ライフサイエンスコーパス: liver damage

1 ategy for preventing and treating IR-induced liver damage.

2 X-linked-dominant protoporphyria (XLP) cause liver damage.

3 , indicating a conserved response to chronic liver damage.

4 4 contribute to acetaminophen (APAP)-induced liver damage.

5 d with the fibrogenic response during severe liver damage.

6 ling pathway protected against virus-induced liver damage.

7 ce from NKT cell-mediated induction of acute liver damage.

8 cell population, in hosts that have suffered liver damage.

9 le CD8(+) and NKT cells cooperatively induce liver damage.

10 of the 598 evaluable subjects had persistent liver damage.

11 ing strategy for prevention of toxin-induced liver damage.

12 death as a novel mechanism of NLRP3-mediated liver damage.

13 iltration into adipose tissue, and decreased liver damage.

14 ish, thereby leading to recovery from severe liver damage.

15 ntial to protect mice from poly(I:C)-induced liver damage.

16 ivating compounds are used for prevention of liver damage.

17 acetamide, were also ineffective in inducing liver damage.

18 s and increased thereafter proportionally to liver damage.

19 atic differentiation of ductular cells after liver damage.

20 ter define the mechanisms behind accelerated liver damage.

21 es displayed a mild increase in ConA-induced liver damage.

22 ced oxidative stress, lipid accumulation and liver damage.

23 r activated T cells in the pathomechanism of liver damage.

24 lso be involved in control of HCV-associated liver damage.

25 els of alanine transaminase, an indicator of liver damage.

26 ary viral response and marked improvement of liver damage.

27 duce HBV replication, causing only transient liver damage.

28 mpared with controls, causing only transient liver damage.

29 control virus replication but can also cause liver damage.

30 gn and reversible, inflammation can increase liver damage.

31 during the early response upon experimental liver damage.

32 gh levels of interleukin-22, which prevented liver damage.

33 en species that might exacerbate cholestatic liver damage.

34 thway plays a significant role in preventing liver damage.

35 phil infiltration, hepatocyte apoptosis, and liver damage.

36 ti-fibrotic therapies to counter HCV-induced liver damage.

37 nodeficiency and is variably associated with liver damage.

38 immune response, and the effect of these on liver damage.

39 NS5B-expression also results in liver damage.

40 lationship between HH-pathway activation and liver damage.

41 nvolved in liver fibrogenesis in response to liver damage.

42 phil infiltration, hepatocyte apoptosis, and liver damage.

43 d the liver against lipopolysaccharide (LPS) liver damage.

44 into the liver in Il22bp-deficient mice upon liver damage.

45 e progression of metabolic and viral chronic liver damage.

46 es massive hepatocyte apoptosis and/or fatal liver damage.

47 in ethanol binge and chronic ethanol-induced liver damage.

48 o induce FGF15 expression in intestine after liver damage.

49 own to promote liver regeneration upon acute liver damage.

50 ers but were not correlated with severity of liver damage.

51 r infiltration by neutrophils and subsequent liver damage.

52 neutrophil depletion significantly prevented liver damage.

53 +4 ligand-induced inflammatory cell-mediated liver damage.

54 , reduced Gsk3 phosphorylation and augmented liver damage.

55 egulating the initial fibrogenic response to liver damage.

56 ng low-choline diets develop fatty liver and liver damage.

57 ng an inflammatory response that exacerbates liver damage.

58 ndings that YCHT significantly decreased the liver damage.

59 sed erythrocyte delivery leads to kidney and liver damage.

60 lication but also regulate acute and chronic liver damage.

61 de of innate immune activation, resulting in liver damage.

62 trators of hepatic inflammation underpinning liver damage.

63 n hepatocytes and protects against oxidative liver damage.

64 nsaminase (ALT) levels, indicative of severe liver damage.

65 ued disease symptoms such as weight loss and liver damage.

66 n implicated or observed in diverse forms of liver damage.

67 in diseases outside of those associated with liver damage.

68 ere activated, they only partially mitigated liver damage.

69 riant on the predisposition to steatosis and liver damage.

70 imals against alcohol-induced, ROS-mediated, liver damage.

71 or trigger immune-mediated necroinflammatory liver damage.

72 er was the most frequent cause of persistent liver damage (65.4%).

73 pression protects from acetaminophen-induced liver damage, a paradigm for glutathione-mediated acute

74 , we found that APAP overdose in mice caused liver damage accompanied by significant thrombocytopenia

75 oprotection against preservation-association liver damage, accompanied by enhanced TIM-3 expression i

76 mice deficient in Cx32 are protected against liver damage, acute inflammation and death caused by liv

77 ugated hyperbilirubinemia without structural liver damage, affecting about 10% of the white populatio

78 which is highly associated with histological liver damage, affects IgG opsonizing activity and can be

79 evels of bile acids, and protected mice from liver damage after ethanol challenge.

80 d PP does not hamper liver function or cause liver damage after extended laparoscopic procedures.

81 factor that regulates apoptosis and induces liver damage after I/R.

82 hemolysis showed a positive correlation with liver damage along with the increased accumulation of fr

83 ubjects and to test their ability to predict liver damage also in comparison with the NAFLD fibrosis

84 that Tnc-deficient mice have a reduction in liver damage and a significant improvement in liver rege

85 aimed to assess whether TM6SF2 E167K affects liver damage and cardiovascular outcomes in subjects at

86 ion made mice resistant to TNF-alpha-induced liver damage and caused an alteration of the intrahepati

87 howed elevated serum markers associated with liver damage and cholestasis, extensive bile duct prolif

88 r results showed that HO-1 induction reduced liver damage and chronic inflammation by regulating immu

89 addition, we show that NKG2D contributes to liver damage and consequent hepatocyte proliferation kno

90 ve stress as a key mediator of virus-induced liver damage and describe a mechanism of innate-immunity

91 , whereas albumin was reduced, demonstrating liver damage and dysfunction.

92 on steatosis severity and is associated with liver damage and fibrosis in patients with CHC.

93 involved in amplifying and perpetuating the liver damage and fibrosis resulting from NLRP3 activatio

94 tion, premalignant dKO livers showed reduced liver damage and fibrosis, in association with decreased

95 ese mechanisms may contribute to progressive liver damage and impaired viral clearance in NASH.

96 it is shown to protect against Jo-2 induced liver damage and improve glucose tolerance in diabetic m

97 ntent in the 2 cohorts, and with more severe liver damage and increased risk of fibrosis compared wit

98 ss selectively in hepatocytes exhibited less liver damage and increased survival compared to mice wit

99 CCs), which arise on a background of chronic liver damage and inflammation, express c-Fos, a componen

100 icroRNAs (miRNAs) may serve as biomarkers of liver damage and inflammation.

101 ivery of small interfering RNA caused severe liver damage and inhibition of cell proliferation after

102 liver disease (NAFLD) is a leading cause of liver damage and is characterized by steatosis.

103 o in mice, BV provides protection from acute liver damage and is dependent on the availability of NO.

104 by either mechanism is associated with least liver damage and is therefore more beneficial for diseas

105 Serum bile acids are elevated after liver damage and may disrupt the blood-brain barrier and

106 ted with an IDO antagonist underwent greater liver damage and mortality compared with mock-treated IL

107 Liver damage and necrosis were greatly reduced in P2Y(2)

108 ce test-derived indexes were associated with liver damage and OGIS was the best predictor of signific

109 uantities of BAs are cytotoxic and can cause liver damage and promote gastrointestinal cancers.

110 ime in the hepatic vein during toxin-induced liver damage and regeneration in rodents.

111 Liver damage and regeneration were quantified by determi

112 The results showed that only BMSCs remitted liver damage and rescued ALF in ConA-treated mice.

113 Increasing autophagy might ameliorate liver damage and restore mitochondrial function after I/

114 individuals who abuse alcoholic beverages to liver damage and subsequent pathological conditions.

115 egulates TNF-alpha production in LPS-induced liver damage and suggest potential cell-specific therape

116 oactive lipid metabolites in alcohol-induced liver damage and tested the potential of targeting arach

117 tivation of NLRP3 inflammasome contribute to liver damage and the activation of innate immunity durin

118 oved glucose tolerance, reduced weight gain, liver damage and the development of hepatic steatosis in

119 to enter the extent and spatial patterns of liver damage and then calculate the outflow concentratio

120 Hepatitis B virus is not cytopathic; both liver damage and viral control--and therefore clinical o

121 ty is highly correlated with the severity of liver damage and with metabolic syndrome parameters that

122 gan dysfunction (including lung, kidney, and liver damage), and lymphocyte apoptosis.

123 resulted in excessive inflammation, massive liver damage, and a marked mortality increase, which hig

124 knockout mice were resistant to ConA-induced liver damage, and anti-interferon beta antibody mitigate

125 can activate effector cells, thus amplifying liver damage, and by modifying the hepatic cellular and

126 a was identified as an essential mediator of liver damage, and CD4 and CD8 T cells but not NK, NKT, o

127 ROV replication, hypercytokinemia, extensive liver damage, and death, whereas WT congenic animals fai

128 and hepatic arterial inflow, aggravates the liver damage, and delays the recovery process after FHVO

129 proliferation and intrahepatic biliary mass, liver damage, and inflammation, whereas blocking galanin

130 s C virus (HCV) infection synergize to cause liver damage, and microRNA-122 (miR-122) appears to play

131 ypes, including hepatic copper accumulation, liver damage, and mitochondrial impairment.

132 Enzyme replacement prevents neonatal death, liver damage, and osteoporosis in murine homocystinuria.

133 ere significantly correlated with markers of liver damage, and SIV-infected animals consistently had

134 platelets participate in the progression of liver damage, and that the direct thrombin inhibitor lep

135 njected into FRG mice, which develop chronic liver damage, and tumor growth was monitored.

136 luding lymphopenia, thrombocytopenia, marked liver damage, and uncontrolled viremia.

137 KT cell cytokine production and NKT-mediated liver damage are highly dependent on activation of this

138 e additional assays are done and measures of liver damage are taken into account.

139 t least in mice, persistence and subclinical liver damage are unique features of A. terreus infection

140 ted with a reduced inflammatory response and liver damage as indicated by lower levels of TCDD-induce

141 monitored tannic acid intake, body mass and liver damage as measured by serum alanine aminotransfera

142 ciated with known metabolic risk factors and liver damage, as determined by ALT levels.

143 Using mouse genetics, histology, liver damage assays and transcriptomics we discovered th

144 n TRPM2 knockout mice, acetaminophen-induced liver damage, assessed by the blood concentration of liv

145 ce the detergent-like property of BAs causes liver damage at high concentrations, hepatic BA levels m

146 been identified as fundamental mediators of liver damage both in mouse models and in humans.

147 navalin A (ConA) causes immune cell-mediated liver damage, but the contribution of resident nonparenc

148 We found that in the absence of IRAK-M, liver damage by alcohol was worse with higher alanine tr

149 cell receptors, which likely act to minimize liver damage by cytotoxic T cells during viral clearance

150 Tregs mitigated immunomediated liver damage by down-regulating the antiviral activity o

151 The enhancement of LPS-induced liver damage by ethanol preexposure was associated with

152 Type I IFN signaling protects from severe liver damage by recruitment of monocytic MDSCs and maint

153 The amelioration of liver damage by systemic application of Cxcl9 might offe

154 could distinguish between healthy liver and liver damaged by acetaminophen.

155 uate compensatory regeneration, overwhelming liver damage can cause acute liver failure (ALF) and dea

156 This mechanism might limit the amount of liver damage caused by activated CD8(+) T cells in patie

157 nine aminotransferase (ALT) increases in the liver damage caused by alcohol, APAP, and TLR9 (CpG)+4 (

158 te liver cancer in mice and humans that have liver damage caused by alcohol, viruses, or carcinogens.

159 In autoimmune hepatitis (AIH), liver-damaging CD4 T cell responses are associated with

160 e was associated with significantly elevated liver damage compared to transfer of wild-type NK cells.

161 bile duct ligation (BDL) displayed increased liver damage compared to wildtype BDL mice.

162 tenance of body mass and lower indicators of liver damage compared with control animals.

163 isualized whether, where, and to what extent liver damage compromised ammonia detoxification.

164 ll and BMDC B7-H1 expression was involved in liver damage control.

165 We found that a history of liver damage corresponds with transmission of an epigene

166 IFNAR-deficient mice from poly(I:C)-induced liver damage, directly linking the deregulated IL-1beta

167 ointestinal bleeding, vitamin deficiency, or liver-damaging diseases, such as infection and alcohol i

168 ures are increasingly applied to investigate liver damage due to drug exposure in toxicology.

169 HDV enhances liver damage during concomitant infection with HBV.

170 to favor neutrophil infiltration in inducing liver damage during hemolytic conditions in malaria.

171 Ccr8(-/-) mice displayed attenuated liver damage (e.g., ALT, histology, and TUNEL) compared

172 Tregs limit immunomediated liver damage early after an acute infection of the liver

173 howed significant increases in biomarkers of liver damage, endotoxemia, and MT indexes and a trend fo

174 y ticks, is often associated with pronounced liver damage, especially in fatal cases.

175 Heavy alcohol use can lead to progressive liver damage, especially in individuals with chronic hep

176 ng with a blocking mAb (RMT1-10) ameliorated liver damage, evidenced by reduced sALT levels and well-

177 f 145 nondiabetic NAFLD subjects to identify liver damage (fibrosis and nonalcoholic steatohepatitis)

178 ing aberrant pre-messenger RNA splicing with liver damage, fibrosis, and HCC.

179 n of an anti-MIR122 worsened the severity of liver damage following ethanol feeding in mice.

180 DAR1 significantly enhanced inflammation and liver damage following IRI, which was accompanied by sig

181 on of bile acids, and protected animals from liver damage from a diet high in levels of bile acids.

182 n limiting hepatic inflammation or resolving liver damage have not been fully understood.

183 address the contribution of serum markers of liver damage, high aspartate (AST, >49.9 IU/L) and alani

184 -/-) mice compared with WT mice, showed more liver damage, higher mortality, and ineffective CO rescu

185 with A. hydrophila die because of kidney and liver damage, hypoglycemia, and thrombocytopenia.

186 lustered in clinical phases with biochemical liver damage (IA and ENEG phases), whereas T-cell activi

187 erase inhibition with neostigmine diminishes liver damage in acute liver failure via the cholinergic

188 m was demonstrated to influence histological liver damage in alcoholic liver disease, nonalcoholic fa

189 tribute to the induction and perpetuation of liver damage in autoimmune hepatitis (AIH) and autoimmun

190 eficient mice were more susceptible to acute liver damage in both models.

191 ein, we examine some potential mechanisms of liver damage in brucellosis.

192 alpha in peritoneal CD11b+ monocytes reduced liver damage in C57BL/6 mice and significantly delayed a

193 re, microbiota transplantation revealed more liver damage in chimeric mice fed CTRL diet, but receivi

194 specific immune effector responses can cause liver damage in chronic infection.

195 I148M) in the PNPLA3 gene is associated with liver damage in chronic liver diseases.

196 Finding specific biomarkers of liver damage in clinical evaluations could increase the

197 le of reducing the fulminant immune-mediated liver damage in cremtg mice to wt level.

198 (IL)-17 axis and that this axis can regulate liver damage in diverse contexts prompted us to address

199 epatotoxic, and acute exposure causes severe liver damage in humans and animals.

200 Liver damage in humans is induced by various insults inc

201 One dose of 10-15 g causes severe liver damage in humans, whereas repeated exposure to ace

202 ted further to prevent acute alcohol-induced liver damage in humans.

203 n analyses showed increased inflammation and liver damage in mice given bone marrow transplants from

204 ld increase in parallel with the severity of liver damage in NAFLD.

205 with oval cells that expressed NEMO reversed liver damage in Nemo(Deltahepa) mice.

206 fat and predisposes to the full spectrum of liver damage in nonalcoholic fatty liver disease (NAFLD)

207 th an increased risk of significant/advanced liver damage in nondiabetic subjects with NAFLD.

208 h adoptive transfer of CD4 T cells triggered liver damage in otherwise IR-resistant RAG(-/-) mice, ad

209 Strikingly, PKA inhibition readily restored liver damage in otherwise IR-resistant, PACAP-conditione

210 downregulation of Sod1 and caused oxidative liver damage in Sod1(-/-) and wild-type mice.

211 ibute to insufficient antiviral response and liver damage in steatohepatitis.

212 Importantly, Fra-1 attenuates liver damage in the 3,5-diethoxycarbonyl-1,4-dihydrocoll

213 iently reversed mitochondrial impairment and liver damage in the acute stages of liver copper accumul

214 ient interferon-gamma production may promote liver damage in the setting of chronic infection.

215 We found extensive liver damage in these animals, with mortality over sever

216 stranded RNA (poly(I:C)), we observed severe liver damage in type I IFN-receptor (IFNAR) chain 1-defi

217 ng in HCC development depends on the mode of liver damage; in the case of HBsAg-driven hepatocarcinog

218 blockade exacerbated local inflammation and liver damage, indicating the importance of TIM-3-Gal-9 s

219 (HO-1), has been shown to protect mice from liver damage induced by acute inflammation.

220 Upon chronic liver damage induced by CCl4 or methionine-choline-defic

221 bp-deficient mice and murine models of acute liver damage induced by ischemia reperfusion and N-acety

222 dependent vasoprotective programs, prevented liver damage, inflammation, and oxidative stress and imp

223 ed hyperplastic cholangiocyte proliferation, liver damage, inflammation, and subsequent fibrosis.

224 Hgd and lacking Fah were exposed to chronic liver damage, injury-resistant nodules consisting of Hgd

225 Alcohol-induced liver damage is a major burden for most societies, and m

226 ic hepatitis in whom the underlying cause of liver damage is adequately treated.

227 Liver damage is believed to result from ductal cholestas

228 Liver damage is in most cases idiosyncratic and unpredic

229 -choline-deficient (MCD) diet, the degree of liver damage is related to dietary sugar content, which

230 points for the evaluation of the severity of liver damage-key for comparison of models of injury, tes

231 We investigated whether ancestral liver damage leads to heritable reprogramming of hepatic

232 parenchymal cells led to markedly attenuated liver damage, loss of Bim in the lymphoid compartment mo

233 The Model for Acetaminophen-induced Liver Damage (MALD) uses a patient's aspartate aminotran

234 Significant alleviation of liver damage manifested by a marked decrease in ALT, and

235 age-related cataract, and to assess whether liver damage mediates the hepatitis-cataract association

236 of NASH development by decreasing steatosis, liver damage, monocyte infiltration, and the production

237 n resistant, the MUP-uPA mice exhibited more liver damage, more immune infiltration, and increased li

238 Liver damage, neurological decline, and molecular analys

239 ter adjustment for biomarkers of preexisting liver damage, nor chronic infection with hepatitis B or

240 ese findings could account for the increased liver damage observed in female Ppargc1a(f/+)Alb-cre(+/0

241 ntribute to explaining some of mechanisms of liver damage observed in human brucellosis.

242 ich may explain some potential mechanisms of liver damage observed in human brucellosis.

243 that the 434K hampered the association with liver damage of the 148M allele (P = 0.006).

244 y a vital and beneficial role in response to liver damage or acute infection, the effects of chronic

245 osis development in vivo after BDL, reducing liver damage, oxidative stress, inflammation, and collag

246 eatosis and inherited host factors influence liver damage progression in chronic hepatitis C (CHC).

247 NPLA3) polymorphism predisposes to NAFLD and liver damage progression in NASH and chronic hepatitis C

248 ne to pregnant mice induced hypertension and liver damage, promoted abnormal labyrinth vascularizatio

249 y liver disease (NAFLD) covers a spectrum of liver damage ranging from simple steatosis to nonalcohol

250 Liver damage, reactive oxygen species (ROS) and paracrin

251 activation of NF-kappaB signaling, moderate liver damage, recruitment of inflammatory cells, hepatoc

252 rces and mechanisms of inflammasome-mediated liver damage remain poorly understood.

253 n dependence on hepatocyte response to acute liver damage remains to be defined.

254 ver failure and the leading cause of chronic liver damage requiring liver transplantation in develope

255 Iterative liver damage, secondary to any cause of liver injury, re

256 cles in the field, detailing the spectrum of liver damage seen in different models, and how they rela

257 lcohol- and lipopolysaccharide (LPS)-induced liver damage, serum ALT elevation, hepatomegaly, and lip

258 ple presented with muscle damage rather than liver damage; several effect alleles in SLC44A1 (rs78739

259 sociated liver pathologies such as extensive liver damage, steatohepatitis and fibrosis.

260 an any other serum marker with apoptosis and liver damage, such as ballooning (r = 0.65; P < 0.001),

261 ional sites of infection, and more extensive liver damage than did wild-type mice.

262 mice generally produce a milder phenotype of liver damage than those using genetically modified mice,

263 terol, Lats2-CKO mice manifested more severe liver damage than wild-type mice.

264 that autoantibody formation accompanies the liver damage that associates with K8/K18 absence.

265 ntribute to the pathogenesis and sequelae of liver damage that develops with metabolic syndrome.

266 e specific, but synergistic functions during liver damage that regulate cellular immune responses and

267 hepa)/p21(-/-) animals displayed accelerated liver damage that was not associated with alterations in

268 ence of weight gain, fructose rapidly causes liver damage that we suggest is secondary to endotoxemia

269 phen- or carbon tetrachloride (CCl4)-induced liver damage; the level of activation correlates with th

270 of IFN-alpha released by liver pDC to induce liver damage through hepatic IRF-1 up-regulation after I

271 gh the FGF15 axis and prevent progression of liver damage to HCC even in the absence of hepatic FXR.

272 L-33 in Kupffer cells, presumably because of liver damage triggered by TRAIL/FasL.

273 ession of HCV replication and HCV-associated liver damage underpinning the role of NK cells in the im

274 production of circulating HDL and increased liver damage upon high-dose LPS challenge.

275 ibited increased inflammation and aggravated liver damage upon viral infection, which was independent

276 ALOX15 knockout prevented alcohol-induced liver damage via attenuation of oxidative stress, ER str

277 hat IL-22BP plays a protective role in acute liver damage, via controlling IL-22-induced Cxcl10 expre

278 The more pronounced liver damage was accompanied by increased and prolonged

279 nsgenic mice, the severity of the subsequent liver damage was ameliorated by neutralization of IL-22.

280 Liver damage was assessed by hematoxylin and eosin and a

281 Liver damage was assessed by serum parameters, histopath

282 interstrain variability in severity of NAFLD liver damage was associated with dysregulation of genes

283 Short-term CCl4 liver damage was earlier and more efficiently repaired i

284 Liver damage was evaluated in 1,201 patients who underwe

285 Liver damage was fully abrogated when macrophage activat

286 eceiving the microbiota of HFD-treated mice; liver damage was further enhanced by transplantation of

287 The impact of rs368234815 on liver damage was generally more marked in nonobese indiv

288 s similar in mice with and without MDA5, but liver damage was increased in MDA5(-/-) mice, suggesting

289 Liver damage was induced in female mice by placing them

290 Liver damage was induced in male mice by placing them on

291 TNF-mediated liver damage was inhibited by two independent mechanisms

292 BDL-induced liver damage was reduced in BDL Kit(W-sh) mice, whereas

293 Acetaminophen-induced liver damage was reduced in P2Y(2)R(-/-) mice.

294 In the presence of chronic liver damage, we show that ablation of a p53-dependent s

295 stemic and local inflammatory responses, and liver damage were associated with bacterial levels.

296 , and FIB-4 scores (a noninvasive measure of liver damage) were examined.

297 vated FXR in the intestine protected against liver damage, whereas absence of FXR promoted progressio

298 ustained high levels of OROV replication and liver damage, whereas WT mice reconstituted with Ifnar(-

299 Burn injury induced significant liver damage, which was indicated by striking levels of

300 etabolic capacity from a specific pattern of liver damage with conventional techniques.