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1 history (24 never-smokers, 16 smokers, and 8 ex-smokers).
2 ion scores compared with both nonsmokers and ex-smokers.
3 GRQ Total, Symptoms, and Impacts scores than ex-smokers.
4 ation was reduced in smokers but enhanced in ex-smokers.
5 k task (2BT)] in 11 abstinent smokers and 11 ex-smokers.
6 O) levels, independent of whether current or ex-smokers.
7 a: r = 0.62 and P < .001) but not in healthy ex-smokers.
8 between mGluR5 binding and relapse in recent ex-smokers.
9 arker expression in COPD current compared to ex-smokers.
10 ater response was observed in smokers versus ex-smokers.
11 GFR mutation compared with 29% of 14 smokers/ex-smokers.
12  all the never-smokers or all the smokers or ex-smokers.
13 , 20.4% were current smokers, and 19.2% were ex-smokers.
14 ng cessation increases the risk of asthma in ex-smokers.
15  at baseline as occasional, experimental, or ex-smokers.
16 al D2R did not differ between nonsmokers and ex-smokers.
17 agnosis were significantly more likely to be ex-smokers.
18 hemoprevention of lung cancer in smokers and ex-smokers.
19  apart were 0.51 for never smokers, 0.48 for ex-smokers, 0.56 for men who smoked < 1 pack/day, and 0.
20 er in current smokers (25.9%, P = 0.008) and ex-smokers (28.2%, P = 0.022) than in nonsmokers (38.5%)
21 o be RF positive at baseline (47%) than were ex-smokers (34%) and never smokers (31%).
22 -15.6 coughs/h]), almost double that of COPD ex-smokers (4.9 [2.3-8.7] coughs/h; P = 0.018) and healt
23 active tPA (current smokers, 31+/-23 IU/min; ex-smokers, 50+/-33 IU/min; nonsmokers 202+/-73 IU/min;
24 e gray matter mGluR5 DVR between smokers and ex-smokers (9.2%; P < 0.01).
25 iction by investigating a group of long-term ex-smokers (abstinence >1.5 years), and to explore assoc
26                                       In all ex-smokers, ADC values were significantly elevated in re
27                                AM taken from ex-smokers also failed to secrete significantly increase
28                                              Ex-smokers also had lower risk-taking to rewards compare
29 urrent smokers, 1.96 (95% CI 1.27 to 3.0) in ex-smokers and 1.27 (95% CI 0.87 to 1.86) in non-smokers
30  odds ratios were 2.5 (95% CI: 1.1, 5.4) for ex-smokers and 1.4 (95% CI: 0.7, 2.9) for current smoker
31  the epsilon3 allele was 1.74 (1.10-2.77) in ex-smokers and 1.68 (1.01-2.83) in smokers, whereas in m
32                 Alveolar macrophages of COPD ex-smokers and active smokers had impaired complement-in
33 posure, sex differences were present in both ex-smokers and current smokers for cigarettes per day (P
34 rease in creatinine clearance was greater in ex-smokers and current smokers than in nonsmokers.
35                                    Long-term ex-smokers and individuals who had never smoked showed n
36        Lung cancer prevention among smokers, ex-smokers and lifetime nonsmokers can be enhanced as we
37  there was no significant difference between ex-smokers and non-smokers in terms of time to Expanded
38 xhibited greater premature responding versus ex-smokers and nonsmokers.
39 jects with colonized COPD when compared with ex-smokers and nonsmokers.
40         In addition, nearly one third of the ex-smokers and smokers classified with the never-smoker-
41  65.6 +/- 6.7 yr; 67.6% male; 23 smokers; 45 ex-smokers) and 24 healthy volunteers (mean age, 57.5 +/
42 ble COPD (COPD), 20 ex-smokers without COPD (ex-smokers), and 15 healthy nonsmokers (nonsmokers).
43 al tobacco smoke exposure, 53 (7.2%) passive ex-smokers, and 121 (16.4%) smokers.
44 ailability measures of 8 current smokers, 10 ex-smokers, and 18 nonsmokers who were scanned with posi
45 21 (21%) were current smokers, 37 (37%) were ex-smokers, and 43 (43%) had never smoked.
46 61) were current smokers, 28% (328,417) were ex-smokers, and 52% (619,774) were never-smokers.
47 patient cohorts identified as never-smokers, ex-smokers, and current smokers.
48  asked at entry whether they were current or ex-smokers, and how many cigarettes they currently smoke
49 at > or = 100 cfu/ml in 34.6% of COPD, 0% of ex-smokers, and in 6.7% of nonsmokers (p = 0.003).
50 n driving COPD-related inflammation, even in ex-smokers, and might result in activation of the proinf
51  to be married, more likely to be current or ex-smokers, and more likely to be politically liberal th
52                               Those who were ex-smokers at both entry and the 3-year resurvey and had
53 ype 5 (mGluR5) binding in smokers and recent ex-smokers (average abstinence duration of 25 weeks).
54 kers had deeper probing depths than non- and ex-smokers, but pockets were reduced significantly and c
55 ate, putamen, and ventral striatum) and with ex-smokers (caudate and putamen).
56 al significance, as both current smokers and ex-smoker chronic obstructive pulmonary disease (COPD) p
57 nd the decreased down-regulation seen in the ex-smokers could be due to incomplete recovery of the re
58                    Smokers, non-smokers, and ex-smokers did not differ significantly in PI, BOP, CAL,
59 males and females; however, among current or ex-smokers, female first-degree relatives had significan
60 orticosteroids, and had never smoked or were ex-smokers for 1 year or more with 10 pack-years or less
61              Compared with 14 nonsmokers, 14 ex-smokers had global reductions in the average gray mat
62                                    Long-term ex-smokers, however, still had higher white blood cell c
63 s (ventilation defects), and gas trapping in ex-smokers in whom FEV1 may be normal and in patients wi
64 cess mortality remains among these long-term ex-smokers, it is only 3% and 10% of the excess mortalit
65  of chronic obstructive pulmonary disease in ex-smokers may be driven, in part, by tobacco anti-idiot
66   These results suggest that with abstinence ex-smokers may recover from low striatal D2R availabilit
67  March 2014 to December 2014 and included 58 ex-smokers (mean age, 73 years +/- 9) with (n = 32; mean
68 tonin metabolism) in current smokers but not ex-smokers might provide clues, but interpretations shou
69 nificantly higher mGluR5 binding than recent ex-smokers, most prominently in the frontal cortex (42%)
70 ges, obtained from nonsmokers (n = 20), COPD ex-smokers (n = 32), and COPD active smokers (n = 64), w
71 confidence interval (CI): 1.08 to 1.42]) and ex-smokers (n = 9,381; HR: 1.32 [95% CI: 1.18 to 1.47])
72 y more common in smokers (13%) compared with ex-smokers/never smokers (4%), a relationship which pers
73 er aspirin was seen in the combined group of ex-smokers/never-smoked patients (10.4% vs. 10.6%; HR: 0
74 Patients aged 40 years or older, smokers, or ex-smokers of 10 pack-years or more with spirometrically
75 kers (OR = 0.3, 95% CI: 0.1, 0.7) than among ex-smokers (OR = 0.6, 95% CI: 0.4, 0.9), and there was a
76 status was stronger in women (odds ratio for ex-smokers [ORex], 1.44; ORcurrent, 3.45) than in men (O
77  AM from smokers compared with nonsmokers or ex-smokers (P < 0.01).
78 MC among COPD active smokers (P < .0001) and ex-smokers (P = .028).
79  greater in current smokers than in non- and ex-smokers (P<0.005).
80 ver, in the placebo condition, activation in ex-smokers predominated in the left hemisphere, whereas
81 s overall were driven by current smokers and ex-smokers, probably because of residual confounding by
82         HRs for death in current smokers and ex-smokers relative to never smokers were 2.70 (95% CI 1
83  smokers (RR = 0.93; 95% CI = 0.76-1.14) nor ex-smokers (RR = 0.98; 95% CI = 0.75-1.28) were at incre
84 rs (RR, 1.51; 95% CI, 1.04-2.21) and passive ex-smokers (RR, 2.21; 95% CI, 1.39-3.50).
85                                    Long-term ex-smokers showed significantly higher mGluR5 binding th
86 nd chronic bronchitis, limited to current or ex-smokers, suggests genetic risk factor(s) for COPD tha
87 ents were significantly different in healthy ex-smokers than they were in ex-smokers with COPD.
88 or moderate dysplasia were more likely to be ex-smokers than those with grades of regular metaplasia
89 h the benefits, yet for most nonsmokers (and ex-smokers), the benefits of radiotherapy far outweigh t
90 choscopic sampling of NBECs from smokers and ex-smokers then will allow susceptible individuals to be
91                  After excluding current and ex-smokers there were 226 cases and 450 disease-free con
92 ceptor binding were acquired in 14 long-term ex-smokers, using positron emission tomography with radi
93                                       In all ex-smokers, VDP was correlated with PRM gas trapping (r
94 r-smokers, risk of coronary heart disease in ex-smokers was 1.34 (95% CI 0.86-2.08) and in smokers it
95 ery of the receptors, especially because the ex-smokers were abstinent for only 25 wk on average.
96                                              Ex-smokers who had stopped by choice (only 3% of ever-sm
97                                        Among ex-smokers who had stopped permanently at ages 25-34 yea
98                                              Ex-smokers who stopped smoking either before or after th
99 topped because of illness, but not the other ex-smokers, who are described as having stopped by choic
100    We analyzed the nuclear lung proteomes of ex-smokers with and without the disease.
101                                              Ex-smokers with asthma appeared to have evidence of an o
102                                              Ex-smokers with asthma had a significant improvement in
103  placebo for 2 weeks in smokers with asthma, ex-smokers with asthma, and never-smokers with asthma.
104 never smokers and CCL5 and CXCL10 reduced in ex-smokers with asthma.
105 prednisolone) in 22 current, 21 never and 10 ex-smokers with asthma.
106                                   Twenty-two ex-smokers with combined chronic obstructive pulmonary d
107 as also significantly correlated with PRM in ex-smokers with COPD (gas trapping: r = 0.47 and P = .03
108 ers with (n = 14) and without COPD (n = 17), ex-smokers with COPD (n = 13), and nonsmokers (n = 12).
109 lood and alveolar macrophages--obtained from ex-smokers with COPD (n = 14), ex-smokers without COPD (
110 th neutrophilic airway lumen inflammation in ex-smokers with COPD and could contribute to progression
111                                  Conversely, ex-smokers with COPD showed an increase in ac-H3 (p < 0.
112 rent in healthy ex-smokers than they were in ex-smokers with COPD.
113 tes as chemopreventive agents in smokers and ex-smokers with early lung lesions.
114 moking history of at least 30 pack-years and ex-smokers with less than 15 years since quitting.
115                            Never smokers and ex-smokers with MS had similar mortality rates compared
116 risks that compared categories of smokers or ex-smokers with otherwise similar never-smokers.
117 ed from nonsmoking patients with SA, smokers/ex-smokers with severe asthma, nonsmoking patients with
118                     We studied 23 current or ex-smokers with similar smoking histories with COPD (n =
119 as performed in three groups of subjects: 26 ex-smokers with stable COPD (COPD), 20 ex-smokers withou
120 s: 26 ex-smokers with stable COPD (COPD), 20 ex-smokers without COPD (ex-smokers), and 15 healthy non
121 obtained from ex-smokers with COPD (n = 14), ex-smokers without COPD (n = 15), and nonsmokers (n = 9)
122 , 92 (12.5%) passive nonsmokers, 157 (21.3%) ex-smokers without environmental tobacco smoke exposure,
123 tality rates compared with never smokers and ex-smokers without MS in the male British doctors cohort

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