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 olarization), ND(3) (3%), PhCH(2)NH(2) (
5%),
NaN(3) (3%), and NO(3)(-) (0.1%)).
8 nstant for singlet oxygen quenching by
added NaN(3) depend on whether Chl or TMPyP was the photosensi
9 ltiphasic [Na+]i changes were observed
after NaN3 and 0 glucose saline with only reduced [Na+]e.
10 er anhydrous conditions with TFA/NaNO(2)
and NaN(3) gave 3e in 87% yield.
11 The role of PhN(3)
and NaN(3) in copper-free click chemistry is exemplified for
12 The protocol is, apart from CuCl
and NaN(3), additive free and allows the isolation of versat
13 andatory, affording RFTA(*-) (from DABCO
and NaN(3)) or RFTAH(*) (from Et(3)N).
14 raacetate) and additives (DABCO, Et(3)N,
and NaN(3)) employed.
15 domain (e.g., spatially dependent oxygen
and NaN(3) diffusion coefficients), thereby providing eviden
16 Similarly, CRP
and NaN3 alone caused equivalent concentration-dependent dec
17 CRP
and NaN3 alone exhibited equivalent concentration-dependent,
18 In the presence of 2-deoxyglucose
and NaN3, amino acids were unable to stimulate insulin relea
19 ospray ionization of solutions of UO2Cl2
and NaN3.
20 [3 + 2] cycloaddition between sodium
azide (
NaN(3)) and organic nitrile derivatives.
21 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.
22 Vehicle or sodium
azide (
NaN3) (25-100 mM) was added to these QCMs while continuo
23 RP (dCRP) to remove azide, and sodium
azide (
NaN3) alone at equivalent concentrations to the undialyz
24 on or metabolic poisoning with sodium
azide (
NaN3).
25 Ms with untreated cells or without cells
but NaN3.
26 Displacement of the chloride
by NaN(3) in acetone/water formed the acyl azide.
27 ity upon partial inhibition of complex IV
by NaN(3).
28 bined glycolytic and respiratory blockage
by NaN3 and 0 glucose saline caused [Na+]i to increase by 2
29 thylthio)sulfonium tetrafluoroborate (
DMTSF)/
NaN(3) with a variety of cyclopentene substrates has bee
30 At these
doses,
NaN3 alters mitochondrial membrane permeability and caus
31 designs, and no requirement for using
excess NaN3.
32 The reaction of 1 a/1 b with
excess NaN3 under inert atmosphere resulted in the formation of
33 y, onset of respiration inhibition
following NaN(3) exposure is determined optically using an O(2)-se
34 If NaN3 was added to either cell type within QCMs, 5 to 8 m
35 ation or NaN3 application and was blocked
in NaN3 and 0 glucose.
36 The reaction of phenyl
isothiocyanate,
NaN(3), and amine (primary aliphatic, aromatic, and alip
37 K(ir)2.2 was inhibited by 10
mm NaN(3).
38 emoval or chemical hypoxia (induced by 10
mM NaN3) for 60 min increased [Na+]i from a baseline of 8.3
39 d recordings, metabolic inhibition with 1
mM NaN3 revealed the presence of a tolbutamide-sensitive ch
40 P[5]-TePh, benzyl bromides reacted with
NaCN/
NaN(3) in water, yielding organic nitriles/azides.
41 and inhibited by catalase and NADH, but
not NaN(3).
42 Addition of 0.5 equiv
of NaN(3) to U[NR(2)](3) (R = SiMe(3)) affords the metallac
43 n convert to the E isomer in the presence
of NaN(3).
44 The synthetic utility
of NaN(3) as the azide component in the [3 + 2] annulation
45 and was decreased to 70% in the presence
of NaN3 or in the absence of extracellular Na+.
46 ained when SMP were treated only with KCN
or NaN(3), reagents that inhibit cytochrome oxidase, not co
47 rganic phosphate and alkaline phosphatase
or NaN(3) treatment further support the involvement of a ph
48 was attenuated during glucose deprivation
or NaN3 application and was blocked in NaN3 and 0 glucose.
49 ic; dipyridamole, a nucleoside inhibitor;
or NaN3, a metabolic inhibitor or under Ca(2+)-free conditi
50 oom temperature with the available
reagents:
NaN(3), N-hydroxy compounds, and PhI(OAc)(2) as the oxid
51 converted to alkyl azides with bench-
stable NaN(3) in the presence of FeCl(3).6H(2)O under blue-ligh
52 Here we report
that NaN(3) caused profound and sustained depolarization attr
53 reactive astrocytes (NRAs) after exposure
to NaN(3), which depletes cellular ATP.
54 complex also with respect to sensitivity
to NaN(3), as well as a mercurial, p-chloromercuribenzosulf
55 c in vivo ischemia, we exposed astrocytes
to NaN3 and 0 glucose saline containing L-lactate and gluta
56 pported (Trapen(TMS))Ce(IV)Cl complex 2
with NaN(3).
57 nto 4-azidotetrafluoronitrobenzene (3b)
with NaN(3) in 93% yield and was used without further purific
58 ing of propargylic epoxy alcohol anti-5
with NaN(3)/NH(4)Cl.
59 The reaction of aldehydes
with NaN(3) and TfOH furnishes the corresponding nitriles in
60 ithin 30 s, and its subsequent reaction
with NaN(3) leads to the detection of hyperpolarized PhN(3) (
61 omplex 4 is thermally stable but reacts
with NaN(3) to form 3, implying a bis-azide intermediate, [(T
62 Complex 1 reacts
with NaN(3) to form the V(V) nitride-azide complex [(Tp(tBu,M
63 Contrary to 1, complex 2 reacts
with NaN(3) to produce an azide-bridged dimer, [{(Tp(tBu,Me))
64 Compound 18 reacts
with NaN3 to yield azide-substituted CB[7] 19 in 81% yield, w