Authors Xiu X. Puskar N.L. Shanata J.A.P. Lester H.A. Dougherty D.A

NICOTINE <1> Database EMBASE Accession Number 2009160327 Authors Xiu X. Puskar N.L. Shanata J.A.P. Lester H.A. Dougherty D.A. Institution (Xiu, Puskar, Shanata, Dougherty) Division of Chemistry and Chemical Engineering, California Institute of Technology, 1200 East California Boulevard, Pasadena, CA 91125, United States. (Lester) Division of Biology, California Institute of Technology, 1200 East California Boulevard, Pasadena, CA 91125, United States. Country of Publication United Kingdom Title Nicotine binding to brain receptors requires a strong cation- interaction. Source Nature. 458(7237)(pp 534-537), 2009. Date of Publication: 26 Mar 2009. Publisher Nature Publishing Group Abstract Nicotine addiction begins with high-affinity binding of nicotine to acetylcholine (ACh) receptors in the brain. The end result is over 4,000,000 smoking-related deaths annually worldwide and the largest source of preventable mortality in developed countries. Stress reduction, pleasure, improved cognition and other central nervous system effects are strongly associated with smoking. However, if nicotine activated ACh receptors found in muscle as potently as it does brain ACh receptors, smoking would cause intolerable and perhaps fatal muscle contractions. Despite extensive pharmacological, functional and structural studies of ACh receptors, the basis for the differential action of nicotine on brain compared with muscle ACh receptors has not been determined. Here we show that at the alpha4B2 brain receptors thought to underlie nicotine addiction, the high affinity for nicotine is the result of a strong cation- interaction to a specific aromatic amino acid of the receptor, TrpB. In contrast, the low affinity for nicotine at the muscle-type ACh receptor is largely due to the fact that this key interaction is absent, even though the immediate binding site residues, including the key amino acid TrpB, are identical in the brain and muscle receptors. At the same time a hydrogen bond from nicotine to the backbone carbonyl of TrpB is enhanced in the neuronal receptor relative to the muscle type. A point mutation near TrpB that differentiates alpha4B2 and muscle-type receptors seems to influence the shape of the binding site, allowing nicotine to interact more strongly with TrpB in the neuronal receptor. ACh receptors are established therapeutic targets for Alzheimers disease, schizophrenia, Parkinsons disease, smoking cessation, pain, attention-deficit hyperactivity disorder, epilepsy, autism and depression. Along with solving a chemical mystery in nicotine addiction, our results provide guidance for efforts to develop drugs that target specific types of nicotinic receptors. copyright 2009 Macmillan Publishers Limited. All rights reserved. ISSN 0028-0836 Publication Type Journal: Article Journal Name Nature Volume 458 Issue Part 7237 Page 534-537 Year of Publication 2009 Date of Publication 26 Mar 2009

NICOTINE <13> Database EMBASE Accession Number 2009231388 Authors Conway J.L.C. Institution (Conway) MRC SGDP Centre, Institute of Psychiatry, Denmark Hill, London, SE5 8AF, United Kingdom. Country of Publication United Kingdom Title Exogenous nicotine normalises sensory gating in schizophrenia; therapeutic implications. Source Medical Hypotheses. 73(2)(pp 259-262), 2009. Date of Publication: August 2009. Publisher Churchill Livingstone Abstract There is a current popular recognition that cigarette smoking is deleterious to health. Although this is very clearly the case for physical health, the situation regarding mental health is, however, rather more complicated. This piece concentrates on the role of smoking in schizophrenia: it is important to consider why schizophrenia, exceptionally amongst the severe and enduring mental illnesses, is associated with increased cigarette consumption. People who suffer from schizophrenia consequently have a greater risk of the complications to physical health caused by this addiction and clearly, it is important to understand why this occurs. Numerous investigators have found that both neuroleptic-naive, first-onset schizophrenics, together with chronic sufferers of the illness, consume more cigarettes and extract a greater amount of nicotine from them. Researchers have further determined that there is deficient endogenous central nicotinic neurotransmission in schizophrenia, which causes a disruption of sensory gating. This disrupted sensory gating is a reasonable explanation for the delusional misinterpretation of consequent cerebral events. This is the principal reason for the markedly increased rate of cigarette smoking in people with schizophrenia: tobacco cigarette smoking represents an attempt at self-medication in schizophrenia, because the additional nicotine so provided alleviates the hypofunctional sensory gating seen in this illness. Nicotine has been proposed to alleviate negative symptoms. The hypothesis here proposes that as nicotine alleviates positive symptoms, it consequently also - ultimately - prevents negative symptoms caused by the apoptotic effects of excitotoxicity. It would be worthwhile to investigate the therapeutic effects, if any, of additional exogenous nicotine delivered in a less toxic form than cigarettes. copyright 2009 Elsevier Ltd. All rights reserved. ISSN 0306-9877 Publication Type Journal: Article Journal Name Medical Hypotheses Volume 73 Issue Part 2 Page 259-262 Year of Publication 2009 Date of Publication August 2009

NICOTINE <15> Database EMBASE Accession Number 2009247727 Authors Weimer D.L. Vining A.R. Thomas R.K. Institution (Weimer) University of Wisconsin-Madison, Robert M. La Follette School of Public Affairs, 1225 Observatory Drive, Madison, WI 53706, United States. (Vining) Simon Fraser University, Vancouver, BC, Canada. (Thomas) Harris Interactive, Rochester, NY, United States. Country of Publication United Kingdom Title Cost benefit analysis involving addictive goods: Contingent valuation to estimate willingness-to-pay for smoking cessation. Source Health Economics. 18(2)(pp 181-202), 2009. Date of Publication: 2009. Publisher John Wiley and Sons Ltd Abstract The valuation of changes in consumption of addictive goods resulting from policy interventions presents a challenge for cost-benefit analysts. Consumer surplus losses from reduced consumption of addictive goods that are measured relative to market demand schedules overestimate the social cost of cessation interventions. This article seeks to show that consumer surplus losses measured using a non-addicted demand schedule provide a better assessment of social cost. Specifically, (1) it develops an addiction model that permits an estimate of the smoker's compensating variation for the elimination of addiction; (2) it employs a contingent valuation survey of current smokers to estimate their willingness-to-pay (WTP) for a treatment that would eliminate addiction; (3) it uses the estimate of WTP from the survey to calculate the fraction of consumer surplus that should be viewed as consumer value; and (4) it provides an estimate of this fraction. The exercise suggests that, as a tentative first and rough rule-of-thumb, only about 75% of the loss of the conventionally measured consumer surplus should be counted as social cost for policies that reduce the consumption of cigarettes. Additional research to estimate this important rule-of-thumb is desirable to address the various caveats relevant to this study. Copyright copyright 2008 John Wiley & Sons, Ltd. ISSN 1057-9230 Publication Type Journal: Article Journal Name Health Economics Volume 18 Issue Part 2 Page 181-202 Year of Publication 2009 Date of Publication 2009

NICOTINE (A) <19> Database EMBASE Accession Number 2009249823 Authors Marcinkiewcz C.A. Prado M.M. Isaac S.K. Marshall A. Rylkova D. Bruijnzeel A.W. Institution (Marcinkiewcz, Prado, Isaac, Marshall, Rylkova, Bruijnzeel) Department of Psychiatry, College of Medicine, University of Florida, Gainesville, FL, United States. (Bruijnzeel) Department of Psychiatry, University of Florida, 100 S. Newell Dr, Gainesville, FL 32610, United States. Country of Publication United Kingdom Title Corticotropin-releasing factor within the central nucleus of the amygdala and the nucleus accumbens shell mediates the negative affective state of nicotine withdrawal in rats. Source Neuropsychopharmacology. 34(7)(pp 1743-1752), 2009. Date of Publication: June 2009. Publisher Nature Publishing Group Abstract Tobacco addiction is a chronic disorder that is characterized by a negative affective state upon smoking cessation and relapse after periods of abstinence. Previous research has shown that an increased central release of corticotropin-releasing factor (CRF) at least partly mediates the deficit in brain reward function associated with nicotine withdrawal in rats. The aim of these studies was to investigate the role of CRF in the central nucleus of the amygdala (CeA), the lateral bed nucleus of the stria terminalis (BNST), and the nucleus accumbens shell (Nacc shell) in the deficit in brain reward function associated with precipitated nicotine withdrawal. The intracranial self-stimulation procedure was used to assess the negative affective aspects of nicotine withdrawal. Elevations in brain reward thresholds are indicative of a deficit in brain reward function. In all experiments, the nicotinic receptor antagonist mecamylamine (3mgkg) elevated the brain reward thresholds of the nicotine-dependent rats (9mgkg per day of nicotine salt) and did not affect the brain reward thresholds of the saline- treated control rats. The administration of the nonspecific CRF12 receptor antagonist D-Phe CRF((12-41)) into the CeA and the Nacc shell prevented the mecamylamine-induced elevations in brain reward thresholds in the nicotine-dependent rats. Blockade of CRF12 receptors in the lateral BNST did not prevent the mecamylamine-induced elevations in brain reward thresholds in the nicotine-dependent rats. These studies indicate that the negative emotional state associated with precipitated nicotine withdrawal is at least partly mediated by an increased release of CRF in the CeA and the Nacc shell. copyright 2009 Nature Publishing Group. ISSN 0893-133X Publication Type Journal: Article Journal Name Neuropsychopharmacology Volume 34 Issue Part 7 Page 1743-1752 Year of Publication 2009 Date of Publication June 2009

NICOTINE <30> Database EMBASE Accession Number 2009228036 Authors Gehricke J.-G. Potkin S.G. Leslie F.M. Loughlin S.E. Whalen C.K. Jamner L.D. Mbogori J. Fallon J.H. Institution (Gehricke, Potkin, Mbogori) Department of Psychiatry and Human Behavior, University of California, Irvine, 19722 MacArthur Blvd., Irvine, CA 92612, United States. (Leslie, Loughlin) Department of Pharmacology, University of California, Irvine, 19722 MacArthur Blvd., Irvine, CA 92612, United States. (Whalen, Jamner) Department of Psychology and Social Behavior, University of California, Irvine, 19722 MacArthur Blvd., Irvine, CA 92612, United States. (Fallon) Department of Anatomy and Neurobiology, University of California, Irvine, 19722 MacArthur Blvd., Irvine, CA 92612, United States. Country of Publication United Kingdom Title Nicotine-induced brain metabolism associated with anger provocation. Source Behavioral and Brain Functions. 5, 2009. Article Number: 19. Date of Publication: 24 Apr 2009. Publisher BioMed Central Ltd. Abstract Cortico-limbic brain activity associated with anger may be susceptible to nicotine and, thus, may contribute to smoking initiation and nicotine addiction. The purpose of the study was to identify the brain regions that are most reactive to nicotine and show the greatest association with anger task performance. Twenty adult nonsmokers (9 women, 11 men) participated in two laboratory sessions to assess brain metabolism with fluoro deoxy-glucose Positron Emission Topography (FDG-PET) in response to nicotine and placebo patches during an anger provocation task. Outcome variables for the anger provocation task were reaction time, intensity and length of retaliation. Reaction time was associated with nicotine-induced changes in the left thalamus. Length of retaliation was associated with a functionally linked set of cortical and subcortical structures such as right frontal lobe, right anterior cingulate (BA 24), right uncus, left parietal lobe, left BA 11, left cingulate, left BA 25, left amygdala, left BA 30, left BA 38 and BA 9. These findings reveal the underlying brain circuitry targeted by nicotine during anger provocation. copyright 2009 Gehricke et al; licensee BioMed Central Ltd. ISSN 1744-9081 Publication Type Journal: Article Journal Name Behavioral and Brain Functions Volume 5 Year of Publication 2009 Date of Publication 24 Apr 2009

NICOTINE <36> Database EMBASE Accession Number 2009217009 Authors Goto R. Takahashi Y. Nishimura S. Ida T. Institution (Ida) Graduate School of Economics, Kyoto University, Yoshida, Sakyo, Kyoto 606-8501, Japan. (Goto) Faculty of Economics, Konan University, Okamoto, Kobe, Japan. (Takahashi) Health Service, Nara Women's University, Kitauoyahigashi-cho, Nara, Japan. (Nishimura, Ida) Graduate School of Economics, Kyoto University, Yoshida, Kyoto, Japan. Country of Publication United Kingdom Title A cohort study to examine whether time and risk preference is related to smoking cessation success. Source Addiction. 104(6)(pp 1018-1024), 2009. Date of Publication: June 2009. Publisher Blackwell Publishing Ltd Abstract Aim: To identify whether time and risk preference predicts relapse among smokers trying to quit. Design: A cohort study of smokers who had recently started to quit. Time and risk preference parameters were estimated using a discrete choice experiment (DCE). Participants: A total of 689 smokers who began quitting smoking within the previous month. Measurements: Time discount rate, coefficient of risk-aversion measured at study entry and duration of smoking cessation measured for 6 months. Findings: In the unadjusted model, Cox's proportional hazard regression showed that those with a high time discount rate were more likely to relapse [hazard ratio: 1.18, 95% confidence interval (CI): 1.11-1.25]. A high coefficient of risk-aversion reduced the hazard of relapse (0.96, 0.96-0.97). When adjusted for other predictors of relapse (age, gender, self-efficacy of quitting, health status, mood variation, past quitting experience, the use of nicotine replacement therapy, nicotine dependence), the hazard ratios of time discount rate and the coefficient of risk-aversion is 1.17 (95% CI: 1.10-1.24) and 0.98 (95% CI: 0.97-0.99), respectively. Conclusions: Those who emphasize future rewards (time-patient preference) and those who give more importance to rewards that are certain (higher risk-aversion) were significantly more likely to continue to abstain from smoking. copyright 2009 Society for the Study of Addiction. ISSN 0965-2140 Publication Type Journal: Article Journal Name Addiction Volume 104 Issue Part 6 Page 1018-1024 Year of Publication 2009 Date of Publication June 2009

NICOTINE <43> Database EMBASE Accession Number 2009217001 Authors Hall S.M. Humfleet G.L. Munoz R.F. Reus V.I. Robbins J.A. Prochaska J.J. Institution (Hall) University of California, San Francisco, Box 0984, 401 Parnassus Avenue, San Francisco, CA 94143-0984, United States. (Hall) University of California, San Francisco, CA, United States. Country of Publication United Kingdom Title Extended treatment of older cigarette smokers. Source Addiction. 104(6)(pp 1043-1052), 2009. Date of Publication: June 2009. Publisher Blackwell Publishing Ltd Abstract Aims: Tobacco dependence treatments achieve abstinence rates of 25-30% at 1 year. Low rates may reflect failure to conceptualize tobacco dependence as a chronic disorder. The aims of the present study were to determine the efficacy of extended cognitive behavioral and pharmacological interventions in smokers [greater-than or equal to] 50 years of age, and to determine if gender differences in efficacy existed. Design: Open randomized clinical trial. Setting: A free-standing, smoking treatment research clinic. Participants: A total of 402 smokers of [greater-than or equal to] 10 cigarettes per day, all 50 years of age or older. Intervention: Participants completed a 12-week treatment that included group counseling, nicotine replacement therapy (NRT) and bupropion. Participants, independent of smoking status, were then assigned randomly to follow-up conditions: (i) standard treatment (ST; no further treatment); (ii) extended NRT (E-NRT; 40 weeks of nicotine gum availability); (iii) extended cognitive behavioral therapy (E-CBT; 11 cognitive behavioral sessions over a 40- week period); or (iv) E-CBT plus E-NRT (E-combined; 11 cognitive behavioral sessions plus 40 weeks nicotine gum availability). Measurements: Primary outcome variable was 7-day point prevalence cigarette abstinence verified biochemically at weeks 24, 52, 64 and 104. Findings: The most clinically important findings were significant main effects for treatment condition, time and the treatment x time interaction. The E-CBT condition produced high cigarette abstinence rates that were maintained throughout the 2-year study period [(week 24 (58%), 52 (55%), 64 (55%) and 104 (55%)], and was significantly more effective than E-NRT and ST across that period. No other treatment condition was significantly different to ST. No effects for gender were found. Conclusions: Extended cognitive behavioral treatments can produce high and stable cigarette abstinence rates for both men and women. NRT does not add to the efficacy of extended CBT, and may hamper its efficacy. Research is needed to determine if these results can be replicated in a sample with a greater range of ages, and improved upon with the addition of medications other than NRT. copyright 2009 Society for the Study of Addiction. ISSN 0965-2140 Publication Type Journal: Article Journal Name Addiction Volume 104 Issue Part 6 Page 1043-1052 Year of Publication 2009 Date of Publication June 2009

NICOTINE <44> Database EMBASE Accession Number 2009217000 Authors Bricker J.B. Otten R. Liu J.L. Peterson A.V. Institution (Bricker) Fred Hutchinson Cancer Research Center, Division of Public Health Sciences M3-B821, PO Box 19024, Seattle, WA 98109-1024, United States. (Bricker, Liu, Peterson) Cancer Prevention Research Program, Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA, United States. (Bricker) Department of Psychology, University of Washington, Seattle, WA, United States. (Otten) Behavioural Science Institute, Radboud University Nijmegen, Nijmegen, Netherlands. (Peterson) Department of Biostatistics, University of Washington, Seattle, WA, United States. Country of Publication United Kingdom Title Parents who quit smoking and their adult children's smoking cessation: A 20-year follow-up study. Source Addiction. 104(6)(pp 1036-1042), 2009. Date of Publication: June 2009. Publisher Blackwell Publishing Ltd Abstract Aims: Extending our earlier findings from a longitudinal cohort study, this study examines parents' early and late smoking cessation as predictors of their young adult children's smoking cessation. Design: Parents' early smoking cessation status was assessed when their children were aged 8 years; parents' late smoking cessation was assessed when their children were aged 17 years. Young adult children's smoking cessation, of at least 6 months duration, was assessed at age 28 years. Setting: Forty Washington State school districts. Participants and measurements: Participants were 991 at least weekly smokers at age 17 whose parents were ever regular smokers and who also reported their smoking status at age 28. Questionnaire data were gathered on parents and their children (49% female and 91% Caucasian) in a longitudinal cohort (84% retention). Findings: Among children who smoked daily at age 17, parents' quitting early (i.e. by the time their children were aged 8) was associated with a 1.7 times higher odds of these children quitting by age 28 compared to those whose parents did not quit [odds ratio (OR) 1.70; 95% confidence interval (CI) 1.23, 2.36]. Results were similar among children who smoked weekly at age 17 (OR 1.91; 95% CI 1.41, 2.58). There was a similar, but non-significant, pattern of results among those whose parents quit late. Conclusions: Supporting our earlier findings, results suggest that parents' early smoking cessation has a long-term influence on their adult children's smoking cessation. Parents who smoke should be encouraged to quit when their children are young. copyright 2009 Society for the Study of Addiction. ISSN 0965-2140 Publication Type Journal: Article Journal Name Addiction Volume 104 Issue Part 6 Page 1036-1042 Year of Publication 2009 Date of Publication June 2009

NICOTINE (A) <73> Database EMBASE Accession Number 2009191292 Authors Iiguez S.D. Warren B.L. Parise E.M. Alcantara L.F. Schuh B. Maffeo M.L. Manojlovic Z. Bolaos-Guzman C.A. Institution (Iiguez, Warren, Parise, Alcantara, Schuh, Maffeo, Manojlovic, Bolaos-Guzman) Program in Neuroscience, Department of Psychology, Florida State University, Tallahassee, FL, United States. (Bolaos-Guzman) Program in Neuroscience, Department of Psychology, Florida State University, 1107 West Call Street, Tallahassee, FL 32306-4301, United States. Country of Publication United Kingdom Title Nicotine exposure during adolescence induces a depression-like state in adulthood. Source Neuropsychopharmacology. 34(6)(pp 1609-1624), 2009. Date of Publication: May 2009. Publisher Nature Publishing Group Abstract There is a strong link between tobacco consumption and mood disorders. It has been suggested that afflicted individuals smoke to manage mood, however, there is evidence indicating that tobacco consumption can induce negative mood. This study was designed to investigate whether nicotine exposure during adolescence influences emotionality/behavioral functioning later in life. Adolescent (postnatal days, PD 30-44) male rats were treated with twice-daily injections of nicotine (0, 0.16, 0.32, or 0.64 mg/kg) for 15 consecutive days, and their behavioral reactivity to various behavioral paradigms (the elevated plus maze (EPM), sucrose preference, locomotor activity in the open field, and forced swim test (FST) was assessed 24 h (short term) or 1-month (long term) after exposure. Separate groups of adult rats received nicotine (0.32 mg/kg) to control for age-dependent effects. We report that nicotine exposure during adolescencebut not adulthoodleads to a depression-like state manifested in decreased sensitivity to natural reward (sucrose), and enhanced sensitivity to stress- (FST) and anxiety-eliciting situations (EPM) later in life. Our data show that behavioral dysregulation can emerge 1 week after drug cessation, and that a single day of nicotine exposure during adolescence can be sufficient to precipitate a depression-like state in adulthood. We further demonstrate that these deficits can be normalized by subsequent nicotine (0.32 mg/kg) or antidepressant (ie fluoxetine or bupropion; 10 mg/kg) treatment in adulthood. These data suggest that adolescent exposure to nicotine results in a negative emotional state rendering the organism significantly more vulnerable to the adverse effects of stress. Within this context, our findings, together with others indicating that nicotine exposure during adolescence enhances risk for addiction later in life, could serve as a potential model of comorbidity. copyright 2009 Nature Publishing Group. ISSN 0893-133X Publication Type Journal: Article Journal Name Neuropsychopharmacology Volume 34 Issue Part 6 Page 1609-1624 Year of Publication 2009 Date of Publication May 2009

NICOTINE <76> Database EMBASE Accession Number 2009177415 Authors Freund M. Campbell E. Paul C. Sakrouge R. Lecathelinais C. Knight J. Wiggers J. Walsh R.A. Jones T. Girgis A. Nagle A. Institution (Freund) Newcastle Institute of Public Health, University of Newcastle, Hunter New England Population Health Service, Locked Bag 10, Wallsend, NSW 2287, Australia. (Freund, Campbell, Sakrouge, Lecathelinais, Knight, Wiggers) Hunter New England Area Health Service, Department of Health, NSW, Australia. (Paul, Lecathelinais, Walsh, Girgis) Centre for Health Research and Psycho-Oncology, Cancer Council of NSW, University of Newcastle, NSW, Australia. (Jones) Greater Western Population Health, NSW Department of Health, NSW, Australia. (Nagle) National Heart Foundation, NSW Division, NSW, Australia. (Freund, Campbell, Paul, Lecathelinais, Knight, Wiggers, Walsh, Girgis) Hunter Medical Research Institute, NSW, Australia. Country of Publication United Kingdom Title Increasing hospital-wide delivery of smoking cessation care for nicotine-dependent in-patients: A multi-strategic intervention trial. Source Addiction. 104(5)(pp 839-849), 2009. Date of Publication: May 2009. Publisher Blackwell Publishing Ltd Abstract Aims, design and intervention Smoking care provision to in-patients is important in assisting smoking cessation and for management of nicotine withdrawal. Limited studies have reported the effectiveness of interventions designed to increase the hospital-wide provision of such care. A quasi-experimental matched-pair trial, involving two intervention and two control hospitals in NSW, Australia, investigated whether a multi-strategic intervention increased hospital-wide smoking care provision. Participants and measurements Patient surveys (n = 274-347 per experimental condition), medical notes audits (n = 181-228) and health professional surveys (n = 229-302) were used to collect outcome data at baseline and follow- up. Findings Significantly greater increases in intervention hospitals compared to control hospitals were found for patient-reported offer of nicotine replacement therapy (NRT) (intervention 34% versus control 12%), provision of NRT (16% versus 4%) and provision of written resources (11% versus 2%), and for the recording in medical notes of smoking management discussion (13% versus 3%), offer of NRT (24% versus 3%) and provision of NRT (21% versus 5%). Intervention group health professionals reported significantly greater increases in the mean estimate of patients who: had their smoking management discussed (30% versus 17%); were offered or provided with NRT (30% versus 18%); were asked their intention to smoke post-discharge (22% versus 10%); and were provided with discharge NRT (21% versus 4%). Conclusions Implementation of a multi-strategic intervention is effective in increasing hospital smoking care delivery, particularly the provision of NRT. Research is required to identify methods to increase further the delivery of this and other forms of smoking care. copyright 2009 Society for the Study of Addiction. ISSN 0965-2140 Publication Type Journal: Article Journal Name Addiction Volume 104 Issue Part 5 Page 839-849 Year of Publication 2009 Date of Publication May 2009

NICOTINE <79> Database EMBASE Accession Number 2009171368 Authors Siru R. Hulse G.K. Tait R.J. Institution (Hulse) University School of Psychiatry and Clinical Neurosciences, University of Western Australia, QE II Medical Centre (MPC 521), Nedlands, WA 6009, Australia. (Siru, Hulse, Tait) School of Psychiatry and Clinical Neurosciences, University OfWestern Australia, QE II Medical Centre, Nedlands, WA, Australia. Country of Publication United Kingdom Title Assessing motivation to quit smoking in people with mental illness. Source Addiction. 104(5)(pp 719-733), 2009. Date of Publication: May 2009. Publisher Blackwell Publishing Ltd Abstract Background People with mental health (MH) disorders smoke at higher rates, are more nicotine-dependent and suffer greater morbidity and mortality from smoking-related illnesses than the general population. Helping these people to quit smoking is a public health priority; however, many MH professionals assume that those with mental illness are not motivated to quit. Objectives To use predetermined criteria to identify, review critically and evaluate empirically all English language, peer-reviewed data on motivation to quit smoking in MH populations. Methods A systematic search was conducted and key data on subject characteristics, measures of motivation and other variables abstracted. chi2 analyses were used to compare motivation between MH and general populations, between in-patients and out-patients and between people with depression and people with psychotic disorders. Results Evidence suggests that people with MH disorders are as motivated to quit smoking as the general population, although those with psychotic disorders may be less motivated than individuals with depression. Although readiness to cease smoking was assessed in 14 studies, only two evaluated motivation to quit smoking in in-patient populations. Conclusions People with MH disorders are motivated to quit smoking, although more research is needed looking at in-patient populations. The commonly held false belief that people with MH disorders are not motivated to cease smoking means that opportunities to encourage smoking cessation among this disenfranchised group are being missed. copyright 2009 Society for the Study of Addiction. ISSN 0965-2140 Publication Type Journal: Review Journal Name Addiction Volume 104 Issue Part 5 Page 719-733 Year of Publication 2009 Date of Publication May 2009

NICOTINE <80> Database EMBASE Accession Number 2009171366 Authors Sargent J.D. Hanewinkel R. Institution (Sargent) Cancer Control Research Program, Norris Cotton Cancer Center, Lebanon, NH 03756, United States. (Sargent) Norris Cotton Cancer Center, Dartmouth Medical School, Lebanon, NH, United States. (Hanewinkel) Institute for Therapy and Health Research, IFT-Nord, Kiel, Germany. Country of Publication United Kingdom Title Comparing the effects of entertainment media and tobacco marketing on youth smoking in Germany. Source Addiction. 104(5)(pp 815-823), 2009. Date of Publication: May 2009. Publisher Blackwell Publishing Ltd Abstract Aims To examine differential effects of smoking in films and tobacco advertising on adolescent smoking. We hypothesize that movie smoking will have greater effects on smoking initiation, whereas tobacco advertising receptivity will primarily affect experimentation. Design Longitudinal observational study of adolescents. Setting School- based surveys conducted in Schleswig-Holstein, Germany. Participants A total of 4384 adolescents age 11-15 years at baseline and re-surveyed 1 year later; ever smoking prevalence was 38% at time 1. Measurements The main outcome variable combined two items assessing life-time and current smoking (alpha = 0.87). Baseline never smokers were analyzed separately from those who had tried smoking (ever smokers). Exposure to smoking in 398 internationally distributed US movies was modeled as a continuous variable, with 0 corresponding to the 5th percentile and 1 to the 95th percentile of exposure. Tobacco marketing receptivity consisted of naming a brand for a favorite tobacco advertisement. Ordinal logistic regressions controlled for socio-demographics, other social influences, personality characteristics of the adolescent and parenting style. Findings Whereas 34% of ever smokers were receptive to tobacco marketing at time 1, only 6% of never smokers were. Among time 1 never smokers, exposure to movie smoking was a significantly stronger predictor of higher time 2 smoking level [adjusted proportional odds ratio = 2.76, 95% confidence interval (1.84, 4.15)] than was tobacco marketing receptivity (1.53 [1.07, 2.20]). Among time 1 ever smokers, both tobacco marketing receptivity and exposure to movie smoking predicted higher levels of time 2 smoking [2.17 (1.78, 2.63) and 1.62 (1.18, 2.23), respectively], and the two estimates were not significantly different. Conclusions In this longitudinal study, exposure to movie smoking was a stronger predictor of smoking initiation than tobacco marketing receptivity, which was more common among ever smokers. The results suggest that entertainment media smoking should be emphasized in programs aimed at preventing onset, and both exposures should be emphasized in programs aimed at experimental smokers. copyright 2009 Society for the Study of Addiction. ISSN 0965-2140 Publication Type Journal: Article Journal Name Addiction Volume 104 Issue Part 5 Page 815-823 Year of Publication 2009 Date of Publication May 2009

NICOTINE<82> Database EMBASE Accession Number 2009171364 Authors Grosshans M. Mutschler J. Hermann D. Mann K. Diehl A. Institution (Diehl) Department of Addictive Behavior and Addiction Medicine, Central Institute of Mental Health, D-68159 Mannheim, Germany. (Grosshans, Mutschler, Hermann, Mann, Diehl) Department of Addictive Behavior and Addiction Medicine, Central Institute of Mental Health, Mannheim, Germany. Country of Publication United Kingdom Title Reduced affective symptoms during tobacco dependence treatment with varenicline. Source Addiction. 104(5)(pp 859-861), 2009. Date of Publication: May 2009. Publisher Blackwell Publishing Ltd Abstract Background The nicotinic acetylcholine receptor partial agonist varenicline has been shown to be effective in the treatment of tobacco dependence, but has been reported to induce exacerbations of psychiatric symptoms in subjects with pre-existing psychiatric disorders. Case description We report a tobacco-dependent patient who developed depression and suicidal tendencies during several cessation attempts, but was finally able to stay nicotine- abstinent by taking varenicline. Conclusion In this case varenicline did not lead to exacerbation but appeared to improve the affective symptoms. copyright 2009 Society for the Study of Addiction. ISSN 0965-2140 Publication Type Journal: Article Journal Name Addiction Volume 104 Issue Part 5 Page 859-861 Year of Publication 2009 Date of Publication May 2009

NICOTINE <87> Database EMBASE Accession Number 2009171358 Authors Dawkins L. Powell J.H. Pickering A. Powell J. West R. Institution (Dawkins) School of Psychology, University of East London, Stratford Campus, Romford Road, Stratford, London E15 4LN, United Kingdom. (Dawkins) University of East London, Stratford Campus, Stratford, London, United Kingdom. (Powell, Pickering) Goldsmiths, University of London, London, United Kingdom. (Powell) Institute of Psychiatry, London, United Kingdom. (West) University College London, London, United Kingdom. Country of Publication United Kingdom Title Patterns of change in withdrawal symptoms, desire to smoke, reward motivation and response inhibition across 3 months of smoking abstinence. Source Addiction. 104(5)(pp 850-858), 2009. Date of Publication: May 2009. Publisher Blackwell Publishing Ltd Abstract Aims We have demonstrated previously that acute smoking abstinence is associated with lowered reward motivation and impaired response inhibition. This prospective study explores whether these impairments, along with withdrawal-related symptoms, recover over 3 months of sustained abstinence. Design Participants completed a 12-hour abstinent baseline assessment and were then allocated randomly to quit unaided or continue smoking. All were re-tested after 7 days, 1 month and 3 months. Successful quitters' scores were compared with those of continuing smokers, who were tested after ad libitum smoking. Setting Goldsmiths, University of London. Participants A total of 33 smokers who maintained abstinence to 3 months, and 31 continuing smokers. Measurements Indices demonstrated previously in this cohort of smokers to be sensitive to the effect of nicotine versus acute abstinence: reward motivation [Snaith-Hamilton pleasure scale (SHAPS), Card Arranging Reward Responsivity Objective Test (CARROT), Stroop], tasks of response inhibition [anti-saccade task; Continuous Performance Task (CPT)], clinical indices of mood [Hospital Anxiety and Depression Scale (HADS)], withdrawal symptoms [Mood and Physical Symptoms Scale (MPSS)] and desire to smoke. Findings SHAPS anhedonia and reward responsivity (CARROT) showed significant improvement and plateaued after a month of abstinence, not differing from the scores of continuing smokers tested in a satiated state. Mood, other withdrawal symptoms and desire to smoke all declined from acute abstinence to 1 month of cessation and were equivalent to, or lower than, the levels reported by continuing, satiated smokers. Neither group showed a change in CPT errors over time while continuing smokers, but not abstainers, showed improved accuracy on the anti-saccade task at 3 months. Conclusion Appetitive processes and related affective states appear to improve in smokers who remain nicotine-free for 3 months, whereas response inhibition does not. Although in need of replication, the results suggest tentatively that poor inhibitory control may constitute a long-term risk factor for relapse and could be a target for intervention. copyright 2009 Society for the Study of Addiction. ISSN 0965-2140 Publication Type Journal: Article Journal Name Addiction Volume 104 Issue Part 5 Page 850-858 Year of Publication 2009 Date of Publication May 2009

NICOTINE <103> Database EMBASE Accession Number 2009170315 Authors Rovina N. Nikoloutsou I. Dima E. Michailidou M. Roussos C. Gratziou C. Institution (Rovina, Nikoloutsou, Dima, Michailidou, Gratziou) Smoking Cessation Clinic, Pulmonary and Critical Care Department, Evgenidion Hospital, 20 Papadiamantopoulou Str., 11528 Athens, Greece. (Roussos) Department of Pulmonary and Critical Care Medicine, Evgenidio Hospital, University of Athens, 20 Papadiamantopoulou Str., 11528 Athens, Greece. (Roussos) Department of Critical Care and Pulmonary Services, Evangelismos Hospital, University of Athens, 20 Papadiamantopoulou Str., 11528 Athens, Greece. Country of Publication United Kingdom Title Smoking cessation treatment in a real-life setting: The Greek experience. Source Therapeutic Advances in Respiratory Disease. 1(2)(pp 93-104), 2007. Date of Publication: 2007. Publisher SAGE Publications Ltd Abstract Objectives: The aim of this study was to estimate the clinical efficacy of counseling combined with currently used pharmacotherapy for smoking cessation (bupropion SR and nicotine replacement therapy, NRT) in actual clinical practice, and to identify predictors of successful abstinence at the end of therapy, as well as predictors of sustained abstinence in one year. Methods: 895 smokers, self-motivated to quit, received bupropion SR for 7 or 19 weeks and/or nicotine replacement therapy (NRT) (nicotine patch) for 9 weeks in combination with individual behavioural therapy. An intensive program including repetitive visits and telephone contacts during treatment and one year's follow-up period was available for supporting and motivating smokers to prevent relapse. Results: Post-treatment abstinence rates were 71.6% and 53.2% in bupropion SR groups for 7 and 19 weeks of treatment, respectively, (p < 0.001), 63.4% in bupropion SR plus nicotine patch group and 45% (p < 0.001) in nicotine patch group. One year's follow-up abstinence rates were 43.1%, 29.6%, 30.4% and 18.4% (p < 0.05), respectively. Predictors of successful abstinence at the end of therapy included (a) bupropion SR, (b) lower DSM IV symptom score, and (c) lower nicotine addiction, while predictors for sustained abstinence in one year included: (a) bupropion SR, (b) lower nicotine addiction, and (c) smoker's motivation. Conclusions: Smoking cessation interventions implementing intensive multi-component programs and constant smokers' motivation in health care settings of actual practice seem promising for increasing short and long-term abstinence rates. copyright SAGE Publications 2007. ISSN 1753-4658 Publication Type Journal: Article Journal Name Therapeutic Advances in Respiratory Disease Volume 1 Issue Part 2 Page 93-104 Year of Publication 2007 Date of Publication 2007

NICOTINE <105> Database EMBASE Accession Number 2009168934 Authors Levy D.E. Biener L. Rigotti N.A. Institution (Levy, Rigotti) Tobacco Research and Treatment Center, Institute for Health Policy, Department of Medicine, Boston, MA, United States. (Levy, Rigotti) Massachusetts General Hospital, Department of Medicine, Harvard Medical School, Boston, MA, United States. (Biener) Center for Survey Research, University of Massachusetts, Boston, MA, United States. (Levy) MGH Institute for Health Policy, 50 Staniford Street, Boston, MA 02114, United States. Country of Publication United Kingdom Title The natural history of light smokers: A population-based cohort study. Source Nicotine and Tobacco Research. 11(2)(pp 156-163), 2009. Date of Publication: 2009. Publisher Oxford University Press Abstract Introduction: Among cigarette smokers, lower levels of consumption, defined as smoking fewer cigarettes per day (CPD) or not smoking daily, are becoming more common. The relationship between cigarette consumption and smoking frequency (daily or nondaily) is not well characterized, and the natural history of light smoking (defined here as smoking [less- than or equal to]10 CPD) is poorly understood. Methods: We assessed changes in CPD and smoking frequency over time among light smokers ([less-than or equal to]10 CPD) and very light smokers ([less-than or equal to]5 CPD), using a population-based longitudinal survey of 3,083 adult smokers in Massachusetts who were interviewed three times over a 4-year follow- up period (in 2000-2001, 2002-2003, and 2005-2006). We used logistic regression to identify factors associated with light smokers' progression to heavier smoking or smoking reduction/quitting. Results: Seventy percent of very light smokers were nondaily smokers. Very light nondaily smokers differed from very light daily smokers by younger age, higher socioeconomic status, a social smoking pattern, later smoking initiation, less evidence of nicotine addiction, and more recent and planned cessation efforts. Very light nondaily smokers and smokers consuming 6-10 CPD were more likely to remain in the same smoking category and were less likely to increase consumption than were very light daily smokers. Factors independently associated with increasing consumption among very light smokers were smoking daily, nicotine dependence, White ethnicity, social smoking, and having more friends who smoked; among smokers consuming 6-10 CPD, male gender and lack of quitting self-efficacy were associated with increasing consumption. Conclusion: Our findings indicate that most light smoking is not a gateway to heavier smoking. copyright The Author 2009. Published by Oxford University Press on behalf of the Society for Research on Nicotine and Tobacco. All rights reserved. ISSN 1462-2203 Publication Type Journal: Article Journal Name Nicotine and Tobacco Research Volume 11 Issue Part 2 Page 156-163 Year of Publication 2009 Date of Publication 2009

NICOTINE (A) <109> Database EMBASE Accession Number 2009147937 Authors Sakoori K. Murphy N.P. Institution (Sakoori, Murphy) Molecular Neuropathology Group, RIKEN Brain Science Institute, 2-1 Hirosawa, Wakoshi, Saitama, 351-0198, Japan. Country of Publication United Kingdom Title Enhanced nicotine sensitivity in nociceptin/orphanin FQ receptor knockout mice. Source Neuropharmacology. 56(5)(pp 896-904), 2009. Date of Publication: April 2009. Publisher Elsevier Ltd Abstract The opioid peptide nociceptin (orphanin FQ) has been implicated in reward, reinforcement and addiction. The current study sought evidence of a role of endogenous nociceptin in nicotine responses by studying nociceptin receptor (NOP) knockout mice. The results were: (1) NOP receptor knockout mice showed enhanced anxiety-like behavior on an elevated plus maze. Whereas nicotine (0.05-0.5 mg/kg) tended to be anxiogenic in wild-type mice, NOP receptor KO mice were resistant to this effect, though interpretation was confounded by their stronger anxiety-like behavior. (2) When presented increasing nicotine concentrations (3-50 mug/ml) in a bottle choice drinking paradigm, there were no genotype-dependent differences in nicotine preference. However, NOP receptor knockout mice consumed more 3 mug/ml nicotine solution when considered in absolute terms. (3) NOP receptor knockout mice showed stronger hypothermic responses to nicotine (1 or 2 mg/kg) administration. (4) There was modest evidence that NOP receptor KO mice showed attenuated behavioral sensitization to a low dose of nicotine (0.05 mg/kg) during repeated daily treatment. (5) NOP receptor knockout mice more rapidly tolerated the sedative effect of nicotine (1 mg/kg), due partially to slightly lower locomotion on first treatment. (6) NOP receptor knockout mice, unlike wild-type mice, showed a significant mecamylamine (2.5 mg/kg) induced conditioned place aversion to nicotine (24 mg/kg/day) withdrawal. These results show that mice lacking the influence of endogenous N/OFQ mice are hypersensitive to nicotine in most measures, showing a role of endogenous nociceptin in modulating or mediating the acute effects of nicotine, and possibly nicotine addiction. copyright 2009 Elsevier Ltd. All rights reserved. ISSN 0028-3908 Publication Type Journal: Article Journal Name Neuropharmacology Volume 56 Issue Part 5 Page 896-904 Year of Publication 2009 Date of Publication April 2009

NICOTINE (A) <120> Database EMBASE Accession Number 2009116150 Authors Leao R.M. Cruz F.C. Planeta C.S. Institution (Leao, Cruz, Planeta) Laboratory of Pharmacology, School of Pharmaceutical Sciences, Sao Paulo State University (UNESP), Araraquara, Sao Paulo, Brazil. (Planeta) Laboratory of Pharmacology, School of Pharmaceutical Sciences, Sao Paulo State University (UNESP), Araraquara, Sao Paulo 14801 -902, Brazil. Country of Publication United Kingdom Title Exposure to acute restraint stress reinstates nicotine-induced place preference in rats. Source Behavioural Pharmacology. 20(1)(pp 109-113), 2009. Date of Publication: February 2009. Publisher Lippincott Williams and Wilkins Abstract Tobacco addiction is associated with high rates of relapse to drug use even after prolonged periods of abstinence. Relapse can occur upon reexposure to the drug of abuse, exposure to stress or to stimuli associated with drug consumption. The reinstatement of conditioning place preference (CPP) provides a simple and easy approach to investigate the mechanisms for drug relapse. We evaluated whether exposure to restraint stress could reinstate nicotine- induced CPP 1 or 15 days after its extinction. Nicotine produced place preference to the compartment paired with its injections during conditioning (0.16 mg/kg, subcutaneous; four drug sessions). Once established, nicotine CPP was extinguished by alternate exposure to each compartment after a saline injection (four exposures to each compartment). After this extinction phase, the reinstatement of place conditioning was investigated. For this purpose, rats were exposed to 30-min restraint stress 1 or 15 days after the extinction test, then immediately tested for reinstatement of CPP. Our results show that exposure to restraint stress reinstated CPP 1 and 15 days after extinction. Our study indicates for the first time that the vulnerability to stress-induced reinstatement of nicotine CPP is long-lasting, corroborating clinical studies showing that stress is positively associated with relapse to tobacco use even after a long period of nicotine withdrawal. copyright 2009 Wolters Kluwer Health. ISSN 0955-8810 Publication Type Journal: Article Journal Name Behavioural Pharmacology Volume 20 Issue Part 1 Page 109-113 Year of Publication 2009 Date of Publication February 2009

NICOTINE (A) <122> Database EMBASE Accession Number 2009131174 Authors Anney R.J.L. Lotfi-Miri M. Olsson C.A. Reid S.C. Hemphill S.A. Patton G.C. Institution (Anney) Neuropsychiatric Genetics Research Group, Department of Psychiatry, Trinity College Dublin, Dublin, Ireland. (Anney, Lotfi-Miri, Olsson) Behavioural Genetics Laboratory, Murdch Childrens Research Institute, Parkville, VIC, Australia. (Olsson, Reid, Hemphill, Patton) Centre for Adolescent Health, Murdoch Childrens Research Institute, Parkville, VIC, Australia. (Patton) Department of Paediatrics, University of Melbourne, Melbourne, VIC, Australia. Country of Publication United Kingdom Title Variation in the gene coding for the M5 Muscarinic receptor (CHRM5) influences cigarette dose but is not associated with dependence to drugs of addiction: Evidence from a prospective population based cohort study of young adults. Source BMC Genetics. 8, 2007. Article Number: 46. Date of Publication: 03 Jul 2007. Publisher BioMed Central Ltd. Abstract Background: The mesolimbic structures of the brain are important in the anticipation and perception of reward. Moreover, many drugs of addiction elicit their response in these structures. The M5 muscarinic receptor (M5R) is expressed in dopamine-containing neurones of the substantia nigra pars compacta and ventral tegmental area, and regulates the release of mesolimbic dopamine. Mice lacking M5R show a substantial reduction in both reward and withdrawal responses to morphine and cocaine. The CHRM5, the gene that codes for the M5R, is a strong biological candidate for a role in human addiction. We screened the coding and core promoter sequences of CHRM5 using denaturing high performance liquid chromatography to identify common polymorphisms. Additional polymorphisms within the coding and core promoter regions that were identified through dbSNP were validated in the test population. We investigated whether these polymorphisms influence substance dependence and dose in a cohort of 1947 young Australians. Results: Analysis was performed on 815 participants of European ancestry who were interviewed at wave 8 of the cohort study and provided DNA. We observed a 26.8% increase in cigarette consumption in carriers of the rs7162140 T-allele, equating to 20.1 cigarettes per week (p = 0.01). Carriers of the rs7162140 T-allele were also found to have nearly a 3-fold increased risk of developing cannabis dependence (OR = 2.9 (95%CI 1.1-7.4); p = 0.03). Conclusion: Our data suggest that variation within the CHRM5 locus may play an important role in tobacco and cannabis but not alcohol addiction in European ancestry populations. This is the first study to show an association between CHRM5 and substance use in humans. These data support the further investigation of this gene as a risk factor in substance use and dependence. copyright 2007 Anney et al; licensee BioMed Central Ltd. Publication Type Journal: Article Journal Name BMC Genetics Volume 8 Year of Publication 2007 Date of Publication 03 Jul 2007

NICOTINE <124> Database EMBASE Accession Number 2009130018 Authors Siddiqi K. Lee A.C.K. Institution (Siddiqi) Nuffield Centre for International Health and Development, University of Leeds, 71-75 Clarendon Road, Leeds LS2 9LP, United Kingdom. (Siddiqi) Nuffield Centre for International Health and Development, University of Leeds, Leeds, United Kingdom. (Lee) Section of Public Health, School of Health and Related Research, University of Sheffield, Sheffield, United Kingdom. Country of Publication United Kingdom Title An integrated approach to treat tobacco addiction in countries with high tuberculosis incidence. Source Tropical Medicine and International Health. 14(4)(pp 420-428), 2009. Date of Publication: April 2009. Publisher Blackwell Publishing Ltd Abstract Communicable diseases as well as maternal and child health in low- and middle-income countries continue to be the main focus of global attention. There are also rising trends in the prevalence of non-communicable diseases and further increases are predicted. Several countries are facing this 'dual burden of disease'. There is therefore a need to find ways to integrate the prevention and control of non-communicable diseases into the current health agenda. Tobacco treatment interventions in patients suspected with tuberculosis (TB) offer one such opportunity for a linked healthcare response. Many countries with a high incidence of TB are doubly burdened by an epidemic of tobacco use and tobacco-related diseases. Tobacco use increases the risk of TB infection and is associated with poor treatment compliance, increases in relapse rates and higher secondary mortality. In countries where TB is epidemic, this modest relative risk of infection leads to a significant attributable risk. Regular clinical contact with patients suspected with TB during the diagnosis and treatment phases provides considerable opportunity for health promotion to influence their tobacco- related behaviour. Consequently, treating tobacco addiction in patients suspected with TB is likely to improve the control of TB and prevent tobacco-related diseases. However, despite a high prevalence of tobacco use among TB patients, the treatment of tobacco addiction has not been a priority of TB control programmes. In countries with the dual epidemics of TB and tobacco use, considerable health and economic gains could potentially be made. If effective, such an approach would be highly desirable. We argue that further research assessing the cost-effectiveness and feasibility of linking healthcare interventions such as the treatment of tobacco addiction among TB suspects should receive high priority. copyright 2009 Blackwell Publishing Ltd. ISSN 1360-2276 Publication Type Journal: Article Journal Name Tropical Medicine and International Health Volume 14 Issue Part 4 Page 420-428 Year of Publication 2009 Date of Publication April 2009