Diets of European polecat Mustela putorius in Great Britain during fifty years of population recovery

Following nineteenth-century declines, polecats Mustela putorius are recolonising Great Britain. Polecat diet relates to two potential risks to recovery. First, rabbits Oryctolagus cuniculus, which are important prey for polecats, have experienced extreme population fluctuations, with near extirpation due to myxomatosis in the 1950s, recovery in 1960s–1990s and declines in 1990s–2010s. Second, polecats are secondarily exposed to anticoagulant rodenticides by eating contaminated rodents, and the frequency of polecat exposure to rodenticides is increasing. We analysed stomach contents from 99 polecats collected in 2012–2016 and compared results with earlier studies. Lagomorphs were the most abundant prey (66% frequency of occurrence, 95% confidence interval 53–74%), followed by other mammals (12%, 4–18%), amphibians (10%, 3–16%) and birds (7%, 1–13%). Diet varied seasonally; lagomorph occurrence was highest in spring and summer and lowest in autumn. Dietary niche breadth was greater in the 1960s, when rabbits were scarce, than in other decades, but did not differ between the 1990s and 2010s, indicating that diets have not diversified with recent rabbit declines. This may be because rabbit abundance is not yet low enough to cause dietary diversification or because polecats were collected in areas where rabbits were still abundant. Rodents did not increase in diet between the 1990s and 2010s and still occur with < 10% frequency, indicating that rodents need not contribute much to diet to expose polecats to rodenticides. This potentially limits the effectiveness of management actions designed to minimise polecat exposure to contaminated rodent prey

Reducing publication delay to improve the efficiency and impact of conservation science.

Evidence-based decision-making is most effective with comprehensive access to scientific studies. If studies face significant publication delays or barriers, the useful information they contain may not reach decision-makers in a timely manner. This represents a potential problem for mission-oriented disciplines where access to the latest data is required to ensure effective actions are undertaken. We sought to analyse the severity of publication delay in conservation science-a field that requires urgent action to prevent the loss of biodiversity. We used the Conservation Evidence database to assess the length of publication delay (time from finishing data collection to publication) in the literature that tests the effectiveness of conservation interventions. From 7,447 peer-reviewed and non-peer-reviewed studies of conservation interventions published over eleven decades, we find that the raw mean publication delay was 3.2 years (±2SD = 0.1) and varied by conservation subject. A significantly shorter delay was observed for studies focused on Bee Conservation, Sustainable Aquaculture, Management of Captive Animals, Amphibian Conservation, and Control of Freshwater Invasive Species (Estimated Marginal Mean range from 1.4-1.9 years). Publication delay was significantly shorter for the non-peer-reviewed literature (Estimated Marginal Mean delay of 1.9 years ± 0.2) compared to the peer-reviewed literature (i.e., scientific journals; Estimated Marginal Mean delay of 3.0 years ± 0.1). We found publication delay has significantly increased over time (an increase of ~1.2 years from 1912 (1.4 years ± 0.2) to 2020 (2.6 years ± 0.1)), but this change was much weaker and non-significant post-2000s; we found no evidence for any decline. There was also no evidence that studies on more threatened species were subject to a shorter delay-indeed, the contrary was true for mammals, and to a lesser extent for birds. We suggest a range of possible ways in which scientists, funders, publishers, and practitioners can work together to reduce delays at each stage of the publication process

Investigating infectious disease threats to the recovery of the European polecat in Britain

The European polecat (Mustela putorius) almost became extinct in Britain in the early twentieth century, but populations are now recovering. As seen in other endangered carnivore populations, disease is one potential threat to recovery. This study assessed exposure of wild polecats (n = 149) to three, multi-host pathogens which could limit reproduction and/or cause morbidity and mortality. Serum, lung and brain samples were collected from polecats which died from 2011 to 2016 across Britain. Exposure to Toxoplasma gondii and 12 Leptospira serovars was assessed serologically by antibody detection using the latex agglutination test and microscopic agglutination test, respectively, and the presence of canine distemper virus (CDV) RNA in lung and brain tissue samples was assessed using PCR. Generalised linear models were used to test for relationships between exposure to each pathogen and season, sex, age, and location. All organ samples tested PCR negative for CDV (95% CI 0.00–0.05%). There was evidence of frequent exposure to T. gondii with a recorded seroprevalence of 71.8% (95% CI 64.2–79.4%) and moderate exposure to Leptospira serovars, 14.5% (95% CI 8.6–20.4%). Season, sex, age, and location were not significantly associated with exposure to T. gondii or Leptospira serovars. Evidence of exposure to T. gondii and Leptospira serovars in European polecats could potentially affect mortality, longevity or fecundity. Further studies are warranted to assess the impact of these pathogens on polecat populations in Britain

Long-term increase in secondary exposure to anticoagulant rodenticides in European polecats Mustela putorius in Great Britain

As a result of legal protection and population recovery, European polecats (Mustela putorius) in Great Britain are expanding into areas associated with greater usage of second-generation anticoagulant rodenticides (SGARs). We analysed polecat livers collected from road casualties from 2013 to 2016 for residues of five SGARs. We related variation in residues to polecat traits and potential exposure pathways, by analysing stable isotopes of carbon (δ13C) and nitrogen (δ15N) in their whiskers. 54 of 68 (79%) polecats had detectable residues of at least one SGAR. Bromadiolone (71%) was the most frequently detected compound, followed by difenacoum (53%) and brodifacoum (35%). Applying historical limits of detection to allow comparison between these new data and previous assessments, we show that in the 25 years from 1992 to 2016 inclusive, the rate of detection of SGARs in polecats in Britain has increased by a factor of 1.7. The probability of SGAR detection was positively related to increasing values of δ15N, suggesting that polecats feeding at a higher trophic level were more likely to be exposed. Total concentrations of SGARs in polecats with detectable residues were higher in polecats collected in arable compared to pastoral habitats, and in the west compared to the east of Britain. The number of compounds detected and total concentrations of SGARs increased with polecat age. There was no evidence of regional or seasonal variation in the probability of detecting SGARs, suggesting that the current risk of exposure to SGARs does not vary seasonally and has increased (from that in the 1990s) throughout the polecat's range. We recommend quantification of current practices in rodenticide usage, particularly in the light of recent regulatory changes, to enable assessment and mitigation of the risks of secondary exposure to rodenticides in non-target wildlife

A solution scan of societal options to reduce transmission and spread of respiratory viruses: SARS-CoV-2 as a case study.

Societal biosecurity - measures built into everyday society to minimize risks from pests and diseases - is an important aspect of managing epidemics and pandemics. We aimed to identify societal options for reducing the transmission and spread of respiratory viruses. We used SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) as a case study to meet the immediate need to manage the COVID-19 pandemic and eventually transition to more normal societal conditions, and to catalog options for managing similar pandemics in the future. We used a 'solution scanning' approach. We read the literature; consulted psychology, public health, medical, and solution scanning experts; crowd-sourced options using social media; and collated comments on a preprint. Here, we present a list of 519 possible measures to reduce SARS-CoV-2 transmission and spread. We provide a long list of options for policymakers and businesses to consider when designing biosecurity plans to combat SARS-CoV-2 and similar pathogens in the future. We also developed an online application to help with this process. We encourage testing of actions, documentation of outcomes, revisions to the current list, and the addition of further options

Tapping into non-English-language science for the conservation of global biodiversity.

The widely held assumption that any important scientific information would be available in English underlies the underuse of non-English-language science across disciplines. However, non-English-language science is expected to bring unique and valuable scientific information, especially in disciplines where the evidence is patchy, and for emergent issues where synthesising available evidence is an urgent challenge. Yet such contribution of non-English-language science to scientific communities and the application of science is rarely quantified. Here, we show that non-English-language studies provide crucial evidence for informing global biodiversity conservation. By screening 419,679 peer-reviewed papers in 16 languages, we identified 1,234 non-English-language studies providing evidence on the effectiveness of biodiversity conservation interventions, compared to 4,412 English-language studies identified with the same criteria. Relevant non-English-language studies are being published at an increasing rate in 6 out of the 12 languages where there were a sufficient number of relevant studies. Incorporating non-English-language studies can expand the geographical coverage (i.e., the number of 2° × 2° grid cells with relevant studies) of English-language evidence by 12% to 25%, especially in biodiverse regions, and taxonomic coverage (i.e., the number of species covered by the relevant studies) by 5% to 32%, although they do tend to be based on less robust study designs. Our results show that synthesising non-English-language studies is key to overcoming the widespread lack of local, context-dependent evidence and facilitating evidence-based conservation globally. We urge wider disciplines to rigorously reassess the untapped potential of non-English-language science in informing decisions to address other global challenges. Please see the Supporting information files for Alternative Language Abstracts

Mammographic surveillance in women younger than 50 years who have a family history of breast cancer: tumour characteristics and projected effect on mortality in the prospective, single-arm, FH01 study.

BACKGROUND: Evidence supports a reduction in mortality from breast cancer with mammographic screening in the general population of women aged 40-49 years, but the effect of family history is not clear. We aimed to establish whether screening affects the disease stage and projected mortality of women younger than 50 years who have a clinically significant family history of breast cancer. METHODS: In the single-arm FH01 study, women at intermediate familial risk who were younger than 50 years were enrolled from 76 centres in the UK, and received yearly mammography. Women with BRCA mutations were not explicitly excluded, but would be rare in this group. To compare the FH01 cohort with women not receiving screening, two external comparison groups were used: the control group of the UK Age Trial (106,971 women aged 40-42 years at recruitment, from the general population [ie, average risk], followed up for 10 years), and a Dutch study of women with a family history of breast cancer (cancer cases aged 25-77 years, diagnosed 1980-2004). Study endpoints were size, node status, and histological grade of invasive tumours, and estimated mortality calculated from the Nottingham prognostic index (NPI) score, and adjusted for differences in underlying risk between the FH01 cohort and the control group of the UK Age Trial. This study is registered with the National Research Register, number N0484114809. FINDINGS: 6710 women were enrolled between Jan 16, 2003, and Feb 28, 2007, and received yearly mammography for a mean of 4 years (SD 2) up until Nov 30, 2009; surveillance and reporting of cancers is still underway. 136 women were diagnosed with breast cancer: 105 (77%) at screening, 28 (21%) symptomatically in the interval between screening events, and three (2%) symptomatically after failing to attend their latest mammogram. Invasive tumours in the FH01 study were significantly smaller (p=0·0094), less likely to be node positive (p=0·0083), and of more favourable grade (p=0·0072) than were those in the control group of the UK Age Trial, and were significantly less likely to be node positive than were tumours in the Dutch study (p=0·012). Mean NPI score was significantly lower in the FH01 cohort than in the control group of the UK Age Trial (p=0·00079) or the Dutch study (p<0·0001). After adjustment for underlying risk, predicted 10-year mortality was significantly lower in the FH01 cohort (1·10%) than in the control group of the UK Age Trial (1·38%), with relative risk of 0·80 (95% CI 0·66-0·96; p=0·022). INTERPRETATION: Yearly mammography in women with a medium familial risk of breast cancer is likely to be effective in prevention of deaths from breast cancer

Whole-genome sequencing reveals host factors underlying critical COVID-19

Altres ajuts: Department of Health and Social Care (DHSC); Illumina; LifeArc; Medical Research Council (MRC); UKRI; Sepsis Research (the Fiona Elizabeth Agnew Trust); the Intensive Care Society, Wellcome Trust Senior Research Fellowship (223164/Z/21/Z); BBSRC Institute Program Support Grant to the Roslin Institute (BBS/E/D/20002172, BBS/E/D/10002070, BBS/E/D/30002275); UKRI grants (MC_PC_20004, MC_PC_19025, MC_PC_1905, MRNO2995X/1); UK Research and Innovation (MC_PC_20029); the Wellcome PhD training fellowship for clinicians (204979/Z/16/Z); the Edinburgh Clinical Academic Track (ECAT) programme; the National Institute for Health Research, the Wellcome Trust; the MRC; Cancer Research UK; the DHSC; NHS England; the Smilow family; the National Center for Advancing Translational Sciences of the National Institutes of Health (CTSA award number UL1TR001878); the Perelman School of Medicine at the University of Pennsylvania; National Institute on Aging (NIA U01AG009740); the National Institute on Aging (RC2 AG036495, RC4 AG039029); the Common Fund of the Office of the Director of the National Institutes of Health; NCI; NHGRI; NHLBI; NIDA; NIMH; NINDS.Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care or hospitalization after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes-including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)-in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease