PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
23532682-1	2013	DAI is a leading cause of the patient"s death or lasting vegetable state following severe TBI, and up to now the detailed mechanism of axonal injury after head trauma is still unclear.	Thioacetazone	90-93	Z-DNA binding protein 1	Homo sapiens	0-3
24102571-9	2013	The percentage of CBF reduction was greater in the CON group than in the TBI group (difference = 13.9%, 95% CI = 5.5-22.2%, p = 0.002).	Thioacetazone	73-76	CCAAT enhancer binding protein zeta	Homo sapiens	18-21
22421507-1	2013	Numerous experimental studies in recent years have suggested that erythropoietin (EPO) is an endogenous mediator of neuroprotection in various central nervous system disorders, including TBI.	Thioacetazone	187-190	erythropoietin	Homo sapiens	66-80
22421507-1	2013	Numerous experimental studies in recent years have suggested that erythropoietin (EPO) is an endogenous mediator of neuroprotection in various central nervous system disorders, including TBI.	Thioacetazone	187-190	erythropoietin	Homo sapiens	82-85
22421507-2	2013	Many characteristics of EPO neuroprotection that have been defined in TBI experimental models suggest that it is an attractive candidate for a new treatment of TBI.	Thioacetazone	70-73	erythropoietin	Homo sapiens	24-27
22421507-2	2013	Many characteristics of EPO neuroprotection that have been defined in TBI experimental models suggest that it is an attractive candidate for a new treatment of TBI.	Thioacetazone	160-163	erythropoietin	Homo sapiens	24-27
22421507-3	2013	EPO targets multiple mechanisms known to cause secondary injury after TBI, including anti-excitotoxic, antioxidant, anti-edematous, and anti-inflammatory mechanisms.	Thioacetazone	70-73	erythropoietin	Homo sapiens	0-3
25379227-7	2013	Negative correlations between endorsement of an inappropriate behavior and anticipation of negative emotional consequences were significant for both TBI-ASB and control subjects, but not for TBI-ISB subjects.	Thioacetazone	149-152	arylsulfatase B	Homo sapiens	153-156
23318965-5	2012	An MRD was unavailable for this patient, so we decided on emergent transplantation and successfully performed CB transplantation (CBT) using a low-dose TBI conditioning regimen.	Thioacetazone	152-155	opsin 1, short wave sensitive	Homo sapiens	130-133
23710117-7	2013	In addition, neurological and motor deficits, cerebral contusion, and increased brain TNF-alpha contents caused by TBI can be attenuated by etanercept therapy.	Thioacetazone	115-118	tumor necrosis factor	Rattus norvegicus	86-95
23483949-4	2013	TBI resulted in an increase in anxiety-like behavior and its molecular counterpart NPY1R, a hallmark of PTSD, but these effects were more pronounced in the animals exposed to n-3 deficient diet and switched to WD.	Thioacetazone	0-3	neuropeptide Y receptor Y1	Rattus norvegicus	83-88
23318965-5	2012	An MRD was unavailable for this patient, so we decided on emergent transplantation and successfully performed CB transplantation (CBT) using a low-dose TBI conditioning regimen.	Thioacetazone	152-155	opsin 1, short wave sensitive	Homo sapiens	110-128
23656249-7	2013	In patients with CPHB, increased PDCD5 levels correlated well with AST, TBI, DBIL, and IBIL.	Thioacetazone	72-75	programmed cell death 5	Homo sapiens	33-38
23756974-4	2013	The aim of the present study was to examine the changes in the plasma adiponectin levels and the immunoreactivity of adiponectin in the brain after TBI.	Thioacetazone	148-151	adiponectin, C1Q and collagen domain containing	Rattus norvegicus	117-128
23756974-10	2013	CONCLUSION: Our findings suggest that adiponectin might participate in the pathophysiological process occurring after TBI.	Thioacetazone	118-121	adiponectin, C1Q and collagen domain containing	Rattus norvegicus	38-49
22827467-7	2012	These findings suggest that the activation of the JaK/STAT and Egr3 pathways after TBI may regulate injury-related changes in GABA(A)R subunit expression.	Thioacetazone	83-86	early growth response 3	Rattus norvegicus	63-67
22327727-9	2012	A single dose of AF-16 maintained the raised ICP after a TBI lowered during 3-9 h. The AF protein, enriched in egg yolk, similarly lowered the post-traumatically raised ICP in rats.	Thioacetazone	57-60	proteasome 26S subunit ubiquitin receptor, non-ATPase 4	Rattus norvegicus	17-19
22691970-5	2012	METHODS: Effect of a mouse anti-VEGF antibody was monitored on acute toxicity studying radiation-induced intestinal ulceration (12 Gy TBI); on subacute toxicity using a model of oral mucositis (16.5 Gy); on late radiation injuries by monitoring lung fibrosis (bleomycin and 19 Gy).	Thioacetazone	134-137	vascular endothelial growth factor A	Mus musculus	32-36
22914361-3	2012	Here, the ex vivo phenotype of CD4(+) and CD8(+) T cells and the frequency and phenotype of gamma interferon (IFN-gamma)- and interleukin 17 (IL-17)-producing cells elicited in short-term and long-term cultures following CFP-10 and purified protein derivative (PPD) stimulation were determined in noninfected persons (non-TBi), latently infected persons (LTBi), and patients with active tuberculosis (ATB).	Thioacetazone	322-325	interleukin 17A	Homo sapiens	142-147
22485176-5	2012	METHODOLOGY/PRINCIPAL FINDINGS: The results revealed that NADPH oxidase activity in the cerebral cortex and hippocampal CA1 region increases rapidly following controlled cortical impact in male mice, with an early peak at 1 h, followed by a secondary peak from 24-96 h after TBI.	Thioacetazone	275-278	carbonic anhydrase 1	Mus musculus	120-123
22725661-1	2012	OBJECTIVES: To evaluate the ability of S100B to predict severity of TBI and abnormal cranial CT results for children with TBI.	Thioacetazone	68-71	S100 calcium binding protein B	Homo sapiens	39-44
22725661-4	2012	The mean S100B levels were higher in children with moderate/severe TBI as compared to children with mild TBI based GCS score (0.281 microg L(-1), 95%CI = 0.101, 0.461 vs 0.053, 95%CI = 0.010, 0.095).	Thioacetazone	67-70	S100 calcium binding protein B	Homo sapiens	9-14
22725661-4	2012	The mean S100B levels were higher in children with moderate/severe TBI as compared to children with mild TBI based GCS score (0.281 microg L(-1), 95%CI = 0.101, 0.461 vs 0.053, 95%CI = 0.010, 0.095).	Thioacetazone	105-108	S100 calcium binding protein B	Homo sapiens	9-14
22725661-5	2012	S100B levels were significantly elevated in children following TBI with abnormal cranial CT as compared to children with a normal cranial CT (0.210 microg L(-1), SD = 0.313 vs 0.036 microg L(-1), SD = 0.046, p = 0.03).	Thioacetazone	63-66	S100 calcium binding protein B	Homo sapiens	0-5
22725661-6	2012	Area under the curve for S100B was also significant (0.72, 95%CI = 0.58, 0.86) for prediction of abnormal cranial CT for children with TBI.	Thioacetazone	135-138	S100 calcium binding protein B	Homo sapiens	25-30
22725661-8	2012	CONCLUSIONS: For children following TBI, S100B appears to predict severity of TBI; however, it may not be clinically useful as an independent screening test to select children with mild TBI who need a cranial CT.	Thioacetazone	36-39	S100 calcium binding protein B	Homo sapiens	41-46
22794497-1	2012	OBJECTIVE: To evaluate microtubule-associated proteins (MAP-2), a dendritic marker of both acute damage and chronic neuronal regeneration after injury, in serum of survivors after severe TBI and examine the association with long-term outcome.	Thioacetazone	187-190	microtubule associated protein 2	Homo sapiens	56-61
22794497-4	2012	RESULTS: Severe TBI patients had significantly higher serum MAP-2 concentrations than normal controls with no history of TBI (p = 0.008) at 6 months post-injury.	Thioacetazone	16-19	microtubule associated protein 2	Homo sapiens	60-65
22794497-8	2012	CONCLUSIONS: Severe TBI results in a chronic release of MAP-2 into the peripheral circulation in patients with higher levels of consciousness, suggesting that remodelling of synaptic junctions and neuroplasticity processes occur several months after injury.	Thioacetazone	20-23	microtubule associated protein 2	Homo sapiens	56-61
22529521-1	2012	It has been proved that Nrf2 depletion enhances inflammatory process through activation of NF-kappaB in the brain after TBI, but little is known about the relationship between Nrf2 and NF-kappaB in astrocytes after TBI.	Thioacetazone	120-123	nuclear factor, erythroid derived 2, like 2	Mus musculus	24-28
22529521-1	2012	It has been proved that Nrf2 depletion enhances inflammatory process through activation of NF-kappaB in the brain after TBI, but little is known about the relationship between Nrf2 and NF-kappaB in astrocytes after TBI.	Thioacetazone	120-123	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	91-100
22529521-1	2012	It has been proved that Nrf2 depletion enhances inflammatory process through activation of NF-kappaB in the brain after TBI, but little is known about the relationship between Nrf2 and NF-kappaB in astrocytes after TBI.	Thioacetazone	215-218	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	185-194
22485176-10	2012	In addition, a NOX2-specific inhibitor, gp91ds-tat was also shown to exert neuroprotection against TBI.	Thioacetazone	99-102	cytochrome b-245, beta polypeptide	Mus musculus	15-19
23336085-7	2011	Posttraumatic hypothermia significantly reduced the number of CC1 positive oligodendrocytes lost after normothermia TBI in white matter tracts (p<0.01).	Thioacetazone	116-119	Cardiac cell morphology QTL 1	Rattus norvegicus	62-65
22015765-0	2011	Different quantitative EEG alterations induced by TBI among patients with different APOE genotypes.	Thioacetazone	50-53	apolipoprotein E	Homo sapiens	84-88
22015765-1	2011	Although several studies have revealed the EEG alterations in AD and TBI patients, the influence of APOE (apolipoprotein E) genotype in EEG at the early stage of TBI has not been reported yet.	Thioacetazone	162-165	apolipoprotein E	Homo sapiens	100-104
22015765-1	2011	Although several studies have revealed the EEG alterations in AD and TBI patients, the influence of APOE (apolipoprotein E) genotype in EEG at the early stage of TBI has not been reported yet.	Thioacetazone	162-165	apolipoprotein E	Homo sapiens	106-122
22015765-2	2011	We have previously studied EEG alterations caused by TBI among different APOE genotype carriers.	Thioacetazone	53-56	apolipoprotein E	Homo sapiens	73-77
22015765-3	2011	In this study, we firstly investigated the relationship between APOE polymorphisms and quantitative EEG (QEEG) changes after TBI.	Thioacetazone	125-128	apolipoprotein E	Homo sapiens	64-68
22015765-8	2011	APOE gene did not influence brain electrical activity under normal conditions, but TBI can induce different alterations among different APOE gene carriers, and APOEe4 allele enhances the EEG abnormalities at the early stage of TBI.	Thioacetazone	83-86	apolipoprotein E	Homo sapiens	136-140
22015765-8	2011	APOE gene did not influence brain electrical activity under normal conditions, but TBI can induce different alterations among different APOE gene carriers, and APOEe4 allele enhances the EEG abnormalities at the early stage of TBI.	Thioacetazone	227-230	apolipoprotein E	Homo sapiens	0-4
21596098-2	2011	In this study, we aimed to survey the role of JAK2/STAT pathway in the progress of TBI.	Thioacetazone	83-86	Janus kinase 2	Rattus norvegicus	46-50
21596098-6	2011	Western blotting revealed that expression of p-JAK2, p-STAT1 and p-STAT3 increased immediately, peaked at 3h after TBI and decreased thereafter, and the activation could be inhibited by AG490.	Thioacetazone	115-118	Janus kinase 2	Rattus norvegicus	47-51
21596098-6	2011	Western blotting revealed that expression of p-JAK2, p-STAT1 and p-STAT3 increased immediately, peaked at 3h after TBI and decreased thereafter, and the activation could be inhibited by AG490.	Thioacetazone	115-118	signal transducer and activator of transcription 1	Rattus norvegicus	55-60
21596098-6	2011	Western blotting revealed that expression of p-JAK2, p-STAT1 and p-STAT3 increased immediately, peaked at 3h after TBI and decreased thereafter, and the activation could be inhibited by AG490.	Thioacetazone	115-118	signal transducer and activator of transcription 3	Rattus norvegicus	67-72
21596098-7	2011	Immunohistochemical study showed that JAK2/STAT pathway was activated in both neurons and astrocytes at 3h after TBI.	Thioacetazone	113-116	Janus kinase 2	Rattus norvegicus	38-42
21596098-10	2011	Our results suggest that the JAK2/STAT pathway is activated in pericontusional cortex of rats, and may be involved in the neurological function recovery after TBI.	Thioacetazone	159-162	Janus kinase 2	Rattus norvegicus	29-33
21466884-1	2011	AIM: Antioxidant transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) has been shown in our previous studies to play a crucial role in protection against TBI induced inflammatory response in the brain.	Thioacetazone	173-176	nuclear factor, erythroid derived 2, like 2	Mus musculus	38-81
21466884-1	2011	AIM: Antioxidant transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) has been shown in our previous studies to play a crucial role in protection against TBI induced inflammatory response in the brain.	Thioacetazone	173-176	nuclear factor, erythroid derived 2, like 2	Mus musculus	83-87
21466884-2	2011	The objective of this study was to test whether tert-butylhydroquinone (tBHQ), a novel Nrf2 activator, can protect mice brain against TBI-induced inflammatory damage.	Thioacetazone	134-137	telomerase reverse transcriptase	Mus musculus	48-52
21466884-2	2011	The objective of this study was to test whether tert-butylhydroquinone (tBHQ), a novel Nrf2 activator, can protect mice brain against TBI-induced inflammatory damage.	Thioacetazone	134-137	nuclear factor, erythroid derived 2, like 2	Mus musculus	87-91
21265299-1	2010	The Traumatic Brain Injury Screening Instrument (TBISI) was implemented in Veterans Affairs medical facilities in an attempt to identify Operation Enduring Freedom and Operation Iraqi Freedom (OEF/OIF) veterans with possible mild TBI.	Thioacetazone	49-52	osteoglycin	Homo sapiens	197-200
21219958-2	2011	Previously, IGF-1 (Insulin like growth factor 1) administration prevented TBI-induced damage.	Thioacetazone	74-77	insulin-like growth factor 1	Mus musculus	12-17
21219958-2	2011	Previously, IGF-1 (Insulin like growth factor 1) administration prevented TBI-induced damage.	Thioacetazone	74-77	insulin-like growth factor 1	Mus musculus	19-47
21265299-3	2010	The current study reports preliminary findings on the test-retest reliability of the TBISI in 44 OEF/OIF veterans referred for neuropsychological evaluation following a positive TBI screen.	Thioacetazone	85-88	osteoglycin	Homo sapiens	101-104
20062090-6	2010	Patients conditioned with 4 Gy TBI had higher TNFR1 day 7/baseline ratio than those conditioned with 2 Gy TBI (median 1.65 versus 1.25; P=0.01).	Thioacetazone	31-34	TNF receptor superfamily member 1A	Homo sapiens	46-51
19718070-6	2010	TBI alone significantly upregulated transforming growth factor-beta (TGF-beta), IL-6 and p19 mRNA levels in host BALB/c mice, possibly providing the milieu to induce IL-17 in p19-/- donor cells.	Thioacetazone	0-3	interleukin 6	Mus musculus	80-84
20205514-9	2010	These data suggest a protective role for TNFR2/Fas in the pathogenesis of TBI.	Thioacetazone	74-77	tumor necrosis factor receptor superfamily, member 1a	Mus musculus	41-46
19842078-4	2010	Serum S100 beta appears to be a poor predictor of the outcome following mild TBI.	Thioacetazone	77-80	S100 calcium binding protein B	Homo sapiens	6-15
19718070-6	2010	TBI alone significantly upregulated transforming growth factor-beta (TGF-beta), IL-6 and p19 mRNA levels in host BALB/c mice, possibly providing the milieu to induce IL-17 in p19-/- donor cells.	Thioacetazone	0-3	interleukin 23, alpha subunit p19	Mus musculus	89-92
19718070-6	2010	TBI alone significantly upregulated transforming growth factor-beta (TGF-beta), IL-6 and p19 mRNA levels in host BALB/c mice, possibly providing the milieu to induce IL-17 in p19-/- donor cells.	Thioacetazone	0-3	interleukin 17A	Mus musculus	166-171
19718070-6	2010	TBI alone significantly upregulated transforming growth factor-beta (TGF-beta), IL-6 and p19 mRNA levels in host BALB/c mice, possibly providing the milieu to induce IL-17 in p19-/- donor cells.	Thioacetazone	0-3	interleukin 23, alpha subunit p19	Mus musculus	175-178
20448310-1	2010	OBJECTIVE: to determine the potential impacts of Operation Enduring Freedom (OEF) and Operation Iraqi Freedom (OIF) on the incidence of TBI-related hospitalization in the active duty US Army.	Thioacetazone	136-139	osteoglycin	Homo sapiens	111-114
19812958-6	2010	Following brain injury, S100B levels were significantly increased in the serum (p < 0.05 in SAH day 2-5, TBI day 1-8) and excessively increased in the CSF (p < 0.05 in SAH and TBI day 1-10).	Thioacetazone	108-111	S100 calcium binding protein B	Homo sapiens	24-29
19812958-6	2010	Following brain injury, S100B levels were significantly increased in the serum (p < 0.05 in SAH day 2-5, TBI day 1-8) and excessively increased in the CSF (p < 0.05 in SAH and TBI day 1-10).	Thioacetazone	182-185	S100 calcium binding protein B	Homo sapiens	24-29
20235763-1	2010	PRIMARY OBJECTIVE: To study the predictive capacity of early S100beta samples for long-term outcome prediction after severe TBI.	Thioacetazone	124-127	S100 calcium binding protein B	Homo sapiens	61-69
20235763-4	2010	S100beta concentration was quantified at admission and 24, 48 and 72 hours post-TBI (days 0, 1, 2 and 3).	Thioacetazone	80-83	S100 calcium binding protein B	Homo sapiens	0-8
20235763-11	2010	CONCLUSIONS: A temporal profile of S100beta release from admission to 72 hours post-TBI is strongly recommended for use in identifying patients at risk of developing a worse outcome.	Thioacetazone	84-87	S100 calcium binding protein B	Homo sapiens	35-43
20235763-12	2010	The S100beta protein might be an early biomarker for predicting long-term outcome in patients with acute severe TBI.	Thioacetazone	112-115	S100 calcium binding protein B	Homo sapiens	4-12
19833158-13	2010	In addition elevated C/EBPdelta levels following TBI in the aged brain may play a role in the link between TBI and Alzheimer"s disease.	Thioacetazone	49-52	CCAAT/enhancer binding protein (C/EBP), delta	Mus musculus	21-31
19833158-13	2010	In addition elevated C/EBPdelta levels following TBI in the aged brain may play a role in the link between TBI and Alzheimer"s disease.	Thioacetazone	107-110	CCAAT/enhancer binding protein (C/EBP), delta	Mus musculus	21-31
20448310-7	2010	The increases in TBI hospitalizations coincided with the occurrence of OEF/OIF.	Thioacetazone	17-20	osteoglycin	Homo sapiens	71-78
20448310-8	2010	During OEF/OIF, the Army"s hospitalization rates for moderate and severe TBIs were lower than civilian rates; however, the Army"s hospitalization rate for mild TBIs was higher than civilian rates.	Thioacetazone	73-77	osteoglycin	Homo sapiens	0-14
20448310-9	2010	CONCLUSION: OEF/OIF appear to have had a substantial impact on TBI-related hospitalization rates in the active duty US Army but differences between Army and civilian rates were not as excessive as expected.	Thioacetazone	63-66	osteoglycin	Homo sapiens	12-19
19308039-1	2009	Impairment of glucose metabolism (in particular insulin resistance and type 2 diabetes mellitus) has been reported in patients who have undergone hematopoietic SCT (HSCT) during childhood, especially those treated with TBI.	Thioacetazone	219-222	insulin	Homo sapiens	48-55
19308039-8	2009	Insulin resistance is frequently observed in adult survivors of HSCT treated with TBI in childhood.	Thioacetazone	82-85	insulin	Homo sapiens	0-7
18948378-2	2009	We report here that human flavin-containing monooxygenase 2.1 (FMO2.1), which is expressed predominantly in the lung, catalyzes oxygenation of TAZ.	Thioacetazone	143-146	flavin containing dimethylaniline monoxygenase 2	Homo sapiens	63-67
19257803-16	2009	ROC analysis demonstrated a significant relationship between Q(A) and serum S100B concentrations at 12 h after TBI (AUC = 0.800; SE 0.147, 95% CI 0.511-1.089).	Thioacetazone	111-114	S100 calcium binding protein B	Homo sapiens	76-81
19257803-18	2009	We conclude that serum S100B concentrations accurately indicate BBB dysfunction at 12 h after TBI.	Thioacetazone	94-97	S100 calcium binding protein B	Homo sapiens	23-28
19501075-9	2009	Our microarray based analysis of microRNA expression in rat cerebral cortex after traumatic brain injury has shown that some microRNA such as miR-21 could be involved in the intricate process of TBI course.	Thioacetazone	195-198	microRNA 21	Rattus norvegicus	142-148
19210118-1	2009	The expression of the neutrophil chemokine macrophage inflammatory protein-2 (MIP-2/CXCL2) and the monocyte chemokine monocyte chemotactic protein-1 (MCP-1/CCL2) have been described in glial cells in vitro but their origin following TBI has not been established.	Thioacetazone	233-236	C-C motif chemokine ligand 2	Rattus norvegicus	150-155
19329348-10	2009	Conclusions were drew that there is no expression of MMP-3 in normal brain, that the expression of MMP-3 appears 6h after TBI, and that there is a relationship between the expression of MMP-3 and the time course after TBI, and MMP-3 would be used as an indicator for estimating the age of traumatic brain contusion in forensic pathology.	Thioacetazone	122-125	matrix metallopeptidase 3	Rattus norvegicus	99-104
19329348-10	2009	Conclusions were drew that there is no expression of MMP-3 in normal brain, that the expression of MMP-3 appears 6h after TBI, and that there is a relationship between the expression of MMP-3 and the time course after TBI, and MMP-3 would be used as an indicator for estimating the age of traumatic brain contusion in forensic pathology.	Thioacetazone	122-125	matrix metallopeptidase 3	Rattus norvegicus	99-104
19329348-10	2009	Conclusions were drew that there is no expression of MMP-3 in normal brain, that the expression of MMP-3 appears 6h after TBI, and that there is a relationship between the expression of MMP-3 and the time course after TBI, and MMP-3 would be used as an indicator for estimating the age of traumatic brain contusion in forensic pathology.	Thioacetazone	122-125	matrix metallopeptidase 3	Rattus norvegicus	99-104
19329348-10	2009	Conclusions were drew that there is no expression of MMP-3 in normal brain, that the expression of MMP-3 appears 6h after TBI, and that there is a relationship between the expression of MMP-3 and the time course after TBI, and MMP-3 would be used as an indicator for estimating the age of traumatic brain contusion in forensic pathology.	Thioacetazone	218-221	matrix metallopeptidase 3	Rattus norvegicus	99-104
19329348-10	2009	Conclusions were drew that there is no expression of MMP-3 in normal brain, that the expression of MMP-3 appears 6h after TBI, and that there is a relationship between the expression of MMP-3 and the time course after TBI, and MMP-3 would be used as an indicator for estimating the age of traumatic brain contusion in forensic pathology.	Thioacetazone	218-221	matrix metallopeptidase 3	Rattus norvegicus	99-104
19329348-10	2009	Conclusions were drew that there is no expression of MMP-3 in normal brain, that the expression of MMP-3 appears 6h after TBI, and that there is a relationship between the expression of MMP-3 and the time course after TBI, and MMP-3 would be used as an indicator for estimating the age of traumatic brain contusion in forensic pathology.	Thioacetazone	218-221	matrix metallopeptidase 3	Rattus norvegicus	99-104
19585776-1	2009	This pilot study sought to determine if creatine kinase isoenzyme BB (CK-BB) levels might serve as a biological marker of injury severity in mild TBI (mTBI).	Thioacetazone	146-149	creatine kinase B	Homo sapiens	40-68
19585776-1	2009	This pilot study sought to determine if creatine kinase isoenzyme BB (CK-BB) levels might serve as a biological marker of injury severity in mild TBI (mTBI).	Thioacetazone	146-149	creatine kinase B	Homo sapiens	70-75
18789503-7	2009	With the recent interest in clinical trials of EPO in human stroke, it is both timely and prudent to consider the use of this pharmaceutical avenue in TBI in man.	Thioacetazone	151-154	erythropoietin	Homo sapiens	47-50
18552214-9	2008	These results confirm the association of MBL status with risk of infection in myeloablative, TBI-conditioned transplantation.	Thioacetazone	93-96	mannose binding lectin 2	Homo sapiens	41-44
18380546-12	2009	Higher levels of serum protein S-100B and IL-6 correlated with ultrastructural changes of endothelial cells, and with inflammatory response following TBI, respectively.	Thioacetazone	150-153	S100 calcium binding protein B	Homo sapiens	23-37
18380546-12	2009	Higher levels of serum protein S-100B and IL-6 correlated with ultrastructural changes of endothelial cells, and with inflammatory response following TBI, respectively.	Thioacetazone	150-153	interleukin 6	Homo sapiens	42-46
18976151-4	2009	These parameters were augmentation of cAMP production (TSAb activity), inhibition of bovine thyrotropin (bTSH)-induced cAMP production (TBAb activity), and inhibition of bTSH binding to the TSH receptor (TSHR) (TBI activity).	Thioacetazone	211-214	thyroid stimulating hormone receptor	Bos taurus	190-202
19008173-4	2008	Therefore, the aim was to analyze Il-10 in CSF and serum of patients early after TBI.	Thioacetazone	81-84	interleukin 10	Homo sapiens	34-39
19008173-16	2008	CONCLUSIONS: We demonstrated an analysis of IL-10 CSF and serum concentration after TBI.	Thioacetazone	84-87	interleukin 10	Homo sapiens	44-49
19008173-18	2008	Although the significant increase of IL-10 might indicate a bad outcome of TBI, responsible mechanisms still have to be elucidated.	Thioacetazone	75-78	interleukin 10	Homo sapiens	37-42
17935704-3	2007	This study was conducted to validate whether treatment with recombinant human EPO (rHuEPO) would limit the extent of injury following experimental TBI.	Thioacetazone	147-150	erythropoietin	Homo sapiens	78-81
18273869-7	2008	Antithrombin deficiency correlated with underlying malignancy, donor HLA-mismatch, and TBI, whereas decreased PC activity demonstrated a trend of association with lack of T-cell depletion and TBI.	Thioacetazone	87-90	serpin family C member 1	Homo sapiens	0-12
18325424-11	2008	CONCLUSIONS: These patients with TBI had findings consistent with CSW with elevated BNP levels in the setting of normal cardiac function.	Thioacetazone	33-36	natriuretic peptide B	Homo sapiens	84-87
18325424-14	2008	Further studies are necessary to establish a causative role for BNP in TBI-induced CSW.	Thioacetazone	71-74	natriuretic peptide B	Homo sapiens	64-67
18629743-0	2008	Overlap of mild TBI and mental health conditions in returning OIF/OEF service members and veterans.	Thioacetazone	16-19	osteoglycin	Homo sapiens	62-65
17935704-12	2007	EPO, administered in its recombinant form, affords significant neuroprotection in experimental TBI model and may hold promise for future clinical applications.	Thioacetazone	95-98	erythropoietin	Homo sapiens	0-3
16322908-3	2006	The purpose of the present study was to evaluate trends in BNP plasma concentrations during the acute phase following severe (traumatic brain injury) TBI.	Thioacetazone	150-153	natriuretic peptide B	Homo sapiens	59-62
17826908-0	2007	Neurosteroids reduce inflammation after TBI through CD55 induction.	Thioacetazone	40-43	CD55 molecule (Cromer blood group)	Rattus norvegicus	52-56
17586022-9	2007	CONCLUSIONS: EPO has protective effects after moderate TBI, and this effect seems better than MPSS on antiapoptotic gene expression and LPO.	Thioacetazone	55-58	erythropoietin	Rattus norvegicus	13-16
17586022-11	2007	This experimental study indicates that the benefits of EPO in the management of TBI have promising results and prompts further studies on the difference between EPO and MPSS in histopathological findings at the subcellular level.	Thioacetazone	80-83	erythropoietin	Rattus norvegicus	55-58
17711401-10	2007	Treatment with INO-1001 prevented NAD+ depletion and improved outcome, although modestly, identifying PARP-mediated energy failure as a contributor to the pathological sequelae of TBI.	Thioacetazone	180-183	poly (ADP-ribose) polymerase family, member 1	Mus musculus	102-106
17060133-8	2006	CONCLUSIONS: These findings show that measurement of serum protein S-100 may further aid in the identification of individuals with severe TBI who are likely to experience cognitive difficulties.	Thioacetazone	138-141	S100 calcium binding protein B	Homo sapiens	67-72
16809208-8	2006	CONCLUSIONS: Initial serum S-100B and C-tau levels appear to be poor predictors of 3-month outcome after mild TBI.	Thioacetazone	110-113	S100 calcium binding protein B	Homo sapiens	27-33
16322908-6	2006	FINDINGS: The initial BNP plasma concentrations (42+/-36.9 pg/ml) were 7.3 fold (p<0.01) higher in TBI patients as compared to the control group (5.78+/-1.90 pg/ml).	Thioacetazone	102-105	natriuretic peptide B	Homo sapiens	22-25
16322908-10	2006	Further studies should be undertaken to evaluate the role of BNP in TBI pathophysiology.	Thioacetazone	68-71	natriuretic peptide B	Homo sapiens	61-64
16544950-0	2006	Oxidative activation of thiacetazone by the Mycobacterium tuberculosis flavin monooxygenase EtaA and human FMO1 and FMO3.	Thioacetazone	24-36	flavin containing dimethylaniline monoxygenase 1	Homo sapiens	107-111
16445913-8	2006	Our results can be taken to show that the expression of AQP4 protein after TBI is time-dependent, region-specific, and possibly implicated in the formation and resolution of TBI-induced cerebral edema.	Thioacetazone	75-78	aquaporin 4	Rattus norvegicus	56-60
16445913-8	2006	Our results can be taken to show that the expression of AQP4 protein after TBI is time-dependent, region-specific, and possibly implicated in the formation and resolution of TBI-induced cerebral edema.	Thioacetazone	174-177	aquaporin 4	Rattus norvegicus	56-60
16544950-0	2006	Oxidative activation of thiacetazone by the Mycobacterium tuberculosis flavin monooxygenase EtaA and human FMO1 and FMO3.	Thioacetazone	24-36	flavin containing dimethylaniline monoxygenase 3	Homo sapiens	116-120
16122007-9	2005	The sensitivity and specificity of initial NSE and S100B and peak myelin basic protein concentrations for identifying TBI at ROC curve-defined cutoffs were 71 and 64% (NSE), 77 and 72% (S100B), and 44 and 96% (myelin basic protein), respectively.	Thioacetazone	118-121	enolase 2	Homo sapiens	43-46
16084512-8	2005	TBI led to a significant neuronal loss in frontal cortex (P < 0.001), as well as hippocampal CA3 (P = 0.017) and CA1 (P = 0.002) at 9 days after the trauma; however, cytoskeletal architecture was preserved as indicated by normal betaAPP- and MAP-2 staining.	Thioacetazone	0-3	microtubule-associated protein 2	Rattus norvegicus	245-250
16122007-9	2005	The sensitivity and specificity of initial NSE and S100B and peak myelin basic protein concentrations for identifying TBI at ROC curve-defined cutoffs were 71 and 64% (NSE), 77 and 72% (S100B), and 44 and 96% (myelin basic protein), respectively.	Thioacetazone	118-121	S100 calcium binding protein B	Homo sapiens	51-56
16122007-9	2005	The sensitivity and specificity of initial NSE and S100B and peak myelin basic protein concentrations for identifying TBI at ROC curve-defined cutoffs were 71 and 64% (NSE), 77 and 72% (S100B), and 44 and 96% (myelin basic protein), respectively.	Thioacetazone	118-121	myelin basic protein	Homo sapiens	66-86
11320592-9	2001	ET-1 expression was further increased at 24 h after TBI.	Thioacetazone	52-55	endothelin 1	Rattus norvegicus	0-4
15150870-8	2004	The expressions of COX-2 mRNA appeared to be darkly stained 15 min after TBI for extended periods of time and reached the maximum (P < 0.05) at 1 d post-injury, reached another peak (P < 0.05) at 3 d post-injury, and significant differences (P < 0.05) even presented between control and 7 d post-injury, but not 15 d post-injury.	Thioacetazone	73-76	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	19-24
15150870-9	2004	CONCLUSION: The results of this study indicated that the expression of COX-2 mRNA and protein had a possible relationship with the extended periods of time after TBI.	Thioacetazone	162-165	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	71-76
15150870-10	2004	It might have some relationship between the expression of COX-2 and secondary brain injury after TBI.	Thioacetazone	97-100	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	58-63
15150872-3	2004	RESULTS: Up-regulating of caspase-3 expression was found in tissue from traumatic brain injury compared with controls in early 1 hour after TBI, and lasted for 14 days.	Thioacetazone	140-143	caspase 3	Rattus norvegicus	26-35
15150872-5	2004	CONCLUSION: The increasing of caspase-3 expression indicates that TBI exists.	Thioacetazone	66-69	caspase 3	Rattus norvegicus	30-39
12482117-9	2002	These data suggest that ICAM-1 may be involved in neutrophil invasion and neurological dysfunction after TBI, but also implicate a role for a nonspecific antibody effect in improved functional outcome.	Thioacetazone	105-108	intercellular adhesion molecule 1	Rattus norvegicus	24-30
12389628-7	2002	The allografts from (Jak3-/-) C57BL/6 (H-2b) mice rescued MHC-disparate recipient BALB/c mice (H-2d) of the lethal toxicity of TBI without causing fatal GVHD.	Thioacetazone	127-130	Janus kinase 3	Mus musculus	21-25
14753448-0	2003	Modulation of aquaporin-4 water transport in a model of TBI.	Thioacetazone	56-59	aquaporin 4	Rattus norvegicus	14-25
14753454-6	2003	Double immunostaining showed that phospho-ERK was prominent in astrocytes 6 hrs after TBI.	Thioacetazone	86-89	Eph receptor B1	Rattus norvegicus	42-45
12725156-3	2003	RESULTS: Up-regulating of caspase-1 expression was found in tissue from traumatic brain injury compared with controls in early 1 hour after TBI, and lasted for 2 weeks.	Thioacetazone	140-143	caspase 1	Rattus norvegicus	26-35
12725156-6	2003	The increasing of caspase-1 expression indicates that the TBI exists.	Thioacetazone	58-61	caspase 1	Rattus norvegicus	18-27
11509930-14	2001	This study showed that in pediatric patients with AML consolidation of CR1 with high-dose melphalan allows survival and EFS to be obtained comparable to other auto-HSCT or chemotherapy published series with a potential sparing effect both on duration of treatment (with respect to chemotherapy) and on long-term side-effects (with respect to auto-HSCT with TBI or busulfan containing regimens).	Thioacetazone	357-360	complement C3b/C4b receptor 1 (Knops blood group)	Homo sapiens	71-74
9459642-6	1997	The TBI activity in the purified TBIP was significantly decreased by either etnylene glycol tetraacetate (EGTA) (1 mmol/L) or antibody to calmodulin (CaM) in the TSH receptor assay.	Thioacetazone	4-7	calmodulin 1	Homo sapiens	138-148
10937894-4	2000	Chronic prophylactic hyperventilation therapy should be avoided during the first 5 days after severe TBI and particularly during the first 24 h. CBF measurements in patients with severe TBI demonstrate that blood flow early after injury is low and strongly suggest that in the first few hours after injury the absolute values approach those consistent with ischemia.	Thioacetazone	186-189	CCAAT enhancer binding protein zeta	Homo sapiens	145-148
10808202-4	2000	CR1 patients treated with CY/TBI (n = 7) had 3- and 5-year disease-free survival (DFS) rates of 71% and 57%.	Thioacetazone	29-32	complement C3b/C4b receptor 1 (Knops blood group)	Homo sapiens	0-3
9831863-2	1998	TPO was highly effective in rhesus monkeys exposed to the mid-lethal dose of 5 Gy (300 kV x-rays) TBI, a model in which it alleviated thrombocytopenia, promoted red cell reconstitution, accelerated reconstitution of immature CD34+ bone marrow cells, and potentiated the response to growth factors such as GM-CSF and G-CSF.	Thioacetazone	98-101	thrombopoietin	Macaca mulatta	0-3
9831863-4	1998	In the 5 Gy model, a single dose of TPO augmented by GM-CSF 24 h after TBI was effective in preventing thrombocytopenia.	Thioacetazone	71-74	thrombopoietin	Mus musculus	36-39
11012161-5	1998	During hemopoietic reconstitution following a cytotoxic insult such as results from a midlethal dose of TBI, PB CD34+ cell numbers appeared to be correlated to those of BM, suggesting that PB CD34+ cells may reflect reconstitution of BM CD34+ cells.	Thioacetazone	104-107	CD34 molecule	Macaca mulatta	192-196
11012161-5	1998	During hemopoietic reconstitution following a cytotoxic insult such as results from a midlethal dose of TBI, PB CD34+ cell numbers appeared to be correlated to those of BM, suggesting that PB CD34+ cells may reflect reconstitution of BM CD34+ cells.	Thioacetazone	104-107	CD34 molecule	Macaca mulatta	192-196
11012185-5	1998	In the 5-Gy model, a single dose of TPO 24 h after TBI was effective in preventing thrombocytopenia and was augmented by GM-CSF.	Thioacetazone	51-54	thrombopoietin	Macaca mulatta	36-39
11787527-10	2001	Compared to animals receiving a similar TBI-based conditioning regimen, overall levels of chimerism were significantly lower in the CTX-plus-TI-conditioned animals.	Thioacetazone	40-43	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	132-135
10936210-11	2000	Our findings also suggest a contributory role of activated caspase-3 in neuronal and glial apoptotic degeneration after experimental TBI in vivo.	Thioacetazone	133-136	caspase 3	Rattus norvegicus	59-68
10444519-9	1999	TNF-alpha and IL-1beta decreased the uptake of TBI; however, the uptake of NTBI was increased.	Thioacetazone	47-50	tumor necrosis factor	Homo sapiens	0-9
10444519-9	1999	TNF-alpha and IL-1beta decreased the uptake of TBI; however, the uptake of NTBI was increased.	Thioacetazone	47-50	interleukin 1 beta	Homo sapiens	14-22
10444519-11	1999	Coexposure to TNF-alpha and NTBI, but not to TBI, induced MDA accumulation and greater cytotoxicity (MTT and lactate dehydrogenase release) than TNF-alpha alone.	Thioacetazone	29-32	tumor necrosis factor	Homo sapiens	145-154
10444519-12	1999	These findings indicate that TNF-alpha and IL-1beta modulate iron uptake by A549 cells, with differing effects on TBI and NTBI, as well as on H-ferritin synthesis.	Thioacetazone	114-117	tumor necrosis factor	Homo sapiens	29-38
10444519-12	1999	These findings indicate that TNF-alpha and IL-1beta modulate iron uptake by A549 cells, with differing effects on TBI and NTBI, as well as on H-ferritin synthesis.	Thioacetazone	114-117	interleukin 1 beta	Homo sapiens	43-51
10382950-7	1999	bFGF was below detectability in 22%, 30% and 45% of patients pre-TBI, during TBI or post-TBI respectively.	Thioacetazone	65-68	fibroblast growth factor 2	Homo sapiens	0-4
10382950-7	1999	bFGF was below detectability in 22%, 30% and 45% of patients pre-TBI, during TBI or post-TBI respectively.	Thioacetazone	77-80	fibroblast growth factor 2	Homo sapiens	0-4
10382950-7	1999	bFGF was below detectability in 22%, 30% and 45% of patients pre-TBI, during TBI or post-TBI respectively.	Thioacetazone	77-80	fibroblast growth factor 2	Homo sapiens	0-4
10382950-8	1999	Mean circulating plasma levels of bFGF decreased from a median of 52 pg/ml pre-TBI to 26 pg/ml during TBI, and to 5 pg/ml post-TBI.	Thioacetazone	79-82	fibroblast growth factor 2	Homo sapiens	34-38
10382950-8	1999	Mean circulating plasma levels of bFGF decreased from a median of 52 pg/ml pre-TBI to 26 pg/ml during TBI, and to 5 pg/ml post-TBI.	Thioacetazone	102-105	fibroblast growth factor 2	Homo sapiens	34-38
10382950-8	1999	Mean circulating plasma levels of bFGF decreased from a median of 52 pg/ml pre-TBI to 26 pg/ml during TBI, and to 5 pg/ml post-TBI.	Thioacetazone	102-105	fibroblast growth factor 2	Homo sapiens	34-38
10382950-10	1999	Naturally high levels of bFGF were observed in some patients undergoing fractionated TBI.	Thioacetazone	85-88	fibroblast growth factor 2	Homo sapiens	25-29
9731052-8	1998	The addition of G-CSF resulted in a significant decrease in stem cell content when compared with no G-CSF administration in animals treated with chlorambucil, BCNU, or TBI.	Thioacetazone	168-171	colony stimulating factor 3 (granulocyte)	Mus musculus	16-21
9624626-9	1998	These results suggest a role for hsp70 in human cortex following TBI.	Thioacetazone	65-68	heat shock protein family A (Hsp70) member 4	Homo sapiens	33-38
9459642-6	1997	The TBI activity in the purified TBIP was significantly decreased by either etnylene glycol tetraacetate (EGTA) (1 mmol/L) or antibody to calmodulin (CaM) in the TSH receptor assay.	Thioacetazone	4-7	calmodulin 1	Homo sapiens	150-153
9384474-2	1997	The efficacy of an intensified regimen, TAM (TBI, high-dose cytosine arabinoside and melphalan), is evaluated by analyzing long-term follow-up of a homogenous group of 42 high-risk ALL patients allografted in first CR.	Thioacetazone	45-48	Myeloproliferative syndrome, transient (transient abnormal myelopoiesis)	Homo sapiens	40-43
32174881-10	2020	Genes related to inflammation were upregulated, including AKT serine/threonine kinase 1 (AKT1), a gene coordinating cellular recovery following TBIs.	Thioacetazone	144-148	AKT serine/threonine kinase 1	Homo sapiens	58-87
1897009-8	1991	Thus, TBI might be able to select and/or activate cells responsible for hematopoietic growth inhibition by a mechanism involving, at least in part, TNF-alpha.	Thioacetazone	6-9	tumor necrosis factor	Homo sapiens	148-157
2905613-2	1988	The number of CFU-S was greatly reduced in TBI + SBMT-Maf mice compared with those in TBI + SBMT mice.	Thioacetazone	43-46	avian musculoaponeurotic fibrosarcoma oncogene homolog	Mus musculus	54-57
2905613-4	1988	The time for immune system regeneration was, however, considerably longer in TBI + SBMT-Maf than in TBI + SBMT mice, as measured by the incidence of Ig+, Thy-1.2+, L3T4+, Lyt-2+, and IL-2R+ cells in the spleens.	Thioacetazone	77-80	avian musculoaponeurotic fibrosarcoma oncogene homolog	Mus musculus	88-91
32149839-12	2020	In contrast, after delayed infection monocytes from TBI + Sp mice had higher levels of interleukin-1beta, tumor necrosis factor-alpha, and reactive oxygen species when compared with Sham + Sp mice.	Thioacetazone	52-55	interleukin 1 beta	Mus musculus	87-133
8101401-10	1993	Levels of galactosylceramidase in livers, spleens, and brains of twitchers transplanted after 35-50 mg/kg of BU or after TBI increased to 30-116% of normal control values by 90 days after HCT.	Thioacetazone	121-124	galactosylceramidase	Mus musculus	10-30
2186521-4	1990	Animals receiving anti-LFA-1 and 1100 cGy total-body irradiation showed improved hemopoietic and immunologic reconstitution one month after BMT when compared with animals receiving TBI alone.	Thioacetazone	181-184	integrin subunit alpha L	Homo sapiens	23-28
3402396-9	1988	Saturation studies revealed that the TBI activities of hCGv and asialo-hCGp were due to a competitive inhibition of bTSH binding at both the high and low affinity bTSH-binding sites, whereas the inhibitory activity of hCGc was exerted primarily at the low affinity binding site.	Thioacetazone	37-40	protein phosphatase 1 regulatory inhibitor subunit 11	Homo sapiens	55-59
3402396-9	1988	Saturation studies revealed that the TBI activities of hCGv and asialo-hCGp were due to a competitive inhibition of bTSH binding at both the high and low affinity bTSH-binding sites, whereas the inhibitory activity of hCGc was exerted primarily at the low affinity binding site.	Thioacetazone	37-40	chorionic gonadotropin subunit beta 5	Homo sapiens	71-75
2891767-6	1988	These heterodimeric Ab conjugates were shown to be able to direct the lysis of CALLA+ targets by TBI-6.	Thioacetazone	97-100	membrane metalloendopeptidase	Homo sapiens	79-84
4143451-0	1974	The sensitivity to thiacetazone of tubercle bacilli isolated from patients with pulmonary tuberculosis in Sri Lanka.	Thioacetazone	19-31	sorcin	Homo sapiens	106-109
32174881-10	2020	Genes related to inflammation were upregulated, including AKT serine/threonine kinase 1 (AKT1), a gene coordinating cellular recovery following TBIs.	Thioacetazone	144-148	AKT serine/threonine kinase 1	Homo sapiens	89-93
31280036-7	2019	The TBI with LOC group also had significantly elevated IL-6 concentrations than both TBI without LOC and control groups.	Thioacetazone	4-7	interleukin 6	Homo sapiens	55-59
30001646-2	2019	Interleukin-1 (IL-1) contributes to experimental adult diffuse and contusion TBI models, and IL-1 antagonists have entered clinical trials for severe TBI in adults; however, no such data exist for adolescent TBI.	Thioacetazone	77-80	interleukin 1 complex	Mus musculus	0-13
30001646-2	2019	Interleukin-1 (IL-1) contributes to experimental adult diffuse and contusion TBI models, and IL-1 antagonists have entered clinical trials for severe TBI in adults; however, no such data exist for adolescent TBI.	Thioacetazone	77-80	interleukin 1 complex	Mus musculus	15-19
30001646-2	2019	Interleukin-1 (IL-1) contributes to experimental adult diffuse and contusion TBI models, and IL-1 antagonists have entered clinical trials for severe TBI in adults; however, no such data exist for adolescent TBI.	Thioacetazone	150-153	interleukin 1 complex	Mus musculus	93-97
30001646-2	2019	Interleukin-1 (IL-1) contributes to experimental adult diffuse and contusion TBI models, and IL-1 antagonists have entered clinical trials for severe TBI in adults; however, no such data exist for adolescent TBI.	Thioacetazone	150-153	interleukin 1 complex	Mus musculus	93-97
31185197-8	2019	Furthermore, serotonin depletion also prevented the TBI-induced bilateral increase in c-Fos positive cells within the Rexed laminae I and II of the dorsal horns.	Thioacetazone	52-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-91
31185197-9	2019	These results indicate that in the weeks following TBI, pain may be responsive to 5-HT3 receptor antagonists or other measures which rebalance descending pain modulation.	Thioacetazone	51-54	5-hydroxytryptamine receptor 3A	Rattus norvegicus	82-96
30802757-1	2019	PURPOSE: Previously, higher circulating levels of matrix metalloproteinase (MMP)-9 and tissue inhibitor matrix metalloproteinases (TIMP)-1 were reported in the first hours after TBI in blood samples from patients with poor prognosis.	Thioacetazone	178-181	matrix metallopeptidase 9	Homo sapiens	50-82
31190315-8	2019	Altogether, our results indicate that increased miR-124-3p in microglial exosomes following TBI may inhibit neuronal autophagy and protect against nerve injury via their transfer into neurons.	Thioacetazone	92-95	microRNA 124a-3	Mus musculus	48-58
31190315-9	2019	Thus, treatment with microglial exosomes enriched with miR-124-3p may represent a novel therapeutic strategy for the treatment of nerve injury after TBI.	Thioacetazone	149-152	microRNA 124a-3	Mus musculus	55-65
30802757-1	2019	PURPOSE: Previously, higher circulating levels of matrix metalloproteinase (MMP)-9 and tissue inhibitor matrix metalloproteinases (TIMP)-1 were reported in the first hours after TBI in blood samples from patients with poor prognosis.	Thioacetazone	178-181	TIMP metallopeptidase inhibitor 1	Homo sapiens	87-138
30802757-2	2019	Thus, the objectives of this study were to determine whether MMP-9 and TIMP-1 levels during the first week of a severe TBI could be used as biomarker predictive of mortality.	Thioacetazone	119-122	matrix metallopeptidase 9	Homo sapiens	61-66
30802757-2	2019	Thus, the objectives of this study were to determine whether MMP-9 and TIMP-1 levels during the first week of a severe TBI could be used as biomarker predictive of mortality.	Thioacetazone	119-122	TIMP metallopeptidase inhibitor 1	Homo sapiens	71-77
30802757-5	2019	RESULTS: TIMP-1 concentrations at days 1 (p < .001), 4 (p = .001), and 8 (p = .01) of TBI were higher in non-surviving (n = 34) than in surviving (n = 90) patients.	Thioacetazone	89-92	TIMP metallopeptidase inhibitor 1	Homo sapiens	9-15
30802757-6	2019	ROC curve analyses showed an area under curve of TIMP-1 concentrations at days 1, 4, and 8 of TBI to predict 30-day mortality of 78% (p < .001), 76% (p < .001) and 71% (p = .02) respectively.	Thioacetazone	94-97	TIMP metallopeptidase inhibitor 1	Homo sapiens	49-55
30802757-7	2019	CONCLUSIONS: The most relevant new findings of our study were that TIMP-1 levels during the first week of a severe TBI were higher in non-surviving than in surviving patients and that could be used as biomarker predictive of mortality.	Thioacetazone	115-118	TIMP metallopeptidase inhibitor 1	Homo sapiens	67-73
30979482-9	2019	CONCLUSION: A G-CSF-combined HDCA/CY/TBI regimen is a promising conditioning in patients with myeloid malignant neoplasms who undergo not only CBT but also BMT or PBSCT.	Thioacetazone	37-40	colony stimulating factor 3	Homo sapiens	14-19
31040769-1	2019	This study aimed to investigate the changes of alpha-synuclein in serum and its relationship with default mode network (DMN) connectivity after acute mild traumatic brain injury (mild TBI).	Thioacetazone	184-187	synuclein alpha	Homo sapiens	47-62
31040769-7	2019	These findings supported that alpha-synuclein may modulate the functional connectivity within the DMN and suggest the feasibility of using alpha-synuclein as an objective biomarker for diagnosis and prognosis of mild TBI.	Thioacetazone	217-220	synuclein alpha	Homo sapiens	30-45
31125969-1	2019	Glasgow Coma Scale-Pupils Score: opening the eyes to new ways of predicting outcomes in TBI.	Thioacetazone	88-91	COMA	Homo sapiens	8-12
31192445-6	2019	RESULTS: MDA levels and CAT activity were significantly higher in the TBI group versus the control group.	Thioacetazone	70-73	catalase	Rattus norvegicus	24-27
30922891-16	2019	Our findings suggest the value of combatting visual system injury after TBI by using CB2 inverse agonists such as SMM-189, which appear to target microglia and bias them away from the pro-inflammatory M1 state, toward the protective M2 state.	Thioacetazone	72-75	cannabinoid receptor 2 (macrophage)	Mus musculus	85-88
31093304-6	2019	Serum glucose level evaluation at presentation in the emergency department may aid CT decision-making in mild TBI.	Thioacetazone	110-113	activation induced cytidine deaminase	Homo sapiens	79-82
30883392-8	2019	Collectively, these findings suggest that the CRF-1 receptor plays an important role in the regulation of anxiety-related behaviors following mTBI induction in mice and support the hypothesis that blockade of the CRF-1 receptor may be a promising therapeutic target for anxiety-related disorders in patients with TBI.	Thioacetazone	143-146	corticotropin releasing hormone receptor 1	Mus musculus	46-60
30883392-8	2019	Collectively, these findings suggest that the CRF-1 receptor plays an important role in the regulation of anxiety-related behaviors following mTBI induction in mice and support the hypothesis that blockade of the CRF-1 receptor may be a promising therapeutic target for anxiety-related disorders in patients with TBI.	Thioacetazone	143-146	corticotropin releasing hormone receptor 1	Mus musculus	213-227
30806852-2	2019	In systemic iron overload, elevated circulating levels of transferrin-bound (TBI) and non-transferrin-bound iron (NTBI) are filtered to the renal proximal tubules, where they may cause injury.	Thioacetazone	77-80	transferrin	Homo sapiens	58-69
30806852-9	2019	Furthermore, ZIP14 silencing decreased 55Fe uptake after 55Fe-Transferrin exposure (p < 0.05), suggesting ZIP14 could be involved in early endosomal transport of TBI-derived iron into the cytosol.	Thioacetazone	165-168	solute carrier family 39 member 14	Homo sapiens	13-18
30806852-9	2019	Furthermore, ZIP14 silencing decreased 55Fe uptake after 55Fe-Transferrin exposure (p < 0.05), suggesting ZIP14 could be involved in early endosomal transport of TBI-derived iron into the cytosol.	Thioacetazone	165-168	transferrin	Homo sapiens	62-73
30806852-9	2019	Furthermore, ZIP14 silencing decreased 55Fe uptake after 55Fe-Transferrin exposure (p < 0.05), suggesting ZIP14 could be involved in early endosomal transport of TBI-derived iron into the cytosol.	Thioacetazone	165-168	solute carrier family 39 member 14	Homo sapiens	109-114
30806852-10	2019	Our data suggest that human proximal tubular epithelial cells take up TBI and NTBI, where ZIP8 and ZIP14 are both involved in NTBI uptake, but ZIP14, not ZIP8, mediates TBI-derived iron uptake.	Thioacetazone	79-82	solute carrier family 39 member 8	Homo sapiens	90-94
30806852-10	2019	Our data suggest that human proximal tubular epithelial cells take up TBI and NTBI, where ZIP8 and ZIP14 are both involved in NTBI uptake, but ZIP14, not ZIP8, mediates TBI-derived iron uptake.	Thioacetazone	79-82	solute carrier family 39 member 14	Homo sapiens	99-104
30864534-0	2019	Longitudinal Changes in Disability Rating Scale Scores: A Secondary Analysis Among Patients With Severe TBI Enrolled in the Epo Clinical Trial.	Thioacetazone	104-107	erythropoietin	Homo sapiens	124-127
30557171-8	2019	Higher CCR7 positive cell counts were found in patients receiving TBI during engraftment and during the whole posttransplant period we found a correlation with an improved outcome.	Thioacetazone	66-69	C-C motif chemokine receptor 7	Homo sapiens	7-11
30864534-7	2019	TBI severity group was found to significantly interact with Epo randomization group on mean DRS recovery curves.	Thioacetazone	0-3	erythropoietin	Homo sapiens	60-63
29488331-1	2018	AIMS: To investigate the roles of Lats1/p-YAP1 pathway in TBI-induced neuronal apoptosis and neurological deficits in rats.	Thioacetazone	58-61	large tumor suppressor kinase 1	Rattus norvegicus	34-39
30031156-9	2018	Together, these data demonstrate that cypin activation is a novel approach for improving outcome after TBI and may provide a new pathway for reducing the deficits associated with TBI in patients.	Thioacetazone	103-106	guanine deaminase	Homo sapiens	38-43
30031156-9	2018	Together, these data demonstrate that cypin activation is a novel approach for improving outcome after TBI and may provide a new pathway for reducing the deficits associated with TBI in patients.	Thioacetazone	179-182	guanine deaminase	Homo sapiens	38-43
30209234-0	2018	Glial fibrillary acidic protein elevations relate to neuroimaging abnormalities after mild TBI.	Thioacetazone	91-94	glial fibrillary acidic protein	Homo sapiens	0-31
30463625-11	2018	In isolated TBI patients, increasing syndecan-1 levels (beta for every 10 ng/ml increase: 0.14; 95% CI: 0.02, 0.26) and hypocoagulability were negatively associated with survival.	Thioacetazone	12-15	syndecan 1	Homo sapiens	37-47
30463625-12	2018	CONCLUSIONS: This study provides evidence of syndecan-1 shedding after TBI supporting the notion that breakdown of the glycocalyx contributes to the physiological derangements after TBI.	Thioacetazone	71-74	syndecan 1	Homo sapiens	45-55
30463625-12	2018	CONCLUSIONS: This study provides evidence of syndecan-1 shedding after TBI supporting the notion that breakdown of the glycocalyx contributes to the physiological derangements after TBI.	Thioacetazone	182-185	syndecan 1	Homo sapiens	45-55
30497133-12	2018	Important predictors of recovery included antioxidant activity in the CSF (superoxide dismutase and total antioxidant capacity).CONCLUSIONSRecovery after TBI was dependent on the resolution of oxidative stress imbalance.	Thioacetazone	154-157	colony stimulating factor 2	Homo sapiens	70-73
29488331-1	2018	AIMS: To investigate the roles of Lats1/p-YAP1 pathway in TBI-induced neuronal apoptosis and neurological deficits in rats.	Thioacetazone	58-61	Yes1 associated transcriptional regulator	Rattus norvegicus	42-46
28692352-8	2018	CONCLUSIONS: CASP scores were responsive to change over time at most measurements and differentiated between groups, particularly severe TBI.	Thioacetazone	137-140	cut like homeobox 1	Homo sapiens	13-17
29488331-2	2018	RESULTS: We found that Lats1 and YAP1 were expressed in cerebral cortex neurons of Sprague-Dawley rats, and the phosphorylation levels of Lats1 and YAP1 in injured regions were significantly increased after TBI.	Thioacetazone	207-210	large tumor suppressor kinase 1	Rattus norvegicus	23-28
29488331-2	2018	RESULTS: We found that Lats1 and YAP1 were expressed in cerebral cortex neurons of Sprague-Dawley rats, and the phosphorylation levels of Lats1 and YAP1 in injured regions were significantly increased after TBI.	Thioacetazone	207-210	Yes1 associated transcriptional regulator	Rattus norvegicus	33-37
29488331-2	2018	RESULTS: We found that Lats1 and YAP1 were expressed in cerebral cortex neurons of Sprague-Dawley rats, and the phosphorylation levels of Lats1 and YAP1 in injured regions were significantly increased after TBI.	Thioacetazone	207-210	large tumor suppressor kinase 1	Rattus norvegicus	138-143
29488331-2	2018	RESULTS: We found that Lats1 and YAP1 were expressed in cerebral cortex neurons of Sprague-Dawley rats, and the phosphorylation levels of Lats1 and YAP1 in injured regions were significantly increased after TBI.	Thioacetazone	207-210	Yes1 associated transcriptional regulator	Rattus norvegicus	148-152
29488331-4	2018	CONCLUSIONS: Our work demonstrates that inhibition of Lats1/p-YAP1 pathway mitigates neuronal apoptosis and neurological deficits in a rat model of TBI.	Thioacetazone	148-151	large tumor suppressor kinase 1	Rattus norvegicus	54-59
29488331-4	2018	CONCLUSIONS: Our work demonstrates that inhibition of Lats1/p-YAP1 pathway mitigates neuronal apoptosis and neurological deficits in a rat model of TBI.	Thioacetazone	148-151	Yes1 associated transcriptional regulator	Rattus norvegicus	62-66
30023445-3	2018	We describe the protocol of a three-arm RCT comparing the effectiveness of three modalities of F-PST to reduce executive dysfunction and behavior problems following TBI in adolescence.	Thioacetazone	165-168	ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyltransferase 4	Homo sapiens	97-100
29973909-6	2018	Results indicated that patients with mild TBI at acute phase exhibited reduced left dorsal caudate-based functional connectivity with ventral lateral prefrontal cortex, dorsal anterior cingulate cortex, and inferior parietal lobule, which mainly distributed in the cognitive control network, and reduced right ventral caudate-based functional connectivity with the dorsal lateral prefrontal cortex, dorsal anterior cingulate cortex (dACC), and bilateral ventral anterior cingulate cortex (vACC), which mainly distributed in the executive network and emotional processing network.	Thioacetazone	42-45	Acetyl-CoA carboxylase	Drosophila melanogaster	433-437
29610275-3	2018	Here, we characterized uptake of transferrin (Tf)-bound iron (TBI) and non-Tf-bound iron (NTBI) by immortalized microglial (IMG) cells.	Thioacetazone	62-65	transferrin	Mus musculus	33-44
29610275-5	2018	In contrast, the anti-inflammatory cytokine interleukin 4 (IL-4) promoted TBI uptake.	Thioacetazone	74-77	interleukin 4	Mus musculus	44-57
29610275-5	2018	In contrast, the anti-inflammatory cytokine interleukin 4 (IL-4) promoted TBI uptake.	Thioacetazone	74-77	interleukin 4	Mus musculus	59-63
29220591-4	2018	Administration of EPO improved 30-day survival, alleviated TBI-induced myelosuppression and pancytopenia, by augmenting lymphocytes and other white blood cells in the peripheral blood of rats, while bone marrow and spleen cellularity were restored.	Thioacetazone	59-62	erythropoietin	Rattus norvegicus	18-21
29545592-0	2018	Efficacy and safety of keratinocyte growth factor (palifermin) for prevention of oral mucositis in TBI-based allogeneic hematopoietic stem cell transplantation.	Thioacetazone	99-102	fibroblast growth factor 7	Homo sapiens	23-49
29142020-0	2018	Time out: NFL conflicts of interest with public health efforts to prevent TBI.	Thioacetazone	74-77	neurofilament light chain	Homo sapiens	10-13
30788389-7	2018	The mean serum level of UCH-L1 was significantly higher in patients with CT-positive than in TBI patients with CT negative (SMD = 1.67, 95% CI: 1.12 to 2.23, I2 = 98.1%; p <0.0001).	Thioacetazone	93-96	ubiquitin C-terminal hydrolase L1	Homo sapiens	24-30
30788389-8	2018	The area under the SROC curve for UCH-L1 in the prediction of intracranial lesions after mild TBI was 0.83 (95% CI: 0.80 to 0.86).	Thioacetazone	94-97	ubiquitin C-terminal hydrolase L1	Homo sapiens	34-40
30788389-10	2018	When the analysis was limited to assessing the serum level of UCH-L1 within the first 6 hours after mild TBI, its sensitivity and specificity increased to 0.99 (95% CI: 0.94 to 1.0) and 0.44 (95% CI: 0.38 to 0.052), respectively.	Thioacetazone	105-108	ubiquitin C-terminal hydrolase L1	Homo sapiens	62-68
30788389-13	2018	It was also found that evaluation of serum/plasma level of UCH-L1 within the first 6 hours following TBI would increase its predictive value.	Thioacetazone	101-104	ubiquitin C-terminal hydrolase L1	Homo sapiens	59-65
29185834-8	2018	TBI exhibited significantly reduced level of IL-2, IL-4, IL-7 and IFN-gamma compared with the control mice and treatment with resveratrol attenuated the reduction.	Thioacetazone	0-3	interleukin 2	Mus musculus	45-49
29185834-8	2018	TBI exhibited significantly reduced level of IL-2, IL-4, IL-7 and IFN-gamma compared with the control mice and treatment with resveratrol attenuated the reduction.	Thioacetazone	0-3	interleukin 4	Mus musculus	51-55
29185834-8	2018	TBI exhibited significantly reduced level of IL-2, IL-4, IL-7 and IFN-gamma compared with the control mice and treatment with resveratrol attenuated the reduction.	Thioacetazone	0-3	interleukin 7	Mus musculus	57-61
29185834-8	2018	TBI exhibited significantly reduced level of IL-2, IL-4, IL-7 and IFN-gamma compared with the control mice and treatment with resveratrol attenuated the reduction.	Thioacetazone	0-3	interferon gamma	Mus musculus	66-75
29889090-3	2018	Insulin-like growth factor-1 (IGF-1) has the potential to improve cognitive function and promote neurogenesis after TBI, but its short half-life in the systemic circulation makes it difficult to maintain a therapeutic concentration.	Thioacetazone	116-119	insulin-like growth factor 1	Mus musculus	0-28
29889090-3	2018	Insulin-like growth factor-1 (IGF-1) has the potential to improve cognitive function and promote neurogenesis after TBI, but its short half-life in the systemic circulation makes it difficult to maintain a therapeutic concentration.	Thioacetazone	116-119	insulin-like growth factor 1	Mus musculus	30-35
28841638-8	2017	Additionally, the level of the Bax in mitochondria (mit) and cytosol was elevated in the TBI-treated group as compared to the sham group.	Thioacetazone	89-92	BCL2-associated X protein	Mus musculus	31-34
28729191-4	2017	Hypothermia treatment significantly increased the expression of PSD93, PSD95 and NR2B one month after TBI in the cortex and hippocampus compared with the normothermia group.	Thioacetazone	102-105	discs large MAGUK scaffold protein 2	Mus musculus	64-69
28729191-4	2017	Hypothermia treatment significantly increased the expression of PSD93, PSD95 and NR2B one month after TBI in the cortex and hippocampus compared with the normothermia group.	Thioacetazone	102-105	glutamate receptor, ionotropic, NMDA2B (epsilon 2)	Mus musculus	81-85
28855570-2	2017	Metabotropic glutamate receptor 5 (mGluR5) has been reported to regulate microglias and astrocytes to affect inflammation after TBI, but its effect on modulating infiltrated peripheral WBCs remains unclear.	Thioacetazone	128-131	glutamate receptor, metabotropic 5	Mus musculus	0-33
28855570-2	2017	Metabotropic glutamate receptor 5 (mGluR5) has been reported to regulate microglias and astrocytes to affect inflammation after TBI, but its effect on modulating infiltrated peripheral WBCs remains unclear.	Thioacetazone	128-131	glutamate receptor, ionotropic, kainate 1	Mus musculus	35-41
28855570-3	2017	In a mouse moderate TBI model, we found that mGluR5 knockout (KO) significantly reduced neutrophil infiltration and inflammatory cytokine expression in the brain at 24 hours post TBI, which was accompanied by improved neurological dysfunction.	Thioacetazone	20-23	glutamate receptor, ionotropic, kainate 1	Mus musculus	45-51
28855570-3	2017	In a mouse moderate TBI model, we found that mGluR5 knockout (KO) significantly reduced neutrophil infiltration and inflammatory cytokine expression in the brain at 24 hours post TBI, which was accompanied by improved neurological dysfunction.	Thioacetazone	179-182	glutamate receptor, ionotropic, kainate 1	Mus musculus	45-51
28855570-6	2017	These results provide insight into the role of mGluR5 in the regulation of inflammation in the acute phase of TBI, which may provide novel clues for TBI therapy.	Thioacetazone	110-113	glutamate receptor, ionotropic, kainate 1	Mus musculus	47-53
28855570-6	2017	These results provide insight into the role of mGluR5 in the regulation of inflammation in the acute phase of TBI, which may provide novel clues for TBI therapy.	Thioacetazone	149-152	glutamate receptor, ionotropic, kainate 1	Mus musculus	47-53
28100103-9	2017	We conclude that the APOE promoter -219G/T polymorphism and the BDNF Met/Met genotype might confer risk for sustaining a TBI.	Thioacetazone	121-124	apolipoprotein E	Homo sapiens	21-25
28938628-1	2017	The dysregulation expression of microRNAs (miRNAs) including miR-144, has been widely documented in TBI.	Thioacetazone	100-103	microRNA 144	Homo sapiens	61-68
28938628-12	2017	Taken together, these findings demonstrated that elevated miR-144 promoted cognitive impairments induced by beta-amyloid accumulation post-TBI through suppressing of ADAM10 expression.	Thioacetazone	139-142	microRNA 144	Homo sapiens	58-65
28938628-12	2017	Taken together, these findings demonstrated that elevated miR-144 promoted cognitive impairments induced by beta-amyloid accumulation post-TBI through suppressing of ADAM10 expression.	Thioacetazone	139-142	ADAM metallopeptidase domain 10	Homo sapiens	166-172
28100103-9	2017	We conclude that the APOE promoter -219G/T polymorphism and the BDNF Met/Met genotype might confer risk for sustaining a TBI.	Thioacetazone	121-124	brain derived neurotrophic factor	Homo sapiens	64-68
28533576-10	2017	The same results were determined for IL-2 responses to ESAT-6/CFP-10 between the 2 groups, while significantly higher IL-2 responses to AlaDH were observed in LTBI than in active TBI.	Thioacetazone	160-163	interleukin 2	Homo sapiens	118-122
28452880-3	2017	The aim of this study was to determine if a select set of miRNAs (miR-21, Let-7i, miR-124a, miR-146a, miR-107) that were previously associated with TBI models and clinical studies would be dysregulated and correlated to inflammatory cytokine abundance in the rat penetrating ballistic-like brain injury (PBBI) model.	Thioacetazone	148-151	microRNA 21	Rattus norvegicus	66-72
28452880-3	2017	The aim of this study was to determine if a select set of miRNAs (miR-21, Let-7i, miR-124a, miR-146a, miR-107) that were previously associated with TBI models and clinical studies would be dysregulated and correlated to inflammatory cytokine abundance in the rat penetrating ballistic-like brain injury (PBBI) model.	Thioacetazone	148-151	microRNA 146a	Rattus norvegicus	92-100
28452880-3	2017	The aim of this study was to determine if a select set of miRNAs (miR-21, Let-7i, miR-124a, miR-146a, miR-107) that were previously associated with TBI models and clinical studies would be dysregulated and correlated to inflammatory cytokine abundance in the rat penetrating ballistic-like brain injury (PBBI) model.	Thioacetazone	148-151	microRNA 107	Rattus norvegicus	102-109
27306759-2	2017	Recently, IRF6 was shown to be upregulated after TBI and could promote neuronal apoptosis under oxidative stress conditions.	Thioacetazone	49-52	interferon regulatory factor 6	Mus musculus	10-14
28533576-12	2017	CONCLUSION: The current study suggests that it may be possible to discriminate LTBI from active TBI by IL-2 responses to AlaDH.	Thioacetazone	80-83	interleukin 2	Homo sapiens	103-107
28429354-9	2017	Furthermore, in the TBI-fracture group, CGRP in both hippocampus and the whole brain showed a noticeable augment in RT-PCR and western blot analysis at 72 and 168 h post-injury, and only in this group, immunohistochemistry analysis indicated that CGRP was present in the hippocampus at 168 hours post-injury.	Thioacetazone	20-23	calcitonin-related polypeptide alpha	Rattus norvegicus	40-44
28419114-5	2017	Heart fatty-acid binding protein (H-FABP) has been highlighted in brain injury models and investigated as a biomarker for stroke and severe TBI, for example.	Thioacetazone	140-143	fatty acid binding protein 3	Homo sapiens	0-32
28419114-5	2017	Heart fatty-acid binding protein (H-FABP) has been highlighted in brain injury models and investigated as a biomarker for stroke and severe TBI, for example.	Thioacetazone	140-143	fatty acid binding protein 3	Homo sapiens	34-40
28429354-9	2017	Furthermore, in the TBI-fracture group, CGRP in both hippocampus and the whole brain showed a noticeable augment in RT-PCR and western blot analysis at 72 and 168 h post-injury, and only in this group, immunohistochemistry analysis indicated that CGRP was present in the hippocampus at 168 hours post-injury.	Thioacetazone	20-23	calcitonin-related polypeptide alpha	Rattus norvegicus	247-251
28030563-3	2016	Mild TBI caused a rapid (within 6 h post-mTBI) upregulation of synthesis of TNF-alpha and IL-1beta in the cerebral cortex and hippocampus, followed by an increase in production of neutrophil (CXCL1-3) and monocyte (CCL2) chemoattractants.	Thioacetazone	5-8	tumor necrosis factor	Rattus norvegicus	76-85
27769642-3	2017	A SNP in catechol-o-methyltransferase (COMT) is suggested to influence development of post-traumatic stress disorder (PTSD), but its role in TBI remains unclear.	Thioacetazone	141-144	catechol-O-methyltransferase	Homo sapiens	9-37
27769642-3	2017	A SNP in catechol-o-methyltransferase (COMT) is suggested to influence development of post-traumatic stress disorder (PTSD), but its role in TBI remains unclear.	Thioacetazone	141-144	catechol-O-methyltransferase	Homo sapiens	39-43
28110075-4	2017	TLR9 agonist ODN1826 stimulation in vitro for 5h induced more B10 cells to express cytoplasmic IL-10 in sub-TBI WT mice than in TLR9-/- mice.	Thioacetazone	108-111	toll-like receptor 9	Mus musculus	0-4
28110075-4	2017	TLR9 agonist ODN1826 stimulation in vitro for 5h induced more B10 cells to express cytoplasmic IL-10 in sub-TBI WT mice than in TLR9-/- mice.	Thioacetazone	108-111	interleukin 10	Mus musculus	95-100
28110075-6	2017	TLR9-dependent signaling molecules, MyD88, TRAF6 and IRF8 are involved in sub-TBI induced Breg/B10 cells development and expansion.	Thioacetazone	78-81	toll-like receptor 9	Mus musculus	0-4
28110075-6	2017	TLR9-dependent signaling molecules, MyD88, TRAF6 and IRF8 are involved in sub-TBI induced Breg/B10 cells development and expansion.	Thioacetazone	78-81	myeloid differentiation primary response gene 88	Mus musculus	36-41
28110075-6	2017	TLR9-dependent signaling molecules, MyD88, TRAF6 and IRF8 are involved in sub-TBI induced Breg/B10 cells development and expansion.	Thioacetazone	78-81	TNF receptor-associated factor 6	Mus musculus	43-48
28110075-6	2017	TLR9-dependent signaling molecules, MyD88, TRAF6 and IRF8 are involved in sub-TBI induced Breg/B10 cells development and expansion.	Thioacetazone	78-81	interferon regulatory factor 8	Mus musculus	53-57
28110075-8	2017	Adoptively transferred sub-TBI induced Breg cells significantly suppress inflammatory T cell responses of TH17 and TH1 types in EAE mice.	Thioacetazone	27-30	negative elongation factor complex member C/D, Th1l	Mus musculus	106-109
28030563-3	2016	Mild TBI caused a rapid (within 6 h post-mTBI) upregulation of synthesis of TNF-alpha and IL-1beta in the cerebral cortex and hippocampus, followed by an increase in production of neutrophil (CXCL1-3) and monocyte (CCL2) chemoattractants.	Thioacetazone	5-8	interleukin 1 beta	Rattus norvegicus	90-98
28030563-3	2016	Mild TBI caused a rapid (within 6 h post-mTBI) upregulation of synthesis of TNF-alpha and IL-1beta in the cerebral cortex and hippocampus, followed by an increase in production of neutrophil (CXCL1-3) and monocyte (CCL2) chemoattractants.	Thioacetazone	5-8	C-X-C motif chemokine ligand 13	Rattus norvegicus	192-199
28030563-3	2016	Mild TBI caused a rapid (within 6 h post-mTBI) upregulation of synthesis of TNF-alpha and IL-1beta in the cerebral cortex and hippocampus, followed by an increase in production of neutrophil (CXCL1-3) and monocyte (CCL2) chemoattractants.	Thioacetazone	5-8	C-C motif chemokine ligand 2	Rattus norvegicus	215-219
27489538-15	2016	These results suggest that inhibiting CypD after TBI is an effective strategy to reduce synaptic hyperexcitation, making it a continued target for potential treatment of network abnormalities.	Thioacetazone	49-52	peptidylprolyl isomerase F (cyclophilin F)	Mus musculus	38-42
27876152-4	2016	Both mild tail trauma and TBI induced similar systemic changes that normalized within 48 hours, including release of substance P.	Thioacetazone	26-29	tachykinin 1	Mus musculus	117-128
27181909-4	2016	Some of the most extensively studied blood biomarkers for TBI include S100beta, neuron-specific enolase, glial fibrillary acidic protein, and Tau.	Thioacetazone	58-61	S100 calcium binding protein B	Homo sapiens	70-78
27181909-4	2016	Some of the most extensively studied blood biomarkers for TBI include S100beta, neuron-specific enolase, glial fibrillary acidic protein, and Tau.	Thioacetazone	58-61	enolase 2	Homo sapiens	80-103
28573162-3	2016	The measurement of tissue transferrin- and non-transferrin-bound iron (TBI and NTBI, respectively) uptake in vivo can be achieved via intravenous administration of 59Fe-labeled TBI or NTBI followed by gamma counting of various organs.	Thioacetazone	71-74	transferrin	Mus musculus	26-37
28573162-3	2016	The measurement of tissue transferrin- and non-transferrin-bound iron (TBI and NTBI, respectively) uptake in vivo can be achieved via intravenous administration of 59Fe-labeled TBI or NTBI followed by gamma counting of various organs.	Thioacetazone	71-74	transferrin	Mus musculus	47-58
28573162-3	2016	The measurement of tissue transferrin- and non-transferrin-bound iron (TBI and NTBI, respectively) uptake in vivo can be achieved via intravenous administration of 59Fe-labeled TBI or NTBI followed by gamma counting of various organs.	Thioacetazone	80-83	transferrin	Mus musculus	26-37
28573162-3	2016	The measurement of tissue transferrin- and non-transferrin-bound iron (TBI and NTBI, respectively) uptake in vivo can be achieved via intravenous administration of 59Fe-labeled TBI or NTBI followed by gamma counting of various organs.	Thioacetazone	80-83	transferrin	Mus musculus	47-58
27530814-7	2016	Network analysis of overlapping genes revealed the effects on tubulins (Tubb2a, Tubb3, Tubb4b), Nfe2l2, S100a4, Cd44, and Nfkb2, all of which are linked to TBI-relevant outcomes, including epileptogenesis and tissue repair.	Thioacetazone	156-159	tubulin, beta 2A class IIa	Rattus norvegicus	72-78
27530814-7	2016	Network analysis of overlapping genes revealed the effects on tubulins (Tubb2a, Tubb3, Tubb4b), Nfe2l2, S100a4, Cd44, and Nfkb2, all of which are linked to TBI-relevant outcomes, including epileptogenesis and tissue repair.	Thioacetazone	156-159	tubulin, beta 3 class III	Rattus norvegicus	80-85
27530814-7	2016	Network analysis of overlapping genes revealed the effects on tubulins (Tubb2a, Tubb3, Tubb4b), Nfe2l2, S100a4, Cd44, and Nfkb2, all of which are linked to TBI-relevant outcomes, including epileptogenesis and tissue repair.	Thioacetazone	156-159	tubulin, beta 4B class IVb	Rattus norvegicus	87-93
27530814-7	2016	Network analysis of overlapping genes revealed the effects on tubulins (Tubb2a, Tubb3, Tubb4b), Nfe2l2, S100a4, Cd44, and Nfkb2, all of which are linked to TBI-relevant outcomes, including epileptogenesis and tissue repair.	Thioacetazone	156-159	NFE2 like bZIP transcription factor 2	Rattus norvegicus	96-102
27530814-7	2016	Network analysis of overlapping genes revealed the effects on tubulins (Tubb2a, Tubb3, Tubb4b), Nfe2l2, S100a4, Cd44, and Nfkb2, all of which are linked to TBI-relevant outcomes, including epileptogenesis and tissue repair.	Thioacetazone	156-159	S100 calcium-binding protein A4	Rattus norvegicus	104-110
27530814-7	2016	Network analysis of overlapping genes revealed the effects on tubulins (Tubb2a, Tubb3, Tubb4b), Nfe2l2, S100a4, Cd44, and Nfkb2, all of which are linked to TBI-relevant outcomes, including epileptogenesis and tissue repair.	Thioacetazone	156-159	CD44 molecule (Indian blood group)	Rattus norvegicus	112-116
27530814-7	2016	Network analysis of overlapping genes revealed the effects on tubulins (Tubb2a, Tubb3, Tubb4b), Nfe2l2, S100a4, Cd44, and Nfkb2, all of which are linked to TBI-relevant outcomes, including epileptogenesis and tissue repair.	Thioacetazone	156-159	nuclear factor kappa B subunit 2	Rattus norvegicus	122-127
27017959-9	2016	Moreover, SB reversed the decrease in occludin and ZO-1 expression induced by TBI.	Thioacetazone	78-81	occludin	Mus musculus	38-46
27017959-9	2016	Moreover, SB reversed the decrease in occludin and ZO-1 expression induced by TBI.	Thioacetazone	78-81	tight junction protein 1	Mus musculus	51-55
27237921-2	2016	BACKGROUND: TBI has been recognized as the "signature Injury" of the OEF/OIF campaigns occurring in 14-20% of deployed soldiers.	Thioacetazone	12-15	osteoglycin	Homo sapiens	73-76
27061159-9	2016	CONCUSIONS: Results provide evidence of convergent validity and internal consistency of the CASP and support its use for assessing participation of children with TBI over time.	Thioacetazone	162-165	cut like homeobox 1	Homo sapiens	92-96
27119554-0	2016	Protective effects of PARP inhibitor, PJ34, is related to down-regulation of calpain and NF-kappaB in a mouse model of TBI.	Thioacetazone	119-122	poly (ADP-ribose) polymerase family, member 1	Mus musculus	22-26
26579945-11	2016	CONCLUSIONS: Many of the pathological and behavioural consequences of TBI might be due to activation of the pro-neurotrophin/p75 toxic pathway overriding the protective mechanisms of the mature neurotrophin/Trk pathway.	Thioacetazone	70-73	nerve growth factor receptor (TNFR superfamily, member 16)	Mus musculus	125-128
26772189-3	2016	The kidney expression of the EET producing enzyme CYP2C11 was lower in rats that received total body irradiation (TBI rat) compared with non-irradiated control.	Thioacetazone	114-117	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	50-57
26579945-11	2016	CONCLUSIONS: Many of the pathological and behavioural consequences of TBI might be due to activation of the pro-neurotrophin/p75 toxic pathway overriding the protective mechanisms of the mature neurotrophin/Trk pathway.	Thioacetazone	70-73	neurotrophic tyrosine kinase, receptor, type 1	Mus musculus	207-210
27834535-8	2016	The probability of TBI was highest in the PCT-related trajectories, with significantly lower probabilities in other trajectories.	Thioacetazone	19-22	calcitonin related polypeptide alpha	Homo sapiens	42-45
27466967-5	2016	RESULTS: Mortality of patients with TBI AIS 3, 4 was 1.9% and 2.9% respectively, comparing with 31.1% among TBI AIS 5+.	Thioacetazone	36-39	AIS3	Homo sapiens	40-45
26579945-12	2016	Targeting p75 can be a novel strategy to counteract the damaging effects of TBI.	Thioacetazone	76-79	nerve growth factor receptor (TNFR superfamily, member 16)	Mus musculus	10-13
27834535-9	2016	CONCLUSIONS: It was found that TBI was most common in PCT-related trajectories, indicating that TBI is commonly comorbid with pain and mental health conditions for both men and women.	Thioacetazone	31-34	calcitonin related polypeptide alpha	Homo sapiens	54-57
27834535-9	2016	CONCLUSIONS: It was found that TBI was most common in PCT-related trajectories, indicating that TBI is commonly comorbid with pain and mental health conditions for both men and women.	Thioacetazone	96-99	calcitonin related polypeptide alpha	Homo sapiens	54-57
26633377-5	2015	We observed that methimazole, thiouracil, methylthiouracil, propylthiouracil, ambazone, and thioacetazone inhibited mushroom tyrosinase.	Thioacetazone	92-105	tyrosinase	Mus musculus	125-135
26671128-10	2015	TBI rats also showed significantly higher levels of IL-6 versus control in both CSF and serum, but no significant difference was observed between each impact group.	Thioacetazone	0-3	interleukin 6	Rattus norvegicus	52-56
26633377-7	2015	Both thioacetazone and ambazone significantly inhibited tyrosinase, with IC50 of 14 and 15 muM, respectively.	Thioacetazone	5-18	tyrosinase	Mus musculus	56-66
26025142-15	2015	The exceeding production of QUIN together with increased IDO1 activation and mRNA expression in brain-injured areas suggests that TBI selectively induces a robust stimulation of the neurotoxic branch of the KP pathway.	Thioacetazone	130-133	indoleamine 2,3-dioxygenase 1	Homo sapiens	57-61
25989749-9	2015	Adiponectin in the HSCT/TBI Group was lower than the Chemotherapy-only group, and correlated negatively with time post HSCT/TBI.	Thioacetazone	24-27	adiponectin, C1Q and collagen domain containing	Homo sapiens	0-11
25989749-9	2015	Adiponectin in the HSCT/TBI Group was lower than the Chemotherapy-only group, and correlated negatively with time post HSCT/TBI.	Thioacetazone	124-127	adiponectin, C1Q and collagen domain containing	Homo sapiens	0-11
26112336-11	2015	The brain measures of IL-1beta, IL-6 and TNF-alpha in TBI were also reduced by estrogen.	Thioacetazone	54-57	interleukin 1 beta	Rattus norvegicus	22-30
26112336-11	2015	The brain measures of IL-1beta, IL-6 and TNF-alpha in TBI were also reduced by estrogen.	Thioacetazone	54-57	interleukin 6	Rattus norvegicus	32-36
26112336-11	2015	The brain measures of IL-1beta, IL-6 and TNF-alpha in TBI were also reduced by estrogen.	Thioacetazone	54-57	tumor necrosis factor	Rattus norvegicus	41-50
26112336-14	2015	Estrogen also elevated IL-10 in TBI.	Thioacetazone	32-35	interleukin 10	Rattus norvegicus	23-28
25779951-6	2015	Furthermore, CD4(+) T-cell counts were significantly lower in TLI than in TBI patients the first 6 months after transplantation.	Thioacetazone	74-77	CD4 molecule	Homo sapiens	13-16
25701255-7	2015	The number of Notch1 or Hes1 (+) and BrdU (+) cells decreased in the subgranular zone (SGZ) of the DG in the hippocampus following TBI.	Thioacetazone	131-134	notch 1	Mus musculus	14-20
25860286-8	2015	Significant post-TBI recovery of hematopoietic cells, particularly leukocytes, was observed in TM+/+ mice (p = 0.003), but not in TMPro/- mice, despite the fact that GT3 induced higher levels of granulocyte colony stimulating factor (G-CSF) in TMPro/- mice (p = 0.0001).	Thioacetazone	17-20	thrombomodulin	Mus musculus	95-97
25860286-9	2015	These data demonstrate a critical, G-CSF-independent, role for endothelial TM in GT3-mediated lethality protection and hematopoietic recovery after exposure to TBI and may point to new strategies to enhance the efficacy of current medical countermeasures in radiological/nuclear emergencies.	Thioacetazone	160-163	thrombomodulin	Mus musculus	75-77
25701255-7	2015	The number of Notch1 or Hes1 (+) and BrdU (+) cells decreased in the subgranular zone (SGZ) of the DG in the hippocampus following TBI.	Thioacetazone	131-134	hes family bHLH transcription factor 1	Mus musculus	24-28
25701255-8	2015	Nevertheless, the number of Ngn2-positive cells in the DG of injured mice was markedly higher than in the DG of non-TBI mice.	Thioacetazone	116-119	neurogenin 2	Mus musculus	28-32
25468272-5	2015	Together, these results support the therapeutic potential of GM-CSF for TBI.	Thioacetazone	72-75	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	61-67
25870583-5	2015	The combined fold-changes in plasma levels of PRDX6, S100b, MCP1, NSE, and BDNF resulted in the formulation of a TBI assessment score that identified mTBI with a receiver operating characteristic (ROC) area under the curve of 0.97, when compared to healthy controls.	Thioacetazone	113-116	peroxiredoxin 6	Homo sapiens	46-51
25870583-5	2015	The combined fold-changes in plasma levels of PRDX6, S100b, MCP1, NSE, and BDNF resulted in the formulation of a TBI assessment score that identified mTBI with a receiver operating characteristic (ROC) area under the curve of 0.97, when compared to healthy controls.	Thioacetazone	113-116	S100 calcium binding protein B	Homo sapiens	53-58
25870583-5	2015	The combined fold-changes in plasma levels of PRDX6, S100b, MCP1, NSE, and BDNF resulted in the formulation of a TBI assessment score that identified mTBI with a receiver operating characteristic (ROC) area under the curve of 0.97, when compared to healthy controls.	Thioacetazone	113-116	C-C motif chemokine ligand 2	Homo sapiens	60-64
25870583-5	2015	The combined fold-changes in plasma levels of PRDX6, S100b, MCP1, NSE, and BDNF resulted in the formulation of a TBI assessment score that identified mTBI with a receiver operating characteristic (ROC) area under the curve of 0.97, when compared to healthy controls.	Thioacetazone	113-116	enolase 2	Homo sapiens	66-69
25870583-5	2015	The combined fold-changes in plasma levels of PRDX6, S100b, MCP1, NSE, and BDNF resulted in the formulation of a TBI assessment score that identified mTBI with a receiver operating characteristic (ROC) area under the curve of 0.97, when compared to healthy controls.	Thioacetazone	113-116	brain derived neurotrophic factor	Homo sapiens	75-79
25379648-0	2015	Quinone reductase 2 is an adventitious target of protein kinase CK2 inhibitors TBBz (TBI) and DMAT.	Thioacetazone	85-88	N-ribosyldihydronicotinamide:quinone reductase 2	Homo sapiens	0-19
26094899-2	2015	Rifampicin, rifabutin, and thioacetazone inhibited one CYP reaction.	Thioacetazone	27-40	peptidylprolyl isomerase G	Homo sapiens	55-58
26417600-6	2015	The IGF-1 blood levels result prone to decrease during both the early and late phases after TBI.	Thioacetazone	92-95	insulin like growth factor 1	Homo sapiens	4-9
26417600-8	2015	We review the mechanisms involving IGF-1 in TBI, analyzing how its expression and metabolism may affect prognosis and outcome in head trauma patients.	Thioacetazone	44-47	insulin like growth factor 1	Homo sapiens	35-40
25417641-5	2014	Our data suggested PSGL and CD68 immunopositivity of microglial cells in both focal and diffuse TBI, predominantly in perivascular space correlated with telolysosome formation in cytoplasma.	Thioacetazone	96-99	CD68 molecule	Homo sapiens	28-32
24968091-5	2014	EMMPRIN expression was markedly up-regulated in the brain tissue surrounding the injured region 6-48 h after TBI, as measured by immunoblot and immunohistochemistry.	Thioacetazone	109-112	basigin (Ok blood group)	Rattus norvegicus	0-7
24968091-8	2014	These data demonstrate, for the first time, changes in CD147 and MMP-9 expression following TBI.	Thioacetazone	92-95	matrix metallopeptidase 9	Rattus norvegicus	65-70
24968091-9	2014	These data also suggest that CD147 and MMP-9 may play a role in vascular injuries after TBI.	Thioacetazone	88-91	matrix metallopeptidase 9	Rattus norvegicus	39-44
25229716-2	2015	We recently demonstrated that TBI induces acquired GABAA receptors channelopathy that associates with hyperexcitability in granule cell layer (GCL).	Thioacetazone	30-33	germ cell-less 2, spermatogenesis associated	Homo sapiens	143-146
25229716-7	2015	In the thalamus, we found decreases in alpha1, alpha4, beta2, gamma2 and delta mRNAs in the laterodorsal thalamus and in the area combining the posterior thalamic nuclear group, ventroposterolateral and ventroposteromedial complex at 6 h to 4 months post-TBI.	Thioacetazone	255-258	adrenoceptor alpha 1D	Homo sapiens	39-53
25229716-7	2015	In the thalamus, we found decreases in alpha1, alpha4, beta2, gamma2 and delta mRNAs in the laterodorsal thalamus and in the area combining the posterior thalamic nuclear group, ventroposterolateral and ventroposteromedial complex at 6 h to 4 months post-TBI.	Thioacetazone	255-258	tryptophanyl-tRNA synthetase 1	Homo sapiens	62-78
25229716-9	2015	However, contralaterally there was up-regulation of the subunits delta and alpha4 6 h and 4 months after TBI, respectively.	Thioacetazone	105-108	immunoglobulin binding protein 1	Homo sapiens	75-81
25229716-10	2015	PCR array analysis suggested a mild long-lasting GABAA receptor channelopathy in the GCL and thalamus after TBI.	Thioacetazone	108-111	germ cell-less 2, spermatogenesis associated	Homo sapiens	85-88
25277076-7	2014	Based on these results, we conclude that the diminished miR21 injury response in the aged brain leads to up-regulation of its targets, with the potential to contribute to the poor prognosis following TBI in aging brain.	Thioacetazone	200-203	microRNA 21a	Mus musculus	56-61
24894113-1	2014	OBJECTIVE: TBI causes localized cerebral ischemia that, in turn, is accompanied by both changes in BBB permeability and recruitment of CD34(+) cells to the injured tissue.	Thioacetazone	11-14	CD34 molecule	Rattus norvegicus	135-139
24894113-3	2014	This study is a preliminary investigation into possible correlations between CD34(+) cell recruitment and BBB permeability following TBI in a rat model.	Thioacetazone	133-136	CD34 molecule	Rattus norvegicus	77-81
24894113-10	2014	CONCLUSIONS: The negative linear correlation between CD34(+) cell recruitment and BBB permeability following TBI provides a support for further study of CD34(+) cell transplantation for BBB repair after TBI.	Thioacetazone	109-112	CD34 molecule	Rattus norvegicus	53-57
24894113-10	2014	CONCLUSIONS: The negative linear correlation between CD34(+) cell recruitment and BBB permeability following TBI provides a support for further study of CD34(+) cell transplantation for BBB repair after TBI.	Thioacetazone	109-112	CD34 molecule	Rattus norvegicus	153-157
24894113-10	2014	CONCLUSIONS: The negative linear correlation between CD34(+) cell recruitment and BBB permeability following TBI provides a support for further study of CD34(+) cell transplantation for BBB repair after TBI.	Thioacetazone	203-206	CD34 molecule	Rattus norvegicus	53-57
24894113-10	2014	CONCLUSIONS: The negative linear correlation between CD34(+) cell recruitment and BBB permeability following TBI provides a support for further study of CD34(+) cell transplantation for BBB repair after TBI.	Thioacetazone	203-206	CD34 molecule	Rattus norvegicus	153-157
25417641-6	2014	Polymorphism of PAI-1, MTHFR, eNOS, VEGF, and Apo E genes in TBI were in patients with SOL were bound to show up leucocyte plugging in capillaries.	Thioacetazone	61-64	serpin family E member 1	Homo sapiens	16-21
25417641-6	2014	Polymorphism of PAI-1, MTHFR, eNOS, VEGF, and Apo E genes in TBI were in patients with SOL were bound to show up leucocyte plugging in capillaries.	Thioacetazone	61-64	methylenetetrahydrofolate reductase	Homo sapiens	23-28
25417641-6	2014	Polymorphism of PAI-1, MTHFR, eNOS, VEGF, and Apo E genes in TBI were in patients with SOL were bound to show up leucocyte plugging in capillaries.	Thioacetazone	61-64	vascular endothelial growth factor A	Homo sapiens	36-40
25417641-6	2014	Polymorphism of PAI-1, MTHFR, eNOS, VEGF, and Apo E genes in TBI were in patients with SOL were bound to show up leucocyte plugging in capillaries.	Thioacetazone	61-64	apolipoprotein E	Homo sapiens	46-51
25191305-4	2014	METHODS: Mild TBI patients without depressive symptoms (mTBI-noD, n = 39), TBI patients with depressive symptoms (mTBI-D, n = 13), and 15 patients with major depressive disorder (MDD), but no TBI were given 99m T-ECD single-photon emission computed tomography (SPECT) scans within 2 weeks of injury.	Thioacetazone	57-60	atrophin 1	Homo sapiens	61-64
25221540-14	2014	High basal levels of CBR expression in young naive females could protect against TBI damage whereas stress-induced CBR deficits could predict a poor outcome of TBI in repeatedly stressed females.	Thioacetazone	81-84	cannabinoid receptor 1	Rattus norvegicus	21-24
24124534-7	2013	Membrane beta catenin is transiently reduced in heat acclimated mice and its recovery 7 days post TBI is accompanied by induction of the synaptic marker synaptophysin.	Thioacetazone	98-101	catenin (cadherin associated protein), beta 1	Mus musculus	9-21
24442476-2	2014	To fill this gap, we have derivatized the scaffold of the promiscuous CK2 inhibitor TBI with a deoxyribose moiety, generating TDB, a selective, cell-permeable inhibitor of CK2 and PIM-1.	Thioacetazone	84-87	Pim-1 proto-oncogene, serine/threonine kinase	Homo sapiens	180-185
24728097-2	2014	Previous studies with small sample size have reported higher circulating MMP-2 and MMP-9 levels in patients with TBI, but no association between those levels and mortality.	Thioacetazone	113-116	matrix metallopeptidase 2	Homo sapiens	73-78
24728097-2	2014	Previous studies with small sample size have reported higher circulating MMP-2 and MMP-9 levels in patients with TBI, but no association between those levels and mortality.	Thioacetazone	113-116	matrix metallopeptidase 9	Homo sapiens	83-88
24728097-3	2014	Thus, the aim of this study was to determine whether serum TIMP-1 and MMP-9 levels are associated with mortality in patients with severe TBI.	Thioacetazone	137-140	TIMP metallopeptidase inhibitor 1	Homo sapiens	59-65
24728097-3	2014	Thus, the aim of this study was to determine whether serum TIMP-1 and MMP-9 levels are associated with mortality in patients with severe TBI.	Thioacetazone	137-140	matrix metallopeptidase 9	Homo sapiens	70-75
24728097-8	2014	RESULTS: Non-surviving TBI patients (n = 27) showed higher serum TIMP-1 levels than survivor ones (n = 73).	Thioacetazone	23-26	TIMP metallopeptidase inhibitor 1	Homo sapiens	65-71
24728097-14	2014	CONCLUSIONS: The most relevant and new findings of our study, the largest series reporting data on TIMP-1 and MMP-9 levels in patients with severe TBI, were that serum TIMP-1 levels were associated with TBI mortality and could be used as a prognostic biomarker of mortality in TBI patients.	Thioacetazone	147-150	TIMP metallopeptidase inhibitor 1	Homo sapiens	99-105
24093437-2	2014	Trauma registry data were used to identify TBI in all RTA victims admitted to hospitals in the mid-West region of the Netherlands from 2003 to 2011.	Thioacetazone	43-46	MAS related GPR family member F	Homo sapiens	54-57
24586573-3	2014	In contrast by altering the scaffold of the promiscuous CK2 inhibitor TBI a new class of HIPK2 inhibitors has been generated.	Thioacetazone	70-73	homeodomain interacting protein kinase 2	Homo sapiens	89-94
24806476-12	2014	Low levels of S100B were able to rule out mTBI and high S100B levels correlated with TBI severity.	Thioacetazone	43-46	S100 calcium binding protein B	Homo sapiens	14-19
24728097-14	2014	CONCLUSIONS: The most relevant and new findings of our study, the largest series reporting data on TIMP-1 and MMP-9 levels in patients with severe TBI, were that serum TIMP-1 levels were associated with TBI mortality and could be used as a prognostic biomarker of mortality in TBI patients.	Thioacetazone	147-150	matrix metallopeptidase 9	Homo sapiens	110-115
24728097-14	2014	CONCLUSIONS: The most relevant and new findings of our study, the largest series reporting data on TIMP-1 and MMP-9 levels in patients with severe TBI, were that serum TIMP-1 levels were associated with TBI mortality and could be used as a prognostic biomarker of mortality in TBI patients.	Thioacetazone	147-150	TIMP metallopeptidase inhibitor 1	Homo sapiens	168-174
24728097-14	2014	CONCLUSIONS: The most relevant and new findings of our study, the largest series reporting data on TIMP-1 and MMP-9 levels in patients with severe TBI, were that serum TIMP-1 levels were associated with TBI mortality and could be used as a prognostic biomarker of mortality in TBI patients.	Thioacetazone	203-206	matrix metallopeptidase 9	Homo sapiens	110-115
24728097-14	2014	CONCLUSIONS: The most relevant and new findings of our study, the largest series reporting data on TIMP-1 and MMP-9 levels in patients with severe TBI, were that serum TIMP-1 levels were associated with TBI mortality and could be used as a prognostic biomarker of mortality in TBI patients.	Thioacetazone	203-206	TIMP metallopeptidase inhibitor 1	Homo sapiens	168-174
24728097-14	2014	CONCLUSIONS: The most relevant and new findings of our study, the largest series reporting data on TIMP-1 and MMP-9 levels in patients with severe TBI, were that serum TIMP-1 levels were associated with TBI mortality and could be used as a prognostic biomarker of mortality in TBI patients.	Thioacetazone	203-206	matrix metallopeptidase 9	Homo sapiens	110-115
24728097-14	2014	CONCLUSIONS: The most relevant and new findings of our study, the largest series reporting data on TIMP-1 and MMP-9 levels in patients with severe TBI, were that serum TIMP-1 levels were associated with TBI mortality and could be used as a prognostic biomarker of mortality in TBI patients.	Thioacetazone	203-206	TIMP metallopeptidase inhibitor 1	Homo sapiens	168-174
24860816-4	2014	In addition, results from our previous research have demonstrated that the bone marrow tyrosine kinase gene in chromosome X (BMX), a member of the Tec family of kinases, is highly expressed in rats with TBI.	Thioacetazone	203-206	BMX non-receptor tyrosine kinase	Rattus norvegicus	125-128
23796971-0	2013	Low brain DHA content worsens sensorimotor outcomes after TBI and decreases TBI-induced Timp1 expression in juvenile rats.	Thioacetazone	76-79	TIMP metallopeptidase inhibitor 1	Rattus norvegicus	88-93
23796971-4	2013	Ccl2, Gfap, and Mmp 9 mRNA levels, and MMP-2 and -9 enzymatic activities were increased after TBI regardless of brain DHA level.	Thioacetazone	94-97	matrix metallopeptidase 2	Rattus norvegicus	39-51
23796971-6	2013	In contrast, TBI-induced Timp1 expression was lower in rats on the Deficient diet and correlated with brain DHA level.	Thioacetazone	13-16	TIMP metallopeptidase inhibitor 1	Rattus norvegicus	25-30
23826409-1	2013	AIMS: Activation of specific signaling pathways in response to mechanical trauma causes delayed neuronal apoptosis; GSK-3beta/beta-catenin signaling plays a critical role in the apoptosis of neurons in CNS diseases, SGK was discovered as a regulator of GSK-3beta/beta-catenin pathway, The goal of this study was to determine if the mechanism of cell death or survival mediated by the SGK/GSK-3beta/beta-catenin pathway is involved in a rat model of TBI.	Thioacetazone	449-452	glycogen synthase kinase 3 beta	Rattus norvegicus	116-125
23826409-1	2013	AIMS: Activation of specific signaling pathways in response to mechanical trauma causes delayed neuronal apoptosis; GSK-3beta/beta-catenin signaling plays a critical role in the apoptosis of neurons in CNS diseases, SGK was discovered as a regulator of GSK-3beta/beta-catenin pathway, The goal of this study was to determine if the mechanism of cell death or survival mediated by the SGK/GSK-3beta/beta-catenin pathway is involved in a rat model of TBI.	Thioacetazone	449-452	catenin beta 1	Rattus norvegicus	126-138
23826409-1	2013	AIMS: Activation of specific signaling pathways in response to mechanical trauma causes delayed neuronal apoptosis; GSK-3beta/beta-catenin signaling plays a critical role in the apoptosis of neurons in CNS diseases, SGK was discovered as a regulator of GSK-3beta/beta-catenin pathway, The goal of this study was to determine if the mechanism of cell death or survival mediated by the SGK/GSK-3beta/beta-catenin pathway is involved in a rat model of TBI.	Thioacetazone	449-452	serum/glucocorticoid regulated kinase 1	Rattus norvegicus	216-219
23826409-5	2013	KEY FINDINGS: Temporally, SGK expression showed an increase pattern after TBI and reached a peak at day 3.	Thioacetazone	74-77	serum/glucocorticoid regulated kinase 1	Rattus norvegicus	26-29
23000648-8	2013	In the DUCBT cohort, the use of TBI and early complete chimerism (<= day 21) were identified as risk factors that predispose the development of peri-ES.	Thioacetazone	32-35	perilipin 1	Homo sapiens	147-151