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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 ed visually and quantitatively) and subtype (centrilobular and paraseptal, assessed visually).
6  clinically significant fibrosis (ie, F>=F2, centrilobular and periportal fibrosis or more severe dis
7 nusoidal dilatation is mainly located in the centrilobular area even in the absence of an outflow blo
8  liver, Redd1 induction is restricted to the centrilobular area, and in primary hepatocytes, mTORC1 i
9 position was a prominent feature in diseased centrilobular areas in Plg(o) livers for at least 30 day
10  significant increase of 3NT staining in the centrilobular areas.
11 ients, a histologic pattern characterized by centrilobular ballooning degeneration developed and prog
12    We conclude that a pattern of progressive centrilobular ballooning degeneration, bridging fibrosis
13 ot only acetaminophen-protein adducts in the centrilobular cells of the liver, but nitrotyrosine-prot
14                  A liver biopsy demonstrated centrilobular cholestasis and focal rosetting of hepatoc
15 erpolyploidization of hepatocytes around the centrilobular (CL) region is demonstrated to be closely
16 l injury with extensive sinusoidal fibrosis, centrilobular congestion, and hepatocyte necrosis.
17 rs from ethanol-fed animals showed increased centrilobular CYP2E1 and protein adducts with acetaldehy
18                                              Centrilobular damage results in a more enhanced oval cel
19 onic obstructive pulmonary disease, the mild centrilobular disease pattern is associated with lower F
20 with opportunistic infection, 28 (65%) had a centrilobular distribution of nodules; only one (6%) of
21 s smaller than 1 cm, especially those with a centrilobular distribution, are typically infectious.
22 e remaining five biopsies, three showed only centrilobular dropout, suggesting a resolution of some p
23 fined emphysema, particularly panlobular and centrilobular emphysema (all P </= 0.01).
24 okers can develop either panlobular (PLE) or centrilobular emphysema (CLE).
25 ), and 12 smokers with subtle CT findings of centrilobular emphysema (SCE).
26             Compared with no emphysema, only centrilobular emphysema (three studies) was associated w
27 as the initial site of tissue destruction in centrilobular emphysema and an attractive target for dis
28                      Regarding subtype, only centrilobular emphysema was significantly associated wit
29                                The extent of centrilobular emphysema was significantly associated wit
30 ed pericentral linking, with accumulation of centrilobular eosinophilic material in injured areas, wh
31 and induced diffuse coagulative necrosis and centrilobular fibrosis in some animals.
32 tosis, and necroinflammation with or without centrilobular fibrosis.
33                              Chest CT showed centrilobular granular shadow and ground glass opacities
34 denudation of LSECs at 24 hours, followed by centrilobular hemorrhagic necrosis at 48 hours.
35 algesic and antipyretic agent known to cause centrilobular hepatic necrosis at toxic doses.
36 denced by markedly reduced serum ALT levels, centrilobular hepatic necrosis, and improved mouse survi
37 rized by significant elevation of serum ALT, centrilobular hepatic necrosis, and increased hepatic in
38                                 By contrast, centrilobular hepatocyte loss should be suspected as a r
39                                              Centrilobular hepatocyte necrosis correlated with hepati
40                     Furthermore, pericentral/centrilobular hepatocyte p50 nuclear translocation is te
41  localized at the membrane of midlobular and centrilobular hepatocytes 10 to 48 hours after CCl4 expo
42 evated expression of luciferase and Hmox1 in centrilobular hepatocytes and in tubular epithelial cell
43  was evaluated in periportal and pericentral/centrilobular hepatocytes isolated using digitonin perfu
44 rocarbons may be differentially expressed in centrilobular hepatocytes of rats.
45  substantial delay in repair, with injury of centrilobular hepatocytes persisting up to 14 days after
46 sity of HUG-Br1 message was observed in some centrilobular hepatocytes surrounding larger central vei
47 Lbp expression being enriched in pericentral/centrilobular hepatocytes.
48 ale/lacy appearance and persistent damage to centrilobular hepatocytes.
49 e droplet fatty change that is restricted to centrilobular hepatocytes.
50 hepatic venular endothelial inflammation and centrilobular inflammation but not with rejection relate
51 , hepatic vein endothelial inflammation, and centrilobular inflammation) were blindly assessed semiqu
52  higher levels of reduced glutathione (GSH), centrilobular inflammation, and a fourfold increase in h
53  and uPA simultaneously, with persistence of centrilobular injury as far out as 35 days.
54                      A histologic pattern of centrilobular injury including increased NIA and increas
55  maximize HSC depletion by combining CCl(4) (centrilobular injury) with allyl alcohol (AA) (periporta
56 n staining in detecting bromobenzene-induced centrilobular lesions and recovery of the hepatocellular
57 he histopathologic interpretive challenge of centrilobular lesions in posttransplant liver biopsies a
58                               The persistent centrilobular lesions were not a consequence of impaired
59  rhIL-11 before Con-A administration reduced centrilobular liver necrosis and enhanced survival.
60 ffer cells, have also been implicated in the centrilobular liver necrosis associated with APAP.
61 gimen resulted in hepatic changes including: centrilobular localization of 3-(cysteine-S-yl)APAP prot
62 jury that has been generally associated with centrilobular localization of the adducts.
63        Her chest CT showed bilateral diffuse centrilobular micronodules.
64 proximately 120%, while CYP1A1/1A2 levels in centrilobular, midzonal, and periportal hepatocytes were
65 n 44%, 56%, and 58% as much CYP1A1/1A2 as do centrilobular, midzonal, and periportal hepatocytes, res
66 erize them as peribronchovascular (n = 2) or centrilobular (n = 7).
67                                              Centrilobular necroinflammation (CLNI) associated with a
68                             We have observed centrilobular necrosis (CLN) in several liver allograft
69                                              Centrilobular necrosis and coincidental destructive chol
70 ce treated with APAP alone developed massive centrilobular necrosis and increased serum alanine amino
71  liver injury ranging from mild to extensive centrilobular necrosis and inflammation.
72   Each patient progressed to MHN with severe centrilobular necrosis and variable portal infiltrate.
73 , and nuclear DNA fragmentation resulting in centrilobular necrosis in C57Bl/6J mice.
74                  These findings suggest that centrilobular necrosis is a manifestation of a rejection
75                                              Centrilobular necrosis is within the histologic spectrum
76                        However, APAP-induced centrilobular necrosis, and its associated mortality, wa
77 00 mg/kg, intraperitoneal) developed typical centrilobular necrosis, which could not, however, be pre
78 ase levels that correlated with increases in centrilobular necrosis.
79 APAP showed a more typical, and less severe, centrilobular necrosis.
80 .6%) was mathematically achieved when severe centrilobular NIA and centrilobular PC ratio of 30% to 5
81                    In multivariate analysis, centrilobular NIA and centrilobular plasma cell (PC) rat
82 odules (64.7%), tree-in-bud pattern (61.8%), centrilobular nodules (44.1 %), consolidations (41.2%),
83      High-resolution chest CT revealed small centrilobular nodules in the right upper lobe in March X
84 er were found to have mosaic air trapping or centrilobular nodules on chest CT.
85 a in a blood test and sputum, poorly defined centrilobular nodules throughout the bilateral lung fiel
86 computed tomographic (HRCT) scans indicating centrilobular nodules with adjoining thickened and dilat
87                         A pattern of diffuse centrilobular nodules with sparing of lung segments with
88                  Features of active PTB were centrilobular nodules, 'tree-in-bud' pattern densities,
89 on, HRCT findings of ground-glass opacities, centrilobular nodules, and mosaic attenuation, with trac
90                                              Centrilobular nodules, large nodules, tree-in-bud appear
91 ography showed ground-glass opacity and some centrilobular nodules.
92 es characterized by ground-glass opacity and centrilobular nodules.
93  tomographic examinations range from nodular centrilobular opacities in acute/subacute disease to inc
94 g bronchial wall thickening, bronchiectasis, centrilobular opacities, and air trapping, compared with
95 dders of hamsters with cholangiofibrosis and centrilobular pancreatitis.
96 y with the presence of cholangiofibrosis and centrilobular pancreatitis; however, further studies are
97 r analysis of volumetric CT images for type (centrilobular, panlobular, and mixed) and extent (on a s
98 y achieved when severe centrilobular NIA and centrilobular PC ratio of 30% to 50% were both present.
99                                              Centrilobular pericellular fibrosis, which has not been
100 sed on these findings, we postulate that the centrilobular phenotype of emphysematous destruction COP
101 s to the cellular and molecular level in the centrilobular phenotype of emphysematous destruction in
102 multivariate analysis, centrilobular NIA and centrilobular plasma cell (PC) ratio of 30% to 50% were
103 e opacities that gradually extend toward the centrilobular region and finally replace the entire lobu
104  small anatomic details (interlobular septa, centrilobular region, and small bronchi and bronchioles)
105  by combining 2-AAF with selective damage of centrilobular regions (carbon tetrachloride [CCl4]) or p
106 richrome staining revealed intense signal in centrilobular regions and electron microscopy showed a m
107 tone H3 lysine-9 (3meH3K9) protein levels in centrilobular regions in both ethanol groups, with no ch
108 acetaminophen (1 g/kg) resulted in damage to centrilobular regions of the liver and increases in seru
109 xpression of these proteins was localized in centrilobular regions of the liver.
110                 Pathologic changes affecting centrilobular regions were described in the context of h
111 ses in phagocytic activity of macrophages in centrilobular regions.
112 r DR migration from the portal tracts to the centrilobular site of injury, in association with an inc
113                   Emphysema is classified as centrilobular (subclassified as trace, mild, moderate, c
114 ioactivation of the APAP challenge dose from centrilobular to periportal regions where CYP2E1 is not
115                                              Centrilobular was the predominant emphysema pattern occu
116 ase is possible, and these patients may have centrilobular zone 3 necrosis.
117 ogical features of AI-ALF predominate in the centrilobular zone.

 
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