ライフサイエンスコーパス: liver damage

1 se NAFLD models to evaluate their effects on liver damage.

2 ng an inflammatory response that exacerbates liver damage.

3 ndings that YCHT significantly decreased the liver damage.

4 sed erythrocyte delivery leads to kidney and liver damage.

5 lication but also regulate acute and chronic liver damage.

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

7 trators of hepatic inflammation underpinning liver damage.

8 n hepatocytes and protects against oxidative liver damage.

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

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

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

12 in diseases outside of those associated with liver damage.

13 develop fewer liver tumors following chronic liver damage.

14 ere activated, they only partially mitigated liver damage.

15 riant on the predisposition to steatosis and liver damage.

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

17 mechanisms through which HIV itself induces liver damage.

18 or trigger immune-mediated necroinflammatory liver damage.

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

20 , indicating a conserved response to chronic liver damage.

21 4 contribute to acetaminophen (APAP)-induced liver damage.

22 notransferase in the plasma, indicating less liver damage.

23 d with the fibrogenic response during severe liver damage.

24 ling pathway protected against virus-induced liver damage.

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

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

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

28 of the 598 evaluable subjects had persistent liver damage.

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

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

31 iltration into adipose tissue, and decreased liver damage.

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

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

34 ivating compounds are used for prevention of liver damage.

35 acetamide, were also ineffective in inducing liver damage.

36 s and increased thereafter proportionally to liver damage.

37 ter define the mechanisms behind accelerated liver damage.

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

39 rrier and exaggerated PAMP translocation and liver damage.

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

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

42 ary viral response and marked improvement of liver damage.

43 duce HBV replication, causing only transient liver damage.

44 mpared with controls, causing only transient liver damage.

45 control virus replication but can also cause liver damage.

46 gn and reversible, inflammation can increase liver damage.

47 during the early response upon experimental liver damage.

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

49 en species that might exacerbate cholestatic liver damage.

50 thway plays a significant role in preventing liver damage.

51 phil infiltration, hepatocyte apoptosis, and liver damage.

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

53 hereby promote liver homeostasis and prevent liver damage.

54 kin photosensitivity and occasionally severe liver damage.

55 ysbiosis becomes the major driver of CCl(4) -liver damage.

56 on, abolished gluconeogenesis, and extensive liver damage.

57 re modestly elevated but without evidence of liver damage.

58 ential to protect the liver from cholestatic liver damage.

59 or the real-time, label-free study of septic liver damage.

60 ids in the liver that actively contribute to liver damage.

61 eliorate alcohol-induced steatohepatitis and liver damage.

62 sustain ongoing viral production and initial liver damage.

63 500 mg/kg of APAP challenge caused acute liver damage.

64 whereas an overdose of APAP can cause severe liver damage.

65 ative phosphorylation parameters and reduced liver damage.

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

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

68 atic differentiation of ductular cells after liver damage.

69 ced oxidative stress, lipid accumulation and liver damage.

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

71 own to promote liver regeneration upon acute liver damage.

72 e compounds in CB can attenuate EtOH-induced liver damages.

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

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

75 Upon liver damage, a potent protective response is mounted to

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

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

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

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

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

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

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

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

84 ectin-like receptor) perpetuates and worsens liver damage after toxic liver injury.

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

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

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

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

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

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

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

94 tion, even after the onset of NASH, improved liver damage and fibrosis.

95 NK-depleted mice displayed lower viremia and liver damage and higher hepatic T cell levels.

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

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

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

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

100 the triad TLR4/P-selectin/complement in the liver damage and its relevance for hemolytic diseases.

101 We employed two mouse liver damage and liver failure models induced by lipopol

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

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

104 gravates immune hyperactivation and promotes liver damage and possibly the development of liver failu

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

106 Liver damage and regeneration were quantified by determi

107 liver function and its loss promotes chronic liver damage and regeneration.

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

109 nts, only NAC reduced histologic features of liver damage and serum levels of aminotransferase, gamma

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

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

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

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

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

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

116 in the C5aR2(-/-) mice correlated with less liver damage and with improved survival of CD4(+) and CD

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

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

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

120 loride (CCl(4)) to induce mutations, chronic liver damage, and carcinogenesis.

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

122 ice caused substantial hepatocyte infection, liver damage, and coagulopathy as defined by virological

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

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

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

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

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

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

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

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

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

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

133 analyzed for HBV-specific immune responses, liver damage, and viral parameters.

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

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

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

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

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

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

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

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

142 Many brain pathologies are associated with liver damage, but a direct link has long remained elusiv

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

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

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

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

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

148 In NAFLD, Escherichia coli LPS may increase liver damage by inducing macrophage and platelet activat

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

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

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

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

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

154 providing a novel target in the treatment of liver damage caused by APAP.

155 on of CAY10594 also significantly attenuated liver damage caused by the APAP challenge, eliciting an

156 ssues and cholangiocytes were collected, and liver damage, changes in biliary mass/senescence, and in

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

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

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

160 ative phosphorylation parameters and reduced liver damage compared with vehicle.

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

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

163 ic viral infection leads to inflammation and liver damage, culminating in cirrhosis, the penultimate

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

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

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

167 HDV enhances liver damage during concomitant infection with HBV.

168 thereby detect liver steatosis as a sign of liver damage earlier as well as to verify amiodarone acc

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

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

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

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

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

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

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

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

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

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

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

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

181 l as increased carbon tetrachloride-mediated liver damage in a mouse model.

182 olism and increase the risk of TCDD-elicited liver damage in a sex-specific manner.

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

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

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

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

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

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

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

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

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

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

193 nistration of APAP increased the severity of liver damage in control mice.

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

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

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

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

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

199 Ranitidine decreases liver damage in Mdr2(-/-) (ATP binding cassette subfamil

200 knockdown of GPR55 was sufficient to improve liver damage in mice fed a high-fat diet and in mice fed

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

202 Liver-specific AMPK knockout aggravated liver damage in mouse NASH models.

203 Thus, the AMPK-caspase-6 axis regulates liver damage in NASH, implicating AMPK and caspase-6 as

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

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

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

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

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

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

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

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

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

213 lation significantly alleviated APAP-induced liver damage in vivo and correspondingly reduced serum a

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

215 Liver biopsies revealed nonspecific liver damage including fibrosis, steatosis, or mild incr

216 sential for regeneration after most types of liver damage, including cholestatic injury.

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

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

219 Liver damage induces periportal LGR5+ putative liver ste

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

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

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

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

224 Liver damage is in most cases idiosyncratic and unpredic

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

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

227 entional understanding has been that chronic liver damage leads to a cycle of cell death, regeneratio

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

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

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

231 Liver damage, mast cell (MC) activation, biliary H2HR, a

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

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

234 Liver damage, neurologic decline, and molecular analyses

235 Liver damage, neurological decline, and molecular analys

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

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

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

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

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

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

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

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

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

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

246 fected patients exhibit rapid progression of liver damage relative to HCV monoinfected patients.

247 molecular mechanisms underlying APAP-induced liver damage remain incompletely understood.

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

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

250 B gene was similarly effective at preventing liver damage, restoring copper homeostasis, and improvin

251 ential new therapeutic option for decreasing liver damage resulting from ischemia reperfusion injury.

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

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

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

255 al autophagy deficiency in adult mice causes liver damage, shortens life span to 3 mo due to neurodeg

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

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

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

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

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

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

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

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

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

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

266 biomarkers of the severity of steatosis and liver damage to aid the identification of high-risk stea

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

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

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

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

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

272 factor receptor (PAFR) in colitis-associated liver damage using dextran sulfate sodium (DSS) and anti

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

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

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

276 Liver damage was also more pronounced and longer lasting

277 Liver damage was assessed by hematoxylin and eosin and a

278 Liver damage was assessed by serum parameters, histopath

279 This liver damage was at least in part complement-dependent,

280 Liver damage was characterized by histologic analysis.

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

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

283 Liver damage was fully abrogated when macrophage activat

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

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

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

287 Liver damage was induced in female mice by placing them

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

289 VPA to increase the severity of APAP-induced liver damage was observed in FRGN mice with humanized li

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

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

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

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

294 mokine release, macrovesicular steatosis and liver damage were attenuated.

295 the protective effects of CO on APAP-induced liver damage were mediated by down-regulation of CHOP at

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

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

298 irus (HCV) infection may lead to progressive liver damage, which can be mitigated by successful treat

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.