ライフサイエンスコーパス: hepatic necrosis

1 in bacterial dissemination to the liver and hepatic necrosis.

2 logical phenotype characterized by increased hepatic necrosis.

3 They also show less evidence of hepatic necrosis.

4 icity phenomena emerge and converge to cause hepatic necrosis.

5 tion in the latter 2 patients showed massive hepatic necrosis.

6 ase expression, peroxynitrite formation, and hepatic necrosis.

7 ed with a lethal dose of LMB-2 showed severe hepatic necrosis.

8 ses a 3-fold decrease in animal toxicity and hepatic necrosis.

9 grafts showed either cirrhosis or confluent hepatic necrosis.

10 r levels of plasma AST, ALT, bile salts, and hepatic necrosis after 3 days of BDL than WT mice.

11 drial permeability transition (MPT) mediates hepatic necrosis after ischemia and reperfusion (I/R).

12 JNK inhibition decreases hepatic necrosis and apoptosis after OLT, suggesting tha

13 he AHR signaling pathway gives rise to fetal hepatic necrosis and consequent liver deformation which

14 had early graft dysfunction, with extensive hepatic necrosis and histological signs of antibody-indu

15 e was found to prevent acetaminophen-induced hepatic necrosis and increases in serum transaminase lev

16 red in ductular reaction, leading to massive hepatic necrosis and mortality after bile duct ligation

17 e JAG1 rescued ductular reaction and reduced hepatic necrosis and mortality.

18 y higher than in WT to WT LTx, with enhanced hepatic necrosis and neutrophil infiltration, indicating

19 ndidates because core biopsy revealed subtle hepatic necrosis and nonspecific hepatitis.

20 ssociated with clinical situations including hepatic necrosis and septic shock.

21 al cell accumulation was accompanied by less hepatic necrosis and steatosis, lower serum aminotransfe

22 Many of these agents produce fulminant hepatic necrosis and, in some cases, were withdrawn from

23 ith striking tissue inflammation, widespread hepatic necrosis, and 100% mortality by week 10, and (ii

24 including changes in vascular permeability, hepatic necrosis, and cellular apoptosis.

25 loss, a phenotype consisting of cholestasis, hepatic necrosis, and fibrosis is observed that is more

26 edly reduced serum ALT levels, centrilobular hepatic necrosis, and improved mouse survival.

27 ficant elevation of serum ALT, centrilobular hepatic necrosis, and increased hepatic inflammatory cel

28 e and aspartate aminotransferases, decreased hepatic necrosis, and increased survival relative to Wt

29 anine aminotransferase (ALT) levels, reduced hepatic necrosis, and lower neutrophil infiltration.

30 Serum transaminases, degree of hepatic necrosis, and neutrophil infiltration were all s

31 nine aminotransferase levels at 24 hours and hepatic necrosis at 48 hours.

32 tipyretic agent known to cause centrilobular hepatic necrosis at toxic doses.

33 yeloid-specific STAT3 knockout mice restored hepatic necrosis but decreased liver inflammation.

34 e protected from toxicity with a decrease in hepatic necrosis following acetaminophen challenge.

35 Fulminant hepatic necrosis ("halothane hepatitis") is an unusual a

36 s ranging from febrile illness to retinitis, hepatic necrosis, hemorrhagic fever, and death.

37 s of leukocyte recruitment to sites of focal hepatic necrosis in vivo.

38 enge, the sham IgG treated mice showed 14.6% hepatic necrosis; in contrast, blockade of HMGB1 signifi

39 level, improved survival of mice, decreased hepatic necrosis, inhibition of messenger RNA (mRNA) exp

40 A large animal model of fulminant hepatic necrosis is necessary to test the efficacy of ar

41 rs proinflammatory innate immune cascade and hepatic necrosis, leading to increased incidence of earl

42 Biopsy demonstrated severe hepatic necrosis, likely from prolonged venous congestio

43 onding to regions of decreased perfusion and hepatic necrosis observed in fetal livers.

44 athogenesis: distinctive patterns of massive hepatic necrosis (present in 42% of sections), presence

45 During the recovery phase from submassive hepatic necrosis, subtraction of the rate of cell death

46 liver and exhibited significantly more focal hepatic necrosis than WT B6 mice.

47 Acute hepatic necrosis was diagnosed in a dog.

48 Severe hepatic necrosis was observed in all animals, but residu

49 Pancreatic and hepatic necrosis were observed on histopathological exam

50 whereas inflammatory cytokine expression and hepatic necrosis were similar to ANIT-challenged wild-ty

51 atty degeneration, fibrosis, infiltrate, and hepatic necrosis were the most frequent terms used as de

52 1(-/-) mice were vulnerable to mortality and hepatic necrosis when challenged with endotoxin.

53 This is the first report of acute hepatic necrosis with liver failure caused by Salmonella

54 histopathology findings included multifocal hepatic necrosis with mild inflammation and hepatocyte p