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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
4 e volume (p < 0.001), as was the presence of centrilobular and paraseptal emphysema.
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
8  significant increase of 3NT staining in the centrilobular areas.
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
12                  A liver biopsy demonstrated centrilobular cholestasis and focal rosetting of hepatoc
13 l injury with extensive sinusoidal fibrosis, centrilobular congestion, and hepatocyte necrosis.
14 rs from ethanol-fed animals showed increased centrilobular CYP2E1 and protein adducts with acetaldehy
15                                              Centrilobular damage results in a more enhanced oval cel
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
20 fined emphysema, particularly panlobular and centrilobular emphysema (all P </= 0.01).
21 okers can develop either panlobular (PLE) or centrilobular emphysema (CLE).
22 ), and 12 smokers with subtle CT findings of centrilobular emphysema (SCE).
23 ed pericentral linking, with accumulation of centrilobular eosinophilic material in injured areas, wh
24 and induced diffuse coagulative necrosis and centrilobular fibrosis in some animals.
25 tosis, and necroinflammation with or without centrilobular fibrosis.
26 denudation of LSECs at 24 hours, followed by centrilobular hemorrhagic necrosis at 48 hours.
27 algesic and antipyretic agent known to cause centrilobular hepatic necrosis at toxic doses.
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
30                                 By contrast, centrilobular hepatocyte loss should be suspected as a r
31                                              Centrilobular hepatocyte necrosis correlated with hepati
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
34 rocarbons may be differentially expressed in centrilobular hepatocytes of rats.
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
37 ale/lacy appearance and persistent damage to centrilobular hepatocytes.
38 e droplet fatty change that is restricted to centrilobular hepatocytes.
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
42  and uPA simultaneously, with persistence of centrilobular injury as far out as 35 days.
43                      A histologic pattern of centrilobular injury including increased NIA and increas
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
47                               The persistent centrilobular lesions were not a consequence of impaired
48  rhIL-11 before Con-A administration reduced centrilobular liver necrosis and enhanced survival.
49 ffer cells, have also been implicated in the centrilobular liver necrosis associated with APAP.
50 gimen resulted in hepatic changes including: centrilobular localization of 3-(cysteine-S-yl)APAP prot
51 jury that has been generally associated with centrilobular localization of the adducts.
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
54 erize them as peribronchovascular (n = 2) or centrilobular (n = 7).
55                                              Centrilobular necroinflammation (CLNI) associated with a
56                             We have observed centrilobular necrosis (CLN) in several liver allograft
57                                              Centrilobular necrosis and coincidental destructive chol
58 ce treated with APAP alone developed massive centrilobular necrosis and increased serum alanine amino
59  liver injury ranging from mild to extensive centrilobular necrosis and inflammation.
60   Each patient progressed to MHN with severe centrilobular necrosis and variable portal infiltrate.
61 , and nuclear DNA fragmentation resulting in centrilobular necrosis in C57Bl/6J mice.
62                  These findings suggest that centrilobular necrosis is a manifestation of a rejection
63                                              Centrilobular necrosis is within the histologic spectrum
64                        However, APAP-induced centrilobular necrosis, and its associated mortality, wa
65 00 mg/kg, intraperitoneal) developed typical centrilobular necrosis, which could not, however, be pre
66 ase levels that correlated with increases in centrilobular necrosis.
67 APAP showed a more typical, and less severe, centrilobular necrosis.
68 .6%) was mathematically achieved when severe centrilobular NIA and centrilobular PC ratio of 30% to 5
69                    In multivariate analysis, centrilobular NIA and centrilobular plasma cell (PC) rat
70 er were found to have mosaic air trapping or centrilobular nodules on chest CT.
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
73                                              Centrilobular nodules, large nodules, tree-in-bud appear
74 es characterized by ground-glass opacity and centrilobular nodules.
75 ography showed ground-glass opacity and some centrilobular nodules.
76 g bronchial wall thickening, bronchiectasis, centrilobular opacities, and air trapping, compared with
77 dders of hamsters with cholangiofibrosis and centrilobular pancreatitis.
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.
81                                              Centrilobular pericellular fibrosis, which has not been
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
91 xpression of these proteins was localized in centrilobular regions of the liver.
92                 Pathologic changes affecting centrilobular regions were described in the context of h
93 ses in phagocytic activity of macrophages in centrilobular regions.
94 r DR migration from the portal tracts to the centrilobular site of injury, in association with an inc
95                   Emphysema is classified as centrilobular (subclassified as trace, mild, moderate, c
96 ioactivation of the APAP challenge dose from centrilobular to periportal regions where CYP2E1 is not
97 ase is possible, and these patients may have centrilobular zone 3 necrosis.
98 ogical features of AI-ALF predominate in the centrilobular zone.

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