ライフサイエンスコーパス: tobacco

1 the OsPIP1;3 gene in Nicotiana benthamiana (tobacco).

2 nse against armyworms (Spodoptera exigua) in tobacco.

3 uterine abnormality and/or current smoker of tobacco.

4 erexpressed for successful PA engineering in tobacco.

5 and RsRubisco ~40% the Rubisco content in WT tobacco.

6 abidopsis thaliana), unlike its orthologs in tobacco.

7 ame cardiovascular health hazards as smoking tobacco.

8 ochemically confirmed 7-day point prevalence tobacco abstinence at 6-month follow-up.

9 ivary glands and saliva of aphids from a non-tobacco-adapted (NTA) aphid lineage, when compared to th

10 ) aphid lineage, when compared to those of a tobacco-adapted lineage.

11 each of several common risk factors of NCDs (tobacco, alcohol use, high systolic blood pressure, diet

12 igarettes (e-cigarettes) are non-combustible tobacco alternatives that aerosolize nicotine and flavou

13 lted in phenotypes similar to that of MIM159 tobacco and activated PR gene expression, verifying the

14 d oropharyngeal squamous cell carcinoma from tobacco and alcohol use-associated squamous cell carcino

15 nd that daily or almost daily consumption of tobacco and alcohol were both significantly associated w

16 ies-most importantly reducing consumption of tobacco and alcohol, obesity control, immunizing populat

17 dex, hormone replacement therapy, and use of tobacco and alcohol.

18 they are associated with the intersection of tobacco and cannabis use.

19 tributable Fraction estimates suggested that tobacco and class-A drug use were, respectively, respons

20 (95%CI: 0.605-0.988); those who never smoked tobacco and did not use spliffs (95%CI: 0.489-0.892); th

21 We used the Population Assessment of Tobacco and Health Study to compare long-term abstinence

22 ally representative Population Assessment of Tobacco and Health Study.

23 Comprehensive tobacco and HPV status should therefore be evaluated pri

24 ubisco activity compared with both wild-type tobacco and lines expressing the Se SSU.

25 Tobacco and marijuana smoke particles are quantitatively

26 For tobacco and marijuana smoke, respectively, 4350 and 2575

27 in evaluating the reduced risk potential of tobacco and nicotine products.

28 nfected citrus also alerted on CLas-infected tobacco and periwinkle, CLas-bearing psyllid insect vect

29 ions in Arabidopsis, inhibition of miR159 in tobacco and rice resulted in pleiotropic defects includi

30 in 60 minutes after waking: those who smoked tobacco and used spliffs (95%CI: 0.605-0.988); those who

31 (95%CI: 0.489-0.892); those who never smoked tobacco and used spliffs (95%CI:0.022-0.915).

32 Compared to those who smoked tobacco and used spliffs, the following spliff use behav

33 reported to be lower in people with alcohol, tobacco, and cocaine use disorders.

34 ally classify individuals' risk for alcohol, tobacco, and drug use based on the content from their In

35 improved the performance of NTA lineages on tobacco, and the propeptide domain of CathB3 was found t

36 tent with the broad defense response, MIM159 tobacco appeared immune to Phytophthora infection.

37 y hemorrhagic telangiectasia (HHT) who smoke tobacco are more prone to PAVM persistence after emboliz

38 ese products may represent a novel source of tobacco-associated disease but may also provide a harm r

39 discovery of stratified medicine options for tobacco-associated NSCLC is a high priority.

40 two pathways, the trnE mutation is lethal in tobacco because it inhibits tRNA processing, thus preven

41 arly localized when ectopically expressed in tobacco BY-2 cell cultures.

42 mato, potato, eggplants, pepper, petunia and tobacco can be inhibited by Avr2 with the exception of t

43 of both zeaxanthin and lutein and show that tobacco can regulate the ratio between the two photosyst

44 A/J mice were intranasally treated with the tobacco carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1

45 KRAS mutations and to form lung tumors after tobacco carcinogen exposure.

46 nges in the lung associated with exposure to tobacco carcinogens and inflammation, A/J mice were intr

47 ealth professionals should be role models in tobacco cessation (75.3%), should provide smoking cessat

48 They were originally envisaged as a tobacco cessation aid, but whether or not they help peop

49 and harms of primary care interventions for tobacco cessation among school-aged children and adolesc

50 se epidemiology and mechanisms in women; and tobacco cessation for people living with HIV.

51 t activities, but there was no difference in tobacco cessation or medication adherence between the tr

52 light a potential risk of using nicotine for tobacco cessation.

53 accumulation of the reporter gene product in tobacco chloroplasts encoded in the second ORF.

54 for THP1.0(T) and THS2.4(T) compared to the tobacco cigarette (C651).

55 s of fine and ultrafine particles similar to tobacco cigarettes (t-cigs).

56 perceived as less harmful than conventional tobacco cigarettes during pregnancy for both the mother

57 and 3 included adult smokers of 7 mg ISO tar tobacco cigarettes, and Group 2 consisted of both solus

58 o decrease the rates of smoking conventional tobacco cigarettes, electronic cigarettes (e-cigarettes)

59 they are perceived as a safer alternative to tobacco cigarettes.

60 e (P<0.001), donor male sex (P<0.001), donor tobacco consumption (P=0.001), recipient dyslipidemia (P

61 years of age and 10 pack-years or greater of tobacco consumption from the general population, 15% ful

62 ted oropharyngeal cancers suggests pervasive tobacco consumption likely generates more aggressive tum

63 women above 58 years old and independent of tobacco consumption or oral hygiene.

64 18/51) were HPV-positive and current or past tobacco consumption was reported in 86.3% (44/51).

65 ears of age with 10 pack-years or greater of tobacco consumption, 1,175 (15%) had early COPD, of whom

66 larynx cancers are generally associated with tobacco consumption, alcohol abuse or both, whereas phar

67 opharyngeal cancers in populations with high tobacco consumption.

68 ears of age with 10 pack-years or greater of tobacco consumption.Measurements and Main Results: Among

69 ole of hospitals and health professionals in tobacco control and expect to receive smoking cessation

70 ole of health professionals and hospitals in tobacco control by asking about their agreement with sev

71 nated with the long-standing, evidence-based tobacco control strategies that have significantly reduc

72 folio, with a low level of implementation in tobacco control, and who stayed in surgical units had hi

73 ces in hybrid and WT RsRubisco biogenesis in tobacco correlated with assembly in Escherichia coli adv

74 nsin Smoking Withdrawal Scale (P = 0.04) and Tobacco Craving Questionnaire (P = 0.014).

75 eptide domain of CathB3 was found to bind to tobacco cytoplasmic kinase ENHANCED DISEASE RESISTANCE 1

76 CHRNA3 risk alleles can increase the risk of tobacco dependence and smoking-related diseases in human

77 (nAChR) subunit, increases vulnerability to tobacco dependence and smoking-related diseases, but lit

78 ptor (nAChR) subunit gene, increases risk of tobacco dependence but underlying mechanisms are unclear

79 ief behavioural support for the treatment of tobacco dependence in patients with tuberculosis.

80 are likely to increase the effectiveness of tobacco-dependence pharmacotherapy.

81 tabolically inactivate nicotine and activate tobacco-derived procarcinogens [e.g., 4-[methylnitrosami

82 lasma membrane and perinuclear space in both tobacco epidermal and soybean root cells.

83 Tobacco etch virus protease (TEV) is one of the most wid

84 Spy-C mice express a TEVp (tobacco etch virus protease) cleavage site and a SpyTag

85 s in OPSCC patients (n = 143) with extensive tobacco exposure (median pack-years = 40).

86 0.001, p < 0.001 respectively) regardless of tobacco exposure and associated strongly with differenti

87 We analyzed the relationship between TIME, tobacco exposure and clinical outcomes in OPSCC patients

88 Tobacco exposure correlated significantly (p < 0.001) wi

89 ificant subset of HPV tumors associated with tobacco exposure have diminished treatment response and

90 l, 3,042 (71.7%) were ever-smokers with mean tobacco exposure of 33 pack-years.

91 However, the impact of tobacco exposure on the TIME in OPSCC patients remains u

92 ideration the potential modifying effects of tobacco exposure on treatment effectiveness and clinical

93 n the same way they are trained to ask about tobacco exposure to assess cancer and heart disease risk

94 the TIME, which is potentially modulated by tobacco exposure.

95 r smokers was strongly related to cumulative tobacco exposure.

96 onyl in the e-cigarette aerosol with Classic Tobacco flavor.

97 ressure, exercise, weight, alimentation, and tobacco (Fuster-BEWAT Score [FBS]), ranging from 0 to 15

98 untranslated-region matched rbcL Additional tobacco genotypes produced here incorporated differing p

99 otine, which is the prominent constituent of tobacco, has negative effects on periodontium cells.

100 (ADC) relating to two commercially available tobacco heating products (THPs) and a prototype electron

101 eat, but in larger caterpillars, such as the tobacco hornworm, Manduca sexta, the movement is a defen

102 r with functional studies in Arabidopsis and tobacco, identify a coevolved module between the EDS1-SA

103 ma users and controls (individuals not using tobacco in any form).

104 oal traditionally is used to heat the hookah tobacco in the waterpipe, hookah smoke delivers tobacco

105 the role of e-cigarettes versus combustible tobacco in vascular disease and implications for blood-b

106 CHED genes play opposing regulatory roles in tobacco lateral branching.

107 by transiently expressing D-type cyclins in tobacco leaf cells.

108 he transporter locates to the tonoplast in a tobacco leaf transient expression system.

109 in wild-type and transgenic oil-accumulating tobacco leaves.

110 yl flux reaction in wild-type and engineered tobacco leaves.

111 am beta-glucuronidase (GUS) reporter gene in tobacco leaves.

112 Other tobacco lines producing RsRubisco containing alternate d

113 s (SSU) and expressed the Se LSU in place of tobacco LSU, with and without CcmM35.

114 These findings suggest that the tobacco miR159-GAMYB pathway functions in the biotic def

115 minimal research around various cannabis and tobacco mixing (spliff usage) behaviours and likeliness

116 phage, pepper mild mottle virus (PMMoV), and tobacco mosaic virus (TMV) as indicators of the reductio

117 mber and flexibility was optimized using the tobacco mosaic virus (TMV) display platform.

118 terfacially bridging covalent network within tobacco mosaic virus (TMV) virus-like particles (VLPs).

119 Previously, we used a Tobacco mosaic virus viral vector to express both GFP an

120 itotically quiescent cells that have avoided tobacco mutagenesis.

121 function of AGOs in the interaction of wild tobacco (Nicotiana attenuata) with a naturally occurring

122 ncers-for its use in transiently transformed tobacco (Nicotiana benthamiana) leaves.

123 iltration in the cells of expanded leaves in tobacco (Nicotiana benthamiana).

124 regulatory roles of five BRC gene members in tobacco (Nicotiana tabacum L.) using CRISPR site-directe

125 Here, miR159 function was inhibited in tobacco (Nicotiana tabacum) and rice (Oryza sativa) usin

126 the carboxysome linker protein CcmM35 within tobacco (Nicotiana tabacum) chloroplasts.

127 Recently, tobacco (Nicotiana tabacum) leaves were engineered to ac

128 Here we develop an RNAi-RbcS tobacco (Nicotiana tabacum) master-line, tobRrDeltaS, fo

129 We generated a series of transplastomic tobacco (Nicotiana tabacum) plants to alter tRNA(Glu) ex

130 nd YFP-tagged transmembrane (TM) proteins in tobacco (Nicotiana tabacum) pollen tubes growing normall

131 pt accumulation and translation in leaves of tobacco (Nicotiana tabacum) seedlings after transfer fro

132 tal system in the dicotyledonous model plant tobacco (Nicotiana tabacum) that allows us to study the

133 iagnosed in the previous 4 weeks, who smoked tobacco on a daily basis and were willing to stop smokin

134 The profound effects of tobacco on the genome of lung cancer cells are well-docu

135 Tobacco- or human papillomavirus- driven oropharyngeal s

136 We tested the fidelities of error prone tobacco organelle DNA polymerases using a novel positive

137 s protease enzymes of allergens, detergents, tobacco, ozone, particulate matter, diesel exhaust, nano

138 ere clinical guidelines, graphic warnings on tobacco packaging, and NCD risk factor surveys.

139 e accumulation of reactive oxygen species in tobacco phloem, thereby suppressing both phloem feeding

140 Tobacco photosynthesis and growth were most impaired in

141 totrophically in the absence of carotenes: a tobacco plant containing only the xanthophyll astaxanthi

142 The LTBentero protein was expressed in tobacco plants at up to 5.29 ug g(-1) fresh leaf tissue

143 The transgenic tobacco plants exhibited higher photosynthesis rates, ro

144 Research on mutant tobacco plants shows that a pigment called beta-carotene

145 We engineered tobacco plants with a fungal bioluminescence system that

146 the fungal pathogen B. cinerea in tomato and tobacco plants, and postharvest products.

147 thus, minimizing nicotine exposure from any tobacco product in youth is important.

148 ms (often known as e-cigarettes) are a novel tobacco product with growing popularity, particularly am

149 atic review newly included e-cigarettes as a tobacco product.

150 Interventions to discourage the use of tobacco products (including electronic nicotine delivery

151 Smokeless tobacco products (STPs) are widely used in certain parts

152 Critically, both combustible tobacco products and e-cigarettes contain nicotine, a hi

153 scents who smoke cigarettes or who use other tobacco products and to understand the effectiveness of

154 trials addressed prevention or cessation of tobacco products other than cigarettes; no trials evalua

155 igarettes, bidis, a water pipe, or smokeless tobacco products since the quit date), confirmed biochem

156 ifestyle-related risk factors such as use of tobacco products, hypertension, and general obesity are

157 Its use via smokeless tobacco products, some of which contain saccharin, is on

158 th solus vapers and dual users of vapour and tobacco products.

159 Using Arabidopsis thaliana and Tobacco rattle virus (TRV), we investigate the antiviral

160 in the tobRsLS::X progeny matched endogenous tobacco Rca levels (~1 umol protomer.m(2)) and enhanced

161 n be inhibited by Avr2 with the exception of tobacco Rcr3.

162 cigarettes may reduce their relative risk of tobacco-related disease.

163 luding amount smoked, smoking cessation, and tobacco-related diseases, are altered by the rate of nic

164 g children and adolescents may help decrease tobacco-related illness and injury.

165 Rs significantly declined for lung and other tobacco-related neoplasms.

166 ts that the use of cannabis and nicotine and tobacco-related products (NTPs) during the adolescent ye

167 cts of individual environmental toxicants in tobacco remain largely unexplored.

168 ion of a miR159-resistant GAMYB transgene in tobacco resulted in phenotypes similar to that of MIM159

169 dy, we explored the possibility of using the tobacco retrotransposon Tnt1 to create a transposon-base

170 nitoring the deleterious health impacts from tobacco smoke and ambient air pollution, as well as the

171 Terpenes are present in tobacco smoke and are used as flavor chemicals in e-liqu

172 ger in mobility diameter than particles from tobacco smoke and contain 3.4x more total mass.

173 between SDP and asthma; rather environmental tobacco smoke and other familial factors seem to explain

174 natures of discontinued exposures, including tobacco smoke and ultraviolet light, were not generated

175 s reported to be associated with exposure to tobacco smoke components, which strongly support our fin

176 nducible factor-2alpha)-regulated genes, and tobacco smoke decreases pulmonary HIF-2alpha concentrati

177 Tobacco smoke exposure also reduces vaccine efficacy.

178 rder, increased use of soaps and detergents, tobacco smoke exposure and psychosomatic factors are oth

179 Tobacco smoke exposure is associated with multiple disea

180 tion and changes in children's self-reported tobacco smoke exposure or respiratory health.

181 sema phenotypes in subjects with significant tobacco smoke exposure using deep gene resequencing and

182 Further adjusting for environmental tobacco smoke exposure, family history of PD, and use of

183 re identified, including ethnicity, prenatal tobacco smoke exposure, history of allergies before 12 m

184 the immunosuppressive effects resulting from tobacco smoke exposure.

185 sses that are activated during recovery from tobacco smoke exposure.

186 rd COPD risk factors (primary and secondhand tobacco smoke exposures, occupational and environmental

187 Multiple non-nicotinic components of tobacco smoke have been identified in e-cigarette aeroso

188 is immunosuppressive, other constituents in tobacco smoke have inflammatory effects.

189 striking similarities between marijuana and tobacco smoke in terms of their physical and chemical pr

190 We conclude that tobacco smoke is a major source of isoprene exposure in

191 Tobacco smoke is a potent inflammatory trigger and is im

192 ted health effects, and its concentration in tobacco smoke is higher in comparison with other metals.

193 Tobacco smoke offers a benchmark given that it has been

194 ults in chronic pulmonary exposure to either tobacco smoke or e-cigarettes despite negative respirato

195 he localized metabolism of inhaled drugs and tobacco smoke procarcinogens.

196 prevalent in patients with light exposure to tobacco smoke(1-3).

197 or more live births, exposure to secondhand tobacco smoke, and ever pregnant or not currently pregna

198 ergens (house dust mites, pets, molds, etc), tobacco smoke, and other pollutants, which have an impac

199 The main risk factor for COPD is tobacco smoke, but other environmental exposures also ma

200 are exceedingly different from conventional tobacco smoke, containing dozens of chemicals not found

201 , race/ethnicity, sex, income, environmental tobacco smoke, controller medication, upper respiratory

202 cy of vaccinations in individuals exposed to tobacco smoke, is a critical unmet clinical problem.

203 e adjuvants with the ability to overcome the tobacco smoke-induced immunosuppressive effects.

204 an the role that nicotine plays in thirdhand tobacco smoke.

205 that are associated with minimal exposure to tobacco smoke.

206 sources such as most heated starchy foods or tobacco smoke.

207 This work compared brain TSPO levels in 20 tobacco smokers (abstinent for at least 2 h) and 20 nons

208 Tobacco smokers and males are overrepresented.

209 Cannabis users who are also tobacco smokers are more likely to exhibit cannabis depe

210 Water pipe tobacco smokers have a higher risk of initiation of ciga

211 ntrations in the brain (measured as SUV) for tobacco smokers than for nonsmokers by demonstrating the

212 Exclusive tobacco smokers were distinguished from non-users using

213 onal survey of 1,521 adults (301 combustible tobacco smokers).

214 y (aHR = 2.757 [1.616-4.704], p < 0.001) and tobacco smoking (aHR = 2.150 [1.319-3.503], p < 0.01) we

215 Given the coincident use of tobacco smoking among HIV-infected intravenous drug user

216 ants of health (SDHs, including drug misuse, tobacco smoking and alcohol), and TB, taking into accoun

217 h decreased risk of ADA development, whereas tobacco smoking and infections during the study were ass

218 Results show tobacco smoking as a risk factor for oral HPV among PLWH

219 The rates of tobacco smoking by people living with HIV vastly exceed

220 Tobacco smoking causes lung cancer(1-3), a process that

221 Associations between tobacco smoking during pregnancy and offspring asthma ha

222 Thus, tobacco smoking increases mutational burden, cell-to-cel

223 Tobacco smoking is common in HIV-infected patients, and

224 Tobacco smoking is highly addictive and causes respirato

225 Tobacco smoking is the leading cause but not the only on

226 ove to be one of the key mechanisms by which tobacco smoking leads to increased periodontitis suscept

227 needed to fully characterize the effects of tobacco smoking on the brain immune system.

228 The effects of tobacco smoking on the immune system of the brain are no

229 Tobacco smoking was the major influence on mutational bu

230 Clinical observations have linked tobacco smoking with increased type 2 diabetes risk.

231 lected on education, household overcrowding, tobacco smoking, alcohol and drugs use, and history of h

232 ,115) and tested the association of RBA with tobacco smoking, alcohol consumption, and genetic varian

233 pollutants, built environment, green spaces, tobacco smoking, and biomarkers of chemical pollutants (

234 Obesity, tobacco smoking, and genetic predisposition increase the

235 in England, including through drugs misuse, tobacco smoking, and homelessness.

236 rence, body mass index, alcohol consumption, tobacco smoking, and physical activity.

237 tios (HRs) for lung cancer incidence by sex, tobacco smoking, asbestos exposure, presence of asbestos

238 losis risk was independently associated with tobacco smoking, drugs use (especially injectable drugs

239 e, calendar period, and diagnoses related to tobacco smoking, obesity, and alcohol overconsumption.

240 tational signatures that are associated with tobacco smoking.

241 ver smoked: these cells had less damage from tobacco-specific mutational processes, were fourfold mor

242 lthymidine, which is a DNA adduct induced by tobacco-specific N-nitrosamines, in vitro and in human c

243 were able to form a hybrid enzyme utilizing tobacco SSU and the Se LSU, allowing slow autotrophic gr

244 d these incorporated small amounts of native tobacco SSU.

245 logy study uses data from the National Youth Tobacco Survey to assess trends in self-reported use of

246 acco in the waterpipe, hookah smoke delivers tobacco toxicants and nicotine plus charcoal combustion

247 ettes appear to be more potent than those in tobacco TPM with respect to hydroxyl radical generation

248 n e-cigarettes was much lower as compared to tobacco TPM.

249 In MIM159 tobacco, transcriptome profiling revealed that genes ass

250 Background: Current tobacco treatment guidelines have established the effica

251 rs have not fully implemented evidence-based tobacco treatment into routine care.

252 ascular disease (2.4% versus 3.3%; P=0.002), tobacco use (36.5% versus 52.3%; P<0.001), and prior car

253 ctors for developing colon pathology include tobacco use (odds ratio (OR), 2.0; 95% confidence interv

254 r brief counseling, to prevent initiation of tobacco use among school-aged children and adolescents.

255 -feasible interventions for the cessation of tobacco use among school-aged children and adolescents.

256 l strategies that have significantly reduced tobacco use and initiation in the United States.

257 history, systemic co-morbidities, alcohol or tobacco use as well as serum levels of calcium and vitam

258 Weight loss >= 5%, tobacco use at LEMS onset and age at onset >= 50 years w

259 Tobacco use initiation; tobacco use cessation; health outcomes; harms.

260 , P < 10(-30)), followed by individuals with tobacco use disorder (TUD) (AOR = 8.222 ([7.925-8.530],

261 was significantly inversely associated with tobacco use disorder comorbidities (adjusted odds ratio

262 ne the co-occurrence of past-year alcohol or tobacco use disorder with past-year anxiety disorders, m

263 rders, largely driven by an association with tobacco use disorder.

264 among those who met criteria for a past-year tobacco use disorder.

265 es associated with alcohol use disorders and tobacco use disorders among heterosexual, bisexual, and

266 ed annual 480 000 deaths are attributable to tobacco use in adults, including from secondhand smoke.

267 nificantly higher smoking and male smokeless tobacco use in most Appalachian disparity states.

268 weden 2005-2012 with information on maternal tobacco use in pregnancy, followed until December 2015.

269 ng education or brief counseling, to prevent tobacco use in school-aged children and adolescents have

270 never having smoked a full cigarette, and no tobacco use in the prior 3 years.

271 Tobacco use initiation; tobacco use cessation; health ou

272 cological interventions with no or a minimal tobacco use intervention control group (eg, usual care,

273 but whether or not they help people to quit tobacco use is controversial.

274 Tobacco use is the leading cause of preventable death in

275 Tobacco use is the leading preventable cause of mortalit

276 total and direct causal roles of alcohol and tobacco use on CVD risk factors and events.

277 Using serum cotinine values to classify tobacco use showed that smokers have higher serum concen

278 ong children in the US since the late 1990s, tobacco use via electronic cigarettes (e-cigarettes) is

279 Tobacco use was observed to be associated with a lower r

280 complications, high triglyceride levels, and tobacco use were additional independent predictors for g

281 d risk factors for NCDs (such as obesity and tobacco use).

282 Tobacco use, a primary HNSCC risk factor, was evaluated

283 d with a cluster of behavioural factors (ie, tobacco use, alcohol, diet, physical activity, and sodiu

284 d the health risks associated with nicotine, tobacco use, and electronic nicotine delivery systems in

285 tors, including excess sugar consumption and tobacco use, as well as underlying infection and inflamm

286 ace and ethnicity or those with a history of tobacco use, asthma, or diabetes mellitus type II.

287 Age, sex, race/ethnicity, tobacco use, chronic conditions, influenza vaccination,

288 Risk factors include tobacco use, coronary artery disease, and respiratory fa

289 odels included adjustment for race, obesity, tobacco use, hypertension (HTN), atrial fibrillation (AF

290 ed model regarding the effects of emotion on tobacco use, in particular, as well as on addictive beha

291 ic blood pressure, diastolic blood pressure, tobacco use, statin use, body mass index, urine microalb

292 Older age, tobacco use, underlying cardiovascular disease, diabetes

293 ppressants and other medications, and 4% for tobacco use, with 31% clinic appointment nonadherence in

294 etes, and 19.4% reported current or previous tobacco use.

295 sex, body mass index, recent infection, and tobacco use.

296 etes, and 19.4% reported current or previous tobacco use.

297 amily history, obesity, type 2 diabetes, and tobacco use.

298 symptoms representing a major burden to quit tobacco use.

299 consistent associations among ever and never tobacco users, men and women, and individuals with lower

300 rovide a harm reduction strategy for current tobacco users.