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1 ptake, they do not enhance pulse velocity or basal secretion.
2 69 nmol/l are considered to represent normal basal secretion.
3 m-tomosyn-2 was novel in strongly augmenting basal secretion.
4 he inhibitory effects on stimulated, but not basal, secretion.
5 mature secretory granules, with no effect on basal secretion; a cell-permeant control peptide (Kal-C-
6 rovide a foundation for defining pathways of basal secretion and AASIS, augmenting our understanding
10 nd to regulate angiotensin II-stimulated and basal secretion, expression and promoter activity of BNP
14 antation may be due to increased less potent basal secretion in the fasting state and less frequent,
20 palmitate levels to simultaneously increase basal secretion of glucagon and insulin positions elevat
22 atinocytes, EPA and DHA were shown to reduce basal secretion of IL-8 by 66% and 63%, respectively (p<
26 data using intact GH3 cells demonstrate that basal secretion of SRIF-related material is largely calc
27 PS stimulation, but no evidence of increased basal secretion of these cytokines, or alterations in ba
29 181+/-8 microg (n=26, mean +/- S.E.M.), and basal secretion rate, 4.4+/-0.4 microg h(-1), indicated
31 to 1 mmol/L glucose, resulting in very high basal secretion rates that were inhibited by diazoxide a
32 f duodenal HCO(3)(-) secretion proposes that basal secretion results from Cl(-)/HCO(3)(-) exchange, w
33 ffusion hypothesis, auxin pulse velocity and basal secretion should increase with decreasing cell wal
34 der 5 conditions: unstimulated (to determine basal secretion), stimulated with forskolin, stimulated
38 d protein secretion was not stimulated above basal secretion, whereas alpha1-adrenergic-agonist-stimu
39 sed 2-3-fold above the already high level of basal secretion, whereas lysosomal SMase activity was de
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