ライフサイエンスコーパス: NaN(3)

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1 NaN(3)-treated beads retained full affinity for at least

2 NaN3 increased cytotoxicity to >90% only when neutrophil

3 er/0.02% NaN(3); and SEC-50 mM NaNO(3)/0.02% NaN(3) and multi detection.

4 ght scattering detector) and SEC-water/0.02% NaN(3); and SEC-50 mM NaNO(3)/0.02% NaN(3) and multi det

5 as to perform large-scale experiments, 0.1% NaN(3) was added.

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

7 nstant for singlet oxygen quenching by added NaN(3) depend on whether Chl or TMPyP was the photosensi

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

9 er anhydrous conditions with TFA/NaNO(2) and NaN(3) gave 3e in 87% yield.

10 domain (e.g., spatially dependent oxygen and NaN(3) diffusion coefficients), thereby providing eviden

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

12 CRP and NaN3 alone exhibited equivalent concentration-dependent,

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

14 ospray ionization of solutions of UO2Cl2 and NaN3.

15 K(ir)2.3 was inhibited by 3 mm sodium azide (NaN(3)), whereas K(ir)2.1 and K(ir)2.2 were not.

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

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

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

19 Ms with untreated cells or without cells but NaN3.

20 Displacement of the chloride by NaN(3) in acetone/water formed the acyl azide.

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

22 thylthio)sulfonium tetrafluoroborate (DMTSF)/NaN(3) with a variety of cyclopentene substrates has bee

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

24 designs, and no requirement for using excess NaN3.

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

26 y, onset of respiration inhibition following NaN(3) exposure is determined optically using an O(2)-se

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

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

29 K(ir)2.2 was inhibited by 10 mm NaN(3).

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

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

32 and inhibited by catalase and NADH, but not NaN(3).

33 Addition of 0.5 equiv of NaN(3) to U[NR(2)](3) (R = SiMe(3)) affords the metallac

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

35 ained when SMP were treated only with KCN or NaN(3), reagents that inhibit cytochrome oxidase, not co

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

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

38 Here we report that NaN(3) caused profound and sustained depolarization attr

39 reactive astrocytes (NRAs) after exposure to NaN(3), which depletes cellular ATP.

40 complex also with respect to sensitivity to NaN(3), as well as a mercurial, p-chloromercuribenzosulf

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

42 nto 4-azidotetrafluoronitrobenzene (3b) with NaN(3) in 93% yield and was used without further purific

43 ing of propargylic epoxy alcohol anti-5 with NaN(3)/NH(4)Cl.

44 The reaction of aldehydes with NaN(3) and TfOH furnishes the corresponding nitriles in

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

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