Mindfulness, Acceptance and Defusion Strategies in Smokers: a Systematic Review of Laboratory Studies

The psychological flexibility model (PFM) provides a framework for understanding and treating behavioural dysregulation in addictions. Rather than modulating the intensity of subjective experience, interventions based on, or consistent with, the PFM (PFM interventions) seek to alter the individual’s relationship to internal states, such as craving, negative affect and drug-related thoughts, using mindfulness, acceptance and related strategies. Experimental (non-clinical) studies in smokers have examined the effects of specific isolated strategies informed by or consistent with the PFM (PFM strategies). Here, we systematically review these studies and determine the extent to which they conform to methodological standards indicative of high levels of internal validity. Eligible studies were identified through electronic database searches and assessed for the presence of specific methodological features. Provisional aggregate effect sizes were determined depending on availability of data. Of 1499 screened publications, 12 met the criteria. All examined aspects of private subjective experience relevant to abstinence (craving n = 12; negative affect n = 10), demonstrating effects favouring PFM strategies relative to inactive control conditions. However, only six assessed outcome domains consistent with the PFM and provided no consistent evidence favouring PFM strategies. Overall, most studies had methodological limitations. As such, high-quality experimental studies continue to be needed to improve our understanding of necessary and/or sufficient constituents of PFM-guided smoking cessation interventions. Recommendations for future research are discussed

Restructuring Reward Mechanisms in Nicotine Addiction: A Pilot fMRI Study of Mindfulness-Oriented Recovery Enhancement for Cigarette Smokers

The primary goal of this pilot feasibility study was to examine the effects of Mindfulness-Oriented Recovery Enhancement (MORE), a behavioral treatment grounded in dual-process models derived from cognitive science, on frontostriatal reward processes among cigarette smokers. Healthy adult (N=13; mean (SD) age 49 ± 12.2) smokers provided informed consent to participate in a 10-week study testing MORE versus a comparison group (CG). All participants underwent two fMRI scans: pre-tx and after 8-weeks of MORE. Emotion regulation (ER), smoking cue reactivity (CR), and resting-state functional connectivity (rsFC) were assessed at each fMRI visit; smoking and mood were assessed throughout. As compared to the CG, MORE significantly reduced smoking (d=2.06) and increased positive affect (d=2.02). MORE participants evidenced decreased CR-BOLD response in ventral striatum (VS; d=1.57) and ventral prefrontal cortex (vPFC; d=1.7) and increased positive ER-BOLD in VS (dVS=2.13) and vPFC (dvmPFC=2.66). Importantly, ER was correlated with smoking reduction (r’s = .68 to .91) and increased positive affect (r’s = .52 to .61). These findings provide preliminary evidence that MORE may facilitate the restructuring of reward processes and play a role in treating the pathophysiology of nicotine addiction

The Pneumococcal Serine-Rich Repeat Protein Is an Intra-Species Bacterial Adhesin That Promotes Bacterial Aggregation In Vivo and in Biofilms

The Pneumococcal serine-rich repeat protein (PsrP) is a pathogenicity island encoded adhesin that has been positively correlated with the ability of Streptococcus pneumoniae to cause invasive disease. Previous studies have shown that PsrP mediates bacterial attachment to Keratin 10 (K10) on the surface of lung cells through amino acids 273–341 located in the Basic Region (BR) domain. In this study we determined that the BR domain of PsrP also mediates an intra-species interaction that promotes the formation of large bacterial aggregates in the nasopharynx and lungs of infected mice as well as in continuous flow-through models of mature biofilms. Using numerous methods, including complementation of mutants with BR domain deficient constructs, fluorescent microscopy with Cy3-labeled recombinant (r)BR, Far Western blotting of bacterial lysates, co-immunoprecipitation with rBR, and growth of biofilms in the presence of antibodies and competitive peptides, we determined that the BR domain, in particular amino acids 122–166 of PsrP, promoted bacterial aggregation and that antibodies against the BR domain were neutralizing. Using similar methodologies, we also determined that SraP and GspB, the Serine-rich repeat proteins (SRRPs) of Staphylococcus aureus and Streptococcus gordonii, respectively, also promoted bacterial aggregation and that their Non-repeat domains bound to their respective SRRPs. This is the first report to show the presence of biofilm-like structures in the lungs of animals infected with S. pneumoniae and show that SRRPs have dual roles as host and bacterial adhesins. These studies suggest that recombinant Non-repeat domains of SRRPs (i.e. BR for S. pneumoniae) may be useful as vaccine antigens to protect against Gram-positive bacteria that cause infection

Molecular Mechanisms Associated with Nicotine Pharmacology and Dependence.

Tobacco dependence is a leading cause of preventable disease and death worldwide. Nicotine, the main psychoactive component in tobacco cigarettes, has also been garnering increased popularity in its vaporized form, as derived from e-cigarette devices. Thus, an understanding of the molecular mechanisms underlying nicotine pharmacology and dependence is required to ascertain novel approaches to treat drug dependence. In this chapter, we review the field's current understanding of nicotine's actions in the brain, the neurocircuitry underlying drug dependence, factors that modulate the function of nicotinic acetylcholine receptors, and the role of specific genes in mitigating the vulnerability to develop nicotine dependence. In addition to nicotine's direct actions in the brain, other constituents in nicotine and tobacco products have also been found to alter drug use, and thus, evidence is provided to highlight this issue. Finally, currently available pharmacotherapeutic strategies are discussed, along with an outlook for future therapeutic directions to achieve to the goal of long-term nicotine cessation

Regulation of proteinaceous effector expression in phytopathogenic fungi

Effectors are molecules used by microbial pathogens to facilitate infection via effector-triggered susceptibility or tissue necrosis in their host. Much research has been focussed on the identification and elucidating the function of fungal effectors during plant pathogenesis. By comparison, knowledge of how phytopathogenic fungi regulate the expression of effector genes has been lagging. Several recent studies have illustrated the role of various transcription factors, chromosome-based control, effector epistasis, and mobilisation of endosomes within the fungal hyphae in regulating effector expression and virulence on the host plant. Improved knowledge of effector regulation is likely to assist in improving novel crop protection strategies

A systematic review of cannabis health warning research

Background: Cannabis legalization provides an opportunity to communicate with consumers through mandated health warnings on cannabis packaging. However, research on cannabis health warnings is a nascent field. Therefore, a review is needed to synthesize cannabis health warning research and inform ongoing policy discussions. Methods: This paper used systematic review guidelines to search online databases, including PubMed Central, Scopus, Web of Science, Jstor, Communication and Mass Media Complete, Medline, PsycINFO, and Google Scholar. Search strings combined the terms “cannabis” or “marijuana” with “health warning” or “health warning message” or “warning label” or “health warning label” or “health information label.” Results were synthesized narratively. Results: The search identified 90 research articles. After screening, 17 studies on the impact of cannabis health warnings were retained. Retained studies focused on the hypothetical effects of cannabis health warnings (n = 11; 64.7 %) and “real world” effects of implementing warnings post-legalization (n = 6; 35.3 %). Evidence indicated mandated cannabis health warnings improved noticing and recall of health warning content. Cannabis health warnings describing risks of addiction were consistently rated the least effective. Pictorial cannabis health warnings generally outperformed text-only warnings when displayed on their own, while experiments with warnings on products had mixed results. Cannabis health warnings decreased product appeal, mainly when package branding was minimized. Conclusions: Health warnings on cannabis packaging are an important strategy to communicate risk to consumers. Mandating warnings increased notice, recall, and health knowledge. Warnings with pictures and describing specific risks were most effective, as was showing warnings without product branding

Effects of Experimental Negative Affect Manipulations on \u3cem\u3eAd Libitum\u3c/em\u3e Smoking: a Meta-analysis

Aims: To quantify the effect of negative affect (NA), when manipulated experimentally, upon smoking as measured within laboratory paradigms. Quantitative meta-analyses tested the effects of NA versus neutral conditions on (1) latency to smoke and (2) number of puffs taken. Methods: Twelve experimental studies tested the influence of NA induction, relative to a neutral control condition (n = 1190; range = 24–235). Those providing relevant data contributed to separate random-effects meta-analyses to examine the effects of NA on two primary smoking measures: (1) latency to smoke (nine studies) and (2) number of puffs taken during ad libitum smoking (11 studies). Hedge\u27s g was calculated for all studies through the use of post-NA cue responses relative to post-neutral cue responses. This effect size estimate is similar to Cohen\u27s d, but corrects for small sample size bias. Results: NA reliably decreased latency to smoke (g = –0.14; CI = –0.23 to –0.04; P = 0.007) and increased number of puffs taken (g = 0.14; CI = 0.02 to 0.25; P = 0.02). There was considerable variability across studies for both outcomes (I2 = 51 and 65% for latency and consumption, respectively). Potential publication bias was indicated for both outcomes, and adjusted effect sizes were smaller and no longer statistically significant. Conclusions: In experimental laboratory studies of smokers, negative affect appears to reduce latency to smoking and increase number of puffs taken, but this could be due to publication bias