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1 fluid transport in primary cultures of human alveolar epithelial type II cells.
2 d receptors on the apical plasma membrane of alveolar epithelial type II cells.
3 immortalized mouse lung epithelial cells and alveolar epithelial type II cells.
4 uring the exocytosis of lamellar bodies from alveolar epithelial type II cells.
5 t levels in fibroblasts, myofibroblasts, and alveolar epithelial type II cells.
6 n across primary cultures of polarized human alveolar epithelial type II cells after an inflammatory
7 fication associated with a reduced number of alveolar epithelial type II cells and exhibit persistent
10 ation channels are functionally expressed in alveolar epithelial type II cells, and suggest that thes
12 es using small molecule inhibitors in murine alveolar epithelial type II cells (C10) and primary lung
13 n of B-RAF in C-RAF BxB-expressing embryonic alveolar epithelial type II cells did not block adenoma
14 loride transport genes and proteins in human alveolar epithelial type II cells, effects that were ass
16 ty decreased at the basolateral membranes of alveolar epithelial type II cells incubated with scorpio
17 There was no difference in cell injury in alveolar epithelial type II cells incubated with scorpio
19 ypothesis, A549 cells (an immortalized human alveolar epithelial type II cell-like fine) were infecte
20 ed from haemorrhaged rats or by A549 and rat alveolar epithelial type II cell monolayers stimulated w
22 report a cell-specific RNAi system using an alveolar epithelial type II cell-specific promoter--the
23 n did not affect the production of NO by rat alveolar epithelial type II cells that were stimulated w
25 and net fluid transport across rat and human alveolar epithelial type II cells via a reduction in the
26 a,K-ATPase activity and protein abundance in alveolar epithelial type II cells via the alpha(1)- and
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