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Predation is a fundamental ecological and evolutionary process that varies in space, and the avoidance of predation risk is of central importance in foraging theory. While there has been a recent growth of approaches to spatially model predation risk, these approaches lack an adequate mechanistic framework that can be applied to real landscapes. In this paper we show how predation risk can be decomposed into encounter and attack stages, and modeled spatially using resource selection functions (RSF) and resource selection probability functions (RSPF). We use this approach to compare the effects of landscape attributes on the relative probability of encounter, the conditional probability of death given encounter, and overall wolf and elk resource selection to test whether predation risk is simply equivalent to location of the predator. We then combine the probability of encounter and conditional probability of death into a spatially explicit function of predation risk following Lima and Dill's reformulation of Holling's functional response. We illustrate this approach in a wolf–elk system in and adjacent to Banff National Park, Alberta, Canada. In this system we found that the odds of elk being encountered by wolves was 1.3 times higher in pine forest and 4.1 times less in grasslands than other habitats. The relative odds of being killed in pine forests, given an encounter, increased by 1.2. Other habitats, such as grasslands, afforded elk reduced odds (4.1 times less) of being encountered and subsequently killed (1.4 times less) by wolves. Our approach illustrates that predation risk is not necessarily equivalent to just where predators are found. We show that landscape attributes can render prey more or less susceptible to predation and effects of landscape features can differ between the encounter and attack stages of predation. We conclude by suggesting applications of our approach to model predator–prey dynamics using spatial predation risk functions in theoretical and applied settings. [ABSTRACT FROM AUTHOR]

The International Classification of Diseases, Ninth Revision (ICD-9) was released in the 1970s and adopted in Canada for physician billing claims in 1979 (CIHI n.d.b.; WHO & International Conference for the Ninth Revision of the International Classification of Diseases 1977). ICD-9 is no longer adequate for representing our modern healthcare environment and patient needs. We summarize the findings from a small survey of ICD-9 users across Canada - such as family physicians, researchers and decision makers - who describe the limitations of ICD-9 and the features that they would desire in a new or updated classification system., (Copyright © 2022 Longwoods Publishing.)

Aim: Group A streptococcus (GAS) pharyngitis is a common clinical infection with significant morbidity but remains understudied. Materials & methods: We sought to assess the rates of testing and incidence of GAS pharyngitis in Calgary, Alberta based on age and sex. Results: A total of 1,074,154 tests were analyzed (58.8% female, mean age 24.8 years) of which 16.6% were positive. Age-standardized testing and positivity was greatest in the 5-14 years age group and lowest in persons over 75 years. Females had greater rates of testing and positivity throughout. Testing rates (incidence rate ratios: 1.40, 95% CI: 1.39-1.41) and case rates (incidence rate ratios: 1.36, 95% CI: 1.33-1.39) increased over time. Conclusion: Future studies should focus on evaluating disparities in testing and treatment outcomes to optimize the approach to this infection.

Background: Healthcare systems generate substantial carbon footprints that may be targeted to decrease greenhouse gas emissions. Outreach clinics may represent tools to assist in this reduction by optimizing patient related travel. Therefore, we sought to estimate the carbon footprint savings associated with a head and neck surgery outreach clinic., Methods: This study was a cross-sectional survey of patient travel patterns to a surgical outreach clinic compared to a regional cancer treatment centre from December 2019 to February 2020. Participants completed a self-administered survey of 12 items eliciting travel distance, vehicle details, and ability to combine medical appointments. Canadian datasets of manufacturer provided vehicular efficiency were used to estimate carbon emissions for each participant. Geographic information systems were used for analyses., Results: One hundred thirteen patients were included for analysis. The majority of patients (85.8%) used their own personal vehicle to travel to the outreach clinic. The median distance to the clinic and regional centre were 29.0 km (IQR 6.0-51.9) and 327.0 km (IQR 309.0-337.0) respectively. The mean carbon emission reduction per person was therefore 117,495.4 g (SD: 29,040.0) to 143,570.9 g (SD: 40,236.0). This represents up to 2.5% of an average individual's yearly carbon footprint. Fewer than 10% of patients indicated they were able to carpool or group their appointments., Conclusion: Surgical outreach clinics decrease carbon footprints associated with patient travel compared to continued care at a regional centre. Further research is needed to determine possible interventions to further reduce carbon emissions associated with the surgical care of patients.

Objectives: Antipsychotic medications are often used for the first-line management of behavioral and psychological symptoms of dementia (BPSD) contrary to guideline recommendations. The Optimizing Practices, Use, Care and Services-Antipsychotics (OPUS-AP) strategy aims to improve the well-being of long-term care (LTC) residents with major neurocognitive disorder (MNCD) by implementing a resident-centered approach, nonpharmacologic interventions, and antipsychotic deprescribing in inappropriate indications., Design: Prospective, closed cohort supplemented by a developmental evaluation., Setting and Participants: Residents of designated wards in 24 LTC centers in Québec, Canada., Methods: Provincial guidelines were disseminated, followed by the implementation of an integrated knowledge translation and mobilization strategy, including training, coaching, clinical tools, evaluation of clinical practices, and a change management strategy. Antipsychotic, benzodiazepine, and antidepressant prescriptions; BPSD; and falls were evaluated every 3 months, for 9 months, from January to October 2018. Semistructured interviews (n = 20) were conducted with LTC teams to evaluate the implementation of OPUS-AP., Results: Of 1054 residents, 78.3% had an MNCD diagnosis and 51.7% an antipsychotic prescription. The cohort included 464 residents with both MNCD and antipsychotic prescription. Antipsychotic deprescribing (cessation or dose decrease) was attempted in 220 of the 344 residents still admitted at 9 months. Complete cessation was observed in 116 of these residents (52.7%) and dose reduction in 72 (32.7%), for a total of 188 residents (85.5%; 95% confidence interval: 80.1%, 89.8%). A decrease in benzodiazepine prescriptions and improvements in Cohen-Mansfield Agitation Inventory scores were observed among residents who had their antipsychotics deprescribed. Caregivers and clinicians expressed satisfaction as a result of observing an improved quality of life among residents., Conclusions and Implications: Antipsychotic deprescribing was successful in a vast majority of LTC residents with MNCD without worsening of BPSD. Based on this success, phase 2 of OPUS-AP is now under way in 129 LTC centers in Québec., (Copyright © 2019 AMDA – The Society for Post-Acute and Long-Term Care Medicine. Published by Elsevier Inc. All rights reserved.)

Background: Understanding the complex interaction of risk factors that increase the likelihood of developing common diseases is challenging. The Canadian Partnership for Tomorrow Project (CPTP) is a prospective cohort study created as a population-health research platform for assessing the effect of genetics, behaviour, family health history and environment (among other factors) on chronic diseases., Methods: Volunteer participants were recruited from the general Canadian population for a confederation of 5 regional cohorts. Participants were enrolled in the study and core information obtained using 2 approaches: attendance at a study assessment centre for all study measures (questionnaire, venous blood sample and physical measurements) or completion of the core questionnaire (online or paper), with later collection of other study measures where possible. Physical measurements included height, weight, percentage body fat and blood pressure. Participants consented to passive follow-up through linkage with administrative health databases and active follow-up through recontact. All participant data across the 5 regional cohorts were harmonized., Results: A total of 307 017 participants aged 30-74 from 8 provinces were recruited. More than half provided a venous blood sample and/or other biological sample, and 33% completed physical measurements. A total of 709 harmonized variables were created; almost 25% are available for all participants and 60% for at least 220 000 participants., Interpretation: Primary recruitment for the CPTP is complete, and data and biosamples are available to Canadian and international researchers through a data-access process. The CPTP will support research into how modifiable risk factors, genetics and the environment interact to affect the development of cancer and other chronic diseases, ultimately contributing evidence to reduce the global burden of chronic disease., Competing Interests: Competing interests: Trevor Dummer reports grants from the Canadian Partnership Against Cancer during the conduct of the study. Sébastien Jacquemont reports grants from the Canadian Institutes of Health Research, grants from Genome Quebec, funding from the Cable Public Affairs Channel during the conduct of the study, and funding from Novartis and GW Pharmaceuticals outside the submitted work. Treena McDonald reports grants from Canadian Partnership Against Cancer during the conduct of the study. Paula Robson reports grants from the Alberta Cancer Foundation, grants from Government of Alberta via the Alberta Cancer Prevention Legacy Fund, grants from Alberta Innovates — Health Solutions via the Alberta Cancer Prevention Legacy Fund and grants from Canadian Partnership Against Cancer during the conduct of the study. Ma’n Zawati reports grants from Canadian Partnership Against Cancer during the conduct of the study., (© 2018 Joule Inc. or its licensors.)

Asthma, atopy, and related phenotypes are heterogeneous complex traits, with both genetic and environmental risk factors. Extensive research has been conducted and over hundred genes have been associated with asthma and atopy phenotypes, but many of these findings have failed to replicate in subsequent studies. To separate true associations from false positives, candidate genes need to be examined in large well-characterized samples, using standardized designs (genotyping, phenotyping and analysis). In an attempt to replicate previous associations we amalgamated the power and resources of four studies and genotyped 5,565 individuals to conduct a genetic association study of 93 previously associated candidate genes for asthma and related phenotypes using the same set of 861 single-nucleotide polymorphisms (SNPs), a common genotyping platform, and relatively harmonized phenotypes. We tested for association between SNPs and the dichotomous outcomes of asthma, atopy, atopic asthma, and airway hyperresponsiveness using a general allelic likelihood ratio test. No SNP in any gene reached significance levels that survived correction for all tested SNPs, phenotypes, and genes. Even after relaxing the usual stringent multiple testing corrections by performing a gene-based analysis (one gene at a time as if no other genes were typed) and by stratifying SNPs based on their prior evidence of association, no genes gave strong evidence of replication. There was weak evidence to implicate the following: IL13, IFNGR2, EDN1, and VDR in asthma; IL18, TBXA2R, IFNGR2, and VDR in atopy; TLR9, TBXA2R, VDR, NOD2, and STAT6 in airway hyperresponsiveness; TLR10, IFNGR2, STAT6, VDR, and NPSR1 in atopic asthma. Additionally we found an excess of SNPs with small effect sizes (OR < 1.4). The low rate of replication may be due to small effect size, differences in phenotypic definition, differential environmental effects, and/or genetic heterogeneity. To aid in future replication studies of asthma genes a comprehensive database was compiled and is available to the scientific community at http://genapha.icapture.ubc.ca/.