ライフサイエンスコーパス: nitric oxide

1 osolic calcium, reactive oxygen species, and nitric oxide.

2 cture may switch mitoNEET and Miner1 to bind nitric oxide.

3 associated with an increase in production of nitric oxide.

4 hondrial O2(. -), and diminished endothelial nitric oxide.

5 , oxidative stress, and limited bioavailable nitric oxide.

6 onmental signals such as oxygen, nitrate and nitric oxide.

7 nd subsequent chemiluminescence detection of nitric oxide.

8 ants (50.2% male [n = 115]) received inhaled nitric oxide.

9 ulosis infections in response to hypoxia and nitric oxide.

10 tile or rapidly diffusing substances such as nitric oxide.

11 against the antiviral effector mechanism of nitric oxide.

12 ers in Miner2, with each cluster binding one nitric oxide.

13 cellular cascades involved Ca(2+) stores and nitric oxide.

14 fied human mitoNEET and Miner1 fails to bind nitric oxide, a single mutation of Asp-96 to Val in mito

15 Modulation of nitric oxide activity through blockade of CD47 signaling

16 In addition, MSCs secreted nitric oxide after Mtb infection, and inhibition of NO b

17 e guanylyl cyclase (sGC) is the receptor for nitric oxide and a highly sought-after therapeutic targe

18 eover, we highlighted the cross-talk between nitric oxide and H2S in several bilogical contexts.

19 Aortic nitric oxide and Nos2 levels were higher in Adamts1-defi

20 reactivity in OZR reflects a loss in venular nitric oxide and PGI2 bioavailability, associated with t

21 indicating downstream signaling through both nitric oxide and prostaglandins.

22 nces in sputum neutrophil counts and exhaled nitric oxide and serum IgE levels.

23 ing lipopolysaccharide (LPS)-stimulated ROS, nitric oxide and TNFalpha production, which translated i

24 ural sleep included tidal breathing, exhaled nitric oxide, and multiple breath washout measures.

25 eral vascular resistance and the increase in nitric oxide are impaired or absent in salt sensitivity,

26 ic studies demonstrated that adiponectin and nitric oxide are released after activation of adipocyte-

27 Since then, the discovery of nitric oxide as a biological effector and better underst

28 f blood eosinophil count, fractional exhaled nitric oxide, Asthma Control Questionnaire, medication u

29 NEET or Asp-123 to Val in Miner1 facilitates nitric oxide binding in the [2Fe-2S] cluster, indicating

30 ss spectrometry analyses further reveal that nitric oxide binds to the reduced [2Fe-2S] clusters in M

31 y contested given their ability to transduce nitric oxide bioactivity within the microcirculation.

32 dative stress (94.7 +/- 6.2%) and normalised nitric oxide bioavailability (115.6 +/- 22.3%) in the fe

33 e 5 expression (167 +/- 13.7%) and decreased nitric oxide bioavailability (54.7 +/- 6.1%) in the feta

34 s benefits on dilatory function and baseline nitric oxide bioavailability.

35 nted in ECSHIP2(Delta/+) mice, as was aortic nitric oxide bioavailability.

36 SOV of FAs reflects the local production of nitric oxide by the endothelium in response to luminal s

37 ee known small molecule bioregulators (SMBs) nitric oxide, carbon monoxide, and hydrogen sulfide were

38 guanylyl cyclase (sGC), a key enzyme in the nitric oxide/cGMP signaling pathway.

39 ounds, oxygen, carbon dioxide, ethylene, and nitric oxide, change during the submergence of plant org

40 The nitric oxide concentration and nuclear factor-kappa B (N

41 Nitric oxide contributes to protection from tuberculosis

42 inine synthesis in urea cycle and citrulline-nitric oxide cycle.

43 effects of organic nitrate therapy, via both nitric oxide-dependent and -independent mechanisms.

44 ect on T-cell responses that was mediated by nitric oxide-dependent depletion of l-arginine.

45 itrosylation is therefore revealed here as a nitric oxide-dependent host strategy involved in plant i

46 rated fatty acids react with nitric oxide or nitric oxide-derived species.

47 on-PN intermediate in the catalytic cycle of nitric oxide dioxygenase (NOD) enzymes, which facilitate

48 The identity of the specific nitric oxide dioxygenase (NOD) that serves as the main i

49 n of ADP-induced platelet aggregation by the nitric oxide donor sodium nitroprusside and the phosphod

50 balance between various mediators, including nitric oxide, endothelin, and prostanoids, among others.

51 P2 receptors on endothelial cells to produce nitric oxide, endothelium-derived hyperpolarizing factor

52 Exhaled nitric oxide (eNO) is a biomarker of airway inflammation

53 nction, respiratory symptoms, exhaled breath nitric oxide [eNO], exhaled carbon monoxide [eCO], and h

54 onal responses, detectable within minutes of nitric oxide exposure, typically took several hours to m

55 and distribution of GABAergic parvalbumin or nitric oxide-expressing and cholinergic interneurons wer

56 otoxemia, persistent pulmonary hypertension, nitric oxide, extracorporeal membrane oxygenation, and A

57 ociation between baseline fractional exhaled nitric oxide (FeNO) and the response to inhaled corticos

58 The fraction of exhaled nitric oxide (FENO) is a useful marker of asthma control

59 On the other hands, the fraction of exhaled nitric oxide (FENO) is a useful noninvasive marker of eo

60 ible biomarkers included fraction of exhaled nitric oxide (Feno) values, blood eosinophil (bEOS) coun

61 tor reversibility >/=12%, fractional exhaled nitric oxide [FeNO] >/=35 parts per billion, and peak ex

62 The nitric oxide formation from selected N-nitrosamines was

63 onises endothelial dysfunction by increasing nitric oxide formation, activating anti-inflammatory pat

64 esidues in proteins are readily disrupted by nitric oxide forming a protein-bound dinitrosyl iron com

65 cuss novel approaches to improve endothelial nitric oxide generation and preserve its bioavailability

66 onchodilator response and fractional exhaled nitric oxide had good sensitivity and specificity for pr

67 mission from rotational-vibrational bands of nitric oxide, hydroxyl and molecular oxygen as signature

68 ur proteins are among the primary targets of nitric oxide in cells.

69 pacity (HDL ability to induce the release of nitric oxide in endothelial cells).

70 sicians, and the fractional concentration of nitric oxide in exhaled air (FeNO) was measured.

71 ractions stimulate FA endothelium to release nitric oxide in response to elevated shear stress second

72 The results suggest that binding of nitric oxide in the CDGSH-type [2Fe-2S] clusters in mito

73 Binding of nitric oxide in the reduced Miner2 [2Fe-2S] clusters pro

74 Placebo (nitrogen) or inhaled nitric oxide initiated at 20 ppm was decreased to 10 ppm

75 Inhaled nitric oxide, initiated at 20 ppm on postnatal days 5 to

76 , the transient one-electron reduced form of nitric oxide, is a significant challenge owing to its hi

77 s sputum eosinophilia and fractional exhaled nitric oxide levels, along with oral corticosteroid use,

78 inophils, as well as high fractional exhaled nitric oxide levels, exacerbation rates, and oral cortic

79 ilator responsiveness and fractional exhaled nitric oxide levels.

80 c oxide synthase downregulation, and reduced nitric oxide-mediated inhibition of platelet aggregation

81 quired for VSMC recruitment during increased nitric oxide-mediated vasodilatation and angiopoietin si

82 Pronounced elevations in trough levels of nitric oxide metabolites occurred with KNO3 (visit 2: 19

83 re examined for their analytical response to nitric oxide (NO(*)).

84 Nitric oxide (NO) activates the NO-sensitive soluble gua

85 tosis was accompanied by decreased levels of nitric oxide (NO) and inducible NO synthase (iNOS) in ce

86 mined the kinetics of growth and turnover of nitric oxide (NO) and N2 O at low cell densities of Nitr

87 ll removed through chemical decomposition to nitric oxide (NO) and nitrate.

88 g bacteria (AOB) emit substantial amounts of nitric oxide (NO) and nitrous oxide (N2O), both of which

89 potassium channels (KIR ), and synthesis of nitric oxide (NO) and prostaglandins (PG).

90 Although the wound healing effects of nitric oxide (NO) are known, the mechanism by which NO m

91 mic analysis in endothelial cells identified nitric oxide (NO) as major mediator of this phenotype in

92 f these heme-silk films for the detection of nitric oxide (NO) at nanomolar levels in the presence an

93 understood, interventions aimed at enhancing nitric oxide (NO) bioavailability remain a key area of i

94 Hepatic and systemic hemodynamic, nitric oxide (NO) bioavailability, LF, HSC activation, a

95 ABSTRACT: Endothelial nitric oxide (NO) controls cardiac oxygen (O2 ) consumpt

96 KEY POINTS: In the heart, endothelial nitric oxide (NO) controls oxygen consumption in the wor

97 an plasma and cells serve important roles in nitric oxide (NO) dependent as well as NO independent si

98 ypothesized that Trpc6 would help to mediate nitric oxide (NO) dysregulation and that this would be m

99 Nitric oxide (NO) exerts pleiotropic effects on plant de

100 ssive degradation of its [4Fe-4S] cluster on nitric oxide (NO) exposure.

101 oxide synthase (NOS) uncoupling with reduced nitric oxide (NO) formation and greater oxidative and ni

102 nd direct approach to investigate sources of nitric oxide (NO) formed in soils.

103 Nitric oxide (NO) has been known to promote physiologica

104 und that Cavin-2 regulates the production of nitric oxide (NO) in endothelial cells by controlling th

105 The importance of nitric oxide (NO) in many biological processes has garne

106 els regulate flow-induced vasodilatation via nitric oxide (NO) in mouse mesenteric resistance arterie

107 cible nitric oxide synthase (iNOS) generates nitric oxide (NO) in myeloid cells that acts as a defens

108 Nitric oxide (NO) is a key messenger in plant stress res

109 Nitric oxide (NO) is a regulatory molecule in the vascul

110 Nitric oxide (NO) is able to lower intraocular pressure

111 Nitric oxide (NO) is an important regulator of inflammat

112 Nitric oxide (NO) is an intercellular messenger involved

113 Nitric oxide (NO) is an intermediate of the nitrogen cyc

114 itrification, a respiratory process in which nitric oxide (NO) is an intermediate.

115 Nitric oxide (NO) is generated from arginine and oxygen

116 Host nitric oxide (NO) is important in controlling TB infecti

117 Nitric oxide (NO) is inactivated by cell-free hemoglobin

118 The signaling molecule nitric oxide (NO) is synthesized in animals by structura

119 INTRODUCTION: Increased exhaled nitric oxide (NO) levels in asthma are suggested to be t

120 mammalian globin cytoglobin (CYGB) regulates nitric oxide (NO) metabolism and cell death.

121 he relationship between circulating arginine-nitric oxide (NO) metabolites and CTRCD remains unstudie

122 x species and it elucidates the influence of nitric oxide (NO) on sulfur trioxide (SO3) generation.

123 the reactive ammonia-oxidation intermediates nitric oxide (NO) or hydroxylamine (NH2OH) for N2O produ

124 , we demonstrate that bdMphi fail to produce nitric oxide (NO) or upregulate inducible nitric oxide s

125 his; however, the association of endothelial nitric oxide (NO) pathways with disease severity is unkn

126 a sigma (sigma) receptor pharmacophore and a nitric oxide (NO) photodonor.

127 Nitric oxide (NO) produced by endothelial cells in respo

128 ed to lower blood pressure, possibly through nitric oxide (NO) production in skin.

129 pendent activation of nitric oxide synthase, nitric oxide (NO) production, NO-dependent S-nitrosylati

130 ty is associated with elevated intracellular nitric oxide (NO) production, which promotes nitrosative

131 mulating these glutamate receptors increases nitric oxide (NO) production, which stimulates matrix me

132 and significant inhibitory activity against nitric oxide (NO) production.

133 otes is linked through a single mechanism to nitric oxide (NO) sensing [3, 4].

134 he inhibitory phosphorylation of endothelial nitric oxide (NO) synthase (eNOS) at Thr497 (eNOS(pThr49

135 Neurons expressing nitric oxide (NO) synthase (nNOS) and thus capable of sy

136 m the nitric oxide produced by the inducible nitric oxide (NO) synthase of macrophages.

137 n transport chain, and uncoupled endothelial nitric oxide (NO) synthase.

138 bryonic fibroblasts via mechanisms involving nitric oxide (NO) synthesis and posttranslational modifi

139 hemoglobin from ongoing hemolysis scavenges nitric oxide (NO) to create an NO deficiency which can a

140 asing evidence for the potential function of nitric oxide (NO) to overcome MDR.

141 yte colony-stimulating factor (G-CSF) and of nitric oxide (NO) upon challenge with corynebacterial gl

142 parent activity in the ready eliminateion of nitric oxide (NO) via facile redox reactions, and the el

143 emical sensor for the selective detection of nitric oxide (NO), a critical cancer biomarker.

144 troglycerin-mediated dilation (GMD), urinary nitric oxide (NO), and inflammatory markers were measure

145 production of pro-inflammatory cytokines and nitric oxide (NO), in response to LPS and alpha-synuclei

146 NOS), which generates the potent vasodilator nitric oxide (NO), is decreased.

147 e synthase (eNOS) and its bioactive product, nitric oxide (NO), mediate many endothelial cell functio

148 Reactions between nitric oxide (NO), nitrite (NO2-), and unsaturated fatty

149 Multiple lines of evidence point to impaired nitric oxide (NO)-cGMP bioavailability as playing a cent

150 s on glucose and lipid metabolism, has shown nitric oxide (NO)-dependent vasodilator properties in ex

151 KEY POINTS: Combining nitric oxide (NO)-mediated increased blood flow with ang

152 ferentially to neovascularization induced by nitric oxide (NO)-mediated vasodilatation, by comparing

153 e accompanied by increased soil emissions of nitric oxide (NO).

154 idamide, dihydrochloride (AAPH) radicals and nitric oxide (NO).

155 rdiovascular system, many of which depend on nitric oxide (NO).

156 several HDACs are subjected to regulation by nitric oxide (NO); in plants, however, it is unknown whe

157 m reaction of superoxide anion (O2(*-)) with nitric oxide (.NO) and has been suggested to form an as-

158 ulfur limits so questions were posed whether nitric oxide (NOx) and particulate matter (PM) emissions

159 rmed when unsaturated fatty acids react with nitric oxide or nitric oxide-derived species.

160 crophage function, we assessed cytotoxicity, nitric oxide or reactive oxygen species production, and

161 percent predicted FEV1, fraction of exhaled nitric oxide, or asthma symptoms.

162 tility of pharmacological stimulation of the nitric oxide pathway as a therapeutic strategy.

163 ipids, indicate that both the urea cycle and nitric oxide pathways are dysregulated at early stages i

164 In contrast, we report that nitric oxide primarily protects mice by repressing an in

165 ve nitrogen species (RNS) generated from the nitric oxide produced by the inducible nitric oxide (NO)

166 synthesis, restored cellular BH4 levels and nitric oxide production and decreased radiation-induced

167 Blocking CX3CR1 or nitric oxide production during G-CSF treatment reduces e

168 g either CD23 upregulation or CD23-dependent nitric oxide production eliminated the enhanced antifung

169 educed by 30% cytokine-induced apoptosis and nitric oxide production in INS-1E cells.

170 pression profiles, oxygen consumption rates, nitric oxide production levels, shear stress responses,

171 ne stimulation in these cells also activated nitric oxide production that was blocked by sigma1-recep

172 lcium signals in primary cells that activate nitric oxide production to increase ciliary beating and

173 a stronger bactericidal activity with higher nitric oxide production, a more proinflammatory polarize

174 and Ca(2+) influx, which activates low-level nitric oxide production, increases apical membrane Cl(-)

175 euronal nitric oxide synthase activation and nitric oxide production.

176 ation, reduced HO-1 expression and increased nitric oxide production.

177 to HAT as implausible for the reaction with nitric oxide radical in all the solvents investigated.

178 l-1,3-butadiene) carrying nearly unperturbed nitric oxide radical to form [((R)DDB)Fe(NO)2((*)NO)](+)

179 se, one contained genes for both nitrate and nitric oxide reductase, and one had nitrate and nitrite

180 ights regarding the mechanism of flavodiiron nitric oxide reductases.

181 g as the terminal components to dioxygen and nitric oxide reductive scavenging pathways in these orga

182 lium-dependent vascular relaxation through a nitric oxide-related mechanism.

183 a combination of adenosine triphosphate and nitric oxide, respectively.

184 ted with markers of systemic vasodilatation (nitric oxide, rho = -0.66, P = 0.06; diastolic blood pre

185 city, oxygen radical absorbance capacity and nitric oxide scavenging assays.

186 itive balance between heme-free, ferric, and nitric oxide-sensitive ferrous sGC in cells and tissues,

187 required to allow beneficial effects of both nitric oxide-sensitive guanylyl cyclase activation and i

188 y inflammation, including fractional exhaled nitric oxide, serum IgE, periostin, and blood and sputum

189 are genetic variants in 2 genes that mediate nitric oxide signaling (Nitric Oxide Synthase 3 [NOS3] a

190 enal function via activation of Akt-mediated nitric oxide signaling in the kidney.

191 A genetic predisposition to enhanced nitric oxide signaling is associated with reduced risks

192 Pharmacological stimulation of nitric oxide signaling may prove useful in the preventio

193 chondrial protein Miner2 may represent a new nitric oxide signaling mode in cells.

194 pact of a genetic predisposition to enhanced nitric oxide signaling on risk for cardiovascular diseas

195 Nitric oxide signaling plays a key role in the regulatio

196 tion studies, we examined the effect of this nitric oxide signaling score on cardiometabolic and othe

197 lves a non-canonical mechanism of retrograde nitric oxide signalling, which is triggered by Ca(2+) in

198 on the cell surface appear to also modulate nitric oxide signalling; both signalling pathways affect

199 han in generating an immediate resistance to nitric oxide stress, suggesting that survival of M. tube

200 than or equal to 10 mum in diameter (PM10), nitric oxide, sulfur dioxide, and nitrogen dioxide in di

201 t-translational modifications of endothelial nitric oxide synthase (eNOS) lead to impaired nitric oxi

202 dysfunction, which is caused by endothelial nitric oxide synthase (eNOS) uncoupling, is an initial s

203 Instead, expression of endothelial nitric oxide synthase (eNOS), which generates the potent

204 OPE also had higher NO, inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX-2)

205 complex 1 (mTORC1), HIF1alpha and inducible nitric oxide synthase (iNOS) coordinates DC metabolism a

206 of the NF-kappaB subunit p65; and inducible nitric oxide synthase (iNOS) expression.

207 by genetic deletion of inducible isoform of nitric oxide synthase (iNOS) from VCP TG mouse and by ph

208 Inducible nitric oxide synthase (iNOS) generates nitric oxide (NO)

209 ported that Sal-1 targets cellular inducible nitric oxide synthase (iNOS) in a miRNA manner, leading

210 lyze the role of NADPH oxidase and inducible nitric oxide synthase (iNOS) in a murine model of A. act

211 ce nitric oxide (NO) or upregulate inducible nitric oxide synthase (iNOS) mRNA following Toll-like re

212 aB p65-responsive genes, including inducible nitric oxide synthase (iNOS), interleukin-6 (IL-6), and

213 proximately 60% of which expressed inducible nitric oxide synthase (iNOS).

214 teins cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS).

215 s and markedly decreased levels of inducible nitric oxide synthase (iNOS).

216 1 (CB1R) and inhibitory effect on inducible nitric oxide synthase (iNOS).

217 SC were treated with inhibitors of inducible nitric oxide synthase (L-NAME and NCX-4016).

218 6) and decreased the expression of inducible nitric oxide synthase (M1 marker).

219 el of human enteric neuropathy, the neuronal nitric oxide synthase (nNOS(-/-)) deficient mouse model,

220 he nitric oxide synthesizing enzyme neuronal nitric oxide synthase (nNOS) in nerve fibers of the muri

221 Inhibition of neuronal nitric oxide synthase (nNOS) is a promising therapeutic

222 Neuronal nitric oxide synthase (nNOS) is a target for development

223 tion that depended on activation of neuronal nitric oxide synthase (nNOS).

224 nt expression of NMDA receptors (NMDARs) and nitric oxide synthase (NOS) and is therefore much more s

225 oduction from the amino acid l-arginine, via nitric oxide synthase (NOS) enzymes, research in recent

226 ytotoxic effects, which are inhibited by the nitric oxide synthase (NOS) inhibitor L-NIO, and genetic

227 e dystrophin-sarcoglycan complex delocalizes nitric oxide synthase (NOS) to alter its signaling, and

228 Oxidative stress and nitric oxide synthase (NOS) uncoupling are thought to co

229 This imbalance leads to nitric oxide synthase (NOS) uncoupling with reduced nitr

230 hat protein kinase Cbeta (PKCbeta) and brain nitric oxide synthase (NOS1), both identified by proteom

231 the metalloproteinase ADAMTS1 and inducible nitric oxide synthase (NOS2) as therapeutic targets in i

232 racellular adhesion molecule 1 (ICAM-1), and nitric oxide synthase (NOS2), developed leukostasis and

233 crosis factor-alpha (P = 0.04) and inducible nitric oxide synthase (P = 0.02) in skin biopsy specimen

234 uM(vgat/vglut2)) and another also expressing nitric oxide synthase (SuM(Nos1/Vglut2)).

235 h is located at 11p14, potentially affecting nitric oxide synthase 3 (NOS3) expression, as shown by m

236 2 genes that mediate nitric oxide signaling (Nitric Oxide Synthase 3 [NOS3] and Guanylate Cyclase 1,

237 d indomethacin and inhibition of endothelial nitric oxide synthase abolished the effects of therapeut

238 nd isoform-specific endothelial and neuronal nitric oxide synthase activation and nitric oxide produc

239 nucleotide phosphate-oxidase 2 and inducible nitric oxide synthase and enhanced lung concentrations o

240 SIRT1-regulated Akt, endothelial nitric oxide synthase and GLUT4 levels were also induced

241 ased glutathione levels, increased inducible nitric oxide synthase and heme-oxygenase 1 expression, a

242 ased glutathione levels, increased inducible nitric oxide synthase and heme-oxygenase 1 expression, a

243 is attributable to preservation of neuronal nitric oxide synthase and sarcoplasmic reticulum Ca(2+)

244 by the sigma1-receptor antagonist or various nitric oxide synthase blockers.

245 mitogen-activated protein kinase (MAPK), and nitric oxide synthase deactivation.

246 n, shedding of procoagulant MPs, endothelial nitric oxide synthase downregulation, and reduced nitric

247 rotyrosine formation and increased inducible nitric oxide synthase expression.

248 emodelling by over-expression of endothelial nitric oxide synthase in the fat pad of the adult rat me

249 ing loss of ROV and was eliminated following nitric oxide synthase inhibition.

250 Importantly, infusion of the nitric oxide synthase inhibitor l-N(G)-monomethyl-l-argi

251 tric tissues and these were inhibited by the nitric oxide synthase inhibitor L-NNA.

252 dichlorofluorescein diacetate dye, inducible nitric oxide synthase levels determined by Western blot,

253 activation by fluvoxamine triggered the Akt-nitric oxide synthase signaling pathway, resulting in ti

254 capillaries via the NMDA receptors-neuronal nitric oxide synthase signaling pathway.

255 volves the activation of the Akt-endothelial nitric oxide synthase survival pathway, and the inhibiti

256 tion that could be restored by inhibition of nitric oxide synthase via the inhibitor N-nitro-l-methyl

257 e dismutase were increased, whereas those of nitric oxide synthase were decreased, in 7- to 10-week-o

258 c contractions persisted until inhibition of nitric oxide synthase with N(omega) -nitro-l-arginine me

259 triggers calmodulin-dependent activation of nitric oxide synthase, nitric oxide (NO) production, NO-

260 dimerization and phosphorylation of neuronal nitric oxide synthase, sarcoplasmic reticulum Ca(2+) rel

261 actility, tetrahydrobiopterin, the dimers of nitric oxide synthase, sarcoplasmic reticulum Ca(2+) rel

262 ry cytokine tumor necrosis factor, inducible nitric oxide synthase, the M1 activator interferon gamma

263 effects alter the expression of endothelial nitric oxide synthase, the stability of atherosclerotic

264 ssion of proinflammatory proteins (inducible nitric oxide synthase, tumor necrosis factor-alpha, and

265 adhesion molecule-1 (VCAM-1) and endothelial nitric oxide synthase, whereas PDEs had significantly hi

266 )) and triple-negative breast cancer (TNBC), nitric oxide synthase-2 (NOS2) and cyclooxygenase-2 (COX

267 ediators including cytokines, chemokines and nitric oxide synthase-2.

268 st, affects development of DN in endothelial nitric oxide synthase-knockout db/db mice.

269 rons ( approximately 1%) expressing neuronal nitric oxide synthase.

270 obese type 2 diabetic mice by an endothelial nitric oxide synthase/Akt/vascular endothelial growth fa

271 in capillary/arteriole density, endothelial nitric oxide synthase/Akt/vascular endothelial growth fa

272 Endothelial nitric-oxide synthase (eNOS) and its bioactive product,

273 he stability and activity of the endothelial nitric-oxide synthase (eNOS) and that Cavin-2 knockdown

274 s by mitochondria, NADPH oxidase, and type 2 nitric-oxide synthase (NOS-2) and resulted in S-nitrosyl

275 ry cytokines and the mRNA encoding inducible nitric-oxide synthase in both LRP1-expressing and -defic

276 of pro-inflammatory cytokines and inducible nitric-oxide synthase induction in BV2 cells in a concen

277 of capon (C-terminal PDZ ligand of neuronal nitric-oxide synthase protein), apoptosis-associated spe

278 Intriguingly, eNOS activity is regulated by nitric-oxide synthase trafficking inducer (NOSTRIN), whi

279 glial fibrillary acidic protein and neuronal nitric-oxide synthase, and Abeta and p-Tau(Ser-202) also

280 In contrast, inhibition of nitric-oxide synthase, p38 MAPK, and G9a abrogated H3K9m

281 e availability of BH4 leads to uncoupling of nitric oxide synthases and production of highly oxidativ

282 t radiation disrupted BH4, which resulted in nitric oxide synthases uncoupling and augmented radiatio

283 terin (BH4) is an essential cofactor for all nitric oxide synthases.

284 itric oxide synthase (eNOS) lead to impaired nitric oxide synthesis.

285 P (SP), neuropeptide tyrosine (NPY), and the nitric oxide synthesizing enzyme neuronal nitric oxide s

286 nd loss of function of amacrine cells (brain nitric oxide synthetase/tyrosine hydroxylase expression)

287 To test whether administration of inhaled nitric oxide to preterm infants requiring positive press

288 for IgE levels (268 IU), fraction of exhaled nitric oxide values (14.5 ppb), and blood eosinophil cou

289 d eosinophil counts, and fraction of exhaled nitric oxide values in relationship to sputum eosinophil

290 ormed spirometry and had fraction of exhaled nitric oxide values measured twice during the school yea

291 siveness to mannitol and fraction of exhaled nitric oxide values were measured.

292 tinuous inotropic support for >/=14 days, or nitric oxide ventilation for >/=48 hours.

293 However, macrophage ability to produce nitric oxide was defective.

294 On day 4 plasma and urine nitric oxide was increased by 244 +/- 89% and 450 +/- 36

295 ever, after challenging M. tuberculosis with nitric oxide we found that the rapid transcriptional res

296 cid arginine is a physiological precursor to nitric oxide, which is a key mediator of embryonic survi

297 type 5 inhibitor, potentiates the actions of nitric oxide, which leads to vasodilatation of the uteri

298 To carry and deliver nitric oxide with a controlled redox state and rate is c

299 l-venous delivery gradients of intravascular nitric oxide, with deoxyhemoglobin-mediated reduction id

300 al protein Miner2 [2Fe-2S] clusters can bind nitric oxide without disruption of the clusters.