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Language barriers (LB) contribute to coronavirus disease 2019 (COVID-19) health inequities. People with LB were more likely to be SARS-CoV-2 positive despite lower testing and had higher rates of hospitalization. Data on hospital outcomes among immigrants with LB, however, are limited. We aimed to investigate the clinical outcomes of hospitalized COVID-19 cases by LB, immigration status, ethnicity, and access to COVID-19 health information and services prior to admission. Adults with laboratory-confirmed community-acquired COVID-19 hospitalized from March 1 to June 30, 2020, at four tertiary-care hospitals in Montréal, Quebec, Canada were included. Demographics, comorbidities, immigration status, country of birth, ethnicity, presence of LB, and hospital outcomes (ICU admission and death) were obtained through a chart review. Additional socio-economic and access to care questions were obtained through a phone survey. A Fine-Gray competing risk subdistribution hazards model was used to estimate the risk of ICU admission and in-hospital death by immigrant status, region of birth and LB Among 1093 patients, 622 (56.9%) were immigrants and 101 (16.2%) of them had a LB. One third (36%) of immigrants with LB did not have access to an interpreter during hospitalization. Admission to ICU and in-hospital mortality were not significantly different between groups. Prior to admission, one third (14/41) of immigrants with LB had difficulties accessing COVID-19 information in their mother tongue and one third (9/27) of non-white immigrants with a LB had difficulties accessing COVID-19 services. Immigrants with LB were inequitably affected by the first wave of the pandemic in Quebec, Canada. In our study, a large proportion had difficulties accessing information and services related to COVID-19 prior to admission, which may have increased SARS-CoV-2 exposure and hospitalizations. After hospitalization, a large proportion did not have access to interpreters. Providing medical information and care in the language of preference of increasing diverse populations in Canada is important for promoting health equity. [ABSTRACT FROM AUTHOR]

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Background: Although the typical inheritance of spastic paraplegia 7 is recessive, several reports have suggested that SPG7 variants may also cause autosomal dominant hereditary spastic paraplegia (HSP)., Objectives: We aimed to conduct an exome-wide genetic analysis on a large Canadian cohort of HSP patients and controls to examine the association of SPG7 and HSP., Methods: We analyzed 585 HSP patients from 372 families and 1175 controls, including 580 unrelated individuals. Whole-exome sequencing was performed on 400 HSP patients (291 index cases) and all 1175 controls., Results: The frequency of heterozygous pathogenic/likely pathogenic SPG7 variants (4.8%) among unrelated HSP patients was higher than among unrelated controls (1.7%; OR 2.88, 95% CI 1.24-6.66, P = 0.009). The heterozygous SPG7 p.(Ala510Val) variant was found in 3.7% of index patients versus 0.85% in unrelated controls (OR 4.42, 95% CI 1.49-13.07, P = 0.005). Similar results were obtained after including only genetically-undiagnosed patients. We identified four heterozygous SPG7 variant carriers with an additional pathogenic variant in known HSP genes, compared to zero in controls (OR 19.58, 95% CI 1.05-365.13, P = 0.0031), indicating potential digenic inheritance. We further identified four families with heterozygous variants in SPG7 and SPG7-interacting genes (CACNA1A, AFG3L2, and MORC2). Of these, there is especially compelling evidence for epistasis between SPG7 and AFG3L2. The p.(Ile705Thr) variant in AFG3L2 is located at the interface between hexamer subunits, in a hotspot of mutations associated with spinocerebellar ataxia type 28 that affect its proteolytic function., Conclusions: Our results provide evidence for complex inheritance in SPG7-associated HSP, which may include recessive and possibly dominant and digenic/epistasis forms of inheritance. © 2021 International Parkinson and Movement Disorder Society., (© 2021 International Parkinson and Movement Disorder Society.)

Background: Evidence for the impact of the food retailing environment on food-related and obesity outcomes remains equivocal, but only a few studies have attempted to identify sub-populations for whom this relationship might be stronger than others. Genetic polymorphisms related to dopamine signalling have been associated with differences in responses to rewards such as food and may be candidate markers to identify such sub-populations. This study sought to investigate whether genetic variation of the dopamine D4 receptor gene (DRD4 exon III 48 bp VNTR polymorphism) moderated the association between local exposure to food retailers on BMI and diet in a sample of 4 to12-year-old children., Methods: Data collected from a birth cohort and a community cross-sectional study conducted in Montreal, Canada, were combined to provide DRD4 VNTR polymorphism data in terms of presence of the 7-repeat allele (DRD4-7R) for 322 children aged between 4 and 12 (M (SD): 6.8(2.8) y). Outcomes were Body Mass Index (BMI) for age and energy density derived from a Food Frequency Questionnaire. Food environment was expressed as the proportion of local food retailers classified as healthful within 3 km of participants' residence. Linear regression models adjusted for age, sex, income, cohort, and geographic clustering were used to test gene*environment interactions., Results: A significant gene*food environment interaction was found for energy density with results indicating that DRD4-7R carriers had more energy dense diets than non-carriers, with this effect being more pronounced in children living in areas with proportionally more unhealthy food retailers. No evidence of main or interactive effects of DRD4 VNTR and food environment was found for BMI., Conclusions: Results of the present study suggest that a genetic marker related to dopamine pathways can identify children with potentially greater responsiveness to unhealthy local food environment. Future studies should investigate additional elements of the food environment and test whether results hold across different populations.

Research on eating behaviour has identified several potentially relevant eating-related traits captured by different questionnaires. Often, these questionnaires predict Body Mass Index (BMI), but the relationship between them has not been explicitly studied. We studied the unity and diversity of questionnaires capturing five common eating-related traits: Power of Food, Eating Impulsivity, emotional eating, Disinhibition, and binge eating in women from Estonia (n = 740) and Canada (n = 456). Using bifactor analysis, we showed that a) these questionnaires are largely explained by a single factor, and b) relative to this shared factor, only some questionnaires offered additional variance in predicting BMI. Hence, these questionnaires seemed to characterise a common factor, which we label Uncontrolled Eating. Item Response Theory techniques were then applied to demonstrate that c) within this common factor, the questionnaires could be placed on a continuum of Uncontrolled Eating. That is, Eating Impulsivity focused on the milder degree, Power of Food Scale, emotional eating scales, and Disinhibition on intermediate degrees, and the Binge Eating Scale on the most severe degrees of Uncontrolled Eating. In sum, evidence from two samples showed that questionnaires capturing five common BMI-related traits largely reflected the same underlying latent trait - Uncontrolled Eating. In Estonia, some questionnaires focused on different severities of this common construct, supporting a continuum model of Uncontrolled Eating. These findings provide a starting point for developing better questionnaires of the neurobehavioural correlates of obesity, and provide a unifying perspective from which to view the existing literature. R scripts and data used for the analysis are provided., (Copyright © 2015 Elsevier Ltd. All rights reserved.)