RESUMO
INTRODUCTION: There are increased opportunities for public health practitioners (PHPs) in England to shape alcohol availability and reduce harms through a statutory role in licensing processes in local government. However, how public health can effectively influence alcohol licence decision-making is little understood. METHODS: A mixed methods study was conducted to identify challenges faced by PHPs and mechanisms to strengthen their role. This involved a survey of practitioners across London local authorities (n = 18) and four focus group discussions with a range of licensing stakeholders (n = 36). RESULTS: Survey results indicated a varied picture of workload, capacity to respond to licence applications and levels of influence over decision-making among PHPs in London. Practitioners described a felt lack of status within the licence process, and difficulties using and communicating public health evidence effectively, without a health licensing objective. Strategies considered supportive included engaging with other responsible authorities and developing understanding and relationships over time. CONCLUSIONS: Against political and resource constraints at local and national government levels, pragmatic approaches for strengthening public health influence over alcohol licensing are required, including promoting relationships between stakeholders and offering opportunities for PHPs to share best practice about making effective contributions to licensing.
Assuntos
Bebidas Alcoólicas/legislação & jurisprudência , Licenciamento/legislação & jurisprudência , Prática de Saúde Pública , Política Pública , Tomada de Decisões , Inglaterra , Grupos Focais , Humanos , Londres , Saúde PúblicaRESUMO
BACKGROUND: Public health in England has opportunities to reduce alcohol-related harms via shaping the availability and accessibility of alcohol through the licensing function in local government. While the constraints of licensing legislation have been recognised, what is currently little understood are the day-to-day realities of how public health practitioners enact the licensing role, and how they can influence the local alcohol environment. METHODS: To address this, a mixed-methods study was conducted across 24 local authorities in Greater London between 2016 and 17. Data collection involved ethnographic observation of public health practitioners' alcohol licensing work (in eight local authorities); a survey of public health practitioners (n = 18); interviews with licensing stakeholders (n = 10); and analysis of public health licensing data from five local authorities. Fieldnotes and interview transcripts were analysed thematically, and quantitative data were analysed using descriptive statistics. RESULTS: Results indicated that some public health teams struggle to justify the resources required to engage with licensing processes when they perceive little capacity to influence licensing decisions. Other public health teams consider the licensing role as important for shaping the local alcohol environment, and also as a strategic approach for positioning public health within the council. Practitioners use different processes to assess the potential risks of licence applications but also the potential strengths of their objections, to determine when and how actions should be taken. Identifying the direct influence of public health on individual licences is challenging, but the study revealed how practitioners did achieve some level of impact, for example through negotiation with applicants. CONCLUSIONS: This study shows public health impact following alcohol licensing work is difficult to measure in terms of reducing alcohol-related harms, which poses challenges for justifying this work amid resource constraints. However, there is potential added value of the licensing role in strategic positioning of public health in local government to influence broader determinants of health.
Assuntos
Consumo de Bebidas Alcoólicas/legislação & jurisprudência , Bebidas Alcoólicas/provisão & distribuição , Licenciamento , Governo Local , Saúde Pública/legislação & jurisprudência , Redução do Dano , Humanos , Londres , Pesquisa Qualitativa , Inquéritos e QuestionáriosRESUMO
Tumour necrosis factor-alpha (TNF-alpha) signals though two receptors, TNFR1 and TNFR2. TNFR1 has a role in cytotoxicity, whereas TNFR2 regulates death responses or proliferation. TNF activates pro-inflammatory transcription factor nuclear factor-kappaB (NF-kappaB) by uncertain signalling mechanisms. Here we report the contribution of each TNFR towards the NF-kappaB activation processes. In human cells expressing endogenous or exogenous TNFR2, in addition to TNFR1, we found both TNFRs capable of activating NF-kappaB, as measured by IkappaBalpha (inhibitor of NF-kappaB) degradation, electrophoretic mobility shift assay and NF-kappaB gene reporter assays. TNFR2 activation did not degrade IkappaBbeta. However, TNF-effects on NF-kappaB activation occurred predominantly through TNFR1, with TNFR2 activating the transcription factor poorly.
Assuntos
Antígenos CD/metabolismo , Proteínas I-kappa B , NF-kappa B/metabolismo , Receptores do Fator de Necrose Tumoral/metabolismo , Transcrição Gênica/fisiologia , Antígenos CD/genética , Antígenos CD/farmacologia , Linhagem Celular , Proteínas de Ligação a DNA/metabolismo , Ensaio de Desvio de Mobilidade Eletroforética , Genes Reporter , Células HeLa , Humanos , Soros Imunes/farmacologia , Proteínas Quinases JNK Ativadas por Mitógeno , Rim/citologia , Rim/metabolismo , Proteínas Quinases Ativadas por Mitógeno/metabolismo , Inibidor de NF-kappaB alfa , NF-kappa B/antagonistas & inibidores , NF-kappa B/genética , Receptores do Fator de Necrose Tumoral/genética , Receptores Tipo I de Fatores de Necrose Tumoral , Receptores Tipo II do Fator de Necrose Tumoral , Proteínas Recombinantes de Fusão/genética , Proteínas Recombinantes de Fusão/metabolismo , Transdução de Sinais/fisiologia , Transcrição Gênica/efeitos dos fármacos , TransfecçãoRESUMO
Nicotine replacement therapies (NRT) have limited success in smoking cessation. The efficacy of nicotine may be compromised by its main metabolite, cotinine. An anti-cotinine vaccine to remove this antagonism could enhance the efficacy of NRT. We show that cotinine is a weak nicotinic agonist and decreases responses to nicotine, consistent with antagonism through receptor desensitisation. trans-4-Thiol cotinine was coupled to tetanus toxoid, and rats immunised repeatedly. Vaccination raised antibodies specific for cotinine that do not recognise other metabolites or nicotine. Increased serum cotinine concentrations following nicotine administration indicate sequestration of cotinine by antibodies, encouraging further evaluation of this vaccine in behavioural models of nicotine addiction and relapse.