ライフサイエンスコーパス: liver necrosis

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1 e response sufficient to cause fatal massive liver necrosis.

2 resulted in a significant reduction of acute liver necrosis.

3 Crisis was due to extensive liver necrosis accompanied by pleural edema.

4 le duct proliferation, and nearly eliminated liver necrosis after BDL.

5 idental-overdose group more often had severe liver necrosis (aminotransferase levels, >3500 IU per li

6 NRBF2-deficient mice develop focal liver necrosis and ductular reaction, accompanied by imp

7 ays exacerbated liver injury as reflected by liver necrosis and enhanced apoptosis (p < 0.001).

8 e Con-A administration reduced centrilobular liver necrosis and enhanced survival.

9 impaired liver regeneration characterized by liver necrosis and failure.

10 hepatocytes displayed significantly reduced liver necrosis and inflammation than wild-type mice.

11 h oil/ethanol and corn oil/ethanol) that had liver necrosis and inflammation.

12 after partial hepatectomy, characterized by liver necrosis and reduced and delayed hepatocyte DNA sy

13 livers, partial hepatectomy leads to severe liver necrosis and reduced hepatocyte proliferation.

14 bacterial load was associated with increased liver necrosis and serum alanine aminotransferase levels

15 aEC, developed impaired hepatic vasculature, liver necrosis, and degenerative lesions in cardiac myoc

16 ased levels of blood transaminases, enhanced liver necrosis, and more pronounced neutrophil infiltrat

17 Pathological changes (fatty liver, necrosis, and inflammation) were observed only in

18 d FE showed the most severe pathology (fatty liver, necrosis, and inflammation), those fed CE showed

19 etween 15 and 18 days, with evidence of mild liver necrosis/apoptosis.

20 Thrombosis of the artery and subsequent liver necrosis are indications for retransplantation.

21 al was accompanied by a dramatic increase in liver necrosis (as measured on a scale from 0 to 3) in t

22 ve also been implicated in the centrilobular liver necrosis associated with APAP.

23 e administration caused an intense degree of liver necrosis associated with increases in lipid peroxi

24 collaborate to guide neutrophils to sites of liver necrosis by CXC chemokine receptor 2 (CXCR2) and f

25 -dependent DNA damage is a critical event in liver necrosis caused by alkylating hepatotoxins.

26 hese effects are also accompanied by reduced liver necrosis, correlating with elevated serum interleu

27 Regions of liver necrosis demonstrated low attenuation on CT scans

28 vivo, extensive intestinal inflammation and liver necrosis developed.

29 ve impaired liver regeneration and increased liver necrosis following partial hepatectomy that is cor

30 /alanine aminotransferase levels and reduced liver necrosis formation.

31 owever, the primary Ca2+ target resulting in liver necrosis has not been determined.

32 ononuclear cellular infiltration, multifocal liver necrosis, hepatomegaly, and splenomegaly were foun

33 a dominant role in the development of severe liver necrosis in IRF3-deficient mice.

34 del, we show that inflammation may attenuate liver necrosis induced by carbon tetrachloride (CCl(4))

35 ral LPS administration potentiates alcoholic liver necrosis, inflammation, and fibrosis despite effic

36 either fish oil or corn oil developed fatty liver, necrosis, inflammation, and central vein collagen

37 lated specificity, but they do not cause the liver necrosis that is associated with T cell eliminatio

38 lobes pedicle (24% liver mass), resulting in liver necrosis; the remaining two omental lobes (8% live

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