ライフサイエンスコーパス: hepatocellular injury

1 hepatic neutrophil accumulation, edema, and hepatocellular injury.

2 ne of three treated animals without apparent hepatocellular injury.

3 at mediates activation of coagulation during hepatocellular injury.

4 ependent inflammatory phenotype and leads to hepatocellular injury.

5 the progression of hepatic inflammation and hepatocellular injury.

6 f HO-1 overexpression on HCV replication and hepatocellular injury.

7 en-induced liver toxicity, causing fulminant hepatocellular injury.

8 itical for IR-induced liver inflammation and hepatocellular injury.

9 to its previously documented central role in hepatocellular injury.

10 flammatory response and significantly reduce hepatocellular injury.

11 lpha), liver accumulation of neutrophils, or hepatocellular injury.

12 patic intra cellular oxygenation and reduced hepatocellular injury.

13 and reduced tissue oxygenation and increased hepatocellular injury.

14 n accumulation of leukocytes and significant hepatocellular injury.

15 ages of fibrosis caused by either biliary or hepatocellular injury.

16 liver regeneration in the setting of ongoing hepatocellular injury.

17 as been no evidence of rosiglitazone-induced hepatocellular injury.

18 ounted for by biomarkers of inflammation and hepatocellular injury.

19 Rosiglitazone may be associated with hepatocellular injury.

20 ttern for HCV genomic RNA and any indices of hepatocellular injury.

21 Liver function tests revealed severe hepatocellular injury.

22 r tissue may be a significant determinant of hepatocellular injury.

23 route toward suppressing fibrosis caused by hepatocellular injuries.

24 Absence of Smad3 significantly blunted hepatocellular injury 9 hours post ConA injection, which

25 between HCV replication in liver tissue and hepatocellular injury, a strand-specific in situ hybridi

26 ceptor antagonists convey protection against hepatocellular injury accompanied by a decrease in nitri

27 t HMGB1-HC-KO mice had significantly greater hepatocellular injury after I/R, compared to control mic

28 erfusion there was a significant increase in hepatocellular injury and a delay in recovery compared t

29 crosis factor (TNF)-alpha causes much of the hepatocellular injury and cell death that follows toxin-

30 In conclusion, JNK2 contributes to hepatocellular injury and death after I/R in association

31 found that IL-6-/- mice developed increased hepatocellular injury and defective regeneration with si

32 ced activation of the coagulation system and hepatocellular injury and diminished hepatic fibrin depo

33 atocellular proliferation and an increase of hepatocellular injury and endoplasmic reticulum stress.

34 eatosis, to steatohepatitis with evidence of hepatocellular injury and fibrosis, to cirrhosis.

35 indromatosis (CYLD), confers protection from hepatocellular injury and fibrosis.

36 Immediately after reperfusion, hepatocellular injury and function were improved in HMP

37 statin pretreatment significantly attenuated hepatocellular injury and increased survival of male mic

38 of hepatic steatosis but leads to increased hepatocellular injury and inflammation that may be due i

39 onic ethanol consumption can cause sustained hepatocellular injury and inhibit the subsequent regener

40 ated by oxidants and cytokines and regulates hepatocellular injury and insulin resistance, suggesting

41 iver neutrophil recruitment by up to 72% and hepatocellular injury and liver edema were each reduced

42 IL-33 significantly reduced hepatocellular injury and liver neutrophil accumulation

43 of a transgenic line of sickle cell mice for hepatocellular injury and localization of two isoforms o

44 The basis of hepatocellular injury and progressive fibrosis in a subs

45 Cholestasis contributes to hepatocellular injury and promotes liver carcinogenesis.

46 polysaccharide and peptidoglycan resulted in hepatocellular injury and renal dysfunction.

47 livers harvested to determine the degree of hepatocellular injury and the induction of TNF-, IL-1bet

48 Altered hepatic lipid homeostasis, hepatocellular injury, and inflammation are features of

49 t increases in liver neutrophil recruitment, hepatocellular injury, and liver edema, as defined by li

50 , leading to hepatic neutrophil recruitment, hepatocellular injury, and liver edema.

51 hrs in hypotension, acute renal dysfunction, hepatocellular injury, and lung injury.

52 mice would increase cholestasis, steatosis, hepatocellular injury, and mortality and impair hepatocy

53 ing in these models and results in increased hepatocellular injury, apoptosis, and death.

54 howed improved survival, there was extensive hepatocellular injury as indicated by large LDH release

55 ted liver glycogen and significantly reduced hepatocellular injury as measured by LDH release and AST

56 ion, Ad-based IL-13 significantly diminished hepatocellular injury, assessed by serum glutamic oxaloa

57 postnatal week and increased DNA damage and hepatocellular injury at 1-2 weeks of age.

58 urs, followed by predominantly centrolobular hepatocellular injury at 24 hours.

59 ely on the histologic findings of steatosis, hepatocellular injury (ballooning, Mallory bodies), and

60 lly susceptible K8tg mice, HF diet triggered hepatocellular injury, ballooning, apoptosis, inflammati

61 owed no significant changes in steatosis and hepatocellular injury, but a approximately 50% reduction

62 IL-10 KO and IL-10/IL-4 KO mice experienced hepatocellular injury, but only IL-10 KO mice advanced t

63 liferation have the disadvantage of inducing hepatocellular injury by delivery of toxins or by surgic

64 e at reperfusion, stimulated by PAF, mediate hepatocellular injury by triggering leukocyte accumulati

65 CD8+ T cells can cause hepatocellular injury by two distinct mechanisms.

66 irst time the construction of a hypothetical hepatocellular injury cascade for this disease involving

67 ated the renal dysfunction, lung injury, and hepatocellular injury caused by lipoteichoic acid/peptid

68 start of nefazodone therapy suggested severe hepatocellular injury caused by the drug.

69 CD8 and L-selectin, but not CD4, ameliorated hepatocellular injury, confirming that CD8(+) cells are

70 ukin-6 null (IL-6-/-) mice develop increased hepatocellular injury, defective regeneration, delayed w

71 Histological analysis correlated with the hepatocellular injury determined with transaminases and

72 s intrinsic cLT production may contribute to hepatocellular injury during inflammation.

73 following ischemia/reperfusion is a cause of hepatocellular injury during transplantation.

74 but attenuated the renal dysfunction and the hepatocellular injury/dysfunction caused by LTA/PepG.

75 Hepatocellular injury, female sex, high levels of TBL, a

76 tial proportion of HCC arises as a result of hepatocellular injury from NASH.

77 ory biomarker IL-6 and for the biomarkers of hepatocellular injury glutamate dehydrogenase, alanine a

78 histology from 128 patients presenting with hepatocellular injury had more severe inflammation, necr

79 The central role of T cell activation in hepatocellular injury has been well documented.

80 ell-characterized DILI [n = 35, including 19 hepatocellular injury (HC) and 16 cholestatic/mixed inju

81 is characterized by cholestasis, steatosis, hepatocellular injury, impaired regeneration, a decrease

82 ypothesized that Btk inhibition would reduce hepatocellular injury in a murine model of liver warm he

83 Neutrophils contribute to hepatocellular injury in a number of acute inflammatory

84 BTKB66 treatment ameliorated hepatocellular injury in a well-established model of liv

85 Because nefazodone seems to cause severe hepatocellular injury in an idiosyncratic manner, routin

86 l therapy and therapeutic protection against hepatocellular injury in HCV infection.

87 CLP induced cholestasis, steatosis, and hepatocellular injury in interleukin-6 -/-, but not inte

88 f c-Jun kinase, a process that may cause the hepatocellular injury in nonalcoholic steatohepatitis.

89 pha); to correlate inversely with markers of hepatocellular injury in patients with liver ischemia; a

90 acterial lipopolysaccharide (LPS) results in hepatocellular injury in rats, the onset of which occurs

91 drial dysfunction may be important causes of hepatocellular injury in the steatotic liver.

92 TNFalpha, liver neutrophil accumulation, and hepatocellular injury in wild-type mice.

93 mmation-mediated STAT3 activation attenuates hepatocellular injury induced by CCl(4) in myeloid-speci

94 observed conditions included renal failure, hepatocellular injury, infections, and hematologic malig

95 In contrast, biomarkers of hepatocellular injury, inflammatory gene induction, and

96 Hepatocellular injury is caused by toxicity of the mutan

97 Drug-induced hepatocellular injury is identified internationally by a

98 One such protective pathway to reduce hepatocellular injury is the up-regulation of heme oxyge

99 erase, alanine aminotransferase (markers for hepatocellular injury), lipase (indicator of pancreatic

100 patocytes, suggesting that in these settings hepatocellular injury may be altered by the decrease in

101 of infection in humans, including prolonged hepatocellular injury, necrosis, hyperplasia, and an ele

102 om mild necrosis and inflammation to extreme hepatocellular injury, nodular regeneration, and bile du

103 tic hepatitis and 12 patients presented with hepatocellular injury, of which six had an autoimmune ph

104 Histologic features including hepatocellular injury (P = .005), Mallory-Denk bodies (P

105 ted in hypotension, acute renal dysfunction, hepatocellular injury, pancreatic injury, and increased

106 The remaining HDS cases presented as hepatocellular injury, predominantly in middle-aged wome

107 on of deleted vectors in mice resulted in no hepatocellular injury relative to that seen with first-g

108 isms by which lysosomal iron participates in hepatocellular injury remain uncertain.

109 accumulation at 6 hours correlated with the hepatocellular injury seen at 24 hours.

110 ttenuate further the small level of residual hepatocellular injury seen in leukopenic rats.

111 ent of renal dysfunction (serum creatinine), hepatocellular injury (serum alanine aminotransferase an

112 ligation, FAAH(-/-) mice displayed increased hepatocellular injury, suggesting that FAAH protects hep

113 kout-transgenic SCD mice indicated extensive hepatocellular injury that was accompanied by increased

114 In retrorsine-induced hepatocellular injury the capacity of fully differentiat

115 Endotoxin (LPS) can cause hepatocellular injury under several circumstances, and l

116 Hepatocellular injury was assessed by alanine aminotrans

117 n antibody-treated mice were fed an HFD, and hepatocellular injury was assessed by histology, propidi

118 tic neutrophil recruitment, liver edema, and hepatocellular injury were all significantly reduced by

119 s of T cell immunity, virus replication, and hepatocellular injury were studied in two HAV-infected c

120 Steatotic liver responds with increased hepatocellular injury when exposed to an ischemic-reperf

121 NO stimulation reduced hepatocellular injury, whereas inhibition of nitric oxid