A qualitative study of using nicotine products for smoking cessation after discharge from residential drug and alcohol treatment in Australia.

INTRODUCTION: Tobacco smoking is highly prevalent among alcohol and other drugs (AOD) service clients and, despite interest in quitting, abstinence is rarely sustained. Nicotine products may assist after discharge from residential treatment services, but little is known about client receptivity to them. This study examined AOD withdrawal service clients' experiences of two types of nicotine products for smoking cessation post-discharge, combination nicotine replacement therapy (cNRT) and nicotine vaping products (NVP). METHODS: We held semi-structured telephone interviews with 31 Australian AOD service clients in a clinical trial of a 12-week smoking cessation intervention using Quitline support plus cNRT or NVP delivered post-discharge from a smoke-free residential service. We asked about health and social factors, nicotine cravings, Quitline experience, and barriers and facilitators to cNRT or NVP, then thematically analysed data. RESULTS: cNRT and NVP were described by participants as feasible and acceptable for smoking cessation. For most participants, cost limited cNRT access post study, as did difficulty navigating NVP prescription access. Quitline support was valued, but not consistently used, with participants noting low assistance with NVP-facilitated cessation. Participants considered both cessation methods acceptable and socially supported, and sought information on decreasing nicotine use via NVP. DISCUSSION AND CONCLUSIONS: AOD service clients highly valued receiving cNRT or NVP with behavioural support for smoking reduction or abstinence. Both interventions were acceptable to service clients. Findings suggest a potential need to examine both whether NVP use should be permitted in this context, and guidance on the individual suitability of cNRT or NVP.

MAPK phosphatase 1 inhibition of p38α within lung myofibroblasts is essential for spontaneous fibrosis resolution.

Fibrosis following tissue injury is distinguished from normal repair by the accumulation of pathogenic and apoptosis-resistant myofibroblasts (MFs), which arise primarily by differentiation from resident fibroblasts. Endogenous molecular brakes that promote MF dedifferentiation and clearance during spontaneous resolution of experimental lung fibrosis may provide insights that could inform and improve the treatment of progressive pulmonary fibrosis in patients. MAPK phosphatase 1 (MKP1) influences the cellular phenotype and fate through precise and timely regulation of MAPK activity within various cell types and tissues, yet its role in lung fibroblasts and pulmonary fibrosis has not been explored. Using gain- and loss-of-function studies, we found that MKP1 promoted lung MF dedifferentiation and restored the sensitivity of these cells to apoptosis - effects determined to be mainly dependent on MKP1's dephosphorylation of p38α MAPK (p38α). Fibroblast-specific deletion of MKP1 following peak bleomycin-induced lung fibrosis largely abrogated its subsequent spontaneous resolution. Such resolution was restored by treating these transgenic mice with the p38α inhibitor VX-702. We conclude that MKP1 is a critical antifibrotic brake whose inhibition of pathogenic p38α in lung fibroblasts is necessary for fibrosis resolution following lung injury.

The Lung Microbiome Predicts Mortality and Response to Azithromycin in Lung Transplant Patients with Chronic Rejection.

RATIONALE: Chronic lung allograft dysfunction (CLAD) is the leading cause of death following lung transplant, and azithromycin has variable efficacy in CLAD. The lung microbiome is a risk factor for developing CLAD, but the relationship between lung dysbiosis, pulmonary inflammation, and allograft dysfunction remains poorly understood. Whether lung microbiota predict outcomes or modify treatment response after CLAD is unknown. OBJECTIVES: To determine whether lung microbiota predict post-CLAD outcomes and clinical response to azithromycin. METHODS: Retrospective cohort study using acellular bronchoalveolar lavage (BAL) fluid prospectively collected from lung transplant recipients within 90 days of CLAD onset. Lung microbiota were characterized using 16S rRNA gene sequencing and ddPCR. In two additional cohorts, causal relationships of dysbiosis and inflammation were evaluated by comparing lung microbiota with CLAD-associated cytokines and measuring ex vivo P. aeruginosa growth in sterilized BAL fluid. MEASUREMENTS AND MAIN RESULTS: Patients with higher bacterial burden had shorter post-CLAD survival, independent of CLAD phenotype, azithromycin treatment, and relevant covariates. Azithromycin treatment improved survival in patients with high bacterial burden, but had negligible impact on patients with low or moderate burden. Lung bacterial burden was positively associated with CLAD-associated cytokines, and ex vivo growth of P. aeruginosa was augmented in BAL fluid from transplant recipients with CLAD. CONCLUSIONS: In lung transplant patients with chronic rejection, increased lung bacterial burden is an independent risk factor for mortality and predicts clinical response to azithromycin. Lung bacterial dysbiosis is associated with alveolar inflammation and may be promoted by underlying lung allograft dysfunction.

GTP Signaling Links Metabolism, DNA Repair, and Responses to Genotoxic Stress.

How cell metabolism regulates DNA repair is incompletely understood. Here, we define a GTP-mediated signaling cascade that links metabolism to DNA repair and has significant therapeutic implications. GTP, but not other nucleotides, regulates the activity of Rac1, a guanine nucleotide-binding protein, which promotes the dephosphorylation of serine 323 on Abl-interactor 1 (Abi-1) by protein phosphatase 5 (PP5). Dephosphorylated Abi-1, a protein previously not known to activate DNA repair, promotes nonhomologous end joining. In patients and mouse models of glioblastoma, Rac1 and dephosphorylated Abi-1 mediate DNA repair and resistance to standard-of-care genotoxic treatments. The GTP-Rac1-PP5-Abi-1 signaling axis is not limited to brain cancer, as GTP supplementation promotes DNA repair and Abi-1-S323 dephosphorylation in nonmalignant cells and protects mouse tissues from genotoxic insult. This unexpected ability of GTP to regulate DNA repair independently of deoxynucleotide pools has important implications for normal physiology and cancer treatment. SIGNIFICANCE: A newly described GTP-dependent signaling axis is an unexpected link between nucleotide metabolism and DNA repair. Disrupting this pathway can overcome cancer resistance to genotoxic therapy while augmenting it can mitigate genotoxic injury of normal tissues. This article is featured in Selected Articles from This Issue, p. 5.

Genetic deficiency of the transcription factor NFAT1 confers protection against fibrogenic responses independent of immune influx.

Idiopathic pulmonary fibrosis (IPF) is marked by unremitting matrix deposition and architectural distortion. Multiple profibrotic pathways contribute to the persistent activation of mesenchymal cells (MCs) in fibrosis, highlighting the need to identify and target common signaling pathways. The transcription factor nuclear factor of activated T cells 1 (NFAT1) lies downstream of second messenger calcium signaling and has been recently shown to regulate key profibrotic mediator autotaxin (ATX) in lung MCs. Herein, we investigate the role of NFAT1 in regulating fibroproliferative responses during the development of lung fibrosis. Nfat1-/--deficient mice subjected to bleomycin injury demonstrated improved survival and protection from lung fibrosis and collagen deposition as compared with bleomycin-injured wild-type (WT) mice. Chimera mice, generated by reconstituting bone marrow cells from WT or Nfat1-/- mice into irradiated WT mice (WT→WT and Nfat1-/-→WT), demonstrated no difference in bleomycin-induced fibrosis, suggesting immune influx-independent fibroprotection in Nfat1-/- mice. Examination of lung tissue and flow sorted lineageneg/platelet-derived growth factor receptor alpha (PDGFRα)pos MCs demonstrated decreased MC numbers, proliferation [↓ cyclin D1 and 5-ethynyl-2'-deoxyuridine (EdU) incorporation], myofibroblast differentiation [↓ α-smooth muscle actin (α-SMA)], and survival (↓ Birc5) in Nfat1-/- mice. Nfat1 deficiency abrogated ATX expression in response to bleomycin in vivo and MCs derived from Nfat1-/- mice demonstrated decreased ATX expression and migration in vitro. Human IPF MCs demonstrated constitutive NFAT1 activation, and regulation of ATX in these cells by NFAT1 was confirmed using pharmacological and genetic inhibition. Our findings identify NFAT1 as a critical mediator of profibrotic processes, contributing to dysregulated lung remodeling and suggest its targeting in MCs as a potential therapeutic strategy in IPF.NEW & NOTEWORTHY Idiopathic pulmonary fibrosis (IPF) is a fatal disease with hallmarks of fibroblastic foci and exuberant matrix deposition, unknown etiology, and ineffective therapies. Several profibrotic/proinflammatory pathways are implicated in accelerating tissue remodeling toward a honeycombed end-stage disease. NFAT1 is a transcriptional factor activated in IPF tissues. Nfat1-deficient mice subjected to chronic injury are protected against fibrosis independent of immune influxes, with suppression of profibrotic mesenchymal phenotypes including proliferation, differentiation, resistance to apoptosis, and autotaxin-related migration.

Effectiveness of nicotine salt vapes, cytisine, and a combination of these products, for smoking cessation in New Zealand: protocol for a three-arm, pragmatic, community-based randomised controlled trial.

BACKGROUND: Combining short-acting nicotine replacement therapy with varenicline increases smoking cessation rates compared with varenicline alone, but not all people tolerate these medications or find them helpful. We aim to investigate the therapeutic potential of an analogous combination, by evaluating the effectiveness, safety, and acceptability of combining nicotine salt e-cigarettes with cytisine, compared to nicotine salt e-cigarettes or cytisine only, on smoking abstinence at six months. METHODS: A pragmatic, community-based, investigator-blinded, randomised superiority trial design will be utilised. Eligible participants will be people who smoke daily (N = 800, 90% power) from throughout New Zealand, who are: aged ≥ 18 years, motivated to quit in the next two weeks, able to provide online consent, willing to use e-cigarettes and/or cytisine, and have daily access to a mobile phone. Recruitment will utilise multi-media advertising. Participants will be randomised (3:3:2 ratio) to 12 weeks of: 1) e-cigarettes (closed pod system, 3% nicotine salt, tobacco flavour) plus cytisine; 2) e-cigarettes alone, or 3) cytisine alone. All groups will receive a six-month, text-message-based behavioural support programme. The primary outcome is self-reported, biochemically verified, continuous abstinence at six months post-quit date. Secondary outcomes, measured at quit date, then one, three, six, and 12 months post-quit date, include self-reported continuous abstinence, 7-day point prevalence abstinence, cigarettes smoked per day, withdrawal and urge to smoke, time to (re)lapse, treatment use and compliance, treatment crossover, dual-use, use of other cessation products, change in e-cigarette products, continuation of product use, acceptability, change in health state, health-related quality of life, change in body mass index, adverse events, and cost per quitter. DISCUSSION: Pragmatic trials are of particular value as they reflect the 'real world' impact of interventions. The trial will provide some of the first evidence on the effectiveness of combining nicotine salt e-cigarettes with cytisine for smoking cessation, in a country with strong tobacco control policy. Findings will be incorporated into relevant systematic reviews, informing practice and policy. TRIAL REGISTRATION: NCT05311085 ClinicalTrials.gov. Registered 5th April, 2022.

Invitation methods for Indigenous New Zealand Maori in lung cancer screening: Protocol for a pragmatic cluster randomized controlled trial.

Lung cancer screening can significantly reduce mortality from lung cancer. Further evidence about how to optimize lung cancer screening for specific populations, including Aotearoa New Zealand (NZ)'s Indigenous Maori (who experience disproportionately higher rates of lung cancer), is needed to ensure it is equitable. This community-based, pragmatic cluster randomized trial aims to determine whether a lung cancer screening invitation from a patient's primary care physician, compared to from a centralized screening service, will optimize screening uptake for Maori. Participating primary care practices (clinics) in Auckland, Aotearoa NZ will be randomized to either the primary care-led or centralized service for delivery of the screening invitation. Clinic patients who meet the following criteria will be eligible: Maori; aged 55-74 years; enrolled in participating clinics in the region; ever-smokers; and have at least a 2% risk of developing lung cancer within six years (determined using the PLCOM2012 risk prediction model). Eligible patients who respond positively to the invitation will undertake shared decision-making with a nurse about undergoing a low dose CT scan (LDCT) and an assessment for Chronic Obstructive Pulmonary Disease (COPD). The primary outcomes are: 1) the proportion of eligible population who complete a risk assessment and 2) the proportion of people eligible for a CT scan who complete the CT scan. Secondary outcomes include evaluating the contextual factors needed to inform the screening process, such as including assessment for Chronic Obstructive Pulmonary Disease (COPD). We will also use the RE-AIM framework to evaluate specific implementation factors. This study is a world-first, Indigenous-led lung cancer screening trial for Maori participants. The study will provide policy-relevant information on a key policy parameter, invitation method. In addition, the trial includes a nested analysis of COPD in the screened Indigenous population, and it provides baseline (T0 screen round) data using RE-AIM implementation outcomes.

GTP signaling links metabolism, DNA repair, and responses to genotoxic stress.

How cell metabolism regulates DNA repair is incompletely understood. Here, we define a GTP-mediated signaling cascade that links metabolism to DNA repair and has significant therapeutic implications. GTP, but not other nucleotides, regulates the activity of Rac1, a G protein, that promotes the dephosphorylation of serine 323 on Abl-interactor 1 (Abi-1) by protein phosphatase 5 (PP5). Dephosphorylated Abi-1, a protein previously not known to activate DNA repair, promotes non-homologous end joining. In patients and mouse models of glioblastoma, Rac1 and dephosphorylated Abi-1 mediate DNA repair and resistance to standard of care genotoxic treatments. The GTP-Rac1-PP5-Abi-1 signaling axis is not limited to brain cancer, as GTP supplementation promotes DNA repair and Abi-1-S323 dephosphorylation in non-malignant cells and protects mouse tissues from genotoxic insult. This unexpected ability of GTP to regulate DNA repair independently of deoxynucleotide pools has important implications for normal physiology and cancer treatment.

The mitigating effect of exogenous carbon monoxide on chronic allograft rejection and fibrosis post-lung transplantation.

BACKGROUND: Small airway inflammation and fibrosis or bronchiolitis obliterans (BO) is the predominant presentation of chronic lung allograft dysfunction (CLAD) post-lung transplantation. Carbon monoxide (CO) is a critical endogenous signaling transducer with known anti-inflammatory and anti-fibrotic effects but its therapeutic potential in CLAD remains to be fully elucidated. METHODS: Here we investigate the effect of inhaled CO in modulating chronic lung allograft rejection pathology in a murine orthotopic lung transplant model of BO (B6D2F1/J→DBA/2J). Additionally, the effects of CO on the activated phenotype of mesenchymal cells isolated from human lung transplant recipients with CLAD were studied. RESULTS: Murine lung allografts treated with CO (250 ppm × 30 minutes twice daily from days 7 to 40 post-transplantation) demonstrated decreased immune cell infiltration, fibrosis, and airway obliteration by flow cytometry, trichrome staining, and morphometric analysis, respectively. Decreased total collagen, with levels comparable to isografts, was noted in CO-treated allografts by quantitative hydroxyproline assay. In vitro, CO (250 ppm × 16h) was effective in reversing the fibrotic phenotype of human CLAD mesenchymal cells with decreased collagen I and ß-catenin expression as well as an inhibitory effect on ERK1/2 MAPK, and mTORC1/2 signaling. Sildenafil, a phosphodiesterase 5 inhibitor, partially mimicked the effects of CO on CLAD mesenchymal cells and was partially effective in decreasing collagen deposition in murine allografts, suggesting the contribution of cGMP-dependent and -independent mechanisms in mediating the effect of CO. CONCLUSION: These results suggest a potential role for CO in alleviating allograft fibrosis and mitigating chronic rejection pathology post-lung transplant.

'It's somewhere here, isn't it'? The provision of information and health warnings for alcoholic beverages sold online in New Zealand and the United Kingdom.

INTRODUCTION: Alcohol beverages in many countries are required to display health information and warnings on all product packaging, given the individual and societal harm caused by alcohol. It is unclear whether consumers purchasing alcohol online are able to easily view such information. This study examines the presence, type and location of mandatory and voluntary health information and warnings consumers are exposed to when entering online alcohol retail shopping environments in the United Kingdom (UK) and New Zealand (NZ). METHODS: Using an observational study design, 1407 randomly sampled alcoholic beverages from 14 online alcohol retailers (7 per country) were reviewed to ascertain the visual presence or absence of mandatory and voluntary health information and warnings. RESULTS: UK online alcohol retailers were more compliant than NZ retailers in showing mandatory health information (e.g., alcohol by volume percentage was visible on 92% of alcoholic beverages sold online in the UK, compared to 31% in NZ, p < 0.001). A similar pattern was noted for voluntary health warnings. Online retailers in both countries had a low proportion of alcohol products with the viewable mandatory information, and voluntary health warnings were rarely present and/or viewable. DISCUSSION AND CONCLUSIONS: Mandatory health information and warnings for alcoholic beverages are not fully adhered to within the UK and NZ online retail environments, impacting the ability of consumers to make informed purchase decisions. In both countries, alcohol policy needs to stipulate that mandatory health information and warnings should be clearly viewable on the product page and product imagery of online alcohol retailers.

Vitamin D supplementation in children and young adults with persistent proteinuria secondary to glomerular disease.

BACKGROUND: Vitamin D deficiency is common in glomerular disease. Supplementation may be ineffective due to ongoing urinary losses of vitamin D binding protein. We sought to determine if daily cholecalciferol supplementation would increase vitamin D concentrations in children with glomerular disease and persistent proteinuria, without adverse effects. METHODS: Eighteen participants at least 5 years of age with primary glomerular disease and urine protein:creatinine ratio ≥ 0.5 were enrolled from four pediatric nephrology practices to receive cholecalciferol supplementation: 4,000 IU or 2,000 IU per day for serum 25 hydroxyvitamin vitamin D (25OHD) concentrations < 20 ng/mL and 20 ng/mL to < 30 ng/mL, respectively. Measures of vitamin D and mineral metabolism were obtained at baseline and weeks 6 and 12. Multivariable generalized estimating equation (GEE) regression estimated mean percent changes in serum 25OHD concentration. RESULTS: Median baseline 25OHD was 12.8 ng/mL (IQR 9.3, 18.9) and increased to 27.8 ng/mL (20.5, 36.0) at week 6 (p < 0.001) without further significant increase at week 12. A total of 31% of participants had a level ≥ 30 ng/mL at week 12. Supplementation was stopped in two participants at week 6 for mildly elevated calcium and phosphorus, respectively, with subsequent declines in 25OHD of > 20 ng/mL. In the adjusted GEE model, 25OHD was 102% (95% CI: 64, 141) and 96% (95% CI: 51, 140) higher versus baseline at weeks 6 and 12, respectively (p < 0.001). CONCLUSION: Cholecalciferol supplementation in vitamin D deficient children with glomerular disease and persistent proteinuria safely increases 25OHD concentration. Ideal dosing to fully replete 25OHD concentrations in this population remains unknown. CLINICAL TRIAL: NCT01835639. A higher resolution version of the Graphical abstract is available as Supplementary information.

Incentivised physical activity intervention promoting daily steps among university employees in the workplace through a team-based competition.

Introduction: The benefits of walking on health and well-being is well established and regarded as the most accessible form of physical activity (PA) that most individuals can incorporate into their lives. Despite the benefits, the impact of a competitive walking intervention combined with a prize incentive in the workplace is yet to be established. The aim of this intervention was to promote PA among university employees through teams-based competition with a prize incentive targeted towards the recommended 10,000 steps per day. Methods: A total of 49 employees participated and formed eight departmental teams ranging from Senior Admin management, Educational & Social work, Nursing & Midwifery, Sport & Exercise, Health Sciences, Admin Assistant, Library, and IT to compete in a walking intervention. Each team was handed an ActiGraph wGT3X-BT from Monday to Friday to record their walking steps. Steps. Post intervention participants completed an open-ended survey to provide their views about the intervention. Results: The ActiGraph findings determined that steps increased by 4,799 per day from daily baseline of 5,959 to 10,758 throughout this intervention. The themes from qualitative data showed that the prize incentive and competitive nature of this intervention has motivated staff to walk more, changed their behaviour, enjoyed the team-based competition, and improved perceived productivity in the workplace. Discussion and conclusion: This intervention increased employees' daily steps by 4,799 and met the 10,000 steps guideline. The 'Health Sciences' team recorded the highest steps 531,342 followed by the 'Education and Social Work' accumulating 498,045 steps throughout this intervention. This intervention with prize incentive demonstrated a positive impact on employees personal and work-based outcomes as well as contributed to the workplace PA, health, and wellbeing literature, and more specifically, to the scarce research focused on university settings.

Examination of national survey data regarding academic foundation training during the COVID-19 pandemic second wave.

Aim: We aimed to examine the effect of the second wave of the COVID-19 pandemic on Academic Foundation Programme (AFP) trainees. Methods: A voluntary, anonymous questionnaire was circulated to all UK AFP doctors. Data were collected from February 2021 to April 2021 then analysed. Results: Of a possible 1,096 trainees, 149 responded to the survey: 48% of respondents were at least partially redeployed, 31% lost academic time and 47% had projects cancelled or postponed. In free-text responses, despite some research opportunities, frustration at lost research time and opportunities were common themes. Trainees also highlighted communication and wellbeing issues. Conclusion: These results demonstrate that the overall effect of COVID-19 on this cohort cannot be underestimated. We propose that a series of measures are implemented to protect and support academic trainees. We hope that these measures would encourage high-quality academic output and help secure the development of the academic clinical workforce.

Trial registration and time to publication in a retrospective cohort of publicly funded randomised controlled trials in New Zealand 1999-2017.

OBJECTIVES: To determine how quickly randomised controlled trials funded by the Health Research Council of New Zealand (HRC) were registered and published, and whether time to publication differed by trial result. DESIGN: We created a retrospective cohort of trials offered funding from 1999 to 2017 by seeking lists of candidate studies using the Official Information Act 1982. These lists were supplemented by searching the HRC's online research repository and an open-access database on Figshare. One investigator searched for trial registrations and for dissemination using electronic databases, university websites and ResearchGate. One investigator extracted data from the obtained studies and a second investigator independently corroborated the data entry from a 10% random sample. RESULTS: We identified 258 trials that were offered funding, 252 trials were conducted and 229 (90.9%) were registered, 179 prospectively by the date of the final search (24 March 2022). Overall, 236 trials were completed by the date of the last search and in 209 (88.6%) trials the results had been disseminated, 200 (84.7%) of which were by journal publication. We obtained the results for 214 trials, 91 (42.5%) of which were positive, 120 (56.1%) of which were null and 3 (1.4%) of which were negative. Median time to publication was 22.7 months for positive trials and 21.5 months for combined null or negative trials (log rank test p=0.83). Median time since trial completion in the trials that had not been published was 43.6 months (IQR 17.1-108.2 months). CONCLUSIONS: Between 1999 and 2017, almost 9 out of every 10 HRC-funded trials had been registered and a similar proportion of completed trials had been published with no difference in time to publication based on type of result. However, only a slim majority of trials had published within the 2-year time frame set by the WHO.

Workplace Physical Activity Barriers and Facilitators: A Qualitative Study Based on Employees Physical Activity Levels.

INTRODUCTION: Lack of time, management support, insufficient facilitates, workload balance, and culture are often reported as common barriers to physical activity (PA) participation in the workplace. In comparison, identifying facilitators of PA in the workplace are scarce. A 'one-size-fits-all' approach to overcoming the barriers may also be unsuccessful within university settings where multidisciplinary workforce exists due to the heterogeneity nature of job roles. Thus, the aim of this study was to understand the perceived barriers and facilitators of PA of university employees who were classified as active or inactive based on their job roles. METHODS: Forty-one employees (female = 17; male = 24) participated in focus groups to discuss their perceived barriers and facilitators to PA in the workplace. Participants were categorised based on their PA levels as active and inactive prior analysing the semi-structured focus groups data via using thematic analysis. RESULTS AND DISCUSSION: The results showed that a lack of time was reported by 80% of the participants as a barrier to PA, including 63% inactive and 17% of the active participants. This included 27% administrators' staff, 23% academics, 19% senior management, and 11% professional service staff. Over 75% participants reported a lack of management support as one of the perceived barriers to their PA engagement in the workplace. Approximately 58% also reported workplace culture as a barrier to PA participation. Open access to a gym on campus was perceived to be the main facilitator to engaging in PA in the future. Similarly, increased management support for engaging in PA and having flexibility during working days were perceived as facilitators for PA engagement and a way to reduced sedentary behaviour in the workplace. CONCLUSIONS: These findings contribute to the limited literature in terms of evaluating obstacles and facilitators of university employees to encourage engagement with PA in the workplace. These findings can be applied to form PA, health, and wellbeing-related interventions specifically targeting these identified barriers that are experienced in the workplace and thereby potentially reducing absenteeism and increasing productivity.

Revised Guidelines for smoking cessation in New Zealand, 2021.

AIMS: To summarise the literature underpinning key recommendations made in the 2021 revision of the Ministry of Health's New Zealand Guidelines for Helping People to Stop Smoking. METHODS: A comprehensive literature review of smoking cessation interventions was undertaken in July 2021. Recommendations were formulated from the findings of the literature review and expert advice. RESULTS: Healthcare professionals should ask and briefly advise all people who smoke to stop smoking, regardless of whether they say they are ready to stop smoking or not. They should offer smoking cessation support, which includes both behavioural and pharmacological (e.g., nicotine replacement therapy, nortriptyline, bupropion or varenicline) interventions. The Guidelines also include advice around the use of vaping in smoking cessation. Recommendations are also formulated for priority populations of smokers: Maori, Pacific, pregnant women, and people with mental illness and other addictions. CONCLUSIONS: The guidelines will assist healthcare professionals in providing evidence-based smoking cessation support to people who smoke. To be effective and equitable, the ABC model requires organisational commitment, integration into routine practice, and increased attention to the upstream determinants of smoking and quitting.

Effectiveness of a preschool asthma education programme, compared to usual care, on the frequency of acute asthma events: a community-based cluster randomised trial.

AIM: To determine whether an asthma intervention delivered within preschools can improve asthma outcomes in children aged 2-5 years with asthma or a high probability of asthma. METHODS: Between 2011 and 2013, we undertook a pragmatic, single-blind, cluster randomised trial in Auckland, New Zealand. We randomly assigned (1:1 ratio) preschools, and their children aged 2-5 years with asthma or a high probability of asthma, to receive an asthma intervention (a 12-month respiratory nurse-led asthma assessment using an evidence-based, web-based tool and a class-based asthma education programme for four months), or a control intervention (a class-based science education programme for four months). Both groups received standard asthma management by their primary care physician. The primary outcome was the proportion of children that had at least one unscheduled ("urgent") medical or ED attendance for asthma over 12 months. RESULTS: We randomised 171 preschools, 85 to the intervention (341 children) and 86 to the control (334 children). We found no difference in the primary outcome (intervention: 216/341, 63% vs control: 181/334, 54%: adjusted Odds Ratio=1.36, 95% Confidence Interval=0.95-1.94, p=0.095). However, compared with the control group, the intervention group had improved and sustained asthma control and fewer asthma symptoms over 12 months. CONCLUSIONS: Combining asthma education with a nurse-led, evidence-based asthma assessment and education intervention led to sustained improvements in asthma control in this preschool population, but its effect on acute events remains unclear.

Closing the gaps in tobacco endgame evidence: a scoping review.

OBJECTIVE: Tobacco endgame policies aim to rapidly and permanently reduce smoking to minimal levels. We reviewed evidence syntheses for: (1) endgame policies, (2) evidence gaps, and (3) future research priorities. DATA SOURCES: Guided by JBI scoping review methodology, we searched five databases (PubMed, CINAHL, Scopus, Embase and Web of Science) for evidence syntheses published in English since 1990 on 12 policies, and Google for publications from key national and international organisations. Reference lists of included publications were hand searched. STUDY SELECTION: Two reviewers independently screened titles and abstracts. Inclusion criteria were broad to capture policy impacts (including unintended), feasibility, public and stakeholder acceptability and other aspects of policy implementation. DATA EXTRACTION: We report the results according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses extension for Scoping Reviews checklist. DATA SYNTHESIS: Eight policies have progressed to evidence synthesis stage (49 publications): mandatory very low nicotine content (VLNC) standard (n=26); product standards to substantially reduce consumer appeal or remove the most toxic products from the market (n=1); moving consumers to reduced risk products (n=8); tobacco-free generation (n=4); ending sales (n=2); sinking lid (n=2); tax increases (n=7); and restrictions on tobacco retailers (n=10). Based on published evidence syntheses, the evidence base was most developed for a VLNC standard, with a wide range of evidence synthesised. CONCLUSIONS: VLNC cigarettes have attracted the most attention, in terms of synthesised evidence. Additional focus on policies that reduce the availability of tobacco is warranted given these measures are being implemented in some jurisdictions.