ライフサイエンスコーパス: non-smoker

1 HNP 1-3 when compared with diseased sites of non-smokers.

2 d lower risk-taking to rewards compared with non-smokers.

3 onse patterns were found in both smokers and non-smokers.

4 e implicating the dangers of nCB exposure in non-smokers.

5 PDLSC from teeth extracted from smokers and non-smokers.

6 predicting monetary cues in both smokers and non-smokers.

7 periodontal healing in smokers compared with non-smokers.

8 reduction in clinical outcomes compared with non-smokers.

9 fect is compromised in smokers compared with non-smokers.

10 esis capacity in heavy smokers compared with non-smokers.

11 fferences in performance between smokers and non-smokers.

12 s had 3.5%, 12.8%, and 23.2% greater AL than non-smokers.

13 infected with Porphyromonas gingivalis than non-smokers.

14 ex-smokers and 1.27 (95% CI 0.87 to 1.86) in non-smokers.

15 fferent site profiles among both smokers and non-smokers.

16 P 1-3 than healthy sites in both smokers and non-smokers.

17 lung tissue of current smokers compared with non-smokers.

18 issue, from patients with COPD, smokers, and non-smokers.

19 ic DNA from smokers compared with former and non-smokers.

20 ty Status Scale scores 4 and 6 compared with non-smokers.

21 representative cohorts of adult smokers and non-smokers.

22 across all conditions, compared to non-ADHD non-smokers.

23 ermined in smokers and results compared with non-smokers.

24 tial pathogens as compared with the flora of non-smokers.

25 ation found among younger adults, women, and non-smokers.

26 All participants were non-smokers.

27 reater level of RAGE compared to the matched non-smokers.

28 periodontal disease and COPD among former or non-smokers.

29 rlic, hawthorn and fermented bean curd) than non-smokers.

30 3.0) and severe CAL (RRR = 8.2) compared to non-smokers.

31 smokers of 15 or more cigarettes a day as in non-smokers.

32 lements, may also affect risk, especially in non-smokers.

33 equate for current or recent smokers but not non-smokers.

34 ding and higher number of missing teeth than non-smokers.

35 ly to exhibit the presence of pathogens than non-smokers.

36 significantly more maxillary bone loss than non-smokers.

37 o the model, which included IL-1 genotype in non-smokers.

38 Similar risk estimates were seen among non-smokers.

39 s greater among cigarette smokers than among non-smokers.

40 old risk (women) of tooth loss compared with non-smokers.

41 return to the rate of tooth loss observed in non-smokers.

42 cigarettes but remained higher than those in non-smokers.

43 kers was 2.3 times that of former smokers or non-smokers.

44 ained from periodontally healthy smokers and non-smokers.

45 er adults is more pronounced in smokers than non-smokers.

46 quit lose a decade of life expectancy versus non-smokers.

47 ividuals who had tried smoking compared with non-smokers.

48 delayed loaded (DL) implants in smokers and non-smokers.

49 ng to smokers having 16.8% lower values than non-smokers.

50 osa of the asthmatic smokers compared to the non-smokers.

51 nd soft tissue status in healthy smokers and non-smokers.

52 but only lysine was depleted in biofilm from non-smokers.

53 concentration were significantly lower than non-smokers.

54 ihood of TP in current smokers compared with non-smokers.

55 in the lungs of murine smokers compared with non-smokers.

56 Non-smokers (0- to 10-ng/ml cotinine level) healed with

57 Mean probing reduction was 50% greater among non-smokers (0.6 mm) when compared to smokers (0.4 mm),

58 At 9 months both smokers (0.67 +/- 0.39) and non-smokers (0.78 +/- 0.30) had a significant decrease i

59 0.05) lower in smokers (1.32 +/- 0.45) than non-smokers (1.45 +/- 0.40).

60 hyperresponsiveness after FP was greater in non-smokers (1.5- and twofold doubling dose difference f

61 At baseline, RPS was elicited in all non-smokers (100%) and in only 3 of 15 smokers (20%; P<.

62 -training, RFVOL was smaller in smokers than non-smokers (100.9 +/- 20.2 vs. 108.7 +/- 24.5, p = 0.01

63 red to former cigarette smokers (20.2%), and non-smokers (13.1%).

64 in beyond the threshold were much greater in non-smokers (13.9%) compared to 9.0% in smokers (P <0.01

65 in the smokers (83 ng mL(-1)), compared with non-smokers (212 ng mL(-1), p = 0.013).

66 ed in smokers (331 ng mL(-1)), compared with non-smokers (238 ng mL(-1), p = 0.008).

67 geal Swallow; RPS were studied in 15 healthy non-smokers (24.2+/-3.3 SD y, 7 males) and 15 healthy ch

68 78%, P=0.001) without affecting responses in non-smokers (401+/-80%).

69 more likely female (81% vs 60%; p<0.001) and non-smokers (53% vs 42%; p=0.004).

70 was significantly higher among smokers than non-smokers (62.5% versus 14.3%, respectively).

71 issue biopsies from 120 systemically healthy non-smokers, 65 with CP and 55 with AgP, each contributi

72 s was found in smokers (93.8%) compared with non-smokers (76.9%).

73 he LAR was also attenuated in smokers versus non-smokers (adjusted mean minimum change in FEV1 (L) ov

74 s assessing bone regeneration in smokers and non-smokers after periodontal therapy were selected.

75 ase consisting of 725 self-reported lifelong non-smokers aged 53 to 74 years.

76 We recruited eligible non-smokers (aged 18-65 years) in 28 international study

77 Patients were non-smokers, aged >/=40 years, and using antidiabetic dr

78 Non-smokers also presented the greatest reductions in me

79 ion and similarly, abolishing this reflex in non-smokers also results in laryngeal spillage.

80 ces when analyses were restricted to healthy non-smokers also suggested some residual confounding by

81 Analysis of palatal tissues from 12 non-smokers and 10 smokers identified 830 significantly

82 pulation comprised 15 patients with CP (five non-smokers and 10 smokers).

83 Eighty-seven adult patients (54 non-smokers and 33 smokers) with moderate to advanced pe

84 Among male non-smokers and among females, self-reported heavy drink

85 gh all patients reported they were currently non-smokers and had not smoked for at least 5 years, the

86 its products heavily, deliberately targeting non-smokers and keeps prices low until smoking and local

87 clusively in smokers with AD, in contrast to non-smokers and other lung cancer subtypes.

88 Data analysis (t test) revealed that both non-smokers and smokers had a statistically significant

89 PSV was 0.61+/-0.06 mL and 0.76+/-0.06 mL in non-smokers and smokers respectively (P=.1).

90 as 0.52 mm versus 0.50 mm at (P = 0.845) for non-smokers and smokers respectively.

91 orded, and all individuals were divided into non-smokers and smokers.

92 aired inflammatory functioning compared with non-smokers and that constituents of tobacco smoke other

93 positively associated with age in HNSCC from non-smokers and that larynx SCC from non-smokers have a

94 The volunteers were healthy non-smokers and they were divided according to sex into

95 putum eosinophils were lower in smokers than non-smokers and were suppressed in both groups by FP.

96 ariance was performed, with group (smoker vs non-smoker) and genotype as factors, thereby controlling

97 s at 1 year (41.9% for smokers and 49.3% for non-smokers) and 2 to 5 years follow-up (43.9% for smoke

98 patients with IL implants (16 smokers and 15 non-smokers) and 30 patients with DL implants (17 smoker

99 eline status, age, smoking status (smoker or non-smoker), and full-mouth dental plaque score.

100 Smokers, non-smokers, and ex-smokers did not differ significantly

101 tobacco use, susceptibility to smoking among non-smokers, and exposure to secondhand smoke at home an

102 however, more than 25% of COPD patients are non-smokers, and gene-by-smoking interactions are expect

103 ciation was present overall as well as among non-smokers, and persisted after control for lipid and n

104 The results were analyzed for smokers and non-smokers, and the median time to hemostasis was signi

105 emenopausal women and in smokers compared to non-smokers, and was positively correlated with urinary

106 Seventy-two non-smokers are included in this study: 21 individuals w

107 xcreted in the urine of mice and adult human non-smokers as carnosine-propanols.

108 ssociations were stronger in smokers than in non-smokers, as well as stronger in consumers of high (>

109 reductions in probing depth for smokers and non-smokers at 1 year (41.9% for smokers and 49.3% for n

110 s except for the higher plaque scores in the non-smokers at 6 months (P <0.01).

111 s significantly different (P <0.05) only for non-smokers at 6 months, whereas OPG was not significant

112 th effects of ETS exposure is lung cancer in non-smokers, based on epidemiologic evidence and knowled

113 and planned separate analyses in smokers and non-smokers because of the known effects of smoking on F

114 elicits a modest increase in MSNA in healthy non-smokers but does not change HR, BP, or FVR.

115 % indicated they would prefer to live with a non-smoker) but not smokers (69% had no preference).

116 abetes is far more prevalent in smokers than non-smokers, but the underlying mechanisms of vulnerabil

117 e Early AR was suppressed by FP treatment in non-smokers, but was not impacted in smokers.

118 ers could be successfully distinguished from non smokers by univariate and multivariate statistical a

119 ticola was investigated in 25 smokers and 25 non-smokers by using DNA probes.

120 king and 30% of the lung cancer deaths among non-smokers can be attributed to residential radon expos

121 IL-1 positive non-smokers can be successfully treated and maintained o

122 age 49 years, 43% female, 77% non-white, 91% non-smokers, CD4+ T cell count 590 cells/mm(3), BMI 31 k

123 ngs were obtained from 32 otherwise healthy, non-smoker chronic periodontitis individuals and 25 syst

124 was associated with anthracosis in lungs of non-smokers (coefficient = 6.0; standard error = 2.9; p

125 urrent case series of nodules collected in a non-smoker cohort of patients.

126 5) was statistically significantly higher in non-smokers compared with smokers in both groups.

127 significant differences between smokers and non-smokers comparing probing depth, clinical attachment

128 3051 smokers and 2220 non-smokers completed baseline and follow-up assessments

129 Forty-five participants (30 smokers and 15 non-smokers) completed the study and had usable data.

130 udies, with 30,757 children and 44,432 adult non-smokers, containing SHS exposure and TB outcome data

131 and in smokers without COPD when compared to non-smoker control participants but did not correlate wi

132 d in severe asthma and COPD as compared with non-smoker controls (p < 0.02).

133 amine synthesis capacity between smokers and non-smoker controls in the whole striatum (t28=0.64, p=0

134 In conclusion, compared with current non-smokers, current smokers had lower BMI but higher WC

135 By 9 months only the gingival index of non-smokers decreased significantly compared to baseline

136 Smokers and non-smokers differed in whole-brain SUVs (P=0.006) owing

137 mL/year, 95% CI -38.8 to 32.2; p=0.86) or in non-smokers (difference of -5.6 mL/year, -29.4 to 18.3;

138 llowed a dose-dependent pattern (compared to non-smokers, difference in mean EFW [95% CI] at 40 weeks

139 smokers demonstrated lower muscle mass than non-smokers, differences were abolished with training.

140 Both smokers and non-smokers displayed a significant gain (P < 0.05) in c

141 The same was found among non-smokers except an inverse association was found betw

142 ng in early pregnancy was similar to that of non-smokers, except for a shorter FL and greater AC arou

143 Fewer non-smokers exhibited at least nine of these sites at 3

144 association with smoking status (smokers vs non-smokers), Fagerstrom Test for ND scores or indexed c

145 ation increase in OxGua levels among current non-smokers, female and non-obese participants, respecti

146 eased in smokers, but decreases to that of a non-smoker following tobacco cessation.

147 and gains in clinical attachment compared to non-smokers following periodontal therapy.

148 king performance between regular smokers and non-smokers for older (n = 37, 13 smokers) and younger (

149 x scores remained consistent for smokers and non-smokers for the duration of the study.

150 s follow-up (43.9% for smokers and 48.3% for non-smokers) for the subgroup of patients followed beyon

151 to analyze the periodontal conditions among non-smokers, former smokers and current smokers in the t

152 (FTND) score, in a total of 2037 smokers and non-smokers from 602 nuclear families of African- or Eur

153 ring pregnancy had a smaller fetal size than non-smokers from early gestation (16-20 weeks) through t

154 Smokers with CP benefit less than non-smokers from treatment by the combination of SRP, MT

155 rs were significantly higher in smokers than non-smokers: gingival index, probing depth, and loss of

156 II mucogingival defects were divided into a non-smoker group or smoker group.

157 microbial profile were also observed in the non-smoker group, which showed the lowest proportions of

158 ents were included in each of the smoker and non-smoker groups.

159 antly better responses (P < 0.02); likewise, non-smokers had similarly better response (P < 0.02).

160 CC from non-smokers and that larynx SCC from non-smokers have a greater number of signature 5 mutatio

161 no significant difference between the smoker/non-smoker hazard ratios for those with different APOE g

162 Six months postoperatively, the non-smokers healed with a 0.2-mm mean recession depth co

163 d in human lung airway epithelium of healthy non-smokers, healthy smokers and individuals with chroni

164 ites with CAL > or =3 mm compared to healthy non-smokers, healthy smokers, and non-smokers with diabe

165 ignificantly higher in smokers compared with non-smokers in both groups.

166 probing depth reduction between smokers and non-smokers in either the GBA or GB groups.

167 ignificantly higher in smokers compared with non-smokers in patients with IL and DL dental implants.

168 ignificant difference between ex-smokers and non-smokers in terms of time to Expanded Disability Stat

169 CI 0.04-0.46), compared with 13 (13%) of 99 non-smokers in the mercaptopurine group and 14 (16%) of

170 Non-smokers included individuals with a previous history

171 thylated in smokers compared with former and non-smokers, including an intragenic region of the aryl

172 For non-smokers, incremental lifetime cancer risk (ILCR) and

173 ff levels separately defined for smokers and non-smokers indicated increased risk for compromised tre

174 ve less [(11)C]DAA1106 binding globally than non-smokers, indicating less microglial activation.

175 d 25 systemically and periodontally healthy, non-smoker individuals.

176 We randomized 40 SCZ non-smokers into a double-blind clinical trial with four

177 ated lung cancer, lung cancer among lifetime non-smokers is a leading cause of death in the United St

178 nvironmental tobacco smoke (ETS) exposure of non-smokers is associated with a two- to three-fold incr

179 mbustion of organic material, in smokers and non-smokers is less known.

180 In non-smokers, levels were similar to those reached transi

181 When tested on a series of smoker and non-smoker lung adenocarcinoma data sets, we show that t

182 the molecular differences between smoker and non-smoker lung adenocarcinoma.

183 d on gene expression data from Taiwan female non-smoker lung cancer patients, while there is evidence

184 ore specifically, when applied to smoker and non-smoker lung cancer sets, nDGE results illustrate the

185 the molecular differences between smoker and non-smoker lung cancer.

186 At 9 months non-smokers maintained a mean decrease in probing depth

187 ement of VS/fP values toward values found in non-smokers (mean 58.2% normalization of receptor levels

188 study, we tested 48 participants, a group of non-smokers (n = 12) and three groups of regular smokers

189 age- and gender-matched smokers (n = 14) and non-smokers (n = 14) with periodontitis were measured by

190 tivity, tooth pain, and swelling compared to non-smokers (n = 21).

191 Here, in a sample of smokers (n=35) and non-smokers (n=21), a previously validated parametric fl

192 Non-smokers needing two implants in different quadrants

193 Compared to non-smokers, neither current smokers (RR = 0.93; 95% CI

194 For both smokers and non-smokers, neuroimaging results showed similar increas

195 fluid (GCF) levels of MT in smokers (S) and non-smokers (NS) with chronic periodontitis (CP), and co

196 teer participants consisting of four groups, non-smokers (NS), CS, EC, and dual EC and cigarette smok

197 different in EC and DS groups compared with non-smokers (NS).

198 ndividuals vaping e-cigarettes (e-cigs), and non-smokers (NS).

199 its they were categorized into three groups: non-smokers (NS; n = 95), former smokers (FS; n = 22), a

200 psychotic disorders in daily smokers versus non-smokers of 2.18 (95% CI 1.23-3.85).

201 In adult forms of periodontitis, non-smokers of northern European heritage carrying the "

202 hs and IL-1 levels reduced at 3 months among non-smokers only.

203 gnificantly lower (P <0.05) after OSFMUD for non-smokers only.

204 tinib is highly effective in treating women, non-smoker or former light smoker, advanced non-small ce

205 For non-smokers or former light smokers (<5 pk/yr), IL-1 gen

206 ase of 7.43 (95% CI: 1.20-46.20) compared to non-smokers or former light smokers who were IL-1 genoty

207 Ninety patients, non-smokers or former smokers with less than 10 pack-yea

208 HPV-positive low-risk oropharyngeal cancer (non-smokers or lifetime smokers with a smoking history o

209 ed no cognitive or clinical effect either in non-smokers or smokers.

210 of delay was greater among single patients, non-smokers, or those with stage IV tumors.

211 Additionally, among non-smokers, overall and prostate cancer incidences stat

212 epopulated in the smokers faster than in the non-smokers (P <0.01).

213 ne and so were Gram-positive bacteria in the non-smokers (P <0.01).

214 antly higher in healthy smokers than healthy non-smokers (P <0.05).

215 Smokers had EMF's over double that of non-smokers (p = 0.011).

216 ion of GCF TGF-beta1 at baseline compared to non-smokers (P = 0.03).

217 ater EFW from 32 weeks' gestation onwards in non-smokers (p = 0.03, difference in mean EFW at 40 week

218 ess reduction in mean GCF volume compared to non-smokers (P = 0.04).

219 Fifteen healthy and non-smoker patients (nine males and six females; mean ag

220 Fourteen smoker and 13 non-smoker patients completed the study protocol and rev

221 m change in FEV1 (L) over 4-10 h [95% CI] in non-smokers: placebo -1.01 [1.31, 0.70], FP 100 mug -0.3

222 Seventy-one percent of non-smokers (positive likelihood ratio of 4.22) and 88%

223 Compared with genotype-negative (TT) non-smokers, positivity for the risk genotypes (CC+CT) a

224 Non-smokers presented no change in bone loss, while smok

225 /smoker, prevalence 38%, OR 0.88, P=0.74, CC/non-smoker, prevalence 42% (reference), CC/smoker preval

226 oking appears to abrogate this effect (CT/TT/non-smoker, prevalence of PsA 13%, OR 0.20, P=0.0001; CT

227 The reduction in PD in smokers and non-smokers ranged from 0.76 to 2.05 mm and 1.27 to 2.40

228 2395 (78%) smokers and 1632 (74%) non-smokers recalled seeing at least one Tips advertisem

229 lting in an estimated 4.7 million additional non-smokers recommending cessation services and more tha

230 TP was higher in current smokers relative to non-smokers regardless of sex and periodontitis classifi

231 ving rise to lung adenocarcinomas (LADCs) in non-smokers remain elusive.

232 smoke respond better to immunotherapies than non-smokers, remains poorly understood.

233 pared to IL-1 genotype-negative patients and non-smokers, respectively.

234 Likewise, recent non-smokers respond to periodontal therapy in a manner s

235 The data have shown that smokers and non-smokers responded similarly after 9 months to the li

236 ngeal anesthesia abolished RPS reflex in all non-smokers resulting in laryngeal spillage.

237 et from human epithelial brushes (smoker vs. non-smoker) revealed a high degree of similarity between

238 The smoker versus non-smoker RR of 1.51 (1.40-1.63) for all female mortali

239 7 patients with CP (24 smokers [S+P+] and 23 non-smokers [S-P+]) and 46 periodontally healthy individ

240 ealthy individuals (23 smokers [S+P-] and 23 non-smokers [S-P-]) for a total of 93 participants.

241 None of the non-smokers showed evidence of laryngeal spillage of wat

242 Non-smokers showed lower mean number of sites with probi

243 d attachment gain (delta AL) were greater in non-smoker subjects than smoker subjects.

244 lly and periodontally healthy smokers versus non-smokers suggest lack of adverse effects of smoking o

245 attachment loss and gingival recession than non-smokers, suggesting poorer periodontal health in smo

246 association with PTSD is most pronounced in non-smokers, suggesting the result was independent of sm

247 the genetic instrument with fetal growth in non-smokers suggests that genetic pleiotropy may have ma

248 ogical states, studies of nicotine in normal-non-smokers tend to show deleterious effects.

249 ation closure was comparable for smokers and non-smokers, the proportion of Class II residual defects

250 ette smoking status; compared to children of non-smokers, those whose mothers or both parents smoked

251 sual backward masking in healthy smokers and non-smokers to further understand the effects of nicotin

252 s are approximately three times as likely as non-smokers to have periodontitis.

253 Recommendations by non-smokers to quit grew from 2.6% at baseline to 5.1% a

254 ed children and eight studies assessed adult non-smokers; two studies assessed both populations.

255 were compared between infants of smokers and non-smokers, using generalized linear models.

256 For CAL, the gain in non-smokers versus smokers ranged from 0.29 to 1.6 mm an

257 ly showed an improved treatment effect among non-smokers versus smokers.

258 e mean gain in clinical attachment level for non-smokers was 0.47 mm and 0.59 mm for smokers.

259 first episode of psychosis in smokers versus non-smokers was 3.22 (95% CI 1.63-6.33), with some evide

260 for myocardial infarction in smokers versus non-smokers was 4.6 (4.2-5.1).

261 Baseline probing depth for non-smokers was 5.46 +/- .46 mm and for smokers 5.70 +/-

262 inflammatory mediators levels in smokers and non-smokers was also evaluated.

263 on signatures for lung cancer in smokers and non-smokers we further show that codons 157 and 273 have

264 of the tracheal epithelium from smokers and non-smokers, we generate a comprehensive atlas of epithe

265 ne PD and the delta PD or delta AL among the non-smokers, weak and insignificant relationship existed

266 psychotic illness at an earlier age than did non-smokers (weighted mean difference -1.04 years, 95% C

267 d crossover design was used in which healthy non-smokers were administered placebo and nicotine (2-mg

268 reported results separately for smokers and non-smokers were also included.

269 When only non-smokers were analyzed, a significant moderate positi

270 ive smokers and five age- and gender-matched non-smokers were examined.

271 Eighty non-smokers were included (40 CsA-medicated renal transp

272 und that bronchial and nasal epithelium from non-smokers were most similar in gene expression when co

273 tients with periodontitis, 20 smokers and 20 non-smokers were recruited.

274 Thirty-two smokers and 32 non-smokers were selected and received scaling and root

275 patients with DL implants (17 smokers and 13 non-smokers) were included.

276 Differences were most pronounced in non-smokers, while heavy smokers showed reduced levels o

277 y task during fMRI in cohorts of smokers and non-smokers who completed a two-drug, placebo-controlled

278 Forty-three smokers and thirty-seven non-smokers who met DSM-IV criteria for schizophrenia we

279 neoplasia (CIN) and cancer, as compared with non-smokers who were infected with similar variants and

280 approximately 1.4-fold of the expression in non-smokers (Wilcoxon test; P = 0.031).

281 dministration was significantly higher among non-smokers with ADHD, and their choices of nicotine wer

282 proteinase-8 (MMP-8) patterns in smokers and non-smokers with chronic periodontitis (CP) and test the

283 n oxidative stress biomarkers in smokers and non-smokers with chronic periodontitis (CP).

284 kine signaling 1 (SOCS1) gene in smokers and non-smokers with chronic periodontitis (CP).

285 ly validated (salivary cotinine) smokers and non-smokers with chronic periodontitis (CP: n = 13) or a

286 Non-smokers with CP or AgP had lower levels of saliva TN

287 GCF was collected from smokers and non-smokers with CP, both at baseline and 1 to 2 weeks a

288 roduction was altered in smokers compared to non-smokers with CP.

289 omoter in 45 saliva samples from smokers and non-smokers with CP.

290 to healthy non-smokers, healthy smokers, and non-smokers with diabetes.

291 cillin (AMX) in the treatment of smokers and non-smokers with generalized chronic periodontitis (CP).

292 Ninety systemically healthy non-smokers with moderate to advanced periodontitis (63

293 CF) concentrations of sICAM-1 in smokers and non-smokers with periodontal disease.

294 gression in smokers may differ from those of non-smokers with the same disease classification.

295 plant failures in smokers are twice those of non-smokers, with a higher failure rate in the maxillary

296 periodontitis in smokers, former smokers, or non-smokers, with a subset of specific environmental var

297 iated periodontitis is distinct from that of non-smokers, with significant differences in the prevale

298 se (LAR) was suppressed by FP in smokers and non-smokers; with placebo, the LAR was also attenuated i

299 vations that atherosclerosis often occurs in non-smokers without elevated levels of low-density lipop

300 One hundred fourteen healthy non-smokers, without known clinical atherosclerosis, had