Thermal macrophysiology is an established research field that has led to well-described patterns in the global structuring of climate adaptation and risk. However, since it was developed primarily in ...animals, we lack information on how general these patterns are across organisms. This is alarming if we are to understand how thermal tolerances are distributed globally, improve predictions of climate change, and mitigate effects. We approached this knowledge gap by compiling a geographically and taxonomically extensive database on plant heat and cold tolerances and used this dataset to test for thermal macrophysiological patterns and processes in plants. We found support for several expected patterns: Cold tolerances are more variable and exhibit steeper latitudinal clines and stronger relationships with local environmental temperatures than heat tolerances overall. Next, we disentangled the importance of local environments and evolutionary and biogeographic histories in generating these patterns. We found that all three processes have significantly contributed to variation in both heat and cold tolerances but that their relative importance differs. We also show that failure to simultaneously account for all three effects overestimates the importance of the included variable, challenging previous conclusions drawn from less comprehensive models. Our results are consistent with rare evolutionary innovations in cold acclimation ability structuring plant distributions across biomes. In contrast, plant heat tolerances vary mainly as a result of biogeographical processes and drift. Our results further highlight that all plants, particularly at mid-to-high latitudes and in their nonhardened state, will become increasingly vulnerable to ongoing climate change.
Geographic characters— traits describing the spatial distribution of a species— may both affect and be affected by processes associated with lineage birth and death. This is potentially confounding ...to comparative analyses of species distributions because current models do not allow reciprocal interactions between the evolution of ranges and the growth of phylogenetic trees. Here, we introduce a likelihood-based approach to estimating region-dependent rates of speciation, extinction, and range evolution from a phylogeny, using a new model in which these processes are interdependent. We demonstrate the method with simulation tests that accurately recover parameters relating to the mode of speciation and source-sink dynamics. We then apply it to the evolution of habitat occupancy in Californian plant communities, where we find higher rates of speciation in chaparral than in forests and evidence for expanding habitat tolerances.
Celotno besedilo
Dostopno za:
BFBNIB, DOBA, IZUM, KILJ, NMLJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
There are at least two theoretical reasons to believe antidepressants might help in smoking cessation. Nicotine withdrawal may produce depressive symptoms or precipitate a major depressive episode ...and antidepressants may relieve these. Nicotine may have antidepressant effects that maintain smoking, and antidepressants may substitute for this effect. Alternatively, some antidepressants may have a specific effect on neural pathways underlying nicotine addiction, (e.g. blocking nicotine receptors) independent of their antidepressant effects.
The aim of this review is to assess the effect of antidepressant medications in aiding long-term smoking cessation. The medications include bupropion; doxepin; fluoxetine; imipramine; moclobemide; nortriptyline; paroxetine; sertraline, tryptophan and venlafaxine.
We searched the Cochrane Tobacco Addiction Group trials register which includes trials indexed in MEDLINE, EMBASE, SciSearch and PsycINFO, and other reviews and meeting abstracts, in September 2006.
We considered randomized trials comparing antidepressant medications to placebo or an alternative pharmacotherapy for smoking cessation. We also included trials comparing different doses, using pharmacotherapy to prevent relapse or re-initiate smoking cessation or to help smokers reduce cigarette consumption. We excluded trials with less than six months follow up.
We extracted data in duplicate on the type of study population, the nature of the pharmacotherapy, the outcome measures, method of randomization, and completeness of follow up. The main outcome measure was abstinence from smoking after at least six months follow up in patients smoking at baseline, expressed as an odds ratio (OR). We used the most rigorous definition of abstinence available in each trial, and biochemically validated rates if available. Where appropriate, we performed meta-analysis using a fixed-effect model.
Seventeen new trials were identified since the last update in 2004 bringing the total number of included trials to 53. There were 40 trials of bupropion and eight trials of nortriptyline. When used as the sole pharmacotherapy, bupropion (31 trials, odds ratio OR 1.94, 95% confidence interval CI 1.72 to 2.19) and nortriptyline (four trials, OR 2.34, 95% CI 1.61 to 3.41) both doubled the odds of cessation. There is insufficient evidence that adding bupropion or nortriptyline to nicotine replacement therapy provides an additional long-term benefit. Three trials of extended therapy with bupropion to prevent relapse after initial cessation did not find evidence of a significant long-term benefit. From the available data bupropion and nortriptyline appear to be equally effective and of similar efficacy to nicotine replacement therapy. Pooling three trials comparing bupropion to varenicline showed a lower odds of quitting with bupropion (OR 0.60, 95% CI 0.46 to 0.78). There is a risk of about 1 in 1000 of seizures associated with bupropion use. Concerns that bupropion may increase suicide risk are currently unproven. Nortriptyline has the potential for serious side-effects, but none have been seen in the few small trials for smoking cessation. There were six trials of selective serotonin reuptake inhibitors; four of fluoxetine, one of sertraline and one of paroxetine. None of these detected significant long-term effects, and there was no evidence of a significant benefit when results were pooled. There was one trial of the monoamine oxidase inhibitor moclobemide, and one of the atypical antidepressant venlafaxine. Neither of these detected a significant long-term benefit.
The antidepressants bupropion and nortriptyline aid long-term smoking cessation but selective serotonin reuptake inhibitors (e.g. fluoxetine) do not. Evidence suggests that the mode of action of bupropion and nortriptyline is independent of their antidepressant effect and that they are of similar efficacy to nicotine replacement. Adverse events with both medications are rarely serious or lead to stopping medication.
Healthcare professionals frequently advise patients to improve their health by stopping smoking. Such advice may be brief, or part of more intensive interventions.
The aims of this review were to ...assess the effectiveness of advice from physicians in promoting smoking cessation; to compare minimal interventions by physicians with more intensive interventions; to assess the effectiveness of various aids to advice in promoting smoking cessation, and to determine the effect of anti-smoking advice on disease-specific and all-cause mortality.
We searched the Cochrane Tobacco Addiction Group trials register. Date of the most recent search: September 2007.
Randomized trials of smoking cessation advice from a medical practitioner in which abstinence was assessed at least six months after advice was first provided.
We extracted data in duplicate on the setting in which advice was given, type of advice given (minimal or intensive), and whether aids to advice were used, the outcome measures, method of randomization and completeness of follow up. The main outcome measure was abstinence from smoking after at least six months follow up. We also considered the effect of advice on mortality where long-term follow-up data were available. We used the most rigorous definition of abstinence in each trial, and biochemically validated rates where available. Subjects lost to follow up were counted as smokers. Effects were expressed as relative risks. Where possible, meta-analysis was performed using a Mantel-Haenszel fixed effect model.
We identified 41 trials, conducted between 1972 and 2007, including over 31,000 smokers. In some trials, subjects were at risk of specified diseases (chest disease, diabetes, ischaemic heart disease), but most were from unselected populations. The most common setting for delivery of advice was primary care. Other settings included hospital wards and outpatient clinics, and industrial clinics. Pooled data from 17 trials of brief advice versus no advice (or usual care) detected a significant increase in the rate of quitting (relative risk (RR) 1.66, 95% confidence interval (CI) 1.42 to 1.94). Amongst 11 trials where the intervention was judged to be more intensive the estimated effect was higher (RR 1.84, 95% CI 1.60 to 2.13) but there was no statistical difference between the intensive and minimal subgroups. Direct comparison of intensive versus minimal advice showed a small advantage of intensive advice (RR 1.37, 95% CI 1.20 to 1.56). Direct comparison also suggested a small benefit of follow-up visits. Only one study determined the effect of smoking advice on mortality. This study found no statistically significant differences in death rates at 20 years follow up.
Simple advice has a small effect on cessation rates. Assuming an unassisted quit rate of 2 to 3%, a brief advice intervention can increase quitting by a further 1 to 3%. Additional components appear to have only a small effect, though there is a small additional benefit of more intensive interventions compared to very brief interventions.
The aim of nicotine replacement therapy (NRT) is temporarily to replace much of the nicotine from cigarettes to reduce motivation to smoke and nicotine withdrawal symptoms, thus easing the transition ...from cigarette smoking to complete abstinence.
The aims of this review were:To determine the effect of NRT compared to placebo in aiding smoking cessation, and to consider whether there is a difference in effect for the different forms of NRT (chewing gum, transdermal patches, nasal spray, inhalers and tablets/lozenges) in achieving abstinence from cigarettes. To determine whether the effect is influenced by the dosage, form and timing of use of NRT; the intensity of additional advice and support offered to the smoker; or the clinical setting in which the smoker is recruited and treated. To determine whether combinations of NRT are more likely to lead to successful quitting than one type alone. To determine whether NRT is more or less likely to lead to successful quitting compared to other pharmacotherapies.
We searched the Cochrane Tobacco Addiction Group trials register for papers with 'nicotine' or 'NRT' in the title, abstract or keywords. Date of most recent search July 2007.
Randomized trials in which NRT was compared to placebo or to no treatment, or where different doses of NRT were compared. We excluded trials which did not report cessation rates, and those with follow up of less than six months.
We extracted data in duplicate on the type of participants, the dose, duration and form of nicotine therapy, the outcome measures, method of randomization, and completeness of follow up. The main outcome measure was abstinence from smoking after at least six months of follow up. We used the most rigorous definition of abstinence for each trial, and biochemically validated rates if available. We calculated the risk ratio (RR) for each study. Where appropriate, we performed meta-analysis using a Mantel-Haenszel fixed-effect model.
We identified 132 trials; 111 with over 40,000 participants contributed to the primary comparison between any type of NRT and a placebo or non-NRT control group. The RR of abstinence for any form of NRT relative to control was 1.58 (95% confidence interval CI: 1.50 to 1.66). The pooled RR for each type were 1.43 (95% CI: 1.33 to 1.53, 53 trials) for nicotine gum; 1.66 (95% CI: 1.53 to 1.81, 41 trials) for nicotine patch; 1.90 (95% CI: 1.36 to 2.67, 4 trials) for nicotine inhaler; 2.00 (95% CI: 1.63 to 2.45, 6 trials) for oral tablets/lozenges; and 2.02 (95% CI: 1.49 to 3.73, 4 trials) for nicotine nasal spray. The effects were largely independent of the duration of therapy, the intensity of additional support provided or the setting in which the NRT was offered. The effect was similar in a small group of studies that aimed to assess use of NRT obtained without a prescription. In highly dependent smokers there was a significant benefit of 4 mg gum compared with 2 mg gum, but weaker evidence of a benefit from higher doses of patch. There was evidence that combining a nicotine patch with a rapid delivery form of NRT was more effective than a single type of NRT. Only one study directly compared NRT to another pharmacotherapy. In this study quit rates with nicotine patch were lower than with the antidepressant bupropion.
All of the commercially available forms of NRT (gum, transdermal patch, nasal spray, inhaler and sublingual tablets/lozenges) can help people who make a quit attempt to increase their chances of successfully stopping smoking. NRTs increase the rate of quitting by 50-70%, regardless of setting. The effectiveness of NRT appears to be largely independent of the intensity of additional support provided to the individual. Provision of more intense levels of support, although beneficial in facilitating the likelihood of quitting, is not essential to the success of NRT.
Individual counselling from a smoking cessation specialist may help smokers to make a successful attempt to stop smoking.
The objective of the review is to determine the effects of individual ...counselling.
We searched the Cochrane Tobacco Addiction Group Specialized Register for studies with counsel* in any field. Date of the most recent search: December 2004.
Randomized or quasi-randomized trials with at least one treatment arm consisting of face-to-face individual counselling from a healthcare worker not involved in routine clinical care. The outcome was smoking cessation at follow up at least six months after the start of counselling.
Both authors extracted data. The intervention and population, method of randomization and completeness of follow up were recorded.
We identified 21 trials with over 7000 participants. Eighteen trials compared individual counselling to a minimal behavioural intervention, four compared different types or intensities of counselling. Individual counselling was more effective than control. The odds ratio for successful smoking cessation was 1.56 (95% confidence interval 1.32 to 1.84). In a subgroup of three trials where all participants received nicotine replacement therapy the point estimate of effect was smaller and did not reach significance (odds ratio 1.34, 95% confidence interval 0.98 to 1.83). We failed to detect a greater effect of intensive counselling compared to brief counselling (odds ratio 0.98, 95% confidence interval 0.61 to 1.56).
Smoking cessation counselling can assist smokers to quit.
Healthcare professionals frequently advise patients to improve their health by stopping smoking. Such advice may be brief, or part of more intensive interventions.
The aims of this review were to ...assess the effectiveness of advice from physicians in promoting smoking cessation; to compare minimal interventions by physicians with more intensive interventions; to assess the effectiveness of various aids to advice in promoting smoking cessation and to determine the effect of anti-smoking advice on disease-specific and all-cause mortality.
We searched the Cochrane Tobacco Addiction Group trials register and the Cochrane Central Register of Controlled Trials (CENTRAL). Date of the most recent searches: March 2004.
Randomized trials of smoking cessation advice from a medical practitioner in which abstinence was assessed at least six months after advice was first provided.
We extracted data in duplicate on the setting in which advice was given, type of advice given (minimal or intensive), and whether aids to advice were used, the outcome measures, method of randomization and completeness of follow up. The main outcome measures were abstinence from smoking after at least six months follow up and mortality. We used the most rigorous definition of abstinence in each trial, and biochemically validated rates where available. Subjects lost to follow up were counted as smokers. Where possible, meta-analysis was performed using a Mantel-Haenszel fixed effect model.
We identified 39 trials, conducted between 1972 and 2003, including over 31,000 smokers. In some trials, subjects were at risk of specified diseases (chest disease, diabetes, ischaemic heart disease), but most were from unselected populations. The most common setting for delivery of advice was primary care. Other settings included hospital wards and outpatient clinics, and industrial clinics. Pooled data from 17 trials of brief advice versus no advice (or usual care) revealed a small but significant increase in the odds of quitting (odds ratio 1.74, 95% confidence interval 1.48 to 2.05). This equates to an absolute difference in the cessation rate of about 2.5%. There was insufficient evidence, from indirect comparisons, to establish a significant difference in the effectiveness of physician advice according to the intensity of the intervention, the amount of follow up provided, and whether or not various aids were used at the time of the consultation in addition to providing advice. Direct comparison of intensive versus minimal advice showed a small advantage of intensive advice (odds ratio 1.44, 95% confidence interval 1.24 to 1.67). Direct comparison also suggested a small benefit of follow-up visits. Only one study determined the effect of smoking advice on mortality. It found no statistically significant differences in death rates at 20 years follow up.
Simple advice has a small effect on cessation rates. Additional manoeuvres appear to have only a small effect, though more intensive interventions are marginally more effective than minimal interventions.
Recent genome-wide association studies (GWAS) of striatal volumes and bipolar disorder (BD) indicate these traits are heritable and share common genetic architecture, however little independent work ...has been conducted to help establish this relationship.
Subcortical volumes (mm3) of young, healthy offspring of BD (N= 32) and major depressive disorder (MDD) patients (N= 158) were compared to larger healthy control sample (NRANGE= 925–1052) adjusting for potential confounds, using data from the latest release (S1200) of the Human Connectome Project. Based on recent GWAS findings, it was hypothesised that the accumbens and caudate would be smaller in offspring of BD, but not MDD patients.
After multiple comparison correction, there was a regional and BD specific relationship in the direction expected (Accumbens: F2,1067= 6.244, PFDR-CORRECTED= 0.014).
In line with recent GWAS, there was evidence supporting the hypothesis that reduced striatal volume may be part of the genetic risk for BD, but not MDD.
It cannot be concluded whether this association was specific to BD or consistent with a broader psychosis phenotype, due to a small sample size for offspring of schizophrenia patients. Furthermore, one cannot rule out potential shared environmental influences of parental BD.
The common genetic architecture of BD may confer susceptibility via inherited genetic factors that affect striatal volume. Future work should establish how this relationship relates to specific BD symptomology. This work may also help to dissect clinical heterogeneity and improve diagnosis nosology.
•Genome wide association studies suggest bipolar disorder and striatal brain volumes have shared genetic aetiology.•Little work has explored the impact of familial bipolar risk on subcortical brain structure using large samples.•Reduced ventral striatum volume in offspring of bipolar patients, but not offspring of major depressive disorder patients.•Reduced ventral striatum volume may be a neural antecedent that confers risk specifically to bipolar disorder.•This observation suggests striatal imaging markers may help to dissect clinical heterogeneity in mood disorders.
Telephone services can provide information and support for smokers. Counselling may be provided proactively or offered reactively to callers to smoking cessation helplines.
To evaluate the effect of ...proactive and reactive telephone support to help smokers quit.
We searched the Cochrane Tobacco Addiction Group trials register for studies using free text term 'telephone*' or the keywords 'telephone counselling' or 'Hotlines' or 'Telephone' . Date of the most recent search: January 2006.
Randomized or quasi-randomized controlled trials in which proactive or reactive telephone counselling to assist smoking cessation was offered to smokers or recent quitters.
Trials were identified and data extracted by one person (LS) and checked by a second (TL). The main outcome measure was the odds ratio for abstinence from smoking after at least six months follow up. We selected the strictest measure of abstinence, using biochemically validated rates where available. We considered participants lost to follow-up to be continuing smokers. Where trials had more than one arm with a less intensive intervention we used only the most similar intervention without the telephone component as the control group in the primary analysis. We assessed statistical heterogeneity amongst sub groups of clinically comparable studies using the I(2) statistic. Where appropriate, we pooled studies using a fixed-effect model. A meta-regression was used to investigate the effect of differences in planned number of calls.
Forty-eight trials met the inclusion criteria. Among smokers who contacted helplines, quit rates were higher for groups randomised to receive multiple sessions of call-back counselling (eight studies, >18,000 participants, odds ratio (OR) for long term cessation 1.41, 95% confidence interval (CI) 1.27 to 1.57). Two of these studies showed a significant benefit of more intensive compared to less intensive intervention. Telephone counselling not initiated by calls to helplines also increased quitting (29 studies, >17,000 participants, OR 1.33, 95% CI 1.21 to 1.47). A meta-regression detected a significant association between the maximum number of planned calls and the effect size. There was clearer evidence of benefit in the subgroup of trials recruiting smokers motivated to quit. Of two studies that provided access to a hotline one showed a significant benefit and one did not. Two studies comparing different counselling approaches during a single session did not detect significant differences. A further seven studies were too diverse to contribute to meta-analyses and are discussed separately.
Proactive telephone counselling helps smokers interested in quitting. There is evidence of a dose response; one or two brief calls are less likely to provide a measurable benefit. Three or more calls increases the odds of quitting compared to a minimal intervention such as providing standard self-help materials, brief advice, or compared to pharmacotherapy alone. Telephone quitlines provide an important route of access to support for smokers, and call-back counselling enhances their usefulness.
Many organisms are responding to climate change with dramatic range shifts, involving plastic and genetic changes to cope with novel climate regimes found at higher latitudes. Using experimental ...lineages of the seed beetle Callosobruchus maculatus, we simulated the initial phase of colonisation to progressively cooler and/or more variable conditions, to investigate how adaptation and phenotypic plasticity contribute to shifts in thermal tolerance during colonisation of novel climates.
We show that heat and cold tolerance rapidly evolve during the initial stages of adaptation to progressively cooler and more variable climates. The evolved shift in cold tolerance is, however, associated with maladaptive plasticity under the novel conditions, resulting in a pattern of countergradient variation between the ancestral and novel, fluctuating thermal environment. In contrast, lineages exposed to progressively cooler, but constant, temperatures over several generations expressed only beneficial plasticity in cold tolerances and no evolved response.
We propose that thermal adaptation during a range expansion to novel, more variable climates found at high latitudes and elevations may typically involve genetic compensation arising from maladaptive plasticity in the initial stages of adaptation, and that this form of (countergradient) thermal adaptation may represent an opportunity for more rapid and labile evolutionary change in thermal tolerances than via classic genetic assimilation models for thermal tolerance evolution (i.e., selection on existing reaction norms). Moreover, countergradient variation in thermal tolerances may typically mask cryptic genetic variability for these traits, resulting in apparent evolutionary stasis in thermal traits.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
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