ライフサイエンスコーパス: hepatic injury

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

2 n with decreased energy supply and increased hepatic injury.

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

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

5 -8 (IL-8), which are likely to contribute to hepatic injury.

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

7 o investigate graft-host interactions during hepatic injury.

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

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

10 ver disease independently of the etiology of hepatic injury.

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

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

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

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

15 ts and primarily are associated with chronic hepatic injury.

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

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

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

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

20 ntly enhanced survival and protected against hepatic injury.

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

22 o hemodynamically stable patients with blunt hepatic injury.

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

24 uced histological and biochemical markers of hepatic injury.

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

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

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

28 in hepatocytes, which results in progressive hepatic injury.

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

30 nhibitors are ineffective in preventing this hepatic injury.

31 tis virus coinfection amplify and accelerate hepatic injury.

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

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

34 er failure, and other clinically significant hepatic injury.

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

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

37 present results indicate that lung IR caused hepatic injury.

38 which effectively ameliorates Con A-induced hepatic injury.

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

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

41 critical factor underlying events leading to hepatic injury.

42 mitantly consume or abuse alcohol leading to hepatic injury.

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

44 completely resistant to tyrosinemia-induced hepatic injury.

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

46 perplasia and hepatomegaly in the absence of hepatic injury.

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

48 tion site that coincided with development of hepatic injury.

49 after splenic injection under conditions of hepatic injury.

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

51 unities in devising therapeutics in specific hepatic injuries.

52 7%) of 210 splenic injuries, 71 (34%) of 206 hepatic injuries, 30 (48%) of 63 renal injuries, four (1

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

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

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

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

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

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

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

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

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

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

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

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

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

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

67 Hepatic injury and chronic wounding are characterized by

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

93 uantify transcription factor activity during hepatic injury and repair.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

139 Hepatic injury due to cold storage followed by reperfusi

140 During hepatic injury due to either carbon tetrachloride injury

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

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

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

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

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

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

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

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

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

150 Hepatic injury following ischemia or I/R was investigate

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

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

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

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

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

156 Hepatic injury has been reported following duloxetine us

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

182 Hepatic injury induced by ischemia and reperfusion is an

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

184 Chronic hepatic injury is accompanied by a ductular response tha

185 Hepatic injury is associated with a defective intestinal

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

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

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

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

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

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

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

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

194 Hepatic injury, myeloperoxidase activity, nuclear factor

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

214 Mice received repeated hepatic injuries throughout 12 weeks by intraperitoneal

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

216 MAGL modulates hepatic injury via endocannabinoid and eicosanoid signal

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

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

219 Hepatic injury was associated with neutrophil sequestrat

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

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

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

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

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

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

226 Hepatic injuries were graded with CT-based classificatio

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

228 Hepatic injuries were more common in patients with chest

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

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

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

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

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