Background: People living with schizophrenia are less likely to quit smoking compared with the general population and people living with other psychiatric disorders. Understanding the schizophrenia-specific psychosocial barriers and facilitators to smoking cessation is important for designing effective smoking cessation interventions. We aimed to systematically review research examining psychosocial barriers and facilitators to smoking cessation in people living with schizophrenia.Methods: We followed the PRISMA statement to conduct a systematic literature review examining psychosocial barriers and facilitators to smoking cessation in people living with schizophrenia. We searched EMBASE, Medline, PsycINFO, and CINAHL databases from inception to 14 June 2018 to identify relevant articles. We included peer-reviewed original research articles that examined psychosocial barriers and facilitators to smoking cessation, as well as factors associated with maintenance of smoking habits in people living with schizophrenia spectrum disorders. Qualitative, quantitative, or mixed-methods study designs were included. Three authors screened titles, abstracts, and full-texts using the eligibility criteria. We conducted a narrative synthesis of the data to account for the heterogeneity of study designs. We analyzed qualitative and quantitative studies separately.Results: We identified 685 studies from our systematic search and screened the full-text of 134 articles. The final set of 23 articles included 20 quantitative studies and 3 qualitative studies. The most commonly cited barrier to smoking cessation in people living with schizophrenia was cravings and addiction, followed by a perceived increased risk of negative affect associated with quitting smoking. People living with schizophrenia reported smoking to manage stress and to maintain social relationships. People living with schizophrenia were found to be less likely to receive cessation support from health professionals than smokers without schizophrenia. Health concerns were the most commonly mentioned facilitator to quit smoking.Conclusions: People living with schizophrenia experience a wide range of barriers to smoking cessation. The influence of these barriers on smoking cessation likelihood may be greater among people living with schizophrenia than people without psychiatric disorders. Health professionals play an important role in smoking cessation for people living with schizophrenia and should consider barriers and facilitators identified in this review to support quitting in this vulnerable population.

Recent evidence indicated that alcohol exposure during the fetal period increases the susceptibility to tumor development in mammary and prostate tissues. Whether fetal alcohol exposure increases the susceptibility to prolactin-producing tumor (prolactinoma) development in the pituitary was studied by employing the animal model of estradiol-induced prolactinomas in Fischer 344 female rats. We employed an animal model of fetal alcohol exposure that simulates binge alcohol drinking during the first two trimesters of human pregnancy and involves feeding pregnant rats with a liquid diet containing 6.7% alcohol during gestational day 7 to day 21. Control rats were pair-fed with isocaloric liquid diet or fed ad libitum with rat chow diet. Adult alcohol exposed and control female offspring rats were used in this study on the day of estrus or after estrogen treatment. Results show that fetal alcohol-exposed rats had increased levels of pituitary weight, pituitary prolactin (PRL) protein and mRNA, and plasma PRL. However, these rats show decreased pituitary levels of dopamine D2 receptor (D2R) mRNA and protein and increased pituitary levels of D2R promoter methylation. Also, they show elevated pituitary mRNA levels of DNA methylating genes (DNMT1, DNMT3b, MeCP2) and histone modifying genes (HDAC2, HDAC4, G9a). When fetal alcohol exposed rats were treated neonatally with a DNA methylation inhibitor 5-Aza deoxycytidine and/or a HDAC inhibitor trichostatin-A their pituitary D2R mRNA, pituitary weights and plasma PRL levels were normalized. These data suggest that fetal alcohol exposure programs the pituitary to increase the susceptibility to the development of prolactinomas possibly by enhancing the methylation of the D2R gene promoter and repressing the synthesis and control of D2R on PRL-producing cells.

ObjectivesIt is the aim of the current research to identify some common functionalities of postnatal application, and to determine the quality of the information content of postnatal depression application using validated scales that have been applied for applications in other specialties.Settings and participantsTo determine the information quality of the postnatal depression smartphone applications, the two most widely used smartphone application stores, namely Apple iTunes as well as Google Android Play store, were searched between 20May and 31 May. No participants were involved. The inclusion criteria for the application were that it must have been searchable using the keywords ‘postnatal’, ‘pregnancy’, ‘perinatal’, ‘postpartum’ and ‘depression’, and must be in English language.InterventionThe Silberg Scale was used in the assessment of the information quality of the smartphone applications.Primary and secondary outcomes measureThe information quality score was the primary outcome measure.ResultsOur current results highlighted that while there is currently a myriad of applications, only 14 applications are specifically focused on postnatal depression. In addition, the majority of the currently available applications on the store have only disclosed their last date of modification as well as ownership. There remain very limited disclosures about the information of the authors, as well as the references for the information included in the application itself. The average score for the Silberg Scale for the postnatal applications we have analysed is 3.0.ConclusionsThere remains a need for healthcare professionals and developers to jointly conceptualise new applications with better information quality and evidence base.

Recent statistics released by Alzheimer's Disease International has highlighted how prevalent dementia will become in the next couple of years. Along with the increased incidence of individuals being diagnosed with dementia, there has also been an increment in the number of informal carers for people living with dementia. A recent report highlighted that in Australia, there are an estimated of 200,000 informal carers as of 2011. Caring for people who are living with dementia is not an easy task. Previous studies have highlighted that as much as 65% of caregivers do experience symptoms suggestive of depressive symptoms in the process of care. With the rapid advances in technology, it is of no surprise that information technology and its related innovations have been used in dementia care. A review of the existing literature shows that much of these innovations are focused on the care of patients affiliated with dementia. However, clearly interventions focusing on the needs of the dementia cohort of patient are limited. There are currently more emerging studies demonstrating the efficacy of web-based interventional toolkits for carers who are caring for individuals with dementia. Whilst there are previous studies demonstrating the effectiveness of smartphone interventions for dementia patients, there remains a paucity of smartphone based interventions for caregivers who are living with people with dementia. This technical note describes the conceptualization of an evidence based smartphone intervention for patients living with dementia, as well as for carers of these patients.

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Circadian systems regulate the immune system by various molecular and physiological pathways. Disruption to the circadian temporality of these pathways is associated with disease formation and progression. Circadian clock genes have been shown to regulate pathways involved in cellular proliferation, apoptosis, and DNA damage response, as aberrant rhythms in these genes are associated with various diseases. However, there is growing evidence that specific circadian genes differentially regulate functional pathways of immunocompetent cells. To extend our previous findings of the role of Period 2 in regulating splenocyte rhythms, we report that mice carrying a mutation in the Period 1 gene (Per1 -/ -mice), involved in the negative limb of the molecular clock, display significantly altered rhythms of cytokine (eg, interferon-g) and cytolytic factors (eg, perforin and granzyme B) in splenic natural killer (NK) cells. Altered rhythms of NK cell immune factors were accompanied by changes in circadian expression of circadian clock genes, Bmal1 and Per2. In addition, Per1-/ -circadian running-wheel activity rhythms remained rhythmic during constant darkness, although with a shortened free-running circadian period, suggesting primary involvement of peripheral molecular clocks. These findings indicate that the Per1 gene through NK cellular clocks modulates immune pathways.

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Introduction The QuitNic pilot trial aimed to test the feasibility of providing a nicotine vaping product (NVP) compared with combination nicotine replacement therapy (NRT) to smokers upon discharge from a smoke-free residential substance use disorder (SUD) treatment service. Methods QuitNic was a pragmatic two-arm randomised controlled trial. At discharge from residential withdrawal, 100 clients received telephone Quitline behavioural support and either 12-weeks supply of NRT, or an NVP. Treatment adherence and acceptability, self-reported abstinence, cigarettes smoked per day (CPD), frequency of cravings, and severity of withdrawal symptoms, were assessed at 6-weeks and 12-weeks. Results are reported for complete cases and for abstinence outcomes, Penalized Imputation results are reported where missing is assumed smoking. Results Retention was 63% at 6-weeks and 50% at 12-weeks. At 12-weeks, 68% of the NRT group reported using combination NRT while 96% of the NVP group used the device. Acceptability ratings for the products were high in both groups. At 12-weeks, 14% of the NVP group and 18% of the NRT group reported not smoking at all in the last 7 days. Mean CPD among continued smokers decreased significantly between baseline to 12-weeks in both groups; from 19.91 to 4.72 for the NVP group (p<0.001) and from 20.88 to 5.52 in the NRT group (p<0.001). Cravings and withdrawal symptoms significantly decreased for both groups. Conclusion Clients completing residential withdrawal readily engaged with smoking cessation post-treatment when given the opportunity. Further research is required to identify the most effective treatments post-withdrawal for this population at elevated risk of tobacco-related harm. IMPLICATIONS This pilot study showed that smoking cessation support involving options for nicotine replacement and Quitline-delivered cognitive behavioural counselling is attractive to people after they have been discharged from SUD treatment. Both nicotine vaping products and nicotine replacement therapies were highly acceptable and used by participants who reported reductions in cravings for cigarettes and perceptions of withdrawal symptoms and reductions in number of cigarettes smoked. Some participants self-reported abstinence from cigarettes - around one in five reported having quit smoking cigarettes at 12-weeks post-discharge. The results have significant public health implications for providing quit support following discharge from SUD treatment.