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CPD has fallen in some countries with well developed tobacco control measures, 13 possibly as a result of taxation measures and the introduction of smoke-free laws; but, it has been argued that this does not necessarily mean tobacco dependence is decreasing because CPD is not well correlated with nicotine intake. 13 Many of the prevalence studies also assessed the sociodemographics of hardcore smokers and found that they are more likely to be from a more deprived socioeconomic background. 12 Inequalities and smoking are closely related.

Objective To compare the effects of free nicotine replacement therapy or proactive telephone counselling in addition to standard smoking cessation support offered through a telephone quitline.Design Parallel group, 2×2 factorial, randomised controlled trial.Setting National quitline, England.Participants 2591 non-pregnant smokers aged 16 or more residing in England who called the quitline between February 2009 and February 2010 and agreed to set a quit date: 648 were each randomised to standard support, proactive support, or proactive support with nicotine replacement therapy, and 647 were randomised to standard support with nicotine replacement therapy.Interventions Two interventions were offered in addition to standard support: six weeks’ nicotine replacement therapy, provided free, and proactive counselling sessions (repeat telephone calls from, and interaction with, cessation advisors).Main outcome measures The primary outcome was self reported smoking cessation for six or more months after the quit date. The secondary outcome was cessation validated by exhaled carbon monoxide measured at six or more months.Results At six months, 17.7% (n=229) of those offered nicotine replacement therapy reported smoking cessation compared with 20.1% (n=261) not offered such therapy (odds ratio 0.85, 95% confidence interval 0.70 to 1.04), and 18.2% (n=236) offered proactive counselling reported smoking cessation compared with 19.6% (n=254) offered standard support (0.91, 0.75 to 1.11). Data validated by carbon monoxide readings changed the findings for nicotine replacement therapy only, with smoking cessation validated in 6.6% (85/1295) of those offered nicotine replacement therapy compared with 9.4% (122/1296) not offered such therapy (0.67, 0.50 to 0.90).Conclusions Offering free nicotine replacement therapy or additional (proactive) counselling to standard helpline support had no additional effect on smoking cessation.Trial registration ClinicalTrials.gov NCT00775944.

Table 1 Total N=2591 No NRT N=1296 NRT N=1295 Unadjusted OR (95% CI; p value) Adjusted OR* (95% CI; p value) Adjusted OR[dagger] (95% CI; p value) Outcomes at 6 months, n (%) Prolonged cessation (inc. questionnaire data) (primary outcome) 490 (18.9) 261 (20.1) 229 (17.7) 0.85 (0.70 to 1.04; p=0.11) 0.86 (0.70 to 1.06; p=0.16) 0.84 (0.66 to 1.07; p=0.17) Carbon monoxide validated prolonged cessation 207 (8.0) 122 (9.4) 85 (6.6) 0.67 (0.50 to 0.90; p=0.008) 0.65 (0.48 to 0.88; p=0.005) 0.63 (0.45 to 0.86; p=0.004) Self-reported cessation for >=7 days 531 (20.5) 283 (21.8) 248 (19.1) 0.85 (0.70 to 1.03; p=0.09) 0.85 (0.70 to 1.04; p=0.13) 0.85 (0.67 to 1.07; p=0.17) Carbon monoxide validated cessation for >=7 days 200 (7.7) 119 (9.2) 81 (6.2) 0.66 (0.49 to 0.88; p=0.006) 0.64 (0.47 to 0.87; p=0.004) 0.62 (0.45 to 0.86; p=0.004) Reported cessation for >=3 months 401 (15.5) 216 (16.6) 185 (14.3) 0.83 (0.67 to 1.03; p=0.09) 0.84 (0.67 to 1.05; p=0.14) 0.86 (0.66 to 1.10; p=0.23) Reports one or more quit attempts lasting >24 h[dagger] 594 (22.9) 289 (22.3) 305 (23.5) 1.07 (0.88 to 1.28; p=0.49) 1.05 (0.86 to 1.27; p=0.60) 1.15 (0.88 to 1.50; p=0.30) Median (IQR) no. quit attempts reported 2 (1-3) 2 (1-4) 2 (1-3) n/a n/a n/a Outcomes at 1 month, n (%) Prolonged cessation since quit date 1040 (40.1) 520 (40.1) 520 (40.1) 0.99 (0.85 to 1.16; p=0.93) 1.01 (0.86 to 1.19; p=0.88) 1.00 (0.80 to 1.26; p=0.96) Reported cessation for >=7 days 831 (32.0) 417 (32.2) 414 (32.0) 0.98 (0.83 to 1.16; p=0.85) 0.99 (0.84 to 1.18; p=0.97) 0.97 (0.77 to 1.22; p=0.80) *Adjusted for age, gender, educational level and heaviness of smoking index; 2397 cases included in adjusted analyses. [dagger]Additionally adjusted for all forms of non-trial support.

Background Single-item urges to smoke measures have been contemplated as important measures of nicotine dependence This study aimed to prospectively determine the relationships between measures of craving to smoke and smoking cessation, and compare their ability to predict cessation with the Heaviness of Smoking Index, an established measure of nicotine dependence. Methods We conducted a secondary analysis of data from the randomised controlled PORTSSS trial. Measures of nicotine dependence, ascertained before making a quit attempt, were the HSI, frequency of urges to smoke (FUTS) and strength of urges to smoke (SUTS). Self-reported abstinence at six months after quitting was the primary outcome measure. Multivariate logistic regression and Receiver Operating Characteristic (ROC) analysis were used to assess associations and abilities of the nicotine dependence measures to predict smoking cessation. Results Of 2,535 participants, 53.5% were female; the median (Interquartile range) age was 38 (28–50) years. Both FUTS and HSI were inversely associated with abstinence six months after quitting; for each point increase in HSI score, participants were 16% less likely to have stopped smoking (OR 0.84, 95% C.I 0.78-0.89, p < 0.0001). Compared to participants with the lowest possible FUTS scores, those with greater scores had generally lower odds of cessation (p across frequency of urges categories=0.0026). SUTS was not associated with smoking cessation. ROC analysis suggested the HSI and FUTS had similar predictive validity for cessation. Conclusions Higher FUTS and HSI scores were inversely associated with successful smoking cessation six months after quit attempts began and both had similar validity for predicting cessation.

Background The use of nicotine replacement therapy before quitting smoking is called nicotine preloading. Standard smoking cessation protocols suggest commencing nicotine replacement therapy only on the first day of quitting smoking (quit day) aiming to reduce withdrawal symptoms and craving. However, other, more successful smoking cessation pharmacotherapies are used prior to the quit day as well as after. Nicotine preloading could improve quit rates by reducing satisfaction from smoking prior to quitting and breaking the association between smoking and reward. A systematic literature review suggests that evidence for the effectiveness of preloading is inconclusive and further trials are needed. Methods/Design This is a study protocol for a multicenter, non-blinded, randomized controlled trial based in the United Kingdom, enrolling 1786 smokers who want to quit, funded by the National Institute for Health Research, Health Technology Assessment program, and sponsored by the University of Oxford. Participants will primarily be recruited through general practices and smoking cessation clinics, and randomized (1:1) either to use 21 mg nicotine patches, or not, for four weeks before quitting, whilst smoking as normal. All participants will be referred to receive standard smoking cessation service support. Follow-ups will take place at one week, four weeks, six months and 12 months after quit day. The primary outcome will be prolonged, biochemically verified six-month abstinence. Additional outcomes will include point prevalence abstinence and abstinence of four-week and 12-month duration, side effects, costs of treatment, and markers of potential mediators and moderators of the preloading effect. Discussion This large trial will add substantially to evidence on the effectiveness of nicotine preloading, but also on its cost effectiveness and potential mediators, which have not been investigated in detail previously. A range of recruitment strategies have been considered to try and compensate for any challenges encountered in recruiting the large sample, and the multicentre design means that knowledge can be shared between recruitment teams. The pragmatic study design means that results will give a realistic estimate of the success of the intervention if it were to be rolled out as part of standard smoking cessation service practice. Trial registration Current Controlled Trials ISRCTN33031001 . Registered 27 April 2012.

Yet given Lansley's wish to base policy on evidence and on results, it is surprising that the new Government has started to dismantle important parts of the infrastructure that delivered the gains in public health seen in the past decade, such as the reduction in the number of smokers in England by 25%. Since coming to power in May, 2010, this Government has maintained a freeze on all mass media health campaigns, including those aimed at encouraging smokers to quit and informing them about the services available to help them.

In linear optics, the concept of a mode or eigenmode is well established. Often these modes correspond to a set of fields that are mutually orthogonal with intensity profiles that are invariant as they propagate through a given optical system. More generally, using an eigenmode decomposition, one can define a set of orthogonal modes with respect to an optical measure given that is linear in the intensity of the fields or Hermitian in the fields themselves. However, if the intensity of the light is sufficiently large, the dipole response of an optical medium includes nonlinear terms that cause the eigenmode decomposition to break down. In this work, we introduce the eigenmode decomposition in the presence of these nonlinear source terms by introducing small perturbation fields whose interaction is mediated by some high-intensity background field. Unlike the eigenmodes of linear optics, these novel modes correspond to a set of orthogonal fields that are, in general, distributed across multiple wavelengths. Here, we study the definition and interaction of these eigenmodes for classical electromagnetic fields and multiphoton fields. In the context of classical fields, with our eigenmodes established, we highlight the influence of the high-intensity background field on the symmetry of the eigenmodes. At the multiphoton level, we show that the description of multiphoton fields is simplified by using the propagation eigenmodes while remaining equivalent to the standard approach.

STUDY QUESTION Does offering either free nicotine replacement therapy (NRT) or higher intensity proactive telephone support in addition to standard quitline care increase smoking cessation rates at six months after starting quitline supported cessation attempts? SUMMARY ANSWER Cessation rates at six months were not improved by offering either NRT or higher intensity proactive telephone support in addition to standard quitline support. WHAT IS KNOWN AND WHAT THIS PAPER ADDS Quitlines reach many smokers but optimum methods for providing quitline cessation support need defining. In England, where cessation support is readily available through established health services, offering free NRT or proactive counselling in addition to reactive cessation support provided by the national quitline was ineffective.

Using an in vivo model of pulmonary hypertension (PHT) secondary to left ventricular dysfunction (LVD), the pulmonary arterial response to the nitric oxide synthase (NOS) blocker L‐NAME (30 μmol.min−1 i.v.) and the subsequent responses to cumulatively administered endothelin‐1 (ET‐1) (0.001 – 4 nmol.kg−1 i.v.) or big ET‐1 (0.1 – 2.0 nmol.kg−1 i.v.) were studied. Additionally, the effect of the non‐selective ET‐1 receptor antagonist, SB209670, was investigated. Eight weeks after coronary artery ligation or sham operation, rabbits demonstrated increased mean pulmonary arterial pressure (PAP) accompanied by right ventricular hypertrophy. Blockade of NOS caused a greater increase in basal PAP (increased by 7.7±1.1 mmHg c.f. 3.8±1.0 mmHg in controls, P<0.05) and uncovered a greater pulmonary pressor response to exogenous ET‐1 in rabbits with PHT (increased by 10.2±2.3 mmHg c.f. 4.9±1.0 mmHg in controls, P<0.05). Big ET‐1 evoked a pulmonary pressor effect, in both groups of rabbits, that was increased following blockade of NOS and was more potent in rabbits with PHT. The non‐selective ET‐1 receptor antagonist, SB209670, reduced basal PAP (from 16.9 mmHg to 15.9 mmHg, P<0.05) in rabbits with PHT and blocked the response to ET‐1 in the presence of L‐NAME. In conclusion, the results demonstrate that basal NO activity masks a pulmonary pressor response to exogenously administered ET‐1. An increased responsiveness to ET‐1 was shown in the pulmonary arterial bed of rabbits with PHT secondary to LVD, implicating a pathophysiological role for ET‐1 in this model. British Journal of Pharmacology (2002) 135, 1060–1068; doi:10.1038/sj.bjp.0704529