ライフサイエンスコーパス: NO2

1 NO2 concentrations, a marker of traffic-related air poll

2 NO2 exposure negatively affected beta-cell function, evi

3 NO2 was positively associated with colorectal cancer mor

4 NO2(-) may act by S-nitrosating protein thiols, thereby

5 NO2(-) observed in HAO activity assays is a nonenzymatic

6 NO2-OA inhibited TNFalpha-induced NF-kappaB transcriptio

7 NO2-OA reduced TNBC cell growth and viability in vitro,

8 NO2-PLs were generated by NO2BF4 in hydrophobic environm

9 PM10 (hazard ratio 1.07, 95% CI 1.06-1.08), NO2 (1.09, 1.08-1.10), and CO (1.09, 1.08-1.10).

10 in concentrations of PM10 (1.07, 1.05-1.08), NO2 (1.09, 1.08-1.11), and CO (1.10, 1.08-1.11).

11 in concentrations of PM10 (1.08, 1.07-1.09), NO2 (1.12, 1.10-1.13), and CO (1.09, 1.08-1.10).

12 y available biomarkers only 4 (serum Coll2-1 NO2, CS846, COMP and urinary CTXII) were consistently as

13 10-NO2-OA has been extensively tested in animal models and

14 In particular, 10-nitro oleic acid (10-NO2-OA) potently induces Nrf2-dependent antioxidant gene

15 nd fecal pathways are the main routes for 10-NO2-OA excretion in rats, and allowed the identification

16 Bio-elimination pathways for 10-NO2-OA were evaluated in rats (30 mg/kg.day) and in huma

17 tools for the experimental evaluation of 10-NO2-OA levels in vivo, but importantly they also set the

18 in concentrations of PM10 (1.09, 1.06-1.12), NO2 (1.09, 1.06-1.12), and CO (1.05, 1.02-1.08).

19 riment with (15)NH4NO3, NH4(15)NO3, or Na(15)NO2 amendments, we found distinct (15)N abundances in NO

20 lated sunlight, and [(15)N2]DNAN yielded (15)NO2(-) in leaves.

21 idences since 1990 (PM10 and PM2.5) or 1970 (NO2 and NOx) were estimated using the Danish Eulerian He

22 : 0.27 +/- SD 0.55; Rusheen: 2.46 +/- SD 3.4 NO2(-) microg(-1) g(-1) day(-1), P < 0.001) than in Clew

23 uction, is unreactive toward weakly acidic 4-NO2-phenol, and stronger acids cleave the metal-O bonds,

24 y contrast, LS-4DCHIm forms an adduct with 4-NO2-phenol, which includes an H-bond to the peroxo O-ato

25 n-withdrawing group, such as C(4)-Cl or C(5)-NO2, they rearrange to products 4 in the presence of aqu

26 The production of both 4-Me-5-NO2-L-Trp and 4-Me-7-NO2-L-Trp uncovered remarkable regi

27 ) and N-H BDE = 77.4 kcal mol(-1) for 3-CN,7-NO2-phenoxazine to kinh = 6.6 x 10(8) M(-1) s(-1) and N-

28 oduction of both 4-Me-5-NO2-L-Trp and 4-Me-7-NO2-L-Trp uncovered remarkable regio-promiscuity of nitr

29 MOF-905, MOF-905-Me2, MOF-905-Naph, MOF-905-NO2, and MOF-950.

30 Therefore, major sulfate oxidation through a NO2-mediated pathway is not likely in China, or any othe

31 Findings suggest that absolute NO2 exposure disparities by race-ethnicity decreased fro

32 Nitro-conjugated linoleic acid (NO2-CLA) is preferentially formed, constitutes the most

33 dogenous occurrence of nitro-linolenic acid (NO2-Ln) in Arabidopsis and the modulation of NO2-Ln leve

34 identification of 4-nitro-octanedioic acid (NO2-8:0-diCOOH) as the most abundant metabolite in rat u

35 anti-inflammatory agent 10-nitro-oleic acid (NO2-OA), a component of the Mediterranean diet, reduced

36 itro-octadec-9-enoic acid (nitro-oleic acid, NO2-OA), were investigated in multiple preclinical model

37 ive rise to electrophilic nitro-fatty acids (NO2 -FAs), such as nitro oleic acid (OA-NO2 ) and nitro

38 Typical MS/MS fragmentation pattern of all NO2-PL included a neutral loss of HNO2, product ions ari

39 PM10, 1.312 [1.096, 1.571; p = 0.003]), and NO2 was also associated with deaths from malformations o

40 d States [HR = 1.14 (95% CI:1.02, 1.27)] and NO2 only in the Southern United States [HR = 1.16 (95% C

41 in two-pollutant models including PM2.5 and NO2 and in three-pollutant models with O3.

42 lled vehicles to emissions of both PM2.5 and NO2 emphasises the importance of further controls on emi

43 PM2.5 and NO2 were associated with breast cancer overall [HR = 1.0

44 ression to associate physical activities and NO2 (high/medium/low) with asthma and COPD, and then int

45 tion term between each physical activity and NO2.

46 of the transition state in which the Ar and NO2 groups are anti to each other.

47 mical cell potential for 2 with R = F, H and NO2.

48 osynthetic oxidation of Fe(II), H2 S, H2 and NO2-.

49 At warm temperatures, the HO2 and NO2 come to a rapid steady state with pernitric acid (HO

50 ation of HO2 from observations of HO2NO2 and NO2 in metropolitan Atlanta, US, in winter 2014 and summ

51 th varying concentrations of O2, NH4(+), and NO2(-).

52 space analysis measurements show that NO and NO2 gases are formed within minutes on heating catalytic

53 ter exposure for up to 10 h, although NO and NO2 may have exhibited oxidizing effects (e.g., exposure

54 The results showed that SO2, NO, and NO2 are unlikely to have adsorbed on the surface vanadiu

55 uces levels of gaseous nitrous acid, NO, and NO2 within the model and measurement uncertainty.

56 vidence of interaction between nutrition and NO2 exposure during pregnancy.

57 effects of input uncertainties on ozone and NO2 output, to allow robust global sensitivity analysis

58 Exposure to PM and NO2 air pollution was associated with the prevalence of

59 arting complexes with the release of SO2 and NO2.

60 ups of increasing polarity (-CH3, -CHO, and -NO2) on the imidazole linkers provide control over the d

61 lar headgroup and HNO2, [NO2-FA + H](+) and [NO2-FA - H](-) product ions, and cleavages on the fatty

62 Increased mean annual NO2 exposure was associated with increased risk of atopy

63 ing oxidative addition of LPd(0) into the Ar-NO2 bond.

64 y NO2-OA in TNBC cells were multifaceted, as NO2-OA (a) inhibited the inhibitor of NF-kappaB subunit

65 tes to live in a block group with an average NO2 concentration above the WHO annual guideline in 2010

66 We combined annual average NO2 concentration estimates from a temporal land use reg

67 Estimated annual average NO2 concentrations decreased from 2000 to 2010 for all o

68 dels to estimate neighborhood annual average NO2.

69 umber (PN) (over 5.6 nm); black carbon (BC); NO2; benzene, toluene, ethylbenzene, and xylene (BTEX);

70 face and not from chemical reactions between NO2 and the dielectric/semiconductor components.

71 nally, human serum albumin was found to bind NO2-CLA both non-covalently and to form covalent adducts

72 ikely an important fate for NO3 indoors, but NO2 photolysis could be an important source of indoor O3

73 re, steric obstruction of Cys-119/Cys-162 by NO2-OA pretreatment in Langendorff-perfused murine heart

74 unting for NF-kappaB signaling inhibition by NO2-OA in TNBC cells were multifaceted, as NO2-OA (a) in

75 k of S-nitrosation during anoxia alone or by NO2(-) during normoxia places constraints on how S-nitro

76 ndition that promotes rapid SO2 oxidation by NO2 to form aerosol sulfate concentration consistent wit

77 ification at low O2 levels was stimulated by NO2(-) at levels as low as 0.2 mM.

78 Concentrations of black carbon, NO2, PM10, PM2.5, and ultrafine particles were higher on

79 ially associated with other specific causes: NO2 and PM10 were associated with an increase in infant

80 licated increased methylation in cg08500171 (NO2) and decreased methylation in cg17629796 (PM2.5).

81 nt substituents on the fused benzo ring (Cl, NO2, NH2, CF3, ureido, amido, heterocycles), were synthe

82 Classroom NO2 was collected by means of passive sampling for 1-wee

83 In children with asthma, indoor classroom NO2 levels can be associated with increased airflow obst

84 to determine the effect of indoor classroom NO2 on lung function and symptoms in inner-city school c

85 nships with the temporally nearest classroom NO2 level.

86 We compiled NO2 data from fixed-site monitors, chemical transport mo

87 count for inorganic nutrient concentrations (NO2/3, NH4, PO4) in each respective DOM addition.

88 Studies confirm that cyclopalladated NO2 complexes are rapidly oxidized to the corresponding

89 ated with endocrine causes of infant deaths (NO2, 2.167 [1.539, 3.052; p < 0.001]; PM10, 1.433 [1.066

90 jor roads within 100 m and satellite-derived NO2 were consistently the strongest predictors.

91 The sensor is able to detect NO2(-) in a linear response ranging from 1 to 20 muM wit

92 A new type of nitrogen dioxide (NO2 ) gas sensor based on copper phthalocyanine (CuPc) t

93 icrom (PM2.5) (1999-2004), nitrogen dioxide (NO2) (2006), and ozone (O3) (2002-2004) concentrations w

94 xposure to traffic related nitrogen dioxide (NO2) air pollution is associated with adverse health out

95 ent channels, forming: (1) nitrogen dioxide (NO2) and hydroxyl radical ((*)OH), (2) nitrite (NO2(-))

96 tolysis rate constants for nitrogen dioxide (NO2) and nitrate radicals (NO3) in the presence of the d

97 elevated concentrations of nitrogen dioxide (NO2) and particulate matter with aerodynamic diameter <2

98 bient and home exposure to nitrogen dioxide (NO2) causes asthma symptoms and decreased lung function

99 nd PM10, respectively) and nitrogen dioxide (NO2) concentrations at place of residence using logistic

100 , ultrafine particles, and nitrogen dioxide (NO2) concentrations were measured.

101 Mean annual residential nitrogen dioxide (NO2) exposure was estimated for current residential addr

102 e and rapidly converted to nitrogen dioxide (NO2) in the presence of ozone, making it impossible to d

103 imates we created a global nitrogen dioxide (NO2) land use regression model for 2011 using annual mea

104 urements of urban form and nitrogen dioxide (NO2) to explore relationships between urban form and air

105 nd PM10, respectively) and nitrogen dioxide (NO2) using land-use regression for 47,433 Sister Study p

106 .5), black carbon (BC), or nitrogen dioxide (NO2) variations that were independent of year, month, an

107 in aerodynamic diameter), nitrogen dioxide (NO2), and carbon monoxide (CO) and risk of incident chro

108 2.5 mug/m3 (PM2.5), PM10, nitrogen dioxide (NO2), and nitrogen oxides (NOx) at the nurses' residence

109 diameter <= 10 mum (PM10), nitrogen dioxide (NO2), and sulphur dioxide (SO2) with all-cause infant, n

110 tween maternal exposure to nitrogen dioxide (NO2), dietary intake of methyl nutrients, and the odds o

111 onal air pollutants [e.g., nitrogen dioxide (NO2), elemental carbon (EC), and fine particles with aer

112 ion-related air pollutant, nitrogen dioxide (NO2), in the United States.

113 ated residence-based daily nitrogen dioxide (NO2), ozone, fine particulate, and black carbon concentr

114 e-specific measurements of nitrogen dioxide (NO2), sulfur dioxide (SO2) and volatile organic compound

115 vening-night noise (Lden); nitrogen dioxide (NO2); and particulate matter (PM) with aerodynamic diame

116 meters or less (PM2.5) and nitrogen dioxide (NO2)] predictors, we conducted a nonlinear extension of

117 0.6 ppm), toluene (1 ppm), nitrogen dioxide (NO2; 2 ppm) and sulfur dioxide (SO2; 5.6 ppm), in a whol

118 ting O-O cleavage, giving nitrogen dioxide (.NO2) plus a ferryl compound [(P(Im))Fe(IV) horizontal li

119 exposures (represented by nitrogen dioxide; NO2) from a dispersion model, using residential addresse

120 nsitivities, with NO and isoprene emissions, NO2 photolysis, ozone BCs, and deposition velocity being

121 there is considerable interest in employing NO2 -FAs and other EFAs for the prevention and treatment

122 Electrochemically reduced HA enhanced NO2-to-HONO conversion by a factor of 2 relative to non-

123 , particularly in countries without existing NO2 monitoring data or models.

124 m 0.088 to 0.029 and from 0.115 to 0.076 for NO2.

125 ts, a cavity phase shift analyzer (CAPS) for NO2 measurements, and a UV ozone analyzer.

126 In contrast, for NO2, estimates were higher among ever [1.81 (95% CI: 1.1

127 fant deaths were significantly increased for NO2, PM10, and SO2 (1.066 [1.027, 1.107; p = 0.001], 1.0

128 re already in breach of EU safety limits for NO2, this phenomenon does not seem to be only restricted

129 to be 37% lower for PM2.5 and 63% lower for NO2 than at the residential address.

130 evidence of an association was observed for NO2 or NOx.

131 ensitivity is approximately 50x greater for [NO2 ] = 1 ppm with the UVO-treated TFTs, and a limit of

132 treatment is approximately 400x greater for [NO2 ] = 30 ppm than for those without UVO treatment.

133 the efficiency of the first channel, to form NO2, is well documented, a large range of values have be

134 surrounding rural areas are seeing frequent NO2 concentration violations.

135 The model captured 54% of global NO2 variation, with a mean absolute error of 3.7 ppb.

136 rom Tyrosine (Tyr) by adding a nitro group (-NO2) with nitrating agents.

137 oval through the nitrite pathway (NH4(+) --> NO2(-) --> N2) is favorable for wastewater treatment pla

138 Higher NO2 and PM2.5 exposures over follow-up were also associa

139 Higher NO2 and PM2.5 were associated with a faster decline in S

140 exposure disparities persisted, with higher NO2 concentrations for nonwhites than whites in 2010.

141 ty was also inversely associated with higher NO2 exposure (beta = -22.8; 95% CI, -36.0 to -9.7; P = .

142 gh methionine intake, women with the highest NO2 exposure and lowest methionine intake had the greate

143 reaction of BH4(-) with a large excess of HN(NO2 )2 .

144 eaction of BH4(-) with two equivalents of HN(NO2 )2 afforded the di-substituted borate anion consisti

145 he BH4(-) anion with equimolar amounts of HN(NO2 )2 or of BH3 THF with K[N(NO2 )2 ](-) produced a mon

146 combined loss of polar headgroup and HNO2, [NO2-FA + H](+) and [NO2-FA - H](-) product ions, and cle

147 rnal boundary layer and the enhanced [HONO]/[NO2] ratios observed during dust storms in urban areas.

148 the presence of two electrophilic centers in NO2-CLA located on the beta- and delta-carbons with resp

149 In 2000 and 2010, disparities in NO2 concentrations were larger by race-ethnicity than by

150 between and within-city spatial gradients in NO2 concentrations.

151 2-1.28 per 1 interquartile range increase in NO2 [2.2 ppb]) and current wheeze (aOR, 1.14; 1.02-1.28)

152 ends suggested that there was an increase in NO2 columns in most areas from 2005 to around 2011 which

153 r for every 20-parts-per-billion increase in NO2 exposure.

154 struction, such that each 10-ppb increase in NO2 level was associated with a 5% decrease in FEV1/forc

155 hydroxyl radical ([HO2]/[OH]) and increased [NO2]/[NO] with higher levels of RBS and/or RIS.

156 ytic air pretreatment transforms NO gas into NO2 gas and thereby enhances the absorption of NOx in th

157 th aircraft, railway, and road traffic Lden; NO2; and PM2.5, respectively, with minimally overlapping

158 ve sites on soil surfaces drive ground-level NO2-to-nitrite conversion in the atmospheric boundary la

159 Relative to women with the lowest NO2 exposure and high methionine intake, women with the

160 b in 2000 to 2.9 ppb in 2010, estimated mean NO2 concentrations remained 37% higher for nonwhites tha

161 The mean NO2 value was 11.1 ppb (range, 4.3-29.7 ppb).

162 Although the national nonwhite-white mean NO2 concentration disparity decreased from a difference

163 Moreover, NO2-OA reduced the dephosphorylation of p38alpha by hema

164 2 )2 ](-) produced a mono-substituted [BH3 N(NO2 )2 ](-) anion, which contains a B-N connected dinitr

165 amounts of HN(NO2 )2 or of BH3 THF with K[N(NO2 )2 ](-) produced a mono-substituted [BH3 N(NO2 )2 ](

166 Nitrite accumulation (N-NO2(-)/N-NOX) of 92% was maintained.

167 The salts [H2 N-NO2 H][AsF6 ], [H3 N-NO2 ][SbF6 ], [MeHNNO2 H][SbF6 ], a

168 The salts [H2 N-NO2 H][AsF6 ], [H3 N-NO2 ][SbF6 ], [MeHNNO2 H][SbF6 ], and [Me2 NNO2 H][SbF6

169 to derive improved estimates of neighborhood NO2 concentrations by blending measurements with modeled

170 rom congenital malformations of the nervous (NO2, 1.525 [1.179, 1.974; p = 0.001]; PM10, 1.457 [1.150

171 We identified nine NO2-PCs and one NO2-PE species.

172 Nitrite (NO2(-)) and nitroso compounds (E-NO, E = RS, RO, and R2N

173 Nitrite (NO2(-)) supplementation limits hypoxia-induced oxidative

174 ) and hydroxyl radical ((*)OH), (2) nitrite (NO2(-)) and oxygen atom (O((3)P)), and (3) peroxynitrite

175 Nitrate (NO3(-)) and nitrite (NO2(-)) are known to be cardioprotective and to alter en

176 Excess nitrite (NO2(-)) concentrations in water supplies is considered d

177 eactions between nitric oxide (NO), nitrite (NO2-), and unsaturated fatty acids give rise to electrop

178 cal methods for conversion of NO to nitrite (NO2(-)) and nitrate (NO3(-)) have been proposed for (15)

179 etabolism involves NH3 oxidation to nitrite (NO2(-)) via a single obligate intermediate, hydroxylamin

180 The global inventory of NOx (NOx = NO + NO2) emissions is poorly constrained, with a large porti

181 of nitrogen oxides (NOx identical with NO + NO2) decreases.

182 Resulting maps of annual daytime NO, NO2, and black carbon at 30 m-scale reveal stable, persi

183 fects of minor flue gas components (SO2, NO, NO2, H2O, and O2) on vanadium at 500-600 degrees C were

184 ated with high nitrogen oxide (NOX = [NO] + [NO2]) concentrations.

185 of Dhc 16S rRNA genes, CH4, Fe(2+), NO3(-), NO2(-), and SO4(2-) concentrations, total organic carbon

186 CO3(-), HCO2(-), CH3CO2(-), SO4(2-), NO3(-), NO2(-), BrO3(-), AsO4(-), F(-), Cl(-), and Br(-) and, to

187 with dechlorination potential, with NO3(-), NO2(-), and Fe(2+) concentrations exhibiting precedence

188 arse, PM2.5, and PM2.5abs) and gaseous (NOx, NO2) pollutants were positively associated with prevalen

189 first time at the molecular level that the o-NO2 group contributes less compared to the p-NO2 group t

190 resulting in a very weak -M effect of the o-NO2 group, whereas the 2p orbitals of the N atom of the

191 l of the adjacent ring C atom to which the o-NO2 is attached are inclined at >30 degrees to each othe

192 ids (NO2 -FAs), such as nitro oleic acid (OA-NO2 ) and nitro linoleic acid (LNO2 ).

193 studied the effects of nitro-oleic acid (OA-NO2) on the human endothelial cell transcriptome.

194 , we show that the overexpression of both OA-NO2 and Nrf2 substantially decreased and that Nrf2 silen

195 ects of endothelin-1 (ET-1) is induced by OA-NO2 Inasmuch as ET-1 is one of the key regulators of vas

196 Moreover, OA-NO2 is capable of enhancing regulatory T-cell activity.

197 these results support the development of OA-NO2 as a promising therapeutic for ACD and provides new

198 We evaluated the effect of OA-NO2 on allergic contact dermatitis (ACD) using an establ

199 e to examine in more detail the effect of OA-NO2 on endothelin signaling in human endothelial cells.

200 In vivo SC OA-NO2 significantly inhibits pathways that lead to inflamm

201 We found that subcutaneous (SC) OA-NO2 injections administered 18 h prior to sensitization

202 Based on these results, we propose that OA-NO2 and Nrf2 may alleviate the vasoconstrictive effects

203 mmunoprecipitation analysis revealed that OA-NO2 increased the binding of Nrf2 to an antioxidant resp

204 These data suggest that OA-NO2 modulates endothelin signaling by increasing Nrf2-de

205 Nrf2 was found to regulate the OA-NO2-induced transcription of ET-B in human and mouse end

206 Thus, OA-NO2 treatment results in anti-inflammatory effects capab

207 Thus, we sought to determine whether OA-NO2 , an exemplary nitro-fatty acid, has the capacity to

208 ke significantly modified the association of NO2 exposure and livebirth (P = 0.01).

209 There was no significant association of NO2 levels with percent predicted FEV1, fraction of exha

210 vide new insights into the chemical basis of NO2-CLA signaling actions.

211 th the addition of different concertation of NO2(-).

212 sponsible for the functional consequences of NO2(-) exposure.

213 Conversion of NO2 to HONO in the dark was found to be significant and

214 orm very well in photo-assisted detection of NO2 gas.

215 to the sensitive and selective detection of NO2(-) with increasing concentrations quantifiable by UV

216 ensor could be used for the determination of NO2(-) with a linear range from 0.1-1600microm and a det

217 However, the worldwide distribution of NO2 exposure and associated impacts on health is still l

218 It is shown that the effect of NO2 from road traffic upon premature mortality was ten-f

219 ly contributing to the beneficial effects of NO2(-) on mitochondrial metabolism.

220 ression, and greater MRP1-mediated efflux of NO2-OA-glutathione conjugates.

221 nity tag labeling, to quantify the extent of NO2(-)-dependent S-nitrosation of proteins thiols in viv

222 athways stimulated by low O2, independent of NO2(-) concentrations.

223 pollutants, as well as 23-y running means of NO2 and NOx, with both overall and fatal incident MI.

224 ctrochemical analyzer for the measurement of NO2(-) in hypoxia induced H9c2 cardiac cells using ARM m

225 The mechanism of NO2 reduction on soil surrogates composed of HA and clay

226 NO2-Ln) in Arabidopsis and the modulation of NO2-Ln levels throughout this plant's development by mas

227 e main mechanism is the photodissociation of NO2, which then recombines with the ground electronic st

228 At greater than a threshold of 8 ppb of NO2 and after adjusting for race and season (spirometry

229 In this work, we examined the reactions of NO2-CLA with low molecular weight thiols (glutathione, c

230 Reduction of NO2 on ubiquitous Fe-bearing minerals in soil may explai

231 t there is energy barrier for the release of NO2 which prevent NO oxidation.

232 stepwise mechanisms with thiolate attack on NO2-CLA as rate-controlling step.

233 nd that the combined effect of urban form on NO2 is larger for small cities (beta x IQR = -0.46 for c

234 We identified nine NO2-PCs and one NO2-PE species.

235 -phenyl)pyridine-2,6-dicarboxamide, R = H or NO2, or N,N'-bis(2,6-diisopropylphenyl)-1-methylpiperidi

236 ignificant overall association between PM or NO2 exposures and PD risk.

237 r pollution exposure (represented by outdoor NO2 levels) at the birth address and performed a genome-

238 ctively); PM2.5 absorbance; nitrogen oxides (NO2 and NOx); traffic intensity; and elemental compositi

239 e derivatives were obtained for p-OCH3 and p-NO2 benzaldehyde.

240 ereas the 2p orbitals of the N atom of the p-NO2 group and the adjacent ring C atom are almost coplan

241 Hence, the p-NO2 group contributes largely toward the molecular react

242 NO2 group contributes less compared to the p-NO2 group toward the reactivity of 2,4-DNP-based probes.

243 The attachment of pendant NO2 and NEt2 groups at the opposite positions of the pi-

244 easure an average nitrite quantum yield (Phi(NO2(-))) of (1.1 +/- 0.2)% (313 nm, 50 muM nitrate, pH >

245 , 5.5, 8.1, and 11.5 mug/m3 for PM2.5, PM10, NO2, and NOx, respectively.

246 n between long-term exposure to PM2.5, PM10, NO2, or NOx and overall MI incidence, but we observed po

247 ls to evaluate the association between PM10, NO2, and CO concentrations and risk of incident estimate

248 notonic increasing association between PM10, NO2, and CO concentrations and risk of kidney outcomes.

249 l exposure to higher concentrations of PM10, NO2, and CO is associated with increased risk of inciden

250 ignificantly associated with all pollutants: NO2, 1.108 (1.038, 1.182; p < 0.001); PM10, 1.117 (1.050

251 ences that include increased N2O production, NO2(-) toxicity, and shifts in phytoplankton community c

252 Humic acid (HA) is thought to promote NO2 conversion to nitrous acid (HONO) on soil surfaces d

253 of the MeCN and EtCN solvates of 2 with R = NO2 have been determined.

254 A denitrifier method was used to reduce NO2(-) and NO3(-) in the trapping solution quantitativel

255 12.2 parts per billion) increase in regional NO2 exposure was associated with a 34% increased risk of

256 Notably, higher exposures to regional NO2, acid vapor, and EC were also associated with a high

257 ty decreased from 2000 to 2010, but relative NO2 exposure disparities persisted, with higher NO2 conc

258 influenced model performance and residential NO2 exposure estimates for a cohort of 13679 participant

259 ent), our models suggest that Christchurch's NO2 concentrations would be approximately 60% higher tha

260 and competitively by N3(-), OCN(-), SCN(-), NO2(-), and NO3(-), whereas CO2 reduction is inhibited o

261 metry standardized by age, height, and sex), NO2 levels were associated highly with airflow obstructi

262 oxidation of atmospheric gases such as SO2, NO2, volatile organic compounds, organic and inorganic a

263 elevant toxic chemicals, including NH3, SO2, NO2, H2S, and some volatile organic compounds, with part

264 riging or satellite data to a well-specified NO2 land-use regression model each improves prediction.

265 ion is supported by experiments that studied NO2 reactivity on mineral surfaces coated with the model

266 n to NO2 in excess ozone (O3) and subsequent NO2 collection in a 20% triethanolamine (TEA) solution a

267 iency of NO conversion to NO2 and subsequent NO2 collection in the TEA solution is >98% under a varie

268 6; p = 0.002]) and gastrointestinal systems (NO2, 1.214 [1.006, 1.466; p = 0.043]; PM10, 1.312 [1.096

269 In animal systems, NO2-FAs are considered novel signaling mediators of cell

270 In this study, we found that NO2, PM10, and SO2 were differentially associated with a

271 Bioinformatics analysis revealed that NO2-Ln was also involved in the response to oxidative st

272 thelial MCF-10A and MCF7 cells revealed that NO2-OA more selectively inhibited TNBC function.

273 The NO2 sensitivity of these TFTs with the dielectric surfac

274 The NO2 trends suggested that there was an increase in NO2 c

275 The NO2(-) spiked cultures with an initial COD:N = 11:1 accu

276 r results indicate it is as important as the NO2 channel.

277 In comparison, the NO2(-) spiked cultures with COD:N = 4:1 showed significa

278 show that the efficiency of NO conversion to NO2 and subsequent NO2 collection in the TEA solution is

279 cts soil-emitted NO through NO conversion to NO2 in excess ozone (O3) and subsequent NO2 collection i

280 romium trioxide (CrO3), before conversion to NO2(-) and NO3(-) in an alkaline hydrogen peroxide (H2O2

281 NO3(-) action results from its conversion to NO2(-) by salivary bacteria, but the mechanism(s) by whi

282 Exposure to NO2 also showed positive associations with wheeze and sh

283 However, exposure to NO2(-) in conjunction with ischemia led to extensive S-n

284 ded affinity tag), we found that exposure to NO2(-) under normoxic conditions or exposure to ischemia

285 the corresponding NO3 adducts on exposure to NO2(g).

286 with an increase in during-walk exposure to NO2, ultrafine particles and PM2.5, and an increase in P

287 yzes the four-electron oxidation of NH2OH to NO2(-) We provide evidence that HAO oxidizes NH2OH by on

288 ic features, bacteria able to reduce NO3- to NO2- were isolated from soil, N-oxide gas products were

289 chondrial inner membrane to HNO2, but not to NO2(-), combined with the lack of S-nitrosation during a

290 od in which NO is oxidized quantitatively to NO2 by chromium trioxide (CrO3), before conversion to NO

291 posite shows appropriate selectivity towards NO2(-) in the presence of potentially interfering metal

292 ons and satellite-retrieved CO, tropospheric NO2, and aerosol optical depth (AOD) (R(2) > 0.8).

293 stically significant relationship with urban NO2; their combined effect could be substantial.

294 e NH4(+) to N2 under anoxic conditions using NO2(-).

295 Twice as much HONO was formed when NO2 reacted with HA that was photoreduced by irradiation

296 and Oceania (adjusted R(2) within 11%) where NO2 monitoring data are sparse.

297 vide the only likely set of conditions where NO2-mediated oxidation of SO2 outcompetes with other wel

298 vary bacteria, but the mechanism(s) by which NO2(-) affects metabolism remains obscure.

299 .001]) but not significantly associated with NO2 and PM10 (1.044 [0.998, 1.092; p = 0.059] and 1.008

300 found for BC, and a weaker association with NO2.

301 When combined with NO2(-) shock, this prolonged the duration over which ins

302 increase in PWV and augmentation index with NO2 and ultrafine particles.