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1  dendriform morphology were found within the pericentral and central region of the corneal stroma (20
2 actices may need to be adjusted to recognize pericentral and parafoveal hydroxychloroquine retinopath
3                             Both the dorsal (pericentral) and the lateral (external) nuclei of the in
4                        Central, paracentral, pericentral, and the thinnest corneal thicknesses; anter
5 CO concentrations may be elevated around the pericentral area in the liver after chronic alcohol inge
6 eously distributed with concentration in the pericentral area.
7  periportal regions were well oxygenated but pericentral areas became hypoxic.
8 sively in the liver and predominately around pericentral areas of the hepatic lobule, while there was
9 ixed (retinal changes in both parafoveal and pericentral areas).
10 ures correlated with birth weight (P < .05), pericentral axial curvature did not.
11 ntify key differences between periportal and pericentral cells accounting for higher susceptibility t
12                           The descendants of pericentral cells differentiate into Tbx3-negative, poly
13                                        These pericentral cells express the early liver progenitor mar
14 d to a higher susceptibility to steatosis in pericentral cells in the model simulations.
15                          Furthermore, whilst pericentral cells tend to show higher lipid levels, vari
16  cells provide Wnt signals that maintain the pericentral cells, thereby constituting the niche.
17 ng damage is known to occur more severely in pericentral cells.
18 by splitting the sinusoid into periportal to pericentral compartments.
19                        With the exception of pericentral corneal thickness, all regions of corneal th
20 afoveal changes, 24 (12%) also had a zone of pericentral damage, and 24 (12%) had pericentral retinop
21                                 Finally, the pericentral expression of de novo lipogenesis contribute
22 s, whereas the CM projection also included a pericentral extension around the ventromedial and latera
23 nin in metabolic zonation where it regulates pericentral gene expression and in initiating liver rege
24 ion of hepatic stellate cells, and increased pericentral hepatic apoptosis following CCl(4) injury.
25 pstream effector of beta-catenin activity in pericentral hepatocytes and during LR.
26 L rats, ET-1 was localized in periportal and pericentral hepatocytes and hepatic sinusoidal cells.
27 an early peak of p21 expression occurring in pericentral hepatocytes at 6 h, prior to evidence of inj
28 mily members were predominantly localized in pericentral hepatocytes during liver injury, oval cell a
29 y, indicating that rapid induction of p21 in pericentral hepatocytes following CCl4 injection contrib
30  enhancer 3 activity is highly restricted to pericentral hepatocytes in the adult liver.
31 o that in males, but which then increased in pericentral hepatocytes resulting in a bowl-like distrib
32                   Increased proliferation of pericentral hepatocytes was demonstrated by 5-bromo-2'-d
33 and nuclear translocation of beta-catenin in pericentral hepatocytes with a concomitant increase in c
34 I and EII exhibit high levels of activity in pericentral hepatocytes with a gradual reduction in acti
35 ynthesis in the periphery (including that in pericentral hepatocytes) and glutamine catabolism in (pe
36 bular gradient increasing from periportal to pericentral hepatocytes, claudin 3 is uniformly expresse
37  This results in a cycle of AA-enrichment in pericentral hepatocytes, membrane release of AA, and gen
38  V1a receptors are most heavily expressed on pericentral hepatocytes, or by using 2,5-di(tert-butyl)-
39 ause glucagon receptors are predominantly on pericentral hepatocytes, or by using dibutyryl cAMP, whi
40  the central vein with the weakest signal in pericentral hepatocytes, resulting in a hepatic lobular
41 itially perfused at low-flow rates to induce pericentral hypoxia followed by a 40-minute reperfusion
42                            We postulate that pericentral induction of iNOS under ambient conditions o
43                                      A rapid pericentral inflammatory infiltrate enriched in F4/80(+)
44 n-negative epithelioid cells within zones of pericentral injury.
45 h enhanced keratin solubility; and prominent pericentral keratin network disruption.
46  injections into the lateral dorsal horn and pericentral laminae resulted in the largest number of li
47 eoplastic foci adjacent to portal tracts and pericentral large cell dysplasia.
48 roscopically, Plg(0) livers had a pronounced pericentral linking, with accumulation of centrilobular
49 is, presumably autoimmune in nature, who had pericentral necrosis (zone 3) with relative sparing of t
50 at 60 minutes after reperfusion (P<0.05) and pericentral necrosis at 8 hours after reperfusion (P<0.0
51 nsion of the blind spot extending into large pericentral or other types of scotomata (64%).
52 utamine synthetase-positive, suggestive of a pericentral origin.
53  in a parafoveal (bull's eye) pattern, and a pericentral pattern of damage is especially prevalent am
54                            Patients with the pericentral pattern were taking hydroxychloroquine for a
55 he CDE regimen, whereas TAA-treated mice had pericentral patterns of progressive injury and fibrosis,
56 es with a gradual reduction in activity in a pericentral-periportal direction.
57  abnormality of spikes or sharp waves in the pericentral region (centroparietal, centrofrontal, or ce
58 detaldehyde adduct was located mainly in the pericentral region of the liver.
59 ed increases in NADH autofluorescence in the pericentral region, leukocyte adherence, and nonperfused
60 ed increment in NADH autofluorescence in the pericentral region, relative to control mice.
61 creased, predominantly in hepatocytes in the pericentral region.
62 oximately 5% of hepatocytes clustered in the pericentral region.
63 ) after I/R in these mice, especially in the pericentral region.
64 on (indicating hypoxia), particularly in the pericentral region.
65  of adherent leukocytes in both midzonal and pericentral regions after gut I/R was elevated.
66 s, detected immunochemically, accumulated in pericentral regions in liver.
67 ay account for increased oxidative damage in pericentral regions in NASH.
68  Calretinin immunoreactivity was high in the pericentral regions of the IC, but the central nucleus w
69 tly, juniper berry oil reduced cell death in pericentral regions of the liver lobule by 75%.
70 obule has its reactivity enhanced in hypoxic pericentral regions where the pH is lower.
71 thetase gene is also active, specifically in pericentral regions.
72 d X antigens in the liver, especially in the pericentral regions.
73 ld increase in nitrotyrosine accumulation in pericentral regions.
74 dal space surrounding the periportal and the pericentral regions.
75 Detachment of the posterior hyaloid from the pericentral retina exerts anterior traction on the foveo
76                                              Pericentral retina with normal lamination showed a thinn
77 of ONL in the superior-temporal and temporal pericentral retina.
78 hanges 2 degrees -6 degrees from the fovea), pericentral (retinal changes >/= 8 degrees from the fove
79                                              Pericentral retinopathy alone was seen in 50% of Asian p
80 zone of pericentral damage, and 24 (12%) had pericentral retinopathy without any parafoveal damage.
81                            In some families, pericentral RP or macular dystrophy were found in family
82       A key feature of partial epilepsy with pericentral spikes is a characteristic encephalogram abn
83 his distinctive encephalogram abnormality of pericentral spikes unites these several seizure types in
84 ily epilepsy syndrome, partial epilepsy with pericentral spikes, which we map to chromosome 4p15.
85 ared to increase the subjective intensity of pericentral staining of iNOS.
86 ession of de novo lipogenesis contributed to pericentral steatosis when additionally simulating the i
87 ells accounting for higher susceptibility to pericentral steatosis.
88 ed disease in all three families showed more pericentral than peripheral field dysfunction.
89 n the predominant location of steatosis from pericentral to pan-sinusoidal or azonal.
90  pattern in the TAA model as driven from the pericentral vein region.
91 ve TCF/LEF transcription are confined to the pericentral zone and are not increased in number during
92 pecially beta2SP, from the periportal to the pericentral zone as regeneration nears termination via i
93                                   However, a pericentral zone of preserved architecture was present,
94 compared between the periportal (zone 1) and pericentral (zone 3) regions of the rat liver during reg

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