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1  neutrophil infiltration, NET formation, and liver necrosis.
2 resulted in a significant reduction of acute liver necrosis.
3 e response sufficient to cause fatal massive liver necrosis.
4 ectomy because it is associated with massive liver necrosis.
5 epatocyte transcriptome were associated with liver necrosis.
6 esicular hepatic steatosis, as well as focal liver necrosis.
7                  Crisis was due to extensive liver necrosis accompanied by pleural edema.
8 le duct proliferation, and nearly eliminated liver necrosis after BDL.
9 idental-overdose group more often had severe liver necrosis (aminotransferase levels, >3500 IU per li
10           NRBF2-deficient mice develop focal liver necrosis and ductular reaction, accompanied by imp
11 ays exacerbated liver injury as reflected by liver necrosis and enhanced apoptosis (p < 0.001).
12 e Con-A administration reduced centrilobular liver necrosis and enhanced survival.
13 impaired liver regeneration characterized by liver necrosis and failure.
14 le-mediated Uhrf2 knockdown caused extensive liver necrosis and impaired hepatocyte proliferation aft
15  hepatocytes displayed significantly reduced liver necrosis and inflammation than wild-type mice.
16 h oil/ethanol and corn oil/ethanol) that had liver necrosis and inflammation.
17  after partial hepatectomy, characterized by liver necrosis and reduced and delayed hepatocyte DNA sy
18  livers, partial hepatectomy leads to severe liver necrosis and reduced hepatocyte proliferation.
19 bacterial load was associated with increased liver necrosis and serum alanine aminotransferase levels
20 ity testing based on their ability to induce liver necrosis and, eventually, liver cancer.
21 aEC, developed impaired hepatic vasculature, liver necrosis, and degenerative lesions in cardiac myoc
22 ased levels of blood transaminases, enhanced liver necrosis, and more pronounced neutrophil infiltrat
23                  Pathological changes (fatty liver, necrosis, and inflammation) were observed only in
24 d FE showed the most severe pathology (fatty liver, necrosis, and inflammation), those fed CE showed
25 etween 15 and 18 days, with evidence of mild liver necrosis/apoptosis.
26      Thrombosis of the artery and subsequent liver necrosis are indications for retransplantation.
27 al was accompanied by a dramatic increase in liver necrosis (as measured on a scale from 0 to 3) in t
28 ve also been implicated in the centrilobular liver necrosis associated with APAP.
29 e administration caused an intense degree of liver necrosis associated with increases in lipid peroxi
30 collaborate to guide neutrophils to sites of liver necrosis by CXC chemokine receptor 2 (CXCR2) and f
31 -dependent DNA damage is a critical event in liver necrosis caused by alkylating hepatotoxins.
32 hese effects are also accompanied by reduced liver necrosis, correlating with elevated serum interleu
33                                   Regions of liver necrosis demonstrated low attenuation on CT scans
34  vivo, extensive intestinal inflammation and liver necrosis developed.
35 ve impaired liver regeneration and increased liver necrosis following partial hepatectomy that is cor
36 /alanine aminotransferase levels and reduced liver necrosis formation.
37 owever, the primary Ca2+ target resulting in liver necrosis has not been determined.
38 ononuclear cellular infiltration, multifocal liver necrosis, hepatomegaly, and splenomegaly were foun
39 a dominant role in the development of severe liver necrosis in IRF3-deficient mice.
40 y control mice caused severe cholestasis and liver necrosis in Tjp2-deficient animals.
41 del, we show that inflammation may attenuate liver necrosis induced by carbon tetrachloride (CCl(4))
42 ral LPS administration potentiates alcoholic liver necrosis, inflammation, and fibrosis despite effic
43 sis was CD1d-dependent while steroid-induced liver necrosis, inflammation, and metabolic changes were
44  cholic acid-feeding, evidenced by increased liver necrosis, inflammation, fibrosis, and bile ductula
45  either fish oil or corn oil developed fatty liver, necrosis, inflammation, and central vein collagen
46                 Acetaminophen (APAP)-induced liver necrosis is a form of regulated cell death (RCD) i
47  at postnatal day 15-after the appearance of liver necrosis-led to the incorporation of some transduc
48                           LEI-515 attenuated liver necrosis, oxidative stress and inflammation in a C
49 lated specificity, but they do not cause the liver necrosis that is associated with T cell eliminatio
50 lobes pedicle (24% liver mass), resulting in liver necrosis; the remaining two omental lobes (8% live
51 ent feature selection methods that predicted liver necrosis with high specificity and selectivity in