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1 transports bile salts from hepatocytes into bile canaliculi.
2 ericellular fibrosis, and dilated, misshapen bile canaliculi.
3 croscopy also revealed structures resembling bile canaliculi.
4 the lumina, reminiscent of those seen about bile canaliculi.
5 e apical membrane of the hepatocyte into the bile canaliculi.
6 ence of damage to transgenic hepatocytes and bile canaliculi.
7 d excrete fluorescein diacetate into visible bile canaliculi.
8 hepaticus was noted infrequently and only in bile canaliculi.
9 brosis, and ultrastructural abnormalities of bile canaliculi.
10 e increased secretion of fluorescent PC into bile canaliculi.
11 the mutant protein to reach the membrane of bile canaliculi.
12 cantly higher accumulation of CDF in cells + bile canaliculi (32.3 +/- 2.5 versus 24.4 +/- 4.3 pmol/m
13 hese cells as shown by impaired formation of bile canaliculi, absence of polarity, and reduced secret
14 onally, these mutants develop defects in the bile canaliculi and have marked biliary paucity, suggest
17 ) cultures had epithelial morphology, showed bile canaliculi, and expressed albumin messenger RNA (mR
18 he liver, secreted from hepatocytes into the bile canaliculi, and subsequently stored in the gall bla
21 ntrast, organize their luminal surfaces (the bile canaliculi; BC) between their lateral membranes, an
23 ttle or no effect on ABCB4 expression at the bile canaliculi caused a decrease (F357L, T775M, and G95
24 wing to tissue localization in the placenta, bile canaliculi, colon, small bowel, and brain microvess
25 re rapidly in CP-treated animals, and hybrid bile canaliculi developed even 1 day after cell transpla
26 ane regenesis, with hybrid gap junctions and bile canaliculi forming over 3 to 7 days after cell tran
27 was manifested by sequential progression of bile canaliculi from small structures to a fully branche
28 ron microscopy revealed dilated and tortuous bile canaliculi in KO livers along with decreased canali
29 whereas it rapidly appeared in the abnormal bile canaliculi in LKB1(-/-) mice, confirming that junct
30 pheroids spontaneously assemble a functional bile canaliculi network, extending from the surface to t
32 cobacter hepaticus, infects the intrahepatic bile canaliculi of mice, causing a severe chronic hepati
34 tion of filamentous actin in hepatocytes and bile canaliculi of the ischemic lobes compared with the
35 , present focally, was manifested as dilated bile canaliculi, partial loss of microvilli, and retenti
36 e ultrastructural characteristics, including bile canaliculi, peroxisomes, and glycogen granules, whe
37 hanced cell differentiation and formation of bile canaliculi, probably through an effect on hepatocyt
39 ct, i.e., increase in the mature form at the bile canaliculi, was obtained by cell treatments with cy
40 s possess structural polarity and functional bile canaliculi with normal differentiated function.
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