ライフサイエンスコーパス: hepatic injury

1 stigated the contributions of these cells to hepatic injury.

2 isease severity, and appears to reflect true hepatic injury.

3 hionine choline-deficient diet (MCD)-induced hepatic injury.

4 perplasia and hepatomegaly in the absence of hepatic injury.

5 t to kdsr as a novel genetic risk factor for hepatic injury.

6 on of the liver by oval cells during massive hepatic injury.

7 tion site that coincided with development of hepatic injury.

8 after splenic injection under conditions of hepatic injury.

9 ATII cells in the lung sense and respond to hepatic injury.

10 n with decreased energy supply and increased hepatic injury.

11 synthesis-results that were consistent with hepatic injury.

12 es sustains the link between periodontal and hepatic injury.

13 itor H89 prevented the E2-BSA attenuation of hepatic injury.

14 ulation of ER-alpha and GPR30 and attenuated hepatic injury.

15 -8 (IL-8), which are likely to contribute to hepatic injury.

16 ther examine the role of IL-10 in regulating hepatic injury.

17 o investigate graft-host interactions during hepatic injury.

18 aken off the market because of the danger of hepatic injury.

19 tain a normal functional mass in response to hepatic injury.

20 ver disease independently of the etiology of hepatic injury.

21 is C (CHC) infection could result in greater hepatic injury.

22 al additions to the list of drugs that cause hepatic injury.

23 ed oval cell activation during the height of hepatic injury.

24 ts and primarily are associated with chronic hepatic injury.

25 stress in old animals, leading to increased hepatic injury.

26 that arises as a result of certain forms of hepatic injury.

27 irenz (EFV), has been associated with severe hepatic injury.

28 ntly enhanced survival and protected against hepatic injury.

29 rectly damage cells in early alcohol-induced hepatic injury.

30 o hemodynamically stable patients with blunt hepatic injury.

31 tive as B6 mice to Fas-induced lethality and hepatic injury.

32 uced histological and biochemical markers of hepatic injury.

33 on is inhibited and followed by some type of hepatic injury.

34 ediators play a role in pancreatitis-induced hepatic injury.

35 of superoxide, which may also play a role in hepatic injury.

36 in hepatocytes, which results in progressive hepatic injury.

37 ymptomatic, it has been associated with mild hepatic injury.

38 nhibitors are ineffective in preventing this hepatic injury.

39 ermined at 120 mins of reperfusion to assess hepatic injury.

40 al dysfunction, and cell death, resulting in hepatic injury.

41 nse play in the pathogenesis of this form of hepatic injury.

42 ix (ECM) accumulation in response to chronic hepatic injury.

43 taining function, they do not correlate with hepatic injury.

44 ch could lead to increased bile acid-induced hepatic injury.

45 on parenchymal liver cells protected against hepatic injury.

46 in turn impairs liver perfusion and promotes hepatic injury.

47 NKT, or B cells were essential executors of hepatic injury.

48 ker) in the livers of C57BL/6 mice following hepatic injury.

49 tis virus coinfection amplify and accelerate hepatic injury.

50 A have a beneficial effect on metabolism and hepatic injury.

51 er failure, and other clinically significant hepatic injury.

52 g HBV, decreasing in frequency prior to peak hepatic injury.

53 and salutary effects on cerebral as well as hepatic injury.

54 present results indicate that lung IR caused hepatic injury.

55 which effectively ameliorates Con A-induced hepatic injury.

56 atocyte survival following TNF-alpha-induced hepatic injury.

57 ttenuation of Con A-induced, T-cell-mediated hepatic injury.

58 critical factor underlying events leading to hepatic injury.

59 mitantly consume or abuse alcohol leading to hepatic injury.

60 lved as an adaptive mechanism in response to hepatic injury.

61 completely resistant to tyrosinemia-induced hepatic injury.

62 as well as in response to a wide variety of hepatic injuries.

63 unities in devising therapeutics in specific hepatic injuries.

64 The primary outcome was incidence of "hepatic injury" 20 hours following initiation of acetylc

65 7%) of 210 splenic injuries, 71 (34%) of 206 hepatic injuries, 30 (48%) of 63 renal injuries, four (1

66 y and that pharmacological MIP-2 doses after hepatic injury accelerate hepatic regeneration.

67 s after ischemia-reperfusion for analyses of hepatic injury, adenosine triphosphate levels, mitochond

68 Cot/tpl2 KO mice exhibited reduced hepatic injury after acetaminophen challenge, as evidenc

69 ith Ad-SOD1 increases survival and decreases hepatic injury after liver transplantation.

70 t to determine the frequency and severity of hepatic injury after nonmyeloablative conditioning and i

71 d plasma cytokine storm and reduced lung and hepatic injury after polytrauma.

72 near sequence of the mechanism of consequent hepatic injury after S/R remains to be characterized.

73 er the salutary effects of E2 in attenuating hepatic injury after trauma-hemorrhage are mediated via

74 nongenomic salutary effect of E2 in reducing hepatic injury after trauma-hemorrhage is mediated throu

75 acid may be a useful adjunct for preventing hepatic injury after trauma-hemorrhage via endothelial d

76 lular protein CCN1 (CYR61) is induced during hepatic injuries and functions to restrict and resolve l

77 provide the first link between LPS-mediated hepatic injury and a specific oxidative mtDNA deletion,

78 epatic colorectal metastases (CRM) may cause hepatic injury and affect postoperative outcome.

79 mechanisms to generate patterns of simulated hepatic injury and ALT release that scale (or not) to be

80 enhanced hypothermia, plasma cytokines, and hepatic injury and altered splenic lymphocyte apoptosis

81 ormation of TICs but selection pressure from hepatic injury and cell death, which activates TICs.

82 g/kg/day) added to PN on days 4-14 prevented hepatic injury and cholestasis; reversed the suppressed

83 Hepatic injury and chronic wounding are characterized by

84 vation, which contributes to the severity of hepatic injury and clinical outcome.

85 p21 expression is upregulated in response to hepatic injury and correlates with histologic markers of

86 es that leads to the protection of mice from hepatic injury and death caused by CpG DNA/D-GalN.

87 nd repopulate KO livers, eventually limiting hepatic injury and dysfunction despite increased fibrosi

88 Serum and biliary measures of hepatic injury and dysfunction were measured before and

89 glutamyl transferase, bilirubin (markers for hepatic injury and dysfunction), lipase (indicator of pa

90 c venous thrombi and biochemical evidence of hepatic injury and dysfunction.

91 PTEN loss leads to hepatic injury and establishes selective pressure for tu

92 , demonstrated serum bile salt accumulation, hepatic injury and expansion of the systemic bile salt p

93 atocyte growth factor (HGF), which restrains hepatic injury and facilitates reversibility of fibrotic

94 ta1 expression, which together could promote hepatic injury and fibrogenesis.

95 Notably, C7 effectively alleviates hepatic injury and fibrosis in liver disease models whil

96 on in the liver represents a key trigger for hepatic injury and fibrosis in various liver diseases an

97 Iron overload may cause or contribute to hepatic injury and fibrosis.

98 allowed us to clarify their contributions to hepatic injury and fibrosis.

99 Delineating the mechanisms that drive hepatic injury and hepatocellular carcinoma (HCC) progre

100 Chronic ethanol consumption may produce hepatic injury and impair the ability of the liver to re

101 of mitochondrial complex I activity, reduced hepatic injury and improved gut-liver axis in an aggress

102 hepatocytes (steatosis), is associated with hepatic injury and inflammation and leads to the develop

103 slocation of bacterial products that promote hepatic injury and inflammation.

104 ession of chronic liver disease by promoting hepatic injury and inflammation.

105 h is required to elucidate the mechanism for hepatic injury and its relationship with TIC activation.

106 ensitive biomarkers could reveal subclinical hepatic injury and metabolic dysfunction after surgical

107 cal stress induces age-dependent subclinical hepatic injury and metabolic dysregulation detectable by

108 hepatologists should play more attention to hepatic injury and monitor risk of hepatic failure cause

109 ral construct resulted in significantly more hepatic injury and necrosis after acetaminophen exposure

110 imary effect of AKT2 loss was attenuation of hepatic injury and not inhibition of progenitor-cell pro

111 oes dynamic changes during TNF-alpha-induced hepatic injury and plays a critical role in NF-kappaB ac

112 recent years, may represent risk factors for hepatic injury and portal hypertension.

113 expression data from human liver undergoing hepatic injury and regeneration revealed a 233-gene sign

114 or (TNF) alpha release, leading to localized hepatic injury and remote organ dysfunction.

115 examine the role of beta-catenin in chronic hepatic injury and repair, we exposed WT and KO mice to

116 uantify transcription factor activity during hepatic injury and repair.

117 this cell type's repertoire in orchestrating hepatic injury and repair.

118 Supporting this idea, hepatic injury and steatosis have been noted in patients

119 rs and morbidly obese patients, with minimal hepatic injury and steatosis, displayed higher hepatic e

120 We developed a novel animal model in which hepatic injury and stem cell transplantation lead to the

121 ate that rhIL-11 ameliorates T-cell-mediated hepatic injury and suggests its therapeutic potential to

122 s agonist doses, IL-6+/+ mice developed mild hepatic injury and survived, whereas IL-6-/- mice develo

123 The pathogenesis of hepatic injury and the precise mechanisms underlying vir

124 uire the ability to respond appropriately to hepatic injury and to remove bacteria from the blood str

125 ms by which ducts proliferate in response to hepatic injury and to the hypercholeresis that occurs af

126 haracterize the role of the immune system in hepatic injury and tumor development, we comparatively s

127 be placed in three categories: those without hepatic injury and with no residual acetaminophen to be

128 or thrombocytopenia, 36% (range, 29-44%) for hepatic injury, and 66% (range, 29-84%) for shock.

129 n in the liver, hepatocellular inflammation, hepatic injury, and fibrosis.

130 -dose CR2-Crry resulted in steatosis, severe hepatic injury, and high mortality, whereas low-dose CR2

131 consumption is a well-known risk factor for hepatic injury, and mitochondrial damage plays a signifi

132 iable predictor of the presence or extent of hepatic injury, and persistently increased ALT values fo

133 egree of alpha1-AT expression and associated hepatic injury, and that hepatocytes devoid of alpha1-AT

134 es of mechanisms in viral-host interactions, hepatic injury, and therapeutic developments for hepatit

135 Hepatic fibrosis results from chronic hepatic injury, and we have previously reported that end

136 ete reversal of hepatic steatosis, increased hepatic injury, and worsened fibrosis.

137 h a decrease in ischemia-reperfusion-induced hepatic injury, apoptosis, and necrosis.

138 Using selected aspects of acute hepatic injury as endpoints, we also demonstrate that DR

139 following pulmonary infection and increased hepatic injury as measured by plasma aspartate aminotran

140 storage and before transplantation prevents hepatic injury, as documented by a significant increase

141 Moreover, in a murine model of hepatic injury, ASF transplantation was associated with

142 become activated during the early stages of hepatic injury associated with fibrogenesis.

143 oblast-like cells during the early stages of hepatic injury associated with fibrogenesis.

144 oblast-like cells during the early stages of hepatic injury associated with fibrogenesis.

145 t mediator of the local neutrophil-dependent hepatic injury associated with hepatic ischemia/reperfus

146 Increased iron is suspected to enhance hepatic injury associated with nonalcoholic fatty liver

147 nt study demonstrates that UDCA-LPE improves hepatic injury at different stages of NAFLD.

148 with acute gastroenteritis; - 1 patient with hepatic injury because of a suspected metabolic disease;

149 The Pten-null mice had increasing levels of hepatic injury before proliferation of hepatic progenito

150 During severe or chronic hepatic injury, biliary epithelial cells (BECs) undergo

151 utes of hepatic IR not only developed severe hepatic injury but also developed significant AKI and sm

152 kers not only mirror different mechanisms of hepatic injury, but also are independent predictors of l

153 ponse, as observed in other models of severe hepatic injury, but the localization of this response se

154 Attenuation of hepatic injury by deletion of Akt2 reduced progenitor ce

155 n by Paneth cells to initiate intestinal and hepatic injury by hepatic and systemic delivery of IL-17

156 ant contribution to attenuating inflammatory hepatic injury by inducing fibrosis.

157 etformin and identify a new role of PAI-1 in hepatic injury caused by ethanol.

158 ting neutrophils; they also developed severe hepatic injury, characterized by a 6- to 25-fold increas

159 the adult liver show an aberrant response to hepatic injury, characterized by HNF-4alpha silencing, i

160 with plerixafor and G-CSF demonstrated less hepatic injury compared with control animals.

161 developed increased myocarditis but reduced hepatic injury compared with infected B6.129c1 mice.

162 ated gene expression, resulting in decreased hepatic injury despite an increase in hepatic steatosis.

163 y decreased from 50% to 19% in children with hepatic injuries, despite increasing grade of injury, an

164 ociated with a 5-10-fold higher incidence of hepatic injury, differed significantly from other NSAIDs

165 nted a long-term review of a large series of hepatic injuries, documenting the effect of treatment ch

166 Hepatic injury due to cold storage followed by reperfusi

167 During hepatic injury due to either carbon tetrachloride injury

168 bute, at least in part, in the initiation of hepatic injury during alcohol intoxication.

169 thway in the development of TNFalpha-induced hepatic injury during endotoxemia.

170 activate Kupffer cells, thereby exacerbating hepatic injury during sepsis.

171 d patients alike to the potential for severe hepatic injury (eg, troglitazone, tolcapone).

172 Combination of lineage analysis and hepatic injury experiments showed involvement of Sox9-po

173 e cells mediate various functions, including hepatic injury, fibrogenesis, and carcinogenesis.

174 death, LCR livers had significantly greater hepatic injury (fibrosis and apoptosis).

175 Primary outcome measures include change in hepatic injury (fibrosis and inflammation) and liver fat

176 at risk for HCC probably as a result of the hepatic injury, fibrosis, and eventual cirrhosis resulti

177 approach to evaluate tumor growth following hepatic injury, focusing on ECM remodeling and interacti

178 c-Jun phosphorylation, AP-1 activation, and hepatic injury following I/R in JunD-/- mice but, parado

179 Hepatic injury following ischemia or I/R was investigate

180 e restoration of hepatoprotection by IP, and hepatic injury following ischemia was attenuated by trea

181 nistration on pro-inflammatory responses and hepatic injury following T-H.

182 A database of hepatic injuries from 1975 to 1999 was studied for chang

183 /Delta) mice and Mttp(flox/flox) controls to hepatic injury from Escherichia coli lipopolysaccharides

184 CT-based criteria, including hepatic injury grade, signs of arterial vascular injury,

185 Hepatic injury has been reported following duloxetine us

186 Following hepatic injury, hepatic stellate cells (HSCs) transdiffe

187 ged aPTT and INR, decreased platelet count), hepatic injury (high bilirubin), circulatory shock (low

188 ferate using a 2-acetylaminofluorene (2-AAF)/hepatic injury (i.e., CCl4, partial hepatectomy [PHx]) p

189 Severe or fatal hepatic injury in 46 patients was associated with higher

190 orms of tissue injury--they suffer increased hepatic injury in a model of binge alcohol abuse and in

191 Furthermore, reduced hepatic injury in AdLacZ-infected gammadeltaT-cell-defic

192 nti-BTLA mAb aggravates alpha-GalCer-induced hepatic injury in CD160(-/-) mice, suggesting that both

193 to LPS- and TNF-alpha-mediated lethality and hepatic injury in D-galactosamine-sensitized NOD mice is

194 Nevertheless, the exacerbated hepatic injury in DC-depleted mice challenged with APAP

195 ogical AR inhibition against alcohol-induced hepatic injury in experimental ALD.

196 The pathogenesis of hepatic injury in GH is poorly understood.

197 Administration of CCl4 also induced stronger hepatic injury in Jnk(Deltahepa) mice, based on increase

198 This study examined the mechanisms of acute hepatic injury in lambs treated with systemic administra

199 We investigated Geniposide-induced hepatic injury in male Sprague-Dawley rats after 3-day i

200 recently been implicated as a major cause of hepatic injury in metabolic dysfunction-associated fatty

201 as exogenous gp96 aggravated the symptoms of hepatic injury in mice but not in Kupffer cells-ablated

202 ave been implicated as cellular mediators of hepatic injury in models of inflammation in vivo.

203 In contrast, HO-1 depression restored hepatic injury in otherwise I/R resistant Stat4 KOs.

204 tudy was to determine the effect of IL-10 on hepatic injury in patients with chronic hepatitis C.

205 osamine (DEN) and phenobarbital (PB) induced hepatic injury in rats.

206 nking these two processes mechanistically to hepatic injury in the kdsr(I105R) mutants.

207 mutant hepatocytes, which can be a cause of hepatic injury in the mutant.

208 -risk steatotic liver donors and to evaluate hepatic injury in the postoperative period are discussed

209 Mild hepatic injury in this group may be amenable to lifestyl

210 body 1F12, an anti-CD18 antibody, attenuated hepatic injury in vivo, and in PMN-hepatocyte coculture

211 , decreased oxidative stress, and attenuated hepatic injury in vivo.

212 um of monocytes that enter a site of sterile hepatic injury in vivo.

213 les ameliorates or worsens the Con A-induced hepatic injury in vivo.

214 ist treatment was associated with attenuated hepatic injury in wild-type, but not in Adora2b(-/-) mic

215 gnificant protection against IV GCDC-induced hepatic injury, in vitro GCDC-induced permeability trans

216 ll death that has been implicated in causing hepatic injury including steatohepatitis/ nonalcoholic s

217 no overt, histologically demonstrable, acute hepatic injury, including inflammation, necrosis, oval c

218 tor alpha (TNFalpha) underlies many forms of hepatic injury, including that from toxins.

219 domethacin to PiZ mice resulted in increased hepatic injury, indicated by increased hepatocellular pr

220 t mediators involved in neutrophil-dependent hepatic injury induced by ischemia and reperfusion in mi

221 Hepatic injury induced by ischemia and reperfusion is an

222 Excess intrauterine lipids may contribute to hepatic injury, inflammation, impaired mitochondrial fun

223 Hepatic injury, intestinal barrier, gut microbiome, and

224 ccurs as a wound-healing response to chronic hepatic injuries irrespective of the underlying etiology

225 Chronic hepatic injury is accompanied by a ductular response tha

226 Hepatic injury is associated with a defective intestinal

227 s of liver repair and regeneration following hepatic injury is complex and relies on a temporally coo

228 Although migration of stellate cells during hepatic injury is essential for wound-healing and fibros

229 Conclusion: Grade 3 or 4 hepatic injury is infrequent in CCS.

230 Hepatic injury is prevalent in CCHF and contributes to t

231 mechanistic insights into the regulation of hepatic injury, liver immunopathology, and transplant to

232 nt Sdc-1 concentrations were correlated with hepatic injury markers from the effluent.

233 These results suggest that hepatic injury may occur in HCV/HIV coinfection through

234 ion, these findings suggest that progressive hepatic injury may result in cognitive problems even bef

235 e also displayed increased injury in a toxic hepatic injury model caused by CCl(4).

236 In 4 murine hepatic injury models, an absence or blockade of functio

237 AFP gene expression compared with the 2-AAF/hepatic injury models.

238 Hepatic injury, myeloperoxidase activity, nuclear factor

239 Moreover, after this hepatic injury, native liver cells were more susceptible

240 ow that in a fully repairing sterile thermal hepatic injury, neutrophils also penetrate the injury si

241 PHx, when DAPM was given 24 hours before the hepatic injury, no oval cell proliferation was seen (his

242 resulting in protoporphyria that models the hepatic injury occurring sporadically in human erythropo

243 in the liver, WD-CO did not appear to affect hepatic injury or damage when compared to WD-B.

244 es of transgenic mice in vivo does not cause hepatic injury or fibrosis per se but renders the livers

245 No patients developed hepatic injury or hepatotoxicity in either group (odds r

246 were stably transduced with no indication of hepatic injury or histopathology.

247 Following hepatic injury or stress, gluconeogenic and acute-phase

248 gnificant, may suggest a higher incidence of hepatic injury other than hepatic-related death or liver

249 Lower systolic arterial pressure (P=0.043), hepatic injury (P=0.049), and suspected/definite infecti

250 ogression of hepatomegaly to steatosis, then hepatic injury phenotype.

251 ury and fibrosis, resulting in a more severe hepatic injury phenotype.

252 nts in intestinal structure and function and hepatic injury, possibly by preserving microvascular per

253 production of pro-inflammatory mediators and hepatic injury produced by flutamide administration foll

254 ctivation of NF-kappaB, a critical signal in hepatic injury, regeneration, and tumor transformation.

255 n and role of LPC in liver physiology and in hepatic injury remains a contentious topic.

256 hanical circulatory support, cardiac arrest, hepatic injury, renal injury, or rising lactate level (>

257 expression by the cells plays a role in the hepatic injury response and in fibrogenesis.

258 us blunted lipid peroxidation and attenuated hepatic injury resulting from ethanol, but had no effect

259 However, the profiles and consequences of hepatic injury resulting from PAH and CTEPH have not bee

260 eration, reduced angiogenesis, and increased hepatic injury, resulting in pronounced vascular endothe

261 n parallel, Rantes, IRF7, NOD1/2, TREM1, and hepatic injury signaling pathways were upregulated.

262 Ethanol-induced hepatic injury, steatosis, and inflammation were exacerb

263 ways, particularly that of Fas-FasL, causing hepatic injury that can eventually proceed to cirrhosis

264 ctivation and the downstream redox-dependent hepatic injury that results from I/R, and may do so by r

265 However, old rats showed widespread hepatic injury that was manifested over a 24 h period af

266 Mice received repeated hepatic injuries throughout 12 weeks by intraperitoneal

267 to block hepatocyte proliferation, and then hepatic injury, to induce oval cell proliferation.

268 ological levels of PUFAs, and mice developed hepatic injury upon consuming a diet enriched in PUFA.

269 MAGL modulates hepatic injury via endocannabinoid and eicosanoid signal

270 ministered IV, and the presence of renal and hepatic injuries was evaluated at day 11 post burn by hi

271 In an in vivo warm ischemia model, hepatic injury was assessed by serum transaminase levels

272 Hepatic injury was associated with neutrophil sequestrat

273 Another factor that could contribute to hepatic injury was MIP2, which was cytotoxic to alcoholi

274 The increase in cytokines/chemokines of hepatic injury was much higher in ConA-treated control m

275 the overall outcome of acetaminophen-induced hepatic injury was not affected.

276 aminotransferase levels rose transiently and hepatic injury was observed histologically, along with d

277 se model developed to reproduce this type of hepatic injury, we found that hepatocyte transplantation

278 To delineate mechanisms of drug-induced hepatic injury, we used transplanted cells as reporters

279 Hepatic injuries were graded with CT-based classificatio

280 Aortic and hepatic injuries were more common in patients with CC fr

281 Hepatic injuries were more common in patients with chest

282 companied by apoptotic rather than senescent hepatic injury, which gave rise to the hepatic inflammat

283 egrin have opposing effects in Con A-induced hepatic injury, which is associated with blocking the re

284 Overdose patients with no or minimal hepatic injury who had normal liver function tests (LTs)

285 des microvesicular steatosis and more severe hepatic injury with confluent necrosis.

286 IRs of other clinically significant hepatic injury without documented alternate etiologies w

287 ntribute to tissue regeneration after severe hepatic injury, yet signals instructing progenitor cell