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1 e donors (such as 1-propamine 3-(2-hydroxy-2-nitroso-1-propylhydrazine (PAPA) NONOate and diethylamin
2 amine [SNAP] or PAPA NONOATE, 3-[2-Hydroxy-2-nitroso-1-propythdrazinol]-1-propanamine], NOC-15 [PAPA-
3  study of the use of the Fe(III)/3-hydroxy-4-nitroso-2,7-naphthalenedisulfonic acid (NRS) complexes o
4 othiazolidine-4-carboxylic acid (NTCA) and N-nitroso-2-methyl-thiazolidine-4-carboxylic acid (NMTCA)
5                          Reactions between 1-nitroso-2-naphthols and alpha-functionalized ketones suc
6 e (MNPZ), nitrosodiethanolamine (NDELA), and nitroso-(2-hydroxyethyl) glycine (NHeGly) were measured
7 in the initial formation of MNX (hexahydro-1-nitroso-3,5-dinitro-1,3,5-triazine).
8 ino-9H-pyrido[2,3-b]indole (HONH-AalphaC), 2-nitroso-9H-pyrido[2,3-b]indole (NO-AalphaC), N-acetyloxy
9 ll in the tandem cycloaddition to afford the nitroso acetal 38a in 77% yield.
10       In addition, the highly functionalized nitroso acetal products can be hydrogenolyzed selectivel
11 be density functional theory calculations on nitroso acetal-to-aminal rearrangements reported by Denm
12  novel dyotropic rearrangement that converts nitroso acetals into tetracyclic aminals was discovered.
13 cycloadditions to form highly functionalized nitroso acetals.
14 m to increasing concentrations of NO donor S-nitroso acetyl penicillamine (SNAP).
15  incorporating the nitric oxide (NO) donor S-nitroso-acetylpenicillamine (SNAP) and silicone oil in c
16 modify tissue constituents, forming S- and N-nitroso adducts and metal nitrosyls implicated in NO sig
17 ArN=O (Ar = 3,5-Me(2)C(6)H(3), Ph) to give C-nitroso adducts that exhibit three different modes of bo
18 ference in S-nitroso-hemoglobin (SNOHb) or S-nitroso-albumin (SNOAlb) using the tri-iodide method and
19  vitro NO donor treatment of human plasma, S-nitroso-albumin did not form with NO exposure <2 microM,
20 is involved in the sequential process, the N-nitroso aldol reaction, followed by Michael addition.
21 1,2-oxazines from phosphinyl- and phosphonyl-nitroso alkenes has been developed.
22  enol ethers to 4-phosphinyl or 4-phosphonyl nitroso alkenes mediated by water itself.
23 (4)(2-), S(2)O(3)(2-) and Co(CN)(6)(3-), and nitroso-amino-pyrimidine receptors in water suggested th
24 er between the Cu center and the coordinated nitroso and diene units.
25 evations resulted in: (1) rapid formation of nitroso and nitrosyl species; (2) moderate short-term ch
26 icantly higher myocardial levels of nitrite, nitroso, and nitrosyl-heme, and displayed a 48% reductio
27 other N-oxidases involved in hydroxylamino-, nitroso-, and/or nitrosugar formation.
28                                            S-nitroso-AS content is regulated by cellular glutathione
29 kyl-substituted allenes to dienes, and final nitroso/butadiene [4 + 2] cycloadditions.
30 t of small molecules and discovered aromatic nitroso, carboxylate, sulfonamide, and arylstibonic acid
31 further advances in the evergreen field of C-nitroso chemistry, including the discovery of new ways t
32                                            S-Nitroso-CoA (SNO-CoA) and its cognate denitrosylases, SN
33  S-nitrosothiols (S-nitroso-GSH (GSNO) and S-nitroso-CoA (SNO-CoA)).
34  its conjugation with nitric oxide to form S-nitroso-CoA (SNO-CoA), and S-nitrosylation of proteins b
35 t (heretofore unknown) that is mediated by S-nitroso-CoA (SNO-CoA).
36 es to conjugated dienes in the presence of a nitroso compound (additive) was studied quantum mechanic
37   Calculated results reveal that the unbound nitroso compound acts as a better proton transferring ag
38 ar hetero-Diels-Alder cycloadduct of an acyl nitroso compound and a 9,10-dimethyl anthracene derivati
39                      We report a method of S-nitroso compound detection using cavity ring-down measur
40 oppose the milk mineral-induced reduction of nitroso compound formation.
41              Several pathways, involving the nitroso compound in a free or bound state to the gold-al
42 g-down detection allows the measurement of S-nitroso compound levels from pico- to nanomole amounts.
43 t appeared that the moderate basicity of the nitroso compound plays a crucial role to reduce the acti
44                                A resin-bound nitroso compound sequestered a single unexpected compone
45 ree radicals, consists of using a nitrone or nitroso compound to "trap" an unstable free radical as a
46   The lower rate of conversion of the (C7-R)-nitroso compound to the corresponding oximes compared wi
47                 The conversion of the (C8-S)-nitroso compound to the E/Z-oximes was approximately 8 t
48 leophilic addition of the protein thiol to a nitroso compound to yield an N-hydroxysulfenamide, which
49   EPR spectroscopic evidence showed that the nitroso compound trapped other transient intermediates t
50 everse isomerization from the oxime to the C-nitroso compound was observed.
51 e structure of the acyl group of the acyloxy nitroso compound.
52                                   Aromatic C-nitroso compounds (Ar-N horizontal lineO) and related sp
53            Fecal content of apparent total N-nitroso compounds (ATNC), nitrosothiols and nitrosyl iro
54                         Nitrite (NO2(-)) and nitroso compounds (E-NO, E = RS, RO, and R2N) in mammali
55  iron, heterocyclic amines, and endogenous N-nitroso compounds (NOC) are proposed to explain this eff
56 a precursor in the endogenous formation of N-nitroso compounds (NOC), which are possible bladder carc
57            Humans are exposed to preformed N-nitroso compounds (NOCs) and endogenous NOCs.
58  been linked to the formation of genotoxic N-nitroso compounds (NOCs) and lipid peroxidation products
59               Metabolic activation of some N-nitroso compounds (NOCs), an important class of DNA dama
60 e exposed to both endogenous and exogenous N-nitroso compounds (NOCs), and many NOCs can be metabolic
61 , heterocyclic aromatic amines (HAAs), and N-nitroso compounds (NOCs).
62 rates of addition of radicals to nitrones or nitroso compounds (spin traps; STs).
63 , we report that appropriately substituted C-nitroso compounds act solely as donors of neutral nitric
64                                    Dietary N-nitroso compounds and endogenous nitrosation are importa
65                         Cured meat increased nitroso compounds and lipoperoxidation in human stools (
66 lative DNA damage rates of three mutagenic N-nitroso compounds and styrene.
67 ction of nitroaromatics to the corresponding nitroso compounds and, subsequently, to hydroxylamine pr
68 ay increase cancer risk as HCAs, PAHs, and N-nitroso compounds are carcinogenic in animal models.
69           After metabolic activation, many N-nitroso compounds are converted into a diazoacetate inte
70                                            C-Nitroso compounds are sources of biologically active neu
71     Together, these results identify acyloxy nitroso compounds as a new class of HNO donors.
72 stry of nitrile oxides, oximes, oxazete, and nitroso compounds as well as S(N)Vin reactions.
73                                       Many N-nitroso compounds can be metabolically activated to give
74                                       Some N-nitroso compounds can be metabolically activated to yiel
75                   These results suggest that nitroso compounds form a general class of thiol-modifyin
76 processed meat could be a strategy to reduce nitroso compounds formed endogenously after consumption.
77                      Humans are exposed to N-nitroso compounds from both endogenous and exogenous sou
78 cient condensation of sulfinic acid and aryl nitroso compounds has been transformed into a chemoselec
79                                    Various N-nitroso compounds have been associated with neural tube
80                                            S-Nitroso compounds have received much attention in biolog
81 approximately 5 pmol of S(15)NO groups for S-nitroso compounds in aqueous solutions.
82 n, milk mineral reduced the concentration of nitroso compounds in feces and small intestinal content.
83 ondary or tertiary amines and amides, form N-nitroso compounds in the presence of nitrite.
84                                These acyloxy nitroso compounds inhibit glyceraldehyde 3-phosphate deh
85 ethod for the synthesis of gem-difluorinated nitroso compounds is described.
86 The most common method to assay biological S-nitroso compounds is to chemically or photochemically re
87                 These results suggest that N-nitroso compounds may influence the risk of ESCC in men,
88 y via endogenous formation of carcinogenic N-nitroso compounds or increased lipid and protein oxidati
89                                            N-nitroso compounds represent a common type of environment
90  agents and highly acidic conditions, form N-nitroso compounds that have been found to be teratogenic
91                      Humans are exposed to N-nitroso compounds through environmental exposure and end
92                    Addition of these acyloxy nitroso compounds to AhpC C165S yields a sulfinic acid a
93 yzed radical addition with in situ-generated nitroso compounds to prepare sterically hindered amines
94  amines, polycyclic aromatic hydrocarbons, N-nitroso compounds, and heme iron.
95  metabolites, phenols, pesticides, nitro and nitroso compounds, and per- and polyfluoroalkyl substanc
96 combined forming the corresponding nitro and nitroso compounds, and the most reactive cis/syn isomer
97                                            N-Nitroso compounds, known animal carcinogens, are formed
98      Nitrate and nitrite are precursors of N-nitroso compounds, which induce tumors of the pancreas i
99 ma by reducing the endogenous formation of N-nitroso compounds.
100 excess carboxylic acid gives various acyloxy nitroso compounds.
101                    Processed meats contain N-nitroso compounds.
102 he acidic medium of stomach to form N- and C-nitroso compounds.
103 nous production of mutagenic aldehydes and N-nitroso compounds.
104 ites because of the increased formation of N-nitroso compounds.
105 ngs and the azo linkage was formed via amine/nitroso condensation; protected forms of three other Abc
106 ed with organic solvent in the presence of a nitroso-containing resin.
107                    [reaction: see text] Acyl nitroso cycloadducts of the alkaloid thebaine undergo an
108 y-alpha,beta-d-glucopyranose-2-)-N2-acetyl-S-nitroso-d,l-penicillaminami de (glycol-SNAP-2) were also
109 NO)(5-MeIm)](+) generates a mixture of the C-nitroso derivative (OEP)Fe(PhNO)(5-MeIm) and (OEP)Fe(Ph)
110 Structures of complexes with the BTZ-derived nitroso derivative CT325 reveal the mode of inhibitor bi
111 ding oximes compared with that of the (C8-S)-nitroso derivative is attributed to the fact that the ac
112 NO or N2O3 as well as the formation of the S-nitroso derivative of hemoglobin, which has also been re
113 e conversion of either the (C7-R)- or (C8-S)-nitroso derivative to the corresponding E/Z-oximes.
114 er (at 40 degrees C) than that of the (C7-R)-nitroso derivative.
115                When we incubated RDX and its nitroso derivatives with XplA, we found that successive
116 es, but could nevertheless degrade all three nitroso derivatives, demonstrating the potential for com
117 ) significantly enhanced the yields of nitro/nitroso derivatives, likely via the production of triple
118 e-7- and -8-oximes and their corresponding C-nitroso derivatives, which are the key intermediates for
119 ticonvulsant drugs, or drugs that may form N-nitroso derivatives.
120 eo- and highly enantioselective synthesis of nitroso Diels-Alder-type bicycloketones using dienamine.
121 troso species in situ, which were trapped in nitroso-Diels-Alder (NDA) reactions with various dienes
122 n accomplished through the one-pot oxidative nitroso-Diels-Alder reaction of N-arylhydroxylamines wit
123  Chiral phosphoric acid-catalyzed asymmetric nitroso-Diels-Alder reaction of nitrosoarenes with carba
124 rse the regioselectivity of the noncatalyzed nitroso-Diels-Alder reaction.
125                                            N-Nitroso-dimethylamine was detected in all examined produ
126                                  The NDA and nitroso-ene reaction pathways of nitroso intermediates w
127 h involves the formation of a C-N bond via a nitroso-ene reaction.
128 ay, 2-nitrosobenzonitrile undergoes a tandem nitroso-ene/intramolecular cyclization to form benzo[c]i
129  Experimental evidence further suggests that nitroso formation occurs substantially by means of oxida
130 e effect of cystine on the transfer of the S-nitroso functional group from the extracellular to the i
131 hanisms by which an S-nitrosothiol (or the S-nitroso functional group) is transferred across cell mem
132 tion between the resulting hydroxylamine and nitroso functional groups.
133 further by increased expression of GFAP by S-nitroso glutathione (GSNO), an NO donor.
134 n of guanylate cyclase but was mimicked by S-nitroso-glutathione (GSNO; an S-nitrosylating agent).
135 ations, GSNO and the constitutively active S-nitroso-glutathione diethyl ester stimulate CFTR transcr
136 d only glyphosate is prone to nitrosation, n-nitroso glyphosate and glufosinate were used as template
137  rotamers with reversed orientation of the 5-nitroso group are observed for compounds with two differ
138 ubstituents; however, the orientation of the nitroso group does not have any influence on the positio
139                                        The 5-nitroso group is able to form strong intramolecular hydr
140                                   The Cys 69 nitroso group is also protected but requires a higher pH
141                     Surprisingly, the Cys 62 nitroso group is completely buried and pointing to the p
142 rotamers differing in the orientation of the nitroso group were observed in the NMR spectra of the co
143   To establish the unique influence of the S-nitroso group, our study describes high resolution three
144             Small molecules containing the N-nitroso group, such as the bacterial natural product str
145  an inert nitro group replacing the reactive nitroso group.
146 2e-, 2H+ oxidation of the hydroxylamine to a nitroso group.
147 hat NH2Cl is the source of the N atom of the nitroso group.
148  X-ray crystallographic analysis reveals the nitroso groups possess a "nitroxyl-like" bent configurat
149 ow-molecular-weight (LMW) S-nitrosothiols (S-nitroso-GSH (GSNO) and S-nitroso-CoA (SNO-CoA)).
150 and amplification of the N-Methyl-N'-nitro-N-nitroso-guanidine (MNNG) HOS transforming gene (MET) onc
151                     Using N-methyl-N-nitro-N-nitroso-guanidine mutagenesis and selection, a mutant st
152 r the complete carcinogen 1-methyl-3-nitro-1-nitroso-guanidine or two-stage initiation and promotion
153 P activation in lungs of N-methyl-N'-nitro-N-nitroso-guanidine-treated mice or H(2)O(2)-treated cells
154 agens, 5-azacytidine and N-methyl-N'-nitro-N-nitroso-guanidine.
155 axation is inhibited by prior depletion of S-nitroso-Hb, potentiated by low-molecular-weight thiols,
156  Quantitatively there was no difference in S-nitroso-hemoglobin (SNOHb) or S-nitroso-albumin (SNOAlb)
157 ic oxidant in the final oxidation of an aryl-nitroso intermediate to the aryl-nitro product.
158                    Mechanisms via a detected nitroso-intermediate are proposed for oxidative cyclizat
159 sent in these compounds to the corresponding nitroso intermediates by addition at the unsubstituted e
160 esting that the formation of highly reactive nitroso intermediates is essential for target inactivati
161                  Research has shown that the nitroso intermediates of BTZs that are generated in vivo
162 The NDA and nitroso-ene reaction pathways of nitroso intermediates with dienes were mapped by DFT com
163 r similar to the von Richter reaction to the nitroso intermediates, to initiate the inhibition of Dpr
164 oarenes to nitroarenes via hydroxylamine and nitroso intermediates.
165 to N(delta)-hydroxy-N(omega)-methyl-N(omega)-nitroso-l-citrulline, the proposed donor of the function
166 sport of amino acid-based S-nitrosothiols (S-nitroso-L-cysteine and S-nitrosohomocysteine) occurs via
167                                      Using S-nitroso-L-cysteine-ethyl ester (SNCEE) and S-nitrosoglut
168                                   By using S-nitroso-l-cysteine-ethyl-ester, an intracellular NO dono
169 on, whereas exposure of RAW 264.7 cells to S-nitroso-l-glutathione, a NO donor, triggered LKB1 S-nitr
170 n vitro by the nitric oxide donor compound S-nitroso-L-glutathione, failed to exhibit glucose-induced
171 st, DDAH-1 is sensitive to inactivation by S-nitroso-L-homocysteine (3.79 M(-1) s(-1)).
172 nhibition by L-homocysteine, H(2)O(2), and S-nitroso-L-homocysteine is quantified.
173 e maintenance of steady-state tissue nitrite/nitroso levels and illustrate the consequences of nitrit
174  terminal NO(2) group, probably to form a Ti-nitroso linkage between NAB and Ti.
175 acterized microbial reservoir of bioactive N-nitroso metabolites.
176 ctive in the oxygenation of p-anisidine to 4-nitroso-methoxybenzene.
177                                            S-Nitroso modifications of cysteines 62 and 69 are clearly
178  substrates providing synthetically useful N-nitroso N-alkyl nitroanilines in excellent yields which
179 s by others showed that administration of 4-(nitroso)-N-(5-methyl-1,2-oxazol-3-yl)benzenesulfonamide
180  of a series of differentially O-protected N-nitroso-N-acetyl sialyl glycosides and of isotopic label
181 hanism of the oxidative deamination of the N-nitroso-N-acetyl sialyl glycosides leading with overall
182 , with an excess of NO(g) or NO-generators S-nitroso-N-acetyl-D,L-pencillamine and diethylamine NONOa
183 oduction fell with both AI and addition of S-nitroso-N-acetyl-d,l-penicillamine (a NO donor) but was
184 EMP levels by 3-fold, whereas the NO donor S-nitroso-N-acetyl-D,L-penicillamine (SNAP) decreased it.
185                                            S-nitroso-N-acetyl-D,L-penicillamine (SNAP), a NO donor, w
186 o acetylcholine and the nitric oxide donor S-nitroso-N-acetyl-D,L-penicillamine that were restored by
187 of nitrosothiols (S-nitrosoglutathione and S-nitroso-N-acetyl-d,l-penicillamine), nitric oxide, oxidi
188 lled release vehicles for NO, the NO donor S-nitroso-N-acetyl-D-penicillamine (SNAP) was encapsulated
189 ctive agents, S-nitrosoglutathione (GSNO), S-nitroso-N-acetyl-dl-penacillamine, and sodium nitropruss
190 e migraine trigger NTG or another NO donor S-nitroso-N-acetyl-DL-penicillamine (SNAP) at doses releva
191                               The NO donor S-nitroso-N-acetyl-DL-penicillamine (SNAP) rapidly reduced
192  SN56) following exposure to the NO donors S-nitroso-N-acetyl-dl-penicillamine (SNAP), 3-morpholinosy
193 nhibition of HDAC activity, since GSNO and S-nitroso-N-acetyl-dl-penicillamine significantly and reve
194                         The NO donor SNAP (S-nitroso-N-acetyl-DL-penicillamine) and a soluble guanyly
195  sensory neurons from the TG the NO donor, S-nitroso-N-acetyl-dl-penicillamine, inhibited M-current.
196 with either vehicle or nitric oxide donor (S-nitroso-N-acetyl-penicillamine [SNAP] or PAPA NONOATE, 3
197                       NAC was converted to S-nitroso-N-acetylcysteine (SNOAC), decreasing erythrocyti
198  deficient fatty acid beta-oxidation, with S-nitroso-N-acetylcysteine induced site-specific S-nitrosy
199 e.g., nitrosocysteine, nitrosoglutathione, S-nitroso-N-acetylcysteine, S-nitrosoalbumin) present in t
200 not higher (100-500 mum), concentration of S-nitroso-N-acetylpenicillamine (SNAP) can reverse the eff
201                               The NO donor S-nitroso-N-acetylpenicillamine (SNAP) induced apoptosis w
202 e (CSNO), S-nitrosoglutathione (GSNO), and S-nitroso-N-acetylpenicillamine (SNAP) reversibly oxidized
203  The vasodilation elicited by the NO donor S-nitroso-N-acetylpenicillamine (SNAP) was inhibited by OD
204 death and nitrite levels at 24 h caused by S-nitroso-N-acetylpenicillamine (SNAP), a direct nitric ox
205 reatment with the nitric oxide (NO) donor, S-nitroso-N-acetylpenicillamine (SNAP), and the phosphodie
206                               The NO donor S-nitroso-N-acetylpenicillamine (SNAP), at all concentrati
207 rons (CGNs) by treatment with the NO donor S-nitroso-N-acetylpenicillamine (SNAP), for short (6 h) or
208 ly enhanced TH17 cell differentiation, and S-nitroso-N-acetylpenicillamine (SNAP), the NO donor, dose
209 were exposed to combinations of NO donors (S-nitroso-N-acetylpenicillamine [SNAP] and others), a cGMP
210 iolate (NOC-18), S-nitrosoglutathione, and S-nitroso-N-acetylpenicillamine also suppressed CYP2B prot
211                               The NO donor S-nitroso-N-acetylpenicillamine decreases ceramide-induced
212  promoter, in which the nitric oxide donor S-nitroso-N-acetylpenicillamine reduces urea transporter-A
213    Increasing levels of nitric oxide using S-nitroso-N-acetylpenicillamine resulted in a decrease in
214 erated by the addition of 400 microM SNAP (S-nitroso-N-acetylpenicillamine) caused a 10-fold increase
215  enhances M1 macrophage polarization while S-nitroso-N-acetylpenicillamine, a NO donor, suppresses M1
216 ced response, the vasodilation elicited by S-nitroso-N-acetylpenicillamine, an NO donor that activate
217 onophore ionomycin, the nitric oxide donor S-nitroso-N-acetylpenicillamine, and the protein kinase G
218 erestingly, treatment of EC with NO donor, S-nitroso-N-acetylpenicillamine, did not activate SREBP, s
219                When FLS were cultured with S-nitroso-N-acetylpenicillamine, the pattern of MMR expres
220 ted the relaxation induced by the NO donor S-nitroso-N-acetylpenicillamine.
221 nic conditions with the nitric oxide donor S-nitroso-N-acetylpenicillamine.
222 ains to the prototypical alkylating agent, N-nitroso-N-ethylurea (ENU).
223                    A three-generation ENU (N-Nitroso-N-ethylurea)-based forward genetic screen was pe
224                Experiments with deuterated N-nitroso-N-methyl-N-ethylamine demonstrated that the lowe
225 ur nitrosamines (N-nitrosodiphenylamine 1, N-nitroso-N-methylaniline 2, N-butyl-N-(4-hydroxybutyl)nit
226 lated crops such as maize, we conducted an N-nitroso-N-methylurea (NMU) mutagenesis of S. viridis and
227 lever rats (n = 20 per group) treated with N-nitroso-N-methylurea and testosterone to induce prostate
228  precedes the NAD(+) depletion in N-methyl-N-nitroso-N-nitroguanidine (MNNG)-treated cortical neurons
229 myotubes treated with nitric oxide donors, S-nitroso-N-penicillamine (SNAP, 25 muM) or diethylenetria
230 rosomorpholine by hydroxylation alpha to the nitroso nitrogen can result in the deposition of a metas
231 mes (ORFs) in in vitro-cultivated 1-methyl-3-nitroso-nitroguanidine (MNNG)-treated and untreated spir
232 ring the ischemic phase, with an increase in nitroso/nitrosyl products in the heart.
233                           Neither the (C7-R)-nitroso- nor (C8-S)-nitrosobicycloheptane system require
234 itrosamino)-1-(3-pyridinyl)-1-butanone and N-nitroso nornicotine were also detected.
235 tures, the nitrene reacts with O2 to produce nitroso O-oxide mainly in its syn conformation.
236 n so that it occurs via the cis/anti form of nitroso oxide independently on the nature of a meta subs
237 dation of 1a, whereas transformations of the nitroso oxide isomers derived from 1b led to a set of st
238 Upon visible light irradiation (450 nm), the nitroso oxide rapidly rearranges to nitrobenzene.
239 e DFT simulation and kinetic modeling of the nitroso oxide transformations as well as the product ana
240 he reaction proceeds via the cis/syn form of nitroso oxide with a regioselectivity of 91%.
241 onds and asymmetric molecule structure these nitroso oxides exist as four conformers (cis/syn, cis/an
242 regioselectivity of the ortho-cyclization of nitroso oxides was explained using theoretical methods.
243 rmed as a result of these transformations of nitroso oxides, are stabilized by [3 + 2] cycloaddition
244 iates of this reaction are the corresponding nitroso oxides, the unimolecular consumption of which oc
245 larities of the consumption of corresponding nitroso oxides, which are the reaction intermediates, we
246                       The formation of nitro/nitroso probe derivatives was evidenced by high-resoluti
247 converts o-aminophenols to the corresponding nitroso product (hydroxyanilinase activity).
248 NOS) expression, nitrate/nitrite production, nitroso product formation, peroxynitrite accumulation, a
249 orates were converted into the corresponding nitroso products in good to excellent yields.
250 luding plasma and red blood cell nitrate and nitroso proteins and plasma nitrite, but lower concentra
251                                     The 29 S-nitroso proteins identified are all enzymes, mostly serv
252  the emission of nitric oxide (NO) and the S-nitroso-proteome of IE and non-isoprene-emitting (NE) gr
253 their S-nitrosylation pattern, the in vivo S-nitroso-proteome of the NE genotype was more susceptible
254 rimidines and the stability of the resulting nitroso radical cations, the structures of which are det
255    The tert-butyl N-hydroxycarbamate-derived nitroso reagent 1 reacted with N-Cbz-protected spirocycl
256 then undertaken to exploit the hydroxylamine/nitroso redox couple using LC-DED detection for the meas
257 lmonary bypass and reperfusion on myocardial nitroso-redox balance in patients undergoing cardiac sur
258 valuated excitation-contraction coupling and nitroso-redox balance in spontaneously hypertensive hear
259 dative stress), and that therapies restoring nitroso-redox balance in the heart could prevent sudden
260 ntrol both the redox- and NO-based pathways (nitroso-redox homeostasis), which subserve innate and ce
261     Together these findings demonstrate that nitroso-redox imbalance causes RyR2 oxidation, hyponitro
262                        Finally, we show that nitroso-redox imbalance due to decreased NOS1 activity s
263                    Our findings suggest that nitroso-redox imbalance is an important mechanism of ven
264 , patient-derived CS cells displayed greater nitroso-redox imbalance than UV(S)S cells.
265 Ca(2+) cycling and contractility impaired by nitroso-redox imbalance, and NTG enhanced contractile ef
266                        We used two models of nitroso-redox imbalance, neuronal NO synthase-deficient
267 yponitrosylated in heart failure, because of nitroso-redox imbalance.
268 of reactive nitrogen species, a situation of nitroso-redox imbalance.
269                          Hence, rescuing the nitroso-redox levels is a potential therapeutic strategy
270 ontractile function in myocytes with altered nitroso-redox levels.
271  myocytes experiencing an imbalance of their nitroso-redox levels.
272                                          The nitroso resin selectively sequestered a single compound,
273 ack-transformation to SMX was observed for 4-nitroso-SMX, indicating that this metabolite may serve a
274 orin heme, but it can also be stored as an S-nitroso (SNO) conjugate of the proximal heme cysteine (C
275 he hemoglobin beta chain (beta93C) to form S-nitroso (SNO) hemoglobin (Hb) is claimed to be essential
276           Evidence for the pivotal role of S-nitroso (SNO) hemoglobin in mediating this response is d
277 s (B3LYP/6-31G*), which showed that the acyl nitroso species are super-reactive and that activation e
278 s considered to result from reduction of the nitroso species back to the hydroxylamine species.
279 pping studies indicate the intermediacy of a nitroso species during this reaction.
280 nd 2-ethyl-2-oxazoline in methanol gave acyl nitroso species in situ, which were trapped in nitroso-D
281 ow, the main decomposition pathway for the S-nitroso species leads to formation of nitric oxide.
282 hot5 null alleles show increased nitrate and nitroso species levels, and the heat sensitivity of both
283 form the nitroso species, hydrolysis of this nitroso species to produce nitroxyl, and reductive nitro
284 ation of hydroxyurea by catalase to form the nitroso species, hydrolysis of this nitroso species to p
285 (TDP)-l-epi-vancosamine to the corresponding nitroso sugar.
286 e four-electron oxidation of amino sugars to nitroso sugars.
287 hus, we have used a T cell-priming assay and nitroso sulfamethoxazole (SMX-NO) as a model Ag to inves
288 zole, sulfamethoxazole beta-D-glucuronide, 4-nitroso sulfamethoxazole, and 4-nitro sulfamethoxazole w
289 llin, and dicloxacillin, but not abacavir or nitroso sulfamethoxazole.
290 (flucloxacillin, amoxicillin, isoniazid, and nitroso-sulfamethoxazole) to characterize the proteins p
291                       However, exosomes from nitroso-sulfamethoxazole-treated hepatocytes selectively
292 dified with amoxicillin, flucloxacillin, and nitroso-sulfamethoxazole.
293 te formation appears to be linked to N --> O nitroso transfer between the N-benzyl-N-nitrosoamides an
294                 Benzo(a)pyrene [B(a)P] and N-nitroso-tris-chloroethylurea (NTCU) were used to induce
295 ight different inbred strains of mice with N-nitroso-tris-chloroethylurea by skin painting and found
296 ces in susceptibility to Lscc induction by N-nitroso-tris-chloroethylurea with NIH Swiss, A/J, and SW
297  in the presence of iron, large amounts of N-nitroso-tryptophan can be formed even at neutral pH, as
298 , enzymes dedicated to the assembly of the N-nitroso unit have not been identified.
299 guanine (O6BG) and N,N'-bis(2-chloroethyl)-N-nitroso-urea (BCNU) stably increased the percentage of t
300 ine, first to the hydroxylamine and then the nitroso, while linked to the carrier protein of PvfC.

 
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