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ABSTRACT Introduction Unhealthy lifestyle factors, such as smoking, high alcohol intake, poor diet and physical inactivity, are key risk factors for premature mortality. How unhealthy lifestyle factors are viewed in the wider context of socioeconomic deprivation is rarely considered. Understanding key stakeholder views on lifestyle factors in the context of deprivation is critical to intervention development and reducing harm in more deprived populations. The aim of this study was to explore public, healthcare professional and policymaker views around unhealthy lifestyle factors in the context of deprivation. The aim was broad to facilitate iterative development of ideas, as the views of this wide range of stakeholders are rarely captured. Methods Twenty‐five adult members of the public in Scotland took part in four focus groups between August 2022 and June 2023. Eighteen semi‐structured interviews were conducted with professionals: 12 primary‐care practitioners and 6 public‐health practitioners and policymakers. Reflexive thematic analysis was undertaken. Results Four main themes were developed: (1) Evolving complexity of lifestyle factors – the number of lifestyle factors that adversely impact health has grown, with increasingly complex interactions, (2) Social determinants of lifestyle – numerous links were made between socioeconomic conditions and unhealthy lifestyle factors by all participants, (3) Poverty as a fundamental social determinant – poverty was identified as a core factor for unhealthy lifestyle factors, and (4) Agency versus structure in relation to lifestyle – individual agency to address lifestyle factors was limited by structural constraints. Among professionals, understanding the challenging social determinants of unhealthy lifestyle factors was countered by a desire to support healthy change in those affected by deprivation. Conclusion Public and professional views around lifestyle highlight an evolving understanding of the new and growing number of lifestyle factors as well as the increasingly complex interplay between lifestyle factors. Views of the social determinants of lifestyle and structural limits to agency strengthen arguments for reduced emphasis on individual‐level responsibility for unhealthy lifestyle factors and for deeper integration of social determinants into lifestyle interventions. In addition to addressing poverty and socioeconomic inequalities directly, innovative policy, planning and legislation that incorporate wider approaches could tackle upstream determinants of numerous unhealthy lifestyle factors simultaneously. Patient or Public Contribution Members of the public who participated in this study have made contributions by sharing their views and perspectives. The National Health Service Research Scotland Primary Care Patient and Public Involvement (NRS PPI) Group contributed to the development of this work. The NRS PPI Group was consulted as part of the preparatory work for H. M. E. F.'s doctoral thesis funding application. The findings of the qualitative work were presented to them, and they informed the interpretation of those findings and related work presented at conferences and public engagement events.

Abstract Background Components of social connection are associated with mortality, but research examining their independent and combined effects in the same dataset is lacking. This study aimed to examine the independent and combined associations between functional and structural components of social connection and mortality. Methods Analysis of 458,146 participants with full data from the UK Biobank cohort linked to mortality registers. Social connection was assessed using two functional (frequency of ability to confide in someone close and often feeling lonely) and three structural (frequency of friends/family visits, weekly group activities, and living alone) component measures. Cox proportional hazard models were used to examine the associations with all-cause and cardiovascular disease (CVD) mortality. Results Over a median of 12.6 years (IQR 11.9–13.3) follow-up, 33,135 (7.2%) participants died, including 5112 (1.1%) CVD deaths. All social connection measures were independently associated with both outcomes. Friends/family visit frequencies

Abstract Background Long-chain acyl-carnitines (ACs) are potential arrhythmogenic metabolites. Their role in atrial fibrillation (AF) remains incompletely understood. Using a systems medicine approach, we assessed the contribution of C18:1AC to AF by analysing its in vitro effects on cardiac electrophysiology and metabolism, and translated our findings into the human setting. Methods and results Human iPSC-derived engineered heart tissue was exposed to C18:1AC. A biphasic effect on contractile force was observed: short exposure enhanced contractile force, but elicited spontaneous contractions and impaired Ca2+ handling. Continuous exposure provoked an impairment of contractile force. In human atrial mitochondria from AF individuals, C18:1AC inhibited respiration. In a population-based cohort as well as a cohort of patients, high C18:1AC serum concentrations were associated with the incidence and prevalence of AF. Conclusion Our data provide evidence for an arrhythmogenic potential of the metabolite C18:1AC. The metabolite interferes with mitochondrial metabolism, thereby contributing to contractile dysfunction and shows predictive potential as novel circulating biomarker for risk of AF.

Predictors of overall epicardial adipose tissue deposition have been found to vary between males and females. Whether similar sex differences exist in epicardial fat cell morphology is currently unknown. This study aimed to determine whether epicardial fat cell size is associated with different clinical measurements in males and females. Fat cell sizes were measured from epicardial, paracardial, and appendix adipose tissues of post-mortem cases (N= 118 total, 37 females). Epicardial, extra-pericardial, and visceral fat volumes were measured by computed tomography from a subset of cases (N= 70, 22 females). Correlation analyses and stepwise linear regression were performed to identify predictors of fat cell size in males and females. Median fat cell sizes in all depots did not differ between males and females. Body mass index (BMI) and age were independently predictive of epicardial, paracardial, and appendix fat cell sizes in males, but not in females. Epicardial and appendix fat cell sizes were associated with epicardial and visceral fat volumes, respectively, in males only. In females, paracardial fat cell size was associated with extra-pericardial fat volume, while appendix fat cell size was associated with BMI only. No predictors were associated with epicardial fat cell size in females at the univariable or multivariable levels. To conclude, no clinical measurements were useful surrogates of epicardial fat cell size in females, while BMI, age, and epicardial fat volume were independent, albeit weak, predictors in males only.

Abstract Background Infection with SARS-CoV-2 virus (COVID-19) impacts disadvantaged groups most. Lifestyle factors are also associated with adverse COVID-19 outcomes. To inform COVID-19 policy and interventions, we explored effect modification of socioeconomic-status (SES) on associations between lifestyle and COVID-19 outcomes. Methods Using data from UK-Biobank, a large prospective cohort of 502,536 participants aged 37–73 years recruited between 2006 and 2010, we assigned participants a lifestyle score comprising nine factors. Poisson regression models with penalised splines were used to analyse associations between lifestyle score, deprivation (Townsend), and COVID-19 mortality and severe COVID-19. Associations between each exposure and outcome were examined independently before participants were dichotomised by deprivation to examine exposures jointly. Models were adjusted for sociodemographic/health factors. Results Of 343,850 participants (mean age > 60 years) with complete data, 707 (0.21%) died from COVID-19 and 2506 (0.76%) had severe COVID-19. There was evidence of a nonlinear association between lifestyle score and COVID-19 mortality but limited evidence for nonlinearity between lifestyle score and severe COVID-19 and between deprivation and COVID-19 outcomes. Compared with low deprivation, participants in the high deprivation group had higher risk of COVID-19 outcomes across the lifestyle score. There was evidence for an additive interaction between lifestyle score and deprivation. Compared with participants with the healthiest lifestyle score in the low deprivation group, COVID-19 mortality risk ratios (95% CIs) for those with less healthy scores in low versus high deprivation groups were 5.09 (1.39–25.20) and 9.60 (4.70–21.44), respectively. Equivalent figures for severe COVID-19 were 5.17 (2.46–12.01) and 6.02 (4.72–7.71). Alternative SES measures produced similar results. Conclusions Unhealthy lifestyles are associated with higher risk of adverse COVID-19, but risks are highest in the most disadvantaged, suggesting an additive influence between SES and lifestyle. COVID-19 policy and interventions should consider both lifestyle and SES. The greatest public health benefit from lifestyle focussed COVID-19 policy and interventions is likely to be seen when greatest support for healthy living is provided to the most disadvantaged groups.

Background: The cGMP-dependent protein kinase G (PKG) phosphorylates the cardiac ryanodine receptor (RyR2) in vitro. We aimed to determine whether modulation of endogenous PKG alters RyR2-mediated spontaneous Ca2+ release and whether this effect is linked to a change in RyR2 phosphorylation. Methods: & Results: Human embryonic kidney (HEK293) cells with inducible RyR2 expression were treated with the cGMP analogue 8-Br-cGMP (100 μM) to activate endogenous PKG. In cells transfected with luminal Ca2+ sensor, D1ER, PKG activation significantly reduced the threshold for RyR2-mediated spontaneous Ca2+ release (93.9 ± 0.4% of store size with vehicle vs. 91.7 ± 0.8% with 8-Br-cGMP, P = 0.04). Mutation of the proposed PKG phosphorylation sites, S2808 and S2030, either individually or as a combination, prevented the decrease in Ca2+ release threshold induced by endogenous PKG activation. Interestingly, despite a functional dependence on expression of RyR2 phosphorylation sites, 8-Br-cGMP activation of PKG did not promote a detectable change in S2808 phosphorylation (P = 0.9). Paradoxically, pharmacological inhibition of PKG with KT 5823 (1 μM) also reduced the threshold for spontaneous Ca2+ release through RyR2 without affecting S2808 phosphorylation. Silencing RNA knockdown of endogenous PKG expression also had no quantifiable effect on RyR2 S2808 phosphorylation (P = 0.9). However, unlike PKG inhibition with KT 5823, PKG knockdown did not alter spontaneous Ca2+ release propensity or luminal Ca2+ handling. Conclusion: In an intact cell model, activation of endogenous PKG reduces the threshold for RyR2-mediated spontaneous Ca2+ release in a manner dependent on the RyR2 phosphorylation sites S2808 and S2030. This study clarifies the regulation of RyR2 Ca2+ release by endogenous PKG and functionally implicates the role of RyR2 phosphorylation.

Macroscopic deposition of epicardial adipose tissue (EAT) has been strongly associated with numerous indices of obesity and cardiovascular disease risk. In contrast, the morphology of EAT adipocytes has rarely been investigated. We aimed to determine whether obesity-driven adipocyte hypertrophy, which is characteristic of other visceral fat depots, is found within EAT adipocytes. EAT samples were collected from cardiac surgery patients (n = 49), stained with haematoxylin & eosin, and analysed for mean adipocyte size and non-adipocyte area. EAT thickness was measured using echocardiography. A significant positive relationship was found between EAT thickness and body mass index (BMI). When stratified into standardized BMI categories, EAT thickness was 58.7% greater (p = 0.003) in patients from the obese (7.3 ± 1.8 mm) compared to normal (4.6 ± 0.9 mm) category. BMI as a continuous variable significantly correlated with EAT thickness (r = 0.56, p < 0.0001). Conversely, no correlation was observed between adipocyte size and either BMI or EAT thickness. No difference in the non-adipocyte area was found between BMI groups. Our results suggest that the increased macroscopic EAT deposition associated with obesity is not caused by adipocyte hypertrophy. Rather, alternative remodelling via adipocyte proliferation might be responsible for the observed EAT expansion.

The release of Ca2+ by ryanodine receptor (RyR2) channels is critical for cardiac function. However, abnormal RyR2 activity has been linked to the development of arrhythmias, including increased spontaneous Ca2+ release in human atrial fibrillation (AF). Clustering properties of RyR2 have been suggested to alter the activity of the channel, with remodeling of RyR2 clusters identified in pre-clinical models of AF and heart failure. Whether such remodeling occurs in human cardiac disease remains unclear. This study aimed to investigate the nanoscale organization of RyR2 clusters in AF patients – the first known study to examine this potential remodeling in diseased human cardiomyocytes. Right atrial appendage from cardiac surgery patients with paroxysmal or persistent AF, or without AF (non-AF) were examined using super-resolution (dSTORM) imaging. Significant atrial dilation and cardiomyocyte hypertrophy was observed in persistent AF patients compared to non-AF, with these two parameters significantly correlated. Interestingly, the clustering properties of RyR2 were remarkably unaltered in the AF patients. No significant differences were identified in cluster size (mean ∼18 RyR2 channels), density or channel packing within clusters between patient groups. The spatial organization of clusters throughout the cardiomyocyte was also unchanged across the groups. RyR2 clustering properties did not significantly correlate with patient characteristics. In this first study to examine nanoscale RyR2 organization in human cardiac disease, these findings indicate that RyR2 cluster remodeling is not an underlying mechanism contributing to altered channel function and subsequent arrhythmogenesis in human AF.

[This corrects the article DOI: 10.1371/journal.pone.0238091.].

A growing number of metabolomic studies have associated high circulating levels of the amphiphilic fatty acid metabolites, long-chain acylcarnitines (LCACs), with cardiovascular disease (CVD) risk. These studies show that plasma LCAC levels can be correlated with the stage and severity of CVD and with indices of cardiac hypertrophy and ventricular function. Complementing these recent clinical associations is an extensive body of basic research that stems mostly from the twentieth century. These works, performed in cardiomyocyte and multicellular preparations from animal and cell models, highlight stereotypical derangements in cardiac electrophysiology induced by exogenous LCAC treatment that promote arrhythmic muscle behavior. In many cases, this is coupled with acute inotropic modulation; however, whether LCACs increase or decrease contractility is inconclusive. Linked to the electromechanical alterations induced by LCAC exposure is an array of effects on cardiac excitation-contraction coupling mechanisms that overload the cardiomyocyte cytosol with Na+ and Ca2+ ions. The aim of this review is to revisit this age-old literature and collate it with recent findings to provide a pathophysiological context for the growing body of metabolomic association studies that link circulating LCACs with CVD.

BackgroundIt is now well recognised that the risk of severe COVID-19 increases with some long-term conditions (LTCs). However, prior research primarily focuses on individual LTCs and there is a lack of data on the influence of multimorbidity (≥2 LTCs) on the risk of COVID-19. Given the high prevalence of multimorbidity, more detailed understanding of the associations with multimorbidity and COVID-19 would improve risk stratification and help protect those most vulnerable to severe COVID-19. Here we examine the relationships between multimorbidity, polypharmacy (a proxy of multimorbidity), and COVID-19; and how these differ by sociodemographic, lifestyle, and physiological prognostic factors.Methods and findingsWe studied data from UK Biobank (428,199 participants; aged 37-73; recruited 2006-2010) on self-reported LTCs, medications, sociodemographic, lifestyle, and physiological measures which were linked to COVID-19 test data. Poisson regression models examined risk of COVID-19 by multimorbidity/polypharmacy and effect modification by COVID-19 prognostic factors (age/sex/ethnicity/socioeconomic status/smoking/physical activity/BMI/systolic blood pressure/renal function). 4,498 (1.05%) participants were tested; 1,324 (0.31%) tested positive for COVID-19. Compared with no LTCs, relative risk (RR) of COVID-19 in those with 1 LTC was no higher (RR 1.12 (CI 0.96-1.30)), whereas those with ≥2 LTCs had 48% higher risk; RR 1.48 (1.28-1.71). Compared with no cardiometabolic LTCs, having 1 and ≥2 cardiometabolic LTCs had a higher risk of COVID-19; RR 1.28 (1.12-1.46) and 1.77 (1.46-2.15), respectively. Polypharmacy was associated with a dose response higher risk of COVID-19. All prognostic factors were associated with a higher risk of COVID-19 infection in multimorbidity; being non-white, most socioeconomically deprived, BMI ≥40 kg/m2, and reduced renal function were associated with the highest risk of COVID-19 infection: RR 2.81 (2.09-3.78); 2.79 (2.00-3.90); 2.66 (1.88-3.76); 2.13 (1.46-3.12), respectively. No multiplicative interaction between multimorbidity and prognostic factors was identified. Important limitations include the low proportion of UK Biobank participants with COVID-19 test data (1.05%) and UK Biobank participants being more affluent, healthier and less ethnically diverse than the general population.ConclusionsIncreasing multimorbidity, especially cardiometabolic multimorbidity, and polypharmacy are associated with a higher risk of developing COVID-19. Those with multimorbidity and additional factors, such as non-white ethnicity, are at heightened risk of COVID-19.

Summary: Background: Combinations of lifestyle factors interact to increase mortality. Combinations of traditional factors such as smoking and alcohol are well described, but the additional effects of emerging factors such as television viewing time are not. The effect of socioeconomic deprivation on these extended lifestyle risks also remains unclear. We aimed to examine whether deprivation modifies the association between an extended score of lifestyle-related risk factors and health outcomes. Methods: Data for this prospective analysis were sourced from the UK Biobank, a prospective population-based cohort study. We assigned all participants an extended lifestyle score, with 1 point for each unhealthy lifestyle factor (incorporating sleep duration and high television viewing time, in addition to smoking, excessive alcohol, poor diet [low intake of oily fish or fruits and vegetables, and high intake of red meat or processed meats], and low physical activity), categorised as most healthy (score 0–2), moderately healthy (score 3–5), or least healthy (score 6–9). Cox proportional hazards models were used to examine the association between lifestyle score and health outcomes (all-cause mortality and cardiovascular disease mortality and incidence), and whether this association was modified by deprivation. All analyses were landmark analyses, in which participants were excluded if they had an event (death or cardiovascular disease event) within 2 years of recruitment. Participants with non-communicable diseases (except hypertension) and missing covariate data were excluded from analyses. Participants were also excluded if they reported implausible values for physical activity, sleep duration, and total screen time. All analyses were adjusted for age, sex, ethnicity, month of assessment, history of hypertension, systolic blood pressure, medication for hypercholesterolaemia or hypertension, and body-mass index categories. Findings: 328 594 participants aged 40–69 years were included in the study, with a mean follow-up period of 4·9 years (SD 0·83) after the landmark period for all-cause and cardiovascular disease mortality, and 4·1 years (0·81) for cardiovascular disease incidence. In the least deprived quintile, the adjusted hazard ratio (HR) in the least healthy lifestyle category, compared with the most healthy category, was 1·65 (95% CI 1·25–2·19) for all-cause mortality, 1·93 (1·16–3·20) for cardiovascular disease mortality, and 1·29 (1·10–1·52) for cardiovascular disease incidence. Equivalent HRs in the most deprived quintile were 2·47 (95% CI 2·04–3·00), 3·36 (2·36–4·76), and 1·41 (1·25–1·60), respectively. The HR for trend for one increment change towards least healthy in the least deprived quintile compared with that in the most deprived quintile was 1·25 (95% CI 1·12–1·39) versus 1·55 (1·40–1·70) for all-cause mortality, 1·30 (1·05–1·61) versus 1·83 (1·54–2·18) for cardiovascular disease mortality, and 1·10 (1·04–1·17) versus 1·16 (1·09–1·23) for cardiovascular disease incidence. A significant interaction was found between lifestyle and deprivation for all-cause and cardiovascular disease mortality (both pinteraction

Introduction: Unhealthy lifestyle factors, such as smoking, high alcohol intake, poor diet and physical inactivity, are key risk factors for premature mortality. How unhealthy lifestyle factors are viewed in the wider context of socioeconomic deprivation is rarely considered. Understanding key stakeholder views on lifestyle factors in the context of deprivation is critical to intervention development and reducing harm in more deprived populations. The aim of this study was to explore public, healthcare professional and policymaker views around unhealthy lifestyle factors in the context of deprivation. The aim was broad to facilitate iterative development of ideas, as the views of this wide range of stakeholders are rarely captured. Methods: Twenty‐five adult members of the public in Scotland took part in four focus groups between August 2022 and June 2023. Eighteen semi‐structured interviews were conducted with professionals: 12 primary‐care practitioners and 6 public‐health practitioners and policymakers. Reflexive thematic analysis was undertaken. Results: Four main themes were developed: (1) Evolving complexity of lifestyle factors – the number of lifestyle factors that adversely impact health has grown, with increasingly complex interactions, (2) Social determinants of lifestyle – numerous links were made between socioeconomic conditions and unhealthy lifestyle factors by all participants, (3) Poverty as a fundamental social determinant – poverty was identified as a core factor for unhealthy lifestyle factors, and (4) Agency versus structure in relation to lifestyle – individual agency to address lifestyle factors was limited by structural constraints. Among professionals, understanding the challenging social determinants of unhealthy lifestyle factors was countered by a desire to support healthy change in those affected by deprivation. Conclusion: Public and professional views around lifestyle highlight an evolving understanding of the new and growing number of lifestyle factors as well as the increasingly complex interplay between lifestyle factors. Views of the social determinants of lifestyle and structural limits to agency strengthen arguments for reduced emphasis on individual‐level responsibility for unhealthy lifestyle factors and for deeper integration of social determinants into lifestyle interventions. In addition to addressing poverty and socioeconomic inequalities directly, innovative policy, planning and legislation that incorporate wider approaches could tackle upstream determinants of numerous unhealthy lifestyle factors simultaneously. Patient or Public Contribution: Members of the public who participated in this study have made contributions by sharing their views and perspectives. The National Health Service Research Scotland Primary Care Patient and Public Involvement (NRS PPI) Group contributed to the development of this work. The NRS PPI Group was consulted as part of the preparatory work for H. M. E. F.'s doctoral thesis funding application. The findings of the qualitative work were presented to them, and they informed the interpretation of those findings and related work presented at conferences and public engagement events. [ABSTRACT FROM AUTHOR]

This article discusses the role of long-chain acylcarnitines (LCACs) in cardiac pathophysiology. Metabolomics studies have identified associations between LCACs and cardiovascular diseases such as heart failure and cardiac arrhythmias. The article focuses on the effects of LCACs on the ryanodine receptor (RyR2), a calcium release channel in cardiomyocytes. The study found that LCACs promote spontaneous calcium release and intracellular calcium accumulation, potentially through increased cytosolic calcium levels. The article also highlights the importance of considering methodological limitations and membrane perturbation effects when studying LCACs. The findings have implications for future research on LCACs and their potential as therapeutic targets for cardiovascular diseases. [Extracted from the article]

Regular population monitoring of imperilled charismatic species such as large carnivores is critical for conservation. However, the role of monitoring in conservation is frequently diminished due to: 1) surveys being implemented in isolation, 2) limited on-ground-capacity leading to infrequent monitoring, and 3) inappropriate methods being applied. Wildlife monitoring is often resource-intensive and the utility and cost of different field protocols is rarely reported. In this study we deployed two standard field protocols aimed at collecting data on African lions within a spatial capture-recapture framework. For our first protocol, we trained Uganda Wildlife Authority rangers in search-encounter techniques, the industry gold standard for monitoring lions. The second protocol involved deploying 32 paired stations of state-of-the-art infra-red camera traps. During the search-encounter protocol, two rangers covered 2939 km in 76 days, recording 102 detections (30 individuals) in a ~ 256 km2 area. The resulting density estimates (13.91 lions/100 km2, posterior SD = 2.34) yielded acceptable precision. Conversely, 64 camera traps over 1601 trap nights yielded two usable lion detections. We argue that where wildlife tourism rangers exist, they could be a powerful addition to future lion and wildlife census attempts across the continent. Our results confirm that the current technology of store-bought infra-red camera traps is not suitable for individual identification of lions, and therefore cannot be applied to analytical models that require unambiguous individual identities. However, we encourage the continued testing and advancement of infra-red camera trap technology since in many instances, this may be preferable to white-flash camera traps, which can yield individual identities for lions. Our study also shows the immense importance of the Nile Delta for African lions in Uganda’s Murchison Falls National Park, a protected area with both oil extraction and high rates of anthropogenic snaring pressure.

Reported mpox cases in England continued at a low but steady frequency during 2023. Of 137 cases reported in 2023, approximately half were acquired overseas and half were in vaccinated persons. Estimated effectiveness of 2-dose vaccine was 80%, and no vaccinated mpox patient was hospitalized.

Abstract Background Sexually transmitted infections (STIs) are a serious public health issue in many countries. Online postal self-sampling (OPSS) is increasingly used to test for STIs, a trend accelerated by the COVID-19 pandemic. There remains limited understanding of how service users experience OPSS and what leads them to access it over clinic-based services, or vice versa. This research seeks to address these gaps, by undertaking a large qualitative study which sits within the ASSIST study, a mixed-methods, realist evaluation of OPSS. Methods Participants were recruited via clinic-based and online sexual health services in three case study areas in England. Purposive sampling was used to over-represent populations disproportionately affected by poor sexual health: young people; people of colour; men who have sex with men; and trans and non-binary people. Semi-structured interviews were analysed using Levesque’s conceptual framework of access to healthcare. Results We interviewed 100 service users. Participants typically became aware of OPSS from sexual health services, the internet or word of mouth. Acceptability of OPSS was facilitated by the perceived privacy it offered over clinic-based services, which some participants found embarrassing to access. OPSS also enabled participants to overcome barriers to reaching clinic-based services, such as a lack of appointment availability, although difficulty obtaining OPSS kits in some areas undermined this. As all services in our case study areas were free to use, affordability did not significantly shape access, although OPSS enabled some participants to avoid costs associated with travelling to clinic-based services. Participants were usually able to engage with OPSS, finding it easy to use and reliable, although blood self-sampling was challenging for most. Participants valued the support offered by clinic-based services beyond STI testing, including the opportunity to access contraception or ask staff questions, and felt this was more appropriate when they had specific concerns about their sexual health, such as STI symptoms. Conclusions Our findings constitute one of the largest qualitative studies to have explored OPSS and offer valuable insights to providers. OPSS shapes access to STI testing in a number of ways, including facilitating access in many circumstances, but users also want to retain access to clinic-based services, particularly for when they believe they need support beyond STI testing.

Monitoring wildlife populations at scale is fraught with logistical and resource constraints. Despite this, estimating wildlife population state variables and vital rates remains crucial for science, and to assess conservation investment and effort. The veracity and transparency of results also helps prevent politicization of wildlife populations. In Uganda, robust estimates of carnivore population size are rare in the literature. To overcome a near two-decade long data gap we initiated a survey of African lions, leopards, and spotted hyenas with the Uganda Wildlife Authority across six important protected areas. Surveys were conducted within a spatial capture-recapture framework, the industry gold-standard for monitoring carnivore populations. For lions, we used unstructured spatial sampling protocols (in the form of vehicle-based searches), while for leopards, and spotted hyenas we deployed camera traps. Our protocols were designed to obtain unambiguous individual identification photographs. This large-scale effort involved data collection by >100 local conservation stakeholders (including lodge guides, trophy hunters, university students, and government rangers). Locally extinct in three areas, we show lion numbers are precariously low in two of three sites where they still occur (Queen Elizabeth abundance=39.72, Posterior standard deviation (PSD)=7.96; Kidepo Valley abundance=22.23, PSD=11.67). Murchison Falls was identified as Uganda’s lion stronghold with an estimate of ∼240 individuals (PSD=34) and average park-wide densities of 7.43 individuals/100 km2 (PSD=1.05). Leopard densities were highest in Lake Mburo and Murchison Falls. In Murchison they reach some of the highest densities in Africa (14.06 individuals/100 km2, PSD=2.65). Spotted hyena densities were high compared to lions (range=6.15–45.31 individuals/100 km2), except in Lake Mburo where densities were markedly lower (park abundance=23 individuals in 370 km2, PSD=5.26). Our work has critical policy implications, and forms the foundation of the new Strategic Action Plan for Large Carnivore Conservation in Uganda (2023–2033). It also illustrates how cutting-edge, transparent and collaborative science, implemented by multiple wildlife conservation stakeholders can help gauge the conservation status of their wildlife resources.

During the 2022 multicountry mpox outbreak, the United Kingdom identified cases beginning in May. UK cases increased in June, peaked in July, then rapidly declined after September 2022. Public health responses included community-supported messaging and targeted mpox vaccination among eligible gay, bisexual, and other men who have sex with men (GBMSM). Using data from an online survey of GBMSM during November–December 2022, we examined self-reported mpox diagnoses, behavioral risk modification, and mpox vaccination offer and uptake. Among 1,333 participants, only 35 (2.6%) ever tested mpox-positive, but 707 (53%) reported behavior modification to avoid mpox. Among vaccine-eligible GBMSM, uptake was 69% (95% CI 65%–72%; 601/875) and was 92% (95% CI 89%–94%; 601/655) among those offered vaccine. GBMSM self-identifying as bisexual, reporting lower educational qualifications, or identifying as unemployed were less likely to be vaccinated. Equitable offer and provision of mpox vaccine are needed to minimize the risk for future outbreaks and mpox-related health inequalities.