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1 m, associated with small airways disease, or centrilobular.
2 seases with peripheral lobular distribution, centrilobular abnormalities, and panlobular abnormalitie
3 (FasL), and CD40 associated with dropout of centrilobular (acinar zone 3) hepatocytes in chronic all
5 nusoidal dilatation is mainly located in the centrilobular area even in the absence of an outflow blo
6 liver, Redd1 induction is restricted to the centrilobular area, and in primary hepatocytes, mTORC1 i
7 position was a prominent feature in diseased centrilobular areas in Plg(o) livers for at least 30 day
9 ients, a histologic pattern characterized by centrilobular ballooning degeneration developed and prog
10 We conclude that a pattern of progressive centrilobular ballooning degeneration, bridging fibrosis
11 ot only acetaminophen-protein adducts in the centrilobular cells of the liver, but nitrotyrosine-prot
14 rs from ethanol-fed animals showed increased centrilobular CYP2E1 and protein adducts with acetaldehy
16 onic obstructive pulmonary disease, the mild centrilobular disease pattern is associated with lower F
17 with opportunistic infection, 28 (65%) had a centrilobular distribution of nodules; only one (6%) of
18 s smaller than 1 cm, especially those with a centrilobular distribution, are typically infectious.
19 e remaining five biopsies, three showed only centrilobular dropout, suggesting a resolution of some p
23 ed pericentral linking, with accumulation of centrilobular eosinophilic material in injured areas, wh
28 denced by markedly reduced serum ALT levels, centrilobular hepatic necrosis, and improved mouse survi
29 rized by significant elevation of serum ALT, centrilobular hepatic necrosis, and increased hepatic in
32 localized at the membrane of midlobular and centrilobular hepatocytes 10 to 48 hours after CCl4 expo
33 evated expression of luciferase and Hmox1 in centrilobular hepatocytes and in tubular epithelial cell
35 substantial delay in repair, with injury of centrilobular hepatocytes persisting up to 14 days after
36 sity of HUG-Br1 message was observed in some centrilobular hepatocytes surrounding larger central vei
39 hepatic venular endothelial inflammation and centrilobular inflammation but not with rejection relate
40 , hepatic vein endothelial inflammation, and centrilobular inflammation) were blindly assessed semiqu
41 higher levels of reduced glutathione (GSH), centrilobular inflammation, and a fourfold increase in h
44 maximize HSC depletion by combining CCl(4) (centrilobular injury) with allyl alcohol (AA) (periporta
45 n staining in detecting bromobenzene-induced centrilobular lesions and recovery of the hepatocellular
46 he histopathologic interpretive challenge of centrilobular lesions in posttransplant liver biopsies a
50 gimen resulted in hepatic changes including: centrilobular localization of 3-(cysteine-S-yl)APAP prot
52 proximately 120%, while CYP1A1/1A2 levels in centrilobular, midzonal, and periportal hepatocytes were
53 n 44%, 56%, and 58% as much CYP1A1/1A2 as do centrilobular, midzonal, and periportal hepatocytes, res
58 ce treated with APAP alone developed massive centrilobular necrosis and increased serum alanine amino
60 Each patient progressed to MHN with severe centrilobular necrosis and variable portal infiltrate.
65 00 mg/kg, intraperitoneal) developed typical centrilobular necrosis, which could not, however, be pre
68 .6%) was mathematically achieved when severe centrilobular NIA and centrilobular PC ratio of 30% to 5
71 a in a blood test and sputum, poorly defined centrilobular nodules throughout the bilateral lung fiel
72 computed tomographic (HRCT) scans indicating centrilobular nodules with adjoining thickened and dilat
76 g bronchial wall thickening, bronchiectasis, centrilobular opacities, and air trapping, compared with
78 y with the presence of cholangiofibrosis and centrilobular pancreatitis; however, further studies are
79 r analysis of volumetric CT images for type (centrilobular, panlobular, and mixed) and extent (on a s
80 y achieved when severe centrilobular NIA and centrilobular PC ratio of 30% to 50% were both present.
82 sed on these findings, we postulate that the centrilobular phenotype of emphysematous destruction COP
83 s to the cellular and molecular level in the centrilobular phenotype of emphysematous destruction in
84 multivariate analysis, centrilobular NIA and centrilobular plasma cell (PC) ratio of 30% to 50% were
85 e opacities that gradually extend toward the centrilobular region and finally replace the entire lobu
86 small anatomic details (interlobular septa, centrilobular region, and small bronchi and bronchioles)
87 by combining 2-AAF with selective damage of centrilobular regions (carbon tetrachloride [CCl4]) or p
88 richrome staining revealed intense signal in centrilobular regions and electron microscopy showed a m
89 tone H3 lysine-9 (3meH3K9) protein levels in centrilobular regions in both ethanol groups, with no ch
90 acetaminophen (1 g/kg) resulted in damage to centrilobular regions of the liver and increases in seru
94 r DR migration from the portal tracts to the centrilobular site of injury, in association with an inc
96 ioactivation of the APAP challenge dose from centrilobular to periportal regions where CYP2E1 is not
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