ライフサイエンスコーパス: basal release

1 low-calcium environment that also inhibited basal release.

2 n of basal neurotransmission causing "leaky" basal release, (2) changes in either the size or mobiliz

3 stributions and signaling are dependent upon basal release and uptake, and on cytoneme-mediated movem

4 Although basal release at low frequency was insensitive to postsy

5 ude that MH-only mutations modestly increase basal release-channel activity in a manner insufficient

6 choline transport, both reduced H82 cell ACh basal release in a dose-dependent manner.

7 These results indicate that, although basal release is not altered, the amount of dopamine tha

8 Basal release of 5-HT prior to stimulation was significa

9 Basal release of a number of important analytes was dete

10 hyperactivated phenotype, hallmarked by the basal release of cytokines and cytotoxic molecules.

11 Basal release of EDNO (determined by endothelium-depende

12 between the number of estrogen receptors and basal release of EDNO in the aorta of mice, and suggest

13 showed a primed phenotype with an increased basal release of IL-8 and MMP-9 and expressed a corticos

14 COPD AMs also showed increased basal release of IL-8 and TNF-alpha, which was poorly su

15 lucose concentration and the abnormally high basal release of insulin were suppressed by treatment wi

16 An extensive basal release of ir-NYP was detected throughout the dors

17 Basal release of nitric oxide after a 60-minute porcine

18 Under normal conditions, basal release of nitric oxide is known to play a crucial

19 in group 3 exhibited better preservation of basal release of nitric oxide, as measured by contractio

20 thermore, storage in this solution preserved basal release of nitric oxide.

21 We conclude that the basal release of NO from the endothelium plays a permiss

22 he proximal colon is tonically suppressed by basal release of NO.

23 The basal release of PGE(2) in g-HCM cells was two- to fivef

24 The basal release of SP during normoxia was 51.0+/-1.5 fmol/

25 poxia-induced SP release (>95%), whereas the basal release of SP was unaffected.

26 microM elicited a 27 +/- 8% decrease in the basal release of SPLI and prevented the increase in the

27 In conclusion, dynorphin(1-8) reduces the basal release of SPLI and prevents the increase in the r

28 orsal horn through the perfusate reduced the basal release of SPLI by 29 +/- 9% and prevented the inc

29 alone elicited a 75 +/- 30% increase in the basal release of SPLI.

30 ate resulted in a 62 +/- 23% increase in the basal release of SPLI.

31 Similar rates of basal release of UDP-glucose and ATP (72 and 81 fmol/min

32 with progressive and significant apical and basal release of up-taken Insulin.

33 roM) and dipyridamole (200 microM) depressed basal releases of glutamate and taurine and the ischemia

34 We have found that injury does not alter basal release or acetylcholine, but it results in a mark

35 h N-cadherin in postsynaptic neurons reduced basal release probability (p(r)) at inputs to the neuron

36 mechanisms by which a given synapse sets its basal release probability are unknown.

37 In THC-tolerant mice, an increase of the basal release probability was found at PF-PC synapses, i

38 ndritic activity is the major determinant of basal release probability, and we suggest that this feed

39 neurotransmission unaltered with respect to basal release probability, Ca2+ dependence of release, s

40 SP14 deficiency impairs PPF without altering basal release probability.

41 In contrast, basal release that is independent of action potential fi

42 95% O(2) and 5% CO(2.) After determining the basal release, the hypothalami were challenged with 0, 0

43 The increase in basal release was 1.8-fold greater in haplotype 2A monoc

44 CRH-stimulated secretion, but not basal release, was inhibited by preincubation with dexam