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1 rnative theory predicts that ASL is normally hyposmotic.
2                                       During hyposmotic (170 mosmol kg-1) exposure there were large,
3 roM) completely protected both isosmotic and hyposmotic (233 mOsm) slices against hypoxic damage.
4                     Cell swelling induced by hyposmotic (250 osmol (l solution)(-1)) bath solution st
5 %, 35%, and 13% recovery rate in slices made hyposmotic (273, 253, and 233 mOsm, respectively).
6                     Cell swelling induced by hyposmotic bath solution stimulated Cl(-) currents in ar
7                                              Hyposmotic cell swelling caused a marked increase in den
8 e inhibitors (calyculin A and okadaic acid), hyposmotic cell swelling failed to further up-regulate I
9 currents were elicited by both isosmotic and hyposmotic cell swelling.
10                              A 50 mosmol l-1 hyposmotic challenge (300 to 250 mosmol l-1) constricted
11                       Cell depolarization or hyposmotic challenge shorten the cell and reduce membran
12  for channel activation were not affected by hyposmotic challenge.
13 ding failed to arise during large (100 mOsm) hyposmotic challenges, underscoring that neuronal swelli
14 lites and synthetic agonists, in addition to hyposmotic challenges.
15 ssion for the ratio of I- permeability under hyposmotic condition to that under isosmotic condition (
16 ignificantly diminished in slices exposed to hyposmotic conditions as 57% of control (isosmotic) slic
17 enopus laevis expressing TcAQP swelled under hyposmotic conditions indicating water permeability, whi
18                     We studied the effect of hyposmotic conditions on three colonic (Caco2, HRT18, HT
19  (Em) was -58 and -32 mV under isosmotic and hyposmotic conditions, respectively.
20 influx, together with Em under isosmotic and hyposmotic conditions, were used to calculate ER.
21  slightly in response to cell swelling under hyposmotic conditions.
22 I- pulses under isosmotic and, subsequently, hyposmotic conditions.
23 ase in activation of the NMDA receptor under hyposmotic conditions.
24 hole-cell configuration in the presence of a hyposmotic gradient.
25                                Exposure to a hyposmotic/hypotonic solution also led to a significant
26  to prevent ingested ice from nucleating the hyposmotic intestinal fluids.
27 after swelling induced by 60 min exposure to hyposmotic media (170 mosmol kg-1) relative to isosmotic
28 or the volume increase of cancer cells under hyposmotic pressure.
29 In addition, P-gp decreased the magnitude of hyposmotic shock required to activate the channels and t
30 ctivated Cl- channels with ER = 4.9 when the hyposmotic shock was 110 +/- 10 mosM.
31  when cells were exposed to a smaller (10 %) hyposmotic shock.
32 Cd2+ had no effect upon RVD following a 30 % hyposmotic shock.
33 VD) within 16 min when exposed to 30 or 10 % hyposmotic shocks.
34 e) while affording substantial protection to hyposmotic slices (233 mOsm), as 54% of the treated slic
35 usly increased the volume of normal cells in hyposmotic solutions by up to 7%, but 9AC had no effect
36 eously reduced the volume of normal cells in hyposmotic solutions by up to approximately 10%, but Gd3
37 ulatory volume decrease (RVD) in response to hyposmotic solutions.
38 e, amiloride, or HOE 694 are consistent with hyposmotic stimulation of apical NHE3 activity and provi
39 ng a greater than 9-fold increase during the hyposmotic stimulus.
40                                         Mild hyposmotic stress (0.9T) resulted in significant cell sw
41                                              Hyposmotic stress induced significant releases of aspart
42                                   Therefore, hyposmotic stress inhibits cell growth and, depending on
43 cells to correct their volume in response to hyposmotic stress via the efflux of inorganic and organi
44 pases and protein kinases in the response to hyposmotic stress were undertaken using an in vivo rat c
45 azoxide eliminated volume change due to mild hyposmotic stress, similar to that previously noted with
46 nted Cdk and cyclin degradation and reversed hyposmotic stress-induced growth arrest, whereas calpain
47  each other when the cells were submitted to hyposmotic stress.
48 the first evidence that NHE3 is regulated by hyposmotic stress.
49 y a delayed regulatory volume decrease after hyposmotic stress.
50 to I- influx were significantly faster under hyposmotic than under isosmotic conditions.

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