ライフサイエンスコーパス: NO donor

1 of 8-bromo-cGMP or sodium nitroprusside (an NO donor).

2 ugs was reversed by S-nitrosoglutathione, an NO donor.

3 dnd1 can be complemented by application of a NO donor.

4 LPS-induced death that was reversed with an NO donor.

5 y better at 34% with a donor versus 25% with no donor.

6 ype could be rescued by the application of a NO donor.

7 ibitory effects on platelet activation by an NO donor.

8 nduces fetal Hb production and can act as an NO donor.

9 endothelial cells, which was prevented by an NO donor.

10 e expression of microglial CD11b by GSNO, an NO donor.

11 of GFAP by S-nitroso glutathione (GSNO), an NO donor.

12 d a donor, or autologous SCT if in MMolR and no donor.

13 h reaccumulated in the presence of exogenous NO donor.

14 han complex and the NO release rate from the NO donor.

15 when MPhi were reoxygenated or exposed to a NO donor.

16 tive manner compared to low molecular weight NO donors.

17 gnificantly inhibited by treatment with both NO donors.

18 and -independent inhibition of platelets by NO donors.

19 ity contribute to the IOP-lowering effect of NO donors.

20 em cells revealed a lack of stimulation with NO donors.

21 er, acquired the ability to be stimulated by NO donors.

22 of cells to the different concentrations of NO donors.

23 nt, all of which increased after exposure to NO donors.

24 lecule-1 (ICAM-1) blockade or treatment with NO donors.

25 of released NO over existing macromolecular NO donors.

26 amine NONOates, which are well-characterized NO donors.

27 ation and myocardial protection activated by NO donors.

28 on of secondary amines to N-diazeniumdiolate NO donors.

29 ut only after prolonged (>5 min) exposure to NO donors.

30 onors show biological effects different from NO donors.

31 g and/or BH4 was markedly potentiated by the NO donor 1-(hydroxy-NNO-azoxy)-l-proline, disodium salt

32 ncrease in Ca(2+) in ICC-MY, whereas SNP (an NO donor, 10 muM) abolished all activity in ICC-MY.

33 of guanylate cyclase (GC) with and without a NO donor; (2) application of stable cGMP analogue; and (

34 n intracellular NO following addition of the NO donor 3-(2-hydroxy-1-methyl-2-nitrosohydrazino)-N-met

35 were also confirmed in vitro using both the NO donor 3-morpholinosydnonimine and peroxynitrite.

36 ntaining furoxanyl subunits as nitric oxide (NO)-donors (3a-g) were designed, synthesized, and evalua

37 Incubation of the cells with an NO donor abrogated the RNS60-mediated upregulation of Fo

38 evolved WT dihydrofolate reductase requires no donor-acceptor distance fluctuations (no gating).

39 iltrate following topical application of the NO donor-acidified nitrite (NO2(-)), has set the paradig

40 lished and was not reversed by nitric oxide (NO) donor administration; endothelial NO synthase (eNOS)

41 However, lower concentrations of NO donors also stimulate rapid and unequivocal nuclear r

42 NONOate, an NO donor, also activated GSK3beta, indicating that NO ma

43 A donor versus no-donor analysis showed that Philadelphia chromosome-ne

44 s part of first-line therapy, a donor versus no-donor analysis was performed of patients treated in t

45 ligible for allogeneic SCT in a donor versus no-donor analysis.

46 the target enzyme, 5a-k,m showed additional NO donor and antioxidant properties, thus emerging as no

47 A NO donor and AT1-R antagonist reversed CAO-enhanced chem

48 oso-l-cysteine-ethyl-ester, an intracellular NO donor and inhibitor of APLT, we showed that PS and CR

49 Blunted dilatory responses to an NO donor and loss of myogenic tone in KW animals were al

50 Interestingly, the NO donor and nitrosylating agent SNAP reversed the depre

51 essary to efficiently decompose the released NO donor and obtain sustained NO release.

52 f IFN-gamma was reproduced by exposure to an NO donor and reversed by the iNOS inhibitor.

53 The addition of an NO donor and rIFN-alpha to RAW 264.7 cells caused HMGB1

54 LC2) mRNA expression on exposure of cells to NO donors and a decrease in mRNA expression of both card

55 east cancer by targeted delivery of NO where NO donors and activators of downstream players could ini

56 mulate cGMP accumulation, the combination of NO donors and BAY 41-2272 stimulated cGMP levels more th

57 s of liver sinusoidal ECs can be mimicked by NO donors and can be reversed by NO inhibitors in vivo a

58 us, these compounds may act as intracellular NO donors and could augment a killing mechanism intrinsi

59 Indeed, both NO donors and endothelial NO synthase overexpression pro

60 ated decomposition of the N-diazeniumdiolate NO donors and greater NO-release payloads.

61 n S-nitrosylation resembling that induced by NO donors and GSNO.

62 drimers allows for the future combination of NO donors and other functionalities on a single molecula

63 Application of specific NO donors and scavengers inhibited the calcium-dependent

64 xpression of marker genes were observed when NO donors and sGC activators were combined.

65 Here, we demonstrate the effect of NO donors and soluble guanylyl cyclase (sGC) activators

66 ric oxide (NO) scavenging and ameliorated by NO donors and the NO-donor properties of hydroxyurea (HU

67 ed for anaerobic defense against exposure to NO donors and to resist NO-dependent effects of gamma in

68 PBMCs were cultured with a nitric oxide (NO) donor and SLE or control plasma, with or without hea

69 inhibited by sodium nitroprusside (SNP), an NO donor, and l-arginine, the endogenous substrate for N

70 mained unchanged in cells subjected to L-NA, NO donors, and bradykinin in a time- and concentration-d

71 and finer therapeutic control over classical NO donors, and may be better suited for oral delivery to

72 s enhanced in wild-type and mutant plants by NO donors, and the heat sensitivity of hot5 mutants can

73 ts of nrfA and ytfE exhibited sensitivity to NO donors, and the ytfE gene was more critical for survi

74 penicillamine (SNAP), a direct nitric oxide (NO) donor, and successfully quenched 1,1-Diphenyl-2-picr

75 r and recipient was classified as D = 0 when no donor antigens were foreign to the recipient vs D >/=

76 that provide both total NO release from the NO donor as well as instantaneous NO concentrations.

77 ota of specific pathogen-free MyD88-negative NOD donors attenuates T1D in germ-free NOD recipients.

78 a will be of relevance to the development of NO donor-based therapies for CF.

79 outcomes on an intention-to-treat, donor vs no-donor basis were identified.

80 on without brain death [n = 5]; and Group 3: no donor brain death with <1 h of ventilation [n = 6]).

81 number of therapies utilizing gaseous NO or NO donors capable of storing and delivering NO have been

82 umbilical vein endothelial cells (HUVECs) to NO donors caused an increase in phosphorylation of both

83 Exposure of human spermatozoa to NO donors caused mobilisation of stored Ca(2+) by a mech

84 We observed that NO donor compound sensitized lymphomas to dendritic cell

85 on with the stimulon of NO released from two NO donor compounds {3-[2-hydroxy-1-(1-methyl-ethyl)-2-ni

86 l utility of NO gas and low molecular weight NO donor compounds.

87 activation of (pro)MMP-9 using a variety of NO-donor compounds and characterized modifications of th

88 damaging and high (500 microM), DNA-damaging NO donor concentrations were shown.

89 g materials, including decreased leaching of NO donor, controlled release of NO, and maintenance of u

90 NO donor DEA-NONOate (1 to 100 nmol/L) reversed thrombin

91 also treated with the same agents +/- and an NO donor (DEA/NO) and cGMP quantified.

92 ld-type protein was allowed to react with an NO donor, DEA/NO, followed by buffer exchange.

93 No donor death occurred and all donors had full recovery

94 Here, we show that iNOS and NO donor decreased IRS-2 protein expression in INS-1/832

95 Incubation with the NO donor DETA-NO inhibited VIC osteogenic differentiatio

96 In this study, we used the NO donor DETA-NO to model NO exposure to cervical epithe

97 Low concentrations of the NO donor, DETA NONOate (<200 microM), exclusively nitrat

98 Finally, the NO donor DETAnonoate causes further vasoconstriction in

99 e cortical astrocytes with the nitric oxide (NO) donor DetaNONOate induced a time-dependent enhanceme

100 When HRP were incubated with an NO. donor, DETANONOATE ((Z)-1-[2-(2-aminoethyl)-N-(2-amm

101 OVA-sensitized mice treated with an NO donor developed more severe airway inflammation.

102 uppressed by inhibition of NO formation, but NO donors did not mimic or occlude channel inhibition by

103 K2 and was prevented by coperfusion with the NO-donor diethylamine NONOate.

104 Consistent with this, an NO donor, diethylamine nitric oxide (DEANO), induced TGF

105 BL/6 mice and determined the abilities of an NO donor, diethylamine NONOate (DEANO), and a single dos

106 type but not iNOS-null mice treated with the NO donor diethylene triamine/NO 24 hours before ischemia

107 r to and after exposure to 250 microM of the NO donor diethyleneamine/nitric oxide adduct (DETA-NO).

108 s of human bronchial epithelial cells to the NO donor diethylenetriaamine NONOate.

109 The NO donor diethylenetriamine/NO recapitulated the effects

110 her pretreatment of hCSCs with a widely used NO donor, diethylenetriamine nitric oxide adduct (DETA-N

111 adipocytes after a chronic treatment with an NO donor: diethylenetriamine-NO (DETA-NO).

112 In contrast, the NO donors dipropylenetriamine NONOate and sodium nitropr

113 how that NO supplementation in the form of a NO donor (dipropylenetriamine NONOate [DPTA-NO]) prevent

114 S-nitroso-N-acetylpenicillamine (SNAP), the NO donor, dosedependently reduced the percentage of IL-1

115 Parent NO donor drug activity was optimized in advance of gluta

116 Here, we developed N-hydroxyguanidine NO donor drugs that were protected against spontaneous N

117 Application of a NO donor effectively rescues many dnd1 senescence-relate

118 hesis was the finding that unlike those from NOD donors, engraftment with B cells from H2g7 MHC-match

119 g a porous structure without leaching of the NO donor, even in serum.

120 Okadaic acid also had no effect on NO donor-evoked adenosine accumulation, which previously

121 Mimicking the action of NO donors, exogenous H2O2 potentiated pinacidil-preactiv

122 Notably, Flt3 ligand (FL) treatment of NOD donors expanded FC total in peripheral blood and res

123 No donor experienced complications related to G-CSF admi

124 No donor experienced more than grade 1 toxicity.

125 The effects of NO donor exposure were antagonized by application of NO

126 Surprisingly, NO donors failed to induce apoptosis in LNCaP cells, sug

127 gesting a possibility of utilizing such live NO donors for research and clinical needs.

128 represent an additional beneficial effect of NO donors for therapy of portal hypertension.

129 a H2S donor) or sodium nitroprusside (SNP, a NO donor) for 2 days (d) could elicit long-lasting primi

130 dinol (SA-2) containing both antioxidant and NO donor functionalities that provide a therapeutic leve

131 dihydroartemisinin scaffold is combined with NO-donor furoxan and NONOate moieties have been synthesi

132 was 16% in the donor group versus 3% in the no-donor group (P < .001).

133 The 3-year RFS rates in the donor and no-donor groups were 71% and 47%, respectively (P = .005

134 148), the 3-year RFS rates in the donor and no-donor groups were 83% and 53%, respectively (P = .004

135 In the presence of NO donors, H(2)O(2)-induced oligomeric forms of cyt c po

136 At study initiation, no donor had detectable CMV replication, five had EBV re

137 No donor had detectable CMV replication; therefore, its

138 e (NO), a new class of glycosidase activated NO donors has been developed.

139 refore, the combination of QS inhibitors and NO donors has the potential to control the development o

140 Nitric oxide (NO) donors have been shown to stimulate and inhibit the

141 deposition, in patients whose sera contained no donor human leukocyte antigen (HLA)-specific antibody

142 Inspired by these ideas, novel fimbrolide-NO donor hybrid compounds were designed and synthesized.

143 Artemisinin-NO-donor hybrid compounds show promise as potential new

144 S-derived NO are reproduced by exogenous NO (NO donors), implying that nitrates can upregulate cardia

145 lly to localize sGC that was activated by an NO donor in amacrine, bipolar, and ganglion cells.

146 s and total amounts of NO from commonly used NO donors in commercially available cell media routinely

147 unique advantage over conventional chemical NO donors in generating continuous, readily controllable

148 n cellular environments and (ii) "trackable" NO donors in photodynamic therapy of malignancies (such

149 ethyl-1-propyanamine], validating the use of NO donors in studies of neuronal excitability.

150 S-nitrosoglutathione (GSNO; a physiological NO donor) in astrocytes in vitro settings.

151 tems over previously reported macromolecular NO donors include the ability to (1) store large quantit

152 Exposure to NO donors increased protein glutathiolation in COS-7 or

153 thase (NOS); however, cell pretreatment with NO donors (increasing cellular S-nitrosothiol contents)

154 eNOS in lymphatic endothelial cells and that NO donors induce proliferation and/or survival of cultur

155 For Jurkat cells, poly(I:C) and NO donors induced apoptosis as well as HMGB1 release.

156 A-mediated knockdown significantly prevented NO donor-induced reduction in IRS-2 expression in beta-c

157 hibitors, MG132 and lactacystin, blocked the NO donor-induced reduction in IRS-2 protein expression.

158 The administration of an NO donor inhibited fructose-induced ICAM-1 expression, w

159 A NO donor inhibited OT II T cell receptor recognition of

160 In conclusion, in ischemic myocardium an NO donor inhibits glucose uptake and lactate production

161 The introduction of a nitric oxide (NO) donor into the alkyl side chain of dorzolamide (1) a

162 that S-nitrosylation of MMP-9 propeptide by NO-donors is unrelated to their ability to regulate MMP-

163 ly, treatment of tumor-bearing mice with the NO donor JS-K significantly reduced metastases.

164 Treatment with NO donor led to activation of glycogen synthase kinase-3

165 as) cells with DETA NONOate, a nitric oxide (NO)-donor led to induction of MAP-kinase phosphatase -1

166 NO2)and not mediated by LNO2 decay products, NO donors, linoleic acid (LA), or oxidized LA.

167 dify needle-type glucose biosensors with the NO donor-loaded fibers.

168 st that the context-dependent application of NO donors may hold promise for prevention of metastatic

169 er, recipients of thymi from 7- and 10-d-old NOD donor mice remained diabetes-free and exhibited a pr

170 MMP) inhibitor incorporating a nitric oxide (NO) donor/mimetic group (series 1).

171 The primary analysis was the no-donor-mixture cohort (ie, either all red blood cell t

172 mple type, NO produced from a small-molecule NO donor (N-diazeniumdiolated l-proline, PROLI/NO) and a

173 udy, we investigated the effect of exogenous NO donor (NaNO2) on corneal wound healing.

174 r Ly49 ligand-matched, ligand-mismatched, or no donor NK cells.

175 Bath application of the NO donor NOC-18 increased the single-channel activity of

176 d repair, which was prevented by PEG-SOD and NO donor NOC-18.

177 The NO donor NOC-22 prevented permeability transition in iso

178 are similar to NO release from the chemical NO donor NOC-7 [3-(2-hydroxy-1-methyl-2-nitrosohydazino)

179 The NO donors NOC-18 and N-(2-deoxy-alpha,beta-d-glucopyrano

180 ulates this process utilizing a slow-release NO donor (NOC-18) and studying changes in cellular SNO-G

181 the presence of reduced glutathione and the NO-donor NOC12, with no effect in the presence of oxidiz

182 149 mediated either chemically with a strong NO donor or by trans-nitrosylation with GSNO.

183 ity of arteriolar smooth muscle to dilate to NO donor or contract to ET-1 was unaffected throughout t

184 n or c-Jun deficiency, but aggravated by the NO donor or iNOS-inducing cytokines.

185 d endogenously in response to exposure to an NO donor or oxidized low-density lipoproteins (oxLDL) in

186 xyhemoglobin prevents formation from either *NO donor or S-nitrosocysteine, the latter treatment resu

187 and murine endothelial cells in response to NO donors or bradykinin.

188 lts indicate that peroxynitrite arising from NO donors or pathological stimuli such as oxLDL triggers

189 d tube formation in GSNOR(-/-) MSCs, whereas NO donors or PDGFR antagonist reduced tube formation app

190 abolished cGMP production induced by either NO donors or platelet agonists, caused a marked defect i

191 c peptides), trepostinil, inorganic nitrate (NO donor), or a PDE5 inhibitor.

192 An NO donor, or saline, was injected intravitreously into n

193 erence is that exposure to the nitric oxide (NO) donor, PAPA-NONOate (1.5 microm), significantly decr

194 The exogenous NO donor PapaNONOate or the cyclic guanosine 3',5'-monop

195 e and (iii) in C57BL/6 mice treated with the NO donor pentaerythritol tetranitrate (PETN), the NOS in

196 utellarin, hemoglobin, DETA/NO (nitric oxide(NO) donor), PITO (NO scavenger), 8-Br-cGMP (cGMP analog)

197 f either atrial natriuretic peptide (ANP) or NO donors potentiated the inhibitory effects of MPB-fors

198 rogel films modified with N-diazeniumdiolate NO donor precursors and the fluorescent pH indicator sem

199 The addition of exogenous NO using a NO donor prevented the reduction in iNOS levels caused b

200 with high concentrations of a rapid-release NO donor prevents biofilm formation when supplied early

201 This new type of hybrid NO donor prodrug represents an attractive approach for t

202 Ubiquitous small-molecule NO donors promote the AR S-nitrosylation and inhibit gro

203 All compounds (3a-g) demonstrated NO-donor properties at different levels.

204 venging and ameliorated by NO donors and the NO-donor properties of hydroxyurea (HU).

205 Because a topical NO donor raises EVP and a topical NO synthase inhibitor

206 Thus, a simple NO donor recapitulates the vasoregulatory actions of sar

207 e onset of heartbeat; however, nitric oxide (NO) donors regulated HSC number even when treatment occu

208 Generation of NO by an NO donor reproduced the inhibitory effect of the cytokin

209 logeneic EC, and addition of low levels of a NO donor rescues T cell responses.

210 nd a nitric oxide synthase (NOS)-independent NO donor restored NO-dependent vascular reactivity in hu

211 SS-induced EMP levels by 3-fold, whereas the NO donor S-nitroso-N-acetyl-D,L-penicillamine (SNAP) dec

212 ific controlled release vehicles for NO, the NO donor S-nitroso-N-acetyl-D-penicillamine (SNAP) was e

213 ation of the migraine trigger NTG or another NO donor S-nitroso-N-acetyl-DL-penicillamine (SNAP) at d

214 The NO donor S-nitroso-N-acetyl-DL-penicillamine (SNAP) rapi

215 The vasodilation elicited by the NO donor S-nitroso-N-acetylpenicillamine (SNAP) was inhi

216 granule neurons (CGNs) by treatment with the NO donor S-nitroso-N-acetylpenicillamine (SNAP), for sho

217 and prevented the relaxation induced by the NO donor S-nitroso-N-acetylpenicillamine.

218 tured vascular smooth muscle cells, both the NO donor S-nitrosocysteine and atrial natriuretic peptid

219 found that treatment with the physiological NO donor S-nitrosoglutathione (GSNO) increased the abund

220 itch assay, we found that application of the NO donor S-nitrosoglutathione (GSNO) or diethylammonium

221 MKIIdelta) activity after treatment with the NO donor S-nitrosoglutathione (GSNO).

222 However, the NO donor S-nitrosoglutathione induced closure of uvr8-1

223 s that display excessive accumulation of the NO donor S-nitrosoglutathione, it rescued immunity in no

224 expression of dynamin2 or treatment with the NO donor S-nitrosothiols increases, whereas targeted red

225 s created by incorporating the nitric oxide (NO) donor S-nitroso-acetylpenicillamine (SNAP) and silic

226 that in rat sensory neurons from the TG the NO donor, S-nitroso-N-acetyl-dl-penicillamine, inhibited

227 Interestingly, treatment of EC with NO donor, S-nitroso-N-acetylpenicillamine, did not activ

228 tase 1 (GSNOR1) which turns over the natural NO donor, S-nitrosoglutathione (GSNO).

229 The addition of the NO donor, S-nitrosoglutathione, to isolated cell lysates

230 produced by treatment with the nitric oxide (NO) donor, S-nitroso-N-acetylpenicillamine (SNAP), and t

231 has been described that animals treated with NO donors showed increased permeability due to modulatio

232 cells with the iNOS substrate L-arginine and NO donor significantly increased cPLA(2)alpha activity a

233 dition, a one-pot strategy for preparing the NO donor silica allows for straightforward, high-through

234 ic conditions allowed for the preparation of NO donor silica particles of widely varying sizes (d = 2

235 The NO donor SIN-1 and the endogenous NO precursor, L-argini

236 oform, the sensitivity for relaxation to the NO donor SIN-1 and to cGMP was increased in the Day28 lo

237 The NO donor SNAP (S-nitroso-N-acetyl-DL-penicillamine) and

238 posttraining intratelencephalic injection of NO donor SNAP ameliorated anterograde amnestic effects o

239 in vitro thalamic slices, we found that the NO donor SNAP produced a robust, long-lasting depolariza

240 The NO precursor L-arginine or the NO donor SNAP significantly increased the frequency of g

241 vitro to 0.1 micromol/L nitroglycerin or the NO donor SNAP, as compared with control (18.9+/-8.8 and

242 Bromo-cGMP, the NO donor SNAP, the guanylate cyclase activator YC-1, and

243 FVC had been restored by infusion of (ii) an NO donor (SNAP) or (iii) cell-permeant cGMP.

244 In this study, NO donors (SNAP and DETA-NONOate) inhibited DC antigen p

245 Effects of a nitric oxide (NO) donor (SNAP), NO substrate (l-arginine), and NO synt

246 show that direct nigral administration of a NO donor, SNOG, in the rat produced only local toxicity

247 Interestingly, the inhibitory effect of the NO donor SNP on platelet activation was sGC-dependent on

248 The NO donor sodium nitroprusside (SNP) increased intracellu

249 Microinjection of the NO donor sodium nitroprusside (SNP, 1 mM, 50 nl) at a ca

250 ver, vasodilation to endothelium-independent NO donor sodium nitroprusside was unaffected after all t

251 responses to somatosensory stimulation, the NO donor sodium nitroprusside, added within the range of

252 nd A23187 but not to endothelium-independent NO donor sodium nitroprusside.

253 The NO donor sodium nitrprusside (10 mumol l(-1) , n = 8) mi

254 The NO donors sodium nitroprusside and dipropylenetriamine N

255 c C(2)H(4) generation, but the nitric oxide (NO) donor sodium nitroprusside initiated biphasic rises.

256 The nitric oxide (NO) donor sodium nitroprusside was injected intraperiton

257 C), and can be mimicked by the nitric oxide (NO) donor sodium nitroprusside.

258 rough kidney paired donation for whom he had no donor-specific HLA antibody (HLA-DSA).

259 ients were determined to have no HLA-DSA and no donor-specific MICA antibodies pretransplant and at t

260 have treated these cell lines with the same NO donor, spermineNONOate (SPER/NO).

261 against the light from accretion, means that no donor star to date has a measured mass below the hydr

262 analyses revealed a substantial influence of NO-donor stereochemistry and structure on efficiency of

263 T biosensor, eNOS small interfering RNA, and NO donor studies demonstrate NO-induced Src activation a

264 ndard mixtures and single neurons with added NO donor, successfully demonstrate the utility of this a

265 C) receptor antagonist, a NOS inhibitor, and NO donors, suggested that NO released from postsynaptic

266 ion while S-nitroso-N-acetylpenicillamine, a NO donor, suppresses M1 macrophage polarization.

267 es the delivery of engineered nucleases with no donor template to hiPSCs, and genotyping and derivati

268 cited by S-nitroso-N-acetylpenicillamine, an NO donor that activates cGMP signaling, was also inhibit

269 FF than did wild-type DCs, and addition of a NO donor to NOS2(-/-) DCs reduced BAFF production.

270 1-Resf has been employed as a "trackable" NO donor to promote NO-induced apoptosis in MDA-MB-231 h

271 After 50 min, SNP was added as an NO donor to restore baseline CVC at one site.

272 ese studies intentionally used high doses of NO donors to achieve the maximum DNA damage.

273 The administration of NO donors to primary dorsal root ganglion cultures preve

274 ae and Ruminococcaceae, from vehicle-gavaged NOD donors to microbiota-depleted C57BL/6 recipients was

275 C/+NO group also received intraportal SIN-1 (NO donor) to elevate hepatic NO from 180 to 270 min.

276 ffectively block reduced IRS-2 expression in NO donor-treated beta-cells.

277 AW 264.7 cells to S-nitroso-l-glutathione, a NO donor, triggered LKB1 S-nitrosylation.

278 Among the NO-donors used, only S-nitrosocysteine (SNOC) was found

279 silica were converted to N-diazeniumdiolate NO donors via exposure to high pressures of NO (5 atm) u

280 Changes in the AI with addition of a NO donor was longitudinally associated with serum NOx le

281 were removed before hospital discharge, and no donor was readmitted and/or needed outpatient care.

282 The down-regulation by IL-1 or NO donors was abolished by treatments with the proteasom

283 dendritic scaffold using N-diazeniumdiolate NO donors was examined via the reaction of primary amine

284 H(2)O(2)-induced protein-derived radicals by NO donors was shown using direct electron paramagnetic r

285 spectrum was observed after perfusion of the NO-donor was completed, where, if the preconditioning tr

286 T1D transfer by splenocytes from prediabetic NOD donors was observed in Il-2rgamma(null)-NSG versus I

287 nitroso-N-acetyl-D,L-penicillamine (SNAP), a NO donor, was added after removal of GSH-depleting agent

288 zeolite NO (Ze-NO), a chemically inert, pure NO donor, we have shown that NO per se produces little i

289 The inhibitory effects of NO donor were independent of phosphatidylinositol 3-kina

290 ers (7-10) as COX-2 selective inhibitors and NO donors were synthesized and are herein reported.

291 of these powdery biocompatible materials as NO donors where the delivery of NO (a strong antibiotic)

292 larvae upon infection or upon treatment with NO donors, whereas a gain-of-function CanA1 transgene ac

293 mic responses, and that it is reversed by an NO donor, which indicates a role for NO deficiency in th

294 Chronic application of an NO donor while inhibiting endogenous NO synthesis rescue

295 o were hepatitis C virus (HCV) positive, and no donors who were positive for the HIV.

296 effects produced by NO release from chemical NO donors with those elicited by physiological NO releas

297 DETA-NONOate, a long acting NO donor, with a half-life of 20 h, was used.

298 st wall leads to excellent entrapment of the NO donor within the porous host.

299 tment with oral sodium nitrate, an inorganic NO donor without a NSIAD moiety, restores sympatholysis

300 Intravitreous injection of the NO donor without PDT also induced substantial photorecep

301 O-dependent, and treatment of cells with the NO donors (Z)-1-[2-(2-aminoethyl)-N-(2-ammonioethyl) ami