Disease relevance of Smoking Cessation

• Our data also suggest that the weight gain that often follows smoking cessation may be influenced not only by nicotine intake but also by the level of physical activity a smoker typically engages in while smoking [1].
• OBJECTIVE: To review the evidence for efficacy of three contemporary treatments for intermittent claudication: pentoxifylline, exercise programs, and smoking cessation [2].
• For women, reducing cholesterol to 200 mg/dl would have the greatest estimated impact-a gain of 0.8 years-whereas smoking cessation, blood pressure control, or weight loss would yield population-wide gains of 0.7, 0.4, and 0.4 years, respectively [3].
• These results indicate that aberrant promoter hypermethylation of the p16 gene, and to a lesser extent, DAP kinase, occurs frequently in the bronchial epithelium of lung cancer cases and cancer-free controls and persists after smoking cessation [4].
• PURPOSE: To evaluate the effects of randomly assigning smokers who have early chronic obstructive pulmonary disease (COPD) to a smoking-cessation intervention on the symptoms of chronic cough, chronic phlegm production, wheezing and shortness of breath, and to determine the effects of quitting smoking on these symptoms [5].

Psychiatry related information on Smoking Cessation

• The effect of 2-mg nicotine chewing gum as an adjunct to group therapy for smoking cessation was studied in a placebo-controlled, double-blind, randomized trial [6].
• Lung cancer risk reduction after smoking cessation: observations from a prospective cohort of women [7].
• In a double-blind, randomized, placebo-controlled trial, we determined the effects of buspirone on the withdrawal symptoms associated with smoking cessation in 40 long-term cigarette smokers [8].
• Although this study did not demonstrate a significant effect of clonidine on smoking cessation, a beneficial trend was detected and therefore further trials with transcutaneous delivery of this agent in combination with behavior modification techniques are warranted [9].
• We compared sustained-release (SR) bupropion with placebo for smoking cessation in patients with schizophrenic disorders [10].

High impact information on Smoking Cessation

• Lack of efficacy of transdermal nicotine in smoking cessation [11].
• A controlled trial of sustained-release bupropion, a nicotine patch, or both for smoking cessation [12].
• RESULTS: At the end of seven weeks of treatment, the rates of smoking cessation as confirmed by carbon monoxide measurements were 19.0 percent in the placebo group, 28.8 percent in the 100-mg group, 38.6 percent in the 150-mg group, and 44.2 percent in the 300-mg group (P<0.001) [13].
• DESIGN--Group analyses from a prospective, randomized smoking-cessation intervention trial using cotinine levels to assess smoking cessation and reduction [14].
• Randomized, controlled trial of clonidine for smoking cessation in a primary care setting [15].

Chemical compound and disease context of Smoking Cessation

• Sustained-release bupropion for smoking cessation [16].
• Smoking cessation was measured by self-report after one year and validated using saliva cotinine measures [17].
• Clonidine, depression, and smoking cessation [18].
• OBJECTIVE: To compare a sustained-release form of bupropion hydrochloride (bupropion SR) with placebo for smoking cessation among African Americans [19].
• In agreement, clinical trials have suggested that the CB(1) cannabinoid antagonist rimonabant can cause smoking cessation [20].
• Because the upregulation of the nAChRs of the smokers after chronic exposure of the nicotine was downregulated to the nonsmokers' level by around 21 d after smoking cessation, the upregulation is a temporary effect [21].

Biological context of Smoking Cessation

• All participants were randomized to receive either usual care (no intervention) or special intervention, consisting of intensive smoking cessation counseling and the prescription of a metered-dose inhaler containing either ipratropium bromide or placebo (two inhalations three times daily) [22].
• The results indicate that heart rate exhibits a pattern of transient change after smoking cessation which seems to be a physiological effect of nicotine withdrawal [23].
• The hypothesis presented in this paper--that nicotine acts as both a primary reinforcer and an enhancer of other nonnicotine reinforcers--provides important direction for future investigations into the neurobiology of nicotine reinforcement and treatments for smoking cessation [24].
• AIMS: Prescribing nicotine replacement therapy (NRT) or bupropion for smoking cessation is of considerable importance to public health but little is known about prescribing practices [25].
• The efficacy of nicotine gum in group-centered smoking cessation therapy in a family practice [26].

Anatomical context of Smoking Cessation

• When subjects were divided according to their current smoking status, levels of sTNF-R55, sTNF-R75, and IL-8 in sputum were significantly elevated in ex-smoking versus currently smoking patients with COPD, suggesting ongoing inflammation in airways and circulation of patients with COPD after smoking cessation [27].
• OBJECTIVE: The purpose of the present study was to investigate the effect of smoking cessation on the peripheral neutrophil mRNA expression levels for inflammatory cytokines, chemokine, growth factor and matrix metalloproteinase (MMP) [28].
• Our data indicate that smoking cessation is associated with a significant decrease in the symptomatology of COPD, and that change in T lymphocyte beta 2-receptor density is a good marker of change in pulmonary response to beta 2-agonists [29].
• The reactivity of the brachial artery was evaluated using flow-mediated dilation immediately after smoking cessation, before the application of a 21-mg nicotine patch or placebo patch, and 24 hours after patch placement [30].
• Bupropion sustained release (SR) is the first non-nicotine pharmacological treatment approved for smoking cessation and is thought to be effective because of its dopaminergic activity on the pleasure and reward pathways in the mesolimbic system and nucleus accumbens [31].

Gene context of Smoking Cessation

• Platelet MAO-B activity increased after smoking cessation but without a significant difference [32].
• A reversible monoamine oxidase A inhibitor (moclobemide) facilitates smoking cessation and abstinence in heavy, dependent smokers [32].
• Nicotine induces CYP2B1 in rat brain and in humans polymorphic variation in CYP2B6 affects smoking cessation rates [33].
• For male former vs never smokers, there were no differences in mean IGF-I and IGFBP-3 concentrations, suggesting that smoking cessation is associated with normalisation of peptide concentrations [34].
• These results suggest that subsensitivity of the HPA axis to stress during nicotine withdrawal may be implicated in the precipitation of depression during smoking cessation, although GR and CRH in the HPA axis do not appear to play a significant role [35].

Analytical, diagnostic and therapeutic context of Smoking Cessation

• Effect of nicotine chewing gum in smoking cessation. A randomized, placebo-controlled, double-blind study [6].
• Meta-analysis on efficacy of nicotine replacement therapies in smoking cessation [36].
• Proportional hazard models compared the association between mental disorders and mortality before and after adjusting 5 established quality indicators: reperfusion, aspirin, beta-blockers, angiotensin-converting enzyme inhibitors, and smoking cessation counseling [37].
• Early diagnosis of COPD offers the best opportunity to slow the progression of the disease through smoking cessation [38].
• Pharmacotherapy remains a popular choice of smoking cessation intervention for many smokers, and both NRT and bupropion SR, combined with behavioural interventions, achieve 1.5- to >2-fold increases in smoking cessation rates [39].

References