ライフサイエンスコーパス: NaN3

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1 NaN3 increased cytotoxicity to >90% only when neutrophil

2 sion of azide to nitride to cyanate using 4, NaN3 and CO is presented.

3 ltiphasic [Na+]i changes were observed after NaN3 and 0 glucose saline with only reduced [Na+]e.

4 Similarly, CRP and NaN3 alone caused equivalent concentration-dependent dec

5 CRP and NaN3 alone exhibited equivalent concentration-dependent,

6 In the presence of 2-deoxyglucose and NaN3, amino acids were unable to stimulate insulin relea

7 ospray ionization of solutions of UO2Cl2 and NaN3.

8 Vehicle or sodium azide (NaN3) (25-100 mM) was added to these QCMs while continuo

9 RP (dCRP) to remove azide, and sodium azide (NaN3) alone at equivalent concentrations to the undialyz

10 on or metabolic poisoning with sodium azide (NaN3).

11 Ms with untreated cells or without cells but NaN3.

12 bined glycolytic and respiratory blockage by NaN3 and 0 glucose saline caused [Na+]i to increase by 2

13 At these doses, NaN3 alters mitochondrial membrane permeability and caus

14 designs, and no requirement for using excess NaN3.

15 The reaction of 1 a/1 b with excess NaN3 under inert atmosphere resulted in the formation of

16 If NaN3 was added to either cell type within QCMs, 5 to 8 m

17 ation or NaN3 application and was blocked in NaN3 and 0 glucose.

18 d recordings, metabolic inhibition with 1 mM NaN3 revealed the presence of a tolbutamide-sensitive ch

19 emoval or chemical hypoxia (induced by 10 mM NaN3) for 60 min increased [Na+]i from a baseline of 8.3

20 and was decreased to 70% in the presence of NaN3 or in the absence of extracellular Na+.

21 was attenuated during glucose deprivation or NaN3 application and was blocked in NaN3 and 0 glucose.

22 ic; dipyridamole, a nucleoside inhibitor; or NaN3, a metabolic inhibitor or under Ca(2+)-free conditi

23 c in vivo ischemia, we exposed astrocytes to NaN3 and 0 glucose saline containing L-lactate and gluta

24 Compound 18 reacts with NaN3 to yield azide-substituted CB[7] 19 in 81% yield, w

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