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1 ectly accessible to sporozoites entering the liver sinusoid.
2 gher levels of serum IgA and IgA deposits in liver sinusoids.
3 ent engulfment of B cells circulating in the liver sinusoids.
4 esulted in enlarged hepatocytes and narrowed liver sinusoids.
5 a large intravascular macrophage bed in the liver sinusoids.
6 ion/aggregation and subsequent entrapment in liver sinusoids.
7 gh both vessels are largely derived from the liver sinusoids.
8 d that 56% of portal blood flow bypasses the liver sinusoids.
9 d can profoundly contribute to remodeling of liver sinusoids.
10 olling portal blood flow and pressure within liver sinusoids.
11 ominant IL-17A(+) T cell subset in the human liver sinusoids.
12 erved in portal vein radicles, as well as in liver sinusoids, albeit integration of cells in the live
13 finity binding of circulating HCV within the liver sinusoids allowing subsequent transfer of the viru
14 transplanted hepatocytes immediately entered liver sinusoids, along with attenuation of portal vein r
15 ce also showed significant dilatation of the liver sinusoids and an increase in inflammatory cells su
16 initial arrest, CD8 TE actively crawl along liver sinusoids and probe sub-sinusoidal hepatocytes for
18 g to collagen type IV (highly exposed in the liver sinusoids) and collagen type IV-dependent activati
19 t that LPS-induced structural changes in the liver sinusoid are mediated by an LPS-induced Kupffer ce
20 After transplantation, hepatocytes entering liver sinusoids are engrafted, whereas cells entrapped i
21 lymphocytes travel via lung capillaries and liver sinusoids at an extremely rapid rate with the aver
22 e show that circulating CD8 TE arrest within liver sinusoids by docking onto platelets previously adh
23 transplanted cells are rapidly cleared from liver sinusoids by proinflammatory cytokines/chemokines/
24 dothelial cell signaling for angiogenesis or liver sinusoid capillarization, the mechanism for initia
25 In previous work, two anatomically distinct-liver sinusoid endothelial cells (LEC): LEC-1 and LEC-2,
26 C-SIGNR, a type 2 C-type lectin expressed on liver sinusoids, has been shown to bind with high affini
28 novel mechanism by which the destruction of liver sinusoids, induced by the Jo2-mediated co-engageme
30 em able to micropattern the self-assembly of liver sinusoid-like structures with micrometer resolutio
31 tablishes an inductive vascular niche in the liver sinusoids of the Id1(-/-) mice, initiating and res
32 lation of receptor-mediated cell adhesion in liver sinusoids or the manipulation of blood flow-depend
33 related receptor found on the endothelium of liver sinusoids, placental capillaries, and lymph nodes,
34 ort here that neutrophils accumulated in the liver sinusoids suppress cytokine and chemokine mRNA exp
35 fluoresence shows high protein expression in liver sinusoids, the venous sinuses of the red pulp in s
36 must penetrate cell barriers in the skin and liver sinusoid to reach their target cell, the hepatocyt
37 electron-microscopic examination of the rat liver sinusoid was performed in this study after in vivo
40 is largely expressed on endothelial cells in liver sinusoids, whereas DC-SIGN is expressed on dendrit
41 ycerine increased transplanted cell entry in liver sinusoids, whereas labetalol, nifedipine, CGRP, an
43 d shortly after deposition of hepatocytes in liver sinusoids, with clearance of a significant fractio
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