PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
15843462-6	2005	Instead, PGRP-LCa can form heterodimers with LCx when the latter is bound to monomeric peptidoglycan.	lcx	45-48	Peptidoglycan recognition protein LC	Drosophila melanogaster	9-17
14992878-13	2004	Regional wall motion at rest and peak stress in the LCx region demonstrated small but statistically significant improvements by 6 months in the IM bFGF and IV VEGF(165) groups only; no improvement was seen in the IM VEGF(165), IM vehicle, or sham groups.	lcx	52-55	vascular endothelial growth factor A	Sus scrofa	159-163
9595411-2	1998	In vehicle-treated animals, i.e. endothelin (ET)-1 produced an initial hyperemic response in the LCX, followed by a secondary reduction in flow.	lcx	97-100	endothelin 1	Canis lupus familiaris	33-50
12124344-0	2002	LCX, leukemia-associated protein with a CXXC domain, is fused to MLL in acute myeloid leukemia with trilineage dysplasia having t(10;11)(q22;q23).	lcx	0-3	maleless	Drosophila melanogaster	65-68
9869490-2	1998	Because inhibiting the Na-H exchanger (NHE) limits intracellular sodium ([Na]i) and subsequent [Ca]i accumulation, we hypothesized that NHE inhibition would attenuate regional dysfunction in response to 25 cycles of ischemia (I, 2-min) and reperfusion (R, 8-min) of the left circumflex coronary artery (LCx) in conscious swine.	lcx	303-306	solute carrier family 9 member A2	Sus scrofa	23-37
9869490-2	1998	Because inhibiting the Na-H exchanger (NHE) limits intracellular sodium ([Na]i) and subsequent [Ca]i accumulation, we hypothesized that NHE inhibition would attenuate regional dysfunction in response to 25 cycles of ischemia (I, 2-min) and reperfusion (R, 8-min) of the left circumflex coronary artery (LCx) in conscious swine.	lcx	303-306	solute carrier family 9 member A2	Sus scrofa	39-42
9869490-2	1998	Because inhibiting the Na-H exchanger (NHE) limits intracellular sodium ([Na]i) and subsequent [Ca]i accumulation, we hypothesized that NHE inhibition would attenuate regional dysfunction in response to 25 cycles of ischemia (I, 2-min) and reperfusion (R, 8-min) of the left circumflex coronary artery (LCx) in conscious swine.	lcx	303-306	solute carrier family 9 member A2	Sus scrofa	136-139
9893720-7	1998	RESULTS: All three VEGF treatment groups but not the control animals demonstrated a significant increase in the left-to-left (but not right-to-left) collateral index, myocardial blood flow (pre-therapy LCX vs. LAD (average of all groups): 0.76 +/- 0.35 vs. 0.96 +/- 0.38 ml*min-1*g-1, p = 0.03; post-therapy: LCX vs. LAD: 1.16 +/- 0.39 vs. 1.15 +/- 0.28 ml*min-1*g-1, p = NS) and coronary vasodilatory reserve 3 weeks after growth factor administration.	lcx	202-205	vascular endothelial growth factor A	Sus scrofa	19-23
9347213-7	1997	RESULTS: The plasma VIP concentrations in all three vessels were increased after 60 min of LCx occlusion.	lcx	91-94	vasoactive intestinal peptide	Canis lupus familiaris	20-23
9400370-9	1997	The increase in MAPK activity over that in control arteries ranged from 4.5- to 31.7-fold (mean +/- SEM, 10.7 +/- 5.3) in the LAD and 1.8- to 31.3-fold (mean +/- SEM, 9.7 +/- 5.7) in the LCx.	lcx	187-190	mitogen-activated protein kinase 1	Homo sapiens	16-20
8839224-6	1995	In three dogs with residual perfusion in the LCX central area ITF 296 also increased blood flow.	lcx	45-48	trefoil factor 3	Canis lupus familiaris	62-65
8899558-8	1996	A slight but significant increase in NPY levels was observed in both territories (LAD: from 190 +/- 27 to 349 +/- 62 pmol/l, LCX: 146 +/- 30 to 257 +/- 52 pmol/l) suggesting moderate stimulation of cardiac sympathetic nerve activity following LAD occlusion.	lcx	125-128	neuropeptide Y	Sus scrofa	37-40
8770115-6	1996	Microvascular relaxations to both VEGF or bFGF were significantly greater in vessels harvested from the collateral-perfused LCX region, compared with those taken from the normally perfused LAD region.	lcx	124-127	vascular endothelial growth factor A	Sus scrofa	34-38
8928888-5	1996	VEGF-treated animals demonstrated higher flow in the LCX territory during both rest and pacing compared with untreated controls (rest: 1.35 +/- 0.1 vs. 0.80 +/- 0.09 ml.min-1.g-1; pacing; 2.01 +/- 0.37 vs. 1.01 +/- 0.07 ml.min-1.g-1, P < 0.05, VEGF vs. controls).	lcx	53-56	vascular endothelial growth factor A	Sus scrofa	0-4
8928888-6	1996	The observed improvement in regional coronary flow in VEGF-treated animals resulted in better preservation of endothelium-dependent microvessel relaxation as well as fractional LV shortening in the LCX territory during pacing in the VEGF-treated than in control animals (controls: 7.1 +/ 2.6 vs. 3.6 +/- 2.0%, rest vs. pacing; VEGF: 6.9 +/- 2.9 vs. 6.3 +/- 2.9%, rest vs. pacing).	lcx	198-201	vascular endothelial growth factor A	Sus scrofa	54-58
8928888-6	1996	The observed improvement in regional coronary flow in VEGF-treated animals resulted in better preservation of endothelium-dependent microvessel relaxation as well as fractional LV shortening in the LCX territory during pacing in the VEGF-treated than in control animals (controls: 7.1 +/ 2.6 vs. 3.6 +/- 2.0%, rest vs. pacing; VEGF: 6.9 +/- 2.9 vs. 6.3 +/- 2.9%, rest vs. pacing).	lcx	198-201	vascular endothelial growth factor A	Sus scrofa	233-237
8928888-6	1996	The observed improvement in regional coronary flow in VEGF-treated animals resulted in better preservation of endothelium-dependent microvessel relaxation as well as fractional LV shortening in the LCX territory during pacing in the VEGF-treated than in control animals (controls: 7.1 +/ 2.6 vs. 3.6 +/- 2.0%, rest vs. pacing; VEGF: 6.9 +/- 2.9 vs. 6.3 +/- 2.9%, rest vs. pacing).	lcx	198-201	vascular endothelial growth factor A	Sus scrofa	233-237
7630126-7	1995	Chronic treatment with VEGF normalized responses to isoproterenol, NaF, and forskolin in the collateral-dependent LCx region.	lcx	114-117	vascular endothelial growth factor A	Sus scrofa	23-27
7630126-9	1995	The absolute increase in LCx blood flow was greater in the VEGF group than in the control group at rest (P < 0.05), but not during rapid pacing.	lcx	25-28	vascular endothelial growth factor A	Sus scrofa	59-63
9139993-2	1997	ET-1 and PGF2alpha were applied topically (100 microl every 3 min) to the external surface of the left circumflex coronary artery (LCx) in anesthetized dogs or to the bathing medium of isolated canine LCx rings in parallel in vitro experiments.	lcx	131-134	endothelin 1	Canis lupus familiaris	0-4
7521496-5	1994	NPY decreased LCX flow and increased CVR dose dependently in both groups, and there was no significant difference in the dose-response relation between the two groups.	lcx	14-17	neuropeptide Y	Canis lupus familiaris	0-3
7514110-4	1994	Beginning 10 days after placement of an LCx-constricting device, VEGF 45 micrograms (n = 9) or saline (n = 12) was administered daily via an indwelling catheter in the distal LCx, at a point just beyond the occlusion.	lcx	175-178	vascular endothelial growth factor A	Canis lupus familiaris	65-69
8293769-4	1993	Acetylcholine bradykinin and adenosine caused dose-dependent increases in CBF and LCX.	lcx	82-85	kininogen 1	Canis lupus familiaris	14-24
8293769-6	1993	Captopril potentiated the vasodilating effects of bradykinin and acetylcholine on LCX and CBF significantly (P < or = 0.05) and those of adenosine slightly.	lcx	82-85	kininogen 1	Canis lupus familiaris	50-60
7684576-3	1993	Ten weeks later V1 receptor blockade with the use of [d(CH2)5Tyr-(Me)]arginine vasopressin (10-12 micrograms/kg iv) increased resting transmural flow (radioactive microspheres) in the LCX region, indicating the presence of V1 receptors.	lcx	184-187	vasopressin	Sus scrofa	79-90
34652422-5	2022	We detected the point on the mitral annulus closest to the LCX (X point) and measured the minimum distance from the LCX to the mitral annulus (mCAD).	lcx	116-119	congenital cataract	Mus musculus	143-147
1800477-9	1991	Coronary angiography revealed that filling defects of dye were propagated from the third or distal branches to those of more proximal arteries when the doses of endothelin-1 were cumulatively infused into the LCX.	lcx	209-212	endothelin 1	Canis lupus familiaris	161-173
1772671-8	1991	The maximum LCX flow following PAPA 0.3 mg was comparable to peak reactive hyperaemia, but 10-15% higher after injection of 0.6-5.0 mg papaverine.	lcx	12-15	pappalysin 1	Homo sapiens	31-35
3248190-10	1988	In LSS, 50 to 92% increase of rCBF were noted as follows; LA: 79.7 23.7, RA: 66.1 18.1, RH: 58.6 17.6, LCx: 91.4 17.8 (ml/100 g/min).	lcx	103-106	CCAAT/enhancer binding protein zeta	Rattus norvegicus	30-34
3197695-5	1988	During limbic seizure in which spike discharges propagated to the LCx, rCBF in the LA, RA, LCx and LH increased to 220%, 130%, 120% and 190%, respectively.	lcx	66-69	CCAAT/enhancer binding protein zeta	Rattus norvegicus	71-75
30546626-3	2016	The 3D OCT, after the inflation of the jailed ostium of the LCx following the stent deployment to the LAD crossing the LCx, could clearly demonstrate a stent deformation and incomplete apposition at an opposite site of the LCx, which may cause high rates of restenosis and stent thrombosis.	lcx	60-63	plexin A2	Homo sapiens	7-10
3891380-8	1985	bradykinin-induced increases in LCX flow were augmented after captopril.	lcx	32-35	kininogen 1	Canis lupus familiaris	0-10
6387356-7	1984	RS was suppressed by 80% (P less than 0.05) 5 min after injection of BK into the LCx.	lcx	81-84	kininogen 1	Canis lupus familiaris	69-71
6387356-10	1984	These results indicate that BK injection into the LCx causes a prompt reduction in the rate of RS and that this response is reflexively mediated by the renal nerves.	lcx	50-53	kininogen 1	Canis lupus familiaris	28-30
31377485-14	2019	Notably, the expression of CTSL was significantly increased in postangioplasty LCx of vitamin D-deficient swine compared with the vitamin D-sufficient or vitamin D-supplemented animal groups.	lcx	79-82	cathepsin L1	Sus scrofa	27-31
28258851-10	2017	TLS was able to discriminate between coronary stenosis in the LAD, LCX or RCA.	lcx	67-70	FUS RNA binding protein	Homo sapiens	0-3
30546626-3	2016	The 3D OCT, after the inflation of the jailed ostium of the LCx following the stent deployment to the LAD crossing the LCx, could clearly demonstrate a stent deformation and incomplete apposition at an opposite site of the LCx, which may cause high rates of restenosis and stent thrombosis.	lcx	119-122	plexin A2	Homo sapiens	7-10
30546626-3	2016	The 3D OCT, after the inflation of the jailed ostium of the LCx following the stent deployment to the LAD crossing the LCx, could clearly demonstrate a stent deformation and incomplete apposition at an opposite site of the LCx, which may cause high rates of restenosis and stent thrombosis.	lcx	119-122	plexin A2	Homo sapiens	7-10
20935147-6	2010	Using a novel interstitial microdialysis method, MT1-MMP was directly measured and was over threefold higher in the LCx region and over twofold higher in the LAD region in the MI group compared with the no MI group at baseline.	lcx	116-119	matrix metallopeptidase 14	Sus scrofa	49-56
26995415-8	2015	Predilatation of LCX lesion was done with 2.5 x 08 mm NC Trek balloon.	lcx	17-20	potassium two pore domain channel subfamily K member 2	Homo sapiens	57-61
20935147-7	2010	MT1-MMP fluorogenic activity was persistently elevated in the LCx region in the MI and I/R group but remained unchanged in the LAD region.	lcx	62-65	matrix metallopeptidase 14	Sus scrofa	0-7
18046183-6	2007	LCX reactivity to acetylcholine (ACh), endothelin (ET-1), bradykinin (BK), and sodium nitroprusside (SNP) was assessed in vitro using standard techniques.	lcx	0-3	endothelin-1	Sus scrofa	51-55
19815231-1	2010	BACKGROUND: ST-segment depression in lead aVR in acute inferior wall ST-segment elevation myocardial infarction (STEMI) has recently been suggested as a predictor of left circumflex (LCx) artery involvement.	lcx	183-186	NLR family pyrin domain containing 6	Homo sapiens	42-45
19815231-5	2010	RESULTS: The sensitivity and specificity of aVR depression as a predictor of LCx infarction were 53% and 86%, respectively.	lcx	77-80	NLR family pyrin domain containing 6	Homo sapiens	44-47
19959766-9	2010	Our results suggest that exercise training significantly reduces familial hypercholesterolemic pig LCX maximal contractile responses to the endogenous constrictor ET-1, independent of PAT.	lcx	99-102	endothelin-1	Sus scrofa	163-167
18046183-7	2007	RESULTS: The results demonstrate that both ACh and ET-1 elicited dose-dependent increases in tension from LCX rings from all groups.	lcx	106-109	endothelin-1	Sus scrofa	51-55
18046183-9	2007	In contrast, removal of PAT increased ET-1-induced tension in LCX from NF-SED, HF-SED, and HF-EX but not NF-EX.	lcx	62-65	endothelin-1	Sus scrofa	38-42
18046183-12	2007	CONCLUSION: PAT blunts contractions induced by ET-1 in LCX from NF and HF pigs.	lcx	55-58	endothelin-1	Sus scrofa	47-51
17234725-10	2007	In EX LCX arterioles, vasodilation to NOS activators was slightly inhibited by L-NAME but abolished by catalase.	lcx	6-9	catalase	Homo sapiens	103-111