Scoping future research for air pollution recovery indicators (APRI). (Workshop report)

Atmospheric nitrogen (N) pollution is a major and ongoing cause of biodiversity loss across the UK, but in some locations N pollution pressures have been declining. In response to these dynamics, JNCC requested a workshop to help to scope Phase 2 of the Air Pollution Recovery Indicators (APRI) project. The damaging effects of excess N load and of gaseous ammonia on many ecosystems are clear. However, the processes and timescales of ecosystem recovery following a decrease in pollution pressure are less well understood. The APRI project aims to take practical steps to fill this knowledge gap by delivering new scientific research focused on indicators of ecosystem and species recovery from N pollution. In Phase 1, predominantly below-ground responses are being studied at a dry heathland site where experimental additions of N were made between 1998 and 2011, revealing lingering effects on soil chemistry, the soil fungi community and vegetation structure (Kowal et al. 2024). The effect on mycorrhizal fungi, and using these fungi as recovery indicators, is being examined in more detail with recently established assessment methods (Arrigoni et al. 2023). Phase 2 of APRI will consider recovery from N impacts more broadly, e.g. by studying other habitats or species. Further empirical research may be commissioned to better understand recovery pathways from air pollution. A workshop was held on 7–8 November 2023 to help develop an action plan for the remainder of the APRI project. This report summarises the workshop discussion and ensuing work. We note that the focus of the APRI project is on assessing recovery. It is therefore essential to contrast responses of ecosystems subject to decreased pollution pressure with indicators from ecosystems experiencing ongoing pollution. Properties that have been used previously to assess impacts can be used to understand recovery, and novel indicators of ecosystem change are also likely to be useful for assessing recovery. Whatever indicators are chosen to assess change, benchmarking data will be needed to assess the range of potential values and relationships with N deposition. Results from the workshop and subsequent discussions include: • Eleven criteria to help choose appropriate indicators in relation to declining N deposition: Speed of response, Sensitivity of response, Specificity of response, Generality to multiple habitats, Relatedness to recovery endpoints, Previous use, Breadth of pollution gradient, Added value to other policy areas, Resilience in face of anticipated change, Feasibility of collection, Measurement uncertainty. • The need to consider a basket of indicators to indicate recovery from N pollution. Such a basket could include examples from different categories e.g. indicators of pressure, biogeochemical response indicators, and biotic response indicators, with individual indicators likely responding over different timescales. The exact choice may depend on the habitat concerned and the availability of prior data, as well as the question being posed and/or policy goal. • Explicit recommendations on sites to target in APRI Phase 2 to gain information on recovery indicator trajectories, namely (i) well-designed field experiments where N addition has ceased, and (ii) point sources of emissions that have ceased to operate, preferably with a super-imposition of an experimental treatment or treatments. Given uncertainties associated with modelled historical, contemporary, and future N deposition and the potential for confounding variables, analysing survey data from across the UK will be unlikely to provide robust information within the timeframes of the APRI Phase 2. We recommend further assessments may help develop detailed plans for empirical work in Phase 2 of APRI. Potential next steps are to: • Finalise a list of potential and priority indicators of recovery from air pollution (which may differ by habitat type), specifically from high levels of N deposition and/or high atmospheric reactive N concentrations. This finalisation could be done through active participation of the air pollution community and the completion of ‘live’ spreadsheets that address potential indicator criteria. • Summarise relevant data on recovery indicators, across key semi-natural habitats. This summary should include data available from other countries with similar environmental contexts, to help disentangle drivers of change in the UK context. This evidence will help understand recovery pathways from air pollution. As above, this could be done through the active participation of the air pollution community and the completion of ‘live’ spreadsheets. Such an approach could also enable gap analyses, for example identifying where we are missing information by habitat and/or environmental conditions. • Identify areas where co-located monitoring of N with existing habitat/species monitoring could enhance the likelihood for establishing recovery indicators. This should enhance other similar activity such as through the Natural Capital and Ecosystem Assessment programme and the UK Air Pollution Impacts on Ecosystems Networks (APIENs). • Develop a list of priority habitats and sites where empirical research is needed to better understand recovery pathways, including a gap analysis of habitats, methods and/or indicators. • Encourage activities that enhance understanding of ammonia emission sources at local scale (e.g. 1 km or less), to help better identify areas where N pollution has decreased, and recovery might be detected. This could include intensive monitoring or collating and sharing information about permitted N sources. • Develop case studies, including potentially from APRI Phase 1, to demonstrate how existing evidence on localised recovery in semi-natural habitats of conservation importance can be used by policy- and decision-makers to help drive policy toward continued reductions in emissions of reactive N

Age at symptom onset and death and disease duration in genetic frontotemporal dementia : an international retrospective cohort study

Background: Frontotemporal dementia is a heterogenous neurodegenerative disorder, with about a third of cases being genetic. Most of this genetic component is accounted for by mutations in GRN, MAPT, and C9orf72. In this study, we aimed to complement previous phenotypic studies by doing an international study of age at symptom onset, age at death, and disease duration in individuals with mutations in GRN, MAPT, and C9orf72. Methods: In this international, retrospective cohort study, we collected data on age at symptom onset, age at death, and disease duration for patients with pathogenic mutations in the GRN and MAPT genes and pathological expansions in the C9orf72 gene through the Frontotemporal Dementia Prevention Initiative and from published papers. We used mixed effects models to explore differences in age at onset, age at death, and disease duration between genetic groups and individual mutations. We also assessed correlations between the age at onset and at death of each individual and the age at onset and at death of their parents and the mean age at onset and at death of their family members. Lastly, we used mixed effects models to investigate the extent to which variability in age at onset and at death could be accounted for by family membership and the specific mutation carried. Findings: Data were available from 3403 individuals from 1492 families: 1433 with C9orf72 expansions (755 families), 1179 with GRN mutations (483 families, 130 different mutations), and 791 with MAPT mutations (254 families, 67 different mutations). Mean age at symptom onset and at death was 49\ub75 years (SD 10\ub70; onset) and 58\ub75 years (11\ub73; death) in the MAPT group, 58\ub72 years (9\ub78; onset) and 65\ub73 years (10\ub79; death) in the C9orf72 group, and 61\ub73 years (8\ub78; onset) and 68\ub78 years (9\ub77; death) in the GRN group. Mean disease duration was 6\ub74 years (SD 4\ub79) in the C9orf72 group, 7\ub71 years (3\ub79) in the GRN group, and 9\ub73 years (6\ub74) in the MAPT group. Individual age at onset and at death was significantly correlated with both parental age at onset and at death and with mean family age at onset and at death in all three groups, with a stronger correlation observed in the MAPT group (r=0\ub745 between individual and parental age at onset, r=0\ub763 between individual and mean family age at onset, r=0\ub758 between individual and parental age at death, and r=0\ub769 between individual and mean family age at death) than in either the C9orf72 group (r=0\ub732 individual and parental age at onset, r=0\ub736 individual and mean family age at onset, r=0\ub738 individual and parental age at death, and r=0\ub740 individual and mean family age at death) or the GRN group (r=0\ub722 individual and parental age at onset, r=0\ub718 individual and mean family age at onset, r=0\ub722 individual and parental age at death, and r=0\ub732 individual and mean family age at death). Modelling showed that the variability in age at onset and at death in the MAPT group was explained partly by the specific mutation (48%, 95% CI 35\u201362, for age at onset; 61%, 47\u201373, for age at death), and even more by family membership (66%, 56\u201375, for age at onset; 74%, 65\u201382, for age at death). In the GRN group, only 2% (0\u201310) of the variability of age at onset and 9% (3\u201321) of that of age of death was explained by the specific mutation, whereas 14% (9\u201322) of the variability of age at onset and 20% (12\u201330) of that of age at death was explained by family membership. In the C9orf72 group, family membership explained 17% (11\u201326) of the variability of age at onset and 19% (12\u201329) of that of age at death. Interpretation: Our study showed that age at symptom onset and at death of people with genetic frontotemporal dementia is influenced by genetic group and, particularly for MAPT mutations, by the specific mutation carried and by family membership. Although estimation of age at onset will be an important factor in future pre-symptomatic therapeutic trials for all three genetic groups, our study suggests that data from other members of the family will be particularly helpful only for individuals with MAPT mutations. Further work in identifying both genetic and environmental factors that modify phenotype in all groups will be important to improve such estimates. Funding: UK Medical Research Council, National Institute for Health Research, and Alzheimer's Society

A systematic map of studies testing the relationship between temperature and animal reproduction

1. Exposure to extreme temperatures can negatively affect animal reproduction, by disrupting the ability of individuals to produce any offspring (fertility), or the number of offspring produced by fertile individuals (fecundity). This has important ecological consequences, because reproduction is the ultimate measure of population fitness: a reduction in reproductive output lowers the population growth rate and increases the extinction risk. Despite this importance, there have been no large-scale summaries of the evidence for effect of temperature on reproduction. 2. We provide a systematic map of studies testing the relationship between temperature and animal reproduction. We systematically searched for published studies that statistically test for a direct link between temperature and animal reproduction, in terms of fertility, fecundity or indirect measures of reproductive potential (gamete and gonad traits). 3. Overall, we collated a large and rich evidence base, with 1654 papers that met our inclusion criteria, encompassing 1191 species. 4. The map revealed several important research gaps. Insects made up almost half of the dataset, but reptiles and amphibians were uncommon, as were non-arthropod invertebrates. Fecundity was the most common reproductive trait examined, and relatively few studies measured fertility. It was uncommon for experimental studies to test exposure of different life stages, exposure to short-term heat or cold shock, exposure to temperature fluctuations, or to independently assess male and female effects. Studies were most often published in journals focusing on entomology and pest control, ecology and evolution, aquaculture and fisheries science, and marine biology. Finally, while individuals were sampled from every continent, there was a strong sampling bias towards mid-latitudes in the Northern Hemisphere, such that the tropics and polar regions are less well sampled. 5. This map reveals a rich literature of studies testing the relationship between temperature and animal reproduction, but also uncovers substantial missing treatment of taxa, traits, and thermal regimes. This database will provide a valuable resource for future quantitative meta-analyses, and direct future studies aiming to fill identified gaps

Geographical and temporal distribution of SARS-CoV-2 clades in the WHO European Region, January to June 2020

We show the distribution of SARS-CoV-2 genetic clades over time and between countries and outline potential genomic surveillance objectives. We applied three available genomic nomenclature systems for SARS-CoV-2 to all sequence data from the WHO European Region available during the COVID-19 pandemic until 10 July 2020. We highlight the importance of real-time sequencing and data dissemination in a pandemic situation. We provide a comparison of the nomenclatures and lay a foundation for future European genomic surveillance of SARS-CoV-2.Peer reviewe

A global research priority agenda to advance public health responses to fatty liver disease

Background & aims An estimated 38% of adults worldwide have non-alcoholic fatty liver disease (NAFLD). From individual impacts to widespread public health and economic consequences, the implications of this disease are profound. This study aimed to develop an aligned, prioritised fatty liver disease research agenda for the global health community. Methods Nine co-chairs drafted initial research priorities, subsequently reviewed by 40 core authors and debated during a three-day in-person meeting. Following a Delphi methodology, over two rounds, a large panel (R1 n = 344, R2 n = 288) reviewed the priorities, via Qualtrics XM, indicating agreement using a four-point Likert-scale and providing written feedback. The core group revised the draft priorities between rounds. In R2, panellists also ranked the priorities within six domains: epidemiology, models of care, treatment and care, education and awareness, patient and community perspectives, and leadership and public health policy. Results The consensus-built fatty liver disease research agenda encompasses 28 priorities. The mean percentage of ‘agree’ responses increased from 78.3 in R1 to 81.1 in R2. Five priorities received unanimous combined agreement (‘agree’ + ‘somewhat agree’); the remaining 23 priorities had >90% combined agreement. While all but one of the priorities exhibited at least a super-majority of agreement (>66.7% ‘agree’), 13 priorities had 90% combined agreement. Conclusions Adopting this multidisciplinary consensus-built research priorities agenda can deliver a step-change in addressing fatty liver disease, mitigating against its individual and societal harms and proactively altering its natural history through prevention, identification, treatment, and care. This agenda should catalyse the global health community’s efforts to advance and accelerate responses to this widespread and fast-growing public health threat. Impact and implications An estimated 38% of adults and 13% of children and adolescents worldwide have fatty liver disease, making it the most prevalent liver disease in history. Despite substantial scientific progress in the past three decades, the burden continues to grow, with an urgent need to advance understanding of how to prevent, manage, and treat the disease. Through a global consensus process, a multidisciplinary group agreed on 28 research priorities covering a broad range of themes, from disease burden, treatment, and health system responses to awareness and policy. The findings have relevance for clinical and non-clinical researchers as well as funders working on fatty liver disease and non-communicable diseases more broadly, setting out a prioritised, ranked research agenda for turning the tide on this fast-growing public health threat

Reducing the environmental impact of surgery on a global scale: systematic review and co-prioritization with healthcare workers in 132 countries

Background Healthcare cannot achieve net-zero carbon without addressing operating theatres. The aim of this study was to prioritize feasible interventions to reduce the environmental impact of operating theatres. Methods This study adopted a four-phase Delphi consensus co-prioritization methodology. In phase 1, a systematic review of published interventions and global consultation of perioperative healthcare professionals were used to longlist interventions. In phase 2, iterative thematic analysis consolidated comparable interventions into a shortlist. In phase 3, the shortlist was co-prioritized based on patient and clinician views on acceptability, feasibility, and safety. In phase 4, ranked lists of interventions were presented by their relevance to high-income countries and low–middle-income countries. Results In phase 1, 43 interventions were identified, which had low uptake in practice according to 3042 professionals globally. In phase 2, a shortlist of 15 intervention domains was generated. In phase 3, interventions were deemed acceptable for more than 90 per cent of patients except for reducing general anaesthesia (84 per cent) and re-sterilization of ‘single-use’ consumables (86 per cent). In phase 4, the top three shortlisted interventions for high-income countries were: introducing recycling; reducing use of anaesthetic gases; and appropriate clinical waste processing. In phase 4, the top three shortlisted interventions for low–middle-income countries were: introducing reusable surgical devices; reducing use of consumables; and reducing the use of general anaesthesia. Conclusion This is a step toward environmentally sustainable operating environments with actionable interventions applicable to both high– and low–middle–income countries

Do hoverflies (Diptera: Syrphidae) sound like the Hymenoptera they morphologically resemble?

It has long been recognized that many hoverfly species (Diptera: Syrphidae) mimic the morphological appearance of defended Hymenoptera, such as wasps and bees. However, it has also been repeatedly suggested that some mimetic hoverflies respond with sounds on attack that resemble the warning or startle sounds of their hymenopteran models. In this study, we set out to quantitatively compare the spectral characteristics of the sounds produced by a range of nonmimetic flies, wasps, bumblebees, honeybees, and their hoverfly mimics when they were artificially attacked. The sounds made by wasps and honeybees after simulated attacks were statistically distinguishable from their hoverfly mimics. Bumblebee models of their hoverfly mimics share some similarities in the sound they produce on attack, but they were no closer acoustically to their model than a range of other hoverfly species that morphologically resemble other models. All the mimetic hoverflies tested in this study tended to sound similar to one another, regardless of the model they resemble morphologically. Overall, we found little evidence that mimetic hoverflies sound like their hymenopteran models on attack, and we question whether acoustic mimicry has evolved in this complex. Copyright 2009, Oxford University Press.