ライフサイエンスコーパス: non-smoker

1 s follow-up (31.3% for smokers and 41.8% for non-smokers).

2 in 53 patients (15 cigarette smokers and 38 non-smokers).

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

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

5 infected with Porphyromonas gingivalis than non-smokers.

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

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

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

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

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

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

12 representative cohorts of adult smokers and non-smokers.

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

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

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

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

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

18 3.0) and severe CAL (RRR = 8.2) compared to non-smokers.

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

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

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

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

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

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

25 significantly more maxillary bone loss than non-smokers.

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

27 Similar risk estimates were seen among non-smokers.

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

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

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

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

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

33 -surgical periodontal therapy is compared to non-smokers.

34 reatment of intrabony defects in smokers and non-smokers.

35 cted with certain periodontal pathogens than non-smokers.

36 of infection with Bacteroides forsythus than non-smokers.

37 concentration were significantly lower than non-smokers.

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

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

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

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

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

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

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

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

46 periodontal healing in smokers compared with non-smokers.

47 reduction in clinical outcomes compared with non-smokers.

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

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

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

51 fferences in performance between smokers and non-smokers.

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

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

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

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

56 0.05) lower in smokers (1.32 +/- 0.45) than non-smokers (1.45 +/- 0.40).

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

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

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

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

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

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

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

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

65 ere maintained for both smokers (2.7 mm) and non-smokers (3.4 mm).

66 an PD were observed for smokers (3.0 mm) and non-smokers (3.8 mm) at the 1-year follow-up.

67 78%, P=0.001) without affecting responses in non-smokers (401+/-80%).

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

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

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

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

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

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

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

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

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

77 Non-smokers also presented the greatest reductions in me

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

94 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

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

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

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

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

99 rs had higher fibrinogen concentrations than non-smokers, and moderate alcohol consumers had lower co

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

120 3051 smokers and 2220 non-smokers completed baseline and follow-up assessments

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

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

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

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

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

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

127 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;

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

147 likely to subgingivally infect smokers than non-smokers; however, there was not a significantly high

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

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

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

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

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

153 Non-smokers included individuals with a previous history

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

176 t had quit by the initial exam (n = 10); and non-smokers (NS) had never smoked (n = 18).

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

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

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

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

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

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

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

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

185 ne oxidase B (MAO B; EC 1.4.3.4) relative to non-smokers or former smokers.

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

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

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

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

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

191 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

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

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

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

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

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

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

198 2395 (78%) smokers and 1632 (74%) non-smokers recalled seeing at least one Tips advertisem

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

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

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

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

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

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

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

206 7 patients with CP (24 smokers [S+P+] and 23 non-smokers [S-P+]) and 46 periodontally healthy individ

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

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

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

210 significant (p = 0.0001) between smokers and non-smokers, showing no overlap between the groups.

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

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

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

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

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

216 elayed, gingival bleeding when compared with non-smokers; therefore smoking needs to be controlled fo

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

239 evaluation (29.2% for smokers and 42.5% for non-smokers) were sustained in the subgroup of patients

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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