ライフサイエンスコーパス: nonsmoker

1 57.5 +/- 8.9 yr; 37.5% male; 12 smokers; 12 nonsmokers).

2 cts undergoing lung resection (59 smokers, 8 nonsmokers).

3 oderately dependent cigarette smokers and 13 nonsmokers).

4 hol intake, healthy diet, physically active, nonsmoker.

5 4 years), long-term quitter (>4 years), and nonsmoker.

6 condary to POHS are almost 3 times that of a nonsmoker.

7 She was a nonsmoker.

8 n the COPDGene Study, including 103 lifetime nonsmokers.

9 ker and less fatigue resistant than those of nonsmokers.

10 o of in-hospital mortality in smokers versus nonsmokers.

11 sive smoke exposure increased the risk among nonsmokers.

12 All participants were otherwise healthy and nonsmokers.

13 and 18.8% met combined ABC targets and were nonsmokers.

14 flow variability between active smokers and nonsmokers.

15 The study did not allow for evaluation of nonsmokers.

16 tal tracers, and estimated health impacts to nonsmokers.

17 r premature responding versus ex-smokers and nonsmokers.

18 group differences between adult smokers and nonsmokers.

19 er quality-adjusted life-year, especially in nonsmokers.

20 itude % mean (10.0% vs. 6.4%; P = 0.02) than nonsmokers.

21 dings were consistent among both smokers and nonsmokers.

22 ate myocardial layers in healthy smokers and nonsmokers.

23 a associated with long-term weight change in nonsmokers.

24 ted in the microbiome of healthy smokers and nonsmokers.

25 night-shift work among smokers but not among nonsmokers.

26 ,847 patients with COPD, 298 smokers and 204 nonsmokers.

27 bestos increases lung cancer mortality among nonsmokers.

28 %) had a history of smoking; 239 donors were nonsmokers.

29 100 person-examinations (95% CI, 2.0-3.0) in nonsmokers.

30 ularly in populations that include women and nonsmokers.

31 wal, as similar effects were not detected in nonsmokers.

32 connectivity strength among smokers but not nonsmokers.

33 ith weight change at the 1-y follow-up in 16 nonsmokers.

34 in regions associated with weight changes in nonsmokers.

35 sues and urine are higher in smokers than in nonsmokers.

36 concentrations, benefiting both smokers and nonsmokers.

37 ipients of grafts from smokers compared with nonsmokers.

38 ifferentiated patients with lung cancer from nonsmokers.

39 dence linking SHS exposure to lung cancer in nonsmokers.

40 lial cells from active smokers compared with nonsmokers.

41 he associations were similar for smokers and nonsmokers.

42 f the TP53 mutations in human lung cancer in nonsmokers.

43 smokers, but did not increase risk of HCC in nonsmokers.

44 generally had poorer treatment outcomes than nonsmokers.

45 )*-nicotinic acetylcholine receptors than do nonsmokers.

46 rs, and remained elevated when restricted to nonsmokers.

47 bacteria was observed in smokers but not in nonsmokers.

48 ten healthy, visually normal adults who were nonsmokers.

49 ith lower niche saturation than that seen in nonsmokers.

50 higher risk of recurrent disease compared to nonsmokers.

51 oalveolar lavage fluid compared with that of nonsmokers.

52 ha(4)beta(2)* nAChR occupancy in smokers and nonsmokers.

53 y, approximately 1% for smokers and 0.3% for nonsmokers.

54 in risk of bladder cancer, particularly for nonsmokers.

55 isolated from humans who smoke compared with nonsmokers.

56 mokers, who, in turn, had higher levels than nonsmokers.

57 and overweight subjects, and in smokers and nonsmokers.

58 ased risk of CVD incidence in ARIC cigarette nonsmokers.

59 rterioles (P = 0.035) compared with those in nonsmokers.

60 ry function, but it appears to be limited to nonsmokers.

61 also confer a greater bleeding risk than in nonsmokers.

62 smokers of >or=10 cigarettes per day and 30 nonsmokers.

63 of 2.47 (95% CI, 1.24 to 4.92) compared with nonsmokers.

64 AU, P = 0.02) mRNA expression compared with nonsmokers.

65 sms underlying the genesis of lung cancer in nonsmokers.

66 ractional synthesis rate (FSR) compared with nonsmokers.

67 e seen in samples from smokers but rarely in nonsmokers.

68 computed tomography scans of adult lungs of nonsmokers.

69 ronic airflow obstruction but is composed of nonsmokers.

70 els on average up to eight times higher than nonsmokers.

71 of 1.76 (95% CI, 1.23 to 2.51) compared with nonsmokers.

72 and no confounding medication use, and were nonsmokers.

73 he extent of chlorination at alpha-Tyr-24 in nonsmokers.

74 resonance imaging data in 66 smokers and 92 nonsmokers.

75 ficantly lower for smokers compared with the nonsmokers.

76 -Met-32 significantly in all subjects and in nonsmokers.

77 rom smoking mothers compared with those from nonsmokers.

78 up; n = 42), each stratified for smokers and nonsmokers.

79 entrations of serum endotoxin than asthmatic nonsmokers (0.25 EU/mL [IQR, 0.09-0.39 EU/mL] vs 0.08 EU

80 .04]) but reversed during adenosine stress (nonsmokers, 0.89 [P = .03]; smokers, 0.92 [P = .42]).

81 dial-to-epicardial gradient existed at rest (nonsmokers, 1.10 [P = .002]; smokers, 1.30 [P = .01]) an

82 .00) for all subjects, 1.75 (1.16, 2.65) for nonsmokers, 1.15 (0.58, 2.30) for current smokers, 2.42

83 P = .002]; smokers, 1.30 [P = .01]) and CPT (nonsmokers, 1.19 [P < .001] smokers, 1.28 [P = .04]) but

84 men; mean [SD] age, 35.8 [9.9] years) and 20 nonsmokers (10 women and 10 men; mean [SD] age, 30.4 [7.

85 in 18 daily smokers (7 women, 11 men) and 19 nonsmokers (10 women, 9 men).

86 Twenty-nine healthy volunteers (19 nonsmokers, 10 smokers; mean age +/- standard deviation,

87 Compared with 14 nonsmokers, 14 ex-smokers had global reductions in the a

88 mokers (reference group), 92 (12.5%) passive nonsmokers, 157 (21.3%) ex-smokers without environmental

89 ons in insulin action in smokers compared to nonsmokers, 2) increased saturation of IMTG and DAG in s

90 8) and ex-smokers (28.2%, P = 0.022) than in nonsmokers (38.5%).

91 : 11.0, 64.4; P = .006), smoking (smokers vs nonsmokers, 45.2 mm(3); 95% CI: 7.1, 83.4; P = .020), an

92 y-dense food, were measured in a group of 27 nonsmokers (5 men).

93 -year survival than recipients of lungs from nonsmokers (65.8% vs. 48.3%, P<0.05), but recipients of

94 data from 51,080 current smokers and 190,178 nonsmokers (87% European descent) to identify loci influ

95 ly reduced the P50 sensory gating deficit in nonsmokers after long-term treatment (P = .006), (2) red

96 and urinary NNAL increased significantly in nonsmokers after outdoor SHS exposure.

97 re "normalized" in smokers (and increased in nonsmokers) after acute nicotine administration.

98 ed in the smoker AgP group compared with the nonsmoker AgP group, in the CP group, phospholipid, prot

99 restricting the population to term births to nonsmokers, along with other restrictions, to isolate th

100 Nonsmokers' AM generated significantly more tumor necros

101 Both smokers' and nonsmokers' AM induced FoxP3(+) T regulatory cell phenot

102 A healthy lifestyle was defined as being a nonsmoker and physically active (>/=150 min/wk), and hav

103 Compared with both nonsmoker and smoker control subjects, during long-term

104 PGE2 receptors EP2 and EP4 as compared with nonsmoker and smoker control subjects.

105 al community compositions: one common to the nonsmoker and smoker groups, a second to the GOLD 4 grou

106 with relative VOC levels was up to 99.8% for nonsmokers and 100.0% for smokers.

107 [(18)F]fluoro-L-DOPA (FDOPA)-PET scans in 15 nonsmokers and 30 nicotine-dependent smokers, who either

108 Baseline striatal D2R did not differ between nonsmokers and ex-smokers.

109 higher aggression scores compared with both nonsmokers and ex-smokers.

110 availability (binding potential, BPND) than nonsmokers and exhibit greater smoking-induced striatal

111 h BPND in the caudate nucleus and putamen in nonsmokers and female smokers but not in male smokers an

112 Prevalence of chronic rhinitis was lowest in nonsmokers and highest in very heavy smokers (18.5% vs 3

113 Nonsmokers and patients with a higher baseline lung tumo

114 hy smokers were intermediate between healthy nonsmokers and patients with COPD.

115 rs (control), non-pregnant smokers, pregnant nonsmokers and pregnant smokers and sequenced using 16S-

116 ward responsiveness relative to both control nonsmokers and rMDD smokers; conversely, smokers with rM

117 Mouth communities differed between nonsmokers and smokers in species such as Porphyromonas,

118 Macrophages from nonsmokers and smokers were CD163(+), CD206(+), CD14(+),

119 nsive to budesonide compared with those from nonsmokers and smokers when stimulated with LPS.

120 Participants were nonsmokers and smokers without significant comorbidities

121 decade for U.S. children, teens, and adults (nonsmokers and smokers) and, if so, factors influencing

122 ly, this effect is observed independently in nonsmokers and smokers, although the circuit strength di

123 The mouth microbiome differs in nonsmokers and smokers, but lung communities were not si

124 hich were 0.67 and 0.65 for SNR case-matched nonsmokers and smokers, respectively.

125 nome-wide methylation analysis of SAE DNA of nonsmokers and smokers, the data identified 204 unique g

126 developed with measurements from 78 healthy nonsmokers and subsequently validated in a group of 21 o

127 association in other populations, especially nonsmokers and women.

128 rapy may outweigh the benefits, yet for most nonsmokers (and ex-smokers), the benefits of radiotherap

129 se), participant characteristics (smokers or nonsmokers), and drug manipulation employed (pharmacolog

130 for the effect of obesity on mortality among nonsmokers, and 1.97 (95% CI: 1.73, 2.22) for the joint

131 We enrolled 40 subjects with asthma, 13 nonsmokers, and 16 smokers.

132 identified as smokers, 28 were identified as nonsmokers, and 3 were identified as unknown.

133 y diet, 66% were physically active, 95% were nonsmokers, and 55% had low stress.

134 The group with improved eGFR had more women, nonsmokers, and a lower cardiac index.

135 ND-E/I ratio was greater in smokers than in nonsmokers, and it progressively increased from mild to

136 egative subjects, nondrinkers, nondiabetics, nonsmokers, and nonobese individuals indicated a signifi

137 with body mass index 22 to 40, disease-free, nonsmokers, and nonusers of exogenous hormones.

138 tory: nonsusceptible nonsmokers, susceptible nonsmokers, and smokers.

139 onal criteria together with healthy smokers, nonsmokers, and subjects with moderate chronic obstructi

140 e-wide DNA methylation changes compared with nonsmokers, and whether changes in SAE DNA methylation w

141 or long-term continuing smokers and 0.3% for nonsmokers; and cardiac mortality, approximately 1% for

142 5% CI, 1.2-58.6) and to susceptibility among nonsmokers (AOR, 8.5; 95% CI, 1.3-57.2).

143 differences that this approach reveals among nonsmokers, asymptomatic smokers, and patients with chro

144 3 subjects were separated into three groups: nonsmokers, asymptomatic smokers, and symptomatic smoker

145 Compared with nonsmokers, beta(2)*-nAChR availability in the striatum,

146 thickness of the insula in 18 smokers and 24 nonsmokers between the ages of 16 and 21 years.

147 urned to control levels in alcohol-dependent nonsmokers, but alcohol-dependent smokers had significan

148 3-pyridyl)-1-butanol identified 27 of the 28 nonsmokers by history either as active smokers (n = 6, 2

149 In nonsmokers, by contrast, the shift from health to mucosi

150 ower striatal D2R availability compared with nonsmokers (caudate, putamen, and ventral striatum) and

151 antly higher in asymptomatic smokers than in nonsmokers (change in the standard deviation of Pao2 = 7

152 urrent smoking and for passive smoking among nonsmokers compared with a reference category of never a

153 e likely to be older, female, sedentary, and nonsmokers compared with those without SMI.

154 Nicotine-dependent smokers and nonsmokers completed a probabilistic reversal learning t

155 from patients with COPD and from smoker and nonsmoker control subjects.

156 cally and periodontally healthy non-pregnant nonsmokers (control), non-pregnant smokers, pregnant non

157 range of covariates, high SHS exposure among nonsmokers (cotinine level >0.70 and <15.00 microg/L) wa

158 and nucleic acid content were found between nonsmoker CP and AgP groups.

159 Based on these variations, nonsmoker CP and AgP patients were discriminated from ea

160 groups, however, pregnant women (smokers and nonsmokers) demonstrated higher levels of gram-positive

161 received placebo, whereas alcohol use among nonsmokers did not vary by naltrexone assignment.

162 measurements above the LOD, with smoker and nonsmoker DNA containing 3.1 and 1.3 BPDE-N(2)-dG adduct

163 5, P < .001) but no between-group (smoker vs nonsmoker) effect.

164 ajor randomized trial data demonstrated that nonsmokers experience less or no benefit from clopidogre

165 the major locations outside of the home for nonsmokers' exposure to secondhand smoke (SHS).

166 e but not male smokers than in corresponding nonsmokers (F1, 32=5.089, p=0.03).

167 decreased reward sensitivity in smokers (vs nonsmokers; familywise error-corrected P < .05) in the d

168 obtained 10 minutes apart in 25 subjects: 10 nonsmokers (five men, five women; mean +/- standard devi

169 stinent smokers was restored to the level of nonsmokers following stimulation of nicotinic acetylchol

170 nd from 15 individuals who had never smoked (nonsmokers) following 1, 2, 4, and 7 days of undisturbed

171 related to reduced lung function in current nonsmokers (forced expiratory flow midexpiratory phase [

172 Meta-analysis of 7 studies conducted among nonsmokers found a summary relative risk of 0.59 (95% co

173 % methylation difference between placebo and nonsmoker groups were restored (by at least 50%) toward

174 A subgroup of pregnant smokers and nonsmokers had genotyping performed.

175 ailability relative to comparison group, and nonsmokers had lower beta2*-nAChR availability relative

176 As hypothesized, rMDD nonsmokers had lower reward responsiveness relative to b

177 risk taking, and impulsivity in smokers and nonsmokers have not been investigated.

178 re significantly higher in smoker homes than nonsmoker homes (by concentration: 990 ng/g vs 756 ng/g,

179 r in-hospital mortality among smokers versus nonsmokers hospitalized for these events.

180 ctor for lung cancer development in lifelong nonsmokers; however, the mechanistic involvement of SHS

181 The risk reduction was limited to nonsmokers (HR = 0.58, 95% CI: 0.41, 0.83) (P(trend) = 0

182 gher beta(2)*-nAChR availability than female nonsmokers in any region.

183 d over a period of ~45 h in 56 residences of nonsmokers in Copenhagen, Denmark.

184 w remarkable differences between smokers and nonsmokers in levels of a leukocyte formaldehyde-DNA add

185 emale nonsmokers showed higher BEN than male nonsmokers in prefrontal cortex, insula, and precuneus,

186 ly higher in male smokers compared with male nonsmokers in striatum, cortex, and cerebellum, but fema

187 Among the nonsmokers in the ABT-126 25 mg group (N=19), significan

188 used a case-cohort design of postmenopausal nonsmokers in the multiethnic Women's Health Initiative

189 with a variety of adverse health outcomes in nonsmokers, including emphysema (a chronic obstructive p

190 distinctly divergent pathways in smokers and nonsmokers, indicating a need for personalized therapeut

191 els successfully differentiated smokers from nonsmokers, irrespective of periodontal status, with 100

192 Compared with nonsmokers, K was 15% to 20% lower in the caudate nuclei

193 k is at least 2-fold higher when compared to nonsmokers lacking these risk alleles.

194 p to 1 month of abstinence and normalizes to nonsmoker levels by 6 to 12 weeks of abstinence from tob

195 roups were restored (by at least 50%) toward nonsmoker levels with vitamin C treatment.

196 s cotinine levels, we classified patients as nonsmokers (< 3.1 ng/mL), light smokers (3.1-20.9 ng/mL)

197 e combined and applied to current smoker and nonsmoker lung cancer and cardiac mortality rates in pop

198 f all types of mutations in the TP53 gene of nonsmokers' lung tumors and in the cII transgene of lung

199 antiplatelet response in clopidogrel-treated nonsmokers may provide an explanation for the smokers' p

200 ter in HCs than SCZ smokers (n = 11) and SCZ nonsmokers (n = 14).

201 RESEARCH DESIGN AND Nonsmokers (n = 18, aged 20 +/- 0.5 years, BMI 22 +/- 0.

202 Alveolar macrophages, obtained from nonsmokers (n = 20), COPD ex-smokers (n = 32), and COPD

203 COPD (n = 32), smokers (n = 7), and healthy nonsmokers (n = 25).

204 In young to middle-aged (predominately male) nonsmokers (n = 30) and smokers (n = 35), N-acetylaspart

205 led, crossover study of objectively assessed nonsmokers (n = 56) and smokers (n = 54) with stable cor

206 (10th to 12th order) epithelium from healthy nonsmokers (n = 60), healthy smokers (n = 73), and smoke

207 ession in 178 individuals, including healthy nonsmokers (n = 60), healthy smokers (n = 82), and COPD

208 A from lung tissue samples was obtained from nonsmokers (n = 8); smokers without COPD (n = 8); patien

209 i, lateral geniculate body, and thalamus for nonsmokers (n = 9) but were less than 1 in the nAChR-poo

210 from baseline to final MCCB composite score: nonsmokers (N=69) demonstrated a difference from placebo

211 (1940s to 1980s) and three smoking history (nonsmokers, never-dependent smokers and ever-dependent s

212 OR of 2.68 (95% CI, 2.03-3.54) compared with nonsmokers of blood type O.

213 If all U.S. adults became nonsmokers of normal weight by 2020, we forecast that th

214 half the sample) significantly differed from nonsmokers on several demographic and drinking-related v

215 Ten smokers were matched with the 10 nonsmokers on the basis of signal-to-noise ratio (SNR).

216 nce of smoking status (smokers compared with nonsmokers) on the brain response to food in regions ass

217 ly performed in nine subjects: three healthy nonsmokers (one man, two women; mean age, 45 years +/- 4

218 hree separate models were generated: one for nonsmokers, one for the SNR-matched smokers, and one for

219 i in chronic cigarette smokers compared with nonsmokers, only a few studies assessed brain spontaneou

220 ificantly more AM from smokers compared with nonsmokers or ex-smokers (P < 0.01).

221 youth, if they increase the likelihood that nonsmokers or former smokers will use combustible tobacc

222 effects may be influenced by smoking status (nonsmokers OR, 0.65; 95% CI, 0.26-1.22 vs current smoker

223 ronounced among women who were younger, were nonsmokers, or had optimal weight.

224 jects with COPD, 9.5% of smokers, and 10% of nonsmokers (P < 0.001).

225 COPD and smokers with asthma than in healthy nonsmokers (P = .003 and P = .035, respectively) but sim

226 ssel arteriovenous ratio between smokers and nonsmokers (P = 0.243).

227 < 0.001), and regular smoking (-0.27 mum vs. nonsmokers; P = 0.02).

228 ge-matched male (n = 26) and female (n = 30) nonsmokers participated in a [(123)I]5-IA SPECT imaging

229 Thirteen healthy and 13 MDD nonsmokers participated in two [(11)C]ABP688 positron em

230 2 periodontitis groups as well as smoker and nonsmoker patients could be differentiated from each oth

231 A subset of subjects (n = 23/20; smokers/nonsmokers) performed the monetary incentive delay task,

232 In both smokers and nonsmokers, peri-implant mucositis appears to be a pivot

233 Ptrend < 0.001), with no association seen in nonsmokers (Pinteraction = 0.03).

234 Patients who were female, elderly, nonsmokers, poorly educated, with low income, and those

235 circuit strength distinguishes smokers from nonsmokers, predicts addiction severity in smokers, and

236 s increased by asbestos exposure alone among nonsmokers (rate ratio = 3.6 [95% confidence interval (C

237 nterval (CI), 1.7-7.6]), by asbestosis among nonsmokers (rate ratio = 7.40 [95% CI, 4.0-13.7]), and b

238 to live with another smoker (compared with a nonsmoker (referent)) increased the odds of smoking (OR

239 te exposure and PD effects of clopidogrel in nonsmokers relative to smokers.

240 Nonsmokers responded to CPT with a 47% increase in MBF (

241 operative morbidity was increased in passive nonsmokers (RR, 1.51; 95% CI, 1.04-2.21) and passive ex-

242 group of age-, sex- and body weight-matched nonsmokers selected from the pool of nonsmokers who part

243 ory analyses indicated that both smokers and nonsmokers showed activity decreases in the vmPFC and PC

244 Female nonsmokers showed higher BEN than male nonsmokers in pre

245 stratum of current smokers, but not that of nonsmokers, showed significant improvement versus placeb

246 Compared with nonsmokers, smokers had a greater response to milk shake

247 Compared with nonsmokers, smokers showed greater activity in left ante

248 ns were isolated from human lung tissue from nonsmokers, smokers, and patients with COPD by using Per

249 lls isolated from bronchoscopic brushings of nonsmokers, smokers, and smokers with chronic obstructiv

250 astatic prostate cancer more frequently than nonsmokers, suggesting that a tobacco-derived factor is

251 ic states along a trajectory: nonsusceptible nonsmokers, susceptible nonsmokers, and smokers.

252 and platelet reactivity index were higher in nonsmokers than in smokers (p = 0.043, p = 0.005, and p

253 rs were more likely to be older, leaner, and nonsmokers than nonretainers/nonengagers.

254 platelet aggregation (IPA) trended lower in nonsmokers than smokers (least squares mean treatment di

255 Compared with nonsmokers, the most striking change was for TLR5, which

256 Among nonsmokers, the risk of death was lowest for a BMI of 20

257 okers and 78.4 years (95% CI, 70.8-84.0) for nonsmokers; the numbers of life-years lost in associatio

258 We characterized the exposure of nonsmokers to secondhand smoke (SHS) outside a restauran

259 rmation on current trends in the exposure of nonsmokers to SHS across various occupational groups is

260 esign, 24 overnight-abstinent smokers and 20 nonsmokers underwent approximately 17 days of vareniclin

261 ipe-only smokers in comparison with lifelong nonsmokers using clinical parameters of cough and sputum

262 smokers microg/mg dry wt, DAG 0.34 +/- 0.02 nonsmokers vs. 0.35 +/- 0.02 smokers microg/mg dry wt) o

263 wt) or IMTG FSR between groups (0.66 +/- 0.1 nonsmokers vs. 0.55 +/- 0.09 smokers %/hr).

264 rator-activated receptor-gamma (1.76 +/- 0.1 nonsmokers vs. 1.42 +/- 0.11 smokers arbitrary units [AU

265 IMTG or DAG concentration (IMTG 24.2 +/- 3.4 nonsmokers vs. 27.2 +/- 5.9 smokers microg/mg dry wt, DA

266 onocyte chemotactic protein-1 (3.11 +/- 0.41 nonsmokers vs. 4.83 +/- 0.54 smokers AU, P = 0.02) mRNA

267 patients and with passive smoking in 41% of nonsmokers (vs 20% and 40% in general population, respec

268 ss MR per 1000 person-years among current vs nonsmokers was 17.6 (95% CI, 13.3-21.9) for HIV patients

269 The difference between smokers and nonsmokers was not driven by mutations in known driver g

270 Seventeen right-handed smokers and 17 nonsmokers watched a popular movie while undergoing func

271 Compared with nonsmokers, waterpipe smokers had more cough and sputum

272 10(8) normal nucleotides, while those in 20 nonsmokers were 0.19 +/- 0.87, 4.1 +/- 13.3, and 1.0 +/-

273 Thirty-three healthy nonsmokers were exposed to 1 of 2 low levels of aged SHS

274 the present study, 55 smokers and 49 healthy nonsmokers were included.

275 er placement of a nicotine or placebo patch; nonsmokers were scanned twice without nicotine manipulat

276 placebo treated) and 76 newborns of pregnant nonsmokers were studied with newborn PFTs.

277 y-2 (AHSMOG-2), a cohort of health conscious nonsmokers where 81% have never smoked.

278 ime intensity-years of passive smoking among nonsmokers, whereas it decreased with greater alcohol co

279 nd temporal variability in Pao2 than did the nonsmokers, which suggests that this parameter allows de

280 ut the risk of non-Hodgkin lymphoma (NHL) in nonsmokers who are exposed to environmental tobacco smok

281 large airways and bronchopulmonary LNs of 11 nonsmokers who died from an asthma exacerbation (fatal a

282 matched nonsmokers selected from the pool of nonsmokers who participated in study 1.

283 with COPD, 24 ever-smokers without COPD, 32 nonsmokers who underwent a renal biopsy or nephrectomy,

284 of 8 current smokers, 10 ex-smokers, and 18 nonsmokers who were scanned with positron emission tomog

285 dy for up to 235 hr per participant among 50 nonsmokers with coronary artery disease who were >/= 71

286 Selected patients, nonsmokers with less advanced nodal stage, may be overtr

287 Compared with nonsmokers with no other healthy lifestyle factors (heal

288 subjects with moderate COPD and smokers and nonsmokers with normal lung function with rhinovirus.

289 dontal pathology in 120 systemically healthy nonsmokers with periodontitis, with available data on cl

290 Relative to nonsmokers with schizophrenia, smokers with schizophreni

291 ke exposure as measured by the proportion of nonsmokers with undetectable levels of cotinine and by g

292 scover adducts that distinguish smokers from nonsmokers with untargeted adductomics indicates that th

293 thylated in SAE DNA of smokers compared with nonsmokers, with 67% of the regions with differential me

294 s demonstrated less microbial diversity than nonsmokers, with differences in relative abundances of O

295 metalloproteinase 9 compared with cells from nonsmokers, with no difference between the remaining fra

296 all significantly higher in smokers than in nonsmokers, with pvalues of 0.0004, 0.0009, and 0.0004,

297 mokers exhibited lower diversity compared to nonsmokers, with significant enrichment for disease-asso

298 pect to mortality.For healthier agers (i.e., nonsmokers without disease-associated weight loss), havi

299 ugment cognition among cigarette smokers and nonsmokers, yet the systems-level neurobiological mechan

300 Women, nonsmokers, younger participants, and those with hyperte