Peary caribou (Rangifer tarandus pearyi) and muskoxen (Ovibos moschatus) on northwest Victoria Island, Northwest Territories

An aerial population survey of Peary caribou (Rangifer tarandus pearyi) and muskoxen (Ovibus moschatus) on Victoria Island, Northwest Territories, was conducted in July 2010. The population estimate of adult Peary caribou was 150 ± 104 (95% Confidence Interval [CI]) was not significantly different than the 2005 estimate of 66 ± 61 (P < 0.05). There was also an estimate of 430 ± 214 (95% CI) adult Dolphin-Union caribou (R. t. groenlandicus x pearyi) in the study area. However, these caribou represent only a small portion of the Dolphin-Union herd.  The population estimate of 11 442 ± 1637 (95% CI) adult muskoxen is not significantly different than the 2005 estimate of 12 062 ± 2156 (P < 0.05)

Moose (Alces alces) population size and density in the Inuvik Region of the Northwest Territories, Canada

Responding to community concerns, the Gwich’in Renewable Resources Board (GRRB) and the Government of the Northwest Territories Department of Environment and Natural Resources (ENR) conducted an aerial moose (Alces alces) survey in the Inuvik region of the Northwest Territories, Canada to estimate moose density and distribution. The survey was flown in March 2011 and a random stratified sample design was used. Local knowledge was incorporated in to the stratification of survey cells. Moose density in survey blocks ranged from 9.66 moose/100 km2 in the Ikhil Pipeline block to 0 in the Peel River block with a coarse overall moose density 2.24 moose/100 km2. Densities found were low but within expected range for the species in this region of North America based on past surveys

Population survey of Peary caribou (Rangifer tarandus pearyi) and muskoxen (Ovibos moschatus) on Banks Island, Northwest Territories, July 2010

We conducted a systematic aerial transect survey of Peary caribou (Rangifer tarandus pearyi) and muskoxen (Ovibus moschatus) on Banks Island, Northwest Territories, in July 2010. The population estimate of adult Peary caribou was 1097 ± 343 (95% Confidence Interval: CI), which is not significantly different from the 2005 estimate of 929 ± 289 (95% CI; P < 0.05). The current number, however, is a 4- to 9-fold decrease since the 1980s. The adult muskoxen population estimate was 36 676 ± 4031 (95% CI), which is significantly lower than the 2005 estimate of 47 209 ± 3997 (95% CI; P < 0.05)

Estimates of caribou herd size using post-calving surveys in the Northwest Territories and Nunavut, Canada: A meta-analysis

Post-calving surveys to estimate herd size of barren-ground caribou (Rangifer tarandus groenlandicus, R. t. granti, and R. t. caribou) have been used for caribou herds in Alaska, Yukon, Northwest Territories, Nunavut, and Québec/Labrador. The main field procedure uses relocation of collared caribou to locate aggregated groups of hundreds or thousands of caribou during times of high insect harassment that usually occur in July. These groups are then pho­tographed to obtain a count of the caribou in the aggregated groups. Often some caribou are missed, and the count of caribou may be a negatively biased estimate of total herd size, unless a high proportion of the herd is found and photographed. To address this, some previous studies have used the Lincoln-Petersen estimator, which estimates the proportion of the herd counted based on the percentage of available collared caribou found during the survey. However, this estimator assumes equal probabilities of all groups of caribou being found, regardless of group size and the numbers of collared caribou in the group. These assumptions may not be valid, as larger groups are more likely to be found than smaller groups, particularly if there are several collared caribou present. This may lead to estimates that are biased low, along with an estimate of variance that may also be biased low. A two phase estimator developed by Rivest et al., in 1998 became available in R statistical software in 2012. We analyzed 20 data sets from post-calving surveys in the NWT and NU carried out between 2000 and 2015 using the Rivest estimator to explore working characteristics of this estimator. We compared the Rivest estimates with Lincoln-Petersen estimates and total counts on each survey. We considered factors that influence precision of the Rivest estimator with a focus on sampling factors such as the proportion of collars found, the number of collars available, and natural factors such as the degree of aggregation of caribou in each survey (as indexed by the negative binomial dispersion parameter). In general, the Rivest estimator displayed acceptable preci­sion when high proportions of caribou groups with collars were detected and counted, collar numbers were sufficient, and aggregation was adequate. Notable exceptions occurred in years of lower aggregation which resulted in many small groups with 0 or few collared caribou, and in these cases herd estimates had large variances and low precision. Estimates from the Rivest estimator, Lincoln-Petersen estimator, and total counts converged when sampling effort was high, collar numbers relative to herd size were high, and caribou were well aggregated in a limited number of groups. In other cases, estimates of the Rivest estimator were generally higher than Lincoln-Petersen estimates, presumably due to negative bias with the Lincoln-Petersen estimator. We provide a set of working recommendations to optimize field sampling to ensure reliable estimates of herd size using post-calving methods

Bacterial genomics reveal the complex epidemiology of an emerging pathogen in Arctic and boreal ungulates

Northern ecosystems are currently experiencing unprecedented ecological change, largely driven by a rapidly changing climate. Pathogen range expansion, and emergence and altered patterns of infectious disease, are increasingly reported in wildlife at high latitudes. Understanding the causes and consequences of shifting pathogen diversity and host-pathogen interactions in these ecosystems is important for wildlife conservation, and for indigenous populations that depend on wildlife. Among the key questions are whether disease events are associated with endemic or recently introduced pathogens, and whether emerging strains are spreading throughout the region. In this study, we used a phylogenomic approach to address these questions of pathogen endemicity and spread for Erysipelothrix rhusiopathiae, an opportunistic multi-host bacterial pathogen associated with recent mortalities in arctic and boreal ungulate populations in North America. We isolated E. rhusiopathiae from carcasses associated with large-scale die-offs of muskoxen in the Canadian Arctic Archipelago, and from contemporaneous mortality events and/or population declines among muskoxen in northwestern Alaska and caribou and moose in western Canada. Bacterial genomic diversity differed markedly among these locations; minimal divergence was present among isolates from muskoxen in the Canadian Arctic, while in caribou and moose populations, strains from highly divergent clades were isolated from the same location, or even from within a single carcass. These results indicate that mortalities among northern ungulates are not associated with a single emerging strain of E. rhusiopathiae, and that alternate hypotheses need to be explored. Our study illustrates the value and limitations of bacterial genomic data for discriminating between ecological hypotheses of disease emergence, and highlights the importance of studying emerging pathogens within the broader context of environmental and host factors

Antibody Inhibition of a Viral Type 1 Interferon Decoy Receptor Cures a Viral Disease by Restoring Interferon Signaling in the Liver

Type 1 interferons (T1-IFNs) play a major role in antiviral defense, but when or how they protect during infections that spread through the lympho-hematogenous route is not known. Orthopoxviruses, including those that produce smallpox and mousepox, spread lympho-hematogenously. They also encode a decoy receptor for T1-IFN, the T1-IFN binding protein (T1-IFNbp), which is essential for virulence. We demonstrate that during mousepox, T1-IFNs protect the liver locally rather than systemically, and that the T1-IFNbp attaches to uninfected cells surrounding infected foci in the liver and the spleen to impair their ability to receive T1-IFN signaling, thus facilitating virus spread. Remarkably, this process can be reversed and mousepox cured late in infection by treating with antibodies that block the biological function of the T1-IFNbp. Thus, our findings provide insights on how T1-IFNs function and are evaded during a viral infection in vivo, and unveil a novel mechanism for antibody-mediated antiviral therapy

A framework of single-session problem solving in elite sport: A longitudinal multi-study investigation

In this six-year, multi-study paper we summarize a new and effective framework of single-session problem-solving developed in an elite sport context at a world leading national institute of sport science and medicine (English Institute of Sport: EIS). In Study 1, we used ethnography (3.5 years) to observe how single-session problem-solving methods were being considered, explored, introduced and developed within the EIS. In Study 2, we used case-study methods split into two parts. A multiple case-study design (10 cases) was employed in Part one to evaluate how the approach was refined into an effective framework of practice. An individual case-study is then illustrated to detail the framework in-action. Collectively, findings realized a framework of single-session problem-solving for use both inside and outside of elite sport that focused on ways to reframe clients’ problems into more ‘solvable’ descriptions. Guidance for psychologists wishing to integrate these problem-solving techniques into their practice are offered

Multiple novel prostate cancer susceptibility signals identified by fine-mapping of known risk loci among Europeans

Genome-wide association studies (GWAS) have identified numerous common prostate cancer (PrCa) susceptibility loci. We have fine-mapped 64 GWAS regions known at the conclusion of the iCOGS study using large-scale genotyping and imputation in 25 723 PrCa cases and 26 274 controls of European ancestry. We detected evidence for multiple independent signals at 16 regions, 12 of which contained additional newly identified significant associations. A single signal comprising a spectrum of correlated variation was observed at 39 regions; 35 of which are now described by a novel more significantly associated lead SNP, while the originally reported variant remained as the lead SNP only in 4 regions. We also confirmed two association signals in Europeans that had been previously reported only in East-Asian GWAS. Based on statistical evidence and linkage disequilibrium (LD) structure, we have curated and narrowed down the list of the most likely candidate causal variants for each region. Functional annotation using data from ENCODE filtered for PrCa cell lines and eQTL analysis demonstrated significant enrichment for overlap with bio-features within this set. By incorporating the novel risk variants identified here alongside the refined data for existing association signals, we estimate that these loci now explain ∼38.9% of the familial relative risk of PrCa, an 8.9% improvement over the previously reported GWAS tag SNPs. This suggests that a significant fraction of the heritability of PrCa may have been hidden during the discovery phase of GWAS, in particular due to the presence of multiple independent signals within the same regio

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

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 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

CD200 receptor restriction of myeloid cell responses antagonizes antiviral immunity and facilitates cytomegalovirus persistence within mucosal tissue

CD200 receptor (CD200R) negatively regulates peripheral and mucosal innate immune responses. Viruses, including herpesviruses, have acquired functional CD200 orthologs, implying that viral exploitation of this pathway is evolutionary advantageous. However, the role that CD200R signaling plays during herpesvirus infection in vivo requires clarification. Utilizing the murine cytomegalovirus (MCMV) model, we demonstrate that CD200R facilitates virus persistence within mucosal tissue. Specifically, MCMV infection of CD200R-deficient mice (CD200R-/-) elicited heightened mucosal virus-specific CD4 T cell responses that restricted virus persistence in the salivary glands. CD200R did not directly inhibit lymphocyte effector function. Instead, CD200R-/- mice exhibited enhanced APC accumulation that in the mucosa was a consequence of elevated cellular proliferation. Although MCMV does not encode an obvious CD200 homolog, productive replication in macrophages induced expression of cellular CD200. CD200 from hematopoietic and non-hematopoietic cells contributed independently to suppression of antiviral control in vivo. These results highlight the CD200-CD200R pathway as an important regulator of antiviral immunity during cytomegalovirus infection that is exploited by MCMV to establish chronicity within mucosal tissue