrow cells were processed for cytogenetic analyses 18h after hCG.	Vanadates	0-8	hypertrichosis 2 (generalised, congenital)	Homo sapiens	191-194
14562685-2	2003	The purified hCG-preparations from various blood group donors were shown to differ in their sialic acid content.	N-Acetylneuraminic Acid	92-103	hypertrichosis 2 (generalised, congenital)	Homo sapiens	13-16
12963106-6	2003	The results show a statistically significant difference for each treatment compared to controls, with the least difference (P&lt;0.05; OR=2.18) for the comparison between hCG treatment group and controls, a significance of P&lt;0.01; OR=3.05 for the comparison between PGF2alpha treatment and controls, and a highly statistically significant difference (P&lt;0.0001; OR=6.37) for the comparison between PGF2alpha plus hCG-treated animals and controls.	Dinoprost	269-278	hypertrichosis 2 (generalised, congenital)	Homo sapiens	171-174
12827456-3	2003	Insertion of CGH into a pentapeptide, N-acetyl-Ala-Cys-Gly-His-Ala-CONH(2), allowed the formation of a square-planar thiolato Cys-Gly-His complex with nickel(II) in an internal position of the peptide.	n-acetyl-ala-cys-gly-his-ala-conh	38-71	hypertrichosis 2 (generalised, congenital)	Homo sapiens	13-16
12827456-3	2003	Insertion of CGH into a pentapeptide, N-acetyl-Ala-Cys-Gly-His-Ala-CONH(2), allowed the formation of a square-planar thiolato Cys-Gly-His complex with nickel(II) in an internal position of the peptide.	thiolato cys-gly-his	117-137	hypertrichosis 2 (generalised, congenital)	Homo sapiens	13-16
12827456-3	2003	Insertion of CGH into a pentapeptide, N-acetyl-Ala-Cys-Gly-His-Ala-CONH(2), allowed the formation of a square-planar thiolato Cys-Gly-His complex with nickel(II) in an internal position of the peptide.	Nickel	151-157	hypertrichosis 2 (generalised, congenital)	Homo sapiens	13-16
12827456-5	2003	Solutions of CGH-CONH(2) with nickel(II) at neutral pH yielded a red nickel-thiolate complex, but at higher pH (8.5 or above) or with exposure to dioxygen, yellow nickel complexes with N-terminal amino coordination were observed.	Nickel	30-36	hypertrichosis 2 (generalised, congenital)	Homo sapiens	13-16
12827456-5	2003	Solutions of CGH-CONH(2) with nickel(II) at neutral pH yielded a red nickel-thiolate complex, but at higher pH (8.5 or above) or with exposure to dioxygen, yellow nickel complexes with N-terminal amino coordination were observed.	Nickel	69-75	hypertrichosis 2 (generalised, congenital)	Homo sapiens	13-16
12827456-5	2003	Solutions of CGH-CONH(2) with nickel(II) at neutral pH yielded a red nickel-thiolate complex, but at higher pH (8.5 or above) or with exposure to dioxygen, yellow nickel complexes with N-terminal amino coordination were observed.	thiolate	76-84	hypertrichosis 2 (generalised, congenital)	Homo sapiens	13-16
12827456-5	2003	Solutions of CGH-CONH(2) with nickel(II) at neutral pH yielded a red nickel-thiolate complex, but at higher pH (8.5 or above) or with exposure to dioxygen, yellow nickel complexes with N-terminal amino coordination were observed.	Oxygen	146-154	hypertrichosis 2 (generalised, congenital)	Homo sapiens	13-16
12827456-5	2003	Solutions of CGH-CONH(2) with nickel(II) at neutral pH yielded a red nickel-thiolate complex, but at higher pH (8.5 or above) or with exposure to dioxygen, yellow nickel complexes with N-terminal amino coordination were observed.	Nickel	69-75	hypertrichosis 2 (generalised, congenital)	Homo sapiens	13-16
12827456-6	2003	The disulfide-bridged dimers formed from Ni(CGH-CONH(2)) in the presence of air were characterized and found to have the typical coordination found in the amino-terminal binding motif of the serum albumins.	Disulfides	4-13	hypertrichosis 2 (generalised, congenital)	Homo sapiens	44-47
12850276-7	2003	Analysis of the signaling properties of these mutants showed that, when corrected for the amount of hCG bound under the conditions of the signaling assay, the maximal ligand-mediated cAMP produced in cells maintained in the buffer of low ionic strength was comparable for wt LHR and the mutants, only the D333A mutant being somewhat elevated.	Cyclic AMP	183-187	hypertrichosis 2 (generalised, congenital)	Homo sapiens	100-103
12850278-1	2003	Measurements of human choriogonadotropin (hCG) isoforms containing core 2 o-glycans may be useful for diagnosis of Down Syndrome pregnancies and trophoblastic disease.	2 o-glycans	72-83	hypertrichosis 2 (generalised, congenital)	Homo sapiens	42-45
12850278-4	2003	Here, we report that monoclonal antibodies B152 and CTP104 recognize the third (Ser132) and fourth (Ser138) o-glycans, respectively, in the carboxyterminal portion of the hCG beta-subunit.	ctp104	52-58	hypertrichosis 2 (generalised, congenital)	Homo sapiens	171-174
12850278-4	2003	Here, we report that monoclonal antibodies B152 and CTP104 recognize the third (Ser132) and fourth (Ser138) o-glycans, respectively, in the carboxyterminal portion of the hCG beta-subunit.	o-glycans	108-117	hypertrichosis 2 (generalised, congenital)	Homo sapiens	171-174
12850278-7	2003	By measuring hCG with CTP104 in the presence and absence of B152, one can quantify both isoforms using the same readily available standard.	ctp104	22-28	hypertrichosis 2 (generalised, congenital)	Homo sapiens	13-16
12812765-8	2003	The same difference was observed between stressed and control male fetuses in the testosterone testicular response to hCG (5.34+/-0.64 vs. 8.73+/-0.40 ng/testis/h, P&lt;0.05).	Testosterone	82-94	hypertrichosis 2 (generalised, congenital)	Homo sapiens	118-121
12699903-4	2003	Dose and time-dependent reductions of human chorionic gonadotropin (hCG)-stimulated testosterone level were observed in the culture medium.	Testosterone	84-96	hypertrichosis 2 (generalised, congenital)	Homo sapiens	68-71
12699903-6	2003	The expression of StAR protein stimulated by hCG was suppressed by manganese chloride at all concentrations (0.01, 0.1, 1.0 mM) and time points (2, 4, 24, 48 h) tested.	manganese chloride	67-85	hypertrichosis 2 (generalised, congenital)	Homo sapiens	45-48
12606479-4	2003	Gonadotropin-stimulated VEGF production was mediated by cAMP-dependent protein kinase A (PKA), as evidenced by the effect of hCG being mimicked by 8Br-cAMP and being abolished in the presence of a PKA-specific inhibitor, H-89.	8-Bromo Cyclic Adenosine Monophosphate	147-155	hypertrichosis 2 (generalised, congenital)	Homo sapiens	125-128
14567394-2	2003	Treatment with human chorionic gonadotrophin (hCG) induces testis descent by stimulating production of testosterone (T).	Testosterone	103-115	hypertrichosis 2 (generalised, congenital)	Homo sapiens	46-49
12606479-4	2003	Gonadotropin-stimulated VEGF production was mediated by cAMP-dependent protein kinase A (PKA), as evidenced by the effect of hCG being mimicked by 8Br-cAMP and being abolished in the presence of a PKA-specific inhibitor, H-89.	N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide	221-225	hypertrichosis 2 (generalised, congenital)	Homo sapiens	125-128
12606479-8	2003	Furthermore, addition of U0126, an inhibitor of MEK 1/2, abolished the increase in VEGF production stimulated by both hCG and 8Br-cAMP.	U 0126	25-30	hypertrichosis 2 (generalised, congenital)	Homo sapiens	118-121
12742549-12	2003	These results demonstrate that in mares: (1) a small elevation of endogenous LH can induce ovulation, (2) ovulation can be postponed approximately 13 days after a 3-day antarelix treatment if initiated just before the preovulatory LH surge, (3) ovulation can be induced by hCG on depressed levels of endogenous LH, (4) the inhibition of the post ovulatory LH surge has no effect either on the corpus luteum or on fertility.	Luteinizing Hormone	77-79	hypertrichosis 2 (generalised, congenital)	Homo sapiens	273-276
12916004-11	2003	In addition, hCG induced a two-fold increase in oestradiol production from perifused tumour explants.	Estradiol	48-58	hypertrichosis 2 (generalised, congenital)	Homo sapiens	13-16
12683930-6	2003	Ovulation induced by hCG in pentobarbital-treated rats was not altered by LY treatment, indicating normal ovarian sensitivity to gonadotrophins.	Pentobarbital	28-41	hypertrichosis 2 (generalised, congenital)	Homo sapiens	21-24
12559722-4	2003	hCG significantly (P&lt;0.05) increased crown-rump length (saline: 11.9+/-0.2 mm; hCG: 12.7+/-0.2 mm), amniotic sac width (saline: 11.4+/-0.4 mm; hCG: 12.0+/-0.3 mm) and the number of placentomes (saline: 90.8+/-7.3; hCG=122.4+/-6.3).	Sodium Chloride	59-65	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
12559722-4	2003	hCG significantly (P&lt;0.05) increased crown-rump length (saline: 11.9+/-0.2 mm; hCG: 12.7+/-0.2 mm), amniotic sac width (saline: 11.4+/-0.4 mm; hCG: 12.0+/-0.3 mm) and the number of placentomes (saline: 90.8+/-7.3; hCG=122.4+/-6.3).	Sodium Chloride	123-129	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
12559722-4	2003	hCG significantly (P&lt;0.05) increased crown-rump length (saline: 11.9+/-0.2 mm; hCG: 12.7+/-0.2 mm), amniotic sac width (saline: 11.4+/-0.4 mm; hCG: 12.0+/-0.3 mm) and the number of placentomes (saline: 90.8+/-7.3; hCG=122.4+/-6.3).	Sodium Chloride	123-129	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
12559722-5	2003	Among the pregnant animals that were slaughtered on 25 days post-mating, ovulation rate tended to be higher in the hCG group compared to controls (saline: 1.16; hCG: 1.54).	Sodium Chloride	147-153	hypertrichosis 2 (generalised, congenital)	Homo sapiens	115-118
12559722-8	2003	The total number of lambs born (saline: 38; hCG: 58) was significantly (P&lt;0.05) greater in hCG group compared to saline-treated controls.	Sodium Chloride	32-38	hypertrichosis 2 (generalised, congenital)	Homo sapiens	94-97
12820351-3	2003	With this study we tested the effects of the phytoestrogens genistein and daidzein in cell proliferation and the production of progesterone and hCG in trophoblast tumour cells of the cell lines BeWo and Jeg3.	Genistein	60-69	hypertrichosis 2 (generalised, congenital)	Homo sapiens	144-147
12820351-11	2003	RESULTS: With this study we could show that the production of the steroid hormone progesterone and the protein hormone hCG is influenced by the phytoestrogens genistein and daidzein in trophoblast tumour cells of the cell lines BeWo and Jeg3.	Genistein	159-168	hypertrichosis 2 (generalised, congenital)	Homo sapiens	119-122
12820351-11	2003	RESULTS: With this study we could show that the production of the steroid hormone progesterone and the protein hormone hCG is influenced by the phytoestrogens genistein and daidzein in trophoblast tumour cells of the cell lines BeWo and Jeg3.	daidzein	173-181	hypertrichosis 2 (generalised, congenital)	Homo sapiens	119-122
12820351-12	2003	We found a correlation between the effects on the proliferation and the production of progesterone and hCG at high concentrations of genistein and daidzein in the cell lines tested.	Genistein	133-142	hypertrichosis 2 (generalised, congenital)	Homo sapiens	103-106
12820351-12	2003	We found a correlation between the effects on the proliferation and the production of progesterone and hCG at high concentrations of genistein and daidzein in the cell lines tested.	daidzein	147-155	hypertrichosis 2 (generalised, congenital)	Homo sapiens	103-106
12820351-13	2003	With low concentrations of genistein and daidzein we observed a stimulation of the production of hCG and a weak inhibition of proliferation in both cell lines BeWo and Jeg3.	Genistein	27-36	hypertrichosis 2 (generalised, congenital)	Homo sapiens	97-100
12820351-13	2003	With low concentrations of genistein and daidzein we observed a stimulation of the production of hCG and a weak inhibition of proliferation in both cell lines BeWo and Jeg3.	daidzein	41-49	hypertrichosis 2 (generalised, congenital)	Homo sapiens	97-100
12820352-0	2003	hCG in trophoblast tumour cells of the cell line Jeg3 and hCG isolated from amniotic fluid and serum of pregnant women carry oligosaccharides of the sialyl Lewis X and sialyl Lewis a type.	Oligosaccharides	125-141	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
12820352-0	2003	hCG in trophoblast tumour cells of the cell line Jeg3 and hCG isolated from amniotic fluid and serum of pregnant women carry oligosaccharides of the sialyl Lewis X and sialyl Lewis a type.	Oligosaccharides	125-141	hypertrichosis 2 (generalised, congenital)	Homo sapiens	58-61
12611494-0	2003	Effect of hCG injection on prostaglandin E concentrations in ram seminal plasma.	Prostaglandins E	27-42	hypertrichosis 2 (generalised, congenital)	Homo sapiens	10-13
12533407-9	2003	Low urinary hCG levels in early pregnancy were significant determinants of a decline in postimplantation progesterone metabolite.	Progesterone	105-117	hypertrichosis 2 (generalised, congenital)	Homo sapiens	12-15
12611494-3	2003	The rams responded 1 week after hCG with a 1.5- to 4-fold increase in seminal plasma PGE.	Prostaglandins E	85-88	hypertrichosis 2 (generalised, congenital)	Homo sapiens	32-35
12611494-4	2003	The PGE peak was temporally separate from the hCG-induced rise in seminal plasma testosterone which was observed after 1 day.	Testosterone	81-93	hypertrichosis 2 (generalised, congenital)	Homo sapiens	46-49
12477522-10	2002	On the seventh day after hCG/recombinant human LH administration, the peripheral vascular resistance was significantly lower and serum progesterone concentrations significantly higher in the hCG group as compared with the recombinant human LH group.	Luteinizing Hormone	47-49	hypertrichosis 2 (generalised, congenital)	Homo sapiens	191-194
12477522-10	2002	On the seventh day after hCG/recombinant human LH administration, the peripheral vascular resistance was significantly lower and serum progesterone concentrations significantly higher in the hCG group as compared with the recombinant human LH group.	Progesterone	135-147	hypertrichosis 2 (generalised, congenital)	Homo sapiens	191-194
12477528-11	2002	CONCLUSION(S): Nitric oxide was found to be involved in the formation of hCG-induced murine follicular cysts and complications associated with these cysts were ameliorated by the NOS inhibitor L-NAME.	Nitric Oxide	15-27	hypertrichosis 2 (generalised, congenital)	Homo sapiens	73-76
12477528-11	2002	CONCLUSION(S): Nitric oxide was found to be involved in the formation of hCG-induced murine follicular cysts and complications associated with these cysts were ameliorated by the NOS inhibitor L-NAME.	NG-Nitroarginine Methyl Ester	193-199	hypertrichosis 2 (generalised, congenital)	Homo sapiens	73-76
12239104-7	2002	We found that forskolin significantly increased STC gene expression and secretion by both rat and bovine TICs, an effect that was only replicated by human (h) chorionic gonadotropin (CG).	Colforsin	14-23	hypertrichosis 2 (generalised, congenital)	Homo sapiens	183-185
12503886-5	2002	P+hCG protocol increased late-midluteal estradiol levels and produced a significantly higher pregnancy rate (31.7%) than P protocol (13.7%).	Estradiol	40-49	hypertrichosis 2 (generalised, congenital)	Homo sapiens	2-5
12503886-6	2002	CONCLUSIONS: hCG in combination with progesterone for luteal support was suggested to benefit women undergoing IVF with low late-midluteal estradiol levels.	Estradiol	139-148	hypertrichosis 2 (generalised, congenital)	Homo sapiens	13-16
12421175-10	2002	Women with an initial plasma chorionic gonadotrophine (p-hCG) between 2000 and 20 000 IU/l and a gestational age less than 75 days had a significantly better response to the medical treatment than those not fulfilling these two criteria.	chorionic gonadotrophine	29-53	hypertrichosis 2 (generalised, congenital)	Homo sapiens	57-60
12202418-0	2002	The kinetics of serum hCG and progesterone in response to oral and vaginal administration of misoprostol during medical termination of early pregnancy.	Misoprostol	93-104	hypertrichosis 2 (generalised, congenital)	Homo sapiens	22-25
12202418-8	2002	Following misoprostol, hCG and progesterone levels declined by 70.5 +/- 8.8% and 61.3 +/- 16.3% (mean +/- SD) respectively, in 24 h. The percentage decline in hCG correlated inversely (P &lt; 0.05) with the time taken to abort.	Misoprostol	10-21	hypertrichosis 2 (generalised, congenital)	Homo sapiens	23-26
12202418-8	2002	Following misoprostol, hCG and progesterone levels declined by 70.5 +/- 8.8% and 61.3 +/- 16.3% (mean +/- SD) respectively, in 24 h. The percentage decline in hCG correlated inversely (P &lt; 0.05) with the time taken to abort.	Misoprostol	10-21	hypertrichosis 2 (generalised, congenital)	Homo sapiens	159-162
12242037-13	2002	We assume that treatment with brefeldin A impaired glycosylation of beta subunit and consequently inhibited the production of hyperglycosylated form of hCG recognized by B152.	Brefeldin A	30-41	hypertrichosis 2 (generalised, congenital)	Homo sapiens	152-155
12107203-3	2002	Plasma testosterone was 3.9 ng/ml (normal range, 0.2-0.8 ng/ml), was not suppressible by 2 mg dexamethasone (4.3 ng/ml), and was increased (6.3 ng/ml) after three daily injections of hCG (5000 IU).	Testosterone	7-19	hypertrichosis 2 (generalised, congenital)	Homo sapiens	183-186
12088925-11	2002	In all boys but one, irrespective of age, hCG induced a marked increase in testosterone into the adult range (from undetectable to 21.8 (7.0-35.4) nmol/l; P&lt;0.001) and completely suppressed FSH and LH levels.	Testosterone	75-87	hypertrichosis 2 (generalised, congenital)	Homo sapiens	42-45
12088925-11	2002	In all boys but one, irrespective of age, hCG induced a marked increase in testosterone into the adult range (from undetectable to 21.8 (7.0-35.4) nmol/l; P&lt;0.001) and completely suppressed FSH and LH levels.	Luteinizing Hormone	201-203	hypertrichosis 2 (generalised, congenital)	Homo sapiens	42-45
12088925-15	2002	We found (a) normal inhibin B levels in prepubertal boys with uni- or bilateral cryptorchidism, (b) that hCG stimulated testosterone markedly and suppressed FSH and LH levels and (c) that hCG treatment stimulated inhibin B levels in the youngest cryptorchid boys.	Testosterone	120-132	hypertrichosis 2 (generalised, congenital)	Homo sapiens	105-108
12088925-15	2002	We found (a) normal inhibin B levels in prepubertal boys with uni- or bilateral cryptorchidism, (b) that hCG stimulated testosterone markedly and suppressed FSH and LH levels and (c) that hCG treatment stimulated inhibin B levels in the youngest cryptorchid boys.	Luteinizing Hormone	165-167	hypertrichosis 2 (generalised, congenital)	Homo sapiens	105-108
12269381-14	2002	Testicular response to hCG stimuli, in terms of testosterone synthesis was not significantly different in the two groups analyzed with respect to the intact animals.	Testosterone	48-60	hypertrichosis 2 (generalised, congenital)	Homo sapiens	23-26
12057723-9	2002	After the hCG test, the mean serum testosterone level was 16.0 +/- 6.3 ng/mL in men with sperm after TESE and 6.7 +/- 5.6 ng/mL in those without sperm.	Testosterone	35-47	hypertrichosis 2 (generalised, congenital)	Homo sapiens	10-13
12050258-0	2002	Trialkyltin compounds enhance human CG secretion and aromatase activity in human placental choriocarcinoma cells.	Trialkyltin Compounds	0-21	hypertrichosis 2 (generalised, congenital)	Homo sapiens	36-38
12050258-2	2002	In the present study, we investigated the effects of trialkyltin compounds, which are suspected endocrine disrupters, on aromatase activity and hCG secretion in human choriocarcinoma JAR, JEG-3, and BeWo cells.	trialkyltin	53-64	hypertrichosis 2 (generalised, congenital)	Homo sapiens	144-147
12050258-6	2002	In all cell lines, both TBT and TPT increased levels of hCG secretion and aromatase activity in a dose- and time-dependent fashion following exposure to nontoxic concentration ranges.	tributyltin	24-27	hypertrichosis 2 (generalised, congenital)	Homo sapiens	56-59
12050258-6	2002	In all cell lines, both TBT and TPT increased levels of hCG secretion and aromatase activity in a dose- and time-dependent fashion following exposure to nontoxic concentration ranges.	triphenyltin	32-35	hypertrichosis 2 (generalised, congenital)	Homo sapiens	56-59
12050258-7	2002	In addition, these trialkyltin compounds enhanced 8-bromo-cAMP-induced hCG secretion and aromatase activity in JAR cells.	8-Bromo Cyclic Adenosine Monophosphate	50-62	hypertrichosis 2 (generalised, congenital)	Homo sapiens	71-74
11923469-0	2002	Lysine 183 and glutamic acid 157 of the TSH receptor: two interacting residues with a key role in determining specificity toward TSH and human CG.	Lysine	0-6	hypertrichosis 2 (generalised, congenital)	Homo sapiens	143-145
12018033-11	2002	In that case the corpus luteum is further stimulated by hCG secreted by the blastocyst and the trophoblast-cells until 8/9 weeks of gestational age, when synthesis and secretion of steroids is taken over by the placenta.	Steroids	181-189	hypertrichosis 2 (generalised, congenital)	Homo sapiens	56-59
11937130-1	2002	OBJECTIVE: To evaluate the efficacy of methotrexate treatment in selected cases of extrauterine pregnancy (EUP) defined by stable or increasing hCG concentration.	Methotrexate	39-51	hypertrichosis 2 (generalised, congenital)	Homo sapiens	144-147
11937130-6	2002	Failure of hCG levels to fall by &gt;/=15% during any successive week resulted in repeated administration of methotrexate.	Methotrexate	109-121	hypertrichosis 2 (generalised, congenital)	Homo sapiens	11-14
11937130-14	2002	CONCLUSION(S): When methotrexate treatment is administrated in a selected group of EUP defined by stable or increasing hCG, it may fail more frequently (26%) when initial hCG levels are &gt;2,000 mIU/mL.	Methotrexate	20-32	hypertrichosis 2 (generalised, congenital)	Homo sapiens	119-122
11937130-14	2002	CONCLUSION(S): When methotrexate treatment is administrated in a selected group of EUP defined by stable or increasing hCG, it may fail more frequently (26%) when initial hCG levels are &gt;2,000 mIU/mL.	Methotrexate	20-32	hypertrichosis 2 (generalised, congenital)	Homo sapiens	171-174
11923469-0	2002	Lysine 183 and glutamic acid 157 of the TSH receptor: two interacting residues with a key role in determining specificity toward TSH and human CG.	Glutamic Acid	15-28	hypertrichosis 2 (generalised, congenital)	Homo sapiens	143-145
11779609-7	2002	RESULT(S): Prenatally androgenized females exhibited increased T and 17alpha-hydroxyprogesterone response to recombinant hCG stimulation, compared to control females.	17-alpha-Hydroxyprogesterone	69-96	hypertrichosis 2 (generalised, congenital)	Homo sapiens	121-124
11889180-4	2002	Despite several days of lowered or absent r-hFSH administration, 70% of hCG-treated patients successfully completed treatment.	r-hfsh	42-48	hypertrichosis 2 (generalised, congenital)	Homo sapiens	72-75
11836309-7	2002	LH levels returned to baseline after 24 h. Subjects receiving hCG showed peak levels of 240 IU/liter hCG 24 h after administration.	Luteinizing Hormone	0-2	hypertrichosis 2 (generalised, congenital)	Homo sapiens	62-65
11874698-14	2002	Also, the early pregnancy hCG appeared to be the same size as later pregnancy hCG as judged by SDS gel electrophoresis.	Sodium Dodecyl Sulfate	95-98	hypertrichosis 2 (generalised, congenital)	Homo sapiens	26-29
11874698-14	2002	Also, the early pregnancy hCG appeared to be the same size as later pregnancy hCG as judged by SDS gel electrophoresis.	Sodium Dodecyl Sulfate	95-98	hypertrichosis 2 (generalised, congenital)	Homo sapiens	78-81
11786377-1	2002	We have previously demonstrated that the release of arachidonic acid (AA) from human chorionic gonadotropin (hCG)-stimulated Leydig cells occurs in a dose- and time-dependent manner.	Arachidonic Acid	52-68	hypertrichosis 2 (generalised, congenital)	Homo sapiens	109-112
11825028-5	2002	When the intact follicles of oocytes were incubated with hCG in both lunar phases, the production of E2 and DHP measured by enzyme immunoassay decreased and increased significantly from the new moon to the first lunar quarter, respectively.	Estradiol	101-103	hypertrichosis 2 (generalised, congenital)	Homo sapiens	57-60
11825028-5	2002	When the intact follicles of oocytes were incubated with hCG in both lunar phases, the production of E2 and DHP measured by enzyme immunoassay decreased and increased significantly from the new moon to the first lunar quarter, respectively.	17 alpha,20 beta-dihydroxypregn-4-en-3-one	108-111	hypertrichosis 2 (generalised, congenital)	Homo sapiens	57-60
11755999-4	2001	We show that treatment of NOD mice with c-hCG before the onset of clinical symptoms lowered the increased blood glucose levels, reversed the established inflammatory infiltrate of pancreatic tissue, and profoundly inhibited the development of diabetes for prolonged time.	Glucose	112-119	hypertrichosis 2 (generalised, congenital)	Homo sapiens	42-45
11786377-8	2002	The inhibitory effect of mepacrine on the release of AA was evident in hCG-treated Leydig cells, but not in the melittin-treated cells.	Quinacrine	25-34	hypertrichosis 2 (generalised, congenital)	Homo sapiens	71-74
11786377-12	2002	Cells treated with PLA(2) inhibitors did not modify cAMP production, but exogenously added AA significantly reduced cAMP production from hCG-treated Leydig cells, in a manner dependent on the concentration of AA and hCG.	Cyclic AMP	116-120	hypertrichosis 2 (generalised, congenital)	Homo sapiens	137-140
12934246-1	2002	UNLABELLED: Several authors have shown the effect of LH or hCG gonadotrophins on steroid secretion in the chick embryo ovary.	Steroids	81-88	hypertrichosis 2 (generalised, congenital)	Homo sapiens	59-62
12934246-12	2002	PROBLEMS: With LH or hCG nerve fibers and nerve endings were observed both in the right gonad and in the medulla of the left ovary in close contact with the steroid-producing interstitial cells.	Steroids	157-164	hypertrichosis 2 (generalised, congenital)	Homo sapiens	21-24
11738634-2	2001	Here, we show that male goldfish also increase milt volume when isolated for 24 h, or when placed with another male injected with human chorionic gonadotropin (hCG) for 12 h. In contrast to the milt increase induced by pheromonal 17,20 beta-P, the milt increase following isolation or exposure to hCG-injected males was not associated with increased serum GTH-II.	beta-p	236-242	hypertrichosis 2 (generalised, congenital)	Homo sapiens	160-163
11701732-1	2001	Cortisol secretion in adrenal Cushing"s syndrome can be regulated by the aberrant adrenal expression of receptors for gastric inhibitory polypeptide, vasopressin, catecholamines, LH/human CG (LH/hCG), or serotonin.	Hydrocortisone	0-8	hypertrichosis 2 (generalised, congenital)	Homo sapiens	188-190
11738634-2	2001	Here, we show that male goldfish also increase milt volume when isolated for 24 h, or when placed with another male injected with human chorionic gonadotropin (hCG) for 12 h. In contrast to the milt increase induced by pheromonal 17,20 beta-P, the milt increase following isolation or exposure to hCG-injected males was not associated with increased serum GTH-II.	gth-ii	356-362	hypertrichosis 2 (generalised, congenital)	Homo sapiens	160-163
11701732-1	2001	Cortisol secretion in adrenal Cushing"s syndrome can be regulated by the aberrant adrenal expression of receptors for gastric inhibitory polypeptide, vasopressin, catecholamines, LH/human CG (LH/hCG), or serotonin.	Hydrocortisone	0-8	hypertrichosis 2 (generalised, congenital)	Homo sapiens	195-198
11769664-11	2001	(5) A significant negative correlation between TSH and hCG levels and a significant positive correlation between hCG and FT4 and TT4/TBG were demonstrated.	Thyrotropin	47-50	hypertrichosis 2 (generalised, congenital)	Homo sapiens	55-58
14666164-5	2001	In vivo administration of hCG decreased vascular resistance in the human uterus and in vitro treatment increased vasodilatory and decreased vasoconstrictive eicosanoids in the vessels.	Eicosanoids	157-168	hypertrichosis 2 (generalised, congenital)	Homo sapiens	26-29
11721831-13	2001	Among 2-yr-olds, pregnancy rates were higher for cows treated with hCG without CR than for cows that received GnRH with calf removal, whereas cows treated with hCG with CR and GnRH without CR were intermediate.	Chromium	169-171	hypertrichosis 2 (generalised, congenital)	Homo sapiens	160-163
11721831-13	2001	Among 2-yr-olds, pregnancy rates were higher for cows treated with hCG without CR than for cows that received GnRH with calf removal, whereas cows treated with hCG with CR and GnRH without CR were intermediate.	Chromium	169-171	hypertrichosis 2 (generalised, congenital)	Homo sapiens	160-163
11599774-10	2001	The results showed the importance of timing of 4-OHA administration, as 5000 microg/rat 4-OHA was able to restore embryo survival in the 40 PMSG hyperstimulated group only when it was administered 24 h before hCG injection.	formestane	88-93	hypertrichosis 2 (generalised, congenital)	Homo sapiens	209-212
11549661-5	2001	Peak levels of serum hCG and thyroid hormone concentrations were attained at 12 wk gestation, when serum TSH was fully suppressed.	Thyrotropin	105-108	hypertrichosis 2 (generalised, congenital)	Homo sapiens	21-24
11769664-11	2001	(5) A significant negative correlation between TSH and hCG levels and a significant positive correlation between hCG and FT4 and TT4/TBG were demonstrated.	CHEMBL179036	121-124	hypertrichosis 2 (generalised, congenital)	Homo sapiens	113-116
11769664-11	2001	(5) A significant negative correlation between TSH and hCG levels and a significant positive correlation between hCG and FT4 and TT4/TBG were demonstrated.	1-Phenyl-1H-1,2,4-triazole-3,5-diamine	129-132	hypertrichosis 2 (generalised, congenital)	Homo sapiens	113-116
11769664-11	2001	(5) A significant negative correlation between TSH and hCG levels and a significant positive correlation between hCG and FT4 and TT4/TBG were demonstrated.	(S)-2-Amino-3,3-dimethylbutanamide	133-136	hypertrichosis 2 (generalised, congenital)	Homo sapiens	113-116
11476781-7	2001	RESULT(S): Administration of hCG to mimic early pregnancy sustained serum progesterone concentrations and extended the luteal phase in control women.	Progesterone	74-86	hypertrichosis 2 (generalised, congenital)	Homo sapiens	29-32
11559906-7	2001	The association between TSH and hCG in unaffected pregnancies was also measured.	Thyrotropin	24-27	hypertrichosis 2 (generalised, congenital)	Homo sapiens	32-35
11559906-8	2001	The Spearman correlation coefficient between TSH and hCG was -0.21 which was statistically significant (p=0.02, 95% confidence interval -0.38 to -0.03).	Thyrotropin	45-48	hypertrichosis 2 (generalised, congenital)	Homo sapiens	53-56
11689154-7	2001	Upon Cd exposure, a dose-dependent decrease in hCG secretion was seen in all JEG-3 cultures, without any correlation to basal MT expression.	Cadmium	5-7	hypertrichosis 2 (generalised, congenital)	Homo sapiens	47-50
11442338-2	2001	Also, in 22 adolescents and in 22 adults from the same sample they evaluated the hCG effect on the gonadal steroids secretion.	Steroids	107-115	hypertrichosis 2 (generalised, congenital)	Homo sapiens	81-84
11442338-5	2001	The gonadal steroid secretion 2, 24, 48, and 72 h post-hCG was significantly lower in the Tanner 4 adolescents.	Steroids	12-19	hypertrichosis 2 (generalised, congenital)	Homo sapiens	55-58
11442338-7	2001	In late puberty the LH response to GnRH stimulus is not related either to age or to sexual development, contrary to the FSH response obtained after GnRH and the gonadal steroid response after hCG stimulus, both of which are related to age and patients" sexual development.	Steroids	169-176	hypertrichosis 2 (generalised, congenital)	Homo sapiens	192-195
11403907-10	2001	Effects of TCDD (1.0 microg/kg) in the H/W fetuses could be confirmed in vitro by human chorionic gonadotropin (hCG) stimulation assay showing the highest response rate in the TCDD exposed testes.	Polychlorinated Dibenzodioxins	11-15	hypertrichosis 2 (generalised, congenital)	Homo sapiens	112-115
11403907-10	2001	Effects of TCDD (1.0 microg/kg) in the H/W fetuses could be confirmed in vitro by human chorionic gonadotropin (hCG) stimulation assay showing the highest response rate in the TCDD exposed testes.	Polychlorinated Dibenzodioxins	176-180	hypertrichosis 2 (generalised, congenital)	Homo sapiens	112-115
11403907-13	2001	In the presence of hCG, DES-exposed testes showed lower in vitro T and cAMP production rates compared to the untreated testes.	Diethylstilbestrol	24-27	hypertrichosis 2 (generalised, congenital)	Homo sapiens	19-22
11403907-13	2001	In the presence of hCG, DES-exposed testes showed lower in vitro T and cAMP production rates compared to the untreated testes.	Cyclic AMP	71-75	hypertrichosis 2 (generalised, congenital)	Homo sapiens	19-22
11356667-4	2001	In contrast, when ERbeta mRNA levels were estimated in granulosa cells that were cultured in the presence of 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole (DRB), an RNA synthesis inhibitor, we observed a significant inhibitory effect of human CG (hCG) on ERbeta mRNA expression at a magnitude similar to that observed in the absence of DRB.	Dichlororibofuranosylbenzimidazole	109-157	hypertrichosis 2 (generalised, congenital)	Homo sapiens	250-253
11356667-12	2001	When granulosa cells were cultured in the presence of cycloheximide, a protein synthesis inhibitor, the inhibitory effects of hCG, FSK, and TPA on ERbeta mRNA levels were abolished.	Cycloheximide	54-67	hypertrichosis 2 (generalised, congenital)	Homo sapiens	126-129
11298843-7	2001	Administration of hCG, but not FSH, caused a rapid increase in blood testosterone levels, which reached a maximum after 72 h (22.2 +/- 2.7-50.1 +/- 4.5 nmol/L, p &lt; 0.001).	Testosterone	69-81	hypertrichosis 2 (generalised, congenital)	Homo sapiens	18-21
11440542-5	2001	Treatment of BeWo cells with forskolin (FSK) for 48-72 h resulted in an 11- to 44-fold increase in the level of hCG secretion and induced cell fusion leading to the formation of multinucleated syncytiotrophoblasts, indicating functional and morphological differentiation.	Colforsin	29-38	hypertrichosis 2 (generalised, congenital)	Homo sapiens	112-115
11440542-5	2001	Treatment of BeWo cells with forskolin (FSK) for 48-72 h resulted in an 11- to 44-fold increase in the level of hCG secretion and induced cell fusion leading to the formation of multinucleated syncytiotrophoblasts, indicating functional and morphological differentiation.	Colforsin	40-43	hypertrichosis 2 (generalised, congenital)	Homo sapiens	112-115
11440542-8	2001	The level of hCG secretion from the FSK-treated cells was further enhanced when the cells were treated in the presence of the NEP inhibitor phosphoramidon.	Colforsin	36-39	hypertrichosis 2 (generalised, congenital)	Homo sapiens	13-16
11440542-8	2001	The level of hCG secretion from the FSK-treated cells was further enhanced when the cells were treated in the presence of the NEP inhibitor phosphoramidon.	phosphoramidon	140-154	hypertrichosis 2 (generalised, congenital)	Homo sapiens	13-16
11356667-4	2001	In contrast, when ERbeta mRNA levels were estimated in granulosa cells that were cultured in the presence of 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole (DRB), an RNA synthesis inhibitor, we observed a significant inhibitory effect of human CG (hCG) on ERbeta mRNA expression at a magnitude similar to that observed in the absence of DRB.	Dichlororibofuranosylbenzimidazole	109-157	hypertrichosis 2 (generalised, congenital)	Homo sapiens	246-248
11337360-1	2001	We have developed a protocol for degenerate oligonucleotide-primed-polymerase chain reaction-based array comparative genomic hybridization (array CGH) that, when combined with a laser microdissection technique, allows the analysis of cancer cell populations isolated from routine, formalin-fixed, paraffin-embedded tissue samples.	Formaldehyde	281-289	hypertrichosis 2 (generalised, congenital)	Homo sapiens	146-149
11337360-1	2001	We have developed a protocol for degenerate oligonucleotide-primed-polymerase chain reaction-based array comparative genomic hybridization (array CGH) that, when combined with a laser microdissection technique, allows the analysis of cancer cell populations isolated from routine, formalin-fixed, paraffin-embedded tissue samples.	Paraffin	297-305	hypertrichosis 2 (generalised, congenital)	Homo sapiens	146-149
11337360-4	2001	The array CGH method described here will allow the genetic analysis of paraffin-embedded human cancer materials for example in the context of clinical trials.	Paraffin	71-79	hypertrichosis 2 (generalised, congenital)	Homo sapiens	10-13
11497290-6	2001	Estradiol was measured in the supernatant after incubation with hCG and FSH, while hCG was measured after FSH incubation.	Estradiol	0-9	hypertrichosis 2 (generalised, congenital)	Homo sapiens	64-67
11145594-4	2001	In addition, extracellular Ca(2+) (1.5 mmol/liter) increased the effect of PRL on human CG (hCG)-stimulated StAR messenger RNA expression and progesterone (P) production.	Progesterone	142-154	hypertrichosis 2 (generalised, congenital)	Homo sapiens	88-90
11238521-2	2001	It has long been believed that hCG can directly induce in vitro decidualization of ESC via cAMP signaling.	Cyclic AMP	91-95	hypertrichosis 2 (generalised, congenital)	Homo sapiens	31-34
11361105-12	2001	There was an increase in plasma testosterone following hCG; however, this increase was very small in aged stallions.	Testosterone	32-44	hypertrichosis 2 (generalised, congenital)	Homo sapiens	55-58
11361105-13	2001	After stimulation with hCG the control and lack of libido stallions had a significant increase (P&lt;0.05) in testosterone production.	Testosterone	110-122	hypertrichosis 2 (generalised, congenital)	Homo sapiens	23-26
10964934-7	2001	Our results show that the C-flanking sequence (hinge region), Thr(250)-Gln(268), of the Leu-rich repeats (LRRs) specifically interacts with hCG, preferentially hCGalpha.	Threonine	62-65	hypertrichosis 2 (generalised, congenital)	Homo sapiens	140-143
10964934-7	2001	Our results show that the C-flanking sequence (hinge region), Thr(250)-Gln(268), of the Leu-rich repeats (LRRs) specifically interacts with hCG, preferentially hCGalpha.	Glutamine	71-74	hypertrichosis 2 (generalised, congenital)	Homo sapiens	140-143
10964934-8	2001	This interaction is inhibited by exoloop 2 of the endodomain but not by exoloops 1 and 3, suggesting an intimate relationship between Thr(250)-Gln(268), exoloop 2, and hCG.	Threonine	134-137	hypertrichosis 2 (generalised, congenital)	Homo sapiens	168-171
10964934-8	2001	This interaction is inhibited by exoloop 2 of the endodomain but not by exoloops 1 and 3, suggesting an intimate relationship between Thr(250)-Gln(268), exoloop 2, and hCG.	Glutamine	143-146	hypertrichosis 2 (generalised, congenital)	Homo sapiens	168-171
11145594-4	2001	In addition, extracellular Ca(2+) (1.5 mmol/liter) increased the effect of PRL on human CG (hCG)-stimulated StAR messenger RNA expression and progesterone (P) production.	Progesterone	142-154	hypertrichosis 2 (generalised, congenital)	Homo sapiens	92-95
11145594-7	2001	The relevance of the PRL effects observed in mLTC-1 cells was supported by demonstration of similar PRL responses in hCG-stimulated testosterone production of isolated mouse Leydig cells.	Testosterone	132-144	hypertrichosis 2 (generalised, congenital)	Homo sapiens	117-120
11394199-6	2001	hCG increased immunoreactive prostaglandin D2 (PGD2) and decreased PGE2 in brain areas controlling activity and sleep.	Prostaglandin D2	29-45	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
11231992-9	2001	After hCG administration, NA UER increased by 250% (P &lt; 0.01) and estradiol (E(2)) UER by 260% (P &lt; 0.001).	Estradiol	69-78	hypertrichosis 2 (generalised, congenital)	Homo sapiens	6-9
11787171-5	2001	Pretreatment with hCG results in a rapid increase in the number of LH receptors and Ca(2+)-naloxone induces G protein activity.	ca(2+)-naloxone	84-99	hypertrichosis 2 (generalised, congenital)	Homo sapiens	18-21
11787171-12	2001	In conclusion, pretreatment with hCG increased the number of LH receptors and Ca(2+)-naloxone antagonized the hypothalamic GnRH opioid block thus inducing the pulsatility of LH leading to fertile oestrus in queens.	ca(2+)-naloxone	78-93	hypertrichosis 2 (generalised, congenital)	Homo sapiens	33-36
11787171-12	2001	In conclusion, pretreatment with hCG increased the number of LH receptors and Ca(2+)-naloxone antagonized the hypothalamic GnRH opioid block thus inducing the pulsatility of LH leading to fertile oestrus in queens.	Luteinizing Hormone	61-63	hypertrichosis 2 (generalised, congenital)	Homo sapiens	33-36
11232027-11	2001	Treatment of hGLCs with PGF(2alpha) significantly inhibited hCG-induced progesterone production.	Prostaglandins F	24-27	hypertrichosis 2 (generalised, congenital)	Homo sapiens	60-63
11232027-11	2001	Treatment of hGLCs with PGF(2alpha) significantly inhibited hCG-induced progesterone production.	Progesterone	72-84	hypertrichosis 2 (generalised, congenital)	Homo sapiens	60-63
11232027-12	2001	The presence of the MEK inhibitor, PD98059, reversed the inhibitory effect of PGF(2alpha) on hCG-induced progesterone production.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	35-42	hypertrichosis 2 (generalised, congenital)	Homo sapiens	93-96
11232027-12	2001	The presence of the MEK inhibitor, PD98059, reversed the inhibitory effect of PGF(2alpha) on hCG-induced progesterone production.	Prostaglandins F	78-81	hypertrichosis 2 (generalised, congenital)	Homo sapiens	93-96
11232027-12	2001	The presence of the MEK inhibitor, PD98059, reversed the inhibitory effect of PGF(2alpha) on hCG-induced progesterone production.	Progesterone	105-117	hypertrichosis 2 (generalised, congenital)	Homo sapiens	93-96
11394199-6	2001	hCG increased immunoreactive prostaglandin D2 (PGD2) and decreased PGE2 in brain areas controlling activity and sleep.	Prostaglandin D2	47-51	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
11394199-6	2001	hCG increased immunoreactive prostaglandin D2 (PGD2) and decreased PGE2 in brain areas controlling activity and sleep.	Dinoprostone	67-71	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
11394199-7	2001	hCG effects were probably mediated via prostaglandin pathways.	Prostaglandins	39-52	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
11394199-11	2001	hCG treatment also had a beneficial effect against stress ulcer, which was prevented by pretreatment with antisense receptor oligonucleotide, suggesting a direct hCG receptor-mediated effect.	Oligonucleotides	125-140	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
11394199-11	2001	hCG treatment also had a beneficial effect against stress ulcer, which was prevented by pretreatment with antisense receptor oligonucleotide, suggesting a direct hCG receptor-mediated effect.	Oligonucleotides	125-140	hypertrichosis 2 (generalised, congenital)	Homo sapiens	162-165
11023800-12	2000	hCG secretion by invading trophoblast appears to be negatively modulated by endothelin-1 (ET-1) and prostaglandin F(2alpha)(PGF2alpha), while tissue growth factors and collagenases are positive modulators of hCG expression.ProalphaC, an inhibin pro-monomer, may have some value in monitoring corpus luteum function.	Prostaglandins F	100-115	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
11282287-8	2000	A decrease in hCG-stimulated testosterone production was observed at 3 and 24 h in all cases.	Testosterone	29-41	hypertrichosis 2 (generalised, congenital)	Homo sapiens	14-17
11282287-10	2000	TNFalpha and IL1beta, two possible inducers of sphingomyelin hydrolysis, produced similar effects on hCG-stimulated testosterone production.	Testosterone	116-128	hypertrichosis 2 (generalised, congenital)	Homo sapiens	101-104
11282287-11	2000	In experiments performed in the presence of C6, inhibition in hCG-stimulated cAMP production was observed.	Cyclic AMP	77-81	hypertrichosis 2 (generalised, congenital)	Homo sapiens	62-65
11282287-15	2000	These results suggest that a ceramide-dependent pathway regulates hCG-stimulated Leydig cell steroidogenesis at the level of cAMP production and at post-cAMP events.	Ceramides	29-37	hypertrichosis 2 (generalised, congenital)	Homo sapiens	66-69
11282287-15	2000	These results suggest that a ceramide-dependent pathway regulates hCG-stimulated Leydig cell steroidogenesis at the level of cAMP production and at post-cAMP events.	Cyclic AMP	125-129	hypertrichosis 2 (generalised, congenital)	Homo sapiens	66-69
11282287-15	2000	These results suggest that a ceramide-dependent pathway regulates hCG-stimulated Leydig cell steroidogenesis at the level of cAMP production and at post-cAMP events.	Cyclic AMP	153-157	hypertrichosis 2 (generalised, congenital)	Homo sapiens	66-69
11056240-8	2000	Incubation of isolated preovulatory follicles for 3 h with hCG or with menadione (a generator of oxygen radicals) reduced ascorbic acid levels.	Ascorbic Acid	122-135	hypertrichosis 2 (generalised, congenital)	Homo sapiens	59-62
11411038-8	2000	Except for oestradiol (E2) from early GCs, hCG generally stimulated progesterone (P) and E2 secretion.	Progesterone	68-80	hypertrichosis 2 (generalised, congenital)	Homo sapiens	43-46
11192177-8	2000	The pregnancy rate was significantly higher (P&lt;0.0001) in the hCG-EB group (59.5%, 379/637) than in PG (44.8%, 285/636).	estradiol 3-benzoate	69-71	hypertrichosis 2 (generalised, congenital)	Homo sapiens	65-68
11023800-12	2000	hCG secretion by invading trophoblast appears to be negatively modulated by endothelin-1 (ET-1) and prostaglandin F(2alpha)(PGF2alpha), while tissue growth factors and collagenases are positive modulators of hCG expression.ProalphaC, an inhibin pro-monomer, may have some value in monitoring corpus luteum function.	Dinoprost	124-133	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
11023800-12	2000	hCG secretion by invading trophoblast appears to be negatively modulated by endothelin-1 (ET-1) and prostaglandin F(2alpha)(PGF2alpha), while tissue growth factors and collagenases are positive modulators of hCG expression.ProalphaC, an inhibin pro-monomer, may have some value in monitoring corpus luteum function.	proalphac	223-232	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
10875642-8	2000	After GnRH antagonist lowered LH concentrations, administration of hCG resulted in increased testosterone and cortisol concentrations.	Testosterone	93-105	hypertrichosis 2 (generalised, congenital)	Homo sapiens	67-70
11004721-4	2000	In macronodular adrenal hyperplasia, we have identified, in addition to GIP-dependent Cushing"s syndrome, other patients in whom cortisol production was regulated abnormally by vasopressin, ss-adrenergic receptor agonists, hCG/LH, or serotonin 5HT-4 receptor agonists.	Hydrocortisone	129-137	hypertrichosis 2 (generalised, congenital)	Homo sapiens	223-226
11129958-6	2000	In presence of hCG, HDL with or without apo E increased testosterone production respectively by 37 and 25%.	Testosterone	56-68	hypertrichosis 2 (generalised, congenital)	Homo sapiens	15-18
10894155-3	2000	The luteotrophic hormone human CG (hCG) was found to decrease the peak amplitude of the sodium current within seconds.	Sodium	88-94	hypertrichosis 2 (generalised, congenital)	Homo sapiens	31-33
10894155-3	2000	The luteotrophic hormone human CG (hCG) was found to decrease the peak amplitude of the sodium current within seconds.	Sodium	88-94	hypertrichosis 2 (generalised, congenital)	Homo sapiens	35-38
12545818-1	2000	The purpose of this study was to determine the effects of hCG on cellular cAMP levels in gastric adenocarcinoma cells(SGC-7901).	Cyclic AMP	74-78	hypertrichosis 2 (generalised, congenital)	Homo sapiens	58-61
12545818-3	2000	The results showed that hCG obviously increased cAMP levels in SGC-7901 cells in a dose-dependent and time-dependent manner.	Cyclic AMP	48-52	hypertrichosis 2 (generalised, congenital)	Homo sapiens	24-27
12545818-4	2000	When the concentration of hCG increased from 10(-11) mol/L to 10(-6) mol/L, the cellular cAMP levels increased from about 2.1 pmol/mg protein to about 10 pmol/mg protein and were significantly different from the control(P &lt; 0.01).	Cyclic AMP	89-93	hypertrichosis 2 (generalised, congenital)	Homo sapiens	26-29
12545818-5	2000	These results suggest that hCG possibly exerts its effects on gastric cancer cells by activating adenylyl cyclase/cAMP signal transduction pathway.	Cyclic AMP	114-118	hypertrichosis 2 (generalised, congenital)	Homo sapiens	27-30
11006156-7	2000	In common with other insectivores, Atelerix appears to be an induced ovulator, as judged by the ovulation of some 6-8 eggs by about 23 h after injection of hCG.	atelerix	35-43	hypertrichosis 2 (generalised, congenital)	Homo sapiens	156-159
10997481-10	2000	Further, the higher dose of hCG appeared to induce greater increases in progesterone over the 24-hour period examined (P &lt; .02).	Progesterone	72-84	hypertrichosis 2 (generalised, congenital)	Homo sapiens	28-31
10997481-12	2000	Unlike the relationship associated with 5,000 mIU hCG, though, the relationship between 10,000 mIU hCG and progesterone levels was not statistically different (P = .10).	Progesterone	107-119	hypertrichosis 2 (generalised, congenital)	Homo sapiens	99-102
10997481-13	2000	CONCLUSIONS: Increasing the dose of hCG used to stimulate oocyte maturity shifts the previously described relationship between progesterone and IVF-ET-cycle outcome.	Progesterone	127-139	hypertrichosis 2 (generalised, congenital)	Homo sapiens	36-39
10875642-8	2000	After GnRH antagonist lowered LH concentrations, administration of hCG resulted in increased testosterone and cortisol concentrations.	Hydrocortisone	110-118	hypertrichosis 2 (generalised, congenital)	Homo sapiens	67-70
10770207-16	2000	In conclusion, our results suggest that both gonadotropins (FSH and hCG) and cytokines (TGFbeta1 and M-CSF) may be involved in the support of luteal function via suppression of apoptosis, and that TNFalpha and PGF2alpha may contribute to ovarian dysfunction and/or luteal regression via its induction in human luteinized granulosa cells.	Dinoprost	210-219	hypertrichosis 2 (generalised, congenital)	Homo sapiens	68-71
10831986-1	2000	OBJECTIVE: To evaluate measurement of levels of urine hyperglycosylated hCG, a form of hCG with abnormally branched oligosaccharide side chains, in conjunction with ultrasound biometry for Down syndrome risk prediction in an at-risk group.	Oligosaccharides	116-131	hypertrichosis 2 (generalised, congenital)	Homo sapiens	72-75
10831986-1	2000	OBJECTIVE: To evaluate measurement of levels of urine hyperglycosylated hCG, a form of hCG with abnormally branched oligosaccharide side chains, in conjunction with ultrasound biometry for Down syndrome risk prediction in an at-risk group.	Oligosaccharides	116-131	hypertrichosis 2 (generalised, congenital)	Homo sapiens	87-90
10822026-2	2000	The present study examined the possible role of progesterone (Pg) in the chorionic gonadotropin (hCG) concentration in GCBD.	Progesterone	48-60	hypertrichosis 2 (generalised, congenital)	Homo sapiens	97-100
10822026-2	2000	The present study examined the possible role of progesterone (Pg) in the chorionic gonadotropin (hCG) concentration in GCBD.	Progesterone	62-64	hypertrichosis 2 (generalised, congenital)	Homo sapiens	97-100
10879180-3	2000	We synthesized PLEG copolymers containing PEG segments with various molecular weight and prepared hCG-loaded PL/PLEG blend microspheres to improve hCG entrapment efficiency.	pleg	15-19	hypertrichosis 2 (generalised, congenital)	Homo sapiens	98-101
10684807-9	2000	Mifepristone did not per se alter progesterone synthesis, but when it was added in conjunction with hCG, a dose-related inhibitory response was seen, with a maximal 47% reduction in progesterone output at a 10 microM addition (P &lt; 0.05, n = 3).	Mifepristone	0-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	100-103
10684807-9	2000	Mifepristone did not per se alter progesterone synthesis, but when it was added in conjunction with hCG, a dose-related inhibitory response was seen, with a maximal 47% reduction in progesterone output at a 10 microM addition (P &lt; 0.05, n = 3).	Progesterone	182-194	hypertrichosis 2 (generalised, congenital)	Homo sapiens	100-103
10694751-6	2000	It is concluded that receptors of bovine cumulus/oocyte complex cells bind specifically to LH/hCG, that binding capacity is inversely proportional to follicle size, and that the behavior of hCG is similar to that of LH, suggesting that hCG can also promote the maturation of bovine oocytes when used in concentrations greater than LH.	Luteinizing Hormone	91-93	hypertrichosis 2 (generalised, congenital)	Homo sapiens	94-97
10706582-1	2000	This study investigates the relationship between the high density lipoprotein (HDL) receptor (scavenger receptors, SR-BI and SR-BII), selective lipoprotein-cholesteryl ester uptake, and testosterone production in Leydig cells of control, hypocholesterolemic and gonadotrophic hormone (hCG) treated rats.	Testosterone	186-198	hypertrichosis 2 (generalised, congenital)	Homo sapiens	285-288
10879180-3	2000	We synthesized PLEG copolymers containing PEG segments with various molecular weight and prepared hCG-loaded PL/PLEG blend microspheres to improve hCG entrapment efficiency.	copolymers	20-30	hypertrichosis 2 (generalised, congenital)	Homo sapiens	98-101
10600792-4	1999	hCG stimulation increased peripheral levels of testosterone, 17OH-progesterone, androstenedione, dehydroepiandrosterone, and 17beta-estradiol, without affecting circulating pregnenolone and progesterone values.	Testosterone	47-59	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
10652208-7	2000	Androstenedione secretion as a result of stimulation by 100 ng/ml hCG was significantly higher in the culture medium of the follicles with theca cells than in those of collagenase-pretreated follicles (p &lt; 0.0001), indicating that the cells attached to the outside of the basement membrane were actually functional theca cells, not interstitial cells.	Androstenedione	0-15	hypertrichosis 2 (generalised, congenital)	Homo sapiens	66-69
10634376-6	2000	Inhibin B and the hCG-induced testosterone increment correlated strongly (r = 0.84; P&lt;0.0001).	Testosterone	30-42	hypertrichosis 2 (generalised, congenital)	Homo sapiens	18-21
10634376-8	2000	Inhibin B and the testosterone response to hCG were low in boys with testicular damage (delayed diagnosis of cryptorchidism; after testicular torsion) and in patients with gonadal dysgenesis, but were normal or increased in children with androgen insensitivity syndrome.	Testosterone	18-30	hypertrichosis 2 (generalised, congenital)	Homo sapiens	43-46
10634376-9	2000	We conclude that basal inhibin B predicts the testosterone response to hCG in boys and therefore gives reliable information about both the presence and function of the testes.	Testosterone	46-58	hypertrichosis 2 (generalised, congenital)	Homo sapiens	71-74
20681137-8	2000	The variation in the interval from PGF2alpha administration to ovulation in ablated mares was reduced further by hCG administration.	Dinoprost	35-44	hypertrichosis 2 (generalised, congenital)	Homo sapiens	113-116
10818405-3	2000	Most of these substances, such as growth factors and cytokines, do not have independent effects on basal androgen production, but exhibit their regulatory potential by modulating hCG- or LH-stimulated steroid production.	Steroids	201-208	hypertrichosis 2 (generalised, congenital)	Homo sapiens	179-182
10796710-19	2000	This as a result of inadequately declining serum hCG concentrations after one single dose of methotrexate necessitating additional methotrexate injections or surgical interventions.	Methotrexate	131-143	hypertrichosis 2 (generalised, congenital)	Homo sapiens	49-52
10796710-23	2000	Only in patients with low initial serum hCG concentrations systemic methotrexate leads to costs savings compared to laparoscopic salpingostomy.	Methotrexate	68-80	hypertrichosis 2 (generalised, congenital)	Homo sapiens	40-43
10698046-7	2000	These results suggest that the expression of KGF, which is induced in endometrial/decidual cells by progesterone, plays an important role in the embryo-endometrial/ decidual interaction by stimulating hCG secretion rather than affecting cell proliferation.	Progesterone	100-112	hypertrichosis 2 (generalised, congenital)	Homo sapiens	201-204
11096352-5	2000	First, MCF-7 cell growth was stimulated by DHEA in a concentration-dependent manner with a maximal effect at 10(-4) M. Although hCG alone did not have a significant proliferative effect, hCG significantly and dose dependently stimulated MCF-7 cell growth in the presence of a submaximal concentration of DHEA (10(-7 )M).	Dehydroepiandrosterone	43-47	hypertrichosis 2 (generalised, congenital)	Homo sapiens	187-190
11096352-5	2000	First, MCF-7 cell growth was stimulated by DHEA in a concentration-dependent manner with a maximal effect at 10(-4) M. Although hCG alone did not have a significant proliferative effect, hCG significantly and dose dependently stimulated MCF-7 cell growth in the presence of a submaximal concentration of DHEA (10(-7 )M).	Dehydroepiandrosterone	304-308	hypertrichosis 2 (generalised, congenital)	Homo sapiens	187-190
11096352-6	2000	This stimulatory effect of DHEA and hCG was blocked by a pure antiestrogen ICI182,780 and an aromatase inhibitor, arimidex.	Anastrozole	114-122	hypertrichosis 2 (generalised, congenital)	Homo sapiens	36-39
11096352-8	2000	These results indicate that MCF-7 cells intrinsically converted DHEA into E(2) upon hCG stimulation, then grew their own cells DHEA- and hCG-dependently.	Dehydroepiandrosterone	64-68	hypertrichosis 2 (generalised, congenital)	Homo sapiens	84-87
10600792-4	1999	hCG stimulation increased peripheral levels of testosterone, 17OH-progesterone, androstenedione, dehydroepiandrosterone, and 17beta-estradiol, without affecting circulating pregnenolone and progesterone values.	17-alpha-Hydroxyprogesterone	61-78	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
10600792-4	1999	hCG stimulation increased peripheral levels of testosterone, 17OH-progesterone, androstenedione, dehydroepiandrosterone, and 17beta-estradiol, without affecting circulating pregnenolone and progesterone values.	Androstenedione	80-95	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
10600792-4	1999	hCG stimulation increased peripheral levels of testosterone, 17OH-progesterone, androstenedione, dehydroepiandrosterone, and 17beta-estradiol, without affecting circulating pregnenolone and progesterone values.	Dehydroepiandrosterone	97-119	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
10600792-4	1999	hCG stimulation increased peripheral levels of testosterone, 17OH-progesterone, androstenedione, dehydroepiandrosterone, and 17beta-estradiol, without affecting circulating pregnenolone and progesterone values.	Estradiol	125-141	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
10600792-4	1999	hCG stimulation increased peripheral levels of testosterone, 17OH-progesterone, androstenedione, dehydroepiandrosterone, and 17beta-estradiol, without affecting circulating pregnenolone and progesterone values.	Progesterone	66-78	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
10600792-6	1999	Moreover, the drug significantly reduced the response of testosterone, 17OH-progesterone, androstenedione, and dehydroepiandrosterone to hCG, as assessed by the mean integrated area under the curve, whereas it did not influence 17beta-estradiol response.	Testosterone	57-69	hypertrichosis 2 (generalised, congenital)	Homo sapiens	137-140
10600792-6	1999	Moreover, the drug significantly reduced the response of testosterone, 17OH-progesterone, androstenedione, and dehydroepiandrosterone to hCG, as assessed by the mean integrated area under the curve, whereas it did not influence 17beta-estradiol response.	17-alpha-Hydroxyprogesterone	71-88	hypertrichosis 2 (generalised, congenital)	Homo sapiens	137-140
10600792-6	1999	Moreover, the drug significantly reduced the response of testosterone, 17OH-progesterone, androstenedione, and dehydroepiandrosterone to hCG, as assessed by the mean integrated area under the curve, whereas it did not influence 17beta-estradiol response.	Androstenedione	90-105	hypertrichosis 2 (generalised, congenital)	Homo sapiens	137-140
10600792-6	1999	Moreover, the drug significantly reduced the response of testosterone, 17OH-progesterone, androstenedione, and dehydroepiandrosterone to hCG, as assessed by the mean integrated area under the curve, whereas it did not influence 17beta-estradiol response.	Dehydroepiandrosterone	111-133	hypertrichosis 2 (generalised, congenital)	Homo sapiens	137-140
10575580-2	1999	However, no data are available to evaluate if patients alter their endometrial thickness and pattern between the day of hCG administration (DhCG) and the day of oocyte retrieval (DRET) and whether these changes adversely affect endometrial receptivity.	dhcg	140-144	hypertrichosis 2 (generalised, congenital)	Homo sapiens	120-123
11360643-1	1999	OBJECTIVE: To investigate the effects of mifepristone on cell proliferation and hCG secretion of human choriocarcinoma cell line JAR and the cytotoxic effects of mifepristone on this cell line.	Mifepristone	41-53	hypertrichosis 2 (generalised, congenital)	Homo sapiens	80-83
10613402-4	1999	The higher concentration of AZT and ddI produced significant (P &lt; 0.025) reductions in cell numbers and growth rate while producing significant increases in hormone production (hCG, E2, and P4).	Zidovudine	28-31	hypertrichosis 2 (generalised, congenital)	Homo sapiens	180-183
10613402-4	1999	The higher concentration of AZT and ddI produced significant (P &lt; 0.025) reductions in cell numbers and growth rate while producing significant increases in hormone production (hCG, E2, and P4).	Didanosine	36-39	hypertrichosis 2 (generalised, congenital)	Homo sapiens	180-183
10544750-17	1999	For thyroid morphology diseases, the problem is generally one of differentiated thyroid cancer, particular as the frequency is probably higher during pregnancy, the course being aggravated by the TSH-like effect of hCG, and curative treatment with radioactive iodine which cannot be started unless there is no risk of pregnancy.	Thyrotropin	196-199	hypertrichosis 2 (generalised, congenital)	Homo sapiens	215-218
10571964-13	1999	CONCLUSION: It was shown that steroid secretory pattern of follicular cells changed during the year and that the three factors used (pituitary homogenate, hCG and 17alpha,20 betaOH-P) exerted direct influence upon steroids secretion.	Steroids	214-222	hypertrichosis 2 (generalised, congenital)	Homo sapiens	155-158
10645245-2	1999	Pre-treatment of the cells with both oestradiol and medroxyprogesterone acetate was required for MAP kinase activation and COX-2 expression to respond to PAF and hCG.	Estradiol	37-47	hypertrichosis 2 (generalised, congenital)	Homo sapiens	162-165
10645245-2	1999	Pre-treatment of the cells with both oestradiol and medroxyprogesterone acetate was required for MAP kinase activation and COX-2 expression to respond to PAF and hCG.	Medroxyprogesterone Acetate	52-79	hypertrichosis 2 (generalised, congenital)	Homo sapiens	162-165
10645245-4	1999	In contrast, hCG-induced MAP kinase activation was sensitive to PD098059 and protein kinase A inhibitor, H-89, but not to wortmannin.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	64-72	hypertrichosis 2 (generalised, congenital)	Homo sapiens	13-16
10645245-4	1999	In contrast, hCG-induced MAP kinase activation was sensitive to PD098059 and protein kinase A inhibitor, H-89, but not to wortmannin.	N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide	105-109	hypertrichosis 2 (generalised, congenital)	Homo sapiens	13-16
10560952-1	1999	In a previous study we observed increased serum levels of a 3,3"-diiodothyronine sulfate (T2S)-like material (compound W) in women who received human chorionic gonadotropin (hCG) treatment.	3,3"-diiodothyronine sulfate	60-88	hypertrichosis 2 (generalised, congenital)	Homo sapiens	174-177
10560952-1	1999	In a previous study we observed increased serum levels of a 3,3"-diiodothyronine sulfate (T2S)-like material (compound W) in women who received human chorionic gonadotropin (hCG) treatment.	t2s	90-93	hypertrichosis 2 (generalised, congenital)	Homo sapiens	174-177
11360643-6	1999	When the JAR cells were exposed to 5 mumol/L mifepristone for 72 h, the expression of Ki-67 antigen was declined and the amount of hCG secretion was decreased significantly at the third day.	Mifepristone	45-57	hypertrichosis 2 (generalised, congenital)	Homo sapiens	131-134
11360643-7	1999	CONCLUSION: In vitro, mifepristone has cytostatic and cytotoxic effects on JAR cell line and may inhibit the secretion of hCG in JAR cells.	Mifepristone	22-34	hypertrichosis 2 (generalised, congenital)	Homo sapiens	122-125
10411533-9	1999	Both in vivo and in vitro, hCG induced expression of the progesterone receptor and the prostaglandin endoperoxide synthase-2 (PGS-2) gene within 3 h. Ovulation could be completely blocked with the anti-progestogen Org-31710 and partially (50%) with the PGS inhibitor indomethacin in vitro and in vivo.	Indomethacin	267-279	hypertrichosis 2 (generalised, congenital)	Homo sapiens	27-30
11776570-2	1999	METHODS: Radioimmunodetection was performed with a cocktail of 131I-labeled mouse anti-hCG monoclonal antibodies to image xenogaft of human trophoblastic cancer in nude mice.	Iodine-131	63-67	hypertrichosis 2 (generalised, congenital)	Homo sapiens	87-90
10497920-1	1999	The present study was designed to investigate the effect of the opioid agonist FK 33-824 on basal and hCG-induced progesterone (P4), cAMP and cGMP secretion and on the phosphoinositide-specific phospholipase C signalling system in separated porcine small (SLCs) and large luteal cells (LLCs).	Progesterone	114-126	hypertrichosis 2 (generalised, congenital)	Homo sapiens	102-105
10497920-1	1999	The present study was designed to investigate the effect of the opioid agonist FK 33-824 on basal and hCG-induced progesterone (P4), cAMP and cGMP secretion and on the phosphoinositide-specific phospholipase C signalling system in separated porcine small (SLCs) and large luteal cells (LLCs).	Cyclic AMP	133-137	hypertrichosis 2 (generalised, congenital)	Homo sapiens	102-105
10497920-1	1999	The present study was designed to investigate the effect of the opioid agonist FK 33-824 on basal and hCG-induced progesterone (P4), cAMP and cGMP secretion and on the phosphoinositide-specific phospholipase C signalling system in separated porcine small (SLCs) and large luteal cells (LLCs).	Cyclic GMP	142-146	hypertrichosis 2 (generalised, congenital)	Homo sapiens	102-105
10497920-8	1999	In the presence of hCG, cAMP secretion by both SLCs and LLCs was many-fold higher than in the control group.	Cyclic AMP	24-28	hypertrichosis 2 (generalised, congenital)	Homo sapiens	19-22
10497920-9	1999	As regards cGMP output, only LLCs showed elevated secretion of this cyclic nucleotide under the influence of hCG.	Nucleotides, Cyclic	68-85	hypertrichosis 2 (generalised, congenital)	Homo sapiens	109-112
10419734-9	1999	Although serum hCG levels progressively decreased during pregnancy in one patient without PTT, hCG levels initially decreased, but subsequently increased or showed a plateau with advancing gestational age in two patients with PTT.	Bialaphos	226-229	hypertrichosis 2 (generalised, congenital)	Homo sapiens	95-98
10532708-4	1999	Although glycoprotein hormones like hCG are mainly hormonogenic, their action in the latter process involves the efflux or conductance of halide ions.	halide	138-144	hypertrichosis 2 (generalised, congenital)	Homo sapiens	36-39
10532708-5	1999	Since the basis of fluid secretion is an active efflux of ions such as chloride stimulated by a humoral agent, accompanied by a passive diffusion of water across a cell wall, I hypothesize that hCG is also a secretory hormone and responsible for fluid fluxes in the above and other clinical situations.	Chlorides	71-79	hypertrichosis 2 (generalised, congenital)	Homo sapiens	194-197
10532708-5	1999	Since the basis of fluid secretion is an active efflux of ions such as chloride stimulated by a humoral agent, accompanied by a passive diffusion of water across a cell wall, I hypothesize that hCG is also a secretory hormone and responsible for fluid fluxes in the above and other clinical situations.	Water	149-154	hypertrichosis 2 (generalised, congenital)	Homo sapiens	194-197
10381263-8	1999	Administration of digitoxin in vitro resulted in an inhibition of both basal and hCG- as well as 8-Br-cAMP-stimulated release of testosterone.	Digitoxin	18-27	hypertrichosis 2 (generalised, congenital)	Homo sapiens	81-84
10381263-7	1999	Intravenous injection of digitoxin decreased hCG-stimulated, but not basal, plasma testosterone levels.	Digitoxin	25-34	hypertrichosis 2 (generalised, congenital)	Homo sapiens	45-48
10381263-9	1999	In addition, digitoxin diminished hCG-stimulated cAMP accumulation in rat testicular interstitial cells.	Digitoxin	13-22	hypertrichosis 2 (generalised, congenital)	Homo sapiens	34-37
10381263-9	1999	In addition, digitoxin diminished hCG-stimulated cAMP accumulation in rat testicular interstitial cells.	Cyclic AMP	49-53	hypertrichosis 2 (generalised, congenital)	Homo sapiens	34-37
10381267-7	1999	After the challenge of hCG or GnRH, the AP-grafted rats showed a suppressed response in testosterone release as compared to those in the CX-grafted group.	Testosterone	88-100	hypertrichosis 2 (generalised, congenital)	Homo sapiens	23-26
10381267-8	1999	The in vitro data from the AP-grafted rats compared to the CX-grafted animals showed a diminished response in testosterone release upon hCG stimulation.	Testosterone	110-122	hypertrichosis 2 (generalised, congenital)	Homo sapiens	136-139
10086936-13	1999	CONCLUSION: Although a positive hCG test excludes biosynthetic defects of testosterone, an inadequate response does not exclude AIS.	Testosterone	74-86	hypertrichosis 2 (generalised, congenital)	Homo sapiens	32-35
10330104-15	1999	In addition, induction of maturation by FSH, hCG, or pyrroline carboxylate was accompanied by a significant increase in the oxidation of [1-14C]glucose but not [6-14C]glucose by OCC, supporting a proposed role for the pentose phosphate pathway in meiotic induction.	Carbon-14	140-143	hypertrichosis 2 (generalised, congenital)	Homo sapiens	45-48
10330104-15	1999	In addition, induction of maturation by FSH, hCG, or pyrroline carboxylate was accompanied by a significant increase in the oxidation of [1-14C]glucose but not [6-14C]glucose by OCC, supporting a proposed role for the pentose phosphate pathway in meiotic induction.	Glucose	144-151	hypertrichosis 2 (generalised, congenital)	Homo sapiens	45-48
10330104-15	1999	In addition, induction of maturation by FSH, hCG, or pyrroline carboxylate was accompanied by a significant increase in the oxidation of [1-14C]glucose but not [6-14C]glucose by OCC, supporting a proposed role for the pentose phosphate pathway in meiotic induction.	Pentosephosphates	218-235	hypertrichosis 2 (generalised, congenital)	Homo sapiens	45-48
10342884-1	1999	The present studies showed that sequential treatment with equine CG (eCG) and hCG not only induced an increase in ovarian weight, but also caused an estimated 4.6-fold increase in the number of ovarian surface epithelial cells.	epicatechin gallate	69-72	hypertrichosis 2 (generalised, congenital)	Homo sapiens	65-67
10336821-7	1999	In vitro treatment with hCG and protein kinase A (PKA) activators (dbcAMP and forskolin) induced ovarian Cx32.2 mRNA levels and OMC.	Bucladesine	67-73	hypertrichosis 2 (generalised, congenital)	Homo sapiens	24-27
10336821-7	1999	In vitro treatment with hCG and protein kinase A (PKA) activators (dbcAMP and forskolin) induced ovarian Cx32.2 mRNA levels and OMC.	Colforsin	78-87	hypertrichosis 2 (generalised, congenital)	Homo sapiens	24-27
10098511-3	1999	The present study was designed to explore the mechanisms of extracellular calcium (Ca2+) involved in the hCG-stimulated expression of StAR protein and steroidogenesis in a mouse Leydig tumor cell line (mLTC-1).	Calcium	74-81	hypertrichosis 2 (generalised, congenital)	Homo sapiens	105-108
10218972-7	1999	PACAP 38 (5 x 10(-9) M), in combination with an approximately half-maximal dose of hCG (1 ng/ml), showed an additive effect on progesterone accumulation.	Progesterone	127-139	hypertrichosis 2 (generalised, congenital)	Homo sapiens	83-86
10098511-5	1999	The potentiating effect of Ca2+ on the hCG-stimulated StAR response correlated with the acute progesterone (P) response.	Progesterone	94-106	hypertrichosis 2 (generalised, congenital)	Homo sapiens	39-42
10098511-6	1999	In accordance, omission of Ca2+ from the extracellular medium by specific Ca2+ chelators, EDTA or EGTA (4 mmol/liter each), markedly diminished the hCG-stimulated P production.	Edetic Acid	90-94	hypertrichosis 2 (generalised, congenital)	Homo sapiens	148-151
10098511-6	1999	In accordance, omission of Ca2+ from the extracellular medium by specific Ca2+ chelators, EDTA or EGTA (4 mmol/liter each), markedly diminished the hCG-stimulated P production.	Egtazic Acid	98-102	hypertrichosis 2 (generalised, congenital)	Homo sapiens	148-151
10098511-7	1999	The Ca2+ effect on hCG-induced StAR mRNA expression was dramatically suppressed by 10 micromol/liter verapamil, a Ca2+ channel blocker.	Verapamil	101-110	hypertrichosis 2 (generalised, congenital)	Homo sapiens	19-22
10098511-8	1999	The Ca2+-mobilizing agonist, potassium (K+; 4 mmol/liter), greatly increased the hCG responses of StAR expression and P production, which conversely were attenuated by Ca2+ antagonists, further supporting the involvement of intracellular free Ca2+ ([Ca2+]i) in these responses.	Potassium	29-38	hypertrichosis 2 (generalised, congenital)	Homo sapiens	81-84
10098511-10	1999	Inhibition of protein synthesis by cycloheximide (CHX) drastically diminished the hCG-induced StAR protein content, indicating the requirement for on-going protein synthesis for hCG action.	Cycloheximide	35-48	hypertrichosis 2 (generalised, congenital)	Homo sapiens	82-85
10098511-10	1999	Inhibition of protein synthesis by cycloheximide (CHX) drastically diminished the hCG-induced StAR protein content, indicating the requirement for on-going protein synthesis for hCG action.	Cycloheximide	50-53	hypertrichosis 2 (generalised, congenital)	Homo sapiens	82-85
10098511-12	1999	[Ca2+]i moderately augmented the response to hCG in fura-2/AM-loaded mLTC-1 cells within 30-40 sec, reaching a plateau within 1-3 min.	Fura-2	52-58	hypertrichosis 2 (generalised, congenital)	Homo sapiens	45-48
10098511-12	1999	[Ca2+]i moderately augmented the response to hCG in fura-2/AM-loaded mLTC-1 cells within 30-40 sec, reaching a plateau within 1-3 min.	mltc-1	69-75	hypertrichosis 2 (generalised, congenital)	Homo sapiens	45-48
10098511-13	1999	Interestingly, the calcium ionophore (A23187) clearly increased (P &lt; 0.01) StAR mRNA expression, in additive fashion with hCG.	Calcium	19-26	hypertrichosis 2 (generalised, congenital)	Homo sapiens	125-128
10098511-13	1999	Interestingly, the calcium ionophore (A23187) clearly increased (P &lt; 0.01) StAR mRNA expression, in additive fashion with hCG.	Calcimycin	38-44	hypertrichosis 2 (generalised, congenital)	Homo sapiens	125-128
10391520-2	1999	In all three cases, hCG in serum was negative but despite this a single injection of methotrexate successfully treated the condition.	Methotrexate	85-97	hypertrichosis 2 (generalised, congenital)	Homo sapiens	20-23
9843781-8	1998	Administration of hCG to female rats in vivo caused a significant increase in HCO-3 and K+ secretion from the duodenum and pancreas.	7 alpha-hydroxy-4-cholesten-3-one	78-81	hypertrichosis 2 (generalised, congenital)	Homo sapiens	18-21
10098511-16	1999	Stimulation of hCG significantly elevated (2.1 +/- 0.3-fold) the SF-1 mRNA level, which was further augmented in the presence of Ca2+, whereas EGTA and verapamil completely abolished the increase caused by Ca2+.	Egtazic Acid	143-147	hypertrichosis 2 (generalised, congenital)	Homo sapiens	15-18
10098511-16	1999	Stimulation of hCG significantly elevated (2.1 +/- 0.3-fold) the SF-1 mRNA level, which was further augmented in the presence of Ca2+, whereas EGTA and verapamil completely abolished the increase caused by Ca2+.	Verapamil	152-161	hypertrichosis 2 (generalised, congenital)	Homo sapiens	15-18
10202883-10	1999	CONCLUSION(S): In a cohort of 192 women, the minimum plasma progesterone concentration on day 7 in women who attained a full-term pregnancy after induction of ovulation with 5,000 IU of hCG was 10.83 ng/mL.	Progesterone	60-72	hypertrichosis 2 (generalised, congenital)	Homo sapiens	186-189
10327141-2	1999	Hyperglycosylated hCG is a form of hCG with more complex oligosaccharide side chains.	Oligosaccharides	57-72	hypertrichosis 2 (generalised, congenital)	Homo sapiens	18-21
10327141-2	1999	Hyperglycosylated hCG is a form of hCG with more complex oligosaccharide side chains.	Oligosaccharides	57-72	hypertrichosis 2 (generalised, congenital)	Homo sapiens	35-38
10327141-13	1999	A trend was observed, hyperglycosylated hCG MoM values decreasing with advancing creatinine concentration (1.77, 1.08, 1.01, 0.73 and 0.60 at 0.25, 0.50, 0.79, 1.11 and 1.73 mg/ml, respectively).	Creatinine	81-91	hypertrichosis 2 (generalised, congenital)	Homo sapiens	40-43
10729013-9	1999	Transfer of 125I-GnRH from the cavernous sinus to the carotid rete was inhibited by hCG in ewes pretreated with estradiol benzoate but not with oil (P&lt;0.005).	125i-gnrh	12-21	hypertrichosis 2 (generalised, congenital)	Homo sapiens	84-87
10729013-9	1999	Transfer of 125I-GnRH from the cavernous sinus to the carotid rete was inhibited by hCG in ewes pretreated with estradiol benzoate but not with oil (P&lt;0.005).	estradiol 3-benzoate	112-130	hypertrichosis 2 (generalised, congenital)	Homo sapiens	84-87
9935138-11	1999	CONCLUSION(S): End-follicular phase elevation in plasma progesterone (&gt;0.9 ng/mL on the day of hCG administration) was associated with a faster increase in endometrial echogenicity during the early luteal phase of COH cycles.	Progesterone	56-68	hypertrichosis 2 (generalised, congenital)	Homo sapiens	98-101
11462118-10	1999	Melatonin reduced estradiol release from hCG stimulated ovaries of middle-aged rats.	Melatonin	0-9	hypertrichosis 2 (generalised, congenital)	Homo sapiens	41-44
11462118-10	1999	Melatonin reduced estradiol release from hCG stimulated ovaries of middle-aged rats.	Estradiol	18-27	hypertrichosis 2 (generalised, congenital)	Homo sapiens	41-44
10850379-2	1999	hCG treatment at different doses (25, 50 and 100 I.U./Kg/day) for 5 days was found to significantly increase the plasma levels of hCG, estradiol and progesterone in a dose-dependent manner, while the concentrations of LH and FSH remained below the detection levels.	Estradiol	135-144	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
10850379-2	1999	hCG treatment at different doses (25, 50 and 100 I.U./Kg/day) for 5 days was found to significantly increase the plasma levels of hCG, estradiol and progesterone in a dose-dependent manner, while the concentrations of LH and FSH remained below the detection levels.	Progesterone	149-161	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
10850379-2	1999	hCG treatment at different doses (25, 50 and 100 I.U./Kg/day) for 5 days was found to significantly increase the plasma levels of hCG, estradiol and progesterone in a dose-dependent manner, while the concentrations of LH and FSH remained below the detection levels.	Luteinizing Hormone	218-220	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
9861323-3	1998	The aim of this study was to determine the occurrence rate of GTH and the relation between serum levels of hCG, free T4 (fT4), and TSH in a large number of pregnant women.	gth	62-65	hypertrichosis 2 (generalised, congenital)	Homo sapiens	107-110
9990229-3	1998	A 29-year-old male was referred to our hospital for the treatment of progressive lung metastases with elevated hCG level, which had recurred after complete remission following 3 courses of BEP chemotherapy and progressed after transient partial regression following 2 courses of intensified EP chemotherapy.	BEP protocol	189-192	hypertrichosis 2 (generalised, congenital)	Homo sapiens	111-114
9745981-5	1998	Melatonin (0.1-10 ng/ml) had no effect on steroid production in the absence of hCG, but melatonin decreased progesterone and estradiol production by preovulatory follicles in a dose-dependent and time-dependent manner in the presence of hCG (100 mIU/ml).	Melatonin	88-97	hypertrichosis 2 (generalised, congenital)	Homo sapiens	237-240
9861323-15	1998	Using regression analyses, the concentration of fT4 was correlated with hCG levels in women with GTH (P &lt; 0.05, r = 0.269), whereas the concentration of TSH was not correlated with hCG or fT4 level.	CHEMBL179036	48-51	hypertrichosis 2 (generalised, congenital)	Homo sapiens	72-75
9840564-1	1998	OBJECTIVE: To evaluate resolution of serum hCG and progesterone in patients with ectopic pregnancy receiving single-dose intramuscular (IM) methotrexate as compared with those undergoing laparoscopic salpingostomy.	Methotrexate	140-152	hypertrichosis 2 (generalised, congenital)	Homo sapiens	43-46
9840564-4	1998	Methotrexate therapy was repeated if posttreatment day 7 hCG levels did not decrease by 15%, as compared with day 4 levels.	Methotrexate	0-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	57-60
9840564-11	1998	Mean time required for hCG concentrations to decrease to less than 15 mIU/mL was significantly less for laparoscopic salpingostomy than for methotrexate therapy: 20.2+/-2.7 and 27.2+/-2.3 days, respectively (P &lt; .05).	Methotrexate	140-152	hypertrichosis 2 (generalised, congenital)	Homo sapiens	23-26
9840564-13	1998	Initial serum hCG levels for patients receiving additional methotrexate doses were 4830+/-1588 mIU/mL as compared with 2133+/-393 mIU/mL for women receiving only one dose (P = .07).	Methotrexate	59-71	hypertrichosis 2 (generalised, congenital)	Homo sapiens	14-17
9840564-16	1998	Initial hCG levels may be a marker for women requiring additional doses of methotrexate.	Methotrexate	75-87	hypertrichosis 2 (generalised, congenital)	Homo sapiens	8-11
9772104-3	1998	Depressed human chorionic gonadotropin (hCG)-stimulated T response was seen over a 48-h culture of testicular interstitial cells obtained from the animals exposed to 20 mg/kg or higher dose of NiSO4, while the basal T production remained unaltered.	nickel sulfate	193-198	hypertrichosis 2 (generalised, congenital)	Homo sapiens	40-43
9772104-7	1998	Dose-dependent depression in hCG-stimulated T production was seen at 125 microM or higher dose of Ni2+, while basal T production was unaffected.	Nickel(2+)	98-102	hypertrichosis 2 (generalised, congenital)	Homo sapiens	29-32
9772104-9	1998	Decreased hCG-stimulated T production was found in the cultures maintained at least for 4 h in the presence of 1000 microM Ni2+, whereas at 250 microM at least 16 h was required to elicit the depression.	Nickel(2+)	123-127	hypertrichosis 2 (generalised, congenital)	Homo sapiens	10-13
9785042-4	1998	The secretion of hCG is activated by the PKC-activator TPA.	Tetradecanoylphorbol Acetate	55-58	hypertrichosis 2 (generalised, congenital)	Homo sapiens	17-20
9785042-5	1998	TPA induces hCG release into the medium, thus causing a decrease in intracellular hCG content.	Tetradecanoylphorbol Acetate	0-3	hypertrichosis 2 (generalised, congenital)	Homo sapiens	12-15
9785042-5	1998	TPA induces hCG release into the medium, thus causing a decrease in intracellular hCG content.	Tetradecanoylphorbol Acetate	0-3	hypertrichosis 2 (generalised, congenital)	Homo sapiens	82-85
9785042-6	1998	In contrast, db-cAMP inhibites hCG secretion into the medium.	Bucladesine	13-20	hypertrichosis 2 (generalised, congenital)	Homo sapiens	31-34
9861323-16	1998	The concentrations (M +/- SD) of fT4, TSH, and hCG in women with GTH were 42.5 +/- 12.3 pmol/l, 0.20 +/- 0.31 mU/l and 190.2 +/- 98.8 x 10(3) IU/l, whereas those of controls were 14.6 +/- 3.8 pmol/l, 1.43 +/- 1.25 mU/l and 60.1 +/- 45.1 x 10(3) IU/l.	gth	65-68	hypertrichosis 2 (generalised, congenital)	Homo sapiens	47-50
9861323-8	1998	Regression analysis was performed for the comparison between hCG, fT4, and TSH levels in women with GTH.	gth	100-103	hypertrichosis 2 (generalised, congenital)	Homo sapiens	61-64
9861323-15	1998	Using regression analyses, the concentration of fT4 was correlated with hCG levels in women with GTH (P &lt; 0.05, r = 0.269), whereas the concentration of TSH was not correlated with hCG or fT4 level.	gth	97-100	hypertrichosis 2 (generalised, congenital)	Homo sapiens	72-75
10732136-3	1998	In prepuberal gilts treated with PMSG/hCG the follicular progesterone level has been shown to increase sharply before ovulation.	Progesterone	57-69	hypertrichosis 2 (generalised, congenital)	Homo sapiens	38-41
9740689-9	1998	Two of them (12.5%) had poor response to MTX with unsatisfactory fall in serum hCG levels requiring change of chemotherapy to actinomycin D.	Methotrexate	41-44	hypertrichosis 2 (generalised, congenital)	Homo sapiens	79-82
9740689-9	1998	Two of them (12.5%) had poor response to MTX with unsatisfactory fall in serum hCG levels requiring change of chemotherapy to actinomycin D.	Dactinomycin	126-139	hypertrichosis 2 (generalised, congenital)	Homo sapiens	79-82
9705964-5	1998	B-hCG maintained its ability to bind specifically to rat testicular membranes and was also bound to streptavidin-coated polypropylene wells.	Polypropylenes	120-133	hypertrichosis 2 (generalised, congenital)	Homo sapiens	2-5
9705964-6	1998	cAMP production was induced in BLT-1 Leydig tumor cells in vitro after stimulation with B-hCG, as a sign of persistent bioactivity.	Cyclic AMP	0-4	hypertrichosis 2 (generalised, congenital)	Homo sapiens	90-93
9793975-1	1998	Hyperglycosylated hCG (H-hCG) is a minor variant of hCG with abnormal oligosaccharide side chains.	Oligosaccharides	70-85	hypertrichosis 2 (generalised, congenital)	Homo sapiens	18-21
9793975-1	1998	Hyperglycosylated hCG (H-hCG) is a minor variant of hCG with abnormal oligosaccharide side chains.	Oligosaccharides	70-85	hypertrichosis 2 (generalised, congenital)	Homo sapiens	25-28
9793975-1	1998	Hyperglycosylated hCG (H-hCG) is a minor variant of hCG with abnormal oligosaccharide side chains.	Oligosaccharides	70-85	hypertrichosis 2 (generalised, congenital)	Homo sapiens	25-28
9696237-11	1998	Serum hCG clearance curves do enable the timely detection of inadequately declining serum hCG concentrations, for which additional methotrexate can be administered.	Methotrexate	131-143	hypertrichosis 2 (generalised, congenital)	Homo sapiens	6-9
9696237-11	1998	Serum hCG clearance curves do enable the timely detection of inadequately declining serum hCG concentrations, for which additional methotrexate can be administered.	Methotrexate	131-143	hypertrichosis 2 (generalised, congenital)	Homo sapiens	90-93
9565650-3	1998	Following binding of eosin isothiocyanate-derivatized ovine LH or human chorionic gonadotropin (hCG), five proteins with molecular weights of 71, 57, 55, 49 and 36 kDa were selectively derivatized with [125I]-INA following 2 h exposure at 22 degreesC to 514 nm light.	eosine-5-isothiocyanate	21-41	hypertrichosis 2 (generalised, congenital)	Homo sapiens	96-99
9674993-7	1998	In further experiments, preincubation of follicles with hCG was found to reduce 5-HT inhibitory action, but when follicles were incubated with either hCG in the presence of a steroidogenesis inhibitor or estradiol-17beta (E2), the 5-HT inhibition was unaffected.	Estradiol	204-220	hypertrichosis 2 (generalised, congenital)	Homo sapiens	56-59
9674993-7	1998	In further experiments, preincubation of follicles with hCG was found to reduce 5-HT inhibitory action, but when follicles were incubated with either hCG in the presence of a steroidogenesis inhibitor or estradiol-17beta (E2), the 5-HT inhibition was unaffected.	Estradiol	222-224	hypertrichosis 2 (generalised, congenital)	Homo sapiens	56-59
9741835-7	1998	Prostaglandin F2alpha (10(-6) M) significantly inhibited hCG (1 IU/mL), Iso (10(-5) M), CTX (1 microg/mL), and forskolin- (10(-5) M) stimulated progesterone production.	Dinoprost	0-21	hypertrichosis 2 (generalised, congenital)	Homo sapiens	57-60
9741835-9	1998	The ability of PGF2alpha to inhibit hCG- or CTX-stimulated progesterone production was attenuated by pertussis toxin (PTX; 50 ng/mL).	Dinoprost	15-24	hypertrichosis 2 (generalised, congenital)	Homo sapiens	36-39
9741835-9	1998	The ability of PGF2alpha to inhibit hCG- or CTX-stimulated progesterone production was attenuated by pertussis toxin (PTX; 50 ng/mL).	Progesterone	59-71	hypertrichosis 2 (generalised, congenital)	Homo sapiens	36-39
9593605-1	1998	STUDY OBJECTIVE: To determine whether human chorionic gonadotropin (hCG) stimulation elicits an exaggerated 17-hydroxyprogesterone (17-OHP) response in patients with functional ovarian hyperandrogenism.	17-alpha-Hydroxyprogesterone	108-130	hypertrichosis 2 (generalised, congenital)	Homo sapiens	68-71
9593605-1	1998	STUDY OBJECTIVE: To determine whether human chorionic gonadotropin (hCG) stimulation elicits an exaggerated 17-hydroxyprogesterone (17-OHP) response in patients with functional ovarian hyperandrogenism.	17-alpha-Hydroxyprogesterone	132-138	hypertrichosis 2 (generalised, congenital)	Homo sapiens	68-71
9593605-5	1998	Steroid hormone responses to hCG stimulation were measured before and 30, 240, and 300 minutes after hCG injection.	Steroids	0-15	hypertrichosis 2 (generalised, congenital)	Homo sapiens	29-32
9593605-9	1998	After hCG stimulation, 17-hydroxyprogesterone concentrations significantly increased in the patients and were unchanged in the healthy controls.	17-alpha-Hydroxyprogesterone	23-45	hypertrichosis 2 (generalised, congenital)	Homo sapiens	6-9
9593605-10	1998	CONCLUSION: hCG stimulation elicited greater 17-hydroxyprogesterone responses in adolescent girls with functional ovarian hyperandrogenism compared with healthy controls.	17-alpha-Hydroxyprogesterone	45-67	hypertrichosis 2 (generalised, congenital)	Homo sapiens	12-15
29645229-12	1998	On the other hand, progesterone selectively inhibited pleise hCG (alpha, beta) mRNAs expression and decreased hCG secretion in normal placental tissues, whereas choriocarcinoma did not respond to progesterone.	Progesterone	19-31	hypertrichosis 2 (generalised, congenital)	Homo sapiens	61-64
9543166-9	1998	hCG testing demonstrated a high rate of conversion of delta4-androstenedione to estrone and of testosterone to estradiol in the propositus and his father.	Androstenedione	54-76	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
9543166-9	1998	hCG testing demonstrated a high rate of conversion of delta4-androstenedione to estrone and of testosterone to estradiol in the propositus and his father.	Estrone	80-87	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
9543166-9	1998	hCG testing demonstrated a high rate of conversion of delta4-androstenedione to estrone and of testosterone to estradiol in the propositus and his father.	Testosterone	95-107	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
9543166-9	1998	hCG testing demonstrated a high rate of conversion of delta4-androstenedione to estrone and of testosterone to estradiol in the propositus and his father.	Estradiol	111-120	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
9546788-3	1998	Using gel permeation chromatography of the clinical grade hCG and urine concentrates from pregnant women, we demonstrate that an as yet unidentified hCG associated factor (HAF) with anti-HIV, anti-SIV, anti-KS and pro-hematopoietic activities elutes as two peaks corresponding to 15-30 kDa and 2-4 kDa.	Potassium	207-209	hypertrichosis 2 (generalised, congenital)	Homo sapiens	149-152
9833610-19	1998	Binding of hCG to the LH/CG receptor are known to induce two signals, one for adenylyl cyclase/ cAMP and the other for phospholipase C/inositol phosphate/diacylglycerol.	Cyclic AMP	96-100	hypertrichosis 2 (generalised, congenital)	Homo sapiens	11-14
9833610-19	1998	Binding of hCG to the LH/CG receptor are known to induce two signals, one for adenylyl cyclase/ cAMP and the other for phospholipase C/inositol phosphate/diacylglycerol.	Cyclic AMP	96-100	hypertrichosis 2 (generalised, congenital)	Homo sapiens	12-14
9833610-19	1998	Binding of hCG to the LH/CG receptor are known to induce two signals, one for adenylyl cyclase/ cAMP and the other for phospholipase C/inositol phosphate/diacylglycerol.	Inositol Phosphates	135-153	hypertrichosis 2 (generalised, congenital)	Homo sapiens	11-14
9833610-19	1998	Binding of hCG to the LH/CG receptor are known to induce two signals, one for adenylyl cyclase/ cAMP and the other for phospholipase C/inositol phosphate/diacylglycerol.	Inositol Phosphates	135-153	hypertrichosis 2 (generalised, congenital)	Homo sapiens	12-14
9833610-19	1998	Binding of hCG to the LH/CG receptor are known to induce two signals, one for adenylyl cyclase/ cAMP and the other for phospholipase C/inositol phosphate/diacylglycerol.	Diglycerides	154-168	hypertrichosis 2 (generalised, congenital)	Homo sapiens	11-14
9833610-19	1998	Binding of hCG to the LH/CG receptor are known to induce two signals, one for adenylyl cyclase/ cAMP and the other for phospholipase C/inositol phosphate/diacylglycerol.	Diglycerides	154-168	hypertrichosis 2 (generalised, congenital)	Homo sapiens	12-14
9833611-12	1998	On the other hand, progesterone selectively inhibited pleise hCG (alpha, beta) mRNAs expression and decreased hCG secretion in normal placental tissues, whereas choriocarcinoma did not respond to progesterone.	Progesterone	19-31	hypertrichosis 2 (generalised, congenital)	Homo sapiens	61-64
9833611-12	1998	On the other hand, progesterone selectively inhibited pleise hCG (alpha, beta) mRNAs expression and decreased hCG secretion in normal placental tissues, whereas choriocarcinoma did not respond to progesterone.	Progesterone	19-31	hypertrichosis 2 (generalised, congenital)	Homo sapiens	110-113
9833611-15	1998	Characterization of choriocarcinoma hCG revealed that there are striking differences in carbohydrate structures between normal hCG and choriocarcinoma hCG.	Carbohydrates	88-100	hypertrichosis 2 (generalised, congenital)	Homo sapiens	36-39
9833611-15	1998	Characterization of choriocarcinoma hCG revealed that there are striking differences in carbohydrate structures between normal hCG and choriocarcinoma hCG.	Carbohydrates	88-100	hypertrichosis 2 (generalised, congenital)	Homo sapiens	127-130
9833611-15	1998	Characterization of choriocarcinoma hCG revealed that there are striking differences in carbohydrate structures between normal hCG and choriocarcinoma hCG.	Carbohydrates	88-100	hypertrichosis 2 (generalised, congenital)	Homo sapiens	127-130
9833611-16	1998	Sialic acid content in choriocarcinoma hCG was extremely lower compared to that in normal hCG.	N-Acetylneuraminic Acid	0-11	hypertrichosis 2 (generalised, congenital)	Homo sapiens	39-42
9833611-17	1998	The detection of the alteration in hCG sugar chains is useful for biochemical diagnosis of choriocarcinoma.	Sugars	39-44	hypertrichosis 2 (generalised, congenital)	Homo sapiens	35-38
29645229-12	1998	On the other hand, progesterone selectively inhibited pleise hCG (alpha, beta) mRNAs expression and decreased hCG secretion in normal placental tissues, whereas choriocarcinoma did not respond to progesterone.	Progesterone	19-31	hypertrichosis 2 (generalised, congenital)	Homo sapiens	110-113
29645229-15	1998	Characterization of choriocarcinoma hCG revealed that there are striking differences in carbohydrate structures between normal hCG and choriocarcinoma hCG.	Carbohydrates	88-100	hypertrichosis 2 (generalised, congenital)	Homo sapiens	36-39
29645229-15	1998	Characterization of choriocarcinoma hCG revealed that there are striking differences in carbohydrate structures between normal hCG and choriocarcinoma hCG.	Carbohydrates	88-100	hypertrichosis 2 (generalised, congenital)	Homo sapiens	127-130
29645229-15	1998	Characterization of choriocarcinoma hCG revealed that there are striking differences in carbohydrate structures between normal hCG and choriocarcinoma hCG.	Carbohydrates	88-100	hypertrichosis 2 (generalised, congenital)	Homo sapiens	127-130
29645229-16	1998	Sialic acid content in choriocarcinoma hCG was extremely lower compared to that in normal hCG.	N-Acetylneuraminic Acid	0-11	hypertrichosis 2 (generalised, congenital)	Homo sapiens	39-42
29645229-17	1998	The detection of the alteration in hCG sugar chains is useful for biochemical diagnosis of choriocarcinoma.	Sugars	39-44	hypertrichosis 2 (generalised, congenital)	Homo sapiens	35-38
29645260-19	1998	Binding of hCG to the LH/CG receptor are known to induce two signals, one for adenylyl cyclase/ cAMP and the other for phospholipase C/inositol phosphate/diacylglycerol.	Cyclic AMP	96-100	hypertrichosis 2 (generalised, congenital)	Homo sapiens	11-14
29645260-19	1998	Binding of hCG to the LH/CG receptor are known to induce two signals, one for adenylyl cyclase/ cAMP and the other for phospholipase C/inositol phosphate/diacylglycerol.	Cyclic AMP	96-100	hypertrichosis 2 (generalised, congenital)	Homo sapiens	12-14
29645260-19	1998	Binding of hCG to the LH/CG receptor are known to induce two signals, one for adenylyl cyclase/ cAMP and the other for phospholipase C/inositol phosphate/diacylglycerol.	Inositol Phosphates	135-153	hypertrichosis 2 (generalised, congenital)	Homo sapiens	11-14
29645260-19	1998	Binding of hCG to the LH/CG receptor are known to induce two signals, one for adenylyl cyclase/ cAMP and the other for phospholipase C/inositol phosphate/diacylglycerol.	Inositol Phosphates	135-153	hypertrichosis 2 (generalised, congenital)	Homo sapiens	12-14
29645260-19	1998	Binding of hCG to the LH/CG receptor are known to induce two signals, one for adenylyl cyclase/ cAMP and the other for phospholipase C/inositol phosphate/diacylglycerol.	Diglycerides	154-168	hypertrichosis 2 (generalised, congenital)	Homo sapiens	11-14
29645260-19	1998	Binding of hCG to the LH/CG receptor are known to induce two signals, one for adenylyl cyclase/ cAMP and the other for phospholipase C/inositol phosphate/diacylglycerol.	Diglycerides	154-168	hypertrichosis 2 (generalised, congenital)	Homo sapiens	12-14
9801271-2	1998	More recently, it has been found that in control OVA nitric oxide (NO) mediates hCG-induced PGE secretion.	Nitric Oxide	53-65	hypertrichosis 2 (generalised, congenital)	Homo sapiens	80-83
9421419-18	1998	In addition, KGF inhibited the ability of hCG to stimulate progesterone production by granulosa cells.	Progesterone	59-71	hypertrichosis 2 (generalised, congenital)	Homo sapiens	42-45
10732104-0	1998	The synchrony of prostaglandin-induced estrus in cows was reduced by pretreatment with hCG.	Prostaglandins	17-30	hypertrichosis 2 (generalised, congenital)	Homo sapiens	87-90
10732104-15	1998	In Experiment 2, cows treated with hCG/500PG and hCG/1000PG had a more variable (P = 0.0007, P = 0.002) day of occurrence of and a longer interval to estrus (4.2 +/- 0.4 d, P = 0.04; 4.1 +/- 0.4 d, P = 0.03) than saline/500PG-treated cows (3.2 +/- 0.1 d).	Sodium Chloride	213-219	hypertrichosis 2 (generalised, congenital)	Homo sapiens	35-38
10732104-15	1998	In Experiment 2, cows treated with hCG/500PG and hCG/1000PG had a more variable (P = 0.0007, P = 0.002) day of occurrence of and a longer interval to estrus (4.2 +/- 0.4 d, P = 0.04; 4.1 +/- 0.4 d, P = 0.03) than saline/500PG-treated cows (3.2 +/- 0.1 d).	Sodium Chloride	213-219	hypertrichosis 2 (generalised, congenital)	Homo sapiens	49-52
10732104-19	1998	This study indicated that treatment of cows with hCG on Day 5 of the estrous cycle reduced the synchrony of PG-induced estrus and that this reduction was not due to the failure of luteal regression.	Prostaglandins	108-110	hypertrichosis 2 (generalised, congenital)	Homo sapiens	49-52
9605514-4	1998	Pre-incubation of the mLTC-1 cells for 48 h with P (1-10 micromol/l) decreased in dose-dependent fashion their specific binding of [125I]iodo-hCG as well as the hCG-induced cAMP production (down to 65 and 40% respectively, of controls, P &lt; 0.01).	Cyclic AMP	173-177	hypertrichosis 2 (generalised, congenital)	Homo sapiens	161-164
9605514-5	1998	Similar effect of P on hCG-induced cAMP production was observed in adult mouse Leydig cells following a 24 h incubation in the presence of P (0.3-10 micromol/l).	Cyclic AMP	35-39	hypertrichosis 2 (generalised, congenital)	Homo sapiens	23-26
9605514-9	1998	Blocking the steroid synthesis of mLTC-1 cells with 86 micromol/l of aminoglutethimide (AMG) partially reversed the down-regulating effect of hCG on the LHR-mRNA.	Steroids	13-20	hypertrichosis 2 (generalised, congenital)	Homo sapiens	142-145
9605514-9	1998	Blocking the steroid synthesis of mLTC-1 cells with 86 micromol/l of aminoglutethimide (AMG) partially reversed the down-regulating effect of hCG on the LHR-mRNA.	Aminoglutethimide	69-86	hypertrichosis 2 (generalised, congenital)	Homo sapiens	142-145
9605514-9	1998	Blocking the steroid synthesis of mLTC-1 cells with 86 micromol/l of aminoglutethimide (AMG) partially reversed the down-regulating effect of hCG on the LHR-mRNA.	Aminoglutethimide	88-91	hypertrichosis 2 (generalised, congenital)	Homo sapiens	142-145
9605514-13	1998	Since Leydig cell P production is dramatically increased during high-dose stimulation with LH/hCG, due to blockade of C21 steroid side chain cleavage, the present findings offer a function for this steroid in the LHR down-regulation.	Steroids	122-129	hypertrichosis 2 (generalised, congenital)	Homo sapiens	94-97
9605514-13	1998	Since Leydig cell P production is dramatically increased during high-dose stimulation with LH/hCG, due to blockade of C21 steroid side chain cleavage, the present findings offer a function for this steroid in the LHR down-regulation.	Steroids	198-205	hypertrichosis 2 (generalised, congenital)	Homo sapiens	94-97
9801271-2	1998	More recently, it has been found that in control OVA nitric oxide (NO) mediates hCG-induced PGE secretion.	Prostaglandins E	92-95	hypertrichosis 2 (generalised, congenital)	Homo sapiens	80-83
9801271-6	1998	L-NMMA prevented the hCG-induced PGE accumulation in control and diabetic OVA, and the quantities of PGE produced were similar to those of control OVA but lower than in diabetic OVA incubated in the absence of hCG.	omega-N-Methylarginine	0-6	hypertrichosis 2 (generalised, congenital)	Homo sapiens	21-24
9801271-6	1998	L-NMMA prevented the hCG-induced PGE accumulation in control and diabetic OVA, and the quantities of PGE produced were similar to those of control OVA but lower than in diabetic OVA incubated in the absence of hCG.	omega-N-Methylarginine	0-6	hypertrichosis 2 (generalised, congenital)	Homo sapiens	210-213
9801271-6	1998	L-NMMA prevented the hCG-induced PGE accumulation in control and diabetic OVA, and the quantities of PGE produced were similar to those of control OVA but lower than in diabetic OVA incubated in the absence of hCG.	Prostaglandins E	33-36	hypertrichosis 2 (generalised, congenital)	Homo sapiens	21-24
9801271-6	1998	L-NMMA prevented the hCG-induced PGE accumulation in control and diabetic OVA, and the quantities of PGE produced were similar to those of control OVA but lower than in diabetic OVA incubated in the absence of hCG.	Prostaglandins E	101-104	hypertrichosis 2 (generalised, congenital)	Homo sapiens	21-24
9349751-6	1997	In addition, PMA inhibited hCG- and CRH-stimulated steroidogenesis in MA-10 cells and CRH-stimulated steroidogenesis in primary Leydig cells, suggesting that activation of the protein kinase C pathway can influence protein kinase A stimulated steroidogenesis.	Tetradecanoylphorbol Acetate	13-16	hypertrichosis 2 (generalised, congenital)	Homo sapiens	27-31
9348220-6	1997	Progesterone production was inhibited by actinomycin D in the hCG-pretreated cells, supporting the proposal that maintaining StAR protein synthesis is required for optimal steroid production in MA-10 mouse Leydig tumor cells.	Progesterone	0-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	62-65
9348220-6	1997	Progesterone production was inhibited by actinomycin D in the hCG-pretreated cells, supporting the proposal that maintaining StAR protein synthesis is required for optimal steroid production in MA-10 mouse Leydig tumor cells.	Dactinomycin	41-54	hypertrichosis 2 (generalised, congenital)	Homo sapiens	62-65
9348220-6	1997	Progesterone production was inhibited by actinomycin D in the hCG-pretreated cells, supporting the proposal that maintaining StAR protein synthesis is required for optimal steroid production in MA-10 mouse Leydig tumor cells.	Steroids	172-179	hypertrichosis 2 (generalised, congenital)	Homo sapiens	62-65
9561722-1	1997	In Percoll purified Leydig cells from mature rat we have demonstrated that the basal testosterone production (9.5 ng/10(6) Leydig cells/24 h) is increased 10-fold in presence of a saturating amount of hCG (1 IU/mL) and diminished in a dose-related manner when larger concentrations of gonadotropin are used to reach 14 ng/10(6) Leydig cells for 50 IU of hCG.	Testosterone	85-97	hypertrichosis 2 (generalised, congenital)	Homo sapiens	201-204
9561722-1	1997	In Percoll purified Leydig cells from mature rat we have demonstrated that the basal testosterone production (9.5 ng/10(6) Leydig cells/24 h) is increased 10-fold in presence of a saturating amount of hCG (1 IU/mL) and diminished in a dose-related manner when larger concentrations of gonadotropin are used to reach 14 ng/10(6) Leydig cells for 50 IU of hCG.	Testosterone	85-97	hypertrichosis 2 (generalised, congenital)	Homo sapiens	354-357
9561722-2	1997	If 40% (v/v) seminiferous tubule medium (STM) is added together with hCG (1 IU/mL) to the incubation medium, a further increase (62%) of testosterone output is noticed.	Testosterone	137-149	hypertrichosis 2 (generalised, congenital)	Homo sapiens	69-72
9561722-3	1997	Obviously, when the testosterone production is low as a consequence of a higher dose of hCG (50 IU/mL), the STM (80%) improves the steroid synthesis five-fold (67.4 ng).	Testosterone	20-32	hypertrichosis 2 (generalised, congenital)	Homo sapiens	88-91
9561722-3	1997	Obviously, when the testosterone production is low as a consequence of a higher dose of hCG (50 IU/mL), the STM (80%) improves the steroid synthesis five-fold (67.4 ng).	Steroids	131-138	hypertrichosis 2 (generalised, congenital)	Homo sapiens	88-91
9561722-6	1997	The obtained results suggest that paracrine factor(s) presents in STM and acting in synergy with LH/hCG generate(s) the rearrangement of cytoskeletal structures which, in turn, facilitates the availability of cholesterol for the mitochondria and finally enhances the testosterone production in the rat Leydig cells.	Cholesterol	209-220	hypertrichosis 2 (generalised, congenital)	Homo sapiens	100-103
9561722-6	1997	The obtained results suggest that paracrine factor(s) presents in STM and acting in synergy with LH/hCG generate(s) the rearrangement of cytoskeletal structures which, in turn, facilitates the availability of cholesterol for the mitochondria and finally enhances the testosterone production in the rat Leydig cells.	Testosterone	267-279	hypertrichosis 2 (generalised, congenital)	Homo sapiens	100-103
9348261-1	1997	OBJECTIVE: To compare expectant management with local instillation of 50% glucose solution for tubal pregnancies with a serum hCG level &lt; or = 2500 mIU/mL.	Glucose	74-81	hypertrichosis 2 (generalised, congenital)	Homo sapiens	126-129
9275046-3	1997	The addition of the NOS inhibitors, aminoguanidine hemisulfate salt (AG) and N-omega-nitro-L-arginine methyl ester (L-NAME), to the perfusate inhibited the ovulation induced by hCG in a dose-dependent manner, whereas D-NAME had no significant effect.	NG-Nitroarginine Methyl Ester	77-114	hypertrichosis 2 (generalised, congenital)	Homo sapiens	177-180
9275046-3	1997	The addition of the NOS inhibitors, aminoguanidine hemisulfate salt (AG) and N-omega-nitro-L-arginine methyl ester (L-NAME), to the perfusate inhibited the ovulation induced by hCG in a dose-dependent manner, whereas D-NAME had no significant effect.	NG-Nitroarginine Methyl Ester	116-122	hypertrichosis 2 (generalised, congenital)	Homo sapiens	177-180
9275046-6	1997	Inhibition of endogenous NOS by AG and L-NAME resulted in a significant elevation in the production of estradiol (E2), but not of progesterone, stimulated by hCG.	NG-Nitroarginine Methyl Ester	39-45	hypertrichosis 2 (generalised, congenital)	Homo sapiens	158-161
9275046-6	1997	Inhibition of endogenous NOS by AG and L-NAME resulted in a significant elevation in the production of estradiol (E2), but not of progesterone, stimulated by hCG.	Estradiol	103-112	hypertrichosis 2 (generalised, congenital)	Homo sapiens	158-161
9275046-7	1997	The concomitant administration of NP significantly reduced the AG-stimulated production of E2 by ovaries perfused in the presence of hCG, which suggests that NO down-regulates ovarian E2 synthesis.	Nitroprusside	34-36	hypertrichosis 2 (generalised, congenital)	Homo sapiens	133-136
9275046-8	1997	Ovarian production of PGE2 and PGF2alpha in response to hCG was significantly blocked by L-NAME, and exogenous administration of NP stimulated the production of PGs in the absence of gonadotropin.	Dinoprostone	22-26	hypertrichosis 2 (generalised, congenital)	Homo sapiens	56-59
9275046-8	1997	Ovarian production of PGE2 and PGF2alpha in response to hCG was significantly blocked by L-NAME, and exogenous administration of NP stimulated the production of PGs in the absence of gonadotropin.	Dinoprost	31-40	hypertrichosis 2 (generalised, congenital)	Homo sapiens	56-59
9275046-8	1997	Ovarian production of PGE2 and PGF2alpha in response to hCG was significantly blocked by L-NAME, and exogenous administration of NP stimulated the production of PGs in the absence of gonadotropin.	NG-Nitroarginine Methyl Ester	89-95	hypertrichosis 2 (generalised, congenital)	Homo sapiens	56-59
9568526-10	1997	Leydig cells from rats with EAO exhibited an enhanced steroidogenic response to hCG in vitro at 80 days (38%) and an increase in basal (77%) and post-hCG testosterone production (115%) at 160 days compared to controls.	Testosterone	154-166	hypertrichosis 2 (generalised, congenital)	Homo sapiens	150-153
9314578-3	1997	In a mouse Leydig cell line (MA-10) we show that hCG and forskolin are effective inducers of progesterone production and P450scc expression.	Progesterone	93-105	hypertrichosis 2 (generalised, congenital)	Homo sapiens	49-52
9314585-3	1997	Nuclei of the eCG and hCG but not the DES group contained a 32/34-kDA DNase I-like endonuclease activity that was Ca2+/Mg(2+)-dependent, stimulated by Mn2+, optimal at pH 7, and identified by anti-DNase I antibody.	magnesium ion	119-125	hypertrichosis 2 (generalised, congenital)	Homo sapiens	22-25
9314585-3	1997	Nuclei of the eCG and hCG but not the DES group contained a 32/34-kDA DNase I-like endonuclease activity that was Ca2+/Mg(2+)-dependent, stimulated by Mn2+, optimal at pH 7, and identified by anti-DNase I antibody.	Manganese(2+)	151-155	hypertrichosis 2 (generalised, congenital)	Homo sapiens	22-25
16728138-6	1997	Reduced testosterone production by Leydig cells from infected and scrotal-insulated rams in response to hCG and 22ROHC suggests that trypanosome-induced pyrexia might be involved in reducing Leydig cell steroidogenesis and subsequent plasma testosterone levels, possibly by affecting enzymes involved in steroid biosynthesis.	Testosterone	8-20	hypertrichosis 2 (generalised, congenital)	Homo sapiens	104-107
9360228-8	1997	Both hCG and progesterone release rates were lowest at high oxygen tensions.	Oxygen	60-66	hypertrichosis 2 (generalised, congenital)	Homo sapiens	5-8
9360228-12	1997	Exposure to higher oxygen tensions results in reduced hCG and progesterone release.	Oxygen	19-25	hypertrichosis 2 (generalised, congenital)	Homo sapiens	54-57
16728138-4	1997	Stimulation of Leydig cell testosterone production with hCG or 22R-hydroxycholesterol (22ROHC) significantly reduced in infected rams at both 28 and 58 d after infection as well as in scrotal-insulated rams on Day 58.	Testosterone	27-39	hypertrichosis 2 (generalised, congenital)	Homo sapiens	56-59
9262009-1	1997	The chloride channel blockers SITS (4-acetamido-4"-isothiocyanostibene-2,2"-disulphonic acid) and DIDS (4,4"-diisothiocyanostilbene-2,2"-disulphonic acid) markedly suppressed progesterone production in the Rana temporaria and Xenopus laevis follicle-enclosed oocytes and oocyte maturation stimulated by the homologous pituitary suspension and hCG, respectively.	4-acetamido-4"-isothiocyanostibene-2,2"-disulphonic acid	36-92	hypertrichosis 2 (generalised, congenital)	Homo sapiens	343-346
9262009-1	1997	The chloride channel blockers SITS (4-acetamido-4"-isothiocyanostibene-2,2"-disulphonic acid) and DIDS (4,4"-diisothiocyanostilbene-2,2"-disulphonic acid) markedly suppressed progesterone production in the Rana temporaria and Xenopus laevis follicle-enclosed oocytes and oocyte maturation stimulated by the homologous pituitary suspension and hCG, respectively.	4,4"-diisothiocyanostilbene-2,2"-disulphonic acid	104-153	hypertrichosis 2 (generalised, congenital)	Homo sapiens	343-346
9215288-8	1997	COS-7 cells transfected with the mutant receptor exhibited a marked impairment of hCG binding, whereas some cAMP production could be observed at high hCG concentrations.	Cyclic AMP	108-112	hypertrichosis 2 (generalised, congenital)	Homo sapiens	150-153
9214555-2	1997	Although the long-term effect of trophic hormones on Leydig cell cholesterol uptake, storage, and deesterification has been well documented, the early effects of the human choriogonadotropin (hCG) on cell cholesterol/lipid distribution are not yet known.	Cholesterol	205-216	hypertrichosis 2 (generalised, congenital)	Homo sapiens	192-195
9306975-0	1997	Significance of oestradiol for follicular development in hypogonadotrophic immature rats treated with FSH and hCG.	Estradiol	16-26	hypertrichosis 2 (generalised, congenital)	Homo sapiens	110-113
9306975-3	1997	To investigate whether this effect of hCG on follicular growth is due to stimulation of oestradiol production, intraovarian concentrations of oestradiol were suppressed by an aromatase inhibitor and oestradiol action was blocked by an oestrogen antagonist; both of these were administered from day 25 until day 29.	Estradiol	88-98	hypertrichosis 2 (generalised, congenital)	Homo sapiens	38-41
9306975-11	1997	From these studies, it is concluded that the effects of hCG on follicular growth and atresia can be largely attributed to the mitotic and anti-atretic effect of oestradiol.	Estradiol	161-171	hypertrichosis 2 (generalised, congenital)	Homo sapiens	56-59
9306975-12	1997	However, part of the effect of hCG cannot be explained on the basis of oestradiol action.	Estradiol	71-81	hypertrichosis 2 (generalised, congenital)	Homo sapiens	31-34
9260834-12	1997	Moreover, the presence of 8Br-cAMP (0.5 or 1 mM) mimicked the stimulation by hCG.	8-Bromo Cyclic Adenosine Monophosphate	26-34	hypertrichosis 2 (generalised, congenital)	Homo sapiens	77-80
9260834-13	1997	Interestingly, H89 (2 microM), a specific protein kinase-A inhibitor, dramatically decreased the responses to hCG (500 mIU/ml) and the 8Br-cAMP (0.5 mM) stimulation of trophoblastic gap junctional communication.	N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide	15-18	hypertrichosis 2 (generalised, congenital)	Homo sapiens	110-113
9139799-7	1997	In addition, tunicamycin-derived, nonglycosylated LHRs were present at the cell surface and exhibited a phenotype consistent with mature receptors due to their capability to mediate hCG-stimulated cAMP production as well as bind oLH with high affinity.	Tunicamycin	13-24	hypertrichosis 2 (generalised, congenital)	Homo sapiens	182-185
9429850-8	1997	Conversely, hLIF dose-dependently inhibited basal and cAMP-stimulated hCG secretion in trophoblasts derived during the second trimester and at term, as well as in cultured JEG-3 choriocarcinoma cells.	Cyclic AMP	54-58	hypertrichosis 2 (generalised, congenital)	Homo sapiens	70-73
9142140-14	1997	Combined exposure to CsA and DES enhanced the stimulatory effect of hCG on the accumulation of 17-OH-P in the media.	Cyclosporine	21-24	hypertrichosis 2 (generalised, congenital)	Homo sapiens	68-71
10074248-3	1997	Further experiments showed that the inhibitory effect of ET on the hCG-stimulated progesterone production could be reversed by rabbit antiserum to ET (ET-A, 1:1000) or cAMP (10(5) mol/L).	Progesterone	82-94	hypertrichosis 2 (generalised, congenital)	Homo sapiens	67-70
10074248-3	1997	Further experiments showed that the inhibitory effect of ET on the hCG-stimulated progesterone production could be reversed by rabbit antiserum to ET (ET-A, 1:1000) or cAMP (10(5) mol/L).	Cyclic AMP	168-172	hypertrichosis 2 (generalised, congenital)	Homo sapiens	67-70
10074248-5	1997	All these findings suggest that ET may be an intraovarian regulatory factor which may inhibit progesterone production stimulated by hCG from rat granulosa cells through inerfering LH/hCG receptor function and cAMP formation.	Progesterone	94-106	hypertrichosis 2 (generalised, congenital)	Homo sapiens	132-135
10074248-5	1997	All these findings suggest that ET may be an intraovarian regulatory factor which may inhibit progesterone production stimulated by hCG from rat granulosa cells through inerfering LH/hCG receptor function and cAMP formation.	Progesterone	94-106	hypertrichosis 2 (generalised, congenital)	Homo sapiens	183-186
10074248-5	1997	All these findings suggest that ET may be an intraovarian regulatory factor which may inhibit progesterone production stimulated by hCG from rat granulosa cells through inerfering LH/hCG receptor function and cAMP formation.	Cyclic AMP	209-213	hypertrichosis 2 (generalised, congenital)	Homo sapiens	132-135
9142140-11	1997	Although CsA did not affect in vitro release of testosterone, it reduced the stimulatory influence of DES pretreatment on testicular responses to hCG in vitro.	Cyclosporine	9-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	146-149
9130068-4	1997	RESULTS: In the tubal disease group, probability of pregnancy was greater in cycles with serum estradiol levels below 1100 pg/ml on the day of hCG (odds ratio, 4.7) and with administration of gonadotropins for less than 10 days (odds ratio, 3.7).	Estradiol	95-104	hypertrichosis 2 (generalised, congenital)	Homo sapiens	143-146
9142140-14	1997	Combined exposure to CsA and DES enhanced the stimulatory effect of hCG on the accumulation of 17-OH-P in the media.	Diethylstilbestrol	29-32	hypertrichosis 2 (generalised, congenital)	Homo sapiens	68-71
9142140-14	1997	Combined exposure to CsA and DES enhanced the stimulatory effect of hCG on the accumulation of 17-OH-P in the media.	17-alpha-Hydroxyprogesterone	95-102	hypertrichosis 2 (generalised, congenital)	Homo sapiens	68-71
9047011-8	1997	Human CG alone had no effect on PGE2 or PGF2 alpha production by dispersed luteal cells in vitro but inhibited IL-1 beta-stimulated PGF2 alpha production.	Dinoprost	132-136	hypertrichosis 2 (generalised, congenital)	Homo sapiens	6-8
9047011-10	1997	Interestingly, IL-1 beta inhibited this hCG stimulation of progesterone production.	Progesterone	59-71	hypertrichosis 2 (generalised, congenital)	Homo sapiens	40-43
9091345-1	1997	OBJECTIVE: To examine the potential role of the L-arginine:nitric oxide pathway in hCG-induced ovulation in the rabbit.	Arginine	48-58	hypertrichosis 2 (generalised, congenital)	Homo sapiens	83-86
9091345-1	1997	OBJECTIVE: To examine the potential role of the L-arginine:nitric oxide pathway in hCG-induced ovulation in the rabbit.	Nitric Oxide	59-71	hypertrichosis 2 (generalised, congenital)	Homo sapiens	83-86
9091345-8	1997	In vivo administration of L-NAME significantly reduced the percentage of large follicles that ovulated in response to hCG (treated 24.6%, control 68.1%).	NG-Nitroarginine Methyl Ester	26-32	hypertrichosis 2 (generalised, congenital)	Homo sapiens	118-121
8977389-7	1997	Furthermore, the cells bound hCG with a normal high affinity and responded to hCG with increased cAMP production normally.	Cyclic AMP	97-101	hypertrichosis 2 (generalised, congenital)	Homo sapiens	29-32
9024272-10	1997	After increasing doses of hCG, levels of serum testosterone and estradiol and total body BMD increased significantly (by paired t test P = 0.001, 0.003, and 0.01, respectively).	Testosterone	47-59	hypertrichosis 2 (generalised, congenital)	Homo sapiens	26-29
9024272-10	1997	After increasing doses of hCG, levels of serum testosterone and estradiol and total body BMD increased significantly (by paired t test P = 0.001, 0.003, and 0.01, respectively).	Estradiol	64-73	hypertrichosis 2 (generalised, congenital)	Homo sapiens	26-29
9024272-12	1997	Serum bone alkaline phosphatase and urinary N-terminal telopeptide of type I collagen/creatinine levels decreased significantly after increasing the dose of hCG.	Creatinine	86-96	hypertrichosis 2 (generalised, congenital)	Homo sapiens	157-160
9024272-13	1997	We conclude that patients with IHH who have serum testosterone within the laboratory reference range may require a higher dose of hCG to normalize BMD and bone turnover.	Testosterone	50-62	hypertrichosis 2 (generalised, congenital)	Homo sapiens	130-133
9129347-10	1997	Libido and hCG-induced serum testosterone concentrations were studied after the cessation of treatments, up to 3 or 4 years of age.	Testosterone	29-41	hypertrichosis 2 (generalised, congenital)	Homo sapiens	11-14
9129347-13	1997	Two years after treatments in experiment I, hCG-induced testosterone levels were higher in treated colts than in untreated controls, but the difference was not statistically significant.	Testosterone	56-68	hypertrichosis 2 (generalised, congenital)	Homo sapiens	44-47
9297859-6	1997	Medical treatment by local or parenteral methotrexate is recommended in patients with clear evidence of an unruptured pregnancy in based on initial hCG and progesterone level, size of hemoperitoneum, ultrasound diameter of hematosalpinx and absence of clinical pain.	Methotrexate	41-53	hypertrichosis 2 (generalised, congenital)	Homo sapiens	148-151
8977389-7	1997	Furthermore, the cells bound hCG with a normal high affinity and responded to hCG with increased cAMP production normally.	Cyclic AMP	97-101	hypertrichosis 2 (generalised, congenital)	Homo sapiens	78-81
8977403-9	1997	In contrast, phorbol 12-myristate 13-acetate inhibited basal as well as hCG- and 8-bromo-cAMP-induced FP receptor mRNA expression and binding of the radiolabeled ligand.	Tetradecanoylphorbol Acetate	13-44	hypertrichosis 2 (generalised, congenital)	Homo sapiens	72-75
8977403-8	1997	Further, hCG and 8-bromo-cAMP increased binding of radiolabeled PGF2 alpha to intact GL cells.	Dinoprost	64-74	hypertrichosis 2 (generalised, congenital)	Homo sapiens	9-12
9027347-10	1996	Lys91 is important for binding and cAMP induction of hCG, and cAMP induction but not binding of FSH.	Cyclic AMP	35-39	hypertrichosis 2 (generalised, congenital)	Homo sapiens	53-56
8995555-4	1997	HCG stimulated the production of cAMP in the superfused tissue of the first case and in the second case the addition of hCG to the incubation medium caused a significant drop in testosterone release by the primary tumor and in androstendione release by the metastasis.	Cyclic AMP	33-37	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
8995555-4	1997	HCG stimulated the production of cAMP in the superfused tissue of the first case and in the second case the addition of hCG to the incubation medium caused a significant drop in testosterone release by the primary tumor and in androstendione release by the metastasis.	Cyclic AMP	33-37	hypertrichosis 2 (generalised, congenital)	Homo sapiens	120-123
8995555-4	1997	HCG stimulated the production of cAMP in the superfused tissue of the first case and in the second case the addition of hCG to the incubation medium caused a significant drop in testosterone release by the primary tumor and in androstendione release by the metastasis.	Testosterone	178-190	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
8995555-4	1997	HCG stimulated the production of cAMP in the superfused tissue of the first case and in the second case the addition of hCG to the incubation medium caused a significant drop in testosterone release by the primary tumor and in androstendione release by the metastasis.	Testosterone	178-190	hypertrichosis 2 (generalised, congenital)	Homo sapiens	120-123
8995555-4	1997	HCG stimulated the production of cAMP in the superfused tissue of the first case and in the second case the addition of hCG to the incubation medium caused a significant drop in testosterone release by the primary tumor and in androstendione release by the metastasis.	Androstenedione	227-241	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
8995555-4	1997	HCG stimulated the production of cAMP in the superfused tissue of the first case and in the second case the addition of hCG to the incubation medium caused a significant drop in testosterone release by the primary tumor and in androstendione release by the metastasis.	Androstenedione	227-241	hypertrichosis 2 (generalised, congenital)	Homo sapiens	120-123
9402247-1	1997	To determine whether nitric oxide (NO) generation mediates human chorionic gonadotrophin (hCG)-induced prostaglandin E (PGE) secretion by oocyte-cumulus complexes (OCC), the secretion of PGE by cultured rat OCC in the presence of NO donors and NO synthase (NOS) inhibitors was characterized.	Nitric Oxide	21-33	hypertrichosis 2 (generalised, congenital)	Homo sapiens	90-93
9402247-1	1997	To determine whether nitric oxide (NO) generation mediates human chorionic gonadotrophin (hCG)-induced prostaglandin E (PGE) secretion by oocyte-cumulus complexes (OCC), the secretion of PGE by cultured rat OCC in the presence of NO donors and NO synthase (NOS) inhibitors was characterized.	Prostaglandins E	103-118	hypertrichosis 2 (generalised, congenital)	Homo sapiens	90-93
9402247-1	1997	To determine whether nitric oxide (NO) generation mediates human chorionic gonadotrophin (hCG)-induced prostaglandin E (PGE) secretion by oocyte-cumulus complexes (OCC), the secretion of PGE by cultured rat OCC in the presence of NO donors and NO synthase (NOS) inhibitors was characterized.	Prostaglandins E	120-123	hypertrichosis 2 (generalised, congenital)	Homo sapiens	90-93
9402247-3	1997	The three NOS inhibitors tested (NG-nitro-L-arginine methyl ester, NG-monomethyl-L-arginine and aminoguanidine) prevented the hCG-induced PGE accumulation in cultured OCC.	NG-Nitroarginine Methyl Ester	33-65	hypertrichosis 2 (generalised, congenital)	Homo sapiens	126-129
9402247-3	1997	The three NOS inhibitors tested (NG-nitro-L-arginine methyl ester, NG-monomethyl-L-arginine and aminoguanidine) prevented the hCG-induced PGE accumulation in cultured OCC.	omega-N-Methylarginine	67-91	hypertrichosis 2 (generalised, congenital)	Homo sapiens	126-129
9402247-3	1997	The three NOS inhibitors tested (NG-nitro-L-arginine methyl ester, NG-monomethyl-L-arginine and aminoguanidine) prevented the hCG-induced PGE accumulation in cultured OCC.	pimagedine	96-110	hypertrichosis 2 (generalised, congenital)	Homo sapiens	126-129
9402247-3	1997	The three NOS inhibitors tested (NG-nitro-L-arginine methyl ester, NG-monomethyl-L-arginine and aminoguanidine) prevented the hCG-induced PGE accumulation in cultured OCC.	Prostaglandins E	138-141	hypertrichosis 2 (generalised, congenital)	Homo sapiens	126-129
9402247-5	1997	The present results suggest that NO mediates the hCG-induced accumulation of PGE in rat OCC, a process which may occur in vivo in preovulatory follicles prior to ovulation.	Prostaglandins E	77-80	hypertrichosis 2 (generalised, congenital)	Homo sapiens	49-52
8977403-10	1997	In summary, hCG, 8-bromo-cAMP, and phorbol 12-myristate 13-acetate modulate the expression of the FP receptor in human GL cells, which may represent a mechanism to regulate the responsiveness of the ovary to PGF2 alpha.	Dinoprost	208-212	hypertrichosis 2 (generalised, congenital)	Homo sapiens	12-15
9276342-1	1997	The objective of presented studies was to investigate whether estradiol and progesterone administered in vivo and/or added in vitro can influence the primary myometrial cell culture and how these steroid hormones can affect hCG stimulated cAMP and inositol phosphate production in the porcine uterine myocytes.	Estradiol	62-71	hypertrichosis 2 (generalised, congenital)	Homo sapiens	224-227
9276342-1	1997	The objective of presented studies was to investigate whether estradiol and progesterone administered in vivo and/or added in vitro can influence the primary myometrial cell culture and how these steroid hormones can affect hCG stimulated cAMP and inositol phosphate production in the porcine uterine myocytes.	Progesterone	76-88	hypertrichosis 2 (generalised, congenital)	Homo sapiens	224-227
9276342-1	1997	The objective of presented studies was to investigate whether estradiol and progesterone administered in vivo and/or added in vitro can influence the primary myometrial cell culture and how these steroid hormones can affect hCG stimulated cAMP and inositol phosphate production in the porcine uterine myocytes.	Steroids	196-212	hypertrichosis 2 (generalised, congenital)	Homo sapiens	224-227
9276342-1	1997	The objective of presented studies was to investigate whether estradiol and progesterone administered in vivo and/or added in vitro can influence the primary myometrial cell culture and how these steroid hormones can affect hCG stimulated cAMP and inositol phosphate production in the porcine uterine myocytes.	Cyclic AMP	239-243	hypertrichosis 2 (generalised, congenital)	Homo sapiens	224-227
9276342-1	1997	The objective of presented studies was to investigate whether estradiol and progesterone administered in vivo and/or added in vitro can influence the primary myometrial cell culture and how these steroid hormones can affect hCG stimulated cAMP and inositol phosphate production in the porcine uterine myocytes.	Inositol Phosphates	248-266	hypertrichosis 2 (generalised, congenital)	Homo sapiens	224-227
9276342-6	1997	The myometrial smooth muscle cells treated with low dose of estradiol and progesterone in vivo responded with much higher accumulation of inositol phosphates to strong (1000 mU/ml) hCG stimulation when compared with those receiving high dose of both steroids.	Estradiol	60-69	hypertrichosis 2 (generalised, congenital)	Homo sapiens	181-184
9276342-6	1997	The myometrial smooth muscle cells treated with low dose of estradiol and progesterone in vivo responded with much higher accumulation of inositol phosphates to strong (1000 mU/ml) hCG stimulation when compared with those receiving high dose of both steroids.	Progesterone	74-86	hypertrichosis 2 (generalised, congenital)	Homo sapiens	181-184
9276342-6	1997	The myometrial smooth muscle cells treated with low dose of estradiol and progesterone in vivo responded with much higher accumulation of inositol phosphates to strong (1000 mU/ml) hCG stimulation when compared with those receiving high dose of both steroids.	Steroids	250-258	hypertrichosis 2 (generalised, congenital)	Homo sapiens	181-184
9276342-8	1997	hCG (0.1 mU/ml) had usually the additive effect on cAMP production in porcine myometrial cells.	Cyclic AMP	51-55	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
9276342-9	1997	The presented paper shows that estradiol and progesterone administration in vivo followed by steroid hormone treatment in vitro affects the primary myometrial cells culture and that both steroid hormones modify the basal accumulation of the second messengers: cAMP and IP3 and their answer to hCG stimuli in pigs.	Estradiol	31-40	hypertrichosis 2 (generalised, congenital)	Homo sapiens	293-296
9276342-9	1997	The presented paper shows that estradiol and progesterone administration in vivo followed by steroid hormone treatment in vitro affects the primary myometrial cells culture and that both steroid hormones modify the basal accumulation of the second messengers: cAMP and IP3 and their answer to hCG stimuli in pigs.	Progesterone	45-57	hypertrichosis 2 (generalised, congenital)	Homo sapiens	293-296
9276342-9	1997	The presented paper shows that estradiol and progesterone administration in vivo followed by steroid hormone treatment in vitro affects the primary myometrial cells culture and that both steroid hormones modify the basal accumulation of the second messengers: cAMP and IP3 and their answer to hCG stimuli in pigs.	Steroids	187-203	hypertrichosis 2 (generalised, congenital)	Homo sapiens	293-296
9027347-14	1996	Therefore, the three amino acids contribute differently in receptor binding and cAMP induction of hCG, FSH and TSH.	Cyclic AMP	80-84	hypertrichosis 2 (generalised, congenital)	Homo sapiens	98-101
9027347-17	1996	To chemically identify the contact site of the alpha C-tail of hCG in the LH/CG receptor, a decamer peptide corresponding to the alpha subunit sequence from His83 to Ser92 (peptide alpha 81-92) was derivatized with UV sensitive reagent, ABG and radio-iodinated.	abg	237-240	hypertrichosis 2 (generalised, congenital)	Homo sapiens	63-66
9027347-17	1996	To chemically identify the contact site of the alpha C-tail of hCG in the LH/CG receptor, a decamer peptide corresponding to the alpha subunit sequence from His83 to Ser92 (peptide alpha 81-92) was derivatized with UV sensitive reagent, ABG and radio-iodinated.	abg	237-240	hypertrichosis 2 (generalised, congenital)	Homo sapiens	64-66
9027347-23	1996	To test the conformational adjustment, ABG was attached to hCG alpha and reassociated with untreated beta to produce ABG-125I-alpha/beta.	abg	39-42	hypertrichosis 2 (generalised, congenital)	Homo sapiens	59-62
9091180-1	1996	In Percoll purified Leydig cells from mature rat incubated for 24 h in Ham F12/DME medium, we demonstrated that the testosterone production (6 ng/10(6) Leydig cells/24 h) is increased 11 fold by a saturating amount of hCG whereas rat Leydig cells the basal output of testosterone is 4.5 ng and increased 2.5 fold by hCG.	Testosterone	116-128	hypertrichosis 2 (generalised, congenital)	Homo sapiens	218-221
9091180-1	1996	In Percoll purified Leydig cells from mature rat incubated for 24 h in Ham F12/DME medium, we demonstrated that the testosterone production (6 ng/10(6) Leydig cells/24 h) is increased 11 fold by a saturating amount of hCG whereas rat Leydig cells the basal output of testosterone is 4.5 ng and increased 2.5 fold by hCG.	Testosterone	116-128	hypertrichosis 2 (generalised, congenital)	Homo sapiens	316-319
9091180-2	1996	In the sulfate-free Ham F12/DME medium used for the proteoglycan (PG) studies, the productions of testosterone are lower but the cells remain sensitive to hCG.	Sulfates	7-14	hypertrichosis 2 (generalised, congenital)	Homo sapiens	155-158
9091180-2	1996	In the sulfate-free Ham F12/DME medium used for the proteoglycan (PG) studies, the productions of testosterone are lower but the cells remain sensitive to hCG.	dimethylethylsilylimidazole	28-31	hypertrichosis 2 (generalised, congenital)	Homo sapiens	155-158
8902207-4	1996	The addition of both Ang II receptor antagonists to the perfusate had no significant effect on the concentration of progesterone in the perfusate of hCG-treated ovaries, whereas PD123319 inhibited the hCG-stimulated production of estradiol.	Estradiol	230-239	hypertrichosis 2 (generalised, congenital)	Homo sapiens	201-204
9363223-4	1996	Both 8-Br-cGMP and 8-Br-cAMP enhanced the expression of hCG in cultured cytotrophoblasts with the differentiation of cytotrophoblasts to syncytiotrophoblasts dose-dependently.	8-bromoguanosino-3',5'-cyclic monophosphorothioate	5-14	hypertrichosis 2 (generalised, congenital)	Homo sapiens	56-59
9363223-4	1996	Both 8-Br-cGMP and 8-Br-cAMP enhanced the expression of hCG in cultured cytotrophoblasts with the differentiation of cytotrophoblasts to syncytiotrophoblasts dose-dependently.	8-Bromo Cyclic Adenosine Monophosphate	19-28	hypertrichosis 2 (generalised, congenital)	Homo sapiens	56-59
9363223-6	1996	hCG, a trophoblast-specific glycoprotein hormone has been identified as a potent growth factor for trophoblasts, also increased [3H]thymidine uptake and the intracellular 3",5"-adenosine monophosphate (cAMP) concentration.	Tritium	129-131	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
9363223-6	1996	hCG, a trophoblast-specific glycoprotein hormone has been identified as a potent growth factor for trophoblasts, also increased [3H]thymidine uptake and the intracellular 3",5"-adenosine monophosphate (cAMP) concentration.	3",5"-adenosine monophosphate	171-200	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
9363223-6	1996	hCG, a trophoblast-specific glycoprotein hormone has been identified as a potent growth factor for trophoblasts, also increased [3H]thymidine uptake and the intracellular 3",5"-adenosine monophosphate (cAMP) concentration.	Cyclic AMP	202-206	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
9363224-6	1996	In animals treated with 4-hydroxy-estradiol, 17 beta-estradiol or prostaglandins, connexin 32 expression started 1 day earlier (day 7 post-hCG) and led to an enhanced connexin 32 expression on day 8 post-hCG compared to control animals.	4-hydroxyestradiol	24-43	hypertrichosis 2 (generalised, congenital)	Homo sapiens	139-142
9363224-6	1996	In animals treated with 4-hydroxy-estradiol, 17 beta-estradiol or prostaglandins, connexin 32 expression started 1 day earlier (day 7 post-hCG) and led to an enhanced connexin 32 expression on day 8 post-hCG compared to control animals.	4-hydroxyestradiol	24-43	hypertrichosis 2 (generalised, congenital)	Homo sapiens	204-207
9363224-6	1996	In animals treated with 4-hydroxy-estradiol, 17 beta-estradiol or prostaglandins, connexin 32 expression started 1 day earlier (day 7 post-hCG) and led to an enhanced connexin 32 expression on day 8 post-hCG compared to control animals.	Estradiol	45-62	hypertrichosis 2 (generalised, congenital)	Homo sapiens	139-142
9363224-6	1996	In animals treated with 4-hydroxy-estradiol, 17 beta-estradiol or prostaglandins, connexin 32 expression started 1 day earlier (day 7 post-hCG) and led to an enhanced connexin 32 expression on day 8 post-hCG compared to control animals.	Estradiol	45-62	hypertrichosis 2 (generalised, congenital)	Homo sapiens	204-207
9363224-6	1996	In animals treated with 4-hydroxy-estradiol, 17 beta-estradiol or prostaglandins, connexin 32 expression started 1 day earlier (day 7 post-hCG) and led to an enhanced connexin 32 expression on day 8 post-hCG compared to control animals.	Prostaglandins	66-80	hypertrichosis 2 (generalised, congenital)	Homo sapiens	139-142
9363224-6	1996	In animals treated with 4-hydroxy-estradiol, 17 beta-estradiol or prostaglandins, connexin 32 expression started 1 day earlier (day 7 post-hCG) and led to an enhanced connexin 32 expression on day 8 post-hCG compared to control animals.	Prostaglandins	66-80	hypertrichosis 2 (generalised, congenital)	Homo sapiens	204-207
8902207-2	1996	The addition to the perfusate of PD123319, a nonpeptide Ang II antagonist with a high affinity for AT2 receptors, inhibited hCG-induced ovulation in a dose-dependent manner, whereas CV-11974, a nonpeptide AT1 receptor antagonist, had no effect.	PD 123319	33-41	hypertrichosis 2 (generalised, congenital)	Homo sapiens	124-127
8902207-3	1996	The majority of ovulated ova and follicular oocytes resumed meiotic maturation in response to hCG; and PD123319, but not CV-11974, significantly inhibited hCG-induced oocyte maturation.	PD 123319	103-111	hypertrichosis 2 (generalised, congenital)	Homo sapiens	155-158
8902207-4	1996	The addition of both Ang II receptor antagonists to the perfusate had no significant effect on the concentration of progesterone in the perfusate of hCG-treated ovaries, whereas PD123319 inhibited the hCG-stimulated production of estradiol.	PD 123319	178-186	hypertrichosis 2 (generalised, congenital)	Homo sapiens	201-204
8902207-5	1996	The production of PGE2 and PGF2 alpha was significantly increased at 6 h in hCG-treated ovaries compared with ovaries before hCG administration.	Dinoprostone	18-22	hypertrichosis 2 (generalised, congenital)	Homo sapiens	76-79
8902207-5	1996	The production of PGE2 and PGF2 alpha was significantly increased at 6 h in hCG-treated ovaries compared with ovaries before hCG administration.	Dinoprostone	18-22	hypertrichosis 2 (generalised, congenital)	Homo sapiens	125-128
8902207-5	1996	The production of PGE2 and PGF2 alpha was significantly increased at 6 h in hCG-treated ovaries compared with ovaries before hCG administration.	Dinoprost	27-31	hypertrichosis 2 (generalised, congenital)	Homo sapiens	76-79
8902207-5	1996	The production of PGE2 and PGF2 alpha was significantly increased at 6 h in hCG-treated ovaries compared with ovaries before hCG administration.	Dinoprost	27-31	hypertrichosis 2 (generalised, congenital)	Homo sapiens	125-128
8902207-6	1996	PD123319 inhibited the hCG-stimulated production of PGs by perfused rabbit ovaries in a dose-dependent manner, indicating that hCG-induced PG synthesis is mediated, at least in part, via the activation of AT2 receptors.	PD 123319	0-8	hypertrichosis 2 (generalised, congenital)	Homo sapiens	23-26
8902207-6	1996	PD123319 inhibited the hCG-stimulated production of PGs by perfused rabbit ovaries in a dose-dependent manner, indicating that hCG-induced PG synthesis is mediated, at least in part, via the activation of AT2 receptors.	PD 123319	0-8	hypertrichosis 2 (generalised, congenital)	Homo sapiens	127-130
8902207-6	1996	PD123319 inhibited the hCG-stimulated production of PGs by perfused rabbit ovaries in a dose-dependent manner, indicating that hCG-induced PG synthesis is mediated, at least in part, via the activation of AT2 receptors.	Phosphatidylglycerols	52-55	hypertrichosis 2 (generalised, congenital)	Homo sapiens	23-26
8902207-6	1996	PD123319 inhibited the hCG-stimulated production of PGs by perfused rabbit ovaries in a dose-dependent manner, indicating that hCG-induced PG synthesis is mediated, at least in part, via the activation of AT2 receptors.	Phosphatidylglycerols	52-55	hypertrichosis 2 (generalised, congenital)	Homo sapiens	127-130
8902207-6	1996	PD123319 inhibited the hCG-stimulated production of PGs by perfused rabbit ovaries in a dose-dependent manner, indicating that hCG-induced PG synthesis is mediated, at least in part, via the activation of AT2 receptors.	Prostaglandins	52-54	hypertrichosis 2 (generalised, congenital)	Homo sapiens	23-26
8902207-6	1996	PD123319 inhibited the hCG-stimulated production of PGs by perfused rabbit ovaries in a dose-dependent manner, indicating that hCG-induced PG synthesis is mediated, at least in part, via the activation of AT2 receptors.	Prostaglandins	52-54	hypertrichosis 2 (generalised, congenital)	Homo sapiens	127-130
8902207-7	1996	Ovulatory efficiency in ovaries perfused with or without PD123319 in the presence of hCG was significantly correlated with PG production by perfused rabbit ovaries 12 h after exposure to hCG (r = 0.6553 for PGE2, p &lt; 0.001; r = 0.4758 for PGF2 alpha, p &lt; 0.05).	PD 123319	57-65	hypertrichosis 2 (generalised, congenital)	Homo sapiens	85-88
8902207-7	1996	Ovulatory efficiency in ovaries perfused with or without PD123319 in the presence of hCG was significantly correlated with PG production by perfused rabbit ovaries 12 h after exposure to hCG (r = 0.6553 for PGE2, p &lt; 0.001; r = 0.4758 for PGF2 alpha, p &lt; 0.05).	PD 123319	57-65	hypertrichosis 2 (generalised, congenital)	Homo sapiens	187-190
8902207-7	1996	Ovulatory efficiency in ovaries perfused with or without PD123319 in the presence of hCG was significantly correlated with PG production by perfused rabbit ovaries 12 h after exposure to hCG (r = 0.6553 for PGE2, p &lt; 0.001; r = 0.4758 for PGF2 alpha, p &lt; 0.05).	Prostaglandins	123-125	hypertrichosis 2 (generalised, congenital)	Homo sapiens	187-190
8902207-7	1996	Ovulatory efficiency in ovaries perfused with or without PD123319 in the presence of hCG was significantly correlated with PG production by perfused rabbit ovaries 12 h after exposure to hCG (r = 0.6553 for PGE2, p &lt; 0.001; r = 0.4758 for PGF2 alpha, p &lt; 0.05).	Dinoprostone	207-211	hypertrichosis 2 (generalised, congenital)	Homo sapiens	187-190
8902207-7	1996	Ovulatory efficiency in ovaries perfused with or without PD123319 in the presence of hCG was significantly correlated with PG production by perfused rabbit ovaries 12 h after exposure to hCG (r = 0.6553 for PGE2, p &lt; 0.001; r = 0.4758 for PGF2 alpha, p &lt; 0.05).	Dinoprost	242-252	hypertrichosis 2 (generalised, congenital)	Homo sapiens	85-88
8902207-7	1996	Ovulatory efficiency in ovaries perfused with or without PD123319 in the presence of hCG was significantly correlated with PG production by perfused rabbit ovaries 12 h after exposure to hCG (r = 0.6553 for PGE2, p &lt; 0.001; r = 0.4758 for PGF2 alpha, p &lt; 0.05).	Dinoprost	242-252	hypertrichosis 2 (generalised, congenital)	Homo sapiens	187-190
8862785-10	1996	Stimulation with hCG (0.1 mg/L) during the 3-day culture caused homologous desensitization of cAMP production, but stimulation with FSH (0.1 mg/L) had no such effect.	Cyclic AMP	94-98	hypertrichosis 2 (generalised, congenital)	Homo sapiens	17-20
8862785-13	1996	The hCG-induced steroidogenesis (progesterone and testosterone production) was not desensitized.	Progesterone	33-45	hypertrichosis 2 (generalised, congenital)	Homo sapiens	4-7
8862785-9	1996	In a similar experiment with 7-day-old ovarian cells, cAMP production was stimulated by both FSH and hCG.	Cyclic AMP	54-58	hypertrichosis 2 (generalised, congenital)	Homo sapiens	101-104
8862785-13	1996	The hCG-induced steroidogenesis (progesterone and testosterone production) was not desensitized.	Testosterone	50-62	hypertrichosis 2 (generalised, congenital)	Homo sapiens	4-7
8857201-4	1996	If male pseudohermaphroditism is suspected on the basis of palpable gonads, we routinely obtain a karyotype, basal adrenal steroid levels, and levels of hCG-stimulated serum testosterone and DHT, then consider a testosterone treatment trial.	Testosterone	174-186	hypertrichosis 2 (generalised, congenital)	Homo sapiens	153-156
8708566-7	1996	RU486 was administered (twice daily for 4 days, 1 mg/injection) to LHRH antagonist-treated rats in which follicular growth and differentiation were stimulated by 10 IU recFSH or by 10 IU recFSH plus 0.5 IU human chorionic gonadotrophin (hCG).	Mifepristone	0-5	hypertrichosis 2 (generalised, congenital)	Homo sapiens	237-240
8708566-8	1996	RU486 had no effect on circulating levels of LH and FSH, but stimulated follicular atresia both in rats treated with recFSH alone and in rats treated with recFSH and hCG.	Mifepristone	0-5	hypertrichosis 2 (generalised, congenital)	Homo sapiens	166-169
9387790-2	1996	0.52 nmol/L hCG 0.1 mumol/L cholera toxin and 10 mumol/L forskolin signifcantly stimulated production of cAMP (Cholera toxin &gt; Forskolin &gt; hCG) and testosterone (no signifcient differences among cholera toxin, Forskolin and hCG).	Colforsin	57-66	hypertrichosis 2 (generalised, congenital)	Homo sapiens	12-15
9387790-2	1996	0.52 nmol/L hCG 0.1 mumol/L cholera toxin and 10 mumol/L forskolin signifcantly stimulated production of cAMP (Cholera toxin &gt; Forskolin &gt; hCG) and testosterone (no signifcient differences among cholera toxin, Forskolin and hCG).	Colforsin	57-66	hypertrichosis 2 (generalised, congenital)	Homo sapiens	145-148
9387790-2	1996	0.52 nmol/L hCG 0.1 mumol/L cholera toxin and 10 mumol/L forskolin signifcantly stimulated production of cAMP (Cholera toxin &gt; Forskolin &gt; hCG) and testosterone (no signifcient differences among cholera toxin, Forskolin and hCG).	Colforsin	57-66	hypertrichosis 2 (generalised, congenital)	Homo sapiens	145-148
8857201-4	1996	If male pseudohermaphroditism is suspected on the basis of palpable gonads, we routinely obtain a karyotype, basal adrenal steroid levels, and levels of hCG-stimulated serum testosterone and DHT, then consider a testosterone treatment trial.	Dihydrotestosterone	191-194	hypertrichosis 2 (generalised, congenital)	Homo sapiens	153-156
9387790-2	1996	0.52 nmol/L hCG 0.1 mumol/L cholera toxin and 10 mumol/L forskolin signifcantly stimulated production of cAMP (Cholera toxin &gt; Forskolin &gt; hCG) and testosterone (no signifcient differences among cholera toxin, Forskolin and hCG).	Cyclic AMP	105-109	hypertrichosis 2 (generalised, congenital)	Homo sapiens	12-15
9387790-2	1996	0.52 nmol/L hCG 0.1 mumol/L cholera toxin and 10 mumol/L forskolin signifcantly stimulated production of cAMP (Cholera toxin &gt; Forskolin &gt; hCG) and testosterone (no signifcient differences among cholera toxin, Forskolin and hCG).	Cyclic AMP	105-109	hypertrichosis 2 (generalised, congenital)	Homo sapiens	145-148
8661355-5	1996	That is, neonatal exposure to phenobarbital enhanced the responsiveness to exogenous hCG as measured by an above-normal increase in testosterone concentration.	Phenobarbital	30-43	hypertrichosis 2 (generalised, congenital)	Homo sapiens	85-88
9387790-2	1996	0.52 nmol/L hCG 0.1 mumol/L cholera toxin and 10 mumol/L forskolin signifcantly stimulated production of cAMP (Cholera toxin &gt; Forskolin &gt; hCG) and testosterone (no signifcient differences among cholera toxin, Forskolin and hCG).	Cyclic AMP	105-109	hypertrichosis 2 (generalised, congenital)	Homo sapiens	145-148
9387790-2	1996	0.52 nmol/L hCG 0.1 mumol/L cholera toxin and 10 mumol/L forskolin signifcantly stimulated production of cAMP (Cholera toxin &gt; Forskolin &gt; hCG) and testosterone (no signifcient differences among cholera toxin, Forskolin and hCG).	Colforsin	130-139	hypertrichosis 2 (generalised, congenital)	Homo sapiens	12-15
9387790-2	1996	0.52 nmol/L hCG 0.1 mumol/L cholera toxin and 10 mumol/L forskolin signifcantly stimulated production of cAMP (Cholera toxin &gt; Forskolin &gt; hCG) and testosterone (no signifcient differences among cholera toxin, Forskolin and hCG).	Colforsin	130-139	hypertrichosis 2 (generalised, congenital)	Homo sapiens	145-148
9387790-2	1996	0.52 nmol/L hCG 0.1 mumol/L cholera toxin and 10 mumol/L forskolin signifcantly stimulated production of cAMP (Cholera toxin &gt; Forskolin &gt; hCG) and testosterone (no signifcient differences among cholera toxin, Forskolin and hCG).	Colforsin	130-139	hypertrichosis 2 (generalised, congenital)	Homo sapiens	145-148
9387790-2	1996	0.52 nmol/L hCG 0.1 mumol/L cholera toxin and 10 mumol/L forskolin signifcantly stimulated production of cAMP (Cholera toxin &gt; Forskolin &gt; hCG) and testosterone (no signifcient differences among cholera toxin, Forskolin and hCG).	Testosterone	154-166	hypertrichosis 2 (generalised, congenital)	Homo sapiens	12-15
9387790-2	1996	0.52 nmol/L hCG 0.1 mumol/L cholera toxin and 10 mumol/L forskolin signifcantly stimulated production of cAMP (Cholera toxin &gt; Forskolin &gt; hCG) and testosterone (no signifcient differences among cholera toxin, Forskolin and hCG).	Testosterone	154-166	hypertrichosis 2 (generalised, congenital)	Homo sapiens	145-148
9387790-2	1996	0.52 nmol/L hCG 0.1 mumol/L cholera toxin and 10 mumol/L forskolin signifcantly stimulated production of cAMP (Cholera toxin &gt; Forskolin &gt; hCG) and testosterone (no signifcient differences among cholera toxin, Forskolin and hCG).	Testosterone	154-166	hypertrichosis 2 (generalised, congenital)	Homo sapiens	145-148
9387790-2	1996	0.52 nmol/L hCG 0.1 mumol/L cholera toxin and 10 mumol/L forskolin signifcantly stimulated production of cAMP (Cholera toxin &gt; Forskolin &gt; hCG) and testosterone (no signifcient differences among cholera toxin, Forskolin and hCG).	Colforsin	216-225	hypertrichosis 2 (generalised, congenital)	Homo sapiens	12-15
9387790-2	1996	0.52 nmol/L hCG 0.1 mumol/L cholera toxin and 10 mumol/L forskolin signifcantly stimulated production of cAMP (Cholera toxin &gt; Forskolin &gt; hCG) and testosterone (no signifcient differences among cholera toxin, Forskolin and hCG).	Colforsin	216-225	hypertrichosis 2 (generalised, congenital)	Homo sapiens	145-148
9387790-2	1996	0.52 nmol/L hCG 0.1 mumol/L cholera toxin and 10 mumol/L forskolin signifcantly stimulated production of cAMP (Cholera toxin &gt; Forskolin &gt; hCG) and testosterone (no signifcient differences among cholera toxin, Forskolin and hCG).	Colforsin	216-225	hypertrichosis 2 (generalised, congenital)	Homo sapiens	145-148
9387790-3	1996	Ovalbumin glycopeptides prepared by extensive pronase digestion significantly inhibited production of cAMP and testosterone of rat testis Leydig cells stimulated by hCG, cholera toxin and forskolin.	Cyclic AMP	102-106	hypertrichosis 2 (generalised, congenital)	Homo sapiens	165-168
9387790-3	1996	Ovalbumin glycopeptides prepared by extensive pronase digestion significantly inhibited production of cAMP and testosterone of rat testis Leydig cells stimulated by hCG, cholera toxin and forskolin.	Testosterone	111-123	hypertrichosis 2 (generalised, congenital)	Homo sapiens	165-168
9387790-4	1996	These results suggest that the carbohydrate moiety of hCG participate in the signal transduction among receptor, G-protein and adenylatecyclase which is inhibited by Asn-linked oligosaccharide chains from ovalbumin glycopeptides.	Carbohydrates	31-43	hypertrichosis 2 (generalised, congenital)	Homo sapiens	54-57
9387790-4	1996	These results suggest that the carbohydrate moiety of hCG participate in the signal transduction among receptor, G-protein and adenylatecyclase which is inhibited by Asn-linked oligosaccharide chains from ovalbumin glycopeptides.	asn-linked oligosaccharide	166-192	hypertrichosis 2 (generalised, congenital)	Homo sapiens	54-57
9387790-4	1996	These results suggest that the carbohydrate moiety of hCG participate in the signal transduction among receptor, G-protein and adenylatecyclase which is inhibited by Asn-linked oligosaccharide chains from ovalbumin glycopeptides.	Glycopeptides	215-228	hypertrichosis 2 (generalised, congenital)	Homo sapiens	54-57
8732685-4	1996	When compared with cells expressing an equivalent density of wild type rLHR (rLHR-wt), concentration-response curves for the hCG-stimulated cAMP accumulation in cells expressing rLRH-D383N- are characterized by an 18-fold increase in the EC50 but no change in the maximal response.	Cyclic AMP	140-144	hypertrichosis 2 (generalised, congenital)	Homo sapiens	125-128
8732685-7	1996	When compared with cells expressing an equivalent density of rLHR-wt, concentration-response curves for the hCG-stimulated cAMP accumulation in cells expressing rLHR-R442H are characterized by a 7-fold increase in the EC50 and a 6- to 10-fold decrease in the maximal response.	Cyclic AMP	123-127	hypertrichosis 2 (generalised, congenital)	Homo sapiens	108-111
8761965-7	1996	Exogenous dibutyryl cAMP increased hCG and progesterone release by normoxic trophoblast but not by hypoxic cells.	Bucladesine	10-24	hypertrichosis 2 (generalised, congenital)	Homo sapiens	35-38
16727857-10	1996	In Experiment 2, the effects of intrauterine infusion of indomethacin on the diameter, function and life span of hCG-induced CL were examined.	Indomethacin	57-69	hypertrichosis 2 (generalised, congenital)	Homo sapiens	113-116
16727857-15	1996	In conclusion, the results suggest that 1) hCG-induced CL are functional but appear to be smaller and secrete less P(4) than spontaneous CL of similar age, and 2) the small size and reduced secretary function observed is not necessarily due to PGF(2alpha) secreted by the uterine endometrium but, probably, to inherent characteristics.	Prostaglandins F	244-247	hypertrichosis 2 (generalised, congenital)	Homo sapiens	43-46
8661355-5	1996	That is, neonatal exposure to phenobarbital enhanced the responsiveness to exogenous hCG as measured by an above-normal increase in testosterone concentration.	Testosterone	132-144	hypertrichosis 2 (generalised, congenital)	Homo sapiens	85-88
8557706-3	1996	We have investigated the role of several ionizable amino acid residues of rat LH/CG-R in human choriogonadotropin (hCG) binding and hCG-mediated cAMP production.	Cyclic AMP	145-149	hypertrichosis 2 (generalised, congenital)	Homo sapiens	132-135
8812244-6	1996	The function of the treated Leydig cell was evaluated by measuring the release of testosterone in response to human chorionic gonadotropin (hCG).	Testosterone	82-94	hypertrichosis 2 (generalised, congenital)	Homo sapiens	140-143
8812244-7	1996	In general, the peroxisome proliferators reduced the hCG-stimulated release of testosterone and either reduced or had no effect on the baseline release of testosterone.	Testosterone	79-91	hypertrichosis 2 (generalised, congenital)	Homo sapiens	53-56
8734477-7	1996	The intracellular concentration of cAMP was increased in response to hCG binding.	Cyclic AMP	35-39	hypertrichosis 2 (generalised, congenital)	Homo sapiens	69-72
8734477-8	1996	In contrast, baculovirus-expressed recombinant hCG only weakly stimulated intracellular cAMP levels at relatively high doses.	Cyclic AMP	88-92	hypertrichosis 2 (generalised, congenital)	Homo sapiens	47-50
8593787-3	1996	IGFBP-3 (100 ng/ml) significantly inhibited the resumption of meiosis in ovulated ova and follicular oocytes in hCG-treated ovaries, as well as the hCG-stimulated production of estradiol (E2), but not progesterone, by the perfused ovaries.	Estradiol	177-186	hypertrichosis 2 (generalised, congenital)	Homo sapiens	148-151
8645633-5	1996	In the present study, we have shown that the time course of synthesis of protein A and its hCG dose-response closely parallel the increase in progesterone production.	Progesterone	142-154	hypertrichosis 2 (generalised, congenital)	Homo sapiens	91-94
9363201-4	1996	At the end of each experiment the DCIP in the decidual culture medium was measured by bioassay: the percentage reduction, from control, of hCG production by JEG-3 cells exposed to 30% DCIP-containing decidual culture medium.	dcip	34-38	hypertrichosis 2 (generalised, congenital)	Homo sapiens	139-142
9363201-4	1996	At the end of each experiment the DCIP in the decidual culture medium was measured by bioassay: the percentage reduction, from control, of hCG production by JEG-3 cells exposed to 30% DCIP-containing decidual culture medium.	dcip	184-188	hypertrichosis 2 (generalised, congenital)	Homo sapiens	139-142
8772614-5	1996	Serum levels of estradiol and hCG were significantly elevated in both the systemic and spermatic veins of patients with NS compared to normal values, but they were within normal limits in patients with S. The histological score count in the contralateral testis was significantly and inversely correlated with the tumor weight and serum levels of hCG and estradiol.	Estradiol	355-364	hypertrichosis 2 (generalised, congenital)	Homo sapiens	30-33
8557159-1	1996	OBJECTIVE: To investigate the capacity of the human corpus luteum (CL) of pregnancy to form cyclic adenosine-3",5"-monophosphate (cAMP) and P in vitro in response to hCG and prostaglandin (PG) E2.	Cyclic AMP	92-128	hypertrichosis 2 (generalised, congenital)	Homo sapiens	166-169
9244169-3	1996	Further studies were performed to determine whether human chorionic gonadotropin (hCG) can interact with the insulin-like growth factor-I (IGF-I) signaling pathway to increase tyrosine phosphorylation of IRS-I.	Tyrosine	176-184	hypertrichosis 2 (generalised, congenital)	Homo sapiens	82-85
9244169-7	1996	The increased tyrosine phosphorylation of IRS-I seen in response to IGF-I stimulation following treatment with either hCG or forskolin was not due to an increase in IRS-I content.	Tyrosine	14-22	hypertrichosis 2 (generalised, congenital)	Homo sapiens	118-121
9244169-9	1996	Thus, we conclude that hCG/LH and IGF-I signaling pathways "cross-talk" to increase the levels of IRS-I tyrosine phosphorylation.	Tyrosine	104-112	hypertrichosis 2 (generalised, congenital)	Homo sapiens	23-26
8557159-1	1996	OBJECTIVE: To investigate the capacity of the human corpus luteum (CL) of pregnancy to form cyclic adenosine-3",5"-monophosphate (cAMP) and P in vitro in response to hCG and prostaglandin (PG) E2.	Cyclic AMP	130-134	hypertrichosis 2 (generalised, congenital)	Homo sapiens	166-169
8557159-8	1996	In pregnancies with plateauing and/or decreasing serum hCG levels, the addition of hCG in vitro significantly stimulated cAMP and P formation, and this stimulatory effect correlated significantly with the preoperative daily change in serum hCG.	Cyclic AMP	121-125	hypertrichosis 2 (generalised, congenital)	Homo sapiens	83-86
8557159-8	1996	In pregnancies with plateauing and/or decreasing serum hCG levels, the addition of hCG in vitro significantly stimulated cAMP and P formation, and this stimulatory effect correlated significantly with the preoperative daily change in serum hCG.	Cyclic AMP	121-125	hypertrichosis 2 (generalised, congenital)	Homo sapiens	83-86
8762457-5	1996	The steroidogenic response of granulosa cells to hCG was inhibited by (+/-) gossypol at 10 and 30 micrograms.ml-1.	Gossypol	70-84	hypertrichosis 2 (generalised, congenital)	Homo sapiens	49-52
8550788-6	1996	Addition of FSH, LH or hCG (30ng/mL) to the incubation medium enhanced progesterone production 2 to 3-fold, but had no effect on aromatase activity.	Progesterone	71-83	hypertrichosis 2 (generalised, congenital)	Homo sapiens	23-26
8984190-3	1996	Fadrozole treatment significantly reduced the number of healthy antral follicles produced and the ovulatory response to exogenous hCG of immature rats primed with pregnant mares" serum gonadotrophin.	Fadrozole	0-9	hypertrichosis 2 (generalised, congenital)	Homo sapiens	130-133
8594297-0	1996	Cocaine inhibits hCG secretion by the human term placental cotyledon perfused in vitro.	Cocaine	0-7	hypertrichosis 2 (generalised, congenital)	Homo sapiens	17-20
8594297-4	1996	This reduction in hCG concentration in the maternal circulation may effect normal steroidogenesis required to maintain pregnancy and may contribute to our understanding of the reproductive toxicology of cocaine.	Cocaine	203-210	hypertrichosis 2 (generalised, congenital)	Homo sapiens	18-21
8527508-6	1995	Nuclei from rat ovaries primed with eCG and hCG, but not DES, substantially degraded their DNA in an apoptotic fashion, and this DNA degradation was Ca2+/Mg(2+)-dependent and inhibited by Zn2+.	magnesium ion	154-160	hypertrichosis 2 (generalised, congenital)	Homo sapiens	44-47
8530405-3	1995	Human choriogonadotropin (hCG) binding was determined, as was hCG-mediated cAMP production.	Cyclic AMP	75-79	hypertrichosis 2 (generalised, congenital)	Homo sapiens	62-65
8530405-5	1995	The most interesting observation was noted with two point mutants of LH/CG-R, Glu332--&gt;Lys and Asp333--&gt;Lys, which bound hCG but failed to give increased cAMP production.	Lysine	110-113	hypertrichosis 2 (generalised, congenital)	Homo sapiens	127-130
8548062-5	1995	At the same time, A II increased the in vitro hCG-stimulated secretion of testosterone by theca.	Testosterone	74-86	hypertrichosis 2 (generalised, congenital)	Homo sapiens	46-49
8548062-6	1995	In granulosa, A II decreased hCG-stimulated aromatization of androstenedione to estradiol but did not alter the release of hCG-stimulated progesterone production.	Androstenedione	61-76	hypertrichosis 2 (generalised, congenital)	Homo sapiens	29-32
8548062-6	1995	In granulosa, A II decreased hCG-stimulated aromatization of androstenedione to estradiol but did not alter the release of hCG-stimulated progesterone production.	Estradiol	80-89	hypertrichosis 2 (generalised, congenital)	Homo sapiens	29-32
8822325-5	1995	Serum testosterone responses to hCG loading were significantly higher in 4-week-old rats treated with GH and/or IGF-I for 1 week than in control rats.	Testosterone	6-18	hypertrichosis 2 (generalised, congenital)	Homo sapiens	32-35
8822325-7	1995	After one-week treatment with GH and/or IGF-I, isolated Leydig cells were prepared from testes of 4-week-old rats and testosterone production by the stimulation of hCG was examined.	Testosterone	118-130	hypertrichosis 2 (generalised, congenital)	Homo sapiens	164-167
8822325-8	1995	Amounts of testosterone production stimulated by hCG were significantly greater in the treated rats than in control rats.	Testosterone	11-23	hypertrichosis 2 (generalised, congenital)	Homo sapiens	49-52
8748135-6	1995	After the cells were washed, cAMP synthesis in response to human chorionic gonadotrophin (hCG) increased by two to three times the control value and this increase was closely correlated with an increase in EGF receptor content.	Cyclic AMP	29-33	hypertrichosis 2 (generalised, congenital)	Homo sapiens	90-93
8748135-8	1995	Induction of EGF potentiation required long-term exposure to EGF, for at least more than 24 h. In addition, progesterone synthesis was sensitive to stimulation with lower doses of hCG.	Progesterone	108-120	hypertrichosis 2 (generalised, congenital)	Homo sapiens	180-183
8527508-6	1995	Nuclei from rat ovaries primed with eCG and hCG, but not DES, substantially degraded their DNA in an apoptotic fashion, and this DNA degradation was Ca2+/Mg(2+)-dependent and inhibited by Zn2+.	Zinc	188-192	hypertrichosis 2 (generalised, congenital)	Homo sapiens	44-47
7578686-5	1995	When a submaximal dosage of CRH was given together with a maximal dosage of hCG, steroid production was stimulated even more highly in MA-10 cells.	Steroids	81-88	hypertrichosis 2 (generalised, congenital)	Homo sapiens	76-79
7675413-3	1995	CASE: A 32-year-old woman had a persistently elevated serum hCG level analyzed by enzyme immunoassay technique before and after being treated with three courses of methotrexate.	Methotrexate	164-176	hypertrichosis 2 (generalised, congenital)	Homo sapiens	60-63
7578698-5	1995	The loss of responsiveness to hCG was not attributable to impaired accumulation of cyclic AMP: basal and hCG-stimulated cyclic AMP concentrations were similar in luteal tissues of estradiol-maintained and estradiol-withdrawn rabbits.	Cyclic AMP	120-130	hypertrichosis 2 (generalised, congenital)	Homo sapiens	105-108
7655650-3	1995	Serum and intratesticular testosterone were at supraphysiological levels in hCG-treated animals and rose even more after combined treatment; a minor elevation of intratesticular testosterone was also observed after FSH treatment.	Testosterone	26-38	hypertrichosis 2 (generalised, congenital)	Homo sapiens	76-79
7660770-8	1995	Eight women in the sonography group received a second glucose injection because of a rising hCG, increasing the success rate in this group to 82.1% (32 of 39 women).	Glucose	54-61	hypertrichosis 2 (generalised, congenital)	Homo sapiens	92-95
8527814-0	1995	The effect of oxytocin on hCG action in phosphoinositide turnover in porcine myometrial smooth muscle cells.	Phosphatidylinositols	40-56	hypertrichosis 2 (generalised, congenital)	Homo sapiens	26-29
8527814-1	1995	The aim of this study was to investigate the effects of hCG, hCG plus oxytocin and oxytocin on [3H] inositol phosphate (IP) formations in porcine myometrial cells obtained from ovariectomized and cyclic gilts.	Tritium	96-99	hypertrichosis 2 (generalised, congenital)	Homo sapiens	61-64
8527814-1	1995	The aim of this study was to investigate the effects of hCG, hCG plus oxytocin and oxytocin on [3H] inositol phosphate (IP) formations in porcine myometrial cells obtained from ovariectomized and cyclic gilts.	Inositol Phosphates	100-118	hypertrichosis 2 (generalised, congenital)	Homo sapiens	56-59
8527814-1	1995	The aim of this study was to investigate the effects of hCG, hCG plus oxytocin and oxytocin on [3H] inositol phosphate (IP) formations in porcine myometrial cells obtained from ovariectomized and cyclic gilts.	Inositol Phosphates	100-118	hypertrichosis 2 (generalised, congenital)	Homo sapiens	61-64
8527814-1	1995	The aim of this study was to investigate the effects of hCG, hCG plus oxytocin and oxytocin on [3H] inositol phosphate (IP) formations in porcine myometrial cells obtained from ovariectomized and cyclic gilts.	Inositol Phosphates	120-122	hypertrichosis 2 (generalised, congenital)	Homo sapiens	56-59
8527814-1	1995	The aim of this study was to investigate the effects of hCG, hCG plus oxytocin and oxytocin on [3H] inositol phosphate (IP) formations in porcine myometrial cells obtained from ovariectomized and cyclic gilts.	Inositol Phosphates	120-122	hypertrichosis 2 (generalised, congenital)	Homo sapiens	61-64
8527814-5	1995	There was also a very significant increase of IP1 after the addition of 1000 mU hCG (p &lt; 0.001) and IP1 and IP3 when 1000 mU hCG plus oxytocin were added (p &lt; 0.001 and p &lt; 0.01, respectively).	Isopenicillin N	46-49	hypertrichosis 2 (generalised, congenital)	Homo sapiens	80-83
8527814-5	1995	There was also a very significant increase of IP1 after the addition of 1000 mU hCG (p &lt; 0.001) and IP1 and IP3 when 1000 mU hCG plus oxytocin were added (p &lt; 0.001 and p &lt; 0.01, respectively).	Isopenicillin N	46-49	hypertrichosis 2 (generalised, congenital)	Homo sapiens	128-131
8527814-9	1995	The highest dose of hCG plus oxytocin provoked accumulation of total [3H]inositol phosphate (p &lt; 0.05) 53% over the basal level on days 21/1 of the estrous cycle.	[3h]inositol phosphate	69-91	hypertrichosis 2 (generalised, congenital)	Homo sapiens	20-23
8527814-10	1995	The present study demonstrates that hCG and oxytocin can increase the accumulation of inositol phosphates in porcine myometrial cells.	Inositol Phosphates	86-105	hypertrichosis 2 (generalised, congenital)	Homo sapiens	36-39
7628372-6	1995	However, introduction of hCG (which has the biological properties of LH) into the cultures on day 1 resulted in follicular degeneration within 3-4 days of culture.	Luteinizing Hormone	69-71	hypertrichosis 2 (generalised, congenital)	Homo sapiens	25-28
7629236-1	1995	There are few critical studies on plasma testosterone (T) and 17 beta-estradiol (E2) levels in men with hCG-producing tumors, and the results are contradictory.	Testosterone	41-53	hypertrichosis 2 (generalised, congenital)	Homo sapiens	104-107
7629236-1	1995	There are few critical studies on plasma testosterone (T) and 17 beta-estradiol (E2) levels in men with hCG-producing tumors, and the results are contradictory.	Estradiol	62-79	hypertrichosis 2 (generalised, congenital)	Homo sapiens	104-107
7629236-9	1995	In patients with increased hCG values (i.e. &gt; 5 IU/L), the mean plasma P, 17-OHP, A, 17-OH delta 5-P, DHEA, T, and E2 levels were higher (P &lt; 0.01 at least) than those in patients whose hCG values were normalized or in controls.	17-alpha-Hydroxyprogesterone	77-83	hypertrichosis 2 (generalised, congenital)	Homo sapiens	27-30
7629236-9	1995	In patients with increased hCG values (i.e. &gt; 5 IU/L), the mean plasma P, 17-OHP, A, 17-OH delta 5-P, DHEA, T, and E2 levels were higher (P &lt; 0.01 at least) than those in patients whose hCG values were normalized or in controls.	17-oh delta 5-p	88-103	hypertrichosis 2 (generalised, congenital)	Homo sapiens	27-30
7629236-10	1995	The patterns of these steroids were very different according to plasma hCG levels.	Steroids	22-30	hypertrichosis 2 (generalised, congenital)	Homo sapiens	71-74
7629236-12	1995	Conversely, for hCG values greater than 3.5 x 10(3) IU/L, hCG levels were negatively correlated (P &lt; 0.05 at least) to all steroid values.	Steroids	126-133	hypertrichosis 2 (generalised, congenital)	Homo sapiens	16-19
7629236-12	1995	Conversely, for hCG values greater than 3.5 x 10(3) IU/L, hCG levels were negatively correlated (P &lt; 0.05 at least) to all steroid values.	Steroids	126-133	hypertrichosis 2 (generalised, congenital)	Homo sapiens	58-61
8554431-6	1995	It is recommended that hCG be administered to patients who undergo varicocelectomy but have persistent subtle Leydig cell dysfunction disclosed by LHRH test to stimulate the intratesticular testosterone production.	Testosterone	190-202	hypertrichosis 2 (generalised, congenital)	Homo sapiens	23-26
8527829-7	1995	In addition to its effect on placental permeability, cocaine decreases the rate of release of hCG into the maternal circulation--reduced from 3.11 (control period) to 1.62 IU/min (test phase, p &lt; .01).	Cocaine	53-60	hypertrichosis 2 (generalised, congenital)	Homo sapiens	94-97
8588072-0	1995	Arachidonic acid inhibits hCG-stimulated progesterone production by corpora lutea of primates: potential mechanism of action.	Arachidonic Acid	0-16	hypertrichosis 2 (generalised, congenital)	Homo sapiens	26-29
8588072-0	1995	Arachidonic acid inhibits hCG-stimulated progesterone production by corpora lutea of primates: potential mechanism of action.	Progesterone	41-53	hypertrichosis 2 (generalised, congenital)	Homo sapiens	26-29
8588072-5	1995	Basal and hCG-stimulated P4 production by luteal cells collected during the midluteal phase was measured after treatment with AA (1, 5, and 10 microM) or linoleic acid (1, 5, and 10 microM).	Linoleic Acid	154-167	hypertrichosis 2 (generalised, congenital)	Homo sapiens	10-13
8580875-6	1995	Dibutyryl cAMP (100 microM) produced an effect similar to that of hCG and both required external calcium for their action.	dibutyryl	0-9	hypertrichosis 2 (generalised, congenital)	Homo sapiens	66-69
7549796-1	1995	Studies of the induction of mammary tumors by 7,12-dimethylbenz(a)anthracene in a rat model show that human chorionic gonadotropin (hCG) administration reduces tumor incidence in a manner comparable to that of a completed pregnancy.	7,12-dimethylbenz(a	46-65	hypertrichosis 2 (generalised, congenital)	Homo sapiens	132-135
7549796-1	1995	Studies of the induction of mammary tumors by 7,12-dimethylbenz(a)anthracene in a rat model show that human chorionic gonadotropin (hCG) administration reduces tumor incidence in a manner comparable to that of a completed pregnancy.	anthracene	66-76	hypertrichosis 2 (generalised, congenital)	Homo sapiens	132-135
7549796-2	1995	On the basis of their studies, Russo and Russo (Cancer Epidemiol., Biomarkers &amp; Prev., 3: 353-364, 1994) have proposed that hCG treatment of young nulliparous women would reduce their breast cancer risk in a manner similar to that of a term pregnancy.	Adenosine Monophosphate	79-82	hypertrichosis 2 (generalised, congenital)	Homo sapiens	128-131
8584891-3	1995	A preliminary survey of the effect of the active oligopeptides on signal systems showed: (1)GY and YG inhibited PLC system; (2)GY and GSK reduced hCG-induced progesterone production in CL cells probably by regulating cellular Ca2+ concentration; (3) GSK decreased TPK activity and GYK increased it in hCG treated CL cell though both of them were inhibitory on progesterone production.	Progesterone	158-170	hypertrichosis 2 (generalised, congenital)	Homo sapiens	146-149
7632848-4	1995	A significant decrease in serum LH, 3 days after hCG injection, was observed for the first time in animals treated on Day 7, but not in those aged 1-6 days.	Luteinizing Hormone	32-34	hypertrichosis 2 (generalised, congenital)	Homo sapiens	49-52
7796925-9	1995	Response of serum testosterone to hCG administration correlated to the maturity of germ cells.	Testosterone	18-30	hypertrichosis 2 (generalised, congenital)	Homo sapiens	34-37
7750599-12	1995	Higher hCG levels may be due to decreased clearance of hCG from the circulation and/or the hCG content of hMG.	Menotropins	106-109	hypertrichosis 2 (generalised, congenital)	Homo sapiens	7-10
8706157-4	1995	Radioimmunodetection was performed using 131I labelled murine anti-hCG McAb.	Iodine-131	41-45	hypertrichosis 2 (generalised, congenital)	Homo sapiens	67-70
9098462-7	1995	In particular, in the patients treated with HMG+hCG, a mean monthly pregnancy rate equal to 10.9% and a cumulative pregnancy rate to 46% at the end of the six cycles were obtained.	Menotropins	44-47	hypertrichosis 2 (generalised, congenital)	Homo sapiens	48-51
7745007-5	1995	Interestingly, JP09 cells were readily stimulated by hCG (20-100 mg/L; 0.52-2.6 x 10(-6) mol/L) to release cAMP, whereas JP26 cells showed little if any response.	Cyclic AMP	107-111	hypertrichosis 2 (generalised, congenital)	Homo sapiens	53-56
7745007-6	1995	Also, cAMP stimulation produced by asialo-hCG was 12-fold in JP09 cells and only 4-fold in JP26 cells compared to 45- and 67-fold stimulations by bTSH, respectively.	Cyclic AMP	6-10	hypertrichosis 2 (generalised, congenital)	Homo sapiens	42-45
7745007-9	1995	Further studies with hCG, asialo-hCG, asialoagalacto-hCG, and deglycosylated hCG revealed that removal of sialic acid caused a marked increase in both its affinity for hTSHr and its cAMP-releasing potency, whereas removal of further carbohydrate, although it slightly enhanced receptor binding, was detrimental to adenylate cyclase activation.	N-Acetylneuraminic Acid	106-117	hypertrichosis 2 (generalised, congenital)	Homo sapiens	21-24
7745007-9	1995	Further studies with hCG, asialo-hCG, asialoagalacto-hCG, and deglycosylated hCG revealed that removal of sialic acid caused a marked increase in both its affinity for hTSHr and its cAMP-releasing potency, whereas removal of further carbohydrate, although it slightly enhanced receptor binding, was detrimental to adenylate cyclase activation.	N-Acetylneuraminic Acid	106-117	hypertrichosis 2 (generalised, congenital)	Homo sapiens	33-36
7745007-9	1995	Further studies with hCG, asialo-hCG, asialoagalacto-hCG, and deglycosylated hCG revealed that removal of sialic acid caused a marked increase in both its affinity for hTSHr and its cAMP-releasing potency, whereas removal of further carbohydrate, although it slightly enhanced receptor binding, was detrimental to adenylate cyclase activation.	N-Acetylneuraminic Acid	106-117	hypertrichosis 2 (generalised, congenital)	Homo sapiens	33-36
7745007-9	1995	Further studies with hCG, asialo-hCG, asialoagalacto-hCG, and deglycosylated hCG revealed that removal of sialic acid caused a marked increase in both its affinity for hTSHr and its cAMP-releasing potency, whereas removal of further carbohydrate, although it slightly enhanced receptor binding, was detrimental to adenylate cyclase activation.	N-Acetylneuraminic Acid	106-117	hypertrichosis 2 (generalised, congenital)	Homo sapiens	33-36
7745007-10	1995	In conclusion, differences in hTSHr expression may cause a variation in the cAMP response to hCG or its glycosylation variants, as does the microheterogeneity of the hormone itself.	Cyclic AMP	76-80	hypertrichosis 2 (generalised, congenital)	Homo sapiens	93-96
8659290-3	1995	This paper reports one case of an infertile male treated with hCG/hMG after surgical correction of a varicocele, which resulted in a feminization effect evidenced by gynaecomastia and severe spermatogenesis blockade.	Menotropins	66-69	hypertrichosis 2 (generalised, congenital)	Homo sapiens	62-65
7798021-4	1995	The three glycoproteins had an inhibitory effect on meningioma proliferation ranging from 5.0-50.0%, 10.0-63.0% and 2.4-34.0% at the highest concentrations of LH (25 mIU/ml), FSH (15 mIU/ml) and hCG (30 IU/ml) respectively.	Luteinizing Hormone	159-161	hypertrichosis 2 (generalised, congenital)	Homo sapiens	195-198
7798031-7	1995	Injection of 50 IU hCG at various times after removal of the implant produced time-dependent changes in CYP17 activity and serum androstenedione levels, when measured 30 h later.	Androstenedione	129-144	hypertrichosis 2 (generalised, congenital)	Homo sapiens	19-22
7852507-7	1995	Asialo-hCG purified from a patient with choriocarcinoma had very potent TSH-like activity (468 microU hTSH/mg).	Thyrotropin	72-75	hypertrichosis 2 (generalised, congenital)	Homo sapiens	7-10
8520182-1	1995	OBJECTIVES: Previous research from this laboratory has suggested that a relationship exists between the increase in circulating progesterone concentrations at the time of hCG administration and cycle outcome in patients undergoing IVF.	Progesterone	128-140	hypertrichosis 2 (generalised, congenital)	Homo sapiens	171-174
8520185-0	1995	Progesterone concentration as a predictor of pregnancy normalcy is the most useful when hCG levels are less than 2000 mIU/mL.	Progesterone	0-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	88-91
8520185-2	1995	Since ultrasound would be the diagnostic tool of choice if hCG was &gt; 2000 mIU/ml, the purpose of the present study was to determine the best predictive value of a single progesterone measurement when hCG levels were &lt; 2000 mIU/ml.	Progesterone	173-185	hypertrichosis 2 (generalised, congenital)	Homo sapiens	203-206
8520185-11	1995	Calculation of the critical ratio z revealed that there is a significant improvement in the predictive value of progesterone when hCG is &lt; 2000 mIU/ml (P &lt; 0.005).	Progesterone	112-124	hypertrichosis 2 (generalised, congenital)	Homo sapiens	130-133
7652182-6	1995	Prostaglandin E2 increased (P &lt; 0.01) at 6 hours after hCG and did not decrease from the peak value until (P &lt; 0.01) 14 hours after hCG.	Dinoprostone	0-16	hypertrichosis 2 (generalised, congenital)	Homo sapiens	58-61
7652182-7	1995	Concentrations of PGF2 alpha increased (P &lt; 0.01) at 4 hours after hCG, but decreased (P &lt; 0.01) from the peak by 10 hours.	Dinoprost	18-22	hypertrichosis 2 (generalised, congenital)	Homo sapiens	70-73
7851573-1	1995	OBJECTIVE: To investigate the clinical performance of local prostaglandin treatment of ectopic pregnancies (EPs) in relation to their biologic activity as determined by preoperative serum hCG levels.	Prostaglandins	60-73	hypertrichosis 2 (generalised, congenital)	Homo sapiens	188-191
7536048-9	1995	Effects of hCG-induced luteinization of cultures on Fas mAb-induced cytotoxicity was examined: combined pretreatment with IFN gamma and hCG induced a synergistic increase in Fas mAb-induced cytotoxicity (40%) over that obtained with IFN gamma-pretreatment alone (15%).	ammonium ferrous sulfate	52-55	hypertrichosis 2 (generalised, congenital)	Homo sapiens	136-139
7852507-10	1995	These in vitro findings suggest that although hCG is reported to exert potent cAMP-stimulating activity on rat thyroid-like cells (FRTL-5) and Chinese hamster ovary cells transfected with hTSH receptor complementary DNA (0.092-0.72 microU hTSH/U hCG), the thyrotropic activity induced by authentic hCG in human thyroid follicles is too weak to cause hyperthyroidism in normal pregnancy.	Cyclic AMP	78-82	hypertrichosis 2 (generalised, congenital)	Homo sapiens	46-49
7618186-0	1995	Re-examination of the effect of hCG on plasma levels and renal excretion of dehydroepiandrosterone sulfate in healthy males.	Dehydroepiandrosterone Sulfate	76-106	hypertrichosis 2 (generalised, congenital)	Homo sapiens	32-35
7572450-7	1995	The hCG group exhibited no signs of heat, and the follicles only reached 5-8 mm in diameter at time of ovulation, which occurred 40h +/- 1h after hCG-injection.	Hydrogen	137-139	hypertrichosis 2 (generalised, congenital)	Homo sapiens	146-149
7618186-4	1995	Contrary to previous findings in normal men, the present study revealed significant DHEAS responses after testicular stimulation with hCG: plasma DHEAS increased from 7.9 +/- 2.3 to 9.6 +/- 2.2 mumol/L (P &lt; 0.05) and urinary DHEAS from 5.7 +/- 3.6 to 9.3 +/- 5.2 mumol/day (P &lt; 0.05).	Dehydroepiandrosterone Sulfate	84-89	hypertrichosis 2 (generalised, congenital)	Homo sapiens	134-137
7618186-4	1995	Contrary to previous findings in normal men, the present study revealed significant DHEAS responses after testicular stimulation with hCG: plasma DHEAS increased from 7.9 +/- 2.3 to 9.6 +/- 2.2 mumol/L (P &lt; 0.05) and urinary DHEAS from 5.7 +/- 3.6 to 9.3 +/- 5.2 mumol/day (P &lt; 0.05).	Dehydroepiandrosterone Sulfate	146-151	hypertrichosis 2 (generalised, congenital)	Homo sapiens	134-137
7618186-4	1995	Contrary to previous findings in normal men, the present study revealed significant DHEAS responses after testicular stimulation with hCG: plasma DHEAS increased from 7.9 +/- 2.3 to 9.6 +/- 2.2 mumol/L (P &lt; 0.05) and urinary DHEAS from 5.7 +/- 3.6 to 9.3 +/- 5.2 mumol/day (P &lt; 0.05).	Dehydroepiandrosterone Sulfate	146-151	hypertrichosis 2 (generalised, congenital)	Homo sapiens	134-137
7618186-7	1995	Significant post-hCG changes were additionally observed for plasma and urinary 3 alpha-androstanediol glucuronide (149% and 79% increases, respectively) and for urinary cortisol (21% decrease).	androstane-3,17-diol glucuronide	79-113	hypertrichosis 2 (generalised, congenital)	Homo sapiens	17-20
7618186-8	1995	Significant correlations were found for the post-hCG percent increases of plasma androstenedione versus plasma DHEAS (r = 0.86) and for the percent increases of plasma testosterone versus urinary DHEAS (r = 0.98), indicating that the extent of gonadal androgen elevations in the circulation of normal men is a determinant of DHEAS increases in blood or urine.	Androstenedione	81-96	hypertrichosis 2 (generalised, congenital)	Homo sapiens	49-52
7618186-8	1995	Significant correlations were found for the post-hCG percent increases of plasma androstenedione versus plasma DHEAS (r = 0.86) and for the percent increases of plasma testosterone versus urinary DHEAS (r = 0.98), indicating that the extent of gonadal androgen elevations in the circulation of normal men is a determinant of DHEAS increases in blood or urine.	Dehydroepiandrosterone Sulfate	111-116	hypertrichosis 2 (generalised, congenital)	Homo sapiens	49-52
7824243-6	1995	The one treatment failure required methotrexate because of rising hCG titers and worsening pain 4 days after the patient was treated with hyperosmolar glucose.	Methotrexate	35-47	hypertrichosis 2 (generalised, congenital)	Homo sapiens	66-69
7536169-1	1994	The possibility of reversing the hypoxanthine induced 2-cell block in mouse embryos when cultured in conditions supplemented with compounds that increase (FSH, hMG, IBMX, hCG) or inhibit (GnRH-analogue) cAMP was assessed.	Hypoxanthine	33-45	hypertrichosis 2 (generalised, congenital)	Homo sapiens	171-174
11322326-3	1995	After injection of hCG into PMSG-primed immature mice, cumulus and mural granulosa cells adjacent to the antrum synthesized a large amount of such glycosaminoglycan, while the outermost layers layers of mural granulosa cells did not.	Glycosaminoglycans	147-164	hypertrichosis 2 (generalised, congenital)	Homo sapiens	19-22
7650310-5	1995	The use of STH to induce spermatogenesis is discussed in light of its capacity to increase testosterone synthesis is response to hCG.	STH	11-14	hypertrichosis 2 (generalised, congenital)	Homo sapiens	129-132
7650310-5	1995	The use of STH to induce spermatogenesis is discussed in light of its capacity to increase testosterone synthesis is response to hCG.	Testosterone	91-103	hypertrichosis 2 (generalised, congenital)	Homo sapiens	129-132
7707285-1	1995	The ability of luteal tissue from rhesus monkeys, collected from spontaneous and prostaglandin F2 alpha (PGF2 alpha) induced luteolytic cycles, to secrete progesterone in response to hCG or dibutyryl cAMP in vitro was assessed.	Progesterone	155-167	hypertrichosis 2 (generalised, congenital)	Homo sapiens	183-186
8775043-3	1995	The administration of HCG resulted in a low response of plasma testosterone.	Testosterone	63-75	hypertrichosis 2 (generalised, congenital)	Homo sapiens	22-25
7695043-8	1994	At 50 mm EtOH, the secretion of hCG in response to EGF was increased 2-fold.	Ethanol	9-13	hypertrichosis 2 (generalised, congenital)	Homo sapiens	32-35
7695043-9	1994	EtOH also increased basal hCG secretion in a dose-dependent manner between 10-50 mM EtOH.	Ethanol	0-4	hypertrichosis 2 (generalised, congenital)	Homo sapiens	26-29
7695043-9	1994	EtOH also increased basal hCG secretion in a dose-dependent manner between 10-50 mM EtOH.	Ethanol	84-88	hypertrichosis 2 (generalised, congenital)	Homo sapiens	26-29
7817723-2	1994	Methotrexate was given in spite of high levels of hCG and appeared to be successful.	Methotrexate	0-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	50-53
7926139-16	1994	The regression curve of hCG plasma levels appeared similar in the four groups with a decrease to pretreatment values between days 6 and 8 after an initial rise after MTX was given.	Methotrexate	166-169	hypertrichosis 2 (generalised, congenital)	Homo sapiens	24-27
7846554-6	1994	However, the suppressive effect of tyrosine on hCG- induced progesterone production was more pronounced in small luteal cells.	Tyrosine	35-43	hypertrichosis 2 (generalised, congenital)	Homo sapiens	47-50
7956942-9	1994	When the cells were treated with the protein synthesis inhibitor cycloheximide (20 micrograms/ml) 20 min before stimulation of the cells with hCG, both basal and hCG-stimulated FS mRNA levels increased at 24 h, indicating stabilization of the transcripts.	Cycloheximide	65-78	hypertrichosis 2 (generalised, congenital)	Homo sapiens	142-145
7956942-9	1994	When the cells were treated with the protein synthesis inhibitor cycloheximide (20 micrograms/ml) 20 min before stimulation of the cells with hCG, both basal and hCG-stimulated FS mRNA levels increased at 24 h, indicating stabilization of the transcripts.	Cycloheximide	65-78	hypertrichosis 2 (generalised, congenital)	Homo sapiens	162-165
7956942-10	1994	However, it did not affect the rapid induction of FS mRNA levels by hCG at 2 h. The decline in FS transcript levels in untreated and hCG-treated cells was studied by blocking the transcription with 5 microM actinomycin-D.	Dactinomycin	207-220	hypertrichosis 2 (generalised, congenital)	Homo sapiens	133-136
7880398-2	1994	This study was designed to determine if suppression by HME was correlated with gestational age, uterine size, or hCG secretion.	elliptinium	55-58	hypertrichosis 2 (generalised, congenital)	Homo sapiens	113-116
7962333-4	1994	After adrenal suppression by dexamethasone combined with gonadal stimulation with hCG, a dramatic decrease in androgens and adrenal steroids was observed in the peripheral blood.	Steroids	132-140	hypertrichosis 2 (generalised, congenital)	Homo sapiens	82-85
7846554-6	1994	However, the suppressive effect of tyrosine on hCG- induced progesterone production was more pronounced in small luteal cells.	Progesterone	60-72	hypertrichosis 2 (generalised, congenital)	Homo sapiens	47-50
16727535-5	1994	Testicular production of testosterone was stimulated by hCG at the stages studied from Day 40 on.	Testosterone	25-37	hypertrichosis 2 (generalised, congenital)	Homo sapiens	56-59
7799316-0	1994	Mechanisms controlling corpus luteum function in the rhesus monkey (Macaca mulatta): inhibitory action of hCG on luteolysis induced by PGF2 alpha.	Dinoprost	135-139	hypertrichosis 2 (generalised, congenital)	Homo sapiens	106-109
7799316-1	1994	The aim of this study was to determine whether daily increasing doses of hCG could overcome luteal regression induced by PGF2 alpha in rhesus monkeys.	Dinoprost	121-125	hypertrichosis 2 (generalised, congenital)	Homo sapiens	73-76
7799316-7	1994	Where intraluteally infused PGF2 alpha resulted in premature, functional luteolysis, hCG always inhibited the luteolytic effect of PGF2 alpha; the secretory patterns of progesterone and oestradiol were augmented, and peak values were reached in concert with the highest concentration of hCG in the blood, and the luteal phase was significantly increased compared with those of untreated monkeys or with monkeys treated with PGF2 alpha alone or vehicle.	Dinoprost	28-32	hypertrichosis 2 (generalised, congenital)	Homo sapiens	85-88
7799316-7	1994	Where intraluteally infused PGF2 alpha resulted in premature, functional luteolysis, hCG always inhibited the luteolytic effect of PGF2 alpha; the secretory patterns of progesterone and oestradiol were augmented, and peak values were reached in concert with the highest concentration of hCG in the blood, and the luteal phase was significantly increased compared with those of untreated monkeys or with monkeys treated with PGF2 alpha alone or vehicle.	Dinoprost	131-135	hypertrichosis 2 (generalised, congenital)	Homo sapiens	85-88
7799316-7	1994	Where intraluteally infused PGF2 alpha resulted in premature, functional luteolysis, hCG always inhibited the luteolytic effect of PGF2 alpha; the secretory patterns of progesterone and oestradiol were augmented, and peak values were reached in concert with the highest concentration of hCG in the blood, and the luteal phase was significantly increased compared with those of untreated monkeys or with monkeys treated with PGF2 alpha alone or vehicle.	Dinoprost	131-135	hypertrichosis 2 (generalised, congenital)	Homo sapiens	85-88
7799316-8	1994	Treatment with hCG alone or with PGF2 alpha vehicle also resulted in maintained luteal function and a significantly longer luteal phase, but both progesterone and oestradiol concentrations began to decline before hCG reached peak values in the circulation.	Dinoprost	33-37	hypertrichosis 2 (generalised, congenital)	Homo sapiens	15-18
7799316-8	1994	Treatment with hCG alone or with PGF2 alpha vehicle also resulted in maintained luteal function and a significantly longer luteal phase, but both progesterone and oestradiol concentrations began to decline before hCG reached peak values in the circulation.	Progesterone	146-158	hypertrichosis 2 (generalised, congenital)	Homo sapiens	15-18
7799316-8	1994	Treatment with hCG alone or with PGF2 alpha vehicle also resulted in maintained luteal function and a significantly longer luteal phase, but both progesterone and oestradiol concentrations began to decline before hCG reached peak values in the circulation.	Estradiol	163-173	hypertrichosis 2 (generalised, congenital)	Homo sapiens	15-18
7890146-3	1994	Membrane lipid rigidity, as determined by fluorescence polarization of DPH, decreased as early as 30 min after injection of a desensitizing dose of hCG.	Phenytoin	71-74	hypertrichosis 2 (generalised, congenital)	Homo sapiens	148-151
7821703-5	1994	The maximal increase in [Ca2+]i in response to hCG (approximately 100 nM) was about one-tenth that induced by PGF2 alpha (approximately 1000 nM).	Dinoprost	110-120	hypertrichosis 2 (generalised, congenital)	Homo sapiens	47-50
7938038-0	1994	Steroid secretion by follicles and cysts from the hypothyroid, hCG-treated rat.	Steroids	0-7	hypertrichosis 2 (generalised, congenital)	Homo sapiens	63-66
7938038-6	1994	After 10 days of treatment with hCG, antral follicles from hypothyroid, hCG-treated rats secreted two to three times more testosterone than similar follicles from euthyroid, saline-treated animals.	Testosterone	122-134	hypertrichosis 2 (generalised, congenital)	Homo sapiens	32-35
7938038-6	1994	After 10 days of treatment with hCG, antral follicles from hypothyroid, hCG-treated rats secreted two to three times more testosterone than similar follicles from euthyroid, saline-treated animals.	Testosterone	122-134	hypertrichosis 2 (generalised, congenital)	Homo sapiens	72-75
7938038-6	1994	After 10 days of treatment with hCG, antral follicles from hypothyroid, hCG-treated rats secreted two to three times more testosterone than similar follicles from euthyroid, saline-treated animals.	Sodium Chloride	174-180	hypertrichosis 2 (generalised, congenital)	Homo sapiens	32-35
7860425-1	1994	We have already reported that the rate of increase in the estradiol/testosterone ratio (E2/T ratio) following human chorionic gonadotropin (hCG) injection has prognostic value in the treatment of oligozoospermia.	Testosterone	68-80	hypertrichosis 2 (generalised, congenital)	Homo sapiens	140-143
7860425-7	1994	The rate of increase in the E2/T ratio during clomiphene citrate treatment showed a statistically positive correlation (r = 0.542) with the rate of increase following hCG injection performed before clomiphene citrate treatment.	Clomiphene	46-64	hypertrichosis 2 (generalised, congenital)	Homo sapiens	167-170
8034070-2	1994	STUDY DESIGN: The number of doublings of hCG per day (1/DT; reciprocal of hCG doubling time) was correlated with serum P using linear and nonlinear models in normal intrauterine pregnancies, spontaneous abortions, and ectopic pregnancies (EPs) conceived spontaneously or after clomiphene citrate (CC).	Clomiphene	277-295	hypertrichosis 2 (generalised, congenital)	Homo sapiens	41-44
8034070-3	1994	RESULTS: Linear correlations between P and 1/DTs of hCG were poor.	Phosphorus	37-38	hypertrichosis 2 (generalised, congenital)	Homo sapiens	52-55
7973829-3	1994	It was demonstrated that high Ca2+/high K+/A23187 significantly enhanced both the basal or hCG-induced progesterone production by rat luteal cells.	Calcimycin	43-49	hypertrichosis 2 (generalised, congenital)	Homo sapiens	91-94
7973829-3	1994	It was demonstrated that high Ca2+/high K+/A23187 significantly enhanced both the basal or hCG-induced progesterone production by rat luteal cells.	Progesterone	103-115	hypertrichosis 2 (generalised, congenital)	Homo sapiens	91-94
7973829-4	1994	To the contrast, decreased Ca2+ concentration in medium/EGTA/verapamil had inhibitory effect on progesterone production in the presence of hCG.	Egtazic Acid	56-60	hypertrichosis 2 (generalised, congenital)	Homo sapiens	139-142
7973829-4	1994	To the contrast, decreased Ca2+ concentration in medium/EGTA/verapamil had inhibitory effect on progesterone production in the presence of hCG.	Verapamil	61-70	hypertrichosis 2 (generalised, congenital)	Homo sapiens	139-142
7973829-4	1994	To the contrast, decreased Ca2+ concentration in medium/EGTA/verapamil had inhibitory effect on progesterone production in the presence of hCG.	Progesterone	96-108	hypertrichosis 2 (generalised, congenital)	Homo sapiens	139-142
7973829-5	1994	Tyr had suppressive effect on hCG-induced progesterone production.	Tyrosine	0-3	hypertrichosis 2 (generalised, congenital)	Homo sapiens	30-33
7973829-5	1994	Tyr had suppressive effect on hCG-induced progesterone production.	Progesterone	42-54	hypertrichosis 2 (generalised, congenital)	Homo sapiens	30-33
8027245-9	1994	Circulating LH-like bioactivity was elevated for more than 48 h after u-hCG.	Luteinizing Hormone	12-14	hypertrichosis 2 (generalised, congenital)	Homo sapiens	72-75
7956173-6	1994	When hCG (2IU/ml) was added to both culture media, the increment in testosterone production hence produced, was greater when cells were cultured in defined medium.	Testosterone	68-80	hypertrichosis 2 (generalised, congenital)	Homo sapiens	5-8
7956173-10	1994	Addition of hCG increased testosterone production by cells cultured in defined medium and enhanced its subsequent response to hCG stimulation.	Testosterone	26-38	hypertrichosis 2 (generalised, congenital)	Homo sapiens	12-15
7956173-13	1994	hCG caused a dose-related increased in testosterone production by cells cultured in defined and serum containing media, but concentrations of hCG above 2 IU/ml depressed testosterone production in the latter group.	Testosterone	39-51	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
7956173-13	1994	hCG caused a dose-related increased in testosterone production by cells cultured in defined and serum containing media, but concentrations of hCG above 2 IU/ml depressed testosterone production in the latter group.	Testosterone	170-182	hypertrichosis 2 (generalised, congenital)	Homo sapiens	142-145
7973337-9	1994	With regard to 17 beta-estradiol levels at the time of administration of hCG, 18 pregnancies (69.23%) were obtained in patients with a 17 beta-estradiol level &gt; or = to 1300, 7 (25.92%) in patients with a 17 beta-estradiol level &gt; or = to 1000 and &lt; or = to 1300 pg/ml and 3 (11.11%) in those with a 17 beta-estradiol level &lt; or = to 900 pg/ml.	Estradiol	15-32	hypertrichosis 2 (generalised, congenital)	Homo sapiens	73-76
7925626-6	1994	When hCG was administered to 5 monkeys in mating season (January), serum testosterone levels increased markedly 30 to 180 min after single administration and showed further increases after continuous administrations for four days.	Testosterone	73-85	hypertrichosis 2 (generalised, congenital)	Homo sapiens	5-8
7973337-9	1994	With regard to 17 beta-estradiol levels at the time of administration of hCG, 18 pregnancies (69.23%) were obtained in patients with a 17 beta-estradiol level &gt; or = to 1300, 7 (25.92%) in patients with a 17 beta-estradiol level &gt; or = to 1000 and &lt; or = to 1300 pg/ml and 3 (11.11%) in those with a 17 beta-estradiol level &lt; or = to 900 pg/ml.	Estradiol	135-152	hypertrichosis 2 (generalised, congenital)	Homo sapiens	73-76
7973337-9	1994	With regard to 17 beta-estradiol levels at the time of administration of hCG, 18 pregnancies (69.23%) were obtained in patients with a 17 beta-estradiol level &gt; or = to 1300, 7 (25.92%) in patients with a 17 beta-estradiol level &gt; or = to 1000 and &lt; or = to 1300 pg/ml and 3 (11.11%) in those with a 17 beta-estradiol level &lt; or = to 900 pg/ml.	Estradiol	135-152	hypertrichosis 2 (generalised, congenital)	Homo sapiens	73-76
7973337-9	1994	With regard to 17 beta-estradiol levels at the time of administration of hCG, 18 pregnancies (69.23%) were obtained in patients with a 17 beta-estradiol level &gt; or = to 1300, 7 (25.92%) in patients with a 17 beta-estradiol level &gt; or = to 1000 and &lt; or = to 1300 pg/ml and 3 (11.11%) in those with a 17 beta-estradiol level &lt; or = to 900 pg/ml.	Estradiol	135-152	hypertrichosis 2 (generalised, congenital)	Homo sapiens	73-76
8156906-7	1994	In contrast, DEX treatment promoted an approximately 3- to 7-fold increase in levels of hCG in both first trimester and term cytotrophoblasts, suggesting that the effects of glucocorticoid on FN and hCG expression are elicited through independent cell-signaling pathways.	Dexamethasone	13-16	hypertrichosis 2 (generalised, congenital)	Homo sapiens	88-91
8017631-8	1994	The enzymatically generated product, aminophenol, is detected immediately by oxidation at the gold electrode (at +0.19 V vs Ag/AgCl), and the magnitude of current is directly proportional to the concentration of hCG in the sample.	Aminophenols	37-48	hypertrichosis 2 (generalised, congenital)	Homo sapiens	212-215
8017631-8	1994	The enzymatically generated product, aminophenol, is detected immediately by oxidation at the gold electrode (at +0.19 V vs Ag/AgCl), and the magnitude of current is directly proportional to the concentration of hCG in the sample.	silver chloride	127-131	hypertrichosis 2 (generalised, congenital)	Homo sapiens	212-215
8013638-2	1994	Membrane lipid rigidity, as determined by fluorescence polarization of DPH, decreased as early as 0.5 h after injection of hCG.	Phenytoin	71-74	hypertrichosis 2 (generalised, congenital)	Homo sapiens	123-126
7515388-5	1994	The median charge and degree of charge heterogeneity of the isoforms of hCG in each serum was determined by electrophoresis in 0.10% agarose suspension.	Sepharose	133-140	hypertrichosis 2 (generalised, congenital)	Homo sapiens	72-75
8198582-1	1994	The functional capacity of the recombinant human LH/hCG receptor was tested on the basis of gonadotropin stimulation of cAMP production by stable transfections of Chinese hamster ovary (CHO) cells.	Cyclic AMP	120-124	hypertrichosis 2 (generalised, congenital)	Homo sapiens	52-55
8198582-2	1994	A CHO cell line expressed with the hLH/hCG receptor cDNA covering the entire amino acid coding region revealed the presence of LH/hCG binding site (Kd: 1.45 x 10(-10)M) on the plasma membrane.	Luteinizing Hormone	36-38	hypertrichosis 2 (generalised, congenital)	Homo sapiens	39-42
8198582-2	1994	A CHO cell line expressed with the hLH/hCG receptor cDNA covering the entire amino acid coding region revealed the presence of LH/hCG binding site (Kd: 1.45 x 10(-10)M) on the plasma membrane.	Luteinizing Hormone	36-38	hypertrichosis 2 (generalised, congenital)	Homo sapiens	130-133
8198582-3	1994	Treatment of transfected cells(CHO-LH/hCGR) with hCG induced dose-dependent increases in intracellular cAMP production, indicating that the expressed human LH/hCG receptor functionally couples with endogenous adenylyl cyclase.	Cyclic AMP	103-107	hypertrichosis 2 (generalised, congenital)	Homo sapiens	38-41
8198582-3	1994	Treatment of transfected cells(CHO-LH/hCGR) with hCG induced dose-dependent increases in intracellular cAMP production, indicating that the expressed human LH/hCG receptor functionally couples with endogenous adenylyl cyclase.	Cyclic AMP	103-107	hypertrichosis 2 (generalised, congenital)	Homo sapiens	49-52
8198582-4	1994	Although hCG induced dose-dependent increases in cAMP production, rat and bovine LH and human FSH did not alter cAMP levels compared to control values.	Cyclic AMP	49-53	hypertrichosis 2 (generalised, congenital)	Homo sapiens	9-12
8198582-6	1994	Preincubation of CHO-LH/hCGR cells with hCG for 16h decreased the subsequent cAMP production caused by a 30min pulse of hCG stimulation.	Cyclic AMP	77-81	hypertrichosis 2 (generalised, congenital)	Homo sapiens	24-27
8198582-6	1994	Preincubation of CHO-LH/hCGR cells with hCG for 16h decreased the subsequent cAMP production caused by a 30min pulse of hCG stimulation.	Cyclic AMP	77-81	hypertrichosis 2 (generalised, congenital)	Homo sapiens	40-43
8156906-7	1994	In contrast, DEX treatment promoted an approximately 3- to 7-fold increase in levels of hCG in both first trimester and term cytotrophoblasts, suggesting that the effects of glucocorticoid on FN and hCG expression are elicited through independent cell-signaling pathways.	Dexamethasone	13-16	hypertrichosis 2 (generalised, congenital)	Homo sapiens	199-202
8064676-4	1994	When oocyte-cumulus complexes were cultured in hormone-free media for 20 h after culture in several combinations of supplemental hormones for the first 20 h period, germinal vesicle breakdown rates and maturation rates were lower in oocytes previously exposed to oestradiol alone or no hormonal supplements (68-70% and 45-49%, respectively) than in oocytes previously exposed to PMSG or hCG (89-99% and 71-89%, respectively).	Estradiol	263-273	hypertrichosis 2 (generalised, congenital)	Homo sapiens	387-390
8206328-5	1994	Only those that recognized hCG albeit weakly, could inhibit binding of 125I-hCG to receptors or hCG action in MA-10 (mouse Leydig tumor cells).	ma-10	110-115	hypertrichosis 2 (generalised, congenital)	Homo sapiens	27-30
8014608-4	1994	The cyclic and PMSG/hCG-treated rats exhibited some similarities and differences in the general pattern of steroid content.	Steroids	107-114	hypertrichosis 2 (generalised, congenital)	Homo sapiens	20-23
8014608-5	1994	Either a presumptive endogenous LH surge or administration of hCG resulted in an increase in the ovarian androgen concentration which preceded a rise in progesterone; the progesterone peak, in turn, was accompanied by a fall in the amount of androgens and oestradiol.	Progesterone	153-165	hypertrichosis 2 (generalised, congenital)	Homo sapiens	62-65
8014608-5	1994	Either a presumptive endogenous LH surge or administration of hCG resulted in an increase in the ovarian androgen concentration which preceded a rise in progesterone; the progesterone peak, in turn, was accompanied by a fall in the amount of androgens and oestradiol.	Progesterone	171-183	hypertrichosis 2 (generalised, congenital)	Homo sapiens	62-65
8014608-5	1994	Either a presumptive endogenous LH surge or administration of hCG resulted in an increase in the ovarian androgen concentration which preceded a rise in progesterone; the progesterone peak, in turn, was accompanied by a fall in the amount of androgens and oestradiol.	Estradiol	256-266	hypertrichosis 2 (generalised, congenital)	Homo sapiens	62-65
8021852-3	1994	Treatment of bats with hCG for 10 days in early delayed implantation induced similar changes in luteal ultrastructure and plasma progesterone concentrations, but did not initiate implantation.	Progesterone	129-141	hypertrichosis 2 (generalised, congenital)	Homo sapiens	23-26
8206328-5	1994	Only those that recognized hCG albeit weakly, could inhibit binding of 125I-hCG to receptors or hCG action in MA-10 (mouse Leydig tumor cells).	ma-10	110-115	hypertrichosis 2 (generalised, congenital)	Homo sapiens	76-79
8206328-5	1994	Only those that recognized hCG albeit weakly, could inhibit binding of 125I-hCG to receptors or hCG action in MA-10 (mouse Leydig tumor cells).	ma-10	110-115	hypertrichosis 2 (generalised, congenital)	Homo sapiens	76-79
8206328-7	1994	As these alpha subunit favoring antibodies easily recognized DG-hCG but not the intact hCG configuration, we suggest that loss of sugars in alpha and beta subunits of DG-hCG was responsible for these alterations.	Sugars	130-136	hypertrichosis 2 (generalised, congenital)	Homo sapiens	64-67
8086275-2	1994	It was found that LH-RH additions (10, 100, 1000 or 10,000 ng/ml medium) increased the number of LH/hCG binding sites in granulosa cells.	Luteinizing Hormone	18-20	hypertrichosis 2 (generalised, congenital)	Homo sapiens	100-103
8086275-3	1994	LH or hCG (0.1, 1, 10 or 100 ng/ml) increased both cAMP and cGMP secretion by the cell culture.	Cyclic AMP	51-55	hypertrichosis 2 (generalised, congenital)	Homo sapiens	6-9
8086275-3	1994	LH or hCG (0.1, 1, 10 or 100 ng/ml) increased both cAMP and cGMP secretion by the cell culture.	Cyclic GMP	60-64	hypertrichosis 2 (generalised, congenital)	Homo sapiens	6-9
8086275-6	1994	The present observations suggest that LH-RH can act as synergist of LH and of hCG increasing a number of LH/hCG receptors and stimulating basal and LH-induced cyclic nucleotide release by ovarian cells.	Luteinizing Hormone	38-40	hypertrichosis 2 (generalised, congenital)	Homo sapiens	78-81
8086275-6	1994	The present observations suggest that LH-RH can act as synergist of LH and of hCG increasing a number of LH/hCG receptors and stimulating basal and LH-induced cyclic nucleotide release by ovarian cells.	Luteinizing Hormone	38-40	hypertrichosis 2 (generalised, congenital)	Homo sapiens	108-111
8086275-6	1994	The present observations suggest that LH-RH can act as synergist of LH and of hCG increasing a number of LH/hCG receptors and stimulating basal and LH-induced cyclic nucleotide release by ovarian cells.	Luteinizing Hormone	68-70	hypertrichosis 2 (generalised, congenital)	Homo sapiens	108-111
8086275-6	1994	The present observations suggest that LH-RH can act as synergist of LH and of hCG increasing a number of LH/hCG receptors and stimulating basal and LH-induced cyclic nucleotide release by ovarian cells.	Nucleotides, Cyclic	159-176	hypertrichosis 2 (generalised, congenital)	Homo sapiens	78-81
7939172-1	1994	Human chorionic gonadotropin (hCG) is a glycoprotein of which sugar chains are considered to show structural changes with malignancy.	Sugars	62-67	hypertrichosis 2 (generalised, congenital)	Homo sapiens	30-33
31936986-11	1994	In the early luteal phase, hCG was distributed symmetrically between both ovaries, and increased the progesterone secretion by the ovulatory ovary only.	Progesterone	101-113	hypertrichosis 2 (generalised, congenital)	Homo sapiens	27-30
31936986-12	1994	In the late luteal phase, hCG was preferentially distributed to the ovulatory ovary, and increased the progesterone secretion by both ovaries.	Progesterone	103-115	hypertrichosis 2 (generalised, congenital)	Homo sapiens	26-29
8306476-7	1994	RESULTS: PGE2 and PGF2 alpha at various concentrations did not have a consistent effect, whereas oestradiol, diethylstilboestrol (and 2-hydroxyoestradiol in early luteal cell cultures) significantly inhibited basal and hCG stimulated progesterone biosynthesis.	Estradiol	97-107	hypertrichosis 2 (generalised, congenital)	Homo sapiens	219-222
8306476-7	1994	RESULTS: PGE2 and PGF2 alpha at various concentrations did not have a consistent effect, whereas oestradiol, diethylstilboestrol (and 2-hydroxyoestradiol in early luteal cell cultures) significantly inhibited basal and hCG stimulated progesterone biosynthesis.	diethylstilboestrol	109-128	hypertrichosis 2 (generalised, congenital)	Homo sapiens	219-222
8306476-7	1994	RESULTS: PGE2 and PGF2 alpha at various concentrations did not have a consistent effect, whereas oestradiol, diethylstilboestrol (and 2-hydroxyoestradiol in early luteal cell cultures) significantly inhibited basal and hCG stimulated progesterone biosynthesis.	2-hydroxyoestradiol	134-153	hypertrichosis 2 (generalised, congenital)	Homo sapiens	219-222
8306476-12	1994	CONCLUSIONS: Oestradiol, at relatively high concentrations, is a potent inhibitor of basal and hCG induced luteal cell steroidogenesis in vitro.	Estradiol	13-23	hypertrichosis 2 (generalised, congenital)	Homo sapiens	95-98
7939172-6	1994	Taken together, these results show that alteration in sugar chain structures of hCG reflect the advanced stage of cervical cancer.	Sugars	54-59	hypertrichosis 2 (generalised, congenital)	Homo sapiens	80-83
7904614-4	1994	In contrast, hCG secretion was stimulated only by terbutaline (5-fold).	Terbutaline	50-61	hypertrichosis 2 (generalised, congenital)	Homo sapiens	13-16
7904614-5	1994	Prorenin and hCG secretory responses were inhibited by corresponding selective receptor antagonists (beta 1-metoprolol and beta 2-ICI 118,551).	beta 1-metoprolol	101-118	hypertrichosis 2 (generalised, congenital)	Homo sapiens	13-16
7939172-2	1994	To study the sugar chain heterogeneity of urinary hCG in patients with gynecological disease, we employed serial lectin affinity chromatography (LAC) using concanavalin A (Con A) and phytohemagglutinin-E (PHA-E) which can separate N-glycoside-linked sugar chains, and Jacalin lectin which is specific for O-glycoside-linked sugar chains.	Sugars	13-18	hypertrichosis 2 (generalised, congenital)	Homo sapiens	50-53
8243314-16	1993	Also, levels of the ovarian cholesterol side-chain cleavage enzyme (CYP 11A) mRNA (2 kilobases) were low in control animals, but increased 20.5- and 14.3-fold after surge doses of rcFSH and hCG, respectively.	Cholesterol	28-39	hypertrichosis 2 (generalised, congenital)	Homo sapiens	190-193
8286613-0	1993	Luminescence luteinizing hormone/choriogonadotropin (LH/CG) bioassay: measurement of serum bioactive LH/CG during early pregnancy in human and macaque.	Luteinizing Hormone	53-55	hypertrichosis 2 (generalised, congenital)	Homo sapiens	104-106
8286613-4	1993	Using 293 cells permanently transfected with the human LH receptor cDNA and a luciferase reporter gene driven by a cAMP-dependent promoter, we have developed a luminescence LH/CG bioassay.	Cyclic AMP	115-119	hypertrichosis 2 (generalised, congenital)	Homo sapiens	176-178
8286613-4	1993	Using 293 cells permanently transfected with the human LH receptor cDNA and a luciferase reporter gene driven by a cAMP-dependent promoter, we have developed a luminescence LH/CG bioassay.	Luteinizing Hormone	55-57	hypertrichosis 2 (generalised, congenital)	Homo sapiens	176-178
8243331-4	1993	The release of 5HT was acutely stimulated by hCG (ED50, 1.1 pM) with maximal stimulation at 10 pM hCG (160%).	Serotonin	15-18	hypertrichosis 2 (generalised, congenital)	Homo sapiens	45-48
8243331-4	1993	The release of 5HT was acutely stimulated by hCG (ED50, 1.1 pM) with maximal stimulation at 10 pM hCG (160%).	Serotonin	15-18	hypertrichosis 2 (generalised, congenital)	Homo sapiens	98-101
8243331-7	1993	Similar increases of 5HT release by hCG were observed in the absence of extracellular Ca2+.	Serotonin	21-24	hypertrichosis 2 (generalised, congenital)	Homo sapiens	36-39
8274420-1	1993	The present in vitro studies using a suspension of Leydig cells from adult rat testis demonstrated that bromocriptine (BR, 2 x 10(-5)M) inhibits hCG-stimulated testosterone production (in the presence of submaximal and maximal doses of hCG), while basal production was unaffected.	Bromocriptine	104-117	hypertrichosis 2 (generalised, congenital)	Homo sapiens	145-148
8274420-1	1993	The present in vitro studies using a suspension of Leydig cells from adult rat testis demonstrated that bromocriptine (BR, 2 x 10(-5)M) inhibits hCG-stimulated testosterone production (in the presence of submaximal and maximal doses of hCG), while basal production was unaffected.	Bromocriptine	104-117	hypertrichosis 2 (generalised, congenital)	Homo sapiens	236-239
8274420-1	1993	The present in vitro studies using a suspension of Leydig cells from adult rat testis demonstrated that bromocriptine (BR, 2 x 10(-5)M) inhibits hCG-stimulated testosterone production (in the presence of submaximal and maximal doses of hCG), while basal production was unaffected.	Bromocriptine	119-121	hypertrichosis 2 (generalised, congenital)	Homo sapiens	145-148
8138106-4	1993	Ultrathin sections of lanthanum-infiltrated samples were observed by transmission electron microscopy at various points during follicular development and hormone-induced maturation: vitellogenic oocytes (&lt; 350 microns), full-grown oocytes (350-400 microns), hCG-stimulated (maturationally competent) oocytes, hCG/MIS-stimulated (early-maturation, hydrating) oocytes, and ovulated oocytes.	Lanthanum	22-31	hypertrichosis 2 (generalised, congenital)	Homo sapiens	261-264
8274420-1	1993	The present in vitro studies using a suspension of Leydig cells from adult rat testis demonstrated that bromocriptine (BR, 2 x 10(-5)M) inhibits hCG-stimulated testosterone production (in the presence of submaximal and maximal doses of hCG), while basal production was unaffected.	Bromocriptine	119-121	hypertrichosis 2 (generalised, congenital)	Homo sapiens	236-239
8138106-4	1993	Ultrathin sections of lanthanum-infiltrated samples were observed by transmission electron microscopy at various points during follicular development and hormone-induced maturation: vitellogenic oocytes (&lt; 350 microns), full-grown oocytes (350-400 microns), hCG-stimulated (maturationally competent) oocytes, hCG/MIS-stimulated (early-maturation, hydrating) oocytes, and ovulated oocytes.	Lanthanum	22-31	hypertrichosis 2 (generalised, congenital)	Homo sapiens	312-315
8274420-1	1993	The present in vitro studies using a suspension of Leydig cells from adult rat testis demonstrated that bromocriptine (BR, 2 x 10(-5)M) inhibits hCG-stimulated testosterone production (in the presence of submaximal and maximal doses of hCG), while basal production was unaffected.	Testosterone	160-172	hypertrichosis 2 (generalised, congenital)	Homo sapiens	145-148
8274420-2	1993	When the cells were exposed to 8-bromo-cAMP either in the presence or absence of hCG, the inhibitory effect of BR was not reversed.	8-Bromo Cyclic Adenosine Monophosphate	31-43	hypertrichosis 2 (generalised, congenital)	Homo sapiens	81-84
7511424-2	1993	Acetylcholine and carbachol as well as nicotine decreased basal and hCG-induced T secretion.	Acetylcholine	0-13	hypertrichosis 2 (generalised, congenital)	Homo sapiens	68-71
7511424-2	1993	Acetylcholine and carbachol as well as nicotine decreased basal and hCG-induced T secretion.	Carbachol	18-27	hypertrichosis 2 (generalised, congenital)	Homo sapiens	68-71
7511424-2	1993	Acetylcholine and carbachol as well as nicotine decreased basal and hCG-induced T secretion.	Nicotine	39-47	hypertrichosis 2 (generalised, congenital)	Homo sapiens	68-71
7511424-3	1993	The ganglionic nicotine antagonist hexamethonium promoted a partial reversal of the inhibitory effect of nicotine on basal or hCG-stimulated T secretion.	Nicotine	15-23	hypertrichosis 2 (generalised, congenital)	Homo sapiens	126-129
7511424-3	1993	The ganglionic nicotine antagonist hexamethonium promoted a partial reversal of the inhibitory effect of nicotine on basal or hCG-stimulated T secretion.	Hexamethonium	35-48	hypertrichosis 2 (generalised, congenital)	Homo sapiens	126-129
7511424-3	1993	The ganglionic nicotine antagonist hexamethonium promoted a partial reversal of the inhibitory effect of nicotine on basal or hCG-stimulated T secretion.	Nicotine	105-113	hypertrichosis 2 (generalised, congenital)	Homo sapiens	126-129
8077313-10	1993	However, a significant augmentation of the effect of hCG on progesterone release was found in incubations of cells on day 5.	Progesterone	60-72	hypertrichosis 2 (generalised, congenital)	Homo sapiens	53-56
8077313-14	1993	Moreover, oxytocin release induced by hCG and a stimulatory effect of oxytocin on the hCG-induced progesterone production during the period of maximal responsiveness of cultured cells were found.	Progesterone	98-110	hypertrichosis 2 (generalised, congenital)	Homo sapiens	86-89
8405904-8	1993	However, both heptanol and octanol at 1 mM blocked the hCG and progesterone induction of maturation in follicle-enclosed Xenopus oocytes.	Heptanol	14-22	hypertrichosis 2 (generalised, congenital)	Homo sapiens	55-58
8308465-4	1993	During the period of pFF treatment, the number of follicles capable of ovulating in response to human chorionic gonadotrophin (hCG) decreased (7.6 +/- 0.7 at 05.00 h on pro-oestrus) and plasma levels of oestradiol showed a peak level 6 h later than in controls treated with 0.5 ml steroid-free porcine serum.	p-Fluorophenylalanine	21-24	hypertrichosis 2 (generalised, congenital)	Homo sapiens	127-130
8308465-6	1993	Supplementary administration of LH throughout the treatment period and 0.5 ml pFF resulted in ovulation of one to three oocytes in response to hCG in only three out of ten animals.	Luteinizing Hormone	32-34	hypertrichosis 2 (generalised, congenital)	Homo sapiens	143-146
8139161-5	1993	The highest number of diploid parthenogenones (20.6%) was obtained in oocytes activated 21.5 hr after hCG injection.	parthenogenones	30-45	hypertrichosis 2 (generalised, congenital)	Homo sapiens	102-105
8276523-11	1993	In both cases, the hCG test repeated after the gonadotrophin treatment showed normal basal and stimulated testosterone levels.	Testosterone	106-118	hypertrichosis 2 (generalised, congenital)	Homo sapiens	19-22
8276523-13	1993	Under such circumstances with persisting hyperprolactinaemia, hCG and/or hCG/hMG combination treatment can induce normal virilization and advance spermatogenesis sufficiently to achieve fertility.	Menotropins	77-80	hypertrichosis 2 (generalised, congenital)	Homo sapiens	73-76
8215690-6	1993	The response of plasma testosterone to the administration of hCG was also significantly decreased in those with sex chromosome aberrations compared with other groups.	Testosterone	23-35	hypertrichosis 2 (generalised, congenital)	Homo sapiens	61-64
8405904-8	1993	However, both heptanol and octanol at 1 mM blocked the hCG and progesterone induction of maturation in follicle-enclosed Xenopus oocytes.	Octanols	27-34	hypertrichosis 2 (generalised, congenital)	Homo sapiens	55-58
7690721-4	1993	Testosterone production by unstimulated cells or in cells stimulated with hCG was not affected by the antagonist.	Testosterone	0-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	74-77
7904497-2	1993	These cells, obtained from IVF patients stimulated by hMG (human menopausal gonadotropin)/hCG (human chorionic gonadotropin), produced estrogen and progesterone under the effects of hCG and FSH (follicle stimulating hormone).	Progesterone	148-160	hypertrichosis 2 (generalised, congenital)	Homo sapiens	90-93
7904497-2	1993	These cells, obtained from IVF patients stimulated by hMG (human menopausal gonadotropin)/hCG (human chorionic gonadotropin), produced estrogen and progesterone under the effects of hCG and FSH (follicle stimulating hormone).	Progesterone	148-160	hypertrichosis 2 (generalised, congenital)	Homo sapiens	182-185
7904497-11	1993	Study III showed that the addition of hCG on days 2-4 produced a 10% increase (p &lt; 0.05) in estradiol production and a 50% increase in progesterone (p &lt; 0.01).	Estradiol	95-104	hypertrichosis 2 (generalised, congenital)	Homo sapiens	38-41
7904497-11	1993	Study III showed that the addition of hCG on days 2-4 produced a 10% increase (p &lt; 0.05) in estradiol production and a 50% increase in progesterone (p &lt; 0.01).	Progesterone	138-150	hypertrichosis 2 (generalised, congenital)	Homo sapiens	38-41
8229992-5	1993	We next evaluated whether hCG might exert its effects through enhanced secretion of testosterone from Leydig cells.	Testosterone	84-96	hypertrichosis 2 (generalised, congenital)	Homo sapiens	26-29
7690721-6	1993	However, cyclic AMP level in cells stimulated with either forskolin or hCG remained unaffected by HS-142-1 even when added at a concentration of 5 micrograms/ml.	Cyclic AMP	9-19	hypertrichosis 2 (generalised, congenital)	Homo sapiens	71-74
8320431-7	1993	The variant forms of hCG have been shown to differ from the native hormone mainly in the carbohydrate moiety, with the more acidic, more glycosylated variants being the ones capable of stimulating the human thyroid and the more alkaline sialic acidic deficient variants on the other hand, being potent thyroid inhibitors.	Carbohydrates	89-101	hypertrichosis 2 (generalised, congenital)	Homo sapiens	21-24
8390677-5	1993	Saturating amounts of human choriogonadotropin (hCG) increased MA-10 progesterone production by 150-fold.	ma-10 progesterone	63-81	hypertrichosis 2 (generalised, congenital)	Homo sapiens	48-51
8390677-7	1993	However, in the presence of Chol-odN antisense to DBI that could reduce DBI levels, MA-10 cells lost their ability to respond to hCG (ED50 = 1 microM).	chol-odn	28-36	hypertrichosis 2 (generalised, congenital)	Homo sapiens	129-132
8390677-8	1993	In these studies the hCG-stimulated cAMP levels and cytochrome P450 side-chain cleavage activity, as measured by metabolism of 22(R)-hydroxycholesterol, were not affected by the Chol-odNs used.	Cyclic AMP	36-40	hypertrichosis 2 (generalised, congenital)	Homo sapiens	21-24
8390677-8	1993	In these studies the hCG-stimulated cAMP levels and cytochrome P450 side-chain cleavage activity, as measured by metabolism of 22(R)-hydroxycholesterol, were not affected by the Chol-odNs used.	(r)-hydroxycholesterol	129-151	hypertrichosis 2 (generalised, congenital)	Homo sapiens	21-24
8393950-1	1993	When ethane dimethanesulphonate (EDS) is administered to rats, Leydig cells are destroyed, and damage to the seminiferous tubules is caused due to lack of testosterone (T), but administration of hCG can prevent this damage.	ethylene dimethanesulfonate	5-31	hypertrichosis 2 (generalised, congenital)	Homo sapiens	195-198
8393950-1	1993	When ethane dimethanesulphonate (EDS) is administered to rats, Leydig cells are destroyed, and damage to the seminiferous tubules is caused due to lack of testosterone (T), but administration of hCG can prevent this damage.	ethylene dimethanesulfonate	33-36	hypertrichosis 2 (generalised, congenital)	Homo sapiens	195-198
8393950-1	1993	When ethane dimethanesulphonate (EDS) is administered to rats, Leydig cells are destroyed, and damage to the seminiferous tubules is caused due to lack of testosterone (T), but administration of hCG can prevent this damage.	Testosterone	155-167	hypertrichosis 2 (generalised, congenital)	Homo sapiens	195-198
8392454-1	1993	OBJECTIVE: We examined the gonadotrophin secretion in patients with increased plasma concentrations of testosterone and oestradiol due to hCG-producing tumours.	Testosterone	103-115	hypertrichosis 2 (generalised, congenital)	Homo sapiens	138-141
8392454-1	1993	OBJECTIVE: We examined the gonadotrophin secretion in patients with increased plasma concentrations of testosterone and oestradiol due to hCG-producing tumours.	Estradiol	120-130	hypertrichosis 2 (generalised, congenital)	Homo sapiens	138-141
8392454-2	1993	DESIGN: Comparison of plasma gonadotrophin concentrations before and after stimulation by GnRH, in eight men with hCG-producing tumours resulting in increased testosterone and oestradiol plasma levels, and in 29 men with Leydig cell tumours resulting in increased oestradiol and normal to low testosterone plasma levels.	Testosterone	159-171	hypertrichosis 2 (generalised, congenital)	Homo sapiens	114-117
8392454-10	1993	CONCLUSIONS: In patients with hCG-secreting germ cell tumours complete suppression of plasma LH and FSH with increased plasma concentrations of both testosterone and oestradiol are often discovered.	Testosterone	149-161	hypertrichosis 2 (generalised, congenital)	Homo sapiens	30-33
8392454-10	1993	CONCLUSIONS: In patients with hCG-secreting germ cell tumours complete suppression of plasma LH and FSH with increased plasma concentrations of both testosterone and oestradiol are often discovered.	Estradiol	166-176	hypertrichosis 2 (generalised, congenital)	Homo sapiens	30-33
8348166-0	1993	A simple and efficacious criterion based on serum LH levels to time hCG administration for human in vitro fertilization.	Luteinizing Hormone	50-52	hypertrichosis 2 (generalised, congenital)	Homo sapiens	68-71
8389756-5	1993	Human chorionic gonadotropin (hCG)-stimulated cAMP accumulation was then measured.	Cyclic AMP	46-50	hypertrichosis 2 (generalised, congenital)	Homo sapiens	30-33
8389756-6	1993	Transfection with Q205LGi2-alpha but not Q205LGo1-alpha resulted in 50-60% inhibition of hCG-stimulated cAMP accumulation of the type 2 adenylyl cyclase.	Cyclic AMP	104-108	hypertrichosis 2 (generalised, congenital)	Homo sapiens	89-92
8389756-8	1993	Treatment with 4 beta-phorbol 12-myristate 13-acetate of cells transfected with the type 2 enzyme cDNA resulted in a 2-fold increase of the hCG-stimulated cAMP accumulation and a complete suppression of the Q205LGi2-alpha inhibition of the type 2 adenylyl cyclase.	Tetradecanoylphorbol Acetate	15-53	hypertrichosis 2 (generalised, congenital)	Homo sapiens	140-143
8389756-8	1993	Treatment with 4 beta-phorbol 12-myristate 13-acetate of cells transfected with the type 2 enzyme cDNA resulted in a 2-fold increase of the hCG-stimulated cAMP accumulation and a complete suppression of the Q205LGi2-alpha inhibition of the type 2 adenylyl cyclase.	Cyclic AMP	155-159	hypertrichosis 2 (generalised, congenital)	Homo sapiens	140-143
7682935-17	1993	hCG in a concentration of 10 ng/ml increased testosterone formation from 0.6 +/- 0.01 to 27.4 +/- 1.01 ng/10(6) cells.h.	Testosterone	45-57	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
7682935-19	1993	IGFBP-3 (0.1, 1, and 2.5 pmol/ml) caused a dose-dependent inhibition of IGF-I- plus hCG-induced testosterone formation.	Testosterone	96-108	hypertrichosis 2 (generalised, congenital)	Homo sapiens	84-87
8485243-2	1993	Bilateral intratesticular injection of increasing doses of naloxone (0.1-10 micrograms/testis) resulted 24 h later in a dose-dependent increase in testosterone production by Leydig cells incubated for 3 h in the presence or absence of hCG (100 ng/ml).	Naloxone	59-67	hypertrichosis 2 (generalised, congenital)	Homo sapiens	235-238
8465984-6	1993	As shown by Western blotting of ovarian effluent, the enzyme appeared following treatment with PMSG and PMSG-hCG; it increased in amount in a time-dependent manner, with a transient decline in the early hours after hCG injection.	pmsg	95-99	hypertrichosis 2 (generalised, congenital)	Homo sapiens	215-218
8387350-4	1993	Coadministration of inhibitors of eicosanoid synthesis into the ovarian bursa (0.5 mg/bursa) markedly augmented the action of hCG on ovarian MPO activity (p &lt; 0.0001).	Eicosanoids	34-44	hypertrichosis 2 (generalised, congenital)	Homo sapiens	126-129
8387350-8	1993	The hCG-stimulated increase in ovarian MPO activity reflects influx of neutrophils into the ovaries during the periovulatory period, and inhibitors of eicosanoid synthesis, which suppress ovulation, further enhance this increase.	Eicosanoids	151-161	hypertrichosis 2 (generalised, congenital)	Homo sapiens	4-7
8485243-3	1993	Unilateral intratesticular injection of naloxone (10 micrograms) similarly enhanced basal and hCG-stimulated testosterone production by Leydig cells, but production was not modified in Leydig cells from the contralateral vehicle-injected testis, nor was it changed when the same dose was injected subcutaneously.	Naloxone	40-48	hypertrichosis 2 (generalised, congenital)	Homo sapiens	94-97
8485243-3	1993	Unilateral intratesticular injection of naloxone (10 micrograms) similarly enhanced basal and hCG-stimulated testosterone production by Leydig cells, but production was not modified in Leydig cells from the contralateral vehicle-injected testis, nor was it changed when the same dose was injected subcutaneously.	Testosterone	109-121	hypertrichosis 2 (generalised, congenital)	Homo sapiens	94-97
8485243-4	1993	Unilateral intratesticular injection of 10 micrograms naloxone led to a dose-dependent increase in the hCG-responsiveness without altering the slope of the hCG dose-response curve.	Naloxone	54-62	hypertrichosis 2 (generalised, congenital)	Homo sapiens	103-106
8395641-4	1993	In vitro release of acetylcholine and hCG from trophoblast tissue of methadone-exposed placentas was not modulated by opioids.	Methadone	69-78	hypertrichosis 2 (generalised, congenital)	Homo sapiens	38-41
8319364-10	1993	Serum free T4 and free T3 were higher in the hyperemesis group (P &lt; 0.01) and the emesis group (P &lt; 0.01), and serum TSH was suppressed to less than 0.1 mU/l in both groups, while serum hCG was not significantly different among these three groups.	Thyrotropin	123-126	hypertrichosis 2 (generalised, congenital)	Homo sapiens	192-195
8458495-13	1993	Twenty-eight of 83 patients treated successfully required more than one injection of MTX (additional doses being given intramuscularly) because of nonresolution of hCG levels.	Methotrexate	85-88	hypertrichosis 2 (generalised, congenital)	Homo sapiens	164-167
7679398-5	1993	A 60-min challenge with hCG evoked dose-dependent stimulation of cAMP and progesterone production.	Cyclic AMP	65-69	hypertrichosis 2 (generalised, congenital)	Homo sapiens	24-27
8462318-5	1993	In the second month, 5,000 IU hCG was administered on cycle day LH+8 and 10,000 hCG on cycle days LH+10 and LH+12, and 200 mg RU 486 on cycle day LH+11, 48 hours prior to the recording.	Luteinizing Hormone	98-100	hypertrichosis 2 (generalised, congenital)	Homo sapiens	30-33
8462318-5	1993	In the second month, 5,000 IU hCG was administered on cycle day LH+8 and 10,000 hCG on cycle days LH+10 and LH+12, and 200 mg RU 486 on cycle day LH+11, 48 hours prior to the recording.	Luteinizing Hormone	98-100	hypertrichosis 2 (generalised, congenital)	Homo sapiens	30-33
8462318-5	1993	In the second month, 5,000 IU hCG was administered on cycle day LH+8 and 10,000 hCG on cycle days LH+10 and LH+12, and 200 mg RU 486 on cycle day LH+11, 48 hours prior to the recording.	Luteinizing Hormone	98-100	hypertrichosis 2 (generalised, congenital)	Homo sapiens	30-33
8462318-9	1993	In the control cycle and following hCG alone, misoprostol had a slight stimulatory effect.	Misoprostol	46-57	hypertrichosis 2 (generalised, congenital)	Homo sapiens	35-38
8096832-3	1993	The number of blood vessel profiles labelled with carbon was increased by hCG in both types of testes, but the response was more sustained in abdominal than in scrotal testes.	Carbon	50-56	hypertrichosis 2 (generalised, congenital)	Homo sapiens	74-77
8392959-5	1993	The stimulatory effects of bGH and hCG on aromatase activity were mimicked by forskolin and dibutyryl cAMP, both of which are known to raise the intracellular level of cAMP.	Colforsin	78-87	hypertrichosis 2 (generalised, congenital)	Homo sapiens	35-38
8392959-5	1993	The stimulatory effects of bGH and hCG on aromatase activity were mimicked by forskolin and dibutyryl cAMP, both of which are known to raise the intracellular level of cAMP.	Cyclic AMP	102-106	hypertrichosis 2 (generalised, congenital)	Homo sapiens	35-38
8392959-5	1993	The stimulatory effects of bGH and hCG on aromatase activity were mimicked by forskolin and dibutyryl cAMP, both of which are known to raise the intracellular level of cAMP.	Cyclic AMP	168-172	hypertrichosis 2 (generalised, congenital)	Homo sapiens	35-38
8392959-6	1993	These results suggest that bGH- as well as hCG-induced increases in aromatase activity are mediated through adenylate cyclase-cAMP-dependent mechanism(s).	Cyclic AMP	126-130	hypertrichosis 2 (generalised, congenital)	Homo sapiens	43-46
8392959-10	1993	The addition of cycloheximide or actinomycin D to the media did not affect the basal production of estradiol but completely blocked the bGH and hCG stimulation of the aromatization of exogenous testosterone to estradiol.	Cycloheximide	16-29	hypertrichosis 2 (generalised, congenital)	Homo sapiens	144-147
8392959-10	1993	The addition of cycloheximide or actinomycin D to the media did not affect the basal production of estradiol but completely blocked the bGH and hCG stimulation of the aromatization of exogenous testosterone to estradiol.	Dactinomycin	33-46	hypertrichosis 2 (generalised, congenital)	Homo sapiens	144-147
8392959-10	1993	The addition of cycloheximide or actinomycin D to the media did not affect the basal production of estradiol but completely blocked the bGH and hCG stimulation of the aromatization of exogenous testosterone to estradiol.	Testosterone	194-206	hypertrichosis 2 (generalised, congenital)	Homo sapiens	144-147
8392959-10	1993	The addition of cycloheximide or actinomycin D to the media did not affect the basal production of estradiol but completely blocked the bGH and hCG stimulation of the aromatization of exogenous testosterone to estradiol.	Estradiol	210-219	hypertrichosis 2 (generalised, congenital)	Homo sapiens	144-147
8388957-6	1993	In contrast, on days 6 and 14 after ovulation, cloprostenol significantly inhibited hCG- and dbcAMP-stimulated progesterone production and the cAMP response to hCG, but had no significant effect on PI turnover.	Cloprostenol	47-59	hypertrichosis 2 (generalised, congenital)	Homo sapiens	84-87
8388957-6	1993	In contrast, on days 6 and 14 after ovulation, cloprostenol significantly inhibited hCG- and dbcAMP-stimulated progesterone production and the cAMP response to hCG, but had no significant effect on PI turnover.	Cloprostenol	47-59	hypertrichosis 2 (generalised, congenital)	Homo sapiens	160-163
8388957-7	1993	Since progesterone production by the marmoset corpus luteum depends on the luteotrophic support of luteinizing hormone (LH), these observations suggest that the luteolytic action of cloprostenol in vivo involves the inhibition of LH/hCG action at sites both prior and subsequent to cAMP accumulation.	Cloprostenol	182-194	hypertrichosis 2 (generalised, congenital)	Homo sapiens	233-236
7679398-5	1993	A 60-min challenge with hCG evoked dose-dependent stimulation of cAMP and progesterone production.	Progesterone	74-86	hypertrichosis 2 (generalised, congenital)	Homo sapiens	24-27
7679398-6	1993	H2O2 dose-dependently inhibited progesterone production (ED50, 50-100 microM) in the absence or presence of hCG and blocked hCG-stimulated cAMP accumulation.	Hydrogen Peroxide	0-4	hypertrichosis 2 (generalised, congenital)	Homo sapiens	108-111
7679398-6	1993	H2O2 dose-dependently inhibited progesterone production (ED50, 50-100 microM) in the absence or presence of hCG and blocked hCG-stimulated cAMP accumulation.	Hydrogen Peroxide	0-4	hypertrichosis 2 (generalised, congenital)	Homo sapiens	124-127
7679398-6	1993	H2O2 dose-dependently inhibited progesterone production (ED50, 50-100 microM) in the absence or presence of hCG and blocked hCG-stimulated cAMP accumulation.	Cyclic AMP	139-143	hypertrichosis 2 (generalised, congenital)	Homo sapiens	124-127
7679398-11	1993	While H2O2 blocked stimulation of cAMP accumulation in response to hCG and cholera toxin, this same response produced by forskolin or aluminum fluoride was unaffected by H2O2.	Hydrogen Peroxide	6-10	hypertrichosis 2 (generalised, congenital)	Homo sapiens	67-70
7679398-11	1993	While H2O2 blocked stimulation of cAMP accumulation in response to hCG and cholera toxin, this same response produced by forskolin or aluminum fluoride was unaffected by H2O2.	Cyclic AMP	34-38	hypertrichosis 2 (generalised, congenital)	Homo sapiens	67-70
7679398-12	1993	Thus, H2O2 appears to uncouple LH (hCG) receptors by interruption of G-protein-dependent activation of adenylate cyclase.	Hydrogen Peroxide	6-10	hypertrichosis 2 (generalised, congenital)	Homo sapiens	35-38
8420926-8	1993	However, if the consensus sequence for N-linked glycosylation at Asn-173 is altered by substitution of Thr-175 with Ala (instead of Asn-173 to Gln), the resulting receptor binds hCG with high affinity although it is still impaired in its ability to be expressed at the plasma membrane.	Nitrogen	39-40	hypertrichosis 2 (generalised, congenital)	Homo sapiens	178-181
8420926-8	1993	However, if the consensus sequence for N-linked glycosylation at Asn-173 is altered by substitution of Thr-175 with Ala (instead of Asn-173 to Gln), the resulting receptor binds hCG with high affinity although it is still impaired in its ability to be expressed at the plasma membrane.	Asparagine	65-68	hypertrichosis 2 (generalised, congenital)	Homo sapiens	178-181
8472852-7	1993	The purified truncated receptor had high binding affinity for human choriogonadotropin (hCG) as indicated by ligand blotting on SDS-PAGE and radioligand receptor assays.	Sodium Dodecyl Sulfate	128-131	hypertrichosis 2 (generalised, congenital)	Homo sapiens	88-91
8420926-9	1993	Furthermore, if all consensus sequences for N-linked glycosylation are mutated collectively while maintaining Asn-173 (by substituting Thr-175 with Ala instead of Asn-173 to Gln), the resulting deglycosylated receptor, although not expressed on the plasma membrane, binds hCG with high affinity.	Nitrogen	44-45	hypertrichosis 2 (generalised, congenital)	Homo sapiens	272-275
1282394-4	1992	On the other hand, hCG injected either at 4 h or at 48 h after birth increases serum T. The administration of 5 micrograms of estradiol 17 beta (E2) to the newborn male rat at the time of birth blocks the expression of the postpartum testosterone surge.	Estradiol	126-143	hypertrichosis 2 (generalised, congenital)	Homo sapiens	19-22
8273931-7	1993	Serum hCG concentrations closely paralleled those of free thyroxine, but the correlation was difficult to assess because of carbimazole.	Thyroxine	58-67	hypertrichosis 2 (generalised, congenital)	Homo sapiens	6-9
8281703-2	1993	LH-RH agonists offer the possibility of manipulating the day of hCG injection and consequently the day of ovum pick-up.	Luteinizing Hormone	0-2	hypertrichosis 2 (generalised, congenital)	Homo sapiens	64-67
8441858-0	1993	LHRH- and (hydroxyproline9) LHRH-stimulated hCG secretion from perifused first-trimester placental cells.	(hydroxyproline9) lhrh	10-32	hypertrichosis 2 (generalised, congenital)	Homo sapiens	44-47
1445932-6	1992	At 4 degrees C, LH receptors occupied by eosin isothiocyanate (EITC)-hCG exhibited a slower RCT (64 microseconds) than did receptors occupied by EITC-oLH (43 microseconds).	eosine-5-isothiocyanate	41-61	hypertrichosis 2 (generalised, congenital)	Homo sapiens	69-72
1330502-2	1992	The light cells were vacuolated and bound 125I-labeled human choriogonadotropin (hCG) with high affinity but upon hCG stimulation in vitro, cAMP and testosterone production by these cells were minimal.	Iodine-125	42-46	hypertrichosis 2 (generalised, congenital)	Homo sapiens	81-84
1293036-1	1992	The role of calcium in regulation of secretion of human chorionic gonadotropin (hCG) by first trimester human placental minces in vitro has been investigated.	Calcium	12-19	hypertrichosis 2 (generalised, congenital)	Homo sapiens	80-83
1293036-2	1992	Depletion of calcium in the medium by addition of EGTA resulted in a drastic decrease in the levels of immunoreactive hCG in the medium with consequent of accumulation of hCG in the tissue.	Calcium	13-20	hypertrichosis 2 (generalised, congenital)	Homo sapiens	118-121
1293036-2	1992	Depletion of calcium in the medium by addition of EGTA resulted in a drastic decrease in the levels of immunoreactive hCG in the medium with consequent of accumulation of hCG in the tissue.	Calcium	13-20	hypertrichosis 2 (generalised, congenital)	Homo sapiens	171-174
1293036-2	1992	Depletion of calcium in the medium by addition of EGTA resulted in a drastic decrease in the levels of immunoreactive hCG in the medium with consequent of accumulation of hCG in the tissue.	Egtazic Acid	50-54	hypertrichosis 2 (generalised, congenital)	Homo sapiens	118-121
1293036-2	1992	Depletion of calcium in the medium by addition of EGTA resulted in a drastic decrease in the levels of immunoreactive hCG in the medium with consequent of accumulation of hCG in the tissue.	Egtazic Acid	50-54	hypertrichosis 2 (generalised, congenital)	Homo sapiens	171-174
1293036-3	1992	Addition of A 23187 which is a calcium ionophore resulted in a dose dose dependent increase in the hCG in the medium and this stimulatory response could not be observed in the absence of calcium.	Calcium	31-38	hypertrichosis 2 (generalised, congenital)	Homo sapiens	99-102
1293036-4	1992	Use of lanthanum (a calcium antagonist) in place of calcium in the medium used resulted in a significant decrease in the levels of hCG in the medium.	Lanthanum	7-16	hypertrichosis 2 (generalised, congenital)	Homo sapiens	131-134
1293036-4	1992	Use of lanthanum (a calcium antagonist) in place of calcium in the medium used resulted in a significant decrease in the levels of hCG in the medium.	Calcium	20-27	hypertrichosis 2 (generalised, congenital)	Homo sapiens	131-134
1293036-4	1992	Use of lanthanum (a calcium antagonist) in place of calcium in the medium used resulted in a significant decrease in the levels of hCG in the medium.	Calcium	52-59	hypertrichosis 2 (generalised, congenital)	Homo sapiens	131-134
1293036-5	1992	Addition of veratridine (a sodium channel activator) stimulated hCG secretion in a dose dependent manner.	Veratridine	12-23	hypertrichosis 2 (generalised, congenital)	Homo sapiens	64-67
1293036-6	1992	These results suggest that calcium is essential for normal secretion of hCG by human placenta.	Calcium	27-34	hypertrichosis 2 (generalised, congenital)	Homo sapiens	72-75
1419894-5	1992	In time-course studies, the serum lipoprotein fraction had no effect on hCG-stimulated testosterone production in vitro at 3.0 or 6.0 h, but partially prevented the normal decline in hCG-stimulated testosterone production after 6.0 h. In contrast, unfractionated serum was stimulatory at all time-points.	Testosterone	198-210	hypertrichosis 2 (generalised, congenital)	Homo sapiens	183-186
1419894-8	1992	The data indicate that (i) the stimulatory effect of serum on short-term hCG-stimulated Leydig cell testosterone production in vitro is predominantly due to the serum lipoprotein fraction, possibly by providing additional precursors for testosterone synthesis, (ii) the biological activity of the lipoproteins is influenced by both stimulatory and inhibitory serum proteins in addition to luteinizing hormone, and (iii) that serum lipoproteins may be involved in supporting Leydig cell steroidogenesis in vivo.	Testosterone	100-112	hypertrichosis 2 (generalised, congenital)	Homo sapiens	73-76
1419894-8	1992	The data indicate that (i) the stimulatory effect of serum on short-term hCG-stimulated Leydig cell testosterone production in vitro is predominantly due to the serum lipoprotein fraction, possibly by providing additional precursors for testosterone synthesis, (ii) the biological activity of the lipoproteins is influenced by both stimulatory and inhibitory serum proteins in addition to luteinizing hormone, and (iii) that serum lipoproteins may be involved in supporting Leydig cell steroidogenesis in vivo.	Testosterone	237-249	hypertrichosis 2 (generalised, congenital)	Homo sapiens	73-76
8431517-7	1993	Both a murine IgG (anti-hCG) and the human anti-tumor IgM 16.88 were conjugated with one to three oligonucleotides via the heterobifunctional cross-linker SMCC.	Oligonucleotides	98-114	hypertrichosis 2 (generalised, congenital)	Homo sapiens	24-27
1337148-6	1992	Transfection of primary cultures of granulosa cells revealed that the activity of the rat pro-DYN promoter [-1858 to 133 base pairs (bp)] was increased 18- to 19-fold by hCG and human FSH treatments and 7-fold by cAMP analog treatment.	Cyclic AMP	213-217	hypertrichosis 2 (generalised, congenital)	Homo sapiens	170-173
1479151-3	1992	hCG bound with high affinity but with a very low capacity and the gonadotropin induced a clear dose response for both testosterone and estradiol production.	Testosterone	118-130	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
1479151-3	1992	hCG bound with high affinity but with a very low capacity and the gonadotropin induced a clear dose response for both testosterone and estradiol production.	Estradiol	135-144	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
1479151-4	1992	The ED50 of hCG on testosterone and estradiol production were 2.5 and 5.0 nM, respectively.	Testosterone	19-31	hypertrichosis 2 (generalised, congenital)	Homo sapiens	12-15
1479151-4	1992	The ED50 of hCG on testosterone and estradiol production were 2.5 and 5.0 nM, respectively.	Estradiol	36-45	hypertrichosis 2 (generalised, congenital)	Homo sapiens	12-15
1479151-5	1992	We conclude that estradiol originates from Leydig cell activity, since estradiol synthesis does not depend on testosterone availability and it shows a clear hCG dose response.	Estradiol	17-26	hypertrichosis 2 (generalised, congenital)	Homo sapiens	157-160
1516981-6	1992	Plasma testosterone levels reached adulthood values during hCG treatment and no statistically significant difference was detected between LTS and STS patients with IHH.	Testosterone	7-19	hypertrichosis 2 (generalised, congenital)	Homo sapiens	59-62
1398554-8	1992	Both corticosterone and dexamethasone inhibited hCG-stimulated T production in a dose-dependent manner.	Corticosterone	5-19	hypertrichosis 2 (generalised, congenital)	Homo sapiens	48-51
1398554-8	1992	Both corticosterone and dexamethasone inhibited hCG-stimulated T production in a dose-dependent manner.	Dexamethasone	24-37	hypertrichosis 2 (generalised, congenital)	Homo sapiens	48-51
1327203-6	1992	Of the serum steroids analyzed, only estradiol and androstenedione concentrations for animals treated with FSH + hCG were consistently elevated above values observed for control HYPOXD rats.	Steroids	13-21	hypertrichosis 2 (generalised, congenital)	Homo sapiens	113-116
1327203-6	1992	Of the serum steroids analyzed, only estradiol and androstenedione concentrations for animals treated with FSH + hCG were consistently elevated above values observed for control HYPOXD rats.	Estradiol	37-46	hypertrichosis 2 (generalised, congenital)	Homo sapiens	113-116
1327203-6	1992	Of the serum steroids analyzed, only estradiol and androstenedione concentrations for animals treated with FSH + hCG were consistently elevated above values observed for control HYPOXD rats.	Androstenedione	51-66	hypertrichosis 2 (generalised, congenital)	Homo sapiens	113-116
1434029-3	1992	TSA, which was detectable in all of 11 women in normal early pregnancy, correlated positively with serum hCG level, but was abolished completely by the pretreatment of serum samples with the solid-phase hCG antibody coupled with Sepharose-4B.	trichostatin A	0-3	hypertrichosis 2 (generalised, congenital)	Homo sapiens	105-108
1434029-3	1992	TSA, which was detectable in all of 11 women in normal early pregnancy, correlated positively with serum hCG level, but was abolished completely by the pretreatment of serum samples with the solid-phase hCG antibody coupled with Sepharose-4B.	trichostatin A	0-3	hypertrichosis 2 (generalised, congenital)	Homo sapiens	203-206
1434029-3	1992	TSA, which was detectable in all of 11 women in normal early pregnancy, correlated positively with serum hCG level, but was abolished completely by the pretreatment of serum samples with the solid-phase hCG antibody coupled with Sepharose-4B.	Sepharose	229-238	hypertrichosis 2 (generalised, congenital)	Homo sapiens	105-108
1434029-4	1992	Total TSA in the model samples of mixture of Graves" and pregnant sera (Gr + Preg), was reduced by the pretreatment with the solid-phase antibody, just corresponding with the reduction in hCG-induced TSA.	trichostatin A	6-9	hypertrichosis 2 (generalised, congenital)	Homo sapiens	188-191
1434029-4	1992	Total TSA in the model samples of mixture of Graves" and pregnant sera (Gr + Preg), was reduced by the pretreatment with the solid-phase antibody, just corresponding with the reduction in hCG-induced TSA.	trichostatin A	200-203	hypertrichosis 2 (generalised, congenital)	Homo sapiens	188-191
1434029-5	1992	Total TSA in early pregnant sera in 15 patients with Graves" disease, decreased significantly but was still positive even by the pretreatment with the hCG antibody.	trichostatin A	6-9	hypertrichosis 2 (generalised, congenital)	Homo sapiens	151-154
1434029-6	1992	Pregnancy-associated changes in TSA was examined serially in a patient with Graves" disease, and hCG-induced TSA increased predominantly along with the serum thyroid hormone in early aggravation period.	trichostatin A	32-35	hypertrichosis 2 (generalised, congenital)	Homo sapiens	97-100
1327203-8	1992	In contrast, these steroids were elevated between Days 3 and 5 of FSH treatment (+/- hCG treatment).	Steroids	19-27	hypertrichosis 2 (generalised, congenital)	Homo sapiens	85-88
1327203-11	1992	Incubates of follicles/cysts from FSH + hCG-treated HYPOXD rats contained more progesterone, androstenedione, and estradiol than incubates of follicles from any other in vivo treatment group.	Progesterone	79-91	hypertrichosis 2 (generalised, congenital)	Homo sapiens	40-43
1327203-11	1992	Incubates of follicles/cysts from FSH + hCG-treated HYPOXD rats contained more progesterone, androstenedione, and estradiol than incubates of follicles from any other in vivo treatment group.	Androstenedione	93-108	hypertrichosis 2 (generalised, congenital)	Homo sapiens	40-43
1327203-11	1992	Incubates of follicles/cysts from FSH + hCG-treated HYPOXD rats contained more progesterone, androstenedione, and estradiol than incubates of follicles from any other in vivo treatment group.	Estradiol	114-123	hypertrichosis 2 (generalised, congenital)	Homo sapiens	40-43
1327203-13	1992	However, only follicles from FSH-treated and FSH + hCG-treated rats responded to cAMP with increased androstenedione and estradiol accumulation in vitro.	Cyclic AMP	81-85	hypertrichosis 2 (generalised, congenital)	Homo sapiens	51-54
1327203-13	1992	However, only follicles from FSH-treated and FSH + hCG-treated rats responded to cAMP with increased androstenedione and estradiol accumulation in vitro.	Androstenedione	101-116	hypertrichosis 2 (generalised, congenital)	Homo sapiens	51-54
1327203-13	1992	However, only follicles from FSH-treated and FSH + hCG-treated rats responded to cAMP with increased androstenedione and estradiol accumulation in vitro.	Estradiol	121-130	hypertrichosis 2 (generalised, congenital)	Homo sapiens	51-54
1327203-14	1992	Inclusion of 400 ng of either androstenedione or testosterone in the incubation medium enhanced progesterone accumulation in follicular incubates from control, hCG-treated, and FSH-treated HYPOXD rats, but did not enhance progesterone accumulation in follicular incubates from FSH + hCG-treated animals.	Androstenedione	30-45	hypertrichosis 2 (generalised, congenital)	Homo sapiens	160-163
1327203-14	1992	Inclusion of 400 ng of either androstenedione or testosterone in the incubation medium enhanced progesterone accumulation in follicular incubates from control, hCG-treated, and FSH-treated HYPOXD rats, but did not enhance progesterone accumulation in follicular incubates from FSH + hCG-treated animals.	Androstenedione	30-45	hypertrichosis 2 (generalised, congenital)	Homo sapiens	283-286
1327203-14	1992	Inclusion of 400 ng of either androstenedione or testosterone in the incubation medium enhanced progesterone accumulation in follicular incubates from control, hCG-treated, and FSH-treated HYPOXD rats, but did not enhance progesterone accumulation in follicular incubates from FSH + hCG-treated animals.	Testosterone	49-61	hypertrichosis 2 (generalised, congenital)	Homo sapiens	160-163
1327203-14	1992	Inclusion of 400 ng of either androstenedione or testosterone in the incubation medium enhanced progesterone accumulation in follicular incubates from control, hCG-treated, and FSH-treated HYPOXD rats, but did not enhance progesterone accumulation in follicular incubates from FSH + hCG-treated animals.	Testosterone	49-61	hypertrichosis 2 (generalised, congenital)	Homo sapiens	283-286
1327203-14	1992	Inclusion of 400 ng of either androstenedione or testosterone in the incubation medium enhanced progesterone accumulation in follicular incubates from control, hCG-treated, and FSH-treated HYPOXD rats, but did not enhance progesterone accumulation in follicular incubates from FSH + hCG-treated animals.	Progesterone	96-108	hypertrichosis 2 (generalised, congenital)	Homo sapiens	160-163
1601748-1	1992	The authors investigated the morphologic characteristics and human chorionic gonadotrophin (hCG)-stimulated testosterone production of adult mouse Leydig cells in vitro, which have different buoyant densities.	Testosterone	108-120	hypertrichosis 2 (generalised, congenital)	Homo sapiens	92-95
1328629-12	1992	The alterations of intraoocyte cAMP contents following exposure to hCG in vivo paralleled those observed in the ovaries perfused with forskolin.	Colforsin	134-143	hypertrichosis 2 (generalised, congenital)	Homo sapiens	67-70
1618405-11	1992	It is concluded that with a complete study of sterility that only shows low seric progesterone and/or endometrium in dysphase or irregular, the diagnosis of DCL is probable and should be treated first with CC plus hCG.	dcl	157-160	hypertrichosis 2 (generalised, congenital)	Homo sapiens	214-217
1378275-2	1992	In vitro [3H]-uridine incorporation into RNA decreased after a high, single dose of hCG (100 IU).	Tritium	10-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	84-87
1378275-2	1992	In vitro [3H]-uridine incorporation into RNA decreased after a high, single dose of hCG (100 IU).	Uridine	14-21	hypertrichosis 2 (generalised, congenital)	Homo sapiens	84-87
1572299-11	1992	Simultaneous perifusion with an LHRH antagonist, (Nal-Glu)LHRH blocked the hCG secretory response to LHRH or (Hyp9)LHRH (equimolar 10(-9) M concentrations; n = 5; P less than 0.05).	2-naphthylalanyl-glutamic acid	49-57	hypertrichosis 2 (generalised, congenital)	Homo sapiens	75-78
1601748-4	1992	In vitro testosterone production of these Leydig cells, in response to different doses of hCG (0, 5, 25, 125, 625, and 3125 pg/mL), was determined by radioimmunoassay.	Testosterone	9-21	hypertrichosis 2 (generalised, congenital)	Homo sapiens	90-93
1601748-6	1992	In Leydig cells of Group 1, testosterone production per cell in vitro in response to 0 and 5 pg/mL hCG was not significantly different (P greater than 0.05).	Testosterone	28-40	hypertrichosis 2 (generalised, congenital)	Homo sapiens	99-102
1569178-5	1992	Further hCG administration (750 IU 24 h later) in both the early and the midluteal phases elicited a clear increase in progesterone concentrations.	Progesterone	119-131	hypertrichosis 2 (generalised, congenital)	Homo sapiens	8-11
1569178-7	1992	Further hCG administration in the midluteal phase resulted in a sharp decline in LH concentrations, brought about mainly by a decrease in LH pulse frequency, this response was not apparent at any other stage of the luteal phase.	Luteinizing Hormone	138-140	hypertrichosis 2 (generalised, congenital)	Homo sapiens	8-11
1601748-8	1992	However, 3125 pg/mL hCG further elevated the testosterone production by those Leydig cells with high buoyant density.	Testosterone	45-57	hypertrichosis 2 (generalised, congenital)	Homo sapiens	20-23
1569178-9	1992	The decline in LH levels following hCG administration in the midluteal phase resembled that seen in spontaneous conception cycles following implantation.	Luteinizing Hormone	15-17	hypertrichosis 2 (generalised, congenital)	Homo sapiens	35-38
1569178-7	1992	Further hCG administration in the midluteal phase resulted in a sharp decline in LH concentrations, brought about mainly by a decrease in LH pulse frequency, this response was not apparent at any other stage of the luteal phase.	Luteinizing Hormone	81-83	hypertrichosis 2 (generalised, congenital)	Homo sapiens	8-11
1601748-9	1992	In Leydig cells in group 2, the patterns of testosterone production in response to hCG doses of 0, 5, and 25 pg/mL were similar to those of Leydig cells in group 1.	Testosterone	44-56	hypertrichosis 2 (generalised, congenital)	Homo sapiens	83-86
1382027-5	1992	Addition to the culture medium of JEG-3 cells slightly increased cAMP secretion only at a concentration of 10(-8) M. The basal level of hCG in the medium was found to be higher in the first-trimester than in the term trophoblast culture, but salmon CT induced an increase in hCG secretion by term placenta cells only.	Cyclic AMP	65-69	hypertrichosis 2 (generalised, congenital)	Homo sapiens	136-139
1536908-2	1992	The number of ova was significantly decreased when RU486 (10 mg/kg) was given from 2 h before to 4 h after the hCG injection.	Mifepristone	51-56	hypertrichosis 2 (generalised, congenital)	Homo sapiens	111-114
1312425-5	1992	The selective 5HT2 receptor agonist (+-)1-[2,5-dimethoxy-4-iodophyryl]2-amino propane hydrochloride (DOI) also stimulated CRF secretion and inhibited hCG-stimulated cAMP generation and testosterone production to control levels (ID50, 7 microM).	(+-)1-[2,5-dimethoxy-4-iodophyryl]2-amino propane hydrochloride	36-99	hypertrichosis 2 (generalised, congenital)	Homo sapiens	150-153
1312425-6	1992	Serotonergic 5HT1A, 5HT1B/1C, 5HT1D, and 5HT3/5HT2 agonists were less effective inhibitors of hCG-stimulated cAMP and testosterone production, while agonists for the 5HT3 receptor had no effect.	Cyclic AMP	109-113	hypertrichosis 2 (generalised, congenital)	Homo sapiens	94-97
1312425-6	1992	Serotonergic 5HT1A, 5HT1B/1C, 5HT1D, and 5HT3/5HT2 agonists were less effective inhibitors of hCG-stimulated cAMP and testosterone production, while agonists for the 5HT3 receptor had no effect.	Testosterone	118-130	hypertrichosis 2 (generalised, congenital)	Homo sapiens	94-97
1312425-10	1992	Also, treatment of cells with ketanserin increased sensitivity to hCG and raised maximal cAMP and testosterone production.	Ketanserin	30-40	hypertrichosis 2 (generalised, congenital)	Homo sapiens	66-69
1312425-16	1992	5HT-stimulated CRF inhibits basal and hCG-induced cAMP generation and steroidogenesis.	Serotonin	0-3	hypertrichosis 2 (generalised, congenital)	Homo sapiens	38-41
1312425-16	1992	5HT-stimulated CRF inhibits basal and hCG-induced cAMP generation and steroidogenesis.	Cyclic AMP	50-54	hypertrichosis 2 (generalised, congenital)	Homo sapiens	38-41
1312425-17	1992	Furthermore, 5HT mediates the stimulatory action of LH/hCG on CRF secretion from Leydig cells and, thus, participates in a negative autoregulatory loop to limit the testosterone response to the gonadotropic stimulus.	Serotonin	13-16	hypertrichosis 2 (generalised, congenital)	Homo sapiens	55-58
1312425-17	1992	Furthermore, 5HT mediates the stimulatory action of LH/hCG on CRF secretion from Leydig cells and, thus, participates in a negative autoregulatory loop to limit the testosterone response to the gonadotropic stimulus.	Testosterone	165-177	hypertrichosis 2 (generalised, congenital)	Homo sapiens	55-58
1385760-2	1992	In 9 cases treated with PG, the method proved to be successful in 89%, as indicated by reduction of human chorionic gonadotropin (hCG) serum values to less than 20 IU/l.	pg	24-26	hypertrichosis 2 (generalised, congenital)	Homo sapiens	130-133
1312425-3	1992	Serotonin stimulated CRF secretion up to 4-fold above basal levels and inhibited basal and hCG-stimulated cAMP generation and testosterone production (ID50, 1 nM).	Serotonin	0-9	hypertrichosis 2 (generalised, congenital)	Homo sapiens	91-94
1312425-3	1992	Serotonin stimulated CRF secretion up to 4-fold above basal levels and inhibited basal and hCG-stimulated cAMP generation and testosterone production (ID50, 1 nM).	Cyclic AMP	106-110	hypertrichosis 2 (generalised, congenital)	Homo sapiens	91-94
1312425-3	1992	Serotonin stimulated CRF secretion up to 4-fold above basal levels and inhibited basal and hCG-stimulated cAMP generation and testosterone production (ID50, 1 nM).	Testosterone	126-138	hypertrichosis 2 (generalised, congenital)	Homo sapiens	91-94
1349590-3	1992	The requirement for treatment was that hCG be given when at least one follicle attained a 17-mm diameter with a serum estradiol level of at least 200 pg/mL per mature follicle.	Estradiol	118-127	hypertrichosis 2 (generalised, congenital)	Homo sapiens	39-42
1536908-3	1992	In addition, its inhibitory action on ovulation was reversed by exogenous progesterone (10 mg/kg) at 2 or 4 h after the hCG injection.	Progesterone	74-86	hypertrichosis 2 (generalised, congenital)	Homo sapiens	120-123
1536908-7	1992	The preovulatory increase of these activities was totally suppressed by RU486 with hCG.	Mifepristone	72-77	hypertrichosis 2 (generalised, congenital)	Homo sapiens	83-86
1536908-8	1992	After administration of progesterone (10 mg/kg) following hCG and RU486 injection, the elevation of proteolytic, enzyme activities in the preovulatory phase was effectively reversed, and levels became similar to those in the control group.	Progesterone	24-36	hypertrichosis 2 (generalised, congenital)	Homo sapiens	58-61
1309346-0	1992	Evidence for a modulation of human chorionic gonadotropin (hCG) subunit messenger ribonucleic acid levels and hCG secretion by gamma-aminobutyric acid in human first trimester placenta in vitro.	gamma-Aminobutyric Acid	127-150	hypertrichosis 2 (generalised, congenital)	Homo sapiens	110-113
1519556-4	1992	Enhanced responsiveness of testosterone (p less than 0.05) and estradiol (p less than 0.05) excretion to hCG injection were observed in patients with oligoasthenoteratozoospermia.	Testosterone	27-39	hypertrichosis 2 (generalised, congenital)	Homo sapiens	105-108
1519556-4	1992	Enhanced responsiveness of testosterone (p less than 0.05) and estradiol (p less than 0.05) excretion to hCG injection were observed in patients with oligoasthenoteratozoospermia.	Estradiol	63-72	hypertrichosis 2 (generalised, congenital)	Homo sapiens	105-108
1516564-5	1992	The binding of 125I-hCG or 125I-LH to spheroplasts of Candida albicans were competitively displaced by hCG, hLH, and PCG.	125i-lh	27-34	hypertrichosis 2 (generalised, congenital)	Homo sapiens	103-106
1516564-5	1992	The binding of 125I-hCG or 125I-LH to spheroplasts of Candida albicans were competitively displaced by hCG, hLH, and PCG.	MY 12-62c	108-111	hypertrichosis 2 (generalised, congenital)	Homo sapiens	20-23
1516564-5	1992	The binding of 125I-hCG or 125I-LH to spheroplasts of Candida albicans were competitively displaced by hCG, hLH, and PCG.	Penicillin G	117-120	hypertrichosis 2 (generalised, congenital)	Homo sapiens	20-23
1309346-4	1992	It was the objective of the present study to find out whether GABA also may influence the biosynthesis and secretion of hCG by human first trimester placenta.	gamma-Aminobutyric Acid	62-66	hypertrichosis 2 (generalised, congenital)	Homo sapiens	120-123
1309346-5	1992	Already one single pulse of GABA (1 h; 0.01-100 microM) stimulated hCG secretion significantly (P less than 0.0001).	gamma-Aminobutyric Acid	28-32	hypertrichosis 2 (generalised, congenital)	Homo sapiens	67-70
1309346-7	1992	The effect on hCG secretion was mimicked by the GABA-A receptor agonist muscimol (P less than 0.002), but under the experimental conditions used (multiple pulses; 1 microM), only the beta mRNA was increased.	Muscimol	72-80	hypertrichosis 2 (generalised, congenital)	Homo sapiens	14-17
1309346-8	1992	The GABA-A receptor antagonist bicuculline (two pulses; 10 microM) suppressed basal hCG secretion (P less than 0.001) and abolished the episodic secretion pattern observed in the control cultures.	Bicuculline	31-42	hypertrichosis 2 (generalised, congenital)	Homo sapiens	84-87
1309346-9	1992	Applying a combination of equimolar amounts of GABA and bicuculline, hCG secretion and the episodic secretion pattern were similar as in control cultures.	gamma-Aminobutyric Acid	47-51	hypertrichosis 2 (generalised, congenital)	Homo sapiens	69-72
1309346-10	1992	The data seem to suggest a regulation of hCG biosynthesis in human first trimester placenta in which GABA is involved, probably acting via GABA-A-like receptor sites.	gamma-Aminobutyric Acid	101-105	hypertrichosis 2 (generalised, congenital)	Homo sapiens	41-44
1730337-1	1992	OBJECTIVE: To examine the possible direct effect of human growth hormone (hGH) on basal and human chorionic gonadodotropin (hCG)-stimulated progesterone (P) production by cultured human luteal cells.	Progesterone	140-152	hypertrichosis 2 (generalised, congenital)	Homo sapiens	124-127
1585012-5	1992	Cells from both types of CL produced inhibin in vitro under basal conditions, but only cells from early to mid CLs responded to hCG with a significant increase in inhibin production.	Chlorine	111-114	hypertrichosis 2 (generalised, congenital)	Homo sapiens	128-131
1585012-6	1992	Both progesterone and oestradiol production were stimulated by hCG in both groups of CL.	Progesterone	5-17	hypertrichosis 2 (generalised, congenital)	Homo sapiens	63-66
1585012-6	1992	Both progesterone and oestradiol production were stimulated by hCG in both groups of CL.	Estradiol	22-32	hypertrichosis 2 (generalised, congenital)	Homo sapiens	63-66
1915960-1	1991	We report a patient undergoing hMG-induced superovulation who demonstrated delayed excretion of hCG, originally believed to be because of successive biochemical pregnancies.	Menotropins	31-34	hypertrichosis 2 (generalised, congenital)	Homo sapiens	96-99
1783364-7	1991	2) The concentration of cholesterol in plasma membrane fraction decreased significantly by hCG stimulation.	Cholesterol	24-35	hypertrichosis 2 (generalised, congenital)	Homo sapiens	91-94
1783364-10	1991	These results indicate the increase of membrane fluidity of the GCs luteinization induced by hCG is due to a decrease of cholesterol/phospholipids ratio.	Cholesterol	121-132	hypertrichosis 2 (generalised, congenital)	Homo sapiens	93-96
1783364-10	1991	These results indicate the increase of membrane fluidity of the GCs luteinization induced by hCG is due to a decrease of cholesterol/phospholipids ratio.	Phospholipids	133-146	hypertrichosis 2 (generalised, congenital)	Homo sapiens	93-96
1787471-5	1991	Within season, there were no differences in testosterone secretion between the two hCG doses, and these responses were similar to those observed after GnRH, but during the rut, testosterone secretion stimulated by both GnRH and hCG was approximately nine times greater than during the nonbreeding season.	Testosterone	177-189	hypertrichosis 2 (generalised, congenital)	Homo sapiens	228-231
1717239-1	1991	To investigate whether LH/human CG (hCG) or progesterone acts as a regulator of estrogen receptors (ER) and progesterone receptors (PR) in granulosa cells, we studied the immunohistochemical expression of both ER and PR in the ovary and the uterus of mature rabbits, during the induction of ovulation by FSH followed by administration of hCG, progesterone, or a progesterone antagonist (RU486) and hCG.	Progesterone	108-120	hypertrichosis 2 (generalised, congenital)	Homo sapiens	32-34
1717239-1	1991	To investigate whether LH/human CG (hCG) or progesterone acts as a regulator of estrogen receptors (ER) and progesterone receptors (PR) in granulosa cells, we studied the immunohistochemical expression of both ER and PR in the ovary and the uterus of mature rabbits, during the induction of ovulation by FSH followed by administration of hCG, progesterone, or a progesterone antagonist (RU486) and hCG.	Progesterone	108-120	hypertrichosis 2 (generalised, congenital)	Homo sapiens	36-39
1660521-3	1991	When human granulosa cells were cultured in the absence of treatment for 3 days, exposure to cloprostenol had no effect on basal progesterone production but inhibited hCG-stimulated progesterone (60% decrease; P less than 0.01), hCG-stimulated cAMP (40% decrease; P less than 0.05) and the progesterone response to dibutyryl cAMP (dbcAMP; 70% decrease; P less than 0.01), suggesting pre- and post-cAMP sites of cloprostenol action.	Cloprostenol	93-105	hypertrichosis 2 (generalised, congenital)	Homo sapiens	167-170
1660521-3	1991	When human granulosa cells were cultured in the absence of treatment for 3 days, exposure to cloprostenol had no effect on basal progesterone production but inhibited hCG-stimulated progesterone (60% decrease; P less than 0.01), hCG-stimulated cAMP (40% decrease; P less than 0.05) and the progesterone response to dibutyryl cAMP (dbcAMP; 70% decrease; P less than 0.01), suggesting pre- and post-cAMP sites of cloprostenol action.	Cloprostenol	93-105	hypertrichosis 2 (generalised, congenital)	Homo sapiens	229-232
1660521-4	1991	The inhibitory actions of cloprostenol were prevented when the granulosa cells were either continuously exposed to treatment from the start of culture or pre-exposed for 3 days to maximum concentrations of LH, hCG, dbcAMP or 8-bromo-cAMP.	Cloprostenol	26-38	hypertrichosis 2 (generalised, congenital)	Homo sapiens	210-213
1660521-5	1991	We conclude that prior exposure either in vivo or in vitro to LH or hCG prevents the subsequent antigonadotrophic action of cloprostenol via a cAMP-dependent mechanism.	Cloprostenol	124-136	hypertrichosis 2 (generalised, congenital)	Homo sapiens	68-71
1660521-5	1991	We conclude that prior exposure either in vivo or in vitro to LH or hCG prevents the subsequent antigonadotrophic action of cloprostenol via a cAMP-dependent mechanism.	Cyclic AMP	143-147	hypertrichosis 2 (generalised, congenital)	Homo sapiens	68-71
1660521-6	1991	Prevention of the antigonadotrophic action of cloprostenol after exposure to hCG may be a mechanism through which CG prevents regression of the corpus luteum in early pregnancy, while the suppressive effect of LH pretreatment may account for the refractory response of the early corpus luteum to cloprostenol following the midcycle LH surge.	Cloprostenol	46-58	hypertrichosis 2 (generalised, congenital)	Homo sapiens	77-80
1660521-6	1991	Prevention of the antigonadotrophic action of cloprostenol after exposure to hCG may be a mechanism through which CG prevents regression of the corpus luteum in early pregnancy, while the suppressive effect of LH pretreatment may account for the refractory response of the early corpus luteum to cloprostenol following the midcycle LH surge.	Cloprostenol	46-58	hypertrichosis 2 (generalised, congenital)	Homo sapiens	78-80
1940555-6	1991	The serum LH level is recommended as a useful parameter in timing hCG administration for IVF.	Luteinizing Hormone	10-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	66-69
1782300-5	1991	The results showed that both small and large luteal cells contained binding sites for LH/hCG, prostaglandin (PG)E2, PGF2 alpha, PGI2, and leukotriene (LT)C4.	Luteinizing Hormone	86-88	hypertrichosis 2 (generalised, congenital)	Homo sapiens	89-92
1744555-4	1991	Human chorionic gonadotrophin (hCG) has been used by some male athletes to stimulate testicular secretion of testosterone.	Testosterone	109-121	hypertrichosis 2 (generalised, congenital)	Homo sapiens	31-34
1744555-6	1991	Administration of hCG resulted in large increases in serum testosterone concentrations and urinary T/LH ratios but small changes in urinary T/E ratios of two subjects (maximum T/E values observed were 0.8 and 1.2 respectively).	Testosterone	59-71	hypertrichosis 2 (generalised, congenital)	Homo sapiens	18-21
1919390-4	1991	In contrast, significant LH/hCG-binding activity was present in Candida cytosol.	Luteinizing Hormone	25-27	hypertrichosis 2 (generalised, congenital)	Homo sapiens	28-31
1713581-3	1991	Although the basal levels of cAMP in the mutant cell lines are comparable to those of the wild-type cells, the increase in cAMP accumulation elicited by human choriogonadotropin (hCG) is severely blunted.	Cyclic AMP	123-127	hypertrichosis 2 (generalised, congenital)	Homo sapiens	179-182
1713581-7	1991	We also show that the ability of these cells to respond to hCG with increased cAMP accumulation and steroid synthesis can be restored with a specific phosphodiesterase inhibitor.	Cyclic AMP	78-82	hypertrichosis 2 (generalised, congenital)	Homo sapiens	59-62
1713581-7	1991	We also show that the ability of these cells to respond to hCG with increased cAMP accumulation and steroid synthesis can be restored with a specific phosphodiesterase inhibitor.	Steroids	100-107	hypertrichosis 2 (generalised, congenital)	Homo sapiens	59-62
1713581-8	1991	These results demonstrate that overexpression of a cAMP-phosphodiesterase in MA-10 cells limits the levels of cAMP attained under hCG stimulation and supresses the steroidogenic response of these cells to hCG.	Cyclic AMP	51-55	hypertrichosis 2 (generalised, congenital)	Homo sapiens	130-133
1713581-8	1991	These results demonstrate that overexpression of a cAMP-phosphodiesterase in MA-10 cells limits the levels of cAMP attained under hCG stimulation and supresses the steroidogenic response of these cells to hCG.	Cyclic AMP	51-55	hypertrichosis 2 (generalised, congenital)	Homo sapiens	205-208
1753171-5	1991	hCG significantly enhanced progesterone (P) and estradiol (E2) production by the cells, however, the addition of LA in concentrations of 10, 100, and 1000 ng/ml had no effect.	Progesterone	27-39	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
1753171-5	1991	hCG significantly enhanced progesterone (P) and estradiol (E2) production by the cells, however, the addition of LA in concentrations of 10, 100, and 1000 ng/ml had no effect.	Estradiol	48-57	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
1716095-7	1991	The initial serum hCG level was high at 460,000 mIU/ml, but fell to 13 mIU/ml after 3 courses of PVP therapy.	Povidone	97-100	hypertrichosis 2 (generalised, congenital)	Homo sapiens	18-21
1919390-11	1991	125I-labelled hLH/hCG binding to Candida membranes was also displaceable by low levels (ng) of partially purified hCG preparations, but much higher levels (micrograms) of highly purified hLH and hCG were required.	MY 12-62c	14-17	hypertrichosis 2 (generalised, congenital)	Homo sapiens	18-21
1919390-11	1991	125I-labelled hLH/hCG binding to Candida membranes was also displaceable by low levels (ng) of partially purified hCG preparations, but much higher levels (micrograms) of highly purified hLH and hCG were required.	MY 12-62c	14-17	hypertrichosis 2 (generalised, congenital)	Homo sapiens	114-117
1919390-11	1991	125I-labelled hLH/hCG binding to Candida membranes was also displaceable by low levels (ng) of partially purified hCG preparations, but much higher levels (micrograms) of highly purified hLH and hCG were required.	MY 12-62c	14-17	hypertrichosis 2 (generalised, congenital)	Homo sapiens	114-117
1904453-8	1991	hCG, including physiological concentrations, stimulated PGE and 6-keto-PGF1 alpha synthesis in placental organ cultures.	Prostaglandins E	56-59	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
1648698-9	1991	In early pregnancy, when hCG concentrations are highest, free thyroid hormones are increased and serum TSH concentration is decreased.	Thyrotropin	103-106	hypertrichosis 2 (generalised, congenital)	Homo sapiens	25-28
1648698-10	1991	An inverse correlation exists between serum hCG and TSH concentrations, but hCG generally correlates poorly with individual thyroid tests.	Thyrotropin	52-55	hypertrichosis 2 (generalised, congenital)	Homo sapiens	44-47
1904453-8	1991	hCG, including physiological concentrations, stimulated PGE and 6-keto-PGF1 alpha synthesis in placental organ cultures.	6-Ketoprostaglandin F1 alpha	64-81	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
1904453-10	1991	A similar hCG-induced stimulation of PGE production occurred in monolayer cultures of trophoblasts.	Prostaglandins E	37-40	hypertrichosis 2 (generalised, congenital)	Homo sapiens	10-13
1904453-12	1991	These data suggest that hCG may have a biological role in the regulation of PG synthesis in early human placenta.	Prostaglandins	76-78	hypertrichosis 2 (generalised, congenital)	Homo sapiens	24-27
2069861-6	1991	Aromatase activity of granulosa-luteal cells was measured from the rate of formation of 3H2O from 1 beta-[3H]androstenedione (1 beta[3H]A) after exposing the cells to hCG, FSH or estradiol (E2) for 48 h. Basal aromatase activity was relatively low, but hCG and FSH stimulated aromatase 8- and 4-fold, respectively.	3h2o	88-92	hypertrichosis 2 (generalised, congenital)	Homo sapiens	167-170
2037112-4	1991	RESULTS: The addition of indomethacin to hCG inhibited ovulation and production of PGs without affecting the follicular microvasculature.	Prostaglandins	83-86	hypertrichosis 2 (generalised, congenital)	Homo sapiens	41-44
1776157-3	1991	Testes isolated from methanol-exposed (200 ppm) rats had the same capability as those from air-exposed rats in synthesizing testosterone whether testes were incubated in the absence or presence of hCG.	Methanol	21-29	hypertrichosis 2 (generalised, congenital)	Homo sapiens	197-200
1651166-5	1991	However, incubation with 1 nM human chorionic gonadotropin (hCG) or 10 nM PGE1 resulted in a significant increase of nuclear volume of small luteal cells by 4 h and that of large luteal cells by 6 h. Small luteal cells were more responsive to hCG than large luteal cells.	Alprostadil	74-78	hypertrichosis 2 (generalised, congenital)	Homo sapiens	243-246
1645252-2	1991	Deglycosylated hCG is a derivative of hCG which retains the ability to bind to the LH/CG receptor, but is unable to activate adenylyl cyclase and thus stimulate cAMP production.	Cyclic AMP	161-165	hypertrichosis 2 (generalised, congenital)	Homo sapiens	15-18
1645252-2	1991	Deglycosylated hCG is a derivative of hCG which retains the ability to bind to the LH/CG receptor, but is unable to activate adenylyl cyclase and thus stimulate cAMP production.	Cyclic AMP	161-165	hypertrichosis 2 (generalised, congenital)	Homo sapiens	38-41
1645252-2	1991	Deglycosylated hCG is a derivative of hCG which retains the ability to bind to the LH/CG receptor, but is unable to activate adenylyl cyclase and thus stimulate cAMP production.	Cyclic AMP	161-165	hypertrichosis 2 (generalised, congenital)	Homo sapiens	16-18
1856522-8	1991	Human chorionic gonadotropin (hCG) also has an action which protects the activity of prostacyclin.	Epoprostenol	85-97	hypertrichosis 2 (generalised, congenital)	Homo sapiens	30-33
1903727-10	1991	CONCLUSION: In hMG-stimulated cycles, a second dose of hCG given during the midluteal phase significantly increases late luteal E2 and P levels and consistently lengthens the luteal phase.	Menotropins	15-18	hypertrichosis 2 (generalised, congenital)	Homo sapiens	55-58
1851591-5	1991	Acute stimulation with hCG increased testosterone levels only slightly in plasma and not in testicular tissues of scorbutic rats, when testosterone levels in ascorbutic rats reached a maximum.	Testosterone	37-49	hypertrichosis 2 (generalised, congenital)	Homo sapiens	23-26
1868150-3	1991	All three fluid samples stimulated both basal and maximal hCG-stimulated testosterone production, although the resulting log dose-response lines of bFF and the hFF extracts were not parallel with those of rTF.	Testosterone	73-85	hypertrichosis 2 (generalised, congenital)	Homo sapiens	58-61
1868150-4	1991	Both rTF and bFF were active over a similar dose range (5.2-150 microliters and 9.7-150 microliters, respectively) and both had a more than additive interaction with hCG on testosterone production.	Testosterone	173-185	hypertrichosis 2 (generalised, congenital)	Homo sapiens	166-169
2014090-2	1991	Methotrexate and citrovorum were given on alternating days until the hCG titer had decreased by 15% on 2 consecutive days.	Leucovorin	17-27	hypertrichosis 2 (generalised, congenital)	Homo sapiens	69-72
1851591-5	1991	Acute stimulation with hCG increased testosterone levels only slightly in plasma and not in testicular tissues of scorbutic rats, when testosterone levels in ascorbutic rats reached a maximum.	Testosterone	135-147	hypertrichosis 2 (generalised, congenital)	Homo sapiens	23-26
1851591-6	1991	Chronic stimulation with hCG increased testosterone levels remarkably in both ascorbutic and scorbutic rats.	Testosterone	39-51	hypertrichosis 2 (generalised, congenital)	Homo sapiens	25-28
1910247-3	1991	This, exacerbated by the long half-life of hCG, causes the principal complications of hMG therapy--multiple pregnancy and hyperstimulation.	hmg	86-89	hypertrichosis 2 (generalised, congenital)	Homo sapiens	43-46
2056229-8	1991	These results suggested that TVU could significantly improve the detection of gestational sacs, and result in a lower hCG threshold than previously established with transabdominal sonography.	N-[1,1-Bis(Oxidanylidene)thian-4-Yl]-7-(3,4-Dimethoxyphenyl)-5-Methyl-4-Oxidanylidene-Thieno[3,2-C]pyridine-2-Carboxamide	29-32	hypertrichosis 2 (generalised, congenital)	Homo sapiens	118-121
1952114-1	1991	The effect of the antiestrogen tamoxifen (Tx) on the acute and chronic hCG administration was evaluated in patients with hypogonadotropic hypogonadism (HH) and in normal men.	Tamoxifen	31-40	hypertrichosis 2 (generalised, congenital)	Homo sapiens	71-74
1952114-5	1991	17OHP rose with hCG alone, but not with hCG + Tx in both groups.	17-alpha-Hydroxyprogesterone	0-5	hypertrichosis 2 (generalised, congenital)	Homo sapiens	16-19
2013870-5	1991	Concentrations of PGF-2 alpha in 9 hourly samples of plasma collected from the posterior vena cava via indwelling catheters were higher on Days 4 through 9 after injection of hCG (P less than 0.05) in the cows with short-lived corpora lutea.	Dinoprost	18-23	hypertrichosis 2 (generalised, congenital)	Homo sapiens	175-178
1848384-2	1991	In the presence of crude immunoglobulin fractions in sera from patients with primary hypothyroidism, cAMP accumulation induced by both crude and purified hCG, and normal pregnant women serum were significantly inhibited compared with that in the presence of normal IgGs.	Cyclic AMP	101-105	hypertrichosis 2 (generalised, congenital)	Homo sapiens	154-157
1848384-5	1991	Binding studies of TSH in FRTL-5 cells also indicated the dose-dependent displacements of [125I]TSH by hCG.	Thyrotropin	19-22	hypertrichosis 2 (generalised, congenital)	Homo sapiens	103-106
1848384-6	1991	Although half-maximal inhibitory concentration of hCG was about 20 times as high as that of TSH on a molar basis, displacement of [125I]TSH was observed at a concentration of hCG of 10(5)IU/l or more, which could be a physiological concentration of hCG in sera of normal pregnant women.	Thyrotropin	136-139	hypertrichosis 2 (generalised, congenital)	Homo sapiens	175-178
1848384-6	1991	Although half-maximal inhibitory concentration of hCG was about 20 times as high as that of TSH on a molar basis, displacement of [125I]TSH was observed at a concentration of hCG of 10(5)IU/l or more, which could be a physiological concentration of hCG in sera of normal pregnant women.	Thyrotropin	136-139	hypertrichosis 2 (generalised, congenital)	Homo sapiens	175-178
1986971-1	1991	The purpose of this study was to analyze follicular fluid (FF) samples for steroid levels from stimulated and unstimulated cycles triggered with human chorionic gonadotropin (hCG) and to assess the influence of controlled ovarian hyperstimulation and luteinizing hormone/hCG on these levels.	Steroids	75-82	hypertrichosis 2 (generalised, congenital)	Homo sapiens	175-178
1996618-8	1991	2 alpha,4 alpha,7-4,5-Epoxy-17-hydroxy-4,17-dimethyl-3-oxo-androstane-2- carbonitrile (epostane), a potent inhibitor of steroid synthesis and ovulation, sharply reduced the synthesis of all five steroids within 30 min after its injection at 3 h after hCG.	2 alpha,4 alpha,7-4,5-epoxy-17-hydroxy-4,17-dimethyl-3-oxo-androstane-2- carbonitrile	0-85	hypertrichosis 2 (generalised, congenital)	Homo sapiens	251-254
1996618-8	1991	2 alpha,4 alpha,7-4,5-Epoxy-17-hydroxy-4,17-dimethyl-3-oxo-androstane-2- carbonitrile (epostane), a potent inhibitor of steroid synthesis and ovulation, sharply reduced the synthesis of all five steroids within 30 min after its injection at 3 h after hCG.	epostane	87-95	hypertrichosis 2 (generalised, congenital)	Homo sapiens	251-254
1996618-8	1991	2 alpha,4 alpha,7-4,5-Epoxy-17-hydroxy-4,17-dimethyl-3-oxo-androstane-2- carbonitrile (epostane), a potent inhibitor of steroid synthesis and ovulation, sharply reduced the synthesis of all five steroids within 30 min after its injection at 3 h after hCG.	Steroids	120-127	hypertrichosis 2 (generalised, congenital)	Homo sapiens	251-254
1900320-5	1991	Coadministration of hCG with the LHRH antagonist prevented the fall in progesterone.	Progesterone	71-83	hypertrichosis 2 (generalised, congenital)	Homo sapiens	20-23
1900320-7	1991	Administration of hCG stimulated progesterone production when given 8 h after the LHRH antagonist but not after 24 h. Cloprostenol prevented the stimulation by hCG.	Cloprostenol	118-130	hypertrichosis 2 (generalised, congenital)	Homo sapiens	18-21
1900320-7	1991	Administration of hCG stimulated progesterone production when given 8 h after the LHRH antagonist but not after 24 h. Cloprostenol prevented the stimulation by hCG.	Cloprostenol	118-130	hypertrichosis 2 (generalised, congenital)	Homo sapiens	160-163
2177626-3	1990	Using percoll-purified mouse Leydig cells, we have demonstrated that several types of histones could almost completely inhibit hCG-stimulated testosterone production and cAMP formation.	Testosterone	142-154	hypertrichosis 2 (generalised, congenital)	Homo sapiens	127-130
1659882-5	1991	LH-stimulated testosterone production was inhibited in the hCG treated rats and dexamethasone caused a further decrease.	Testosterone	14-26	hypertrichosis 2 (generalised, congenital)	Homo sapiens	59-62
1659882-7	1991	HCG, but not dexamethasone, had similar inhibitory effects on LH-stimulated cyclic AMP production.	Luteinizing Hormone	62-64	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
1659882-7	1991	HCG, but not dexamethasone, had similar inhibitory effects on LH-stimulated cyclic AMP production.	Cyclic AMP	76-86	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
1668561-0	1991	[Effect of gossypol acetic acid on hCG-stimulated progesterone production of dissociated rat luteal cells].	gossypol acetic acid	11-31	hypertrichosis 2 (generalised, congenital)	Homo sapiens	35-38
1668561-0	1991	[Effect of gossypol acetic acid on hCG-stimulated progesterone production of dissociated rat luteal cells].	Progesterone	50-62	hypertrichosis 2 (generalised, congenital)	Homo sapiens	35-38
1668561-1	1991	The effect of gossypol acetic acid on hCG-stimulated progesterone synthesis and secretion in isolated rat luteal cells and its possible mechanism were investigated.	gossypol acetic acid	14-34	hypertrichosis 2 (generalised, congenital)	Homo sapiens	38-41
1668561-1	1991	The effect of gossypol acetic acid on hCG-stimulated progesterone synthesis and secretion in isolated rat luteal cells and its possible mechanism were investigated.	Progesterone	53-65	hypertrichosis 2 (generalised, congenital)	Homo sapiens	38-41
1668561-2	1991	When gossypol was used at a concentration of 20 micrograms/ml for one hour, the hCG-stimulated progesterone production and secretion decreased markedly, but the basal progesterone level did not change significantly.	Gossypol	5-13	hypertrichosis 2 (generalised, congenital)	Homo sapiens	80-83
1668561-2	1991	When gossypol was used at a concentration of 20 micrograms/ml for one hour, the hCG-stimulated progesterone production and secretion decreased markedly, but the basal progesterone level did not change significantly.	Progesterone	95-107	hypertrichosis 2 (generalised, congenital)	Homo sapiens	80-83
1668561-6	1991	The present experiment indicates that gossypol acetic acid can inhibit the progesterone production stimulated by hCG in isolated rat luteal cells through direct cellular mechanism.	gossypol acetic acid	38-58	hypertrichosis 2 (generalised, congenital)	Homo sapiens	113-116
1668561-6	1991	The present experiment indicates that gossypol acetic acid can inhibit the progesterone production stimulated by hCG in isolated rat luteal cells through direct cellular mechanism.	Progesterone	75-87	hypertrichosis 2 (generalised, congenital)	Homo sapiens	113-116
1659882-4	1991	It was found that hCG caused a marked increase in prostaglandin F2 alpha formation which was inhibited by treatment with dexamethasone.	Dinoprost	50-72	hypertrichosis 2 (generalised, congenital)	Homo sapiens	18-21
1659882-4	1991	It was found that hCG caused a marked increase in prostaglandin F2 alpha formation which was inhibited by treatment with dexamethasone.	Dexamethasone	121-134	hypertrichosis 2 (generalised, congenital)	Homo sapiens	18-21
1823986-1	1991	Diphenoxylate hydrochloride (R1132) at concentrations of 10 and 20 micrograms/ml or dl-15 methyl-PGF2 alpha methyl ester (PG05) at levels of 5 and 10 micrograms/ml was shown to have no effect on progesterone secretion by luteal cells in vitro in the absence of hCG.	Diphenoxylate	0-27	hypertrichosis 2 (generalised, congenital)	Homo sapiens	261-264
1823986-3	1991	The steroidogenic response of luteal cells to hCG was inhibited by R1132 and PG05.	pg05	77-81	hypertrichosis 2 (generalised, congenital)	Homo sapiens	46-49
2284888-0	1990	Testicular responsiveness to hCG during infancy measured by salivary testosterone.	Testosterone	69-81	hypertrichosis 2 (generalised, congenital)	Homo sapiens	29-32
2177626-3	1990	Using percoll-purified mouse Leydig cells, we have demonstrated that several types of histones could almost completely inhibit hCG-stimulated testosterone production and cAMP formation.	Cyclic AMP	170-174	hypertrichosis 2 (generalised, congenital)	Homo sapiens	127-130
2177626-5	1990	The most potent histone types were H2AS and H8S, both of which could inhibit hCG-stimulated cAMP formation half-maximally at concentrations of 4-5 micrograms/ml.	H8S	44-47	hypertrichosis 2 (generalised, congenital)	Homo sapiens	77-80
2284888-10	1990	A clear stimulatory effect of hCG on testicular testosterone production was found, suggesting that the postnatal increase in serum testosterone concentration in male infants is gonadotropin-mediated.	Testosterone	48-60	hypertrichosis 2 (generalised, congenital)	Homo sapiens	30-33
2284888-10	1990	A clear stimulatory effect of hCG on testicular testosterone production was found, suggesting that the postnatal increase in serum testosterone concentration in male infants is gonadotropin-mediated.	Testosterone	131-143	hypertrichosis 2 (generalised, congenital)	Homo sapiens	30-33
2284888-11	1990	Salivary testosterone concentrations can be increased by hCG, indicating that measurements of salivary testosterone may provide an optional, non-invasive method for assessing gonadal function in children.	Testosterone	9-21	hypertrichosis 2 (generalised, congenital)	Homo sapiens	57-60
2284888-11	1990	Salivary testosterone concentrations can be increased by hCG, indicating that measurements of salivary testosterone may provide an optional, non-invasive method for assessing gonadal function in children.	Testosterone	103-115	hypertrichosis 2 (generalised, congenital)	Homo sapiens	57-60
2177626-5	1990	The most potent histone types were H2AS and H8S, both of which could inhibit hCG-stimulated cAMP formation half-maximally at concentrations of 4-5 micrograms/ml.	Cyclic AMP	92-96	hypertrichosis 2 (generalised, congenital)	Homo sapiens	77-80
2177626-11	1990	Based on the [125I]hCG binding data it is possible to conclude that histone H2AS inhibits the binding of hCG to its receptors on Leydig cells and thereby causes the inhibition of hCG-stimulated cAMP formation and steroidogenesis.	Cyclic AMP	194-198	hypertrichosis 2 (generalised, congenital)	Homo sapiens	19-22
2177626-11	1990	Based on the [125I]hCG binding data it is possible to conclude that histone H2AS inhibits the binding of hCG to its receptors on Leydig cells and thereby causes the inhibition of hCG-stimulated cAMP formation and steroidogenesis.	Cyclic AMP	194-198	hypertrichosis 2 (generalised, congenital)	Homo sapiens	105-108
2177626-11	1990	Based on the [125I]hCG binding data it is possible to conclude that histone H2AS inhibits the binding of hCG to its receptors on Leydig cells and thereby causes the inhibition of hCG-stimulated cAMP formation and steroidogenesis.	Cyclic AMP	194-198	hypertrichosis 2 (generalised, congenital)	Homo sapiens	105-108
2291916-3	1990	Specifically, we determined the in vitro secretion of steroids by intact ovarian follicles of unprimed or hCG-primed fish, the direct effects of steroids on maturational competence, and the effects of steroid (cyanoketone), protein (cycloheximide), and RNA (actinomycin D) synthesis inhibitors on hCG-induced maturational competence and steroidogenesis in vitro.	Steroids	54-61	hypertrichosis 2 (generalised, congenital)	Homo sapiens	106-109
2291916-4	1990	The steroid content of the incubation medium after hCG treatment was measured by RIA.	Steroids	4-11	hypertrichosis 2 (generalised, congenital)	Homo sapiens	51-54
2249634-6	1990	Comparison of the effects of estradiol and hCG on thecal cells from small (less than 5 mm), medium (5-10 mm), and large (greater than 10 mm) antral follicles demonstrated that estradiol stimulated androgen production to a greater extent than hCG with cells from all of these stages of follicle development.	Estradiol	176-185	hypertrichosis 2 (generalised, congenital)	Homo sapiens	43-46
2249634-6	1990	Comparison of the effects of estradiol and hCG on thecal cells from small (less than 5 mm), medium (5-10 mm), and large (greater than 10 mm) antral follicles demonstrated that estradiol stimulated androgen production to a greater extent than hCG with cells from all of these stages of follicle development.	Estradiol	176-185	hypertrichosis 2 (generalised, congenital)	Homo sapiens	242-245
2249634-11	1990	Interestingly, combined treatment of thecal cells with estradiol and hCG resulted in a greater than additive stimulation of androstenedione production, and estradiol decreased the ability of hCG to stimulate progesterone production.	Androstenedione	124-139	hypertrichosis 2 (generalised, congenital)	Homo sapiens	69-72
2249634-11	1990	Interestingly, combined treatment of thecal cells with estradiol and hCG resulted in a greater than additive stimulation of androstenedione production, and estradiol decreased the ability of hCG to stimulate progesterone production.	Estradiol	156-165	hypertrichosis 2 (generalised, congenital)	Homo sapiens	191-194
2249634-11	1990	Interestingly, combined treatment of thecal cells with estradiol and hCG resulted in a greater than additive stimulation of androstenedione production, and estradiol decreased the ability of hCG to stimulate progesterone production.	Progesterone	208-220	hypertrichosis 2 (generalised, congenital)	Homo sapiens	69-72
2249634-11	1990	Interestingly, combined treatment of thecal cells with estradiol and hCG resulted in a greater than additive stimulation of androstenedione production, and estradiol decreased the ability of hCG to stimulate progesterone production.	Progesterone	208-220	hypertrichosis 2 (generalised, congenital)	Homo sapiens	191-194
2226298-2	1990	In vitro stimulation with human CG (hCG) (0.2 IU/ml) caused a 75-fold increase in testosterone production.	cysteinylglycine	32-34	hypertrichosis 2 (generalised, congenital)	Homo sapiens	36-39
2226298-2	1990	In vitro stimulation with human CG (hCG) (0.2 IU/ml) caused a 75-fold increase in testosterone production.	Testosterone	82-94	hypertrichosis 2 (generalised, congenital)	Homo sapiens	36-39
2226298-4	1990	The total cholesterol content of cells stimulated for 4 h with hCG was significantly decreased compared with unstimulated cells (8.4 vs. 17.6 micrograms/mg protein); both free and esterified cholesterol decreased by about 50%.	Cholesterol	10-21	hypertrichosis 2 (generalised, congenital)	Homo sapiens	63-66
2226298-4	1990	The total cholesterol content of cells stimulated for 4 h with hCG was significantly decreased compared with unstimulated cells (8.4 vs. 17.6 micrograms/mg protein); both free and esterified cholesterol decreased by about 50%.	Cholesterol	191-202	hypertrichosis 2 (generalised, congenital)	Homo sapiens	63-66
2226298-5	1990	In unstimulated Leydig cells incubated with [14C]acetate for 12 h, the majority of incorporated [14C] was found in free and esterified cholesterol, whereas, in the hCG-stimulated cells, 80% of incorporated 14C was in testosterone.	14c]acetate	45-56	hypertrichosis 2 (generalised, congenital)	Homo sapiens	164-167
2226298-5	1990	In unstimulated Leydig cells incubated with [14C]acetate for 12 h, the majority of incorporated [14C] was found in free and esterified cholesterol, whereas, in the hCG-stimulated cells, 80% of incorporated 14C was in testosterone.	Carbon-14	45-48	hypertrichosis 2 (generalised, congenital)	Homo sapiens	164-167
2226298-5	1990	In unstimulated Leydig cells incubated with [14C]acetate for 12 h, the majority of incorporated [14C] was found in free and esterified cholesterol, whereas, in the hCG-stimulated cells, 80% of incorporated 14C was in testosterone.	Carbon-14	97-100	hypertrichosis 2 (generalised, congenital)	Homo sapiens	164-167
2226298-5	1990	In unstimulated Leydig cells incubated with [14C]acetate for 12 h, the majority of incorporated [14C] was found in free and esterified cholesterol, whereas, in the hCG-stimulated cells, 80% of incorporated 14C was in testosterone.	Testosterone	217-229	hypertrichosis 2 (generalised, congenital)	Homo sapiens	164-167
2226298-9	1990	HMG-CoA reductase activity induced by hCG was blocked by aminoglutethimide, an inhibitor of the cholesterol side-chain cleavage enzyme.	Aminoglutethimide	57-74	hypertrichosis 2 (generalised, congenital)	Homo sapiens	38-41
2226298-9	1990	HMG-CoA reductase activity induced by hCG was blocked by aminoglutethimide, an inhibitor of the cholesterol side-chain cleavage enzyme.	Cholesterol	96-107	hypertrichosis 2 (generalised, congenital)	Homo sapiens	38-41
2226298-12	1990	During a 6 h incubation, mHDL increased hCG-stimulated testosterone production by 20%, but had no effect on unstimulated testosterone production.	mhdl	25-29	hypertrichosis 2 (generalised, congenital)	Homo sapiens	40-43
2226298-12	1990	During a 6 h incubation, mHDL increased hCG-stimulated testosterone production by 20%, but had no effect on unstimulated testosterone production.	Testosterone	55-67	hypertrichosis 2 (generalised, congenital)	Homo sapiens	40-43
2125284-5	1990	Highly purified human chorionic gonadotropin (hCG) or hLH preparations were much less effective at inhibiting 125I-hLH binding to Drosophila microsomes than partially purified gonadotropins.	125i-hlh	110-118	hypertrichosis 2 (generalised, congenital)	Homo sapiens	46-49
16726883-5	1990	Increases in plasma testosterone levels were determined by a ratio of testosterone concentration before and after hCG injection.	Testosterone	20-32	hypertrichosis 2 (generalised, congenital)	Homo sapiens	114-117
2125284-7	1990	Chromatography of crude hCG preparations clearly resolved the LH-binding inhibitor from hCG.	Luteinizing Hormone	62-64	hypertrichosis 2 (generalised, congenital)	Homo sapiens	24-27
2125284-7	1990	Chromatography of crude hCG preparations clearly resolved the LH-binding inhibitor from hCG.	Luteinizing Hormone	62-64	hypertrichosis 2 (generalised, congenital)	Homo sapiens	88-91
2125284-10	1990	These data suggest that high affinity binding sites for hLH/hCG-like molecules are present in Drosophila microsomes.	MY 12-62c	56-59	hypertrichosis 2 (generalised, congenital)	Homo sapiens	60-63
2271724-4	1990	The luteolytic effect of lilopristone was prevented by exogenous treatment with hCG; however, the animals showed premature menstruation, in spite of high progesterone levels (above 4 ng/ml).	lilopristone	25-37	hypertrichosis 2 (generalised, congenital)	Homo sapiens	80-83
1700569-2	1990	hCG was extracted from the sera using anti-hCG-beta subunit monoclonal antibody-coated microwells, eluted with 2 mol/l guanidine-HCl, and reconstituted with hypotonic Hanks" solution.	Guanidine	119-132	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
1700569-2	1990	hCG was extracted from the sera using anti-hCG-beta subunit monoclonal antibody-coated microwells, eluted with 2 mol/l guanidine-HCl, and reconstituted with hypotonic Hanks" solution.	hanks" solution	167-182	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
1700569-6	1990	cAMP levels were also increased in a dose-dependent manner by adding purified hCG as well as crude hCG and hTSH to FRTL-5 cells.	Cyclic AMP	0-4	hypertrichosis 2 (generalised, congenital)	Homo sapiens	78-81
1700569-6	1990	cAMP levels were also increased in a dose-dependent manner by adding purified hCG as well as crude hCG and hTSH to FRTL-5 cells.	Cyclic AMP	0-4	hypertrichosis 2 (generalised, congenital)	Homo sapiens	99-102
2271732-5	1990	PGE2, PGD2, and 6 beta PGI1 alone stimulated (p less than 0.05) P production to a similar extent (2- to 3-fold over basal) as hCG alone, whereas PGA2 and PGF2 alpha alone had no effect on P production.	Dinoprostone	0-4	hypertrichosis 2 (generalised, congenital)	Homo sapiens	126-129
2253408-4	1990	Following hCG, the luteal phase was prolonged and there were significant increases in the plasma concentrations of inhibin (P less than 0.05), and oestradiol (P less than 0.05).	Estradiol	147-157	hypertrichosis 2 (generalised, congenital)	Homo sapiens	10-13
2167211-7	1990	hCG-stimulated testosterone formation was inhibited in a dose-dependent manner by the addition of IL-2.	Testosterone	15-27	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
2167211-8	1990	IL-2 in a concentration of 100 U/ml decreased hCG-induced testosterone formation from 49.6 +/- 3.6 ng/ml (mean +/- SE) to 8.5 +/- 4.2 ng/ml.	Testosterone	58-70	hypertrichosis 2 (generalised, congenital)	Homo sapiens	46-49
2167211-10	1990	Maximal testosterone production in response to hCG was reduced 40% in the presence of IL-2 (50 U/ml) without alteration of median effective dose (ED50).	Testosterone	8-20	hypertrichosis 2 (generalised, congenital)	Homo sapiens	47-50
2167211-11	1990	IL-2 also inhibited hCG-induced cAMP formation and 8-bromo cAMP- and forskolin-stimulated testosterone production.	Cyclic AMP	32-36	hypertrichosis 2 (generalised, congenital)	Homo sapiens	20-23
2167219-3	1990	Incubation of Leydig cells with a CRF antagonist revealed tonic suppression of basal and hCG-stimulated testosterone production by endogenously produced CRF.	Testosterone	104-116	hypertrichosis 2 (generalised, congenital)	Homo sapiens	89-92
2394770-3	1990	Using a cultured Leydig tumor cell line (MA-10) known to express the CG/LH receptor as the receptor source and polyacrylamide-gel electrophoresis purified hCG as the radioligand, we have established an assay system with the requisite sensitivity (0.04 ng/tube) to measure circulating LH, without significant alteration in total specific binding upon addition of up to 150 microL gonadotropin-free serum when compared to no serum.	polyacrylamide	111-125	hypertrichosis 2 (generalised, congenital)	Homo sapiens	155-158
2273644-6	1990	Moreover, estradiol enhanced the effect of hCG, but tamoxifen did not.	Estradiol	10-19	hypertrichosis 2 (generalised, congenital)	Homo sapiens	43-46
2231546-0	1990	Prostaglandin F-2 alpha causes regression of an hCG-induced corpus luteum before day 5 of its lifespan in cattle.	Dinoprost	0-23	hypertrichosis 2 (generalised, congenital)	Homo sapiens	48-51
2121394-8	1990	hCG resulted in a greater increase of serum testosterone from A to C samples at rest than during the exercise trial (52 vs 33%, P = 0.04).	Testosterone	44-56	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
2117066-0	1990	Alcohol effects on hCG-stimulated gonadal hormones in women.	Alcohols	0-7	hypertrichosis 2 (generalised, congenital)	Homo sapiens	19-22
2117066-10	1990	Since progesterone is essential for the maintenance of pregnancy, alcohol"s attenuation of the expected progesterone response to hCG stimulation could increase the risk of spontaneous abortion.	Alcohols	66-73	hypertrichosis 2 (generalised, congenital)	Homo sapiens	129-132
2117066-11	1990	An alcohol-induced increase in estradiol after hCG administration could contribute to risk for fetal dysmorphology during the first trimester of pregnancy.	Alcohols	3-10	hypertrichosis 2 (generalised, congenital)	Homo sapiens	47-50
2117066-11	1990	An alcohol-induced increase in estradiol after hCG administration could contribute to risk for fetal dysmorphology during the first trimester of pregnancy.	Estradiol	31-40	hypertrichosis 2 (generalised, congenital)	Homo sapiens	47-50
1696941-3	1990	When p-aminobenzamidine, a serine protease inhibitor which inhibits urokinase-type plasminogen activator, was administered together with hCG in the incubation medium, both the permeability increase and PMN extravasation were prevented.	4-aminobenzamidine	5-23	hypertrichosis 2 (generalised, congenital)	Homo sapiens	137-140
2274704-6	1990	When testes fragments were incubated with 0 or 12.5 mIU hCG/ml for 4 h, hCG increased media progesterone levels in rats and control mice, but not in hamsters and hCG-injected mice.	Progesterone	92-104	hypertrichosis 2 (generalised, congenital)	Homo sapiens	56-59
2170316-5	1990	The cells in subfraction I, predominantly damaged Leydig cells, germ cells, and/or residual light cells, bind 125I-labeled hCG with high affinity (Kd 4.09 x 10(-10) mol/L) without producing cAMP and testosterone in response to hCG.	Iodine-125	110-114	hypertrichosis 2 (generalised, congenital)	Homo sapiens	227-230
2170316-5	1990	The cells in subfraction I, predominantly damaged Leydig cells, germ cells, and/or residual light cells, bind 125I-labeled hCG with high affinity (Kd 4.09 x 10(-10) mol/L) without producing cAMP and testosterone in response to hCG.	Testosterone	199-211	hypertrichosis 2 (generalised, congenital)	Homo sapiens	123-126
2170316-7	1990	The cells in subfraction II, identified as typical Leydig cells by electron microscopy, produce cAMP and testosterone in response to hCG but, again, bind only a small amount of hCG (4.5 +/- 0.3 fmol/2 x 10(6) cells/250 microliters/per hour at 37 degrees C).	Cyclic AMP	96-100	hypertrichosis 2 (generalised, congenital)	Homo sapiens	133-136
2170316-7	1990	The cells in subfraction II, identified as typical Leydig cells by electron microscopy, produce cAMP and testosterone in response to hCG but, again, bind only a small amount of hCG (4.5 +/- 0.3 fmol/2 x 10(6) cells/250 microliters/per hour at 37 degrees C).	Testosterone	105-117	hypertrichosis 2 (generalised, congenital)	Homo sapiens	133-136
2167768-1	1990	Prolonged (7-day) hCG infusion caused a remarkable hypertrophy of rat Leydig cells, coupled with a notable enhancement of their basal and stimulated testosterone production in vitro.	Testosterone	149-161	hypertrichosis 2 (generalised, congenital)	Homo sapiens	18-21
2167768-4	1990	Conversely, in chronically hCG-infused animals, 4APP reversed lipid-droplet accumulation and significantly depressed stimulated testosterone production.	4-aminopyrazolo(3,4-d)pyrimidine	48-52	hypertrichosis 2 (generalised, congenital)	Homo sapiens	27-30
2167768-5	1990	The following conclusions are drawn: 1) chronic hCG treatment enhances the ability of rat Leydig cells to take-up exogenous cholesterol from circulating lipoproteins, and to store it in lipid droplets as a reserve material; 2) lipid-droplet stored cholesterol is employed only in the case of intense acute stimulation, since, under basal conditions, endogenous cholesterol synthesis is able to meet the requirements for testosterone production alone.	Cholesterol	124-135	hypertrichosis 2 (generalised, congenital)	Homo sapiens	48-51
2167768-5	1990	The following conclusions are drawn: 1) chronic hCG treatment enhances the ability of rat Leydig cells to take-up exogenous cholesterol from circulating lipoproteins, and to store it in lipid droplets as a reserve material; 2) lipid-droplet stored cholesterol is employed only in the case of intense acute stimulation, since, under basal conditions, endogenous cholesterol synthesis is able to meet the requirements for testosterone production alone.	Cholesterol	248-259	hypertrichosis 2 (generalised, congenital)	Homo sapiens	48-51
2167768-5	1990	The following conclusions are drawn: 1) chronic hCG treatment enhances the ability of rat Leydig cells to take-up exogenous cholesterol from circulating lipoproteins, and to store it in lipid droplets as a reserve material; 2) lipid-droplet stored cholesterol is employed only in the case of intense acute stimulation, since, under basal conditions, endogenous cholesterol synthesis is able to meet the requirements for testosterone production alone.	Cholesterol	248-259	hypertrichosis 2 (generalised, congenital)	Homo sapiens	48-51
2167768-5	1990	The following conclusions are drawn: 1) chronic hCG treatment enhances the ability of rat Leydig cells to take-up exogenous cholesterol from circulating lipoproteins, and to store it in lipid droplets as a reserve material; 2) lipid-droplet stored cholesterol is employed only in the case of intense acute stimulation, since, under basal conditions, endogenous cholesterol synthesis is able to meet the requirements for testosterone production alone.	Testosterone	420-432	hypertrichosis 2 (generalised, congenital)	Homo sapiens	48-51
2387639-7	1990	The deposition of colloidal carbon particles observed in adult rats after hCG-treatment was also not seen in young rats.	Carbon	28-34	hypertrichosis 2 (generalised, congenital)	Homo sapiens	74-77
2170316-2	1990	The light cells were non-steroidogenic and bound 125I-labeled hCG with high affinity (Kd 3.0 x 10(-10) mol/L), whereas the steroidogenic heavier cells (Leydig cells) produced cyclic adenosine monophosphate (cAMP) and testosterone in response to hCG stimulation with very little hCG binding.	Iodine-125	49-53	hypertrichosis 2 (generalised, congenital)	Homo sapiens	62-65
2170316-5	1990	The cells in subfraction I, predominantly damaged Leydig cells, germ cells, and/or residual light cells, bind 125I-labeled hCG with high affinity (Kd 4.09 x 10(-10) mol/L) without producing cAMP and testosterone in response to hCG.	Iodine-125	110-114	hypertrichosis 2 (generalised, congenital)	Homo sapiens	123-126
2274704-6	1990	When testes fragments were incubated with 0 or 12.5 mIU hCG/ml for 4 h, hCG increased media progesterone levels in rats and control mice, but not in hamsters and hCG-injected mice.	Progesterone	92-104	hypertrichosis 2 (generalised, congenital)	Homo sapiens	72-75
2274704-6	1990	When testes fragments were incubated with 0 or 12.5 mIU hCG/ml for 4 h, hCG increased media progesterone levels in rats and control mice, but not in hamsters and hCG-injected mice.	Progesterone	92-104	hypertrichosis 2 (generalised, congenital)	Homo sapiens	72-75
2167228-2	1990	With maximally stimulating concentrations of human choriogonadotropin (hCG) or cyclic AMP, testosterone formation was inhibited by 50% in the presence of 40 microM carbamazepine, 350 microM phenytoin, or greater than 1 mM valproate.	Testosterone	91-103	hypertrichosis 2 (generalised, congenital)	Homo sapiens	71-74
2274704-7	1990	Also, hCG elevated media testosterone levels in control but not in hCG-injected animals.	Testosterone	25-37	hypertrichosis 2 (generalised, congenital)	Homo sapiens	6-9
2167228-2	1990	With maximally stimulating concentrations of human choriogonadotropin (hCG) or cyclic AMP, testosterone formation was inhibited by 50% in the presence of 40 microM carbamazepine, 350 microM phenytoin, or greater than 1 mM valproate.	Carbamazepine	164-177	hypertrichosis 2 (generalised, congenital)	Homo sapiens	71-74
2274704-8	1990	Furthermore, addition of hCG in vitro partially prevented the elevation of media testosterone induced by in vivo hCG.	Testosterone	81-93	hypertrichosis 2 (generalised, congenital)	Homo sapiens	25-28
2167228-2	1990	With maximally stimulating concentrations of human choriogonadotropin (hCG) or cyclic AMP, testosterone formation was inhibited by 50% in the presence of 40 microM carbamazepine, 350 microM phenytoin, or greater than 1 mM valproate.	Phenytoin	190-199	hypertrichosis 2 (generalised, congenital)	Homo sapiens	71-74
2167228-2	1990	With maximally stimulating concentrations of human choriogonadotropin (hCG) or cyclic AMP, testosterone formation was inhibited by 50% in the presence of 40 microM carbamazepine, 350 microM phenytoin, or greater than 1 mM valproate.	Valproic Acid	222-231	hypertrichosis 2 (generalised, congenital)	Homo sapiens	71-74
2274704-8	1990	Furthermore, addition of hCG in vitro partially prevented the elevation of media testosterone induced by in vivo hCG.	Testosterone	81-93	hypertrichosis 2 (generalised, congenital)	Homo sapiens	113-116
2167228-3	1990	With submaximally stimulating concentrations of hCG, leading to physiological testosterone secretion rates, half-maximal inhibition occurred in the presence of 15 microM carbamazepine, 180 microM phenytoin, or 900 microM valproate.	Testosterone	78-90	hypertrichosis 2 (generalised, congenital)	Homo sapiens	48-51
2117002-9	1990	In incubations of 6-OHDA-injected testes, a comparable pattern of T responses to NE and hCG was found only 48 h after injection.	Oxidopamine	18-24	hypertrichosis 2 (generalised, congenital)	Homo sapiens	88-91
2167228-3	1990	With submaximally stimulating concentrations of hCG, leading to physiological testosterone secretion rates, half-maximal inhibition occurred in the presence of 15 microM carbamazepine, 180 microM phenytoin, or 900 microM valproate.	Carbamazepine	170-183	hypertrichosis 2 (generalised, congenital)	Homo sapiens	48-51
2167228-3	1990	With submaximally stimulating concentrations of hCG, leading to physiological testosterone secretion rates, half-maximal inhibition occurred in the presence of 15 microM carbamazepine, 180 microM phenytoin, or 900 microM valproate.	Phenytoin	196-205	hypertrichosis 2 (generalised, congenital)	Homo sapiens	48-51
2167228-3	1990	With submaximally stimulating concentrations of hCG, leading to physiological testosterone secretion rates, half-maximal inhibition occurred in the presence of 15 microM carbamazepine, 180 microM phenytoin, or 900 microM valproate.	Valproic Acid	221-230	hypertrichosis 2 (generalised, congenital)	Homo sapiens	48-51
2347398-4	1990	However, in guanethidine-treated rats, plasma and testis testosterone concentrations after hCG-treatment were significantly decreased.	Guanethidine	12-24	hypertrichosis 2 (generalised, congenital)	Homo sapiens	91-94
2347398-4	1990	However, in guanethidine-treated rats, plasma and testis testosterone concentrations after hCG-treatment were significantly decreased.	Testosterone	57-69	hypertrichosis 2 (generalised, congenital)	Homo sapiens	91-94
2117002-11	1990	Moreover, at 72, 144, and 168 h, the effect of NE &amp; hCG on T production was significantly greater in 6-OHDA-injected testes than in the vehicle injected testes of the same animals.	Adenosine Monophosphate	51-54	hypertrichosis 2 (generalised, congenital)	Homo sapiens	56-59
2117002-11	1990	Moreover, at 72, 144, and 168 h, the effect of NE &amp; hCG on T production was significantly greater in 6-OHDA-injected testes than in the vehicle injected testes of the same animals.	Oxidopamine	105-111	hypertrichosis 2 (generalised, congenital)	Homo sapiens	56-59
2318942-1	1990	Removal of the carbohydrates from hCG results in an antagonist (degly-hCG) that competitively inhibits hCG/LH-stimulated adenylate cyclase in macaque luteal tissue in vitro, but its effect in vivo is controversial.	Carbohydrates	15-28	hypertrichosis 2 (generalised, congenital)	Homo sapiens	34-37
2374116-3	1990	Treatment with hCG resulted in a dose-dependent increase in leucocyte concentration in testicular blood vessels and in the number of blood vessels which could be labelled with intravenously injected carbon particles.	Carbon	199-205	hypertrichosis 2 (generalised, congenital)	Homo sapiens	15-18
2345036-2	1990	Serum testosterone increased 2 to 4-fold over control values 48 h after hCG.	Testosterone	6-18	hypertrichosis 2 (generalised, congenital)	Homo sapiens	72-75
2318942-1	1990	Removal of the carbohydrates from hCG results in an antagonist (degly-hCG) that competitively inhibits hCG/LH-stimulated adenylate cyclase in macaque luteal tissue in vitro, but its effect in vivo is controversial.	Carbohydrates	15-28	hypertrichosis 2 (generalised, congenital)	Homo sapiens	70-73
2318942-1	1990	Removal of the carbohydrates from hCG results in an antagonist (degly-hCG) that competitively inhibits hCG/LH-stimulated adenylate cyclase in macaque luteal tissue in vitro, but its effect in vivo is controversial.	Carbohydrates	15-28	hypertrichosis 2 (generalised, congenital)	Homo sapiens	70-73
2110834-5	1990	Testosterone production stimulated by hCG and forskolin was blocked by addition of PMA but not OAG.	Testosterone	0-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	38-41
1972548-3	1990	In three patients, one injection of 5000 IU hCG resulted in a sharp rise in testosterone.	Testosterone	76-88	hypertrichosis 2 (generalised, congenital)	Homo sapiens	44-47
2110834-7	1990	A23187 had a biphasic effect on stimulated testosterone production: a dosage of 0.25 or 1.0 microM potentiated the action of submaximally effective dosages of hCG or forskolin on testosterone production; a higher dosage of 4 microM inhibited stimulated testosterone production by up to 50%.	Calcimycin	0-6	hypertrichosis 2 (generalised, congenital)	Homo sapiens	159-162
2110834-7	1990	A23187 had a biphasic effect on stimulated testosterone production: a dosage of 0.25 or 1.0 microM potentiated the action of submaximally effective dosages of hCG or forskolin on testosterone production; a higher dosage of 4 microM inhibited stimulated testosterone production by up to 50%.	Testosterone	43-55	hypertrichosis 2 (generalised, congenital)	Homo sapiens	159-162
2110834-7	1990	A23187 had a biphasic effect on stimulated testosterone production: a dosage of 0.25 or 1.0 microM potentiated the action of submaximally effective dosages of hCG or forskolin on testosterone production; a higher dosage of 4 microM inhibited stimulated testosterone production by up to 50%.	Testosterone	179-191	hypertrichosis 2 (generalised, congenital)	Homo sapiens	159-162
2110834-7	1990	A23187 had a biphasic effect on stimulated testosterone production: a dosage of 0.25 or 1.0 microM potentiated the action of submaximally effective dosages of hCG or forskolin on testosterone production; a higher dosage of 4 microM inhibited stimulated testosterone production by up to 50%.	Testosterone	179-191	hypertrichosis 2 (generalised, congenital)	Homo sapiens	159-162
2100104-12	1990	The hCG induced rise of P secretion, however, in the animals treated with 5 and 10 mg/kg bw CdCl2 was diminished and delayed, while in the animals treated with the 15 mg/kg Cd dose a complete lack of response was observed.	Cadmium Chloride	92-97	hypertrichosis 2 (generalised, congenital)	Homo sapiens	4-7
2178300-4	1990	A perfused cystadenofibroma released cAMP, progesterone, estradiol and testosterone into the perfusion medium with an augmented release of cAMP, estradiol and testosterone after the addition of hCG.	Estradiol	145-154	hypertrichosis 2 (generalised, congenital)	Homo sapiens	194-197
2178300-5	1990	hCG also had a stimulating effect on the release of prostanoids from this tumour.	Prostaglandins	52-63	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
2155879-3	1990	Interstitial cells were prepared by collagenase digestion and used to measure 125I-labelled human chorionic gonadotrophin (hCG) binding capacity and androgen production in the presence or absence of hCG or dibutyryl cyclic AMP (dbcAMP).	Iodine-125	78-82	hypertrichosis 2 (generalised, congenital)	Homo sapiens	123-126
2155879-4	1990	At day 2 after EDS treatment, 125I-labelled hCG binding capacity was reduced to 10% of control values, while the production of testosterone and 5 alpha-androstane-3 alpha, 17 beta-diol (adiol) were non-detectable.	Iodine-125	30-34	hypertrichosis 2 (generalised, congenital)	Homo sapiens	44-47
2155879-6	1990	Between days 24 and 40 post-treatment, Leydig cell regeneration occurred, as indicated by a rise in 125I-labelled hCG binding capacity, increased androgen production and the presence of histologically identifiable Leydig cells.	Iodine-125	100-104	hypertrichosis 2 (generalised, congenital)	Homo sapiens	114-117
2155978-1	1990	To investigate the role of progesterone (P) in the ovulatory process, RU486 (RU) (10mg/kg), an antiprogesterone, was administered to PMS-hCG-treated immature female rats (22 days old).	Promethium	133-136	hypertrichosis 2 (generalised, congenital)	Homo sapiens	137-140
2155978-5	1990	By administering RU concomitant with hCG, the preovulatory increase in the CE activities was totally suppressed.	Mifepristone	17-19	hypertrichosis 2 (generalised, congenital)	Homo sapiens	37-40
2178300-3	1990	One ovary, containing a simple cyst, released progesterone into the perfusate, and this release was further increased after the addition of hCG at a concentration of 10 IU/ml.	Progesterone	46-58	hypertrichosis 2 (generalised, congenital)	Homo sapiens	140-143
2100104-12	1990	The hCG induced rise of P secretion, however, in the animals treated with 5 and 10 mg/kg bw CdCl2 was diminished and delayed, while in the animals treated with the 15 mg/kg Cd dose a complete lack of response was observed.	Cadmium	92-94	hypertrichosis 2 (generalised, congenital)	Homo sapiens	4-7
2327831-0	1990	Testicular steroids in spermatic and peripheral veins after single injection of hCG in patients with varicocele.	Steroids	11-19	hypertrichosis 2 (generalised, congenital)	Homo sapiens	80-83
2171385-7	1990	In this format, 50 mIU or more of hCG in urine can be detected in 5 minutes or less, and antibody to Rubella virus at an HAI titer equivalent of 8 or above in serum can be detected in 10 minutes or less.	N-{(1S)-1-{[4-(3-AMINOPROPYL)PIPERAZIN-1-YL]CARBONYL}-4-[(DIAMINOMETHYLENE)AMINO]BUTYL}-3-(TRIFLUOROMETHYL)BENZENESULFONAMIDE	19-22	hypertrichosis 2 (generalised, congenital)	Homo sapiens	34-37
2327831-1	1990	To determine the function of Leydig cells in patients with varicocele, hCG-stimulated levels of progesterone (Prog), 17 alpha-Hydroxy-4-pregnene-3,20-dione (17OHP), 4-Androstene-3,17-dione (A-dione), testosterone (T), and estradiol-17 beta (E2) in both spermatic and peripheral veins were measured.	Progesterone	96-108	hypertrichosis 2 (generalised, congenital)	Homo sapiens	71-74
2327831-1	1990	To determine the function of Leydig cells in patients with varicocele, hCG-stimulated levels of progesterone (Prog), 17 alpha-Hydroxy-4-pregnene-3,20-dione (17OHP), 4-Androstene-3,17-dione (A-dione), testosterone (T), and estradiol-17 beta (E2) in both spermatic and peripheral veins were measured.	Progesterone	110-114	hypertrichosis 2 (generalised, congenital)	Homo sapiens	71-74
2327831-1	1990	To determine the function of Leydig cells in patients with varicocele, hCG-stimulated levels of progesterone (Prog), 17 alpha-Hydroxy-4-pregnene-3,20-dione (17OHP), 4-Androstene-3,17-dione (A-dione), testosterone (T), and estradiol-17 beta (E2) in both spermatic and peripheral veins were measured.	17-alpha-Hydroxyprogesterone	117-155	hypertrichosis 2 (generalised, congenital)	Homo sapiens	71-74
2327831-1	1990	To determine the function of Leydig cells in patients with varicocele, hCG-stimulated levels of progesterone (Prog), 17 alpha-Hydroxy-4-pregnene-3,20-dione (17OHP), 4-Androstene-3,17-dione (A-dione), testosterone (T), and estradiol-17 beta (E2) in both spermatic and peripheral veins were measured.	Androstenedione	165-188	hypertrichosis 2 (generalised, congenital)	Homo sapiens	71-74
2327831-1	1990	To determine the function of Leydig cells in patients with varicocele, hCG-stimulated levels of progesterone (Prog), 17 alpha-Hydroxy-4-pregnene-3,20-dione (17OHP), 4-Androstene-3,17-dione (A-dione), testosterone (T), and estradiol-17 beta (E2) in both spermatic and peripheral veins were measured.	Androstenedione	190-197	hypertrichosis 2 (generalised, congenital)	Homo sapiens	71-74
2327831-1	1990	To determine the function of Leydig cells in patients with varicocele, hCG-stimulated levels of progesterone (Prog), 17 alpha-Hydroxy-4-pregnene-3,20-dione (17OHP), 4-Androstene-3,17-dione (A-dione), testosterone (T), and estradiol-17 beta (E2) in both spermatic and peripheral veins were measured.	Testosterone	200-212	hypertrichosis 2 (generalised, congenital)	Homo sapiens	71-74
2327831-1	1990	To determine the function of Leydig cells in patients with varicocele, hCG-stimulated levels of progesterone (Prog), 17 alpha-Hydroxy-4-pregnene-3,20-dione (17OHP), 4-Androstene-3,17-dione (A-dione), testosterone (T), and estradiol-17 beta (E2) in both spermatic and peripheral veins were measured.	Estradiol	222-239	hypertrichosis 2 (generalised, congenital)	Homo sapiens	71-74
2157976-5	1990	Further, we document that P450arom mRNA and estradiol (E) biosynthesis are regulated by cAMP-dependent mechanisms in granulosa cells of preovulatory (PO) follicles, but are maintained by cAMP-independent mechanisms after LH/hCG-induced luteinization.	Cyclic AMP	88-92	hypertrichosis 2 (generalised, congenital)	Homo sapiens	224-227
2155894-1	1990	In short-term incubations (32 C, 3 h) of purified adult rat Leydig cells, increasing the density from 5000 to 50,000 cells/16 mm diameter culture well caused a significant increase in human chorionic gonadotropin (hCG)-stimulated testosterone secretion/cell.	Testosterone	230-242	hypertrichosis 2 (generalised, congenital)	Homo sapiens	214-217
2155894-4	1990	hCG-stimulated testosterone secretion by Leydig cells incubated at low density was also increased by addition of Leydig cell-conditioned medium.	Testosterone	15-27	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
2284976-3	1990	In the placenta villi cells from early and term gestation in vitro, both exogenous and endogenous hCG showed a stimulatory effect on progesterone secretion, and the effect was approximately proportional to the concentration of the exogenous hCG added.	Progesterone	133-145	hypertrichosis 2 (generalised, congenital)	Homo sapiens	98-101
2108490-3	1990	After only five weeks of hCG/hMG treatment, sperm counts and serum testosterone levels increased dramatically and a child was conceived.	Testosterone	67-79	hypertrichosis 2 (generalised, congenital)	Homo sapiens	25-28
1693508-5	1990	Addition of dibutyryl cAMP from the start or after 96 h of cell culture induced an increase of hCG production and of its free subunits and also stimulated the secretion of hPL.	Cyclic AMP	22-26	hypertrichosis 2 (generalised, congenital)	Homo sapiens	95-98
2284976-3	1990	In the placenta villi cells from early and term gestation in vitro, both exogenous and endogenous hCG showed a stimulatory effect on progesterone secretion, and the effect was approximately proportional to the concentration of the exogenous hCG added.	Progesterone	133-145	hypertrichosis 2 (generalised, congenital)	Homo sapiens	241-244
2686329-4	1989	In the presence of varying concentrations of substrate, the apparent Km for androstenedione was 0.945 mol/l; treatment of cells with insulin, IGF-I and hCG markedly increased the apparent maximal velocity, without modifying Km; peptides were more potent in aromatase stimulation than hCG alone or in combination with either peptides.	Androstenedione	76-91	hypertrichosis 2 (generalised, congenital)	Homo sapiens	152-155
21890190-7	2011	The total number of the CLs was higher (P &lt; 0.05) in animals treated with PGF(2alpha)/PMSG/hCG.	Chlorine	24-27	hypertrichosis 2 (generalised, congenital)	Homo sapiens	94-97
21890190-7	2011	The total number of the CLs was higher (P &lt; 0.05) in animals treated with PGF(2alpha)/PMSG/hCG.	Prostaglandins F	77-80	hypertrichosis 2 (generalised, congenital)	Homo sapiens	94-97
21890190-8	2011	The amount of E(2) and P(4) was lower (P &lt; 0.05, P &lt; 0.001, respectively) in pregnant gilts administrated with PGF(2alpha)/PMSG/hCG.	Prostaglandins F	117-120	hypertrichosis 2 (generalised, congenital)	Homo sapiens	134-137
21890190-12	2011	The PGF(2alpha)/PMSG/hCG treatment resulted in elevated expression of WNT4 (P &lt; 0.001) and CTNNB1 (P &lt; 0.05) in luteal tissue in comparison to the Control gilts.	Prostaglandins F	4-7	hypertrichosis 2 (generalised, congenital)	Homo sapiens	21-24
2607249-4	1989	The thymic fraction caused a dose-dependent decrease in human chorionic gonadotrophin (hCG)-stimulated production of progesterone, oestradiol and testosterone, but had no effect on their synthesis in the absence of hCG.	Progesterone	117-129	hypertrichosis 2 (generalised, congenital)	Homo sapiens	87-90
2607249-4	1989	The thymic fraction caused a dose-dependent decrease in human chorionic gonadotrophin (hCG)-stimulated production of progesterone, oestradiol and testosterone, but had no effect on their synthesis in the absence of hCG.	Estradiol	131-141	hypertrichosis 2 (generalised, congenital)	Homo sapiens	87-90
2607249-4	1989	The thymic fraction caused a dose-dependent decrease in human chorionic gonadotrophin (hCG)-stimulated production of progesterone, oestradiol and testosterone, but had no effect on their synthesis in the absence of hCG.	Testosterone	146-158	hypertrichosis 2 (generalised, congenital)	Homo sapiens	87-90
2607249-5	1989	Similarly, hCG-induced production of these steroids was decreased by TIM and TCM.	Steroids	43-51	hypertrichosis 2 (generalised, congenital)	Homo sapiens	11-14
2607249-7	1989	These results suggest: (1) that the thymus contains a factor with a molecular weight of approximately 28 kDa which interacts with hCG in ovarian cells, (2) that the thymus can release active substances which modify steroid secretion by the ovary in vitro and (3) that the reticuloepithelial cells of the thymus are involved in the secretion of factors which modulate the stimulation by hCG of steroidogenesis in ovarian cells.	Steroids	215-222	hypertrichosis 2 (generalised, congenital)	Homo sapiens	130-133
6299285-2	1983	Incubation of cultured luteal cells or isolated nuclei with fluorescein isothiocyanate conjugated hCG showed concentration of fluorescence in the nuclear region.	Fluorescein-5-isothiocyanate	60-86	hypertrichosis 2 (generalised, congenital)	Homo sapiens	98-101
6299285-6	1983	Radiolabeled hCG bound to the nuclei could also be dissociated by brief exposure to MgCl2 or acidic incubation medium.	Magnesium Chloride	84-89	hypertrichosis 2 (generalised, congenital)	Homo sapiens	13-16
6299285-7	1983	The bound hCG was not extractable with 4M KCl or 2% Triton X-100.	Potassium Chloride	42-45	hypertrichosis 2 (generalised, congenital)	Homo sapiens	10-13
6299285-7	1983	The bound hCG was not extractable with 4M KCl or 2% Triton X-100.	Octoxynol	52-64	hypertrichosis 2 (generalised, congenital)	Homo sapiens	10-13
31087493-4	2019	Consistent with the finding that Leydig cells expressed aldo-keto reductase 1B7 (PGF synthase) and PGE synthase 2, induction of COX-2 by hCG caused a marked increase in testicular PGF 2alpha and PGE 2 levels.	Dinoprostone	195-200	hypertrichosis 2 (generalised, congenital)	Homo sapiens	137-140
2686329-4	1989	In the presence of varying concentrations of substrate, the apparent Km for androstenedione was 0.945 mol/l; treatment of cells with insulin, IGF-I and hCG markedly increased the apparent maximal velocity, without modifying Km; peptides were more potent in aromatase stimulation than hCG alone or in combination with either peptides.	Androstenedione	76-91	hypertrichosis 2 (generalised, congenital)	Homo sapiens	284-287
2602561-9	1989	When the PG synthesis was blocked by indomethacin treatment at 1 h before hCG, ovarian progesterone levels still increased.	Prostaglandins	9-11	hypertrichosis 2 (generalised, congenital)	Homo sapiens	74-77
2559906-6	1989	Testicular cells from arthritic animals secrete significantly less testosterone in vitro compared with cells from non-injected control animals, both basally and in response to dbcAMP and hCG.	Testosterone	67-79	hypertrichosis 2 (generalised, congenital)	Homo sapiens	187-190
2516788-1	1989	In adult men referred with gynaecomastia, the prolonged plasma oestradiol (E2) response to hCG appears to be a useful tool in the diagnosis of feminizing Leydig cell tumour (LCT) of the testis.	Estradiol	63-73	hypertrichosis 2 (generalised, congenital)	Homo sapiens	91-94
2602561-9	1989	When the PG synthesis was blocked by indomethacin treatment at 1 h before hCG, ovarian progesterone levels still increased.	Indomethacin	37-49	hypertrichosis 2 (generalised, congenital)	Homo sapiens	74-77
2550508-7	1989	cAMP significantly increased hCG secretion 48 h after its addition under all conditions.	Cyclic AMP	0-4	hypertrichosis 2 (generalised, congenital)	Homo sapiens	29-32
2591605-6	1989	The increase in testosterone levels induced by hCG (50, 100 and 500 unit/rat s.c.) were also inhibited by intraperitoneal injection of 500 micrograms of PGD2.	Testosterone	16-28	hypertrichosis 2 (generalised, congenital)	Homo sapiens	47-50
2591605-6	1989	The increase in testosterone levels induced by hCG (50, 100 and 500 unit/rat s.c.) were also inhibited by intraperitoneal injection of 500 micrograms of PGD2.	Prostaglandin D2	153-157	hypertrichosis 2 (generalised, congenital)	Homo sapiens	47-50
2550508-12	1989	The results show that cAMP can act as an intracellular messenger in the regulation of both aromatase activity and hCG secretion.	Cyclic AMP	22-26	hypertrichosis 2 (generalised, congenital)	Homo sapiens	114-117
2591605-7	1989	On the other hand, intratesticular injection of hCG (0.01, 0.1 and 1.0 unit/testis) caused an increase in testosterone levels according to dose of hCG.	Testosterone	106-118	hypertrichosis 2 (generalised, congenital)	Homo sapiens	48-51
2804956-3	1989	The volume of mitochondrial and peroxisome compartments, as well as the surface area per cell of mitochondrial cristae and smooth endoplasmic reticulum (SER) were significantly increased after hCG treatment, and showed a highly significant positive linear correlation with both basal and stimulated testosterone production by isolated Leydig cells of the contralateral testis.	Testosterone	299-311	hypertrichosis 2 (generalised, congenital)	Homo sapiens	193-196
2591605-7	1989	On the other hand, intratesticular injection of hCG (0.01, 0.1 and 1.0 unit/testis) caused an increase in testosterone levels according to dose of hCG.	Testosterone	106-118	hypertrichosis 2 (generalised, congenital)	Homo sapiens	147-150
2591605-8	1989	The increase in testosterone levels by hCG was inhibited by simultaneous injection of PGD2 (1.0 micrograms/testis).	Testosterone	16-28	hypertrichosis 2 (generalised, congenital)	Homo sapiens	39-42
2591605-8	1989	The increase in testosterone levels by hCG was inhibited by simultaneous injection of PGD2 (1.0 micrograms/testis).	Prostaglandin D2	86-90	hypertrichosis 2 (generalised, congenital)	Homo sapiens	39-42
2559822-5	1989	hCG preparations within a range of concentrations of 30-300 IU/m elicited 2.3-16.5 times increase in cAMP in a dose-dependent manner.	Cyclic AMP	101-105	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
16726709-0	1989	Ovarian steroid secretion changes after hCG stimulation in early pregnant pigs.	Steroids	8-15	hypertrichosis 2 (generalised, congenital)	Homo sapiens	40-43
16726709-1	1989	Administration of human chorionic gonadotropin (hCG) to promote ovarian steroid secretion near the time of recognition of pregnancy was evaluated.	Steroids	72-79	hypertrichosis 2 (generalised, congenital)	Homo sapiens	48-51
16726709-4	1989	The 1000 IU of hCG group had three-to five-fold greater (P&lt;0.01) estradiol concentrations than controls on Days 14, 15 and 16 post mating.	Estradiol	68-77	hypertrichosis 2 (generalised, congenital)	Homo sapiens	15-18
2608702-4	1989	A single injection of hCG on day 7 after hypophysectomy resulted 12 hrs later in a significant increase in the forming capacity of 13,14H2-PGF2 alpha in WO-CL.	13,14h2	131-138	hypertrichosis 2 (generalised, congenital)	Homo sapiens	22-25
2608702-4	1989	A single injection of hCG on day 7 after hypophysectomy resulted 12 hrs later in a significant increase in the forming capacity of 13,14H2-PGF2 alpha in WO-CL.	Dinoprost	139-143	hypertrichosis 2 (generalised, congenital)	Homo sapiens	22-25
2608702-4	1989	A single injection of hCG on day 7 after hypophysectomy resulted 12 hrs later in a significant increase in the forming capacity of 13,14H2-PGF2 alpha in WO-CL.	wo-cl	153-158	hypertrichosis 2 (generalised, congenital)	Homo sapiens	22-25
2559822-6	1989	Nine pregnant women with serum TSH concentrations less than the lower limit of the normal range (less than 0.25 mU/l) displayed significantly higher values for both thyroid stimulating activities and serum hCG concentrations (P less than 0.001, respectively) compared with those who had normal TSH levels in serum.	Thyrotropin	31-34	hypertrichosis 2 (generalised, congenital)	Homo sapiens	206-209
2531534-3	1989	HCG further augmented 17-OHP production significantly at 96, 144 and 192 hours of culture.	17-alpha-Hydroxyprogesterone	22-28	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
2547583-7	1989	Ovarian 15-HETE production and ovulation were inhibited in a dose-dependent manner when indomethacin was administered sc 1 h after hCG in doses ranging from 0.10-10.0 mg/rat.	15-Hete	8-15	hypertrichosis 2 (generalised, congenital)	Homo sapiens	131-134
2547583-7	1989	Ovarian 15-HETE production and ovulation were inhibited in a dose-dependent manner when indomethacin was administered sc 1 h after hCG in doses ranging from 0.10-10.0 mg/rat.	Indomethacin	88-100	hypertrichosis 2 (generalised, congenital)	Homo sapiens	131-134
2515561-8	1989	Similarly, whereas basal incubation media T levels were unchanged by DES treatment, the steroidogenic response in vitro to hCG was abolished by the presence of DES, and removal of the capsules restored this response.	Diethylstilbestrol	160-163	hypertrichosis 2 (generalised, congenital)	Homo sapiens	123-126
2571598-5	1989	Low clomiphene (10(-9)-10(-7) M) and hCG concentrations appeared to have a synergistic effect on progesterone production.	Progesterone	97-109	hypertrichosis 2 (generalised, congenital)	Homo sapiens	37-40
2516130-2	1989	hCG for 16 days resulted in a significant 163% increase in the number of Leydig cells, and a 9-fold rise in plasma testosterone concentrations.	Testosterone	115-127	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
2571598-3	1989	Clomiphene stimulated progesterone production in both the presence and absence of additional hCG at concentrations less than or equal to 10(7) M. In both the presence and absence of hCG a dose-dependent inhibition of progesterone production was observed with higher concentrations of clomiphene (greater than 10(6) M).	Clomiphene	0-10	hypertrichosis 2 (generalised, congenital)	Homo sapiens	182-185
2571598-3	1989	Clomiphene stimulated progesterone production in both the presence and absence of additional hCG at concentrations less than or equal to 10(7) M. In both the presence and absence of hCG a dose-dependent inhibition of progesterone production was observed with higher concentrations of clomiphene (greater than 10(6) M).	Clomiphene	284-294	hypertrichosis 2 (generalised, congenital)	Homo sapiens	182-185
2571598-4	1989	hCG (1 IU/mL) significantly increased progesterone production in control cells and at all concentrations of clomiphene (10(-9)-10(-5) M) tested.	Clomiphene	108-118	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
2476349-9	1989	Addition of the phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine, increased the stimulation of P4 and cAMP by hCG + PRL in a manner dependent on PRL concentrations.	1-Methyl-3-isobutylxanthine	45-72	hypertrichosis 2 (generalised, congenital)	Homo sapiens	118-121
2476349-9	1989	Addition of the phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine, increased the stimulation of P4 and cAMP by hCG + PRL in a manner dependent on PRL concentrations.	Cyclic AMP	110-114	hypertrichosis 2 (generalised, congenital)	Homo sapiens	118-121
2732296-4	1989	In an effort to understand the regulation of the onset of testosterone formation in the human fetal testis we measured adenylate cyclase activity in response to hCG stimulation in homogenates of fetal testes obtained from first and second trimester human abortuses.	Testosterone	58-70	hypertrichosis 2 (generalised, congenital)	Homo sapiens	161-164
2544411-1	1989	The stimulation of Leydig cells by the administration of a single injection of 100 IU human CG (hCG) to adult male rats caused a significant biphasic stimulation of serum testosterone levels at 2 h and 3 days after injection.	Testosterone	171-183	hypertrichosis 2 (generalised, congenital)	Homo sapiens	92-94
2544411-1	1989	The stimulation of Leydig cells by the administration of a single injection of 100 IU human CG (hCG) to adult male rats caused a significant biphasic stimulation of serum testosterone levels at 2 h and 3 days after injection.	Testosterone	171-183	hypertrichosis 2 (generalised, congenital)	Homo sapiens	96-99
2544411-6	1989	But 2 or 4 weeks after administration of EDS, as a new population of Leydig cells develops in the interstitium, an injection of 100 IU hCG provokes a significant increase in serum testosterone and IR-inhibin levels.	Testosterone	180-192	hypertrichosis 2 (generalised, congenital)	Homo sapiens	135-138
2553431-3	1989	However, both peptides increased hCG-induced testosterone production in a dose-dependent manner.	Testosterone	45-57	hypertrichosis 2 (generalised, congenital)	Homo sapiens	33-36
2553431-7	1989	hGH also enhanced hCG-stimulated cAMP production time dependently, suggesting that the stimulatory effect of hGH on steroidogenesis was due to an increased cAMP production.	Cyclic AMP	33-37	hypertrichosis 2 (generalised, congenital)	Homo sapiens	18-21
2553431-7	1989	hGH also enhanced hCG-stimulated cAMP production time dependently, suggesting that the stimulatory effect of hGH on steroidogenesis was due to an increased cAMP production.	Cyclic AMP	156-160	hypertrichosis 2 (generalised, congenital)	Homo sapiens	18-21
2598478-0	1989	Variable effects of RU 486 on endometrial maintenance in the luteal phase extended by exogenous hCG.	Mifepristone	20-26	hypertrichosis 2 (generalised, congenital)	Homo sapiens	96-99
2598478-1	1989	This study was designed to assess the features and conditions for endometrial bleeding induction with the synthetic antiprogestin and antiglucocorticoid RU 486 during hCG-induced prolongation of the luteal phase.	Mifepristone	153-159	hypertrichosis 2 (generalised, congenital)	Homo sapiens	167-170
2598478-6	1989	In certain cycles, tamoxifen (20 mg/day) was given for 4 consecutive days with hCG, or with hCG and RU 486.	Tamoxifen	19-28	hypertrichosis 2 (generalised, congenital)	Homo sapiens	79-82
2598478-6	1989	In certain cycles, tamoxifen (20 mg/day) was given for 4 consecutive days with hCG, or with hCG and RU 486.	Tamoxifen	19-28	hypertrichosis 2 (generalised, congenital)	Homo sapiens	92-95
2598478-9	1989	Treatment with hCG alone or with the various combinations of RU 486 produced similar serum levels of oestradiol and progesterone which were equivalent to those observed during early pregnancy.	Estradiol	101-111	hypertrichosis 2 (generalised, congenital)	Homo sapiens	15-18
2598478-9	1989	Treatment with hCG alone or with the various combinations of RU 486 produced similar serum levels of oestradiol and progesterone which were equivalent to those observed during early pregnancy.	Progesterone	116-128	hypertrichosis 2 (generalised, congenital)	Homo sapiens	15-18
2598478-10	1989	With hCG alone, the onset of bleeding was on day 21-24 after the LH surge, coinciding with the drop in oestradiol and progesterone.	Estradiol	103-113	hypertrichosis 2 (generalised, congenital)	Homo sapiens	5-8
2598478-10	1989	With hCG alone, the onset of bleeding was on day 21-24 after the LH surge, coinciding with the drop in oestradiol and progesterone.	Progesterone	118-130	hypertrichosis 2 (generalised, congenital)	Homo sapiens	5-8
2780515-13	1989	Both alcohol/water and water extracted adrenal inhibited hCG secretion.	Alcohols	5-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	57-60
2780515-13	1989	Both alcohol/water and water extracted adrenal inhibited hCG secretion.	Water	13-18	hypertrichosis 2 (generalised, congenital)	Homo sapiens	57-60
2780515-13	1989	Both alcohol/water and water extracted adrenal inhibited hCG secretion.	Water	23-28	hypertrichosis 2 (generalised, congenital)	Homo sapiens	57-60
2735400-3	1989	By the time of ovulation (10-12 h after the administration of hCG) both eicosanoids declined to their pre-hCG levels.	Eicosanoids	72-83	hypertrichosis 2 (generalised, congenital)	Homo sapiens	106-109
2550923-7	1989	Secretion of hCG from both attached and unattached cells remained at a low level (less than 200 ng/mg protein) in control cells; in the presence of cAMP, hCG secretion was stimulated by tenfold after 40 h.(ABSTRACT TRUNCATED AT 250 WORDS)	Cyclic AMP	148-152	hypertrichosis 2 (generalised, congenital)	Homo sapiens	13-16
2550923-7	1989	Secretion of hCG from both attached and unattached cells remained at a low level (less than 200 ng/mg protein) in control cells; in the presence of cAMP, hCG secretion was stimulated by tenfold after 40 h.(ABSTRACT TRUNCATED AT 250 WORDS)	Cyclic AMP	148-152	hypertrichosis 2 (generalised, congenital)	Homo sapiens	154-157
2735400-3	1989	By the time of ovulation (10-12 h after the administration of hCG) both eicosanoids declined to their pre-hCG levels.	Eicosanoids	72-83	hypertrichosis 2 (generalised, congenital)	Homo sapiens	62-65
2735400-4	1989	When animals were treated with the cyclooxygenase inhibitor indomethacin at the specific dose of 0.316 mg/rat sc at 1 h before hCG, the ovarian levels of LT B4 and LTs C4/D4/E4 increased to 210% (P less than 0.01) and 113% (P less than 0.05), respectively, above the control levels at 4 h after hCG.	Indomethacin	60-72	hypertrichosis 2 (generalised, congenital)	Homo sapiens	127-130
2735400-4	1989	When animals were treated with the cyclooxygenase inhibitor indomethacin at the specific dose of 0.316 mg/rat sc at 1 h before hCG, the ovarian levels of LT B4 and LTs C4/D4/E4 increased to 210% (P less than 0.01) and 113% (P less than 0.05), respectively, above the control levels at 4 h after hCG.	Indomethacin	60-72	hypertrichosis 2 (generalised, congenital)	Homo sapiens	295-298
2544770-1	1989	The present studies were conducted to determine the effects of gonadotropins (LH and hCG) and prostaglandin F2a (PGF2a) on the production of "second messengers" and progesterone synthesis in purified preparations of bovine small luteal cells.	Progesterone	165-177	hypertrichosis 2 (generalised, congenital)	Homo sapiens	85-88
2505866-3	1989	Testis cells from rats 23, 40, and 90 days of age that were incubated with hCG increased testosterone production when compared with controls.	Testosterone	89-101	hypertrichosis 2 (generalised, congenital)	Homo sapiens	75-78
2505866-4	1989	Preincubation of the cells from postnatal rats with pertussis toxin significantly increased hCG-stimulated testosterone secretion when compared to cells preincubated in medium only at all three ages.	Testosterone	107-119	hypertrichosis 2 (generalised, congenital)	Homo sapiens	92-95
2768115-4	1989	Administration of hCG on d 4 or 7 increased (P less than .05) mean serum progesterone (P4) over the first 16 d of the estrous cycle by .9 and .8 ng/ml, respectively.	Progesterone	73-85	hypertrichosis 2 (generalised, congenital)	Homo sapiens	18-21
2544801-1	1989	The inhibitory effects of recombinant porcine interferon-gamma (IFN gamma) on human CG (hCG)-stimulated testosterone production, and on mRNA concentrations of cholesterol side-chain cleavage (P450scc) and 17 alpha-hydroxylase/C17-20lyase (P450c 17) were investigated using porcine primary Leydig cell culture as a model.	Testosterone	104-116	hypertrichosis 2 (generalised, congenital)	Homo sapiens	84-86
2544801-1	1989	The inhibitory effects of recombinant porcine interferon-gamma (IFN gamma) on human CG (hCG)-stimulated testosterone production, and on mRNA concentrations of cholesterol side-chain cleavage (P450scc) and 17 alpha-hydroxylase/C17-20lyase (P450c 17) were investigated using porcine primary Leydig cell culture as a model.	Testosterone	104-116	hypertrichosis 2 (generalised, congenital)	Homo sapiens	88-91
2544801-2	1989	After preincubation of Leydig cells for 24 h with 1000 pM IFN gamma, hCG-stimulated (10 ng/ml, 2 h) testosterone production was inhibited by 50%, whereas no significant changes were seen in hCG-stimulated cAMP production.	Testosterone	100-112	hypertrichosis 2 (generalised, congenital)	Homo sapiens	69-72
2544801-2	1989	After preincubation of Leydig cells for 24 h with 1000 pM IFN gamma, hCG-stimulated (10 ng/ml, 2 h) testosterone production was inhibited by 50%, whereas no significant changes were seen in hCG-stimulated cAMP production.	Cyclic AMP	205-209	hypertrichosis 2 (generalised, congenital)	Homo sapiens	69-72
2544801-3	1989	Incubation with 10 microM 5-cholestene-3 beta,22(R)-diol or 10 microM 5-cholestene-3 beta,20 alpha-diol together with hCG (10 ng/ml, 2 h) reversed most of the inhibitory effect of IFN gamma, suggesting that IFN gamma inhibits P450scc activity, possibly by inhibiting the substrate (cholesterol) availability for P450scc.	Cholesterol	282-293	hypertrichosis 2 (generalised, congenital)	Homo sapiens	118-121
2505866-5	1989	AVT suppressed hCG-stimulated testosterone secretion, but this suppression was partially reversed in cells from all postnatal ages preincubated with pertussis toxin.	Testosterone	30-42	hypertrichosis 2 (generalised, congenital)	Homo sapiens	15-18
2544801-6	1989	Simultaneous treatment with IFN gamma attenuated these hCG-induced increases in P450scc mRNA (50%) and P450c 17 mRNA (40-100%) concentrations, as well as in testosterone production (77%).	Testosterone	157-169	hypertrichosis 2 (generalised, congenital)	Homo sapiens	55-58
2544770-9	1989	LH (1 microgram/ml) and hCG (20 IU/ml) provoked similar increases in inositol phosphate, cAMP and progesterone accumulation in small luteal cells.	Inositol Phosphates	69-87	hypertrichosis 2 (generalised, congenital)	Homo sapiens	24-27
2544770-9	1989	LH (1 microgram/ml) and hCG (20 IU/ml) provoked similar increases in inositol phosphate, cAMP and progesterone accumulation in small luteal cells.	Cyclic AMP	89-93	hypertrichosis 2 (generalised, congenital)	Homo sapiens	24-27
2544770-9	1989	LH (1 microgram/ml) and hCG (20 IU/ml) provoked similar increases in inositol phosphate, cAMP and progesterone accumulation in small luteal cells.	Progesterone	98-110	hypertrichosis 2 (generalised, congenital)	Homo sapiens	24-27
2754644-0	1989	Effect of pregnancy, injection of oestradiol benzoate or hCG on steroid concentration and release by pig luteal cells.	Steroids	64-71	hypertrichosis 2 (generalised, congenital)	Homo sapiens	57-60
2752075-8	1989	The volume increased to 1.37 +/- 0.26 microL at 4 h after hCG and reached a peak of 4.55 +/- 0.72 microL at 10 h. Indomethacin treatment (0.3-10.0 mg/rat, s.c.) partially inhibited this 7-fold increase in ovarian blood volume.	Indomethacin	114-126	hypertrichosis 2 (generalised, congenital)	Homo sapiens	58-61
2754644-8	1989	The luteal cells from hCG-treated sows produced more progesterone (P less than 0.01) in vitro than did those from the other groups.	Progesterone	53-65	hypertrichosis 2 (generalised, congenital)	Homo sapiens	22-25
2561359-6	1989	LH, hCG and dbcAMP increased the synthesis of pregnenolon twice, and testosterone--three times.	Pregnenolone	46-57	hypertrichosis 2 (generalised, congenital)	Homo sapiens	4-7
2561359-6	1989	LH, hCG and dbcAMP increased the synthesis of pregnenolon twice, and testosterone--three times.	Testosterone	69-83	hypertrichosis 2 (generalised, congenital)	Homo sapiens	4-7
2746064-5	1989	However, the addition of cyclohexamide alone had no effect on progesterone accumulation, but the simultaneous addition of cyclohexamide and hCG blocked the effects of hCG in a dose related manner.	4-[2-(3,5-dimethyl-2-oxocyclohexyl)-2-hydroxyethyl]piperidine-2,6-dione	122-135	hypertrichosis 2 (generalised, congenital)	Homo sapiens	167-170
2494036-5	1989	Granulosa cells from large follicles showed dose-dependent increases in both progesterone accumulation and aromatase activity in response to treatment with hCG.	Progesterone	77-89	hypertrichosis 2 (generalised, congenital)	Homo sapiens	156-159
2494036-8	1989	The effects of both testosterone and DHT on hCG-stimulated aromatase activity and progesterone accumulation by granulosa cells from large preovulatory follicles were inhibitory.	Testosterone	20-32	hypertrichosis 2 (generalised, congenital)	Homo sapiens	44-47
2494036-8	1989	The effects of both testosterone and DHT on hCG-stimulated aromatase activity and progesterone accumulation by granulosa cells from large preovulatory follicles were inhibitory.	Dihydrotestosterone	37-40	hypertrichosis 2 (generalised, congenital)	Homo sapiens	44-47
2626049-1	1989	The acetone extract obtained from the thymuses of 14-day-old rats contains a factor that interacts with hCG in the adult testis cells and inhibits testosterone production.	Acetone	4-11	hypertrichosis 2 (generalised, congenital)	Homo sapiens	104-107
2548285-5	1989	hCG, cAMP and progesterone all could significantly increase the content of tyrosine in the suspensions, suggesting the release of "endogenous tyrosine".	Tyrosine	75-83	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
2548285-5	1989	hCG, cAMP and progesterone all could significantly increase the content of tyrosine in the suspensions, suggesting the release of "endogenous tyrosine".	Tyrosine	142-150	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
2909363-1	1989	Modifications of carbohydrate structures of hCG, such as deglycosylation or desialylation, have been shown to reduce the biological activity of the hormone derivatives in vivo.	Carbohydrates	17-29	hypertrichosis 2 (generalised, congenital)	Homo sapiens	44-47
2909363-2	1989	We posed the question of whether deglycosylated hCG (dg-hCG) and desialylated hCG (ds-hCG) would behave as agonists at the LH/CG receptor in the primate in vivo, as this would bear on their potential clinical utility as LH/CG agonists or antagonists.	Luteinizing Hormone	123-125	hypertrichosis 2 (generalised, congenital)	Homo sapiens	48-51
2724371-10	1989	However, sT and hCG-stimulated sT appeared to be useful indicators of Cd effects on the pituitary-gonadal axis.	Cadmium	70-72	hypertrichosis 2 (generalised, congenital)	Homo sapiens	16-19
2463907-1	1989	To improve our knowledge of the structural features of the alpha-subunit of hCG we have studied the antigenic site recognized by monoclonal antibody (MAb) ECG01 raised against equine CG (eCG) which binds to hormones and alpha-subunits from human and equine species.	epicatechin gallate	187-190	hypertrichosis 2 (generalised, congenital)	Homo sapiens	76-79
2463907-1	1989	To improve our knowledge of the structural features of the alpha-subunit of hCG we have studied the antigenic site recognized by monoclonal antibody (MAb) ECG01 raised against equine CG (eCG) which binds to hormones and alpha-subunits from human and equine species.	epicatechin gallate	187-190	hypertrichosis 2 (generalised, congenital)	Homo sapiens	77-79
2506842-2	1989	Although in two groups treated with different concentrations of hCG the value of 3H-thymidine incorporation into testicular tissue showed no significant difference compared with the untreated control group, treatment with both hCG and hMG induced significant changes in the value of 3H-thymidine incorporation compared with the untreated control group.	3h-thymidine	81-93	hypertrichosis 2 (generalised, congenital)	Homo sapiens	64-67
2506842-2	1989	Although in two groups treated with different concentrations of hCG the value of 3H-thymidine incorporation into testicular tissue showed no significant difference compared with the untreated control group, treatment with both hCG and hMG induced significant changes in the value of 3H-thymidine incorporation compared with the untreated control group.	3h-thymidine	81-93	hypertrichosis 2 (generalised, congenital)	Homo sapiens	227-230
2506842-2	1989	Although in two groups treated with different concentrations of hCG the value of 3H-thymidine incorporation into testicular tissue showed no significant difference compared with the untreated control group, treatment with both hCG and hMG induced significant changes in the value of 3H-thymidine incorporation compared with the untreated control group.	Menotropins	235-238	hypertrichosis 2 (generalised, congenital)	Homo sapiens	64-67
2506842-2	1989	Although in two groups treated with different concentrations of hCG the value of 3H-thymidine incorporation into testicular tissue showed no significant difference compared with the untreated control group, treatment with both hCG and hMG induced significant changes in the value of 3H-thymidine incorporation compared with the untreated control group.	3h-thymidine	283-295	hypertrichosis 2 (generalised, congenital)	Homo sapiens	64-67
2506842-2	1989	Although in two groups treated with different concentrations of hCG the value of 3H-thymidine incorporation into testicular tissue showed no significant difference compared with the untreated control group, treatment with both hCG and hMG induced significant changes in the value of 3H-thymidine incorporation compared with the untreated control group.	3h-thymidine	283-295	hypertrichosis 2 (generalised, congenital)	Homo sapiens	227-230
2492606-5	1989	An injection of hCG on Day 16 of pregnancy, however, induced ovulation in LH-treated animals (6.25-50.0 micrograms LH per injection, s.c. at 12-h intervals from Days 13 to 16).	Luteinizing Hormone	74-76	hypertrichosis 2 (generalised, congenital)	Homo sapiens	16-19
2492606-5	1989	An injection of hCG on Day 16 of pregnancy, however, induced ovulation in LH-treated animals (6.25-50.0 micrograms LH per injection, s.c. at 12-h intervals from Days 13 to 16).	Luteinizing Hormone	115-117	hypertrichosis 2 (generalised, congenital)	Homo sapiens	16-19
2626049-1	1989	The acetone extract obtained from the thymuses of 14-day-old rats contains a factor that interacts with hCG in the adult testis cells and inhibits testosterone production.	Testosterone	147-159	hypertrichosis 2 (generalised, congenital)	Homo sapiens	104-107
2626049-5	1989	30 kDa was found to inhibit the hCG-stimulated production of testosterone.	Testosterone	61-73	hypertrichosis 2 (generalised, congenital)	Homo sapiens	32-35
2644426-0	1989	Seasonal changes in plasma testosterone concentrations in response to administration of hCG in a desert rodent, the sand rat (Psammomys obesus).	Testosterone	27-39	hypertrichosis 2 (generalised, congenital)	Homo sapiens	88-91
2644426-2	1989	Testosterone secretion by the testis of the sand rat was stimulated (by 10-60-fold) throughout the year by exogenously administered hCG (25 i.u.).	Testosterone	0-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	132-135
2472981-3	1989	The results indicated that PRL inhibited, in a dose-dependent manner, hCG-induced cAMP accumulation and 17 beta-estradiol (E2) secretion.	Cyclic AMP	82-86	hypertrichosis 2 (generalised, congenital)	Homo sapiens	70-73
2472981-3	1989	The results indicated that PRL inhibited, in a dose-dependent manner, hCG-induced cAMP accumulation and 17 beta-estradiol (E2) secretion.	Estradiol	104-121	hypertrichosis 2 (generalised, congenital)	Homo sapiens	70-73
2472981-8	1989	The phosphodiesterase (PDE) inhibitor, 3-isobutyl-1-methyl-xanthine, abolished the inhibitory effect of PRL on hCG- and PGE1-induced cAMP accumulation and on hCG-induced E2 secretion, indicating that PRL might be inhibiting cAMP accumulation and steroidogenesis in preovulatory granulosa cells by enhancement of PDE activity.	1-Methyl-3-isobutylxanthine	39-67	hypertrichosis 2 (generalised, congenital)	Homo sapiens	111-114
2472981-8	1989	The phosphodiesterase (PDE) inhibitor, 3-isobutyl-1-methyl-xanthine, abolished the inhibitory effect of PRL on hCG- and PGE1-induced cAMP accumulation and on hCG-induced E2 secretion, indicating that PRL might be inhibiting cAMP accumulation and steroidogenesis in preovulatory granulosa cells by enhancement of PDE activity.	1-Methyl-3-isobutylxanthine	39-67	hypertrichosis 2 (generalised, congenital)	Homo sapiens	158-161
2472981-8	1989	The phosphodiesterase (PDE) inhibitor, 3-isobutyl-1-methyl-xanthine, abolished the inhibitory effect of PRL on hCG- and PGE1-induced cAMP accumulation and on hCG-induced E2 secretion, indicating that PRL might be inhibiting cAMP accumulation and steroidogenesis in preovulatory granulosa cells by enhancement of PDE activity.	Cyclic AMP	133-137	hypertrichosis 2 (generalised, congenital)	Homo sapiens	111-114
2595319-0	1989	Tamoxifen treatment of idiopathic oligozoospermia: effect on hCG-induced testicular steroidogenesis and semen variables.	Tamoxifen	0-9	hypertrichosis 2 (generalised, congenital)	Homo sapiens	61-64
2926195-2	1989	Luteal cells responded to hCG with a significant increase (2- to 4-fold) in progesterone (P) production.	Progesterone	76-88	hypertrichosis 2 (generalised, congenital)	Homo sapiens	26-29
2520509-8	1989	However, an adaptive increase (54%-173%) in the in vivo testosterone response to hCG was seen at ages 26 to 40 days.	Testosterone	56-68	hypertrichosis 2 (generalised, congenital)	Homo sapiens	81-84
2512636-2	1989	During hCG treatment steroid conversion in vitro in testicular biopsy material, as well as serum testosterone concentrations increased dramatically.	Steroids	21-28	hypertrichosis 2 (generalised, congenital)	Homo sapiens	7-10
2512636-4	1989	Combined hCG/hMG treatment seems to be an efficient therapy in well-selected infertile men, whereas increased testosterone production induced by hCG-treatment may be insufficient for restitution of spermatogenesis.	Testosterone	110-122	hypertrichosis 2 (generalised, congenital)	Homo sapiens	145-148
2855024-0	1988	Stimulation of cholesterol side-chain cleavage enzyme activity by cAMP and hCG in MA-10 Leydig tumor cells.	Cholesterol	15-26	hypertrichosis 2 (generalised, congenital)	Homo sapiens	75-78
2638145-9	1989	The addition of hCG at concentration of 10 IU/ml clearly accelerated progesterone production.	Progesterone	69-81	hypertrichosis 2 (generalised, congenital)	Homo sapiens	16-19
2638145-10	1989	Epostane at a concentration of 50 micrograms/ml could significantly inhibit both basic and the hCG-stimulated luteal production of progesterone.	epostane	0-8	hypertrichosis 2 (generalised, congenital)	Homo sapiens	95-98
2638145-10	1989	Epostane at a concentration of 50 micrograms/ml could significantly inhibit both basic and the hCG-stimulated luteal production of progesterone.	Progesterone	131-143	hypertrichosis 2 (generalised, congenital)	Homo sapiens	95-98
2855024-3	1988	However, this stimulation of CSCC activity appears to be of limited significance when compared to the approximately 1000-fold or greater increase observed in progesterone production in the presence of hCG or dbcAMP.	Progesterone	158-170	hypertrichosis 2 (generalised, congenital)	Homo sapiens	201-204
2855024-6	1988	Our observations clearly indicate that given the proper hydroxy substrates (22R-hydroxycholesterol or 25-hydroxycholesterol), MA-10 Leydig cells are able to convert them into progesterone without any stimulation by steroidogenic stimuli, i.e. cAMP or hCG.	22-hydroxycholesterol	76-98	hypertrichosis 2 (generalised, congenital)	Homo sapiens	251-254
2855024-6	1988	Our observations clearly indicate that given the proper hydroxy substrates (22R-hydroxycholesterol or 25-hydroxycholesterol), MA-10 Leydig cells are able to convert them into progesterone without any stimulation by steroidogenic stimuli, i.e. cAMP or hCG.	25-hydroxycholesterol	102-123	hypertrichosis 2 (generalised, congenital)	Homo sapiens	251-254
2855024-6	1988	Our observations clearly indicate that given the proper hydroxy substrates (22R-hydroxycholesterol or 25-hydroxycholesterol), MA-10 Leydig cells are able to convert them into progesterone without any stimulation by steroidogenic stimuli, i.e. cAMP or hCG.	Progesterone	175-187	hypertrichosis 2 (generalised, congenital)	Homo sapiens	251-254
3199379-1	1988	Dispersed horse luteal cells were used to evaluate the ability of horse LH, hCG and PMSG to stimulate progesterone secretion in vitro.	Progesterone	102-114	hypertrichosis 2 (generalised, congenital)	Homo sapiens	76-79
3203757-5	1988	Administration of Gesterol 4 to 6 hours before hCG significantly increased the LH values (19.0 +/- 10.3) compared with those who had Gesterol at the time of hCG (6.8 +/- 2.8, P = 0.0006).	11-hydroxyprogesterone	18-26	hypertrichosis 2 (generalised, congenital)	Homo sapiens	47-50
3215392-1	1988	Injection of adult male rats with human chorionic gonadotrophin (hCG) caused a dose- and time-dependent increase in the levels of immunoactive inhibin in testicular interstitial fluid (IF), which differed from the pattern of change in testosterone levels.	Testosterone	235-247	hypertrichosis 2 (generalised, congenital)	Homo sapiens	65-68
3215392-2	1988	Blockage of the hCG-induced increase in IF levels of testosterone, by administration of aminoglutethimide, only partially attenuated the increase in levels of inhibin.	Testosterone	53-65	hypertrichosis 2 (generalised, congenital)	Homo sapiens	16-19
3215392-2	1988	Blockage of the hCG-induced increase in IF levels of testosterone, by administration of aminoglutethimide, only partially attenuated the increase in levels of inhibin.	Aminoglutethimide	88-105	hypertrichosis 2 (generalised, congenital)	Homo sapiens	16-19
2853976-5	1988	Comparative study of the sugar chains of human chorionic gonadotropin isolated from the urine of pregnant women and of patients with trophoblastic diseases including choriocarcinoma revealed that many new oligosaccharides are included in the tumor hCG.	Oligosaccharides	205-221	hypertrichosis 2 (generalised, congenital)	Homo sapiens	248-251
3206533-6	1988	However, 5000 ng/ml CsA significantly (P less than 0.05) reduced the hCG (1 ng/ml)-stimulated T levels, CSCC and 17,20-desmolase activities.	Cyclosporine	20-23	hypertrichosis 2 (generalised, congenital)	Homo sapiens	69-72
3199379-9	1988	We conclude that the mare corpus luteum is responsive to gonadotrophins in vitro and that exogenous hCG can enhance serum progesterone concentrations throughout the oestrous cycle and early pregnancy.	Progesterone	122-134	hypertrichosis 2 (generalised, congenital)	Homo sapiens	100-103
2852964-8	1988	However, at a maximal dose of human chorionic gonadotropin (hCG), PMA inhibited steroid synthesis at 1 and 2 h but had no significant effect at 3 h. Conversely, PMA had an additive effect on cAMP induced steroidogenesis.	Tetradecanoylphorbol Acetate	66-69	hypertrichosis 2 (generalised, congenital)	Homo sapiens	60-63
2852964-8	1988	However, at a maximal dose of human chorionic gonadotropin (hCG), PMA inhibited steroid synthesis at 1 and 2 h but had no significant effect at 3 h. Conversely, PMA had an additive effect on cAMP induced steroidogenesis.	Steroids	80-87	hypertrichosis 2 (generalised, congenital)	Homo sapiens	60-63
2852964-8	1988	However, at a maximal dose of human chorionic gonadotropin (hCG), PMA inhibited steroid synthesis at 1 and 2 h but had no significant effect at 3 h. Conversely, PMA had an additive effect on cAMP induced steroidogenesis.	Tetradecanoylphorbol Acetate	161-164	hypertrichosis 2 (generalised, congenital)	Homo sapiens	60-63
2852964-8	1988	However, at a maximal dose of human chorionic gonadotropin (hCG), PMA inhibited steroid synthesis at 1 and 2 h but had no significant effect at 3 h. Conversely, PMA had an additive effect on cAMP induced steroidogenesis.	Cyclic AMP	191-195	hypertrichosis 2 (generalised, congenital)	Homo sapiens	60-63
2852964-9	1988	It was further demonstrated that PMA resulted in a decrease in the hCG-induced accumulation of cAMP.	Cyclic AMP	95-99	hypertrichosis 2 (generalised, congenital)	Homo sapiens	67-70
3148558-0	1988	Treatment with an LHRH agonist or hCG increases interstitial fluid volume and permeability to Evans blue in the mouse testis.	Evans Blue	94-104	hypertrichosis 2 (generalised, congenital)	Homo sapiens	34-37
2980250-5	1988	After hCG injection all groups of animals exhibited an increase in plasma testosterone level, although the response was smaller in 12- and 24-month animals compared to the young mature (3 months) ones.	Testosterone	74-86	hypertrichosis 2 (generalised, congenital)	Homo sapiens	6-9
3148558-2	1988	hCG, subcutaneously, resulted in an increase in the permeability to intravenously injected Evans blue into the testicular interstitial space and in the volume of testicular interstitial fluid.	Evans Blue	91-101	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
2844681-4	1988	Leydig cells from adult Hre rats exhibited an enhanced testosterone response to LH and hCG in vitro but not in vivo.	Testosterone	55-67	hypertrichosis 2 (generalised, congenital)	Homo sapiens	87-90
16726496-5	1988	Exposure to either insulin and E2 or insulin, E2 plus hCG resulted in an increase in 3H-thymidine incorporation with the number of primary follicles decreasing at 24 h (P &lt; 0.05) then increasing at 48 h of perifusion (P &lt; 0.05).	Tritium	85-87	hypertrichosis 2 (generalised, congenital)	Homo sapiens	54-57
16726496-5	1988	Exposure to either insulin and E2 or insulin, E2 plus hCG resulted in an increase in 3H-thymidine incorporation with the number of primary follicles decreasing at 24 h (P &lt; 0.05) then increasing at 48 h of perifusion (P &lt; 0.05).	Thymidine	88-97	hypertrichosis 2 (generalised, congenital)	Homo sapiens	54-57
16726496-6	1988	The addition of hCG increased both 3H-thymidine incorporation and the number of primary follicles present after 48 h compared to treatment with insulin and E2 alone (P &lt; 0.05).	Tritium	35-37	hypertrichosis 2 (generalised, congenital)	Homo sapiens	16-19
16726496-6	1988	The addition of hCG increased both 3H-thymidine incorporation and the number of primary follicles present after 48 h compared to treatment with insulin and E2 alone (P &lt; 0.05).	Thymidine	38-47	hypertrichosis 2 (generalised, congenital)	Homo sapiens	16-19
3182393-0	1988	Effects of chronic sulpiride-induced hyperprolactinemia on plasma testosterone and its responses to hCG in normal men.	Sulpiride	19-28	hypertrichosis 2 (generalised, congenital)	Homo sapiens	100-103
3208997-2	1988	FGF enhanced in a dose-dependent manner hCG-stimulated testosterone secretion (ED50 = 11 ng/ml FGF).	Testosterone	55-67	hypertrichosis 2 (generalised, congenital)	Homo sapiens	40-43
3182393-1	1988	To elucidate the effects of sulpiride-induced (300 mg daily) long-term (64 days) hyperprolactinemia on basal and hCG-stimulated plasma testosterone (T), hCG was given to five normal men five times at 2-week intervals (before sulpiride administration and at 2, 4, 6 and 8 weeks).	Testosterone	135-147	hypertrichosis 2 (generalised, congenital)	Homo sapiens	113-116
3411566-7	1988	Between 4 and 8 h after the injection of hCG, labelled glycoconjugates containing [3H]glucosamine, became increasingly associated with the outer surface of the zona pellucida and with the region of the egg plasma membrane, even in Graafian follicles not destined to ovulate.	[3h]glucosamine	82-97	hypertrichosis 2 (generalised, congenital)	Homo sapiens	41-44
2840532-9	1988	hCG, isoproterenol and PGE1 were able to stimulate testosterone production in vitro.	Testosterone	51-63	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
2842496-1	1988	Ovulation induced by hCG in rabbits was reduced significantly (P less than 0.005) by sulpiride-induced hyperprolactinaemia.	Sulpiride	85-94	hypertrichosis 2 (generalised, congenital)	Homo sapiens	21-24
3379138-2	1988	In this study, we tested the thyrotropic activity of purified and commercial hCG and compared its action with that of bovine TSH (bTSH) in cultured rat FRTL-5 cells in regard to stimulation of iodide uptake, activation of adenylate cyclase, and synthesis of DNA.	Iodides	193-199	hypertrichosis 2 (generalised, congenital)	Homo sapiens	77-80
3379138-6	1988	Both purified and commercial hCG produced a dose-related increase in iodide uptake.	Iodides	69-75	hypertrichosis 2 (generalised, congenital)	Homo sapiens	29-32
3379138-8	1988	hCG caused a dose-related increment of adenylate cyclase and [3H]thymidine incorporation.	Tritium	62-64	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
3379138-8	1988	hCG caused a dose-related increment of adenylate cyclase and [3H]thymidine incorporation.	Thymidine	65-74	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
3379138-9	1988	The effect of hCG on iodide uptake and [3H]thymidine incorporation was additive with that of bTSH; hCG was not an antagonist of TSH in these cultured rat thyroid cells.	Iodides	21-27	hypertrichosis 2 (generalised, congenital)	Homo sapiens	14-17
3379138-9	1988	The effect of hCG on iodide uptake and [3H]thymidine incorporation was additive with that of bTSH; hCG was not an antagonist of TSH in these cultured rat thyroid cells.	Tritium	40-42	hypertrichosis 2 (generalised, congenital)	Homo sapiens	14-17
3379138-10	1988	We conclude that hCG has intrinsic thyrotropic activity in FRTL-5 cells in regard to stimulation of iodide uptake, activation of adenylate cyclase, and stimulation of DNA synthesis.	Iodides	100-106	hypertrichosis 2 (generalised, congenital)	Homo sapiens	17-20
3059490-0	1988	Indomethacin inhibits hCG and GnRH agonist-induced secretion of plasminogen activator by granulosa and theca interstitial cells of hypophysectomized rats.	Indomethacin	0-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	22-25
3059490-5	1988	The results indicate that indomethacin can only suppress hCG- and GnRH agonist-induced PA secretion, but not suppress the ovarian content of these enzymes.	Indomethacin	26-38	hypertrichosis 2 (generalised, congenital)	Homo sapiens	57-60
3389053-3	1988	Basal and hCG stimulated testosterone production of rat interstitial cells, and Percoll purified Leydig cells were significantly stimulated by hFF.	Testosterone	25-37	hypertrichosis 2 (generalised, congenital)	Homo sapiens	10-13
3408769-1	1988	Guanyl nucleotides are known to play a dual role in the activation of the adenylate cyclase system of the rat corpus luteum, being required for human choriogonadotropin (hCG) stimulation of the enzyme and modulating hCG binding to some hormone receptors.	guanyl nucleotides	0-18	hypertrichosis 2 (generalised, congenital)	Homo sapiens	170-173
3408769-1	1988	Guanyl nucleotides are known to play a dual role in the activation of the adenylate cyclase system of the rat corpus luteum, being required for human choriogonadotropin (hCG) stimulation of the enzyme and modulating hCG binding to some hormone receptors.	guanyl nucleotides	0-18	hypertrichosis 2 (generalised, congenital)	Homo sapiens	216-219
3408769-2	1988	Current models of adenylate cyclase activation require that guanyl nucleotide binding be enhanced by hormones, and we have examined this binding in rat luteal membrane preparations known to contain guanyl nucleotide-modulated hCG receptors.	guanyl nucleotide	198-215	hypertrichosis 2 (generalised, congenital)	Homo sapiens	226-229
3408769-8	1988	A similar hierarchy was also found for hCG-stimulated adenylate cyclase activity (GMPPnP = GTP greater than ITP) and for modulation of hCG binding (GMPPnP greater than GTP greater than ITP).	Guanylyl Imidodiphosphate	82-88	hypertrichosis 2 (generalised, congenital)	Homo sapiens	39-42
3408769-8	1988	A similar hierarchy was also found for hCG-stimulated adenylate cyclase activity (GMPPnP = GTP greater than ITP) and for modulation of hCG binding (GMPPnP greater than GTP greater than ITP).	Guanosine Triphosphate	91-94	hypertrichosis 2 (generalised, congenital)	Homo sapiens	39-42
3408769-8	1988	A similar hierarchy was also found for hCG-stimulated adenylate cyclase activity (GMPPnP = GTP greater than ITP) and for modulation of hCG binding (GMPPnP greater than GTP greater than ITP).	Inosine Triphosphate	108-111	hypertrichosis 2 (generalised, congenital)	Homo sapiens	39-42
3408769-8	1988	A similar hierarchy was also found for hCG-stimulated adenylate cyclase activity (GMPPnP = GTP greater than ITP) and for modulation of hCG binding (GMPPnP greater than GTP greater than ITP).	Guanylyl Imidodiphosphate	148-154	hypertrichosis 2 (generalised, congenital)	Homo sapiens	135-138
3408769-8	1988	A similar hierarchy was also found for hCG-stimulated adenylate cyclase activity (GMPPnP = GTP greater than ITP) and for modulation of hCG binding (GMPPnP greater than GTP greater than ITP).	Guanosine Triphosphate	168-171	hypertrichosis 2 (generalised, congenital)	Homo sapiens	135-138
3408769-8	1988	A similar hierarchy was also found for hCG-stimulated adenylate cyclase activity (GMPPnP = GTP greater than ITP) and for modulation of hCG binding (GMPPnP greater than GTP greater than ITP).	Inosine Triphosphate	185-188	hypertrichosis 2 (generalised, congenital)	Homo sapiens	135-138
3187563-0	1988	[Effect of twenty-one kinds of amino acids on progesterone production of rat luteal cells induced by hCG].	Progesterone	46-58	hypertrichosis 2 (generalised, congenital)	Homo sapiens	101-104
3392440-2	1988	Treatment with dithiothreitol, neuraminidase, and low pH (3.3) buffer partially dissociated hCG from its receptor with dissociation rates of 42.8%, 35.2%, and 68.7%, respectively.	Dithiothreitol	15-29	hypertrichosis 2 (generalised, congenital)	Homo sapiens	92-95
3392440-10	1988	Treatment with dithiothreitol, neuraminidase, and low pH (3.3) buffer seems feasible for detecting hCG-occupied receptors.	Dithiothreitol	15-29	hypertrichosis 2 (generalised, congenital)	Homo sapiens	99-102
2845837-9	1988	The addition of hCG stimulated cyclic AMP accumulation to a much higher level in the DBCP treated than in controls.	Cyclic AMP	31-41	hypertrichosis 2 (generalised, congenital)	Homo sapiens	16-19
2845837-9	1988	The addition of hCG stimulated cyclic AMP accumulation to a much higher level in the DBCP treated than in controls.	1,2-dibromo-3-chloropropane	85-89	hypertrichosis 2 (generalised, congenital)	Homo sapiens	16-19
2845837-11	1988	Stimulation of hCG increased both DBCP treated and controls to similar levels.	1,2-dibromo-3-chloropropane	34-38	hypertrichosis 2 (generalised, congenital)	Homo sapiens	15-18
2845837-12	1988	Testosterone release into the medium by slices was higher in DBCP treated than in controls and so was also the increment due to hCG stimulation.	Testosterone	0-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	128-131
2845837-12	1988	Testosterone release into the medium by slices was higher in DBCP treated than in controls and so was also the increment due to hCG stimulation.	1,2-dibromo-3-chloropropane	61-65	hypertrichosis 2 (generalised, congenital)	Homo sapiens	128-131
2845837-14	1988	It is suggested that since the major testicular compartment damaged by DBCP is the tubular one, the proportion of the interstitium per testicular unit weight is larger than in controls, thus, cyclic AMP content increment due to hCG stimulation is much higher.	Cyclic AMP	192-202	hypertrichosis 2 (generalised, congenital)	Homo sapiens	228-231
2834186-1	1988	Using a clonal strain of cultured Leydig tumor cells (designated MA-10), we have examined the effects of Ca+2 on the activation of cAMP accumulation and steroid biosynthesis by hCG.	Steroids	153-160	hypertrichosis 2 (generalised, congenital)	Homo sapiens	177-180
2834411-4	1988	A difference was found in the latency, the lag phase until maximal response, and the duration of response between the effects of PGE2 and hCG on both cAMP and P formation.	Cyclic AMP	150-154	hypertrichosis 2 (generalised, congenital)	Homo sapiens	138-141
2834411-7	1988	On the other hand, hCG had less stimulatory effect on cAMP and P formation in CL from early pregnancy compared to CL from the menstrual cycle.	Cyclic AMP	54-58	hypertrichosis 2 (generalised, congenital)	Homo sapiens	19-22
3396759-1	1988	This study was designed to examine the ability of in vivo administration of human chorionic gonadotropin (hCG, 4000 IU) to alter the effects of Lutalyse (PGF2 alpha, 10 mg) in the cow.	Dinoprost	154-164	hypertrichosis 2 (generalised, congenital)	Homo sapiens	106-109
2834186-2	1988	Our results show that addition of Ca+2 ionophores (A23187 or ionomycin) leads to inhibition of the activation of cAMP accumulation by hCG.	Calcimycin	51-57	hypertrichosis 2 (generalised, congenital)	Homo sapiens	134-137
2834186-2	1988	Our results show that addition of Ca+2 ionophores (A23187 or ionomycin) leads to inhibition of the activation of cAMP accumulation by hCG.	Ionomycin	61-70	hypertrichosis 2 (generalised, congenital)	Homo sapiens	134-137
2834186-2	1988	Our results show that addition of Ca+2 ionophores (A23187 or ionomycin) leads to inhibition of the activation of cAMP accumulation by hCG.	Cyclic AMP	113-117	hypertrichosis 2 (generalised, congenital)	Homo sapiens	134-137
2834186-4	1988	A detailed examination of the effects of A23187 and removal of extracellular Ca+2 on the rates of cAMP synthesis and degradation in intact cells revealed that A23187 inhibits the rate of cAMP accumulation activated by hCG, but does not affect the rate of degradation of cAMP.	Cyclic AMP	98-102	hypertrichosis 2 (generalised, congenital)	Homo sapiens	218-221
2834186-4	1988	A detailed examination of the effects of A23187 and removal of extracellular Ca+2 on the rates of cAMP synthesis and degradation in intact cells revealed that A23187 inhibits the rate of cAMP accumulation activated by hCG, but does not affect the rate of degradation of cAMP.	Calcimycin	159-165	hypertrichosis 2 (generalised, congenital)	Homo sapiens	218-221
2834186-4	1988	A detailed examination of the effects of A23187 and removal of extracellular Ca+2 on the rates of cAMP synthesis and degradation in intact cells revealed that A23187 inhibits the rate of cAMP accumulation activated by hCG, but does not affect the rate of degradation of cAMP.	Cyclic AMP	187-191	hypertrichosis 2 (generalised, congenital)	Homo sapiens	218-221
2834186-4	1988	A detailed examination of the effects of A23187 and removal of extracellular Ca+2 on the rates of cAMP synthesis and degradation in intact cells revealed that A23187 inhibits the rate of cAMP accumulation activated by hCG, but does not affect the rate of degradation of cAMP.	Cyclic AMP	187-191	hypertrichosis 2 (generalised, congenital)	Homo sapiens	218-221
2834186-7	1988	Additional experiments show that the effects of A23187 or removal of extracellular Ca+2 on hCG-activated steroidogenesis closely parallel those described for cAMP accumulation.	Calcimycin	48-54	hypertrichosis 2 (generalised, congenital)	Homo sapiens	91-94
2834186-7	1988	Additional experiments show that the effects of A23187 or removal of extracellular Ca+2 on hCG-activated steroidogenesis closely parallel those described for cAMP accumulation.	Cyclic AMP	158-162	hypertrichosis 2 (generalised, congenital)	Homo sapiens	91-94
2834186-8	1988	We conclude that Ca+2 is an inhibitor of the hCG-activated adenylate cyclase in Leydig tumor cells, and that this inhibition imposes a limitation on the ability of hCG to activate steroid biosynthesis.	Steroids	180-187	hypertrichosis 2 (generalised, congenital)	Homo sapiens	164-167
2831035-5	1988	Moreover, combined treatment with both norepinephrine (10(-6) M) and hCG (1 ng/ml) unmasked a synergistic interaction subject to stereospecific blockade by beta (propranolol)- but not alpha (phentolamine)-selective adrenergic antagonists.	(2-benzoylethyl)trimethylammonium	156-160	hypertrichosis 2 (generalised, congenital)	Homo sapiens	69-72
2831035-5	1988	Moreover, combined treatment with both norepinephrine (10(-6) M) and hCG (1 ng/ml) unmasked a synergistic interaction subject to stereospecific blockade by beta (propranolol)- but not alpha (phentolamine)-selective adrenergic antagonists.	Propranolol	162-173	hypertrichosis 2 (generalised, congenital)	Homo sapiens	69-72
2831035-5	1988	Moreover, combined treatment with both norepinephrine (10(-6) M) and hCG (1 ng/ml) unmasked a synergistic interaction subject to stereospecific blockade by beta (propranolol)- but not alpha (phentolamine)-selective adrenergic antagonists.	Phentolamine	191-203	hypertrichosis 2 (generalised, congenital)	Homo sapiens	69-72
2448328-1	1988	Our previous work demonstrated that 8-bromo-cAMP promotes the secretion of both hCG and progesterone by cultured cytotrophoblasts.	8-Bromo Cyclic Adenosine Monophosphate	36-48	hypertrichosis 2 (generalised, congenital)	Homo sapiens	80-83
3279065-5	1988	1) hCG treatment (2000 IU, three times per week) concomitant with weekly plasmapheresis (since the patient"s response to an hCG challenge test was improved after a reduction of antibody titer by plasmapheresis) resulted in only a temporary increase in testosterone production.	Testosterone	252-264	hypertrichosis 2 (generalised, congenital)	Homo sapiens	3-6
2898450-1	1988	Alpha- and beta-momorcharins, which are abortifacient proteins isolated from Momordica charantia seeds, were tested for a possible effect on ovulation and plasma levels of ovarian steroids in mice induced to superovulate by PMSG and hCG.	alpha- and beta-momorcharins	0-28	hypertrichosis 2 (generalised, congenital)	Homo sapiens	233-236
3128487-3	1988	The ability of the heated testis to secrete testosterone in vivo in response to maximal stimulation by hCG was reduced, as judged by testosterone levels in peripheral blood, while there was a supranormal increase in testosterone levels in testicular venous blood.	Testosterone	44-56	hypertrichosis 2 (generalised, congenital)	Homo sapiens	103-106
3128487-3	1988	The ability of the heated testis to secrete testosterone in vivo in response to maximal stimulation by hCG was reduced, as judged by testosterone levels in peripheral blood, while there was a supranormal increase in testosterone levels in testicular venous blood.	Testosterone	133-145	hypertrichosis 2 (generalised, congenital)	Homo sapiens	103-106
3128487-3	1988	The ability of the heated testis to secrete testosterone in vivo in response to maximal stimulation by hCG was reduced, as judged by testosterone levels in peripheral blood, while there was a supranormal increase in testosterone levels in testicular venous blood.	Testosterone	133-145	hypertrichosis 2 (generalised, congenital)	Homo sapiens	103-106
3208576-6	1988	The determination of K" and K was exemplified by obtaining the data of anti-IgG and anti-hCG antibodies (immobilized on triacetyl cellulose membrane) with their antigens.	cellulose triacetate	120-139	hypertrichosis 2 (generalised, congenital)	Homo sapiens	89-92
2833550-4	1988	Binding of 125I-labelled human chorionic gonadotrophin (hCG) to testis homogenate, however, was still less than 10% of normal.	Iodine-125	11-15	hypertrichosis 2 (generalised, congenital)	Homo sapiens	56-59
2448328-6	1988	Forskolin also stimulated adenylate cyclase, cAMP synthesis, and hCG secretion.	Colforsin	0-9	hypertrichosis 2 (generalised, congenital)	Homo sapiens	65-68
2448328-8	1988	8-Bromo-cAMP stimulated cytotrophoblast protein kinase activity, resulting in the increased phosphorylation of a protein with a mol wt of about 70,000, and produced a marked stimulation of hCG secretion.	8-Bromo Cyclic Adenosine Monophosphate	0-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	189-192
2852518-2	1988	Adrenaline enhanced the basal and potentiated the hCG-induced T release.	Epinephrine	0-10	hypertrichosis 2 (generalised, congenital)	Homo sapiens	50-53
3227855-0	1988	Influence of pituitary hormones (hCG, TSH, Pr, GH) on testosterone level and on the functional activity of the Leydig cell in rat fetuses.	Testosterone	54-66	hypertrichosis 2 (generalised, congenital)	Homo sapiens	33-36
3149886-7	1988	The response of plasma testosterone to the administration of hCG was also abnormally low.	Testosterone	23-35	hypertrichosis 2 (generalised, congenital)	Homo sapiens	61-64
2829853-9	1988	These studies show that hCG and db cyclic AMP stimulation of MA-10 cells results in the rapid induction of cycloheximide-sensitive proteins located in the mitochondria which may be instrumental in the acute regulation of steroidogenesis.	Cycloheximide	107-120	hypertrichosis 2 (generalised, congenital)	Homo sapiens	24-27
2852518-4	1988	Although phenylephrine, an alpha 1-agonist, did not alter the basal T secretion, it enhanced hCG-mediated T secretion.	Phenylephrine	9-22	hypertrichosis 2 (generalised, congenital)	Homo sapiens	93-96
2846979-3	1988	Addition of 8-bromo-adenosine-3",5"-monophosphate (8-Br-cAMP), forskolin or cholera toxin (but not 8-Br-cGMP) stimulated hCG and P production by the cultivated placental cells.	8-Bromo Cyclic Adenosine Monophosphate	12-49	hypertrichosis 2 (generalised, congenital)	Homo sapiens	121-124
3121643-1	1988	The time course for LH induction of luteinizing hormone (LH) receptors as reflected in binding of 125I-labeled hCG was investigated in hypophysectomized adult male rats.	Iodine-125	98-102	hypertrichosis 2 (generalised, congenital)	Homo sapiens	111-114
3121643-3	1988	Testicular binding of hCG was determined at different times following the LH injection using Leydig cell membrane preparations from a testicular homogenate.	Luteinizing Hormone	74-76	hypertrichosis 2 (generalised, congenital)	Homo sapiens	22-25
3121643-7	1988	injection increased 125I hCG binding up to 56 +/- 10% of control values within 30 minutes of the LH injection.	Luteinizing Hormone	97-99	hypertrichosis 2 (generalised, congenital)	Homo sapiens	25-28
3075167-8	1988	The addition of hCG caused rounding of the cells and was accompanied by the appearance of microvilli and by pronounced steroid-producing organelles.	Steroids	119-126	hypertrichosis 2 (generalised, congenital)	Homo sapiens	16-19
3346178-12	1988	The single hCG treatment caused significant reversal of the suppression of accessory sex organ weights following melatonin, short days or 35 C temperature.	Melatonin	113-122	hypertrichosis 2 (generalised, congenital)	Homo sapiens	11-14
3346178-14	1988	Animals treated with 35 C or both melatonin and 35 C had lower serum testosterone at 7 weeks of age, released less testosterone after hCG, and had smaller organ weights with or without hCG than long day controls.	Melatonin	34-43	hypertrichosis 2 (generalised, congenital)	Homo sapiens	134-137
3346178-14	1988	Animals treated with 35 C or both melatonin and 35 C had lower serum testosterone at 7 weeks of age, released less testosterone after hCG, and had smaller organ weights with or without hCG than long day controls.	Melatonin	34-43	hypertrichosis 2 (generalised, congenital)	Homo sapiens	185-188
3346178-15	1988	The influence of melatonin treatment and 35 C temperature appears to be additive for testicular weight and testosterone release after hCG.	Melatonin	17-26	hypertrichosis 2 (generalised, congenital)	Homo sapiens	134-137
3346178-15	1988	The influence of melatonin treatment and 35 C temperature appears to be additive for testicular weight and testosterone release after hCG.	Testosterone	107-119	hypertrichosis 2 (generalised, congenital)	Homo sapiens	134-137
3346180-3	1988	The mean change of serum testosterone at 6 hours in the group infused with desialylated hCG (129% of baseline) was significantly greater than that of the controls (69% of baseline).	Testosterone	25-37	hypertrichosis 2 (generalised, congenital)	Homo sapiens	88-91
3346180-5	1988	It was concluded that desialylated hCG, when given as a constant intravenous infusion, can elicit a substantial serum testosterone response comparable to that seen with purified hCG, and thus, that desialylated hCG behaves as an agonist of the LH/CG receptors on human Leydig cells.	Testosterone	118-130	hypertrichosis 2 (generalised, congenital)	Homo sapiens	35-38
3346180-5	1988	It was concluded that desialylated hCG, when given as a constant intravenous infusion, can elicit a substantial serum testosterone response comparable to that seen with purified hCG, and thus, that desialylated hCG behaves as an agonist of the LH/CG receptors on human Leydig cells.	Testosterone	118-130	hypertrichosis 2 (generalised, congenital)	Homo sapiens	36-38
3361073-0	1988	Effect of anticalmodulin drugs on testosterone synthesis in hCG stimulated mouse Leydig cells.	Testosterone	34-46	hypertrichosis 2 (generalised, congenital)	Homo sapiens	60-63
3361073-1	1988	The effect of three anticalmodulin drugs, prepared in this laboratory and a commercially available drug Mastoparan, was tested on the secretion (or synthesis) of testosterone in hCG stimulated Leydig cells.	Testosterone	162-174	hypertrichosis 2 (generalised, congenital)	Homo sapiens	178-181
3361073-2	1988	The results of the use of drugs RN-IV A, RN-IV B and RN-IV C indicated that hCG (10 ng/ml), DbcAMP (0.1 mM) and cholera toxin (2 micrograms/ml)-stimulated testosterone production was inhibited in Leydig cells in a dose dependent manner.	Testosterone	155-167	hypertrichosis 2 (generalised, congenital)	Homo sapiens	76-79
3361073-6	1988	The drug RN-IV B at a concentration of 100 microM, which failed to prevent conversion of exogenous pregnenolone or progesterone to testosterone, otherwise caused complete inhibition of testosterone production in hCG stimulated cells.	Testosterone	185-197	hypertrichosis 2 (generalised, congenital)	Homo sapiens	212-215
3361073-7	1988	Mastoparan also inhibited testosterone production in hCG stimulated cells in a dose dependent manner.	Testosterone	26-38	hypertrichosis 2 (generalised, congenital)	Homo sapiens	53-56
3422321-9	1988	FRP inhibited (P less than 0.05) the hCG-induced increase in 3 beta-HSD activity at 36, 48 and 72 h. HCG enhanced aromatase activity after 48 h while FRP prevented (P less than 0.05) the hCG-induced increase in aromatase activity at 48 and 72 h. Secretion of oestradiol was enhanced (P less than 0.05) at 48 h but inhibited at 72 h by hCG.	Estradiol	259-269	hypertrichosis 2 (generalised, congenital)	Homo sapiens	37-40
3422321-9	1988	FRP inhibited (P less than 0.05) the hCG-induced increase in 3 beta-HSD activity at 36, 48 and 72 h. HCG enhanced aromatase activity after 48 h while FRP prevented (P less than 0.05) the hCG-induced increase in aromatase activity at 48 and 72 h. Secretion of oestradiol was enhanced (P less than 0.05) at 48 h but inhibited at 72 h by hCG.	Estradiol	259-269	hypertrichosis 2 (generalised, congenital)	Homo sapiens	101-104
2846979-1	1988	The present study examined the effects of a cAMP analog on the output of hCG and progesterone (P) in human term trophoblast cells in culture, as well as the conversion of androstenedione and testosterone to estradiol--17 beta and estrone by these cells.	Cyclic AMP	44-48	hypertrichosis 2 (generalised, congenital)	Homo sapiens	73-76
2846979-3	1988	Addition of 8-bromo-adenosine-3",5"-monophosphate (8-Br-cAMP), forskolin or cholera toxin (but not 8-Br-cGMP) stimulated hCG and P production by the cultivated placental cells.	8-Bromo Cyclic Adenosine Monophosphate	51-60	hypertrichosis 2 (generalised, congenital)	Homo sapiens	121-124
2846979-3	1988	Addition of 8-bromo-adenosine-3",5"-monophosphate (8-Br-cAMP), forskolin or cholera toxin (but not 8-Br-cGMP) stimulated hCG and P production by the cultivated placental cells.	Colforsin	63-72	hypertrichosis 2 (generalised, congenital)	Homo sapiens	121-124
3149791-8	1988	These results suggest that hCG stimulation involved the blockade of a potassium current and the activation of a chloride current through an increase of intracellular calcium.	Potassium	70-79	hypertrichosis 2 (generalised, congenital)	Homo sapiens	27-30
3149791-8	1988	These results suggest that hCG stimulation involved the blockade of a potassium current and the activation of a chloride current through an increase of intracellular calcium.	Chlorides	112-120	hypertrichosis 2 (generalised, congenital)	Homo sapiens	27-30
3149791-8	1988	These results suggest that hCG stimulation involved the blockade of a potassium current and the activation of a chloride current through an increase of intracellular calcium.	Calcium	166-173	hypertrichosis 2 (generalised, congenital)	Homo sapiens	27-30
2888559-5	1987	In the other subjects, the hCG test will permit the determination of the presence or absence of testosterone production and in some cases it results in testicular descent.	Testosterone	96-108	hypertrichosis 2 (generalised, congenital)	Homo sapiens	27-30
3119652-5	1987	When stimulated with hCG, the small cells responded with significant increases in progesterone, androstenedione, and testosterone release, but the large cells did not.	Progesterone	82-94	hypertrichosis 2 (generalised, congenital)	Homo sapiens	21-24
3119652-5	1987	When stimulated with hCG, the small cells responded with significant increases in progesterone, androstenedione, and testosterone release, but the large cells did not.	Androstenedione	96-111	hypertrichosis 2 (generalised, congenital)	Homo sapiens	21-24
3119652-5	1987	When stimulated with hCG, the small cells responded with significant increases in progesterone, androstenedione, and testosterone release, but the large cells did not.	Testosterone	117-129	hypertrichosis 2 (generalised, congenital)	Homo sapiens	21-24
3242162-5	1988	Androstenedione and testosterone were elevated two days after the hCG injection but returned to baseline thereafter.	Androstenedione	0-15	hypertrichosis 2 (generalised, congenital)	Homo sapiens	66-69
3242162-5	1988	Androstenedione and testosterone were elevated two days after the hCG injection but returned to baseline thereafter.	Testosterone	20-32	hypertrichosis 2 (generalised, congenital)	Homo sapiens	66-69
3425162-1	1987	The presence of thyroid stimulating activity in partially purified hCG was investigated using, as bioassay system, iodide uptake in rat thyroid FRTL-5 cells.	Iodides	115-121	hypertrichosis 2 (generalised, congenital)	Homo sapiens	67-70
3425162-4	1987	A dose-dependent response, paralleling that evoked by bTSH, was observed in a concentration range of 0.1-4 mumol/l hCG; 1 mumol of hCG was equivalent to 50 pmol of bTSH and 132 pmol of hTSH.	btsh	54-58	hypertrichosis 2 (generalised, congenital)	Homo sapiens	115-118
3425162-4	1987	A dose-dependent response, paralleling that evoked by bTSH, was observed in a concentration range of 0.1-4 mumol/l hCG; 1 mumol of hCG was equivalent to 50 pmol of bTSH and 132 pmol of hTSH.	btsh	164-168	hypertrichosis 2 (generalised, congenital)	Homo sapiens	115-118
3425162-5	1987	The thyrotropic activity coeluted with hCG immunoactivity on Sephadex G-100.	sephadex	61-75	hypertrichosis 2 (generalised, congenital)	Homo sapiens	39-42
2891876-7	1987	The patterns of the steroid response to hCG were similar in both groups: in the testes and in the plasma, they increased acutely following hCG injection (except testicular androstenedione), then, after 72 h, returned to normal values in the plasma but remained higher than the basal values in the testes.	Steroids	20-27	hypertrichosis 2 (generalised, congenital)	Homo sapiens	40-43
2891876-7	1987	The patterns of the steroid response to hCG were similar in both groups: in the testes and in the plasma, they increased acutely following hCG injection (except testicular androstenedione), then, after 72 h, returned to normal values in the plasma but remained higher than the basal values in the testes.	Steroids	20-27	hypertrichosis 2 (generalised, congenital)	Homo sapiens	139-142
2891876-7	1987	The patterns of the steroid response to hCG were similar in both groups: in the testes and in the plasma, they increased acutely following hCG injection (except testicular androstenedione), then, after 72 h, returned to normal values in the plasma but remained higher than the basal values in the testes.	Androstenedione	172-187	hypertrichosis 2 (generalised, congenital)	Homo sapiens	40-43
3119252-5	1987	The fluorescent complex formed on the solid-phase [monoclonal antibody-hCG-monoclonal antibody-biotin-streptavidin-BCPDA-Eu3+] is measured by excitation at 337.1 nm with a nitrogen laser and monitoring the emission at 615 nm in a specially designed gated fluorometer working in a time-resolved mode.	Biotin	95-101	hypertrichosis 2 (generalised, congenital)	Homo sapiens	71-74
3119252-5	1987	The fluorescent complex formed on the solid-phase [monoclonal antibody-hCG-monoclonal antibody-biotin-streptavidin-BCPDA-Eu3+] is measured by excitation at 337.1 nm with a nitrogen laser and monitoring the emission at 615 nm in a specially designed gated fluorometer working in a time-resolved mode.	Nitrogen	172-180	hypertrichosis 2 (generalised, congenital)	Homo sapiens	71-74
3130224-0	1987	Effects of tyrosine and its analogues on hCG-induced progesterone production by rat corpus luteum in vitro.	Tyrosine	11-19	hypertrichosis 2 (generalised, congenital)	Homo sapiens	41-44
3130224-0	1987	Effects of tyrosine and its analogues on hCG-induced progesterone production by rat corpus luteum in vitro.	Progesterone	53-65	hypertrichosis 2 (generalised, congenital)	Homo sapiens	41-44
3430461-5	1987	After both short and longer term exposure to [3H]glucosamine, the maximum uptake of label in preantral follicles occurred 4-8 h after the injection of hCG, indicating that hCG rather than PMSG probably exerts the greatest control over the uptake and incorporation of [3H]glucosamine into the zona pellucida and oocyte of preantral follicles.	[3h]glucosamine	45-60	hypertrichosis 2 (generalised, congenital)	Homo sapiens	151-154
3430461-5	1987	After both short and longer term exposure to [3H]glucosamine, the maximum uptake of label in preantral follicles occurred 4-8 h after the injection of hCG, indicating that hCG rather than PMSG probably exerts the greatest control over the uptake and incorporation of [3H]glucosamine into the zona pellucida and oocyte of preantral follicles.	[3h]glucosamine	45-60	hypertrichosis 2 (generalised, congenital)	Homo sapiens	172-175
3430461-5	1987	After both short and longer term exposure to [3H]glucosamine, the maximum uptake of label in preantral follicles occurred 4-8 h after the injection of hCG, indicating that hCG rather than PMSG probably exerts the greatest control over the uptake and incorporation of [3H]glucosamine into the zona pellucida and oocyte of preantral follicles.	[3h]glucosamine	267-282	hypertrichosis 2 (generalised, congenital)	Homo sapiens	151-154
3430461-5	1987	After both short and longer term exposure to [3H]glucosamine, the maximum uptake of label in preantral follicles occurred 4-8 h after the injection of hCG, indicating that hCG rather than PMSG probably exerts the greatest control over the uptake and incorporation of [3H]glucosamine into the zona pellucida and oocyte of preantral follicles.	[3h]glucosamine	267-282	hypertrichosis 2 (generalised, congenital)	Homo sapiens	172-175
3432304-2	1987	The inhibition of 13,14H2-PGF2-alpha formation and of ovulation induced by a proestrus were completely recovered by an injection of hCG (25 IU/rat) or LH-RH (500 ng/rat) at 15:00 on the same day.	13,14h2	18-25	hypertrichosis 2 (generalised, congenital)	Homo sapiens	132-135
3432304-2	1987	The inhibition of 13,14H2-PGF2-alpha formation and of ovulation induced by a proestrus were completely recovered by an injection of hCG (25 IU/rat) or LH-RH (500 ng/rat) at 15:00 on the same day.	Dinoprost	26-30	hypertrichosis 2 (generalised, congenital)	Homo sapiens	132-135
3116344-6	1987	for 9 days) were unable to modify the tamoxifen effect on the testicular function, while tamoxifen significantly inhibited the increase of the plasma levels of testosterone induced by the administration of moderate doses of hCG (1.5 i.u.	Tamoxifen	89-98	hypertrichosis 2 (generalised, congenital)	Homo sapiens	224-227
3116344-6	1987	for 9 days) were unable to modify the tamoxifen effect on the testicular function, while tamoxifen significantly inhibited the increase of the plasma levels of testosterone induced by the administration of moderate doses of hCG (1.5 i.u.	Testosterone	160-172	hypertrichosis 2 (generalised, congenital)	Homo sapiens	224-227
3116344-11	1987	It is concluded that a prolonged administration of tamoxifen in the rat has, besides an indirect effect resulting from a decrease of the LH levels, a direct inhibitory influence on the testicular testosterone formation, which can be reversed by high doses of hCG.	Tamoxifen	51-60	hypertrichosis 2 (generalised, congenital)	Homo sapiens	259-262
3116344-11	1987	It is concluded that a prolonged administration of tamoxifen in the rat has, besides an indirect effect resulting from a decrease of the LH levels, a direct inhibitory influence on the testicular testosterone formation, which can be reversed by high doses of hCG.	Luteinizing Hormone	137-139	hypertrichosis 2 (generalised, congenital)	Homo sapiens	259-262
3116344-11	1987	It is concluded that a prolonged administration of tamoxifen in the rat has, besides an indirect effect resulting from a decrease of the LH levels, a direct inhibitory influence on the testicular testosterone formation, which can be reversed by high doses of hCG.	Testosterone	196-208	hypertrichosis 2 (generalised, congenital)	Homo sapiens	259-262
2957229-1	1987	Interstitial cells from the testes of the Mongolian gerbil have been used to investigate the effects of serum proteins on testosterone production stimulated by hCG and steroidal precursors.	Testosterone	122-134	hypertrichosis 2 (generalised, congenital)	Homo sapiens	160-163
3666291-6	1987	Plasma testosterone concentration after hCG treatment was not affected by elimination of circulating polymorphonuclear (PMN) leucocytes.	Testosterone	7-19	hypertrichosis 2 (generalised, congenital)	Homo sapiens	40-43
3115021-4	1987	In all cases progesterone synthesis was markedly stimulated by human FSH (10 micrograms/l), human LH (10-100 micrograms/l), hCG (1000 IU/l), forskolin (1 mumol/l) or 8-Bromo-cAMP (1 mmol/l).	Progesterone	13-25	hypertrichosis 2 (generalised, congenital)	Homo sapiens	124-127
3115021-5	1987	In the presence of danazol (1 mg/l) the FSH-, LH- and hCG-stimulated progesterone synthesis was partially inhibited by 55 to 60%.	Danazol	19-26	hypertrichosis 2 (generalised, congenital)	Homo sapiens	54-57
3115021-5	1987	In the presence of danazol (1 mg/l) the FSH-, LH- and hCG-stimulated progesterone synthesis was partially inhibited by 55 to 60%.	Progesterone	69-81	hypertrichosis 2 (generalised, congenital)	Homo sapiens	54-57
3115021-8	1987	It was concluded that not only gonadotropin-stimulated steroid synthesis, as previously demonstrated for hCG, but also forskolin and 8-Bromo-cAMP-stimulated steroidogenesis is sensitive to danazol inhibition.	Steroids	55-62	hypertrichosis 2 (generalised, congenital)	Homo sapiens	105-108
3115021-8	1987	It was concluded that not only gonadotropin-stimulated steroid synthesis, as previously demonstrated for hCG, but also forskolin and 8-Bromo-cAMP-stimulated steroidogenesis is sensitive to danazol inhibition.	Danazol	189-196	hypertrichosis 2 (generalised, congenital)	Homo sapiens	105-108
3109886-10	1987	Results of these studies document unequivocally that the synthesis of prostaglandins that is increased by LH/hCG in rats preceding ovulation is associated with an increased PGS content, that induction of the induced enzyme is transient, and that the enzyme is primarily localized to granulosa cell membrane fractions.	Prostaglandins	70-84	hypertrichosis 2 (generalised, congenital)	Homo sapiens	109-112
3038377-7	1987	In addition, results for serum and urinary hCG correlated well when the latter was expressed in terms of creatinine excretion.	Creatinine	105-115	hypertrichosis 2 (generalised, congenital)	Homo sapiens	43-46
3109887-7	1987	These results suggest that the previously described decreases in CL plasma membrane fluidity and hCG binding in vitro during luteolysis are caused by a synergistic effect of calcium ion and hydrolysis products of phospholipase A activity.	Calcium	174-181	hypertrichosis 2 (generalised, congenital)	Homo sapiens	97-100
3110530-6	1987	5, 8, 11, 14 Eicosatetraynoic acid (ETYA), a general inhibitor of AA metabolism, and Nordihydroguaiaretic acid (NDGA), an inhibitor of the lipoxygenase pathway of AA metabolism, inhibited hCG induced T secretion while indomethacin, an inhibitor of cyclo-oxygenase pathway, had no effect on hCG induced T secretion.	5,8,11,14-Eicosatetraynoic Acid	0-34	hypertrichosis 2 (generalised, congenital)	Homo sapiens	188-191
3110530-0	1987	Arachidonic acid is involved in the regulation of hCG induced steroidogenesis in rat Leydig cells.	Arachidonic Acid	0-16	hypertrichosis 2 (generalised, congenital)	Homo sapiens	50-53
3110530-5	1987	AA also had a biphasic effect on hCG induced cyclic AMP secretion.	Cyclic AMP	45-55	hypertrichosis 2 (generalised, congenital)	Homo sapiens	33-36
3110530-6	1987	5, 8, 11, 14 Eicosatetraynoic acid (ETYA), a general inhibitor of AA metabolism, and Nordihydroguaiaretic acid (NDGA), an inhibitor of the lipoxygenase pathway of AA metabolism, inhibited hCG induced T secretion while indomethacin, an inhibitor of cyclo-oxygenase pathway, had no effect on hCG induced T secretion.	Masoprocol	85-110	hypertrichosis 2 (generalised, congenital)	Homo sapiens	188-191
2439507-5	1987	Initially, it transiently attenuates the increase in intracellular cAMP and steroid biosynthesis provoked by submaximal concentrations of hCG.	Cyclic AMP	67-71	hypertrichosis 2 (generalised, congenital)	Homo sapiens	138-141
2439507-5	1987	Initially, it transiently attenuates the increase in intracellular cAMP and steroid biosynthesis provoked by submaximal concentrations of hCG.	Steroids	76-83	hypertrichosis 2 (generalised, congenital)	Homo sapiens	138-141
2439507-6	1987	At later times, however, it potentiates the stimulatory effects of submaximal concentrations of hCG on steroid biosynthesis in a synergistic fashion.	Steroids	103-110	hypertrichosis 2 (generalised, congenital)	Homo sapiens	96-99
2439507-7	1987	Last, we show that mEGF and submaximal concentrations of cAMP analogues also activate steroidogenesis in a synergistic fashion and that the degree of synergism attained with cAMP analogues plus mEGF is much higher than that attained with hCG plus mEGF.	Cyclic AMP	57-61	hypertrichosis 2 (generalised, congenital)	Homo sapiens	238-241
3656290-0	1987	Terbutaline treatment inhibits the hCG-induced increase in venular permeability in the rat testis.	Terbutaline	0-11	hypertrichosis 2 (generalised, congenital)	Homo sapiens	35-38
3036468-3	1987	hCG treatment increased the formation of type I EPR spectra compared to that obtained with saline-treated controls, and pretreatment with cycloheximide (30 mg/kg BW) before hCG abolished this increase.	Sodium Chloride	91-97	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
3036468-5	1987	The type I EPR signal increased with doses of hCG and correlated well with the pregnenolone production.	Pregnenolone	79-91	hypertrichosis 2 (generalised, congenital)	Homo sapiens	46-49
3036468-7	1987	This suggests that the transport of cholesterol to inner mitochondrial membranes from outer membranes is regulated by hCG.	Cholesterol	36-47	hypertrichosis 2 (generalised, congenital)	Homo sapiens	118-121
2846722-0	1987	The effect of hCG on cyclic AMP in rabbit ciliary processes.	Cyclic AMP	21-31	hypertrichosis 2 (generalised, congenital)	Homo sapiens	14-17
2846722-7	1987	These results dispute the role of cyclic AMP as a mediator of the flow and pressure reducing effects of hCG; however, theoretical and methodological complications relating to this interpretation are discussed.	Cyclic AMP	34-44	hypertrichosis 2 (generalised, congenital)	Homo sapiens	104-107
3656290-3	1987	Carbon-labelling, interstitial fluid volume and leucocyte migration were all reduced in rats treated with hCG+ terbutaline compared to the values in animals given hCG only.	Carbon	0-6	hypertrichosis 2 (generalised, congenital)	Homo sapiens	106-109
3656290-3	1987	Carbon-labelling, interstitial fluid volume and leucocyte migration were all reduced in rats treated with hCG+ terbutaline compared to the values in animals given hCG only.	Terbutaline	111-122	hypertrichosis 2 (generalised, congenital)	Homo sapiens	106-109
3656290-3	1987	Carbon-labelling, interstitial fluid volume and leucocyte migration were all reduced in rats treated with hCG+ terbutaline compared to the values in animals given hCG only.	Terbutaline	111-122	hypertrichosis 2 (generalised, congenital)	Homo sapiens	163-166
3595995-1	1987	This study has evaluated whether the decrease in capacity of Leydig cells to secrete testosterone that occurs during culture or after desensitization with hCG in vivo, is a consequence of the removal of a stimulatory factor(s) in testicular interstitial fluid (IF) to which Leydig cells are normally exposed.	Testosterone	85-97	hypertrichosis 2 (generalised, congenital)	Homo sapiens	155-158
3622921-5	1987	After 3 days of culture, the media were collected, the cells washed and then stimulated with hCG (3 ng/ml) for 3 h. oPRL (1-1000 ng/ml) added at plating, caused a log dose-dependent inhibition of testosterone accumulation during the 3-day culture period; the highest and most consistent inhibition (31%) was with 500 ng/ml oPRL.	Testosterone	196-208	hypertrichosis 2 (generalised, congenital)	Homo sapiens	93-96
3604552-2	1987	Foetuses injected in utero with 52 micrograms/kg hCG had a prompt increase in intratesticular testosterone, demonstrating that the injected substance reached the foetal testis.	Testosterone	94-106	hypertrichosis 2 (generalised, congenital)	Homo sapiens	49-52
3604552-9	1987	Testes from foetuses injected with 52 micrograms/kg hCG 3 days earlier showed an increase in both basal and hCG-stimulated testosterone production during 3 h of incubation when compared with controls.	Testosterone	123-135	hypertrichosis 2 (generalised, congenital)	Homo sapiens	52-55
2824353-0	1987	Effect of PGF2 alpha &amp; cyclic AMP on production of hCG-stimulated progesterone by bovine luteal cells.	pgf2 alpha &amp	10-25	hypertrichosis 2 (generalised, congenital)	Homo sapiens	55-58
2824353-0	1987	Effect of PGF2 alpha &amp; cyclic AMP on production of hCG-stimulated progesterone by bovine luteal cells.	Cyclic AMP	27-37	hypertrichosis 2 (generalised, congenital)	Homo sapiens	55-58
2824353-0	1987	Effect of PGF2 alpha &amp; cyclic AMP on production of hCG-stimulated progesterone by bovine luteal cells.	Progesterone	70-82	hypertrichosis 2 (generalised, congenital)	Homo sapiens	55-58
3305094-1	1987	The LHRH, human chorionic gonadotropin (hCG) or testosterone affected the peripheral serotonin (5HT) concentration in the blood.	Serotonin	85-94	hypertrichosis 2 (generalised, congenital)	Homo sapiens	40-43
3305094-1	1987	The LHRH, human chorionic gonadotropin (hCG) or testosterone affected the peripheral serotonin (5HT) concentration in the blood.	Serotonin	96-99	hypertrichosis 2 (generalised, congenital)	Homo sapiens	40-43
3305094-2	1987	I. p. injection of LHRH or hCG resulted in an increase of testosterone and in a decrease of 5HT levels in the blood.	Testosterone	58-70	hypertrichosis 2 (generalised, congenital)	Homo sapiens	27-30
3305094-2	1987	I. p. injection of LHRH or hCG resulted in an increase of testosterone and in a decrease of 5HT levels in the blood.	Serotonin	92-95	hypertrichosis 2 (generalised, congenital)	Homo sapiens	27-30
3305094-5	1987	On the other hand, treatment of the castrated mice with hCG resulted in an increase of the blood 5HT concentration as wall.	Serotonin	97-100	hypertrichosis 2 (generalised, congenital)	Homo sapiens	56-59
3035053-5	1987	Bound LH/hCG was estimated by elution with acid-citrate buffer, followed by radioimmunoassay of released hormone.	acid-citrate	43-55	hypertrichosis 2 (generalised, congenital)	Homo sapiens	9-12
3595995-2	1987	When Percoll-purified rat Leydig cells were cultured for 3 days in vitro, there was a progressive reduction in their ability to respond to hCG in terms of either testosterone or progesterone production.	Testosterone	162-174	hypertrichosis 2 (generalised, congenital)	Homo sapiens	139-142
3595995-2	1987	When Percoll-purified rat Leydig cells were cultured for 3 days in vitro, there was a progressive reduction in their ability to respond to hCG in terms of either testosterone or progesterone production.	Progesterone	178-190	hypertrichosis 2 (generalised, congenital)	Homo sapiens	139-142
2955060-4	1987	After the combined dexamethasone suppression/hCG stimulation test, the plasma testosterone level rose from 9 ng/ml to 15.1 ng/ml.	Testosterone	78-90	hypertrichosis 2 (generalised, congenital)	Homo sapiens	45-48
3595995-5	1987	Crude Leydig cells from rats injected 24 h previously with 50 IU hCG showed a 70% reduction in their testosterone response to hCG in vitro and, compared to controls, increased testosterone production poorly in response to increasing concentrations of IF.	Testosterone	101-113	hypertrichosis 2 (generalised, congenital)	Homo sapiens	65-68
2955060-9	1987	In incubation of small specimens of tumor tissues in oxygenated Krebs bicarbonate buffer, the release of testosterone into the medium containing hCG was twice as high as that into the medium without hCG.	krebs	64-69	hypertrichosis 2 (generalised, congenital)	Homo sapiens	145-148
2955060-9	1987	In incubation of small specimens of tumor tissues in oxygenated Krebs bicarbonate buffer, the release of testosterone into the medium containing hCG was twice as high as that into the medium without hCG.	Bicarbonates	70-81	hypertrichosis 2 (generalised, congenital)	Homo sapiens	145-148
2955060-9	1987	In incubation of small specimens of tumor tissues in oxygenated Krebs bicarbonate buffer, the release of testosterone into the medium containing hCG was twice as high as that into the medium without hCG.	Testosterone	105-117	hypertrichosis 2 (generalised, congenital)	Homo sapiens	145-148
2955060-10	1987	These results of in vitro and in vivo studies suggest that this tumor was an hCG-dependent testosterone producing Sertoli-Leydig cell tumor.	Testosterone	91-103	hypertrichosis 2 (generalised, congenital)	Homo sapiens	77-80
3595995-5	1987	Crude Leydig cells from rats injected 24 h previously with 50 IU hCG showed a 70% reduction in their testosterone response to hCG in vitro and, compared to controls, increased testosterone production poorly in response to increasing concentrations of IF.	Testosterone	101-113	hypertrichosis 2 (generalised, congenital)	Homo sapiens	126-129
3595995-5	1987	Crude Leydig cells from rats injected 24 h previously with 50 IU hCG showed a 70% reduction in their testosterone response to hCG in vitro and, compared to controls, increased testosterone production poorly in response to increasing concentrations of IF.	Testosterone	176-188	hypertrichosis 2 (generalised, congenital)	Homo sapiens	65-68
3031049-3	1987	Binding sites for 125I-labeled human chorionic gonadotropin (hCG) were preferentially localized in the light cell fraction (apparent Kd = 2.02 X 10(-10) M; Bmax = 1.17 X 10(-5) nmol/2 X 10(6) cells).	Iodine-125	18-22	hypertrichosis 2 (generalised, congenital)	Homo sapiens	61-64
3111113-10	1987	The stimulation of the testosterone biosynthesis is achieved by application of hCG.	Testosterone	23-35	hypertrichosis 2 (generalised, congenital)	Homo sapiens	79-82
3593836-4	1987	injection of hCG at 1600 h on Day 0, 92% of hydroxyflutamide-treated rats ovulated a mean of 8.3 +/- 1.2 oocytes compared to 100% of controls, which ovulated 7.3 +/- 0.4 oocytes per rat: these groups were not significantly different from each other, nor from control rats that received no hCG.	hydroxyflutamide	44-60	hypertrichosis 2 (generalised, congenital)	Homo sapiens	13-16
3593836-4	1987	injection of hCG at 1600 h on Day 0, 92% of hydroxyflutamide-treated rats ovulated a mean of 8.3 +/- 1.2 oocytes compared to 100% of controls, which ovulated 7.3 +/- 0.4 oocytes per rat: these groups were not significantly different from each other, nor from control rats that received no hCG.	hydroxyflutamide	44-60	hypertrichosis 2 (generalised, congenital)	Homo sapiens	289-292
3593836-5	1987	Thus, exogenous hCG completely overcame the inhibitory effect of hydroxyflutamide on ovulation.	hydroxyflutamide	65-81	hypertrichosis 2 (generalised, congenital)	Homo sapiens	16-19
3031049-6	1987	The binding data from this fraction did not obey saturation kinetics, but testosterone levels were elevated 700-800% in the presence of hCG (i.e. basal value 0.22 +/- 0.00 ng/2 X 10(6) cells versus 1.81 +/- 0.04 ng/2 X 10(6) cells in hCG-stimulated cells).	Testosterone	74-86	hypertrichosis 2 (generalised, congenital)	Homo sapiens	136-139
3031050-7	1987	Preferential localization of gonadotropin binding sites was demonstrated on light cells, and the heavier cells produced testosterone in response to hCG without occupancy of high affinity (Kd = 2.02 X 10(-10) M) binding sites.	Testosterone	120-132	hypertrichosis 2 (generalised, congenital)	Homo sapiens	148-151
3295100-4	1987	On its own, LHRH-A stimulated testosterone production by Leydig cells for up to 24 h in culture but inhibited testosterone production stimulated by human chorionic gonadotrophin (hCG) between 24 and 72 h of culture.	Testosterone	110-122	hypertrichosis 2 (generalised, congenital)	Homo sapiens	179-182
3030703-2	1987	Both cholera toxin (CT), which activates adenylate cyclase, and 12-O-tetradecanoyl phorbol-13-acetate (TPA), a protein kinase C activator, stimulated the secretion of hCG in a dose-dependent manner.	Tetradecanoylphorbol Acetate	64-101	hypertrichosis 2 (generalised, congenital)	Homo sapiens	167-170
3030703-2	1987	Both cholera toxin (CT), which activates adenylate cyclase, and 12-O-tetradecanoyl phorbol-13-acetate (TPA), a protein kinase C activator, stimulated the secretion of hCG in a dose-dependent manner.	Tetradecanoylphorbol Acetate	103-106	hypertrichosis 2 (generalised, congenital)	Homo sapiens	167-170
3030703-4	1987	When added together, TPA potentiated the effect of CT on hCG secretion (from 16- to 27-fold) and cAMP accumulation (from 36- to 54-fold) in the medium.	Tetradecanoylphorbol Acetate	21-24	hypertrichosis 2 (generalised, congenital)	Homo sapiens	57-60
3030703-5	1987	TPA (1.0 ng/ml) also caused a 2.0-fold increase in basal cAMP production after 72 h. Time-course studies indicated that the effect of TPA on CT-induced cAMP and hCG productions became significant at 45 min and 6 h, respectively, from the beginning of stimulation.	Tetradecanoylphorbol Acetate	0-3	hypertrichosis 2 (generalised, congenital)	Homo sapiens	161-164
3030703-5	1987	TPA (1.0 ng/ml) also caused a 2.0-fold increase in basal cAMP production after 72 h. Time-course studies indicated that the effect of TPA on CT-induced cAMP and hCG productions became significant at 45 min and 6 h, respectively, from the beginning of stimulation.	Tetradecanoylphorbol Acetate	134-137	hypertrichosis 2 (generalised, congenital)	Homo sapiens	161-164
3030703-7	1987	Our results demonstrate that TPA potentiates CT-induced cAMP and hCG production in cultured human choriocarcinoma cells.	Tetradecanoylphorbol Acetate	29-32	hypertrichosis 2 (generalised, congenital)	Homo sapiens	65-68
3295100-7	1987	On its own, vasopressin stimulated testosterone production for up to 5 h of culture, but not thereafter, while in the presence of hCG, vasopressin inhibited testosterone production beyond 24 h of culture.	Testosterone	157-169	hypertrichosis 2 (generalised, congenital)	Homo sapiens	130-133
3585105-6	1987	Catecholamine-stimulated activity was significantly low and prostaglandin-stimulated activity was significantly high in rabbit endometrium after hCG treatment.	Catecholamines	0-13	hypertrichosis 2 (generalised, congenital)	Homo sapiens	145-148
3585105-6	1987	Catecholamine-stimulated activity was significantly low and prostaglandin-stimulated activity was significantly high in rabbit endometrium after hCG treatment.	Prostaglandins	60-73	hypertrichosis 2 (generalised, congenital)	Homo sapiens	145-148
3455047-6	1987	However, actinomycin D and cycloheximide prevented the effect of hCG.	Dactinomycin	9-22	hypertrichosis 2 (generalised, congenital)	Homo sapiens	65-68
3455047-6	1987	However, actinomycin D and cycloheximide prevented the effect of hCG.	Cycloheximide	27-40	hypertrichosis 2 (generalised, congenital)	Homo sapiens	65-68
3559332-4	1987	The serum estradiol level rose with hCG, and fell with oPRL.	Estradiol	10-19	hypertrichosis 2 (generalised, congenital)	Homo sapiens	36-39
3595728-5	1987	Emetine, cycloheximide and puromycin inhibited both basal and hCG stimulated protein synthesis as well as progesterone production in the cells.	Emetine	0-7	hypertrichosis 2 (generalised, congenital)	Homo sapiens	62-65
3595728-5	1987	Emetine, cycloheximide and puromycin inhibited both basal and hCG stimulated protein synthesis as well as progesterone production in the cells.	Cycloheximide	9-22	hypertrichosis 2 (generalised, congenital)	Homo sapiens	62-65
3595728-5	1987	Emetine, cycloheximide and puromycin inhibited both basal and hCG stimulated protein synthesis as well as progesterone production in the cells.	Puromycin	27-36	hypertrichosis 2 (generalised, congenital)	Homo sapiens	62-65
3033232-0	1987	Inhibition of ovulation in PMSG/hCG-treated immature rats by rotenone, a specific inhibitor of mitochondrial oxidation.	Rotenone	61-69	hypertrichosis 2 (generalised, congenital)	Homo sapiens	32-35
3027492-2	1987	Decapsulated testes from adult rats showed a significant increase in the basal and hCG-stimulated testosterone secretion into the medium in response to 10(-5) M, 10(-6) M, and 10(-7) M Ro5-4864.	Testosterone	98-110	hypertrichosis 2 (generalised, congenital)	Homo sapiens	83-86
3027492-4	1987	When we evaluated the effect of GABA on "in vitro" androgen production at different stages of gonadal maturation we observed that the highest concentration of GABA (10(-6) M) was able to modify the basal and hCG-stimulated androgen production from adult (60 days) and pubertal (45 days) testes.	gamma-Aminobutyric Acid	159-163	hypertrichosis 2 (generalised, congenital)	Homo sapiens	208-211
3027492-5	1987	In addition, when prepubertal testes (31 days) were incubated under basal conditions, 10(-6) M GABA induced a significant increment of androstanediol production, while the stimulatory effect of hCG was reduced in the presence of the same GABA concentration.	gamma-Aminobutyric Acid	95-99	hypertrichosis 2 (generalised, congenital)	Homo sapiens	194-197
3027492-5	1987	In addition, when prepubertal testes (31 days) were incubated under basal conditions, 10(-6) M GABA induced a significant increment of androstanediol production, while the stimulatory effect of hCG was reduced in the presence of the same GABA concentration.	gamma-Aminobutyric Acid	238-242	hypertrichosis 2 (generalised, congenital)	Homo sapiens	194-197
3028794-3	1987	The stimulatory effects of human choriogonadotropin (hCG; 1 nM) on both cAMP and testosterone productions were inhibited by short-term incubation with these drugs.	Cyclic AMP	72-76	hypertrichosis 2 (generalised, congenital)	Homo sapiens	53-56
3028794-3	1987	The stimulatory effects of human choriogonadotropin (hCG; 1 nM) on both cAMP and testosterone productions were inhibited by short-term incubation with these drugs.	Testosterone	81-93	hypertrichosis 2 (generalised, congenital)	Homo sapiens	53-56
3028794-5	1987	The inhibitory effects of PMA on hCG stimulation of both cAMP and testosterone were due mainly to a decrease of the Vmax without modification of the ED50.	Tetradecanoylphorbol Acetate	26-29	hypertrichosis 2 (generalised, congenital)	Homo sapiens	33-36
3028794-5	1987	The inhibitory effects of PMA on hCG stimulation of both cAMP and testosterone were due mainly to a decrease of the Vmax without modification of the ED50.	Cyclic AMP	57-61	hypertrichosis 2 (generalised, congenital)	Homo sapiens	33-36
3028794-5	1987	The inhibitory effects of PMA on hCG stimulation of both cAMP and testosterone were due mainly to a decrease of the Vmax without modification of the ED50.	Testosterone	66-78	hypertrichosis 2 (generalised, congenital)	Homo sapiens	33-36
3028794-7	1987	Pretreatment of Leydig cells with the three drugs for 24 h induced more pronounced modifications, such as a reduction in the number of hCG binding sites and a decreased responsiveness to hCG and forskolin, the testosterone production being drastically reduced.	Testosterone	210-222	hypertrichosis 2 (generalised, congenital)	Homo sapiens	187-190
3028794-8	1987	The effects of PMA were dose- and time-dependent; however, the concentration of PMA required to induce half-maximal effects on hCG receptors (10 nM) was about one order of magnitude higher than those required to reduce cAMP and testosterone productions.	Tetradecanoylphorbol Acetate	15-18	hypertrichosis 2 (generalised, congenital)	Homo sapiens	127-130
3028794-8	1987	The effects of PMA were dose- and time-dependent; however, the concentration of PMA required to induce half-maximal effects on hCG receptors (10 nM) was about one order of magnitude higher than those required to reduce cAMP and testosterone productions.	Testosterone	228-240	hypertrichosis 2 (generalised, congenital)	Homo sapiens	127-130
3028794-9	1987	Further, the inhibitory effects on cAMP and testosterone secretions appeared within the first 3 h, whereas the hCG receptor number remained constant for at least 8 h. It appears therefore, that the main alteration responsible for the steroidogenic refractoriness of PMA-treated Leydig cells is located beyond cAMP formation.	Tetradecanoylphorbol Acetate	266-269	hypertrichosis 2 (generalised, congenital)	Homo sapiens	111-114
3028794-12	1987	Since cycloheximide blocked the effects of PMA on hCG down-regulation, it is likely that the phorbol esters and 1-oleoyl-2-acetyl-sn-glycerol induce the synthesis of some proteins which blocked the recycling of internalized receptors.	Cycloheximide	6-19	hypertrichosis 2 (generalised, congenital)	Homo sapiens	50-53
3028794-12	1987	Since cycloheximide blocked the effects of PMA on hCG down-regulation, it is likely that the phorbol esters and 1-oleoyl-2-acetyl-sn-glycerol induce the synthesis of some proteins which blocked the recycling of internalized receptors.	Phorbol Esters	93-107	hypertrichosis 2 (generalised, congenital)	Homo sapiens	50-53
3028794-12	1987	Since cycloheximide blocked the effects of PMA on hCG down-regulation, it is likely that the phorbol esters and 1-oleoyl-2-acetyl-sn-glycerol induce the synthesis of some proteins which blocked the recycling of internalized receptors.	1-oleoyl-2-acetylglycerol	112-141	hypertrichosis 2 (generalised, congenital)	Homo sapiens	50-53
3560940-0	1987	Comparison of saliva and plasma 17-hydroxyprogesterone time-course response to hCG administration in normal men.	17-alpha-Hydroxyprogesterone	32-54	hypertrichosis 2 (generalised, congenital)	Homo sapiens	79-82
2440666-14	1987	Plasma testosterone levels fluctuated in parallel with the change in plasma hCG levels.	Testosterone	7-19	hypertrichosis 2 (generalised, congenital)	Homo sapiens	76-79
3560940-1	1987	17-Hydroxyprogesterone (17-OHP) time-course response to hCG (5000 IU) was studied simultaneously in the saliva and the plasma of 12 adult healthy men.	17-alpha-Hydroxyprogesterone	0-22	hypertrichosis 2 (generalised, congenital)	Homo sapiens	56-59
3560940-1	1987	17-Hydroxyprogesterone (17-OHP) time-course response to hCG (5000 IU) was studied simultaneously in the saliva and the plasma of 12 adult healthy men.	17-alpha-Hydroxyprogesterone	24-30	hypertrichosis 2 (generalised, congenital)	Homo sapiens	56-59
3480050-1	1987	Quantitation by flow cytofluorometry of the distribution of human choriogonadotropin (hCG)-like material on the surface of various human and mouse tumor cells grown in tissue culture and as solid tumors has been done using fluorescein-tagged rabbit antisera (IgG fraction) to intact hCG and, in one experiment, by use of two monoclonal antibodies specific for hCG.	Fluorescein	223-234	hypertrichosis 2 (generalised, congenital)	Homo sapiens	86-89
3101068-1	1987	This study was undertaken to examine ovarian steroid production during the early stages of hCG-induced ovarian cyst formation in the hypothyroid rat.	Steroids	45-52	hypertrichosis 2 (generalised, congenital)	Homo sapiens	91-94
3101068-6	1987	However, ovaries from hypothyroid, hCG-treated rats secreted significantly more testosterone and estradiol than ovaries from vehicle-treated, hypothyroid rats and euthyroid, hCG-treated rats.	Testosterone	80-92	hypertrichosis 2 (generalised, congenital)	Homo sapiens	35-38
3101068-6	1987	However, ovaries from hypothyroid, hCG-treated rats secreted significantly more testosterone and estradiol than ovaries from vehicle-treated, hypothyroid rats and euthyroid, hCG-treated rats.	Estradiol	97-106	hypertrichosis 2 (generalised, congenital)	Homo sapiens	35-38
3101068-9	1987	In contrast, FSH significantly enhanced testosterone and estradiol secretion by ovaries from hypothyroid, hCG-treated rats.	Testosterone	40-52	hypertrichosis 2 (generalised, congenital)	Homo sapiens	106-109
3101068-10	1987	These results support the hypothesis that increased levels of testosterone and estradiol secretion have a central role in the induction of polycystic ovaries by hCG in the hypothyroid rat.	Testosterone	62-74	hypertrichosis 2 (generalised, congenital)	Homo sapiens	161-164
3122524-7	1987	Serum testosterone significantly increased from 6 to 72 hours following a 200 IU hCG injection.	Testosterone	6-18	hypertrichosis 2 (generalised, congenital)	Homo sapiens	81-84
3780557-12	1987	Ten micrograms of NIH-LH-B9, tested at day 6 of pseudopregnancy, mimicked the effect of hCG.	nih-lh-b9	18-27	hypertrichosis 2 (generalised, congenital)	Homo sapiens	88-91
3609909-4	1987	Hexoprenaline or hCG dose-dependently increased the progesterone production of rat luteal cells and of human cells in mid- and late luteal phase.	Progesterone	52-64	hypertrichosis 2 (generalised, congenital)	Homo sapiens	17-20
2887347-8	1987	After hCG injection, the testosterone response of chronic ULO ram lambs was approx.	Testosterone	25-37	hypertrichosis 2 (generalised, congenital)	Homo sapiens	6-9
3609909-5	1987	Moreover, hexoprenaline further increased the hCG-induced hormone production.	Hexoprenaline	10-23	hypertrichosis 2 (generalised, congenital)	Homo sapiens	46-49
2881817-12	1987	On the other hand, when incubated with hCG, TPA inhibited both cAMP and testosterone production; the ED50s of hCG stimulation increased 4- to 10-fold with both parameters.	Tetradecanoylphorbol Acetate	44-47	hypertrichosis 2 (generalised, congenital)	Homo sapiens	39-42
3820165-7	1987	In hCG-treated animals leucocytes were found adhering to the endothelium in post-capillary venules and in these venular segments dextran was leaking into the interstitium.	Dextrans	129-136	hypertrichosis 2 (generalised, congenital)	Homo sapiens	3-6
3820165-8	1987	Carbon particles were deposited in the walls of post-capillary venules and leucocytes migrated through open interendothelial cell gaps in hCG-treated animals.	Carbon	0-6	hypertrichosis 2 (generalised, congenital)	Homo sapiens	138-141
2881817-12	1987	On the other hand, when incubated with hCG, TPA inhibited both cAMP and testosterone production; the ED50s of hCG stimulation increased 4- to 10-fold with both parameters.	Tetradecanoylphorbol Acetate	44-47	hypertrichosis 2 (generalised, congenital)	Homo sapiens	110-113
2881817-12	1987	On the other hand, when incubated with hCG, TPA inhibited both cAMP and testosterone production; the ED50s of hCG stimulation increased 4- to 10-fold with both parameters.	Cyclic AMP	63-67	hypertrichosis 2 (generalised, congenital)	Homo sapiens	39-42
2881817-12	1987	On the other hand, when incubated with hCG, TPA inhibited both cAMP and testosterone production; the ED50s of hCG stimulation increased 4- to 10-fold with both parameters.	Testosterone	72-84	hypertrichosis 2 (generalised, congenital)	Homo sapiens	39-42
2879749-8	1986	In the hCG/IM/PGF2 alpha-treated ovulatory rabbits (Group 6), PH activity recovered to nearly the level of the hCG-treated rabbits (Group 2).	Dinoprost	14-18	hypertrichosis 2 (generalised, congenital)	Homo sapiens	7-10
16726235-0	1986	Fertility of dairy cattle treated with human chorionic gonadotropin (hCG) to stimulate progesterone secretion.	Progesterone	87-99	hypertrichosis 2 (generalised, congenital)	Homo sapiens	69-72
2879749-9	1986	By addition of PGE2, ovulation did not recover but PH activity was restored to about 70% of the hCG-treated rabbits.	Dinoprostone	15-19	hypertrichosis 2 (generalised, congenital)	Homo sapiens	96-99
3017932-2	1986	In addition, when added at lower doses that did not affect cAMP generation and testosterone responses (100 nM), forskolin caused an increase in sensitivity to hormonal stimulation for all cAMP pools (extracellular, intracellular, and receptor-bound) and a 70% reduction in the ED50 for human chorionic gonadotropin (hCG) stimulation of testosterone production.	Colforsin	112-121	hypertrichosis 2 (generalised, congenital)	Homo sapiens	316-319
3790657-1	1986	The daily administration of human chorionic gonadotropin (hCG) to rats with thiouracil-induced hypothyroidism results in the development of cystic ovaries.	Thiouracil	76-86	hypertrichosis 2 (generalised, congenital)	Homo sapiens	58-61
3017932-5	1986	Such inhibitory actions of low-dose forskolin were prevented by preincubation of Leydig cells with pertussis toxin before addition of forskolin and/or hCG.	Colforsin	36-45	hypertrichosis 2 (generalised, congenital)	Homo sapiens	151-154
3761277-5	1986	Autoradiography of 125I-labelled hCG binding to interstitial cell suspensions at the two ages showed that the gonadotrophin binding per Leydig cell was about 50% lower in the neonatal testis.	Iodine-125	19-23	hypertrichosis 2 (generalised, congenital)	Homo sapiens	33-36
2944979-4	1986	Exposure to ether stress induced a 100% increase in serum prolactin values in androgenized rats with increased serum progesterone levels 4 days after the induction of ovulation and the luteal phase with human chorionic gonadotropin (hCG).	Ether	12-17	hypertrichosis 2 (generalised, congenital)	Homo sapiens	233-236
3013891-3	1986	A novel scheme based on reverse immunoaffinity chromatography using immobilized antibodies to membrane proteins from receptor down-regulated ovary and subsequent two-step affinity purification on hCG-Sepharose was used to isolate homogeneous receptor.	Sepharose	200-209	hypertrichosis 2 (generalised, congenital)	Homo sapiens	196-199
3732138-5	1986	In contrast, treatment with 12.5 IU hCG, although increasing intratesticular testosterone to about 50% of the maximal value, did not increase the volume of IF, and no leukocytes appeared in the interstitial space.	Testosterone	77-89	hypertrichosis 2 (generalised, congenital)	Homo sapiens	36-39
3089339-3	1986	In cells from adult animals, treatment with human chorionic gonadotropin (hCG) (10 ng/ml) significantly increased testosterone and progesterone production relative to their respective controls.	Testosterone	114-126	hypertrichosis 2 (generalised, congenital)	Homo sapiens	74-77
3089339-8	1986	In contrast to the biphasic effect of PRL on production of androgen, PRL treatment enhanced hCG-stimulated production of progesterone in a dose-related manner without exerting an inhibitory effect.	Progesterone	121-133	hypertrichosis 2 (generalised, congenital)	Homo sapiens	92-95
3089339-3	1986	In cells from adult animals, treatment with human chorionic gonadotropin (hCG) (10 ng/ml) significantly increased testosterone and progesterone production relative to their respective controls.	Progesterone	131-143	hypertrichosis 2 (generalised, congenital)	Homo sapiens	74-77
3089339-10	1986	Similarly, in the presence of inhibitors of pregnenolone metabolism, rPRL also enhanced hCG-stimulated production of pregnenolone.	Pregnenolone	44-56	hypertrichosis 2 (generalised, congenital)	Homo sapiens	88-91
3089339-5	1986	Upon addition of 0.1-3 ng/ml of either rPRL or oPRL to the hCG-treated cultures, testosterone production was progressively increased up to a maximum of 70% greater than with hCG alone.	Testosterone	81-93	hypertrichosis 2 (generalised, congenital)	Homo sapiens	59-62
3089339-10	1986	Similarly, in the presence of inhibitors of pregnenolone metabolism, rPRL also enhanced hCG-stimulated production of pregnenolone.	Pregnenolone	117-129	hypertrichosis 2 (generalised, congenital)	Homo sapiens	88-91
3089339-5	1986	Upon addition of 0.1-3 ng/ml of either rPRL or oPRL to the hCG-treated cultures, testosterone production was progressively increased up to a maximum of 70% greater than with hCG alone.	Testosterone	81-93	hypertrichosis 2 (generalised, congenital)	Homo sapiens	174-177
3740485-4	1986	A 2 h administration of hCG (10 mUI/ml) induced a rapid increase in testosterone output while aminoglutethimide (100 microM) decreased it.	Testosterone	68-80	hypertrichosis 2 (generalised, congenital)	Homo sapiens	24-27
3091237-3	1986	hMG in conjunction with clomiphene citrate did not suppress the endogenous LH surge but enhanced the oestradiol levels in the 2 days prior to hCG administration and/or the onset of the LH surge.	hmg	0-3	hypertrichosis 2 (generalised, congenital)	Homo sapiens	142-145
3091237-3	1986	hMG in conjunction with clomiphene citrate did not suppress the endogenous LH surge but enhanced the oestradiol levels in the 2 days prior to hCG administration and/or the onset of the LH surge.	Clomiphene	24-42	hypertrichosis 2 (generalised, congenital)	Homo sapiens	142-145
2874021-3	1986	If only the testosterone concentration in the pre-hCG blood sample was used, this percentage rose to 14 per cent.	Testosterone	12-24	hypertrichosis 2 (generalised, congenital)	Homo sapiens	50-53
3009140-8	1986	Cells grown in serum-free medium on ECM-coated dishes preserved only 50% of LH/hCG receptors and cAMP responsiveness after 48 h. Cells cultured on ECM showed a marked elevation in progesterone production even in the absence of gonadotropin stimulation, whereas cells grown on uncoated dishes almost completely lost their ability to produce progesterone both in the presence and absence of hCG.	Progesterone	180-192	hypertrichosis 2 (generalised, congenital)	Homo sapiens	389-392
3009140-7	1986	Cells grown on ECM had a parallel increase in cAMP responsiveness to hCG stimulation.	Cyclic AMP	46-50	hypertrichosis 2 (generalised, congenital)	Homo sapiens	69-72
2873120-5	1986	When testosterone levels in interstitial fluid were decreased by 75 to 99% either acutely (5-72 hours) or chronically (20-75 days), there was an accompanying increase (P less than 0.001) in the levels of the interstitial fluid factor(s), as determined by the ability of charcoal-stripped interstitial fluid from individual rats to enhance hCG-stimulated testosterone production by Percoll-purified Leydig cells in vitro.	Testosterone	5-17	hypertrichosis 2 (generalised, congenital)	Homo sapiens	339-342
3009152-1	1986	Our previous studies have indicated specificity cross-over between LH/hCG and the TSH receptor.	Luteinizing Hormone	67-69	hypertrichosis 2 (generalised, congenital)	Homo sapiens	70-73
3009152-4	1986	The effect of 10 ug hCG-CR121 was equivalent to 500 +/- 43 (mean +/- SEM) uIU of human TSH (2nd IRP, 80/558) with reference to growth stimulation, as judged by 72-h [3H]-thymidine uptake and to approximately 15 +/- 35 uIU human TSH with reference to receptor activation as judged by cyclic AMP accumulation.	deanol aceglutamate	24-29	hypertrichosis 2 (generalised, congenital)	Homo sapiens	20-23
3459888-0	1986	Changes in the concentration of prostaglandins in preovulatory human follicles after administration of hCG.	Prostaglandins	32-46	hypertrichosis 2 (generalised, congenital)	Homo sapiens	103-106
3709960-7	1986	Denaturation of the fluid or addition of serine protease inhibitor (p-aminobenzamidine) to the fluid prevented the effect of hCG.	4-aminobenzamidine	68-86	hypertrichosis 2 (generalised, congenital)	Homo sapiens	125-128
3724139-0	1986	Saliva testosterone time-course response to hCG in adult normal men.	Testosterone	7-19	hypertrichosis 2 (generalised, congenital)	Homo sapiens	44-47
3724139-2	1986	Testosterone time-course response to 5000 IU hCG was studied simultaneously in the saliva and the plasma of 13 adult normal men.	Testosterone	0-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	45-48
3709960-8	1986	Treatment of the hCG-activated fluid with anti-hCG gamma-globulin Sepharose did not abolish the permeability effect of the fluid.	Sepharose	66-75	hypertrichosis 2 (generalised, congenital)	Homo sapiens	17-20
3005352-2	1986	Estradiol production declined by 70% during the first 48 h in culture and was minimally stimulated by the addition of hCG to the culture medium.	Estradiol	0-9	hypertrichosis 2 (generalised, congenital)	Homo sapiens	118-121
3005352-3	1986	During subsequent culture from 48-120 h estradiol production was significantly increased over control levels by hCG concentrations greater than 0.1 IU/ml.	Estradiol	40-49	hypertrichosis 2 (generalised, congenital)	Homo sapiens	112-115
3005352-5	1986	hCG (0.01-10 IU/ml) stimulated a 3- to 13-fold increase in progesterone production.	Progesterone	59-71	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
3005352-6	1986	However, at hCG concentrations greater than 1 IU/ml, coincubation with testosterone (10(-7) M) significantly inhibited progesterone production.	Testosterone	71-83	hypertrichosis 2 (generalised, congenital)	Homo sapiens	12-15
3005352-6	1986	However, at hCG concentrations greater than 1 IU/ml, coincubation with testosterone (10(-7) M) significantly inhibited progesterone production.	Progesterone	119-131	hypertrichosis 2 (generalised, congenital)	Homo sapiens	12-15
3005352-9	1986	Glycine buffer wash was shown to reversibly remove more than 88% of bound hCG and, in freshly isolated cells, increased [125I]hCG binding by 100%.	Glycine	0-7	hypertrichosis 2 (generalised, congenital)	Homo sapiens	74-77
3005352-9	1986	Glycine buffer wash was shown to reversibly remove more than 88% of bound hCG and, in freshly isolated cells, increased [125I]hCG binding by 100%.	Glycine	0-7	hypertrichosis 2 (generalised, congenital)	Homo sapiens	126-129
3005352-11	1986	At the highest concentration of hCG (5 IU/ml), testosterone (10(-7) M) significantly inhibited the amount of [125I]hCG specifically bound.	Testosterone	47-59	hypertrichosis 2 (generalised, congenital)	Homo sapiens	32-35
3005352-11	1986	At the highest concentration of hCG (5 IU/ml), testosterone (10(-7) M) significantly inhibited the amount of [125I]hCG specifically bound.	Testosterone	47-59	hypertrichosis 2 (generalised, congenital)	Homo sapiens	115-118
3005352-13	1986	In addition, the presence of testosterone (10(-7) M) antagonizes hCG-stimulated progesterone and LH receptor production by these cells.	Testosterone	29-41	hypertrichosis 2 (generalised, congenital)	Homo sapiens	65-68
3005352-13	1986	In addition, the presence of testosterone (10(-7) M) antagonizes hCG-stimulated progesterone and LH receptor production by these cells.	Progesterone	80-92	hypertrichosis 2 (generalised, congenital)	Homo sapiens	65-68
3007125-5	1986	The extent of receptor loss in cells treated with increasing concentrations of hCG was highly correlated with their capacity to stimulate cAMP production.	Cyclic AMP	138-142	hypertrichosis 2 (generalised, congenital)	Homo sapiens	79-82
3007125-11	1986	Cycloheximide and actinomycin D inhibit hCG-mediated and 8-BrcAMP-mediated down-regulation.	Cycloheximide	0-13	hypertrichosis 2 (generalised, congenital)	Homo sapiens	40-43
3007125-11	1986	Cycloheximide and actinomycin D inhibit hCG-mediated and 8-BrcAMP-mediated down-regulation.	Dactinomycin	18-31	hypertrichosis 2 (generalised, congenital)	Homo sapiens	40-43
2938420-5	1986	Four, 8 and 16 h after an s.c. injection of 200 IU hCG the blood flow was continuous and there was leakage of dextran-150 from the microvessels to the interstitial tissue.	dextran-150	110-121	hypertrichosis 2 (generalised, congenital)	Homo sapiens	51-54
3958520-8	1986	The cholesterol content in a 10 day LPPS culture with hCG had a tendency to be lower than that in a 10 day LPPS culture, but there was no statistical difference (p less than 0.1).	Cholesterol	4-15	hypertrichosis 2 (generalised, congenital)	Homo sapiens	54-57
3951333-2	1986	Fractions corresponding to 27-28000 mol wt of the thymus extract diminish the testosterone secretion of Leydig cells stimulated with hCG.	Testosterone	78-90	hypertrichosis 2 (generalised, congenital)	Homo sapiens	133-136
3701705-9	1986	We conclude that entry of LH into antral follicles is restricted and that exposure to an ovulatory dose of hCG results in greater amounts of LH entering preovulatory follicles.	Luteinizing Hormone	26-28	hypertrichosis 2 (generalised, congenital)	Homo sapiens	107-110
3701705-9	1986	We conclude that entry of LH into antral follicles is restricted and that exposure to an ovulatory dose of hCG results in greater amounts of LH entering preovulatory follicles.	Luteinizing Hormone	141-143	hypertrichosis 2 (generalised, congenital)	Homo sapiens	107-110
3958520-11	1986	It was estimated from the results of the present study that hCG enhanced utilization of intracellular cholesterol.	Cholesterol	102-113	hypertrichosis 2 (generalised, congenital)	Homo sapiens	60-63
3014802-4	1986	Granulosa and thecal cells from control and CC-induced follicles all responded to hCG in vitro with increased formation of cAMP.	Cyclic AMP	123-127	hypertrichosis 2 (generalised, congenital)	Homo sapiens	82-85
3093007-3	1986	The concentrate was then specifically retained on an affinity gel with human choriogonadotropin (hCG) covalently grafted by its sugar moiety.	Sugars	128-133	hypertrichosis 2 (generalised, congenital)	Homo sapiens	97-100
3604700-3	1986	Since testicular and epididymal concentrations of testosterone increased after hCG, as expected, the effect might have been mediated by gonadotrophin stimulated testosterone production in Leydig cells.	Testosterone	50-62	hypertrichosis 2 (generalised, congenital)	Homo sapiens	79-82
3604700-3	1986	Since testicular and epididymal concentrations of testosterone increased after hCG, as expected, the effect might have been mediated by gonadotrophin stimulated testosterone production in Leydig cells.	Testosterone	161-173	hypertrichosis 2 (generalised, congenital)	Homo sapiens	79-82
3604700-4	1986	To test this hypothesis, the hCG effect was studied in rats that previously had received aminoglutethimide to block steroidogenesis.	Aminoglutethimide	89-106	hypertrichosis 2 (generalised, congenital)	Homo sapiens	29-32
3093007-5	1986	Prior to coupling, the subunits of hCG were crosslinked with 1-ethyl-3-(dimethylamino propyl) carbodiimide and the sialic acid residues were subjected to periodate oxidation to yield aldehyde groups which could react with the hydrazides of the gel.	Aldehydes	183-191	hypertrichosis 2 (generalised, congenital)	Homo sapiens	35-38
3093007-5	1986	Prior to coupling, the subunits of hCG were crosslinked with 1-ethyl-3-(dimethylamino propyl) carbodiimide and the sialic acid residues were subjected to periodate oxidation to yield aldehyde groups which could react with the hydrazides of the gel.	Isoniazid	226-236	hypertrichosis 2 (generalised, congenital)	Homo sapiens	35-38
3093007-5	1986	Prior to coupling, the subunits of hCG were crosslinked with 1-ethyl-3-(dimethylamino propyl) carbodiimide and the sialic acid residues were subjected to periodate oxidation to yield aldehyde groups which could react with the hydrazides of the gel.	Ethyldimethylaminopropyl Carbodiimide	61-106	hypertrichosis 2 (generalised, congenital)	Homo sapiens	35-38
3093007-5	1986	Prior to coupling, the subunits of hCG were crosslinked with 1-ethyl-3-(dimethylamino propyl) carbodiimide and the sialic acid residues were subjected to periodate oxidation to yield aldehyde groups which could react with the hydrazides of the gel.	N-Acetylneuraminic Acid	115-126	hypertrichosis 2 (generalised, congenital)	Homo sapiens	35-38
3003355-0	1986	Study using in-vivo binding of 125I-labelled hCG, light and electron microscopy of the repopulation of rat Leydig cells after destruction due to administration of ethylene-1,2-dimethanesulphonate.	Iodine-125	31-35	hypertrichosis 2 (generalised, congenital)	Homo sapiens	45-48
3084372-5	1986	Plasma testosterone was elevated 24 h after hCG injection in all types of mice studied, but the increase in diabetic mice was smaller than in normal animals.	Testosterone	7-19	hypertrichosis 2 (generalised, congenital)	Homo sapiens	44-47
3084372-6	1986	However, 72 h after treatment with hCG, plasma testosterone was still elevated in diabetic mice, but not in normal males.	Testosterone	47-59	hypertrichosis 2 (generalised, congenital)	Homo sapiens	35-38
3084372-7	1986	In vitro, hCG stimulated testicular testosterone synthesis in all groups of mice, but the observed increase was smaller in diabetic and obese than in normal animals.	Testosterone	36-48	hypertrichosis 2 (generalised, congenital)	Homo sapiens	10-13
3009971-9	1986	Although TPA and OAG did not increase basal cAMP production, both agents enhanced the cAMP responses stimulated by hCG and forskolin; likewise, phospholipase C alone did not change cAMP production but caused a dose-dependent increase in the cAMP responses to hCG and forskolin.	Cyclic AMP	86-90	hypertrichosis 2 (generalised, congenital)	Homo sapiens	115-118
3009971-9	1986	Although TPA and OAG did not increase basal cAMP production, both agents enhanced the cAMP responses stimulated by hCG and forskolin; likewise, phospholipase C alone did not change cAMP production but caused a dose-dependent increase in the cAMP responses to hCG and forskolin.	Cyclic AMP	86-90	hypertrichosis 2 (generalised, congenital)	Homo sapiens	115-118
3009971-9	1986	Although TPA and OAG did not increase basal cAMP production, both agents enhanced the cAMP responses stimulated by hCG and forskolin; likewise, phospholipase C alone did not change cAMP production but caused a dose-dependent increase in the cAMP responses to hCG and forskolin.	Cyclic AMP	86-90	hypertrichosis 2 (generalised, congenital)	Homo sapiens	115-118
3009971-9	1986	Although TPA and OAG did not increase basal cAMP production, both agents enhanced the cAMP responses stimulated by hCG and forskolin; likewise, phospholipase C alone did not change cAMP production but caused a dose-dependent increase in the cAMP responses to hCG and forskolin.	Colforsin	267-276	hypertrichosis 2 (generalised, congenital)	Homo sapiens	115-118
3003355-5	1986	By 48 h the 125I-labelled hCG binding was negligible and no morphologically recognizable Leydig cells were found at this time.	Iodine-125	12-16	hypertrichosis 2 (generalised, congenital)	Homo sapiens	26-29
3011682-1	1985	The increase in permeability of the testicular blood vessels following an injection of hCG into rats is abolished completely if the animals are treated 3 days earlier with ethane dimethane sulphonate (EDS), a compound that effectively eliminates Leydig cells from the testes.	ethylene dimethanesulfonate	172-199	hypertrichosis 2 (generalised, congenital)	Homo sapiens	87-90
3010006-9	1986	After 12 months of buserelin injections, the changes in hCG-stimulated rat testes are an increased ratio of progesterone/17-OH-progesterone (inhibition of 17-hydroxylase), a reduced capacity for secretion of androstenedione and testosterone (block of 17,20-desmolase), and increased 5 alpha-pregnane-3,20-dione (this steroid inhibits the 17,20-desmolase, similarly to progesterone).	Progesterone	108-120	hypertrichosis 2 (generalised, congenital)	Homo sapiens	56-59
3010006-9	1986	After 12 months of buserelin injections, the changes in hCG-stimulated rat testes are an increased ratio of progesterone/17-OH-progesterone (inhibition of 17-hydroxylase), a reduced capacity for secretion of androstenedione and testosterone (block of 17,20-desmolase), and increased 5 alpha-pregnane-3,20-dione (this steroid inhibits the 17,20-desmolase, similarly to progesterone).	17-alpha-Hydroxyprogesterone	121-139	hypertrichosis 2 (generalised, congenital)	Homo sapiens	56-59
3010006-9	1986	After 12 months of buserelin injections, the changes in hCG-stimulated rat testes are an increased ratio of progesterone/17-OH-progesterone (inhibition of 17-hydroxylase), a reduced capacity for secretion of androstenedione and testosterone (block of 17,20-desmolase), and increased 5 alpha-pregnane-3,20-dione (this steroid inhibits the 17,20-desmolase, similarly to progesterone).	Androstenedione	208-223	hypertrichosis 2 (generalised, congenital)	Homo sapiens	56-59
3010006-9	1986	After 12 months of buserelin injections, the changes in hCG-stimulated rat testes are an increased ratio of progesterone/17-OH-progesterone (inhibition of 17-hydroxylase), a reduced capacity for secretion of androstenedione and testosterone (block of 17,20-desmolase), and increased 5 alpha-pregnane-3,20-dione (this steroid inhibits the 17,20-desmolase, similarly to progesterone).	Testosterone	228-240	hypertrichosis 2 (generalised, congenital)	Homo sapiens	56-59
3010006-9	1986	After 12 months of buserelin injections, the changes in hCG-stimulated rat testes are an increased ratio of progesterone/17-OH-progesterone (inhibition of 17-hydroxylase), a reduced capacity for secretion of androstenedione and testosterone (block of 17,20-desmolase), and increased 5 alpha-pregnane-3,20-dione (this steroid inhibits the 17,20-desmolase, similarly to progesterone).	alpha-pregnane-3,20-dione	285-310	hypertrichosis 2 (generalised, congenital)	Homo sapiens	56-59
3010006-9	1986	After 12 months of buserelin injections, the changes in hCG-stimulated rat testes are an increased ratio of progesterone/17-OH-progesterone (inhibition of 17-hydroxylase), a reduced capacity for secretion of androstenedione and testosterone (block of 17,20-desmolase), and increased 5 alpha-pregnane-3,20-dione (this steroid inhibits the 17,20-desmolase, similarly to progesterone).	Steroids	317-324	hypertrichosis 2 (generalised, congenital)	Homo sapiens	56-59
3010006-9	1986	After 12 months of buserelin injections, the changes in hCG-stimulated rat testes are an increased ratio of progesterone/17-OH-progesterone (inhibition of 17-hydroxylase), a reduced capacity for secretion of androstenedione and testosterone (block of 17,20-desmolase), and increased 5 alpha-pregnane-3,20-dione (this steroid inhibits the 17,20-desmolase, similarly to progesterone).	Progesterone	127-139	hypertrichosis 2 (generalised, congenital)	Homo sapiens	56-59
3938688-3	1985	The steroid replacement regimen can easily be adjusted to maintain pregnancy until the time of luteoplacental shift, based on the close monitoring of the plasma steroid and hCG levels in the pregnant individual.	Steroids	4-11	hypertrichosis 2 (generalised, congenital)	Homo sapiens	173-176
4065036-16	1985	The effect of the hCG was to decrease the preference of progesterone over 17 alpha-OHP as substrate.	Progesterone	56-68	hypertrichosis 2 (generalised, congenital)	Homo sapiens	18-21
4065036-16	1985	The effect of the hCG was to decrease the preference of progesterone over 17 alpha-OHP as substrate.	alpha-ohp	77-86	hypertrichosis 2 (generalised, congenital)	Homo sapiens	18-21
4065036-20	1985	hCG affects the ovarian lyase complex by shifting the relative preference of substrates towards 17 alpha-OHP.	17 alpha-ohp	96-108	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
3934895-9	1985	The beta-adrenergic agonist isoproterenol in preliminary experiments potentiated the stimulatory effect of hCG but had no own stimulatory effect.	Isoproterenol	28-41	hypertrichosis 2 (generalised, congenital)	Homo sapiens	107-110
2999382-6	1985	We conclude that even though GnRHa and LH/hCG seem to elicit similar responses in the ovarian follicle they differ in their kinetics, their efficiency and the mediator of their action.	Luteinizing Hormone	39-41	hypertrichosis 2 (generalised, congenital)	Homo sapiens	42-45
2412804-2	1985	The treatment of Leydig cell cultures with bovine LH (bLH), hCG, or with (Bu)2cAMP elicited a dose- and time-dependent induction of renin activity and a concomitant increase in steroid biosynthesis.	Steroids	177-184	hypertrichosis 2 (generalised, congenital)	Homo sapiens	60-63
2864237-4	1985	Treatment with hCG increased testosterone production 50-fold over control values, whereas treatment with cholinomimetics alone failed to increase androgen production.	Testosterone	29-41	hypertrichosis 2 (generalised, congenital)	Homo sapiens	15-18
2864237-5	1985	Concomitant treatment of testicular cells with nicotinic cholinergic agonists (lobeline, nicotine, and dimethylphenylpiperazinium iodide) inhibited hCG-stimulated androgen biosynthesis in a dose-dependent fashion, with IC50 values of 3 X 10(-5), 1.7 X 10(-4), and greater than 10(-3) M, respectively.	Lobeline	79-87	hypertrichosis 2 (generalised, congenital)	Homo sapiens	148-151
2864237-5	1985	Concomitant treatment of testicular cells with nicotinic cholinergic agonists (lobeline, nicotine, and dimethylphenylpiperazinium iodide) inhibited hCG-stimulated androgen biosynthesis in a dose-dependent fashion, with IC50 values of 3 X 10(-5), 1.7 X 10(-4), and greater than 10(-3) M, respectively.	Nicotine	89-97	hypertrichosis 2 (generalised, congenital)	Homo sapiens	148-151
2864237-5	1985	Concomitant treatment of testicular cells with nicotinic cholinergic agonists (lobeline, nicotine, and dimethylphenylpiperazinium iodide) inhibited hCG-stimulated androgen biosynthesis in a dose-dependent fashion, with IC50 values of 3 X 10(-5), 1.7 X 10(-4), and greater than 10(-3) M, respectively.	Dimethylphenylpiperazinium Iodide	103-136	hypertrichosis 2 (generalised, congenital)	Homo sapiens	148-151
2864237-7	1985	Lobeline (10-4) M) decreased hCG-stimulated testosterone production (50-75%) throughout the 2-day culture period; however, this inhibition was reversible upon removal of the drug.	Lobeline	0-8	hypertrichosis 2 (generalised, congenital)	Homo sapiens	29-32
2864237-7	1985	Lobeline (10-4) M) decreased hCG-stimulated testosterone production (50-75%) throughout the 2-day culture period; however, this inhibition was reversible upon removal of the drug.	Testosterone	44-56	hypertrichosis 2 (generalised, congenital)	Homo sapiens	29-32
2864237-8	1985	Lobeline also inhibited hCG-stimulated cAMP accumulation as well as testosterone production induced by cholera toxin (65% inhibition), forskolin (50% inhibition), or (Bu)2cAMP (70% inhibition).	Lobeline	0-8	hypertrichosis 2 (generalised, congenital)	Homo sapiens	24-27
2864237-8	1985	Lobeline also inhibited hCG-stimulated cAMP accumulation as well as testosterone production induced by cholera toxin (65% inhibition), forskolin (50% inhibition), or (Bu)2cAMP (70% inhibition).	Cyclic AMP	39-43	hypertrichosis 2 (generalised, congenital)	Homo sapiens	24-27
2864237-9	1985	Lobeline inhibition of hCG-stimulated testosterone production was accompanied by decreases in medium accumulation of 17 alpha-hydroxypregnenolone (75%), 17 alpha-hydroxyprogesterone (85%), dehydroepiandrosterone (50%), and androstenedione (61%); however, the medium content of pregnenolone and progesterone were unchanged.	Testosterone	38-50	hypertrichosis 2 (generalised, congenital)	Homo sapiens	23-26
2864237-9	1985	Lobeline inhibition of hCG-stimulated testosterone production was accompanied by decreases in medium accumulation of 17 alpha-hydroxypregnenolone (75%), 17 alpha-hydroxyprogesterone (85%), dehydroepiandrosterone (50%), and androstenedione (61%); however, the medium content of pregnenolone and progesterone were unchanged.	Androstenedione	223-238	hypertrichosis 2 (generalised, congenital)	Homo sapiens	23-26
2864238-6	1985	Testosterone concentration in the spermatic vein was significantly lower on the abdominal side than on the scrotal side in both control and hCG-treated rats.	Testosterone	0-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	140-143
2864238-8	1985	The outflow of testosterone in the spermatic vein was significantly increased at both 8 and 24 h after hCG from both the scrotal and abdominal testes, although it was always smaller from the abdominal testis.	Testosterone	15-27	hypertrichosis 2 (generalised, congenital)	Homo sapiens	103-106
2864238-9	1985	The lower secretion of testosterone from the abdominal testis after hCG was mainly due to reduced blood flow and not to any disability of the Leydig cells of abdominal testes to produce testosterone.	Testosterone	23-35	hypertrichosis 2 (generalised, congenital)	Homo sapiens	68-71
3001418-6	1985	Moreover, treatment with GnRH agonist inhibited hCG-stimulated progesterone production by rat luteal cells incubated in vitro.	Progesterone	63-75	hypertrichosis 2 (generalised, congenital)	Homo sapiens	48-51
3001418-4	1985	GnRH agonist inhibited hCG stimulation of progesterone production and ovarian weight augmentation in hypophysectomized immature female rats in vivo.	Progesterone	42-54	hypertrichosis 2 (generalised, congenital)	Homo sapiens	23-26
3001418-10	1985	On the other hand, GnRH agonist delayed hCG-stimulated accumulation of cyclic AMP in porcine granulosa cells obtained from medium follicles.	Cyclic AMP	71-81	hypertrichosis 2 (generalised, congenital)	Homo sapiens	40-43
3937203-2	1985	We have already shown the advantage of rapid radio-immunological determinations of 17 beta-oestradiol (E2) to induce the releasing action of chorionic gonadotrophic hormone (hCG).	Estradiol	83-101	hypertrichosis 2 (generalised, congenital)	Homo sapiens	174-177
3937203-2	1985	We have already shown the advantage of rapid radio-immunological determinations of 17 beta-oestradiol (E2) to induce the releasing action of chorionic gonadotrophic hormone (hCG).	Estradiol	103-105	hypertrichosis 2 (generalised, congenital)	Homo sapiens	174-177
2995745-7	1985	In the presence of human chorionic gonadotropin (hCG; 12.5 mIU/ml), a lower dose of THC (25 ng/ml), stimulated T production at 0.25 to 1 mM Ca++, but had no effect as Ca++ reached 2.5 mM.	Dronabinol	84-87	hypertrichosis 2 (generalised, congenital)	Homo sapiens	49-52
2995745-11	1985	In the presence of hCG, 25 micrograms THC/ml produced a consistent suppression of T production across glucose concentrations examined.	Glucose	102-109	hypertrichosis 2 (generalised, congenital)	Homo sapiens	19-22
2995745-9	1985	In contrast, in the presence of hCG, a higher THC dose (25 micrograms/ml), suppressed T accumulation at 0.127, and from 1.0 to 12.7, but had no effect at 0.25 mM, or in the absence of Ca++.	Dronabinol	46-49	hypertrichosis 2 (generalised, congenital)	Homo sapiens	32-35
2995745-13	1985	Differential requirements for these divalent cations by the gonadotropins may explain the interactive effects of THC with LH, hCG or FSH.	Dronabinol	113-116	hypertrichosis 2 (generalised, congenital)	Homo sapiens	126-129
2995745-10	1985	In the presence of hCG, the high 25 micrograms/ml dose of THC stimulated T production, in the absence of additional Mg++, and at 0.01 mM Mg++, but THC had no effect at 0.1 mM Mg++, but inhibited T production at 1.1 mM Mg++.	Dronabinol	58-61	hypertrichosis 2 (generalised, congenital)	Homo sapiens	19-22
2995745-11	1985	In the presence of hCG, 25 micrograms THC/ml produced a consistent suppression of T production across glucose concentrations examined.	Dronabinol	38-41	hypertrichosis 2 (generalised, congenital)	Homo sapiens	19-22
4033119-0	1985	Testosterone and dihydrotestosterone levels in epididymis, vas deferens, seminal vesicle and preputial gland of mice after hCG injection.	Testosterone	0-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	123-126
4052531-4	1985	Twelve hours after hCG, the maximal LI (9.02 +/- 0.38%) was seen in OSE cells adjacent to the ovulatory stigma.	serine O-sulfate	68-71	hypertrichosis 2 (generalised, congenital)	Homo sapiens	19-22
2992915-10	1985	Maximal stimulation of cAMP production by hCG was about 10% greater (P less than 0.05) than that by hLH; the activation constant was 12.3 nM for hCG and 28.3 nM for hLH.	Cyclic AMP	23-27	hypertrichosis 2 (generalised, congenital)	Homo sapiens	42-45
2992915-10	1985	Maximal stimulation of cAMP production by hCG was about 10% greater (P less than 0.05) than that by hLH; the activation constant was 12.3 nM for hCG and 28.3 nM for hLH.	Cyclic AMP	23-27	hypertrichosis 2 (generalised, congenital)	Homo sapiens	145-148
2992915-10	1985	Maximal stimulation of cAMP production by hCG was about 10% greater (P less than 0.05) than that by hLH; the activation constant was 12.3 nM for hCG and 28.3 nM for hLH.	MY 12-62c	100-103	hypertrichosis 2 (generalised, congenital)	Homo sapiens	145-148
2994765-3	1985	for 48 h followed by Leydig cell isolation and purification resulted in a decrease in the maxima of hCG-induced cAMP accumulation and testosterone production by approximately 70% and approximately 55%, respectively, when compared to cells of control mice.	Cyclic AMP	112-116	hypertrichosis 2 (generalised, congenital)	Homo sapiens	100-103
2994765-3	1985	for 48 h followed by Leydig cell isolation and purification resulted in a decrease in the maxima of hCG-induced cAMP accumulation and testosterone production by approximately 70% and approximately 55%, respectively, when compared to cells of control mice.	Testosterone	134-146	hypertrichosis 2 (generalised, congenital)	Homo sapiens	100-103
2994765-8	1985	They increased maximal hCG-induced testosterone production not only in desensitized cells, but also in control cells (by 80-100%), whereas their effect on basal testosterone production was negligible.	Testosterone	35-47	hypertrichosis 2 (generalised, congenital)	Homo sapiens	23-26
2994765-9	1985	In desensitized cells from hCG-treated mice (2 micrograms i.p., 48 h) cellular unesterified and esterified cholesterol were decreased by 21% and 81%, respectively, when compared to control cells.	Cholesterol	107-118	hypertrichosis 2 (generalised, congenital)	Homo sapiens	27-30
2994765-11	1985	In conclusion, our data indicate that the impaired steroidogenesis in mouse Leydig cells desensitized in vivo by a single injection of hCG is the result of a depletion in cellular cholesterol, rather than of an impaired conversion of cholesterol to testosterone.	Cholesterol	180-191	hypertrichosis 2 (generalised, congenital)	Homo sapiens	135-138
2994765-11	1985	In conclusion, our data indicate that the impaired steroidogenesis in mouse Leydig cells desensitized in vivo by a single injection of hCG is the result of a depletion in cellular cholesterol, rather than of an impaired conversion of cholesterol to testosterone.	Testosterone	249-261	hypertrichosis 2 (generalised, congenital)	Homo sapiens	135-138
4008604-4	1985	The 24-h incubation with hCG (0-100 ng/ml) also increased the capacity of the cultures to secrete testosterone during a second incubation in a dose-dependent manner even in the absence of hCG (steroidogenic enzyme induction).	Testosterone	98-110	hypertrichosis 2 (generalised, congenital)	Homo sapiens	25-28
4033119-2	1985	The response of circulating T to hCG stimulation was rapid and persisted over a period of 48 h. The temporal changes of androgen content of target organs paralleled the modifications of circulating T. In all organs the high androgen levels attained at 1 or 4 h plateaued until 24 h, decreased thereafter and returned to basal values at 72 h. The concentration of T by sex accessory organs was more accelerated by hCG injection than its conversion into DHT.	Dihydrotestosterone	452-455	hypertrichosis 2 (generalised, congenital)	Homo sapiens	33-36
2862754-7	1985	All the boys with HH had an impaired testosterone response to hCG, and SHBG levels did not decrease after hCG.	Testosterone	37-49	hypertrichosis 2 (generalised, congenital)	Homo sapiens	62-65
4036233-4	1985	24 hours after treatment, however, the response of plasma testosterone to hCG was diminished.	Testosterone	58-70	hypertrichosis 2 (generalised, congenital)	Homo sapiens	74-77
4092719-3	1985	Development of testicular tumors had initially little effect on basal and hCG-stimulated plasma testosterone and androstenedione levels but eventually led to atrophy of the seminal vesicles.	Testosterone	96-108	hypertrichosis 2 (generalised, congenital)	Homo sapiens	74-77
4036234-1	1985	The normal response of testosterone synthesis to hCG has a biphasic pattern.	Testosterone	23-35	hypertrichosis 2 (generalised, congenital)	Homo sapiens	49-52
4092719-3	1985	Development of testicular tumors had initially little effect on basal and hCG-stimulated plasma testosterone and androstenedione levels but eventually led to atrophy of the seminal vesicles.	Androstenedione	113-128	hypertrichosis 2 (generalised, congenital)	Homo sapiens	74-77
2410037-7	1985	Cycloheximide, at a dose of 0.1 mg/rat, was given at 12 h before hCG, immediately after hCG, and at 9 h after hCG.	Cycloheximide	0-13	hypertrichosis 2 (generalised, congenital)	Homo sapiens	65-68
3923029-3	1985	Evidence for the presence of a testis was provided by a plasma testosterone increase after hCG administration (5000 IU/day for 3 days) and its spontaneous response to an endogenous preovulatory LH peak.	Testosterone	63-75	hypertrichosis 2 (generalised, congenital)	Homo sapiens	91-94
3926930-7	1985	After injection of hCG, plasma concentrations of FSH increased significantly by 6 h, reached peak values at 12 h and declined to control levels at 36 h. On the other hand, plasma concentrations of LH were reduced by 6 h and decreased further during the next 36 h. An abrupt fall in plasma concentrations of oestradiol-17 beta occurred within 3 h of the administration of hCG.	Luteinizing Hormone	197-199	hypertrichosis 2 (generalised, congenital)	Homo sapiens	19-22
3926930-7	1985	After injection of hCG, plasma concentrations of FSH increased significantly by 6 h, reached peak values at 12 h and declined to control levels at 36 h. On the other hand, plasma concentrations of LH were reduced by 6 h and decreased further during the next 36 h. An abrupt fall in plasma concentrations of oestradiol-17 beta occurred within 3 h of the administration of hCG.	Luteinizing Hormone	197-199	hypertrichosis 2 (generalised, congenital)	Homo sapiens	371-374
3926930-7	1985	After injection of hCG, plasma concentrations of FSH increased significantly by 6 h, reached peak values at 12 h and declined to control levels at 36 h. On the other hand, plasma concentrations of LH were reduced by 6 h and decreased further during the next 36 h. An abrupt fall in plasma concentrations of oestradiol-17 beta occurred within 3 h of the administration of hCG.	Estradiol	307-325	hypertrichosis 2 (generalised, congenital)	Homo sapiens	19-22
3160620-2	1985	The actions of IF and LHRH-A were similar in showing (1) a delayed onset of action, (2) enhancement of testosterone production in response to a maximally stimulating concentration (5 nM) of hCG, and (3) near cessation of stimulation following their removal from the incubation medium.	Testosterone	103-115	hypertrichosis 2 (generalised, congenital)	Homo sapiens	190-193
3160620-7	1985	Thus, whereas the rate of testosterone production by Leydig cells in response to 5 nM hCG declined progressively from 4 to 20 h, addition of IF attenuated or prevented this decline.	Testosterone	26-38	hypertrichosis 2 (generalised, congenital)	Homo sapiens	86-89
2410037-7	1985	Cycloheximide, at a dose of 0.1 mg/rat, was given at 12 h before hCG, immediately after hCG, and at 9 h after hCG.	Cycloheximide	0-13	hypertrichosis 2 (generalised, congenital)	Homo sapiens	88-91
2410037-7	1985	Cycloheximide, at a dose of 0.1 mg/rat, was given at 12 h before hCG, immediately after hCG, and at 9 h after hCG.	Cycloheximide	0-13	hypertrichosis 2 (generalised, congenital)	Homo sapiens	88-91
2410037-9	1985	Colchicine, at a dose of 0.1 mg/rat, inhibited ovulation, but not PA activity, when it was given 1 h before hCG.	Colchicine	0-10	hypertrichosis 2 (generalised, congenital)	Homo sapiens	108-111
3902663-7	1985	It is concluded that the suppressive effects of short photoperiods on the ability of the hamster testis to produce testosterone and to respond to hCG stimulation are due to reductions in endogenous LH, FSH and prolactin release, with a consequent loss of testicular LH/hCG receptors and decreased activity of enzymes involved in the biosynthesis of testosterone.	Testosterone	349-361	hypertrichosis 2 (generalised, congenital)	Homo sapiens	146-149
2986949-3	1985	It is observed that a tumor promoter, phorbol myristate acetate (PMA), binds specifically to the cells (Ka = 5 X 10(8) M-1; 3.9 X 10(11) receptors/mg), reduces (33%) the affinity but not the number of EGF receptors, and stimulates hCG to the same extent as does EGF.	Tetradecanoylphorbol Acetate	38-63	hypertrichosis 2 (generalised, congenital)	Homo sapiens	231-234
2986949-3	1985	It is observed that a tumor promoter, phorbol myristate acetate (PMA), binds specifically to the cells (Ka = 5 X 10(8) M-1; 3.9 X 10(11) receptors/mg), reduces (33%) the affinity but not the number of EGF receptors, and stimulates hCG to the same extent as does EGF.	Tetradecanoylphorbol Acetate	65-68	hypertrichosis 2 (generalised, congenital)	Homo sapiens	231-234
2986949-4	1985	The relative potencies of PMA (100%), phorbol dibutyrate (25%), and nonesterified phorbol (no effect) to stimulate hCG parallel their known tumor-promoting activities.	Tetradecanoylphorbol Acetate	26-29	hypertrichosis 2 (generalised, congenital)	Homo sapiens	115-118
2986949-4	1985	The relative potencies of PMA (100%), phorbol dibutyrate (25%), and nonesterified phorbol (no effect) to stimulate hCG parallel their known tumor-promoting activities.	Phorbol 12,13-Dibutyrate	38-56	hypertrichosis 2 (generalised, congenital)	Homo sapiens	115-118
2986949-4	1985	The relative potencies of PMA (100%), phorbol dibutyrate (25%), and nonesterified phorbol (no effect) to stimulate hCG parallel their known tumor-promoting activities.	phorbol	38-45	hypertrichosis 2 (generalised, congenital)	Homo sapiens	115-118
2986949-8	1985	Nordihydroguairetic acid (a cyclooxygenase and lipoxygenase inhibitor) reduced by 90% basal and EGF- or PMA-stimulated hCG secretion.	nordihydroguairetic acid	0-24	hypertrichosis 2 (generalised, congenital)	Homo sapiens	119-122
2986949-8	1985	Nordihydroguairetic acid (a cyclooxygenase and lipoxygenase inhibitor) reduced by 90% basal and EGF- or PMA-stimulated hCG secretion.	Tetradecanoylphorbol Acetate	104-107	hypertrichosis 2 (generalised, congenital)	Homo sapiens	119-122
3861290-1	1985	This study examined the effect of epostane, a new antifertility drug, on normal and hCG-stimulated progesterone production during the luteal phase of the menstrual cycle in rhesus monkeys.	epostane	34-42	hypertrichosis 2 (generalised, congenital)	Homo sapiens	84-87
3902663-6	1985	Furthermore, testosterone production in vitro by regressed testes of animals exposed to short photoperiod was increased significantly by one large dose of hCG administered 26 h before killing the animals.	Testosterone	13-25	hypertrichosis 2 (generalised, congenital)	Homo sapiens	155-158
3861290-1	1985	This study examined the effect of epostane, a new antifertility drug, on normal and hCG-stimulated progesterone production during the luteal phase of the menstrual cycle in rhesus monkeys.	Progesterone	99-111	hypertrichosis 2 (generalised, congenital)	Homo sapiens	84-87
3861290-3	1985	Epostane also reduced the elevated luteal phase progesterone levels of animals treated with hCG indicating that the drug acts directly on the corpus luteum.	epostane	0-8	hypertrichosis 2 (generalised, congenital)	Homo sapiens	92-95
4020768-5	1985	In association with this change there was a significant increase in the amounts of a locally-produced factor in interstitial fluid which stimulates basal and hCG-stimulated testosterone production by isolated purified Leydig cells.	Testosterone	173-185	hypertrichosis 2 (generalised, congenital)	Homo sapiens	158-161
3921972-6	1985	These results indicate that in the barbiturate-treated hamster the elevated follicular fluid levels of progesterone precede by 1-2 days the previously reported increase in steroidogenic capability of delayed follicles to produce progesterone in vitro; this correlated with an increase in the ratio of hCG:FSH binding and this was mostly due to a decrease in FSH binding to whole follicles.	barbituric acid	35-46	hypertrichosis 2 (generalised, congenital)	Homo sapiens	301-304
2989027-2	1985	Simultaneous addition of forskolin and hCG resulted in a striking synergistic stimulation of cAMP production.	Cyclic AMP	93-97	hypertrichosis 2 (generalised, congenital)	Homo sapiens	39-42
2989027-4	1985	hCG (3 X 10(-9) M) lowered about 6-fold the ED50 for forskolin-elicited cAMP accumulation and increased the maximal response to forskolin about 16-fold.	Colforsin	53-62	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
2989027-4	1985	hCG (3 X 10(-9) M) lowered about 6-fold the ED50 for forskolin-elicited cAMP accumulation and increased the maximal response to forskolin about 16-fold.	Cyclic AMP	72-76	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
2989027-4	1985	hCG (3 X 10(-9) M) lowered about 6-fold the ED50 for forskolin-elicited cAMP accumulation and increased the maximal response to forskolin about 16-fold.	Colforsin	128-137	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
2989027-6	1985	Moreover, pretreatment with hCG induced only a homologous desensitization of adenylate cyclase, whereas the enzyme became partially resistant to both hCG and forskolin in cells pretreated with forskolin.	Colforsin	158-167	hypertrichosis 2 (generalised, congenital)	Homo sapiens	28-31
2989027-6	1985	Moreover, pretreatment with hCG induced only a homologous desensitization of adenylate cyclase, whereas the enzyme became partially resistant to both hCG and forskolin in cells pretreated with forskolin.	Colforsin	193-202	hypertrichosis 2 (generalised, congenital)	Homo sapiens	28-31
2989027-6	1985	Moreover, pretreatment with hCG induced only a homologous desensitization of adenylate cyclase, whereas the enzyme became partially resistant to both hCG and forskolin in cells pretreated with forskolin.	Colforsin	193-202	hypertrichosis 2 (generalised, congenital)	Homo sapiens	150-153
2989027-7	1985	The homologous hCG-induced desensitization and the partial heterologous one induced by forskolin suggest that more than the catalytic unit of the cyclase is required for the diterpene activation.	Colforsin	87-96	hypertrichosis 2 (generalised, congenital)	Homo sapiens	15-18
2989027-7	1985	The homologous hCG-induced desensitization and the partial heterologous one induced by forskolin suggest that more than the catalytic unit of the cyclase is required for the diterpene activation.	Diterpenes	174-183	hypertrichosis 2 (generalised, congenital)	Homo sapiens	15-18
3921972-6	1985	These results indicate that in the barbiturate-treated hamster the elevated follicular fluid levels of progesterone precede by 1-2 days the previously reported increase in steroidogenic capability of delayed follicles to produce progesterone in vitro; this correlated with an increase in the ratio of hCG:FSH binding and this was mostly due to a decrease in FSH binding to whole follicles.	Progesterone	103-115	hypertrichosis 2 (generalised, congenital)	Homo sapiens	301-304
3971933-3	1985	When the sympathomimetics norepinephrine, epinephrine, and isoproterenol were added to the medium, androgen production in response to hCG was enhanced by 100-300%.	Norepinephrine	26-40	hypertrichosis 2 (generalised, congenital)	Homo sapiens	134-137
3971933-3	1985	When the sympathomimetics norepinephrine, epinephrine, and isoproterenol were added to the medium, androgen production in response to hCG was enhanced by 100-300%.	Epinephrine	29-40	hypertrichosis 2 (generalised, congenital)	Homo sapiens	134-137
3971933-3	1985	When the sympathomimetics norepinephrine, epinephrine, and isoproterenol were added to the medium, androgen production in response to hCG was enhanced by 100-300%.	Isoproterenol	59-72	hypertrichosis 2 (generalised, congenital)	Homo sapiens	134-137
3971933-4	1985	The ability of the catecholamines to stimulate androgen production was dependent on the continuous presence of hCG.	Catecholamines	19-33	hypertrichosis 2 (generalised, congenital)	Homo sapiens	111-114
3971933-8	1985	The acquisition of catecholamine responsiveness was specific to hCG; if theca-interstitial cells were induced to differentiate with either prostaglandin E2 or cholera toxin, then isoproterenol did not enhance androgen synthesis.	Catecholamines	19-32	hypertrichosis 2 (generalised, congenital)	Homo sapiens	64-67
3999743-0	1985	Stimulation of the synthesis of steroids and steroid sulphates in human testicular tissue in vitro by hCG and by 8-bromo-cyclic AMP.	Steroids	32-40	hypertrichosis 2 (generalised, congenital)	Homo sapiens	102-105
2987616-6	1985	Under stimulation with hCG, there was a rapid response in testicular steroidogenesis, initially seen as a rapid increase in the secretion of unconjugated and sulphated steroids.	Steroids	168-176	hypertrichosis 2 (generalised, congenital)	Homo sapiens	23-26
2987616-8	1985	Only high doses of hCG, 10-100 ng/ml, were then able to lead to a net accumulation of unconjugated steroids, at 24-36 h of incubation with hCG.	Steroids	99-107	hypertrichosis 2 (generalised, congenital)	Homo sapiens	19-22
3999743-0	1985	Stimulation of the synthesis of steroids and steroid sulphates in human testicular tissue in vitro by hCG and by 8-bromo-cyclic AMP.	steroid sulphates	45-62	hypertrichosis 2 (generalised, congenital)	Homo sapiens	102-105
2987616-8	1985	Only high doses of hCG, 10-100 ng/ml, were then able to lead to a net accumulation of unconjugated steroids, at 24-36 h of incubation with hCG.	Steroids	99-107	hypertrichosis 2 (generalised, congenital)	Homo sapiens	139-142
3999743-2	1985	The results showed, we believe for the first time, that the production of steroid sulphates as well as of unconjugated steroids can be stimulated in human testis tissue in vitro and they confirm earlier observations in vivo which suggested that testicular production of steroid sulphates can be stimulated by hCG.	steroid sulphates	74-91	hypertrichosis 2 (generalised, congenital)	Homo sapiens	309-312
2982568-1	1985	Cell fractions were obtained by separation on Percoll density gradients after dissociation of mature mouse testes by mechanical or collagenase dispersion, and the ultrastructure, hCG receptor properties, and hCG-stimulated testosterone (T) production of these fractions were compared.	Testosterone	223-235	hypertrichosis 2 (generalised, congenital)	Homo sapiens	208-211
2985225-1	1985	Administration of human chorionic gonadotropin (hCG) to pregnant mare"s serum gonadotropin--hCG primed rats results in the loss of in vitro responsiveness of the ovaries to exogenous gonadotropins for progesterone production.	Progesterone	201-213	hypertrichosis 2 (generalised, congenital)	Homo sapiens	48-51
2985225-1	1985	Administration of human chorionic gonadotropin (hCG) to pregnant mare"s serum gonadotropin--hCG primed rats results in the loss of in vitro responsiveness of the ovaries to exogenous gonadotropins for progesterone production.	Progesterone	201-213	hypertrichosis 2 (generalised, congenital)	Homo sapiens	92-95
2985225-4	1985	Examination of the time course for the loss of lipoprotein response after hCG injection revealed that injection with 50 IU of hCG results in a loss of gonadotropin response as early as 1 h after injection, but exogenous cholesterol-carrying lipoprotein fractions, LDL and HDL, were capable of stimulating progesterone production up to 4 h after hormone injection.	Cholesterol	220-231	hypertrichosis 2 (generalised, congenital)	Homo sapiens	126-129
2985225-4	1985	Examination of the time course for the loss of lipoprotein response after hCG injection revealed that injection with 50 IU of hCG results in a loss of gonadotropin response as early as 1 h after injection, but exogenous cholesterol-carrying lipoprotein fractions, LDL and HDL, were capable of stimulating progesterone production up to 4 h after hormone injection.	Progesterone	305-317	hypertrichosis 2 (generalised, congenital)	Homo sapiens	126-129
3010511-8	1985	The stimulatory effect of hCG was limited to the metabolism of progesterone and was restricted to the sequence: 17-hydroxyprogesterone----androstenedione----testosterone---- dihydrotestosterone.	Progesterone	63-75	hypertrichosis 2 (generalised, congenital)	Homo sapiens	26-29
2581068-0	1985	Changes in plasma steroid levels after single administration of hCG or LHRH agonist analogue in dog and rat.	Steroids	18-25	hypertrichosis 2 (generalised, congenital)	Homo sapiens	64-67
2581068-5	1985	When dogs were injected with hCG, we also observed a marked stimulation of dehydroepiandrosterone levels (20-fold; P less than 0.01) accompanied by a small increase of plasma testosterone concentration (2-fold, P less than 0.01).	Dehydroepiandrosterone	75-97	hypertrichosis 2 (generalised, congenital)	Homo sapiens	29-32
2581068-5	1985	When dogs were injected with hCG, we also observed a marked stimulation of dehydroepiandrosterone levels (20-fold; P less than 0.01) accompanied by a small increase of plasma testosterone concentration (2-fold, P less than 0.01).	Testosterone	175-187	hypertrichosis 2 (generalised, congenital)	Homo sapiens	29-32
2581068-6	1985	In rats injected with either hCG or the LHRH analogue, an increment of plasma testosterone (7-fold, P less than 0.01) is detected in the first hour while plasma dehydroepiandrosterone levels are slightly stimulated.	Testosterone	78-90	hypertrichosis 2 (generalised, congenital)	Homo sapiens	29-32
2581068-6	1985	In rats injected with either hCG or the LHRH analogue, an increment of plasma testosterone (7-fold, P less than 0.01) is detected in the first hour while plasma dehydroepiandrosterone levels are slightly stimulated.	Dehydroepiandrosterone	161-183	hypertrichosis 2 (generalised, congenital)	Homo sapiens	29-32
2581068-7	1985	Moreover, in rats injected with hCG, low plasma steroid levels are present between 4-12 h after injection due to testicular desensitization.	Steroids	48-55	hypertrichosis 2 (generalised, congenital)	Homo sapiens	32-35
2581068-9	1985	Acute testicular steroidogenic responsiveness to hCG on the dog is, however, different: after stimulation, the levels of plasma dehydroepiandrosterone are maintained at a plateau and slowly decline after 24-48 h. Our data indicate that in dogs, stimulation of testicular steroidogenesis leads to an increase of plasma delta 5-steroid levels while the same stimuli cause, in the rat, a stimulation of delta 4-androgen, particularly testosterone.	Dehydroepiandrosterone	128-150	hypertrichosis 2 (generalised, congenital)	Homo sapiens	49-52
2581068-9	1985	Acute testicular steroidogenic responsiveness to hCG on the dog is, however, different: after stimulation, the levels of plasma dehydroepiandrosterone are maintained at a plateau and slowly decline after 24-48 h. Our data indicate that in dogs, stimulation of testicular steroidogenesis leads to an increase of plasma delta 5-steroid levels while the same stimuli cause, in the rat, a stimulation of delta 4-androgen, particularly testosterone.	Steroids	17-24	hypertrichosis 2 (generalised, congenital)	Homo sapiens	49-52
2581068-9	1985	Acute testicular steroidogenic responsiveness to hCG on the dog is, however, different: after stimulation, the levels of plasma dehydroepiandrosterone are maintained at a plateau and slowly decline after 24-48 h. Our data indicate that in dogs, stimulation of testicular steroidogenesis leads to an increase of plasma delta 5-steroid levels while the same stimuli cause, in the rat, a stimulation of delta 4-androgen, particularly testosterone.	Testosterone	431-443	hypertrichosis 2 (generalised, congenital)	Homo sapiens	49-52
3010511-8	1985	The stimulatory effect of hCG was limited to the metabolism of progesterone and was restricted to the sequence: 17-hydroxyprogesterone----androstenedione----testosterone---- dihydrotestosterone.	17-hydroxyprogesterone----androstenedione----testosterone---- dihydrotestosterone	112-193	hypertrichosis 2 (generalised, congenital)	Homo sapiens	26-29
3010511-9	1985	Dexamethasone-suppression, and hCG-stimulation of the intratesticular levels of delta 4-steroids, was mirrored by corresponding changes in the peripheral plasma levels, with the exception of the plasma levels of androstenedione which were not influenced by any of the treatments studied.	delta 4-steroids	80-96	hypertrichosis 2 (generalised, congenital)	Homo sapiens	31-34
2981665-4	1985	The level of ovarian and follicular 3H-Hyp decreased by about 40% on the afternoon of proestrus or after exogenous stimulation of ovulation by human CG (hCG), and this decrease was abolished by blocking the surge of gonadotropins with Nembutal.	Tritium	36-38	hypertrichosis 2 (generalised, congenital)	Homo sapiens	149-151
2981665-4	1985	The level of ovarian and follicular 3H-Hyp decreased by about 40% on the afternoon of proestrus or after exogenous stimulation of ovulation by human CG (hCG), and this decrease was abolished by blocking the surge of gonadotropins with Nembutal.	Tritium	36-38	hypertrichosis 2 (generalised, congenital)	Homo sapiens	153-156
2981665-11	1985	Cysteine effectively inhibited ovulation even when injected 7 h after the hCG stimulus.	Cysteine	0-8	hypertrichosis 2 (generalised, congenital)	Homo sapiens	74-77
2981665-13	1985	Indomethacin (inhibitor of cyclooxygenase) and nordihydroguaiaretic acid (inhibitor of lipoxygenase) blocked ovulation and inhibited hCG-induced ovarian collagenolysis.	Indomethacin	0-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	133-136
2981665-13	1985	Indomethacin (inhibitor of cyclooxygenase) and nordihydroguaiaretic acid (inhibitor of lipoxygenase) blocked ovulation and inhibited hCG-induced ovarian collagenolysis.	Masoprocol	47-72	hypertrichosis 2 (generalised, congenital)	Homo sapiens	133-136
2981670-9	1985	Studies with 125I-labeled hormones further supported the conclusion that hCG differs from all other LHs in being most tightly bound and, hence, least dissociable, while eCG and rLH dissociate most readily; oLH and eLH can be placed in between these hormones in the extent of their dissociability.	Iodine-125	13-17	hypertrichosis 2 (generalised, congenital)	Homo sapiens	73-76
3997269-5	1985	The response of 17-OHP, T, E2 and the 17-OHP/T ratio to hCG was similar in short-term and long-term tamoxifen-treated men as well as in 6 untreated eugonadal male controls.	Tamoxifen	100-109	hypertrichosis 2 (generalised, congenital)	Homo sapiens	56-59
3997273-1	1985	The possible mediation by steroids, prostaglandins or protein synthesis on the hCG-induced increase in hormone uptake and interstial fluid volume in the rat testis in vivo was studied following a single iv injection of hCG.	Steroids	26-34	hypertrichosis 2 (generalised, congenital)	Homo sapiens	79-82
3997269-2	1985	This defect has been attributed to an early rise in oestradiol (E2) following hCG administration.	Estradiol	52-62	hypertrichosis 2 (generalised, congenital)	Homo sapiens	78-81
3997269-5	1985	The response of 17-OHP, T, E2 and the 17-OHP/T ratio to hCG was similar in short-term and long-term tamoxifen-treated men as well as in 6 untreated eugonadal male controls.	17-alpha-Hydroxyprogesterone	16-22	hypertrichosis 2 (generalised, congenital)	Homo sapiens	56-59
3997273-1	1985	The possible mediation by steroids, prostaglandins or protein synthesis on the hCG-induced increase in hormone uptake and interstial fluid volume in the rat testis in vivo was studied following a single iv injection of hCG.	Prostaglandins	36-50	hypertrichosis 2 (generalised, congenital)	Homo sapiens	79-82
3997269-5	1985	The response of 17-OHP, T, E2 and the 17-OHP/T ratio to hCG was similar in short-term and long-term tamoxifen-treated men as well as in 6 untreated eugonadal male controls.	17-alpha-Hydroxyprogesterone	38-44	hypertrichosis 2 (generalised, congenital)	Homo sapiens	56-59
3968512-7	1985	In contrast, hCG dramatically enhanced ovarian secretion of both testosterone and oestradiol without affecting progesterone secretion.	Testosterone	65-77	hypertrichosis 2 (generalised, congenital)	Homo sapiens	13-16
3968512-7	1985	In contrast, hCG dramatically enhanced ovarian secretion of both testosterone and oestradiol without affecting progesterone secretion.	Estradiol	82-92	hypertrichosis 2 (generalised, congenital)	Homo sapiens	13-16
3968512-4	1985	On day 9, blood was obtained from the ovarian vein and corpora lutea and follicles were isolated and incubated in vitro for 2 h. Administration of hCG to intact rats increased ovarian secretion of testosterone and oestradiol dramatically, but did not affect progesterone secretion.	Testosterone	197-209	hypertrichosis 2 (generalised, congenital)	Homo sapiens	147-150
3968512-8	1985	Prolactin administered together with hCG antagonized the stimulation of both testosterone and oestradiol secretion by hCG, yet increased progesterone production.	Testosterone	77-89	hypertrichosis 2 (generalised, congenital)	Homo sapiens	37-40
3968512-4	1985	On day 9, blood was obtained from the ovarian vein and corpora lutea and follicles were isolated and incubated in vitro for 2 h. Administration of hCG to intact rats increased ovarian secretion of testosterone and oestradiol dramatically, but did not affect progesterone secretion.	Estradiol	214-224	hypertrichosis 2 (generalised, congenital)	Homo sapiens	147-150
3968512-8	1985	Prolactin administered together with hCG antagonized the stimulation of both testosterone and oestradiol secretion by hCG, yet increased progesterone production.	Testosterone	77-89	hypertrichosis 2 (generalised, congenital)	Homo sapiens	118-121
3968512-8	1985	Prolactin administered together with hCG antagonized the stimulation of both testosterone and oestradiol secretion by hCG, yet increased progesterone production.	Estradiol	94-104	hypertrichosis 2 (generalised, congenital)	Homo sapiens	37-40
3968512-8	1985	Prolactin administered together with hCG antagonized the stimulation of both testosterone and oestradiol secretion by hCG, yet increased progesterone production.	Estradiol	94-104	hypertrichosis 2 (generalised, congenital)	Homo sapiens	118-121
3968512-8	1985	Prolactin administered together with hCG antagonized the stimulation of both testosterone and oestradiol secretion by hCG, yet increased progesterone production.	Progesterone	137-149	hypertrichosis 2 (generalised, congenital)	Homo sapiens	37-40
3968512-9	1985	When the specific effects of hCG and prolactin administration on follicles and corpora lutea were studied separately, it was found that hCG treatment in vivo greatly stimulated testosterone and oestradiol production by both tissues in vitro.	Testosterone	177-189	hypertrichosis 2 (generalised, congenital)	Homo sapiens	29-32
3968512-9	1985	When the specific effects of hCG and prolactin administration on follicles and corpora lutea were studied separately, it was found that hCG treatment in vivo greatly stimulated testosterone and oestradiol production by both tissues in vitro.	Testosterone	177-189	hypertrichosis 2 (generalised, congenital)	Homo sapiens	136-139
3968512-9	1985	When the specific effects of hCG and prolactin administration on follicles and corpora lutea were studied separately, it was found that hCG treatment in vivo greatly stimulated testosterone and oestradiol production by both tissues in vitro.	Estradiol	194-204	hypertrichosis 2 (generalised, congenital)	Homo sapiens	29-32
3968512-9	1985	When the specific effects of hCG and prolactin administration on follicles and corpora lutea were studied separately, it was found that hCG treatment in vivo greatly stimulated testosterone and oestradiol production by both tissues in vitro.	Estradiol	194-204	hypertrichosis 2 (generalised, congenital)	Homo sapiens	136-139
3968512-10	1985	Since hCG only marginally affected aromatase activity in the follicle, had no effect on aromatase activity in luteal cells and did not increase progesterone synthesis, it appears that hCG acts to increase the formation of androgen substrate for oestradiol biosynthesis.	Estradiol	245-255	hypertrichosis 2 (generalised, congenital)	Homo sapiens	184-187
3968512-11	1985	Prolactin, administered with or without hCG, inhibited both basal and hCG-stimulated testosterone and oestradiol synthesis by the follicle.	Testosterone	85-97	hypertrichosis 2 (generalised, congenital)	Homo sapiens	40-43
3968512-11	1985	Prolactin, administered with or without hCG, inhibited both basal and hCG-stimulated testosterone and oestradiol synthesis by the follicle.	Testosterone	85-97	hypertrichosis 2 (generalised, congenital)	Homo sapiens	70-73
3968512-11	1985	Prolactin, administered with or without hCG, inhibited both basal and hCG-stimulated testosterone and oestradiol synthesis by the follicle.	Estradiol	102-112	hypertrichosis 2 (generalised, congenital)	Homo sapiens	40-43
3968512-11	1985	Prolactin, administered with or without hCG, inhibited both basal and hCG-stimulated testosterone and oestradiol synthesis by the follicle.	Estradiol	102-112	hypertrichosis 2 (generalised, congenital)	Homo sapiens	70-73
3968512-15	1985	However, corpora lutea of rats treated with prolactin responded to the hCG challenge with an increase in testosterone and oestradiol synthesis.	Testosterone	105-117	hypertrichosis 2 (generalised, congenital)	Homo sapiens	71-74
2579862-3	1985	The efficacy of the substances to cause an increase in the hCG medium concentration was in the following order: IBMX less than control less than 8-bromo-cGMP = 8-bromo-cAMP less than cGMP + IBMX less than cAMP + IBMX.	1-Methyl-3-isobutylxanthine	112-116	hypertrichosis 2 (generalised, congenital)	Homo sapiens	59-62
3968512-15	1985	However, corpora lutea of rats treated with prolactin responded to the hCG challenge with an increase in testosterone and oestradiol synthesis.	Estradiol	122-132	hypertrichosis 2 (generalised, congenital)	Homo sapiens	71-74
2579862-3	1985	The efficacy of the substances to cause an increase in the hCG medium concentration was in the following order: IBMX less than control less than 8-bromo-cGMP = 8-bromo-cAMP less than cGMP + IBMX less than cAMP + IBMX.	8-bromocyclic GMP	145-157	hypertrichosis 2 (generalised, congenital)	Homo sapiens	59-62
2579862-5	1985	Only in the presence of 8-bromo-cAMP, 8-bromo-cGMP, and cGMP + IBMX was hCG synthesized, which differs significantly in the investigated properties from hCG of the control cultures.	8-Bromo Cyclic Adenosine Monophosphate	24-36	hypertrichosis 2 (generalised, congenital)	Homo sapiens	72-75
2579862-3	1985	The efficacy of the substances to cause an increase in the hCG medium concentration was in the following order: IBMX less than control less than 8-bromo-cGMP = 8-bromo-cAMP less than cGMP + IBMX less than cAMP + IBMX.	8-Bromo Cyclic Adenosine Monophosphate	160-172	hypertrichosis 2 (generalised, congenital)	Homo sapiens	59-62
2579862-3	1985	The efficacy of the substances to cause an increase in the hCG medium concentration was in the following order: IBMX less than control less than 8-bromo-cGMP = 8-bromo-cAMP less than cGMP + IBMX less than cAMP + IBMX.	Cyclic GMP	153-157	hypertrichosis 2 (generalised, congenital)	Homo sapiens	59-62
2579862-3	1985	The efficacy of the substances to cause an increase in the hCG medium concentration was in the following order: IBMX less than control less than 8-bromo-cGMP = 8-bromo-cAMP less than cGMP + IBMX less than cAMP + IBMX.	Cyclic AMP	168-172	hypertrichosis 2 (generalised, congenital)	Homo sapiens	59-62
2579862-4	1985	The synthesized hCG was examined with respect to its receptor binding activity (LH/hCG receptor of rat testes), the activities to stimulate adenylate cyclase as well as testosterone biosynthesis in purified mouse Leydig cells, the immunological activity, and the microheterogeneity in isoelectric focusing.	Testosterone	169-181	hypertrichosis 2 (generalised, congenital)	Homo sapiens	16-19
2579862-5	1985	Only in the presence of 8-bromo-cAMP, 8-bromo-cGMP, and cGMP + IBMX was hCG synthesized, which differs significantly in the investigated properties from hCG of the control cultures.	8-bromocyclic GMP	38-50	hypertrichosis 2 (generalised, congenital)	Homo sapiens	72-75
2579862-7	1985	In the presence of both 8-bromo-cAMP and 8-bromo-cGMP, microheterogeneity of hCG in isoelectric focusing was diminished and the synthesis of more acidic hCG subpopulations was favoured.	8-Bromo Cyclic Adenosine Monophosphate	24-36	hypertrichosis 2 (generalised, congenital)	Homo sapiens	77-80
2579862-7	1985	In the presence of both 8-bromo-cAMP and 8-bromo-cGMP, microheterogeneity of hCG in isoelectric focusing was diminished and the synthesis of more acidic hCG subpopulations was favoured.	8-Bromo Cyclic Adenosine Monophosphate	24-36	hypertrichosis 2 (generalised, congenital)	Homo sapiens	153-156
2579862-7	1985	In the presence of both 8-bromo-cAMP and 8-bromo-cGMP, microheterogeneity of hCG in isoelectric focusing was diminished and the synthesis of more acidic hCG subpopulations was favoured.	8-bromocyclic GMP	41-53	hypertrichosis 2 (generalised, congenital)	Homo sapiens	77-80
2579862-7	1985	In the presence of both 8-bromo-cAMP and 8-bromo-cGMP, microheterogeneity of hCG in isoelectric focusing was diminished and the synthesis of more acidic hCG subpopulations was favoured.	8-bromocyclic GMP	41-53	hypertrichosis 2 (generalised, congenital)	Homo sapiens	153-156
2981077-1	1985	The receptor binding properties and biological actions of chemically deglycosylated asialo human CG (AHF-hCG) were studied in ovarian granulosa cells from diethylstilbestrol (DES)-treated immature rats.	Diethylstilbestrol	175-178	hypertrichosis 2 (generalised, congenital)	Homo sapiens	97-99
4038724-2	1985	In this present study, we investigated the correlation between the preovulatory increase in progesterone and the periovulatory increase in plasminogen activator (PA) activities was completely suppressed with simultaneous injection with hCG of a minimum effective dose of cycloheximide to block ovulation completely.	Progesterone	92-104	hypertrichosis 2 (generalised, congenital)	Homo sapiens	236-239
4038724-2	1985	In this present study, we investigated the correlation between the preovulatory increase in progesterone and the periovulatory increase in plasminogen activator (PA) activities was completely suppressed with simultaneous injection with hCG of a minimum effective dose of cycloheximide to block ovulation completely.	Cycloheximide	271-284	hypertrichosis 2 (generalised, congenital)	Homo sapiens	236-239
4038724-3	1985	Suppression of hCG-induced acute rise of preovulatory progesterone after simultaneous injection with hCG of a minimum effective dose of cyanoketone to block ovulation completely, was accompanied by an only partial but significant suppression of hCG-induced increase in PA activities.	Cyanoketone	136-147	hypertrichosis 2 (generalised, congenital)	Homo sapiens	15-18
4038724-3	1985	Suppression of hCG-induced acute rise of preovulatory progesterone after simultaneous injection with hCG of a minimum effective dose of cyanoketone to block ovulation completely, was accompanied by an only partial but significant suppression of hCG-induced increase in PA activities.	Cyanoketone	136-147	hypertrichosis 2 (generalised, congenital)	Homo sapiens	101-104
4038724-3	1985	Suppression of hCG-induced acute rise of preovulatory progesterone after simultaneous injection with hCG of a minimum effective dose of cyanoketone to block ovulation completely, was accompanied by an only partial but significant suppression of hCG-induced increase in PA activities.	Cyanoketone	136-147	hypertrichosis 2 (generalised, congenital)	Homo sapiens	101-104
4038724-4	1985	Furthermore this suppression of PA activities after concurrent injection of cyanoketone with hCG was reversed by a supplementary injection of a dose of progesterone which was enough to restore ovulatory responses completely against the inhibitory action of cyanoketone.	Cyanoketone	76-87	hypertrichosis 2 (generalised, congenital)	Homo sapiens	93-96
4038724-4	1985	Furthermore this suppression of PA activities after concurrent injection of cyanoketone with hCG was reversed by a supplementary injection of a dose of progesterone which was enough to restore ovulatory responses completely against the inhibitory action of cyanoketone.	Progesterone	152-164	hypertrichosis 2 (generalised, congenital)	Homo sapiens	93-96
4038724-4	1985	Furthermore this suppression of PA activities after concurrent injection of cyanoketone with hCG was reversed by a supplementary injection of a dose of progesterone which was enough to restore ovulatory responses completely against the inhibitory action of cyanoketone.	Cyanoketone	257-268	hypertrichosis 2 (generalised, congenital)	Homo sapiens	93-96
3931598-5	1985	The MgAC could be stimulated by hormones (FSH, hCG, PGE1, isoproterenol, glucagon), the highest activation being achieved with FSH.	mgac	4-8	hypertrichosis 2 (generalised, congenital)	Homo sapiens	47-50
2981077-4	1985	When added with LH to FSH-treated cells, AHF-hCG inhibited LH-stimulated cAMP formation by 70% but did not alter the elevated level of progesterone production.	Cyclic AMP	73-77	hypertrichosis 2 (generalised, congenital)	Homo sapiens	45-48
2981077-6	1985	When added to freshly prepared granulosa cells which have minimal LH receptors, AHF-hCG decreased FSH-stimulated cAMP production by 20% and reduced progesterone production by 50% and increased cGMP formation by 100% during 48 h of culture.	Cyclic AMP	113-117	hypertrichosis 2 (generalised, congenital)	Homo sapiens	84-87
2981077-6	1985	When added to freshly prepared granulosa cells which have minimal LH receptors, AHF-hCG decreased FSH-stimulated cAMP production by 20% and reduced progesterone production by 50% and increased cGMP formation by 100% during 48 h of culture.	Progesterone	148-160	hypertrichosis 2 (generalised, congenital)	Homo sapiens	84-87
2981077-6	1985	When added to freshly prepared granulosa cells which have minimal LH receptors, AHF-hCG decreased FSH-stimulated cAMP production by 20% and reduced progesterone production by 50% and increased cGMP formation by 100% during 48 h of culture.	Cyclic GMP	193-197	hypertrichosis 2 (generalised, congenital)	Homo sapiens	84-87
2981077-8	1985	In contrast, native hCG did not alter FSH-induced cAMP or progesterone production but reduced the cGMP responses to FSH and choleragen.	Cyclic GMP	98-102	hypertrichosis 2 (generalised, congenital)	Homo sapiens	20-23
3972240-3	1985	The bursal extract inhibited the response of the testis cells to hCG detected as a reduced testosterone secretion.	Testosterone	91-103	hypertrichosis 2 (generalised, congenital)	Homo sapiens	65-68
2981077-10	1985	In choleragen-treated granulosa cells, the increases in cAMP and progesterone synthesis were enhanced by addition of both hCG and AHF-hCG, and cGMP production was increased by AHF-hCG but slightly decreased by hCG.	Cyclic AMP	56-60	hypertrichosis 2 (generalised, congenital)	Homo sapiens	122-125
2981077-10	1985	In choleragen-treated granulosa cells, the increases in cAMP and progesterone synthesis were enhanced by addition of both hCG and AHF-hCG, and cGMP production was increased by AHF-hCG but slightly decreased by hCG.	Cyclic AMP	56-60	hypertrichosis 2 (generalised, congenital)	Homo sapiens	134-137
2981077-10	1985	In choleragen-treated granulosa cells, the increases in cAMP and progesterone synthesis were enhanced by addition of both hCG and AHF-hCG, and cGMP production was increased by AHF-hCG but slightly decreased by hCG.	Cyclic AMP	56-60	hypertrichosis 2 (generalised, congenital)	Homo sapiens	134-137
2981077-10	1985	In choleragen-treated granulosa cells, the increases in cAMP and progesterone synthesis were enhanced by addition of both hCG and AHF-hCG, and cGMP production was increased by AHF-hCG but slightly decreased by hCG.	Cyclic AMP	56-60	hypertrichosis 2 (generalised, congenital)	Homo sapiens	134-137
2981077-10	1985	In choleragen-treated granulosa cells, the increases in cAMP and progesterone synthesis were enhanced by addition of both hCG and AHF-hCG, and cGMP production was increased by AHF-hCG but slightly decreased by hCG.	Progesterone	65-77	hypertrichosis 2 (generalised, congenital)	Homo sapiens	122-125
2981077-10	1985	In choleragen-treated granulosa cells, the increases in cAMP and progesterone synthesis were enhanced by addition of both hCG and AHF-hCG, and cGMP production was increased by AHF-hCG but slightly decreased by hCG.	Progesterone	65-77	hypertrichosis 2 (generalised, congenital)	Homo sapiens	134-137
2981077-10	1985	In choleragen-treated granulosa cells, the increases in cAMP and progesterone synthesis were enhanced by addition of both hCG and AHF-hCG, and cGMP production was increased by AHF-hCG but slightly decreased by hCG.	Progesterone	65-77	hypertrichosis 2 (generalised, congenital)	Homo sapiens	134-137
2981077-10	1985	In choleragen-treated granulosa cells, the increases in cAMP and progesterone synthesis were enhanced by addition of both hCG and AHF-hCG, and cGMP production was increased by AHF-hCG but slightly decreased by hCG.	Progesterone	65-77	hypertrichosis 2 (generalised, congenital)	Homo sapiens	134-137
2981077-11	1985	These results indicate that the enhanced LH receptor affinity caused by removal of the sugar moieties from hCG is accompanied by a relatively greater increase in FSH receptor affinity, and that deglycosylated hCG acts as a partial agonist with the ability to modify granulosa cell responses to both LH and FSH.	Sugars	87-92	hypertrichosis 2 (generalised, congenital)	Homo sapiens	107-110
2987495-0	1985	Relationship between hCG receptors disappearance and steroid accumulation during long term hCG stimulation in porcine Leydig cell cultures.	Steroids	53-60	hypertrichosis 2 (generalised, congenital)	Homo sapiens	21-24
3974230-1	1985	A collagenase dispersed cell suspension from PMSG-hCG primed immature rats responded to exogenously added hCG, cholera enteroxin, prolactin, and 8-Bromocyclic-AMP with increase in progesterone production in a dose dependent manner, and this stimulation was augmented by the plasma lipoprotein fractions hHDL and hLDL.	8-Bromo Cyclic Adenosine Monophosphate	145-162	hypertrichosis 2 (generalised, congenital)	Homo sapiens	50-53
3974230-1	1985	A collagenase dispersed cell suspension from PMSG-hCG primed immature rats responded to exogenously added hCG, cholera enteroxin, prolactin, and 8-Bromocyclic-AMP with increase in progesterone production in a dose dependent manner, and this stimulation was augmented by the plasma lipoprotein fractions hHDL and hLDL.	Progesterone	180-192	hypertrichosis 2 (generalised, congenital)	Homo sapiens	50-53
3974230-5	1985	Although the extent of hCG and prolactin stimulation of progesterone production and its potentiation by lipoprotein fractions was observed to be higher on days 3 and 5 than that seen on day 7, the net amount of progesterone produced was highest on day 7.	Progesterone	56-68	hypertrichosis 2 (generalised, congenital)	Homo sapiens	23-26
2982677-9	1985	hCG also stimulated cAMP release from the mouse thyroid, the increases being approximately 2.3- and 1.8-fold, in the presence of 2270 and 4540 IU/ml (4.5 and 9.0 X 10(-6) M), respectively.	Cyclic AMP	20-24	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
2987495-0	1985	Relationship between hCG receptors disappearance and steroid accumulation during long term hCG stimulation in porcine Leydig cell cultures.	Steroids	53-60	hypertrichosis 2 (generalised, congenital)	Homo sapiens	91-94
2987495-5	1985	A 50% receptor disappearance was obtained for 0.5 ng hCG/ml which led to a steroid accumulation of 50% of the maximal accumulation obtained with 100 ng/ml.	Steroids	75-82	hypertrichosis 2 (generalised, congenital)	Homo sapiens	53-56
6543041-1	1984	The effect of chloroquine injection to rats on in vitro-testosterone secretion stimulated by human chorionic gonadotropin (hCG) and prostaglandin E1 (PGE1) was studied.	Chloroquine	14-25	hypertrichosis 2 (generalised, congenital)	Homo sapiens	123-126
6510500-2	1984	Mice housed with 110 or 55 cm2 of floor space per animal showed the same basal serum testosterone and hCG-induced testosterone release.	Testosterone	114-126	hypertrichosis 2 (generalised, congenital)	Homo sapiens	102-105
6441784-4	1984	The early and late phases of the plasma testosterone to hCG in hyperprolactinaemic patients were comparable to those of the controls, although the maximum and relative increment was somewhat diminished (5.0 +/- 1.2 vs 7.2 +/- 2.1 ng/ml; P less than 0.05, and 1.8 +/- 0.2 vs 2.3 +/- 0.5 ng/ml; P less than 0.02, respectively).	Testosterone	40-52	hypertrichosis 2 (generalised, congenital)	Homo sapiens	56-59
6441784-5	1984	The plasma oestradiol response to hCG was not different between the two groups, but the maximum and relative incement was higher in the hyperprolactinaemic patients (135.9 +/- 20.6 vs 97.1 +/- 11.9 pg/ml; P less than 0.05, and 4.9 +/- 0.6 vs 3.1 +/- 0.5 pg/ml; P less than 0.01, respectively.	Estradiol	11-21	hypertrichosis 2 (generalised, congenital)	Homo sapiens	34-37
6543041-1	1984	The effect of chloroquine injection to rats on in vitro-testosterone secretion stimulated by human chorionic gonadotropin (hCG) and prostaglandin E1 (PGE1) was studied.	Testosterone	56-68	hypertrichosis 2 (generalised, congenital)	Homo sapiens	123-126
6543041-3	1984	Testosterone secretion was stimulated by hCG or PGE1 for 3 h in the removed testis and was measured by radioimmunoassay.	Testosterone	0-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	41-44
6543041-5	1984	However, in pubertal rats chloroquine treatment inhibited testosterone secretion in hCG-stimulated testis.	Chloroquine	26-37	hypertrichosis 2 (generalised, congenital)	Homo sapiens	84-87
6543041-5	1984	However, in pubertal rats chloroquine treatment inhibited testosterone secretion in hCG-stimulated testis.	Testosterone	58-70	hypertrichosis 2 (generalised, congenital)	Homo sapiens	84-87
6542566-10	1984	On d 16 medium follicles from control or hCG-injected gilts were larger, contained more estrogen and less progesterone than those recovered on d 13 (P less than .01).	Progesterone	106-118	hypertrichosis 2 (generalised, congenital)	Homo sapiens	41-44
6542566-9	1984	Tissue from large follicles of hCG-injected gilts produced more progesterone in vitro than did tissue from medium follicles (P less than .05), but estrogen production did not differ.	Progesterone	64-76	hypertrichosis 2 (generalised, congenital)	Homo sapiens	31-34
6090097-7	1984	ADX had no effect, and dexamethasone treatment decreased (16-20%) PRL binding to ventral prostate and hCG binding to rat testis.	Dexamethasone	23-36	hypertrichosis 2 (generalised, congenital)	Homo sapiens	102-105
6487695-7	1984	Yet in rats with decidual tissue, hCG stimulated progesterone production for at least 48 h and maintained the decidual tissue content of decidual luteotropin.	Progesterone	49-61	hypertrichosis 2 (generalised, congenital)	Homo sapiens	34-37
6090495-5	1984	hCG (1 IU/ml) stimulated a significant increase in progesterone production above basal levels after 72 h of culture, which continued to increase until 96 h of culture; 20 alpha-dihydroprogesterone (20 alpha-OH progesterone) production also was increased by hCG (1 IU/ml) at 72 h of culture, but unlike progesterone production, showed no further increase.	Progesterone	51-63	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
6151939-9	1984	The testicular testosterone concentration following stimulation with a low dose of hCG was significantly lower in abdominal testes.	Testosterone	15-27	hypertrichosis 2 (generalised, congenital)	Homo sapiens	83-86
6090495-5	1984	hCG (1 IU/ml) stimulated a significant increase in progesterone production above basal levels after 72 h of culture, which continued to increase until 96 h of culture; 20 alpha-dihydroprogesterone (20 alpha-OH progesterone) production also was increased by hCG (1 IU/ml) at 72 h of culture, but unlike progesterone production, showed no further increase.	alpha-dihydroprogesterone	171-196	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
6090495-5	1984	hCG (1 IU/ml) stimulated a significant increase in progesterone production above basal levels after 72 h of culture, which continued to increase until 96 h of culture; 20 alpha-dihydroprogesterone (20 alpha-OH progesterone) production also was increased by hCG (1 IU/ml) at 72 h of culture, but unlike progesterone production, showed no further increase.	alpha-oh progesterone	201-222	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
6090495-5	1984	hCG (1 IU/ml) stimulated a significant increase in progesterone production above basal levels after 72 h of culture, which continued to increase until 96 h of culture; 20 alpha-dihydroprogesterone (20 alpha-OH progesterone) production also was increased by hCG (1 IU/ml) at 72 h of culture, but unlike progesterone production, showed no further increase.	Progesterone	184-196	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
6090495-7	1984	In addition, progesterone production in the presence of hCG (10 IU/ml) decreased significantly (P less than 0.04) as 20 alpha-OH progesterone levels increased.	Progesterone	13-25	hypertrichosis 2 (generalised, congenital)	Homo sapiens	56-59
6090495-7	1984	In addition, progesterone production in the presence of hCG (10 IU/ml) decreased significantly (P less than 0.04) as 20 alpha-OH progesterone levels increased.	alpha-oh progesterone	120-141	hypertrichosis 2 (generalised, congenital)	Homo sapiens	56-59
6090495-9	1984	These results show that cultured human granulosa-luteal cells are responsive to hCG, with parallel increases in both progesterone production and [125I]hCG receptor binding.	Progesterone	117-129	hypertrichosis 2 (generalised, congenital)	Homo sapiens	80-83
6501084-5	1984	Leydig cells obtained from fetally-irradiated adult rats demonstrated increased basal (1.3 X) and LH-stimulated (4.4 X) testosterone production and increased hCG binding (4.8 X) per histochemically identified Leydig cell, as compared to cells obtained from nonirradiated control animals.	Luteinizing Hormone	98-100	hypertrichosis 2 (generalised, congenital)	Homo sapiens	158-161
6094687-5	1984	Cyclic AMP enhanced hCG secretion more markedly than LH-RH.	Cyclic AMP	0-10	hypertrichosis 2 (generalised, congenital)	Homo sapiens	20-23
6094687-6	1984	3) Retinoic acid had no effect on either cell proliferation or hCG secretion, whereas sodium butyrate inhibited both cell proliferation and hCG secretion.	Butyric Acid	86-101	hypertrichosis 2 (generalised, congenital)	Homo sapiens	140-143
6094687-7	1984	These results suggest that modifiers of hCG secretion may be grouped as follows; agents that inhibited cell proliferation slightly and enhanced hCG secretion markedly (LH-RH, cyclic AMP), agents that inhibited cell proliferation markedly and enhanced hCG secretion slightly (anticancer drugs) and agents that inhibited both cell proliferation and hCG secretion (estradiol, progesterone and sodium butyrate).	Cyclic AMP	175-185	hypertrichosis 2 (generalised, congenital)	Homo sapiens	40-43
6094687-7	1984	These results suggest that modifiers of hCG secretion may be grouped as follows; agents that inhibited cell proliferation slightly and enhanced hCG secretion markedly (LH-RH, cyclic AMP), agents that inhibited cell proliferation markedly and enhanced hCG secretion slightly (anticancer drugs) and agents that inhibited both cell proliferation and hCG secretion (estradiol, progesterone and sodium butyrate).	Estradiol	362-371	hypertrichosis 2 (generalised, congenital)	Homo sapiens	40-43
6094687-7	1984	These results suggest that modifiers of hCG secretion may be grouped as follows; agents that inhibited cell proliferation slightly and enhanced hCG secretion markedly (LH-RH, cyclic AMP), agents that inhibited cell proliferation markedly and enhanced hCG secretion slightly (anticancer drugs) and agents that inhibited both cell proliferation and hCG secretion (estradiol, progesterone and sodium butyrate).	Progesterone	373-385	hypertrichosis 2 (generalised, congenital)	Homo sapiens	40-43
6094687-7	1984	These results suggest that modifiers of hCG secretion may be grouped as follows; agents that inhibited cell proliferation slightly and enhanced hCG secretion markedly (LH-RH, cyclic AMP), agents that inhibited cell proliferation markedly and enhanced hCG secretion slightly (anticancer drugs) and agents that inhibited both cell proliferation and hCG secretion (estradiol, progesterone and sodium butyrate).	Butyric Acid	390-405	hypertrichosis 2 (generalised, congenital)	Homo sapiens	40-43
6477561-0	1984	An oligosaccharide of the O-linked type distinguishes the free from the combined form of hCG alpha subunit.	Oligosaccharides	3-18	hypertrichosis 2 (generalised, congenital)	Homo sapiens	89-92
6086278-3	1984	At 10(-9) M Ins the additive effect on hCG response became apparent (80% of maximal progesterone production).	Progesterone	84-96	hypertrichosis 2 (generalised, congenital)	Homo sapiens	39-42
6146510-3	1984	A biphasic testosterone response was seen in the scrotal (Scr) testis in response to hCG, with maxima at 1 h and 3 days after injection.	Testosterone	11-23	hypertrichosis 2 (generalised, congenital)	Homo sapiens	85-88
6086278-5	1984	hCG maximally stimulated cAMP production at 10(-10) M, whereas Ins neither stimulated cAMP production nor enhanced hCG response.	Cyclic AMP	25-29	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3
6747963-3	1984	However, indomethacin treatment of the recipients (10 mg/kg s.c. every 6 h from 120 to 168 h after hCG) prevented implantation of all transferred blastocysts, although 6 of the 8 rabbits died between Days 9 and 16 of (pseudo)pregnancy.	Indomethacin	9-21	hypertrichosis 2 (generalised, congenital)	Homo sapiens	99-102
6480142-1	1984	Serum testosterone responses to a single sc injection of hCG (25 IU/100 g body weight) were monitored for 5 days in rats throughout sexual maturation (22-70 days).	Testosterone	6-18	hypertrichosis 2 (generalised, congenital)	Homo sapiens	57-60
6735151-2	1984	The testosterone secretion in vitro, measured by radioimmunoassay, was employed to evaluate the response to hCG in testis from 8 to 16 days of incubation.	Testosterone	4-16	hypertrichosis 2 (generalised, congenital)	Homo sapiens	108-111
6735151-4	1984	On the contrary, at 12, 14, and 16 days a clear increase in testosterone secretion has been demonstrated when hCG was added to the culture medium.	Testosterone	60-72	hypertrichosis 2 (generalised, congenital)	Homo sapiens	110-113
6480142-2	1984	Two hours after hCG injection serum testosterone levels rose in 22, 37 and 53 day-old animals and remained elevated for 2 days, returning to control levels on day 3.	Testosterone	36-48	hypertrichosis 2 (generalised, congenital)	Homo sapiens	16-19
6480142-5	1984	Testosterone levels were elevated 2 h after hCG injection (25.4 +/- 2.5 ng/ml) and declined significantly at 12 and 24 h to 17.1 +/- 1.0 and 16.1 +/- 3.4 ng/ml, respectively.	Testosterone	0-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	44-47
6480142-8	1984	In vitro patterns of basal and hCG-stimulated testosterone secretion by decapsulated testes following a single hCG injection also changed during sexual maturation.	Testosterone	46-58	hypertrichosis 2 (generalised, congenital)	Homo sapiens	31-34
6480142-8	1984	In vitro patterns of basal and hCG-stimulated testosterone secretion by decapsulated testes following a single hCG injection also changed during sexual maturation.	Testosterone	46-58	hypertrichosis 2 (generalised, congenital)	Homo sapiens	111-114
6480142-9	1984	In 22 day-old animals the testes exhibited refractoriness to in vitro hCG stimulation at 12 h, but testes from 37 day old rats were refractory from 2 to 24 h. In vitro testosterone responses of testes from 53 and 70 day-old rats were similar to that reported for adult rats with a period of refractoriness from 12 h to 2 days.	Testosterone	168-180	hypertrichosis 2 (generalised, congenital)	Homo sapiens	70-73
6480142-10	1984	This study demonstrates that during sexual maturation in the rat alterations occur in the temporal patterns of testosterone secretion in vivo and in vitro following hCG stimulation.	Testosterone	111-123	hypertrichosis 2 (generalised, congenital)	Homo sapiens	165-168
6715352-5	1984	Under blockade of pregnenolone metabolism using cyanoketone and spironolactone, AVT, like hCG, stimulated pregnenolone accumulation with an ED50 dose of 5.8 +/- 0.3 X 10(-9) M. Similar effects were observed with several related neurohypophysial hormones, but not with nine unrelated peptides.	Pregnenolone	106-118	hypertrichosis 2 (generalised, congenital)	Homo sapiens	90-93
6715352-3	1984	Treatment with arginine vasotocin (AVT; 10(-6) M) over a 10-day period inhibited the human chorionic gonadotropin (hCG)-stimulated testosterone accumulation while enhancing hCG-stimulated progesterone accumulation.	Vasotocin	15-33	hypertrichosis 2 (generalised, congenital)	Homo sapiens	115-118
6726673-3	1984	When stimulated with hCG, testicular blood flow was increased in the low dose group; the testosterone concentrations in peripheral and testicular venous blood were also increased to a greater extent than those of the control group.	Testosterone	89-101	hypertrichosis 2 (generalised, congenital)	Homo sapiens	21-24
6715352-3	1984	Treatment with arginine vasotocin (AVT; 10(-6) M) over a 10-day period inhibited the human chorionic gonadotropin (hCG)-stimulated testosterone accumulation while enhancing hCG-stimulated progesterone accumulation.	Vasotocin	15-33	hypertrichosis 2 (generalised, congenital)	Homo sapiens	173-176
6715352-3	1984	Treatment with arginine vasotocin (AVT; 10(-6) M) over a 10-day period inhibited the human chorionic gonadotropin (hCG)-stimulated testosterone accumulation while enhancing hCG-stimulated progesterone accumulation.	Vasotocin	35-38	hypertrichosis 2 (generalised, congenital)	Homo sapiens	115-118
6715352-3	1984	Treatment with arginine vasotocin (AVT; 10(-6) M) over a 10-day period inhibited the human chorionic gonadotropin (hCG)-stimulated testosterone accumulation while enhancing hCG-stimulated progesterone accumulation.	Vasotocin	35-38	hypertrichosis 2 (generalised, congenital)	Homo sapiens	173-176
6715352-3	1984	Treatment with arginine vasotocin (AVT; 10(-6) M) over a 10-day period inhibited the human chorionic gonadotropin (hCG)-stimulated testosterone accumulation while enhancing hCG-stimulated progesterone accumulation.	Testosterone	131-143	hypertrichosis 2 (generalised, congenital)	Homo sapiens	115-118
6715352-3	1984	Treatment with arginine vasotocin (AVT; 10(-6) M) over a 10-day period inhibited the human chorionic gonadotropin (hCG)-stimulated testosterone accumulation while enhancing hCG-stimulated progesterone accumulation.	Progesterone	188-200	hypertrichosis 2 (generalised, congenital)	Homo sapiens	115-118
6715352-5	1984	Under blockade of pregnenolone metabolism using cyanoketone and spironolactone, AVT, like hCG, stimulated pregnenolone accumulation with an ED50 dose of 5.8 +/- 0.3 X 10(-9) M. Similar effects were observed with several related neurohypophysial hormones, but not with nine unrelated peptides.	Pregnenolone	18-30	hypertrichosis 2 (generalised, congenital)	Homo sapiens	90-93
6430026-6	1984	Five of these patients who had normal testosterone values after three doses of hCG had testosterone values below the normal range after seven doses.	Testosterone	87-99	hypertrichosis 2 (generalised, congenital)	Homo sapiens	79-82
6430026-8	1984	Testosterone values after stimulation with hCG were low in three and very low in the other seven.	Testosterone	0-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	43-46
6734929-6	1984	A single injection of 100 IU hCG induced a biphasic serum testosterone response with peaks in serum testosterone at 2 h and 72 h, the intervening nadir suggesting a period of in vivo refractoriness.	Testosterone	58-70	hypertrichosis 2 (generalised, congenital)	Homo sapiens	29-32
6726684-6	1984	Granulosa cells generated from all follicles responded to hCG treatment with significantly increased progesterone secretion after 4 days in culture.	Progesterone	101-113	hypertrichosis 2 (generalised, congenital)	Homo sapiens	58-61
6734929-6	1984	A single injection of 100 IU hCG induced a biphasic serum testosterone response with peaks in serum testosterone at 2 h and 72 h, the intervening nadir suggesting a period of in vivo refractoriness.	Testosterone	100-112	hypertrichosis 2 (generalised, congenital)	Homo sapiens	29-32
6725154-5	1984	Testosterone secretion rates were increased approximately fourfold during incubation with hCG; tissues from implanted animals secreted testosterone at a higher rate (P less than .05) than control tissues (b = 120.7 +/- 6.0 vs 81.6 +/- 6.0).	Testosterone	0-12	hypertrichosis 2 (generalised, congenital)	Homo sapiens	90-93
6323131-3	1984	Down-regulation was stimulated in FSH-primed granulosa cells by exposure to LH for 1 h. By 24 h after LH exposure, the LH/hCG receptor content, as measured using [125I]iodo-hCG was 70% less than controls.	Luteinizing Hormone	76-78	hypertrichosis 2 (generalised, congenital)	Homo sapiens	122-125
6323131-3	1984	Down-regulation was stimulated in FSH-primed granulosa cells by exposure to LH for 1 h. By 24 h after LH exposure, the LH/hCG receptor content, as measured using [125I]iodo-hCG was 70% less than controls.	Luteinizing Hormone	102-104	hypertrichosis 2 (generalised, congenital)	Homo sapiens	122-125
6323131-4	1984	To determine whether this loss of LH/hCG receptors was due to accelerated receptor degradation, turnover measurements were made using tunicamycin to inhibit LH/hCG receptor synthesis.	Tunicamycin	134-145	hypertrichosis 2 (generalised, congenital)	Homo sapiens	160-163
6323131-5	1984	Under these conditions, there was a small (16%) increase in the rate of degradation of LH/hCG receptors in LH-treated cells compared to controls.	Luteinizing Hormone	87-89	hypertrichosis 2 (generalised, congenital)	Homo sapiens	90-93
6323131-6	1984	By contrast, the rate of LH/hCG receptor synthesis, estimated mathematically, was reduced by 75% in the LH-treated cells.	Luteinizing Hormone	25-27	hypertrichosis 2 (generalised, congenital)	Homo sapiens	28-31
6323131-11	1984	In contrast, NH4Cl inhibited the degradation of receptor-bound [125I]iodo-hCG, suggesting that the ligand and the receptor may be handled differently by the granulosa cell.	Ammonium Chloride	13-18	hypertrichosis 2 (generalised, congenital)	Homo sapiens	74-77
6725154-5	1984	Testosterone secretion rates were increased approximately fourfold during incubation with hCG; tissues from implanted animals secreted testosterone at a higher rate (P less than .05) than control tissues (b = 120.7 +/- 6.0 vs 81.6 +/- 6.0).	Testosterone	135-147	hypertrichosis 2 (generalised, congenital)	Homo sapiens	90-93
6704473-6	1984	Treatment with propranolol or with butoxamine, a nonspecific beta- and a specific beta 2-adrenergic receptor blocker, respectively, antagonized the testicular hyposensitivity to hCG induced by stress.	Propranolol	15-26	hypertrichosis 2 (generalised, congenital)	Homo sapiens	178-181
6704473-6	1984	Treatment with propranolol or with butoxamine, a nonspecific beta- and a specific beta 2-adrenergic receptor blocker, respectively, antagonized the testicular hyposensitivity to hCG induced by stress.	Butoxamine	35-45	hypertrichosis 2 (generalised, congenital)	Homo sapiens	178-181
6317357-9	1984	Leydig cells desensitized in vivo by hCG treatment and isolated by elutriation were also resolved by Metrizamide gradients into 4 bands, but showed a redistribution in the gradient, due to the shift of about 50% of the cells originally present in the heaviest bands to lower density fractions.	Metrizamide	101-112	hypertrichosis 2 (generalised, congenital)	Homo sapiens	37-40
6200387-5	1984	beta hCG levels manifested a 1 to 1.5 log drop over the 8 days of chemotherapy and complete remission was noted within 5 to 6 weeks of the first dose of methotrexate.	Methotrexate	153-165	hypertrichosis 2 (generalised, congenital)	Homo sapiens	5-8
6328403-2	1984	Zn2+ at concentrations of 10(-6) to 10(-4) M enhanced the hCG-stimulated production of cyclic AMP and testosterone, but only in the presence of Ca2+ X [125I]hCG binding to rat testicular tissue was not affected by Zn2+ X Cu2+, Ni2+, Co2+, and Mn2+ did not increase cyclic AMP or testosterone production in concentrations of 10(-7) to 10(-3) M and even inhibited them at a high concentration (10(-2) M).	Zinc	0-4	hypertrichosis 2 (generalised, congenital)	Homo sapiens	58-61
6328403-2	1984	Zn2+ at concentrations of 10(-6) to 10(-4) M enhanced the hCG-stimulated production of cyclic AMP and testosterone, but only in the presence of Ca2+ X [125I]hCG binding to rat testicular tissue was not affected by Zn2+ X Cu2+, Ni2+, Co2+, and Mn2+ did not increase cyclic AMP or testosterone production in concentrations of 10(-7) to 10(-3) M and even inhibited them at a high concentration (10(-2) M).	Zinc	0-4	hypertrichosis 2 (generalised, congenital)	Homo sapiens	157-160
6328403-2	1984	Zn2+ at concentrations of 10(-6) to 10(-4) M enhanced the hCG-stimulated production of cyclic AMP and testosterone, but only in the presence of Ca2+ X [125I]hCG binding to rat testicular tissue was not affected by Zn2+ X Cu2+, Ni2+, Co2+, and Mn2+ did not increase cyclic AMP or testosterone production in concentrations of 10(-7) to 10(-3) M and even inhibited them at a high concentration (10(-2) M).	Cyclic AMP	87-97	hypertrichosis 2 (generalised, congenital)	Homo sapiens	58-61
6328403-2	1984	Zn2+ at concentrations of 10(-6) to 10(-4) M enhanced the hCG-stimulated production of cyclic AMP and testosterone, but only in the presence of Ca2+ X [125I]hCG binding to rat testicular tissue was not affected by Zn2+ X Cu2+, Ni2+, Co2+, and Mn2+ did not increase cyclic AMP or testosterone production in concentrations of 10(-7) to 10(-3) M and even inhibited them at a high concentration (10(-2) M).	Testosterone	102-114	hypertrichosis 2 (generalised, congenital)	Homo sapiens	58-61
6328403-2	1984	Zn2+ at concentrations of 10(-6) to 10(-4) M enhanced the hCG-stimulated production of cyclic AMP and testosterone, but only in the presence of Ca2+ X [125I]hCG binding to rat testicular tissue was not affected by Zn2+ X Cu2+, Ni2+, Co2+, and Mn2+ did not increase cyclic AMP or testosterone production in concentrations of 10(-7) to 10(-3) M and even inhibited them at a high concentration (10(-2) M).	zn2+ x	214-220	hypertrichosis 2 (generalised, congenital)	Homo sapiens	58-61
6328403-2	1984	Zn2+ at concentrations of 10(-6) to 10(-4) M enhanced the hCG-stimulated production of cyclic AMP and testosterone, but only in the presence of Ca2+ X [125I]hCG binding to rat testicular tissue was not affected by Zn2+ X Cu2+, Ni2+, Co2+, and Mn2+ did not increase cyclic AMP or testosterone production in concentrations of 10(-7) to 10(-3) M and even inhibited them at a high concentration (10(-2) M).	zn2+ x	214-220	hypertrichosis 2 (generalised, congenital)	Homo sapiens	157-160
6328403-2	1984	Zn2+ at concentrations of 10(-6) to 10(-4) M enhanced the hCG-stimulated production of cyclic AMP and testosterone, but only in the presence of Ca2+ X [125I]hCG binding to rat testicular tissue was not affected by Zn2+ X Cu2+, Ni2+, Co2+, and Mn2+ did not increase cyclic AMP or testosterone production in concentrations of 10(-7) to 10(-3) M and even inhibited them at a high concentration (10(-2) M).	cupric ion	221-225	hypertrichosis 2 (generalised, congenital)	Homo sapiens	58-61
6328403-2	1984	Zn2+ at concentrations of 10(-6) to 10(-4) M enhanced the hCG-stimulated production of cyclic AMP and testosterone, but only in the presence of Ca2+ X [125I]hCG binding to rat testicular tissue was not affected by Zn2+ X Cu2+, Ni2+, Co2+, and Mn2+ did not increase cyclic AMP or testosterone production in concentrations of 10(-7) to 10(-3) M and even inhibited them at a high concentration (10(-2) M).	cupric ion	221-225	hypertrichosis 2 (generalised, congenital)	Homo sapiens	157-160
6328403-2	1984	Zn2+ at concentrations of 10(-6) to 10(-4) M enhanced the hCG-stimulated production of cyclic AMP and testosterone, but only in the presence of Ca2+ X [125I]hCG binding to rat testicular tissue was not affected by Zn2+ X Cu2+, Ni2+, Co2+, and Mn2+ did not increase cyclic AMP or testosterone production in concentrations of 10(-7) to 10(-3) M and even inhibited them at a high concentration (10(-2) M).	Nickel(2+)	227-231	hypertrichosis 2 (generalised, congenital)	Homo sapiens	58-61
6328403-2	1984	Zn2+ at concentrations of 10(-6) to 10(-4) M enhanced the hCG-stimulated production of cyclic AMP and testosterone, but only in the presence of Ca2+ X [125I]hCG binding to rat testicular tissue was not affected by Zn2+ X Cu2+, Ni2+, Co2+, and Mn2+ did not increase cyclic AMP or testosterone production in concentrations of 10(-7) to 10(-3) M and even inhibited them at a high concentration (10(-2) M).	Nickel(2+)	227-231	hypertrichosis 2 (generalised, congenital)	Homo sapiens	157-160
6328403-2	1984	Zn2+ at concentrations of 10(-6) to 10(-4) M enhanced the hCG-stimulated production of cyclic AMP and testosterone, but only in the presence of Ca2+ X [125I]hCG binding to rat testicular tissue was not affected by Zn2+ X Cu2+, Ni2+, Co2+, and Mn2+ did not increase cyclic AMP or testosterone production in concentrations of 10(-7) to 10(-3) M and even inhibited them at a high concentration (10(-2) M).	Cobalt(2+)	233-237	hypertrichosis 2 (generalised, congenital)	Homo sapiens	58-61
6328403-2	1984	Zn2+ at concentrations of 10(-6) to 10(-4) M enhanced the hCG-stimulated production of cyclic AMP and testosterone, but only in the presence of Ca2+ X [125I]hCG binding to rat testicular tissue was not affected by Zn2+ X Cu2+, Ni2+, Co2+, and Mn2+ did not increase cyclic AMP or testosterone production in concentrations of 10(-7) to 10(-3) M and even inhibited them at a high concentration (10(-2) M).	Cobalt(2+)	233-237	hypertrichosis 2 (generalised, congenital)	Homo sapiens	157-160
6328403-2	1984	Zn2+ at concentrations of 10(-6) to 10(-4) M enhanced the hCG-stimulated production of cyclic AMP and testosterone, but only in the presence of Ca2+ X [125I]hCG binding to rat testicular tissue was not affected by Zn2+ X Cu2+, Ni2+, Co2+, and Mn2+ did not increase cyclic AMP or testosterone production in concentrations of 10(-7) to 10(-3) M and even inhibited them at a high concentration (10(-2) M).	Manganese(2+)	243-247	hypertrichosis 2 (generalised, congenital)	Homo sapiens	58-61
6328403-2	1984	Zn2+ at concentrations of 10(-6) to 10(-4) M enhanced the hCG-stimulated production of cyclic AMP and testosterone, but only in the presence of Ca2+ X [125I]hCG binding to rat testicular tissue was not affected by Zn2+ X Cu2+, Ni2+, Co2+, and Mn2+ did not increase cyclic AMP or testosterone production in concentrations of 10(-7) to 10(-3) M and even inhibited them at a high concentration (10(-2) M).	Manganese(2+)	243-247	hypertrichosis 2 (generalised, congenital)	Homo sapiens	157-160
6328403-2	1984	Zn2+ at concentrations of 10(-6) to 10(-4) M enhanced the hCG-stimulated production of cyclic AMP and testosterone, but only in the presence of Ca2+ X [125I]hCG binding to rat testicular tissue was not affected by Zn2+ X Cu2+, Ni2+, Co2+, and Mn2+ did not increase cyclic AMP or testosterone production in concentrations of 10(-7) to 10(-3) M and even inhibited them at a high concentration (10(-2) M).	Cyclic AMP	265-275	hypertrichosis 2 (generalised, congenital)	Homo sapiens	58-61
6328403-2	1984	Zn2+ at concentrations of 10(-6) to 10(-4) M enhanced the hCG-stimulated production of cyclic AMP and testosterone, but only in the presence of Ca2+ X [125I]hCG binding to rat testicular tissue was not affected by Zn2+ X Cu2+, Ni2+, Co2+, and Mn2+ did not increase cyclic AMP or testosterone production in concentrations of 10(-7) to 10(-3) M and even inhibited them at a high concentration (10(-2) M).	Cyclic AMP	265-275	hypertrichosis 2 (generalised, congenital)	Homo sapiens	157-160
6328403-2	1984	Zn2+ at concentrations of 10(-6) to 10(-4) M enhanced the hCG-stimulated production of cyclic AMP and testosterone, but only in the presence of Ca2+ X [125I]hCG binding to rat testicular tissue was not affected by Zn2+ X Cu2+, Ni2+, Co2+, and Mn2+ did not increase cyclic AMP or testosterone production in concentrations of 10(-7) to 10(-3) M and even inhibited them at a high concentration (10(-2) M).	Testosterone	279-291	hypertrichosis 2 (generalised, congenital)	Homo sapiens	58-61
6328403-2	1984	Zn2+ at concentrations of 10(-6) to 10(-4) M enhanced the hCG-stimulated production of cyclic AMP and testosterone, but only in the presence of Ca2+ X [125I]hCG binding to rat testicular tissue was not affected by Zn2+ X Cu2+, Ni2+, Co2+, and Mn2+ did not increase cyclic AMP or testosterone production in concentrations of 10(-7) to 10(-3) M and even inhibited them at a high concentration (10(-2) M).	Testosterone	279-291	hypertrichosis 2 (generalised, congenital)	Homo sapiens	157-160
6538898-3	1984	(2) Non-fertilized eggs first bisected, and the resulting sister halves activated 17 h after administration of hCG with ethyl alcohol.	Ethanol	120-133	hypertrichosis 2 (generalised, congenital)	Homo sapiens	111-114
6317357-10	1984	However, in spite of their changes in density, the Leydig cell bands still showed similar degrees of receptor down-regulation and impairment of the steroid responses to hCG in vitro.	Steroids	148-155	hypertrichosis 2 (generalised, congenital)	Homo sapiens	169-172
6093423-7	1984	Danazol (10 micrograms/ml) inhibited thecal cAMP production in most short-term experiments but only the hCG-stimulated cAMP production of granulosa cells.	Cyclic AMP	119-123	hypertrichosis 2 (generalised, congenital)	Homo sapiens	104-107
6486617-3	1984	In all children, immunoreactive plasma LH was high (4 to 30 mIU/ml) but non-responsive to LH-RH, due to the presence of hCG (15 to 6,000 mIU/ml).	Luteinizing Hormone	39-41	hypertrichosis 2 (generalised, congenital)	Homo sapiens	120-123
6100037-0	1984	Effects of the antiestrogen CI-628 on hCG-induced desensitization of testosterone in purified Leydig cells.	Nitromifene	28-34	hypertrichosis 2 (generalised, congenital)	Homo sapiens	38-41
6100037-0	1984	Effects of the antiestrogen CI-628 on hCG-induced desensitization of testosterone in purified Leydig cells.	Testosterone	69-81	hypertrichosis 2 (generalised, congenital)	Homo sapiens	38-41
6100037-3	1984	Steroidogenic desensitization to Bt2 cAMP and hCG stimulation in vitro was observed with both doses of hCG administered in vivo.	Bucladesine	33-41	hypertrichosis 2 (generalised, congenital)	Homo sapiens	103-106
6100037-5	1984	CI-628 in combination with hCG treatment in vivo led to testosterone production in vitro that was similar to that observed with hCG treatment alone.	Testosterone	56-68	hypertrichosis 2 (generalised, congenital)	Homo sapiens	27-30
6433822-3	1984	Although, testosterone levels were maintained at higher levels during hCG therapy for more than 10 days, inhibin and FSH levels returned back to pretreatment levels, indicating involvement of hCG in the regulation of circulating levels of inhibin.	Testosterone	10-22	hypertrichosis 2 (generalised, congenital)	Homo sapiens	70-73
6479696-0	1984	Effect of administration of progesterone on beta hCG blood level in early pregnancy.	Progesterone	28-40	hypertrichosis 2 (generalised, congenital)	Homo sapiens	49-52
6420302-6	1984	This azoospermia was not reversed by testosterone (T) replacement therapy, or by addition of HMG to T. In vitro, the crude hCG preparation stimulated cAMP accumulation in rat Sertoli cell cultures indicating that this hCG preparation possesses an "FSH-like" action.	Cyclic AMP	150-154	hypertrichosis 2 (generalised, congenital)	Homo sapiens	123-126
6231277-15	1984	Injection of hCG into control and agonist treated dogs resulted in similar percentage increases in plasma levels of testosterone, although peak levels were greater in control than in treated animals.	Testosterone	116-128	hypertrichosis 2 (generalised, congenital)	Homo sapiens	13-16
6098681-5	1984	Administration of hCG caused a significant increase in plasma testosterone levels in all genotypes.	Testosterone	62-74	hypertrichosis 2 (generalised, congenital)	Homo sapiens	18-21
6098681-6	1984	However, injection of the highest dose of hCG used (0.9 IU/g bw) caused a significantly greater elevation in plasma testosterone in Wx/Wv than in +/+ mice.	Testosterone	116-128	hypertrichosis 2 (generalised, congenital)	Homo sapiens	42-45
6323862-3	1984	The plasma membrane events that are rapidly activated by the specific interaction of LH or hCG with Leydig cell receptors include increased binding of guanyl nucleotide, and stimulation of cAMP-independent, Ca2+-dependent phosphorylation of a 44,500 Mr protein, with the characteristics of the adenylate cyclase nucleotide regulatory unit.	guanyl nucleotide	151-168	hypertrichosis 2 (generalised, congenital)	Homo sapiens	91-94
6323862-3	1984	The plasma membrane events that are rapidly activated by the specific interaction of LH or hCG with Leydig cell receptors include increased binding of guanyl nucleotide, and stimulation of cAMP-independent, Ca2+-dependent phosphorylation of a 44,500 Mr protein, with the characteristics of the adenylate cyclase nucleotide regulatory unit.	Cyclic AMP	189-193	hypertrichosis 2 (generalised, congenital)	Homo sapiens	91-94
6323862-7	1984	Large doses of hCG cause "early" (prior to pregnenolone) and "late" steroidogenic lesions (17 alpha-hydroxylase, 17-20 desmolase) that are independent of receptor loss.	Pregnenolone	43-55	hypertrichosis 2 (generalised, congenital)	Homo sapiens	15-18
6323862-10	1984	After hCG stimulation, an increase in nuclear E2 binding was accompanied by an early rise of RNA polymerase activities within 45 min coincident with the maximal increases in circulating testosterone and estradiol levels.	Testosterone	186-198	hypertrichosis 2 (generalised, congenital)	Homo sapiens	6-9
6323862-10	1984	After hCG stimulation, an increase in nuclear E2 binding was accompanied by an early rise of RNA polymerase activities within 45 min coincident with the maximal increases in circulating testosterone and estradiol levels.	Estradiol	203-212	hypertrichosis 2 (generalised, congenital)	Homo sapiens	6-9
6321273-3	1984	A single injection of 200 IU hCG induced a sharp increase of plasma testosterone which was still evident 24 h later.	Testosterone	68-80	hypertrichosis 2 (generalised, congenital)	Homo sapiens	29-32
6321273-5	1984	A second administration of 200 IU hCG, 48 h after the first injection, showed a similar pattern but on the 5th day there was an increased stimulation of testosterone production with respect to that obtained after a single dose of hCG.	Testosterone	153-165	hypertrichosis 2 (generalised, congenital)	Homo sapiens	34-37
6199440-7	1984	It is, therefore, possible that the temporary elevation of the hCG level observed in vitro after treatment with MTX is the result of an increase in secretion of hCG, rather than cellular damage.	Methotrexate	112-115	hypertrichosis 2 (generalised, congenital)	Homo sapiens	63-66
6199440-0	1984	[Effect of methotrexate on cell growth and the production of hCG, beta-hCG and SP-1 in cultured choriocarcinoma cell lines].	Methotrexate	11-23	hypertrichosis 2 (generalised, congenital)	Homo sapiens	61-64
6199440-6	1984	The ratio of the extra- to the intracellular hCG level was shown to be about 100:1 after the administration of MTX to BeWo and GCH-2.	Methotrexate	111-114	hypertrichosis 2 (generalised, congenital)	Homo sapiens	45-48
6199440-7	1984	It is, therefore, possible that the temporary elevation of the hCG level observed in vitro after treatment with MTX is the result of an increase in secretion of hCG, rather than cellular damage.	Methotrexate	112-115	hypertrichosis 2 (generalised, congenital)	Homo sapiens	161-164
6196179-3	1983	However, treatment with cycloheximide or puromycin before the hCG injection prevented the decrease in the activity of these enzymes by hCG.	Cycloheximide	24-37	hypertrichosis 2 (generalised, congenital)	Homo sapiens	62-65
6325320-0	1984	The effect of varying doses of hCG on the in vivo uptake by rat testis and serum testosterone response.	Testosterone	81-93	hypertrichosis 2 (generalised, congenital)	Homo sapiens	31-34
6325320-5	1984	These results suggest that the in vivo uptake of hCG in the testes is modulated by the hormone dose used and that the mode of early serum testosterone response to varying hCG doses is dose dependent.	Testosterone	138-150	hypertrichosis 2 (generalised, congenital)	Homo sapiens	49-52
6325320-5	1984	These results suggest that the in vivo uptake of hCG in the testes is modulated by the hormone dose used and that the mode of early serum testosterone response to varying hCG doses is dose dependent.	Testosterone	138-150	hypertrichosis 2 (generalised, congenital)	Homo sapiens	171-174
6196179-3	1983	However, treatment with cycloheximide or puromycin before the hCG injection prevented the decrease in the activity of these enzymes by hCG.	Cycloheximide	24-37	hypertrichosis 2 (generalised, congenital)	Homo sapiens	135-138
6196179-3	1983	However, treatment with cycloheximide or puromycin before the hCG injection prevented the decrease in the activity of these enzymes by hCG.	Puromycin	41-50	hypertrichosis 2 (generalised, congenital)	Homo sapiens	62-65
6196179-3	1983	However, treatment with cycloheximide or puromycin before the hCG injection prevented the decrease in the activity of these enzymes by hCG.	Puromycin	41-50	hypertrichosis 2 (generalised, congenital)	Homo sapiens	135-138
6198267-2	1983	We showed previously that sodium butyrate stimulated human chorionic gonadotropin (hCG) measured by radioimmunoassay of medium from human second trimester amniotic fluid cell cultures, termed AF cells.	Butyric Acid	26-41	hypertrichosis 2 (generalised, congenital)	Homo sapiens	83-86
6198267-3	1983	We now find that stimulation of hCG in the presence of sodium butyrate takes as long as 20 h. When AF cells are preincubated with sodium butyrate, hCG levels increase in direct relation to length of the preincubation period.	Butyric Acid	55-70	hypertrichosis 2 (generalised, congenital)	Homo sapiens	32-35
6198267-3	1983	We now find that stimulation of hCG in the presence of sodium butyrate takes as long as 20 h. When AF cells are preincubated with sodium butyrate, hCG levels increase in direct relation to length of the preincubation period.	Butyric Acid	55-70	hypertrichosis 2 (generalised, congenital)	Homo sapiens	147-150
6198267-3	1983	We now find that stimulation of hCG in the presence of sodium butyrate takes as long as 20 h. When AF cells are preincubated with sodium butyrate, hCG levels increase in direct relation to length of the preincubation period.	Butyric Acid	130-145	hypertrichosis 2 (generalised, congenital)	Homo sapiens	32-35
6198267-3	1983	We now find that stimulation of hCG in the presence of sodium butyrate takes as long as 20 h. When AF cells are preincubated with sodium butyrate, hCG levels increase in direct relation to length of the preincubation period.	Butyric Acid	130-145	hypertrichosis 2 (generalised, congenital)	Homo sapiens	147-150
6198267-5	1983	Addition of cycloheximide or Actinomycin D inhibited protein synthesis and RNA synthesis, respectively, and prevented the stimulation of hCG by sodium butyrate.	Cycloheximide	12-25	hypertrichosis 2 (generalised, congenital)	Homo sapiens	137-140
6196179-4	1983	Actinomycin D pretreatment prevented the hCG-induced decrease of C-17-C-20 lyase activity.	Dactinomycin	0-13	hypertrichosis 2 (generalised, congenital)	Homo sapiens	41-44
6198267-5	1983	Addition of cycloheximide or Actinomycin D inhibited protein synthesis and RNA synthesis, respectively, and prevented the stimulation of hCG by sodium butyrate.	Dactinomycin	29-42	hypertrichosis 2 (generalised, congenital)	Homo sapiens	137-140
6198267-5	1983	Addition of cycloheximide or Actinomycin D inhibited protein synthesis and RNA synthesis, respectively, and prevented the stimulation of hCG by sodium butyrate.	Butyric Acid	144-159	hypertrichosis 2 (generalised, congenital)	Homo sapiens	137-140
6196179-5	1983	In correlation with the changes in these enzyme activities induced by hCG, the concentration of ovarian microsomal cytochrome P-450 decreased to barely detectable level after hCG treatment; this decrease was also prevented by pretreatment with cycloheximide.	Cycloheximide	244-257	hypertrichosis 2 (generalised, congenital)	Homo sapiens	70-73
6198267-7	1983	Other agents reported to influence hCG production by different types of cell cultures include dibutyryl cyclic AMP, epidermal growth factor (EGF), methotrexate, and hydroxyurea.	Bucladesine	94-114	hypertrichosis 2 (generalised, congenital)	Homo sapiens	35-38
6196179-5	1983	In correlation with the changes in these enzyme activities induced by hCG, the concentration of ovarian microsomal cytochrome P-450 decreased to barely detectable level after hCG treatment; this decrease was also prevented by pretreatment with cycloheximide.	Cycloheximide	244-257	hypertrichosis 2 (generalised, congenital)	Homo sapiens	175-178
6198267-7	1983	Other agents reported to influence hCG production by different types of cell cultures include dibutyryl cyclic AMP, epidermal growth factor (EGF), methotrexate, and hydroxyurea.	Methotrexate	147-159	hypertrichosis 2 (generalised, congenital)	Homo sapiens	35-38
6198267-7	1983	Other agents reported to influence hCG production by different types of cell cultures include dibutyryl cyclic AMP, epidermal growth factor (EGF), methotrexate, and hydroxyurea.	Hydroxyurea	165-176	hypertrichosis 2 (generalised, congenital)	Homo sapiens	35-38
6668083-3	1983	In the presence of 1.5 X 10(-5) M BR, both basal and hCG-stimulated testosterone production were decreased whereas at lower doses BR was ineffective.	Bromocriptine	34-36	hypertrichosis 2 (generalised, congenital)	Homo sapiens	53-56
6668083-3	1983	In the presence of 1.5 X 10(-5) M BR, both basal and hCG-stimulated testosterone production were decreased whereas at lower doses BR was ineffective.	Testosterone	68-80	hypertrichosis 2 (generalised, congenital)	Homo sapiens	53-56
3317221-0	1987	[Comparison of the kinetics of the response of salivary and plasma 17-hydroxyprogesterone to the administration of HCG in men].	17-alpha-Hydroxyprogesterone	67-89	hypertrichosis 2 (generalised, congenital)	Homo sapiens	115-118
3317221-1	1987	17-hydroxyprogesterone (17-OHP) time course response to hCG (5,000 IU) was studied simultaneously in the saliva and the plasma of 12 adult healthy men.	17-alpha-Hydroxyprogesterone	0-22	hypertrichosis 2 (generalised, congenital)	Homo sapiens	56-59
3317221-1	1987	17-hydroxyprogesterone (17-OHP) time course response to hCG (5,000 IU) was studied simultaneously in the saliva and the plasma of 12 adult healthy men.	17-alpha-Hydroxyprogesterone	24-30	hypertrichosis 2 (generalised, congenital)	Homo sapiens	56-59