240 research outputs found

    Deeper Into the Knight: Exploring Deans Knight and Its Effects on the Canadian GAAR

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    This article discusses the most recent decision of the Supreme Court of Canada in Deans Knight Income Corporation v. Canada (2023) and explores its implications for the Canadian GAAR

    Do cognitive processes mediate the relationship between adverse childhood experiences and health related outcomes?

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    Adverse childhood experiences (ACEs) are stressful life events that occur during development. It is well-established that ACE exposure has negative downstream implications for a broad range of health-related behaviors, ultimately hastening mortality. Underlying mechanisms linking the experience of early life adversity with poor health remain less understood, however, and thus potential targets for intervention remain elusive. This work seeks to fill an important theoretical gap in the ACE literature by evaluating whether executive function (EF) constitute a biologically-plausible mediating mechanism in this causal pathway. To do so, two separate studies were conducted. In Study 1, undergraduate students completed measures of ACE exposure, EF, health-risk behaviors (e.g., smoking, drug and alcohol use, unsafe sexual practices), and psychopathology (e.g., anxiety, depression). Multivariate modeling determined that executive dysfunction in daily life mediated the relationship between childhood adversity exposure and current mental health concerns. EF did not mediate the effect between ACEs and health-risk behaviours. Study 2 sought to replicate and extend this work by narrowing the focus of health-risk behaviours to those most relevant for an undergraduate population (i.e., risky alcohol-related behaviours), and incorporating behavioural measures of EF in addition to self-report questionnaires. EF difficulties in daily life, but not on in-lab tasks, mediated the relationship between ACEs and psychopathology symptoms. The relationship between ACEs and risky alcohol use was not mediated by EF. These results partially support a neurodevelopmental model of ACE exposure vis-à-vis future health, focusing on the role of EF

    Impact of topographic internal lee wave drag on an eddying global ocean model

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    Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/116868/1/ocemod_wavedrag_eddystatistics_trossmanetal_2016.pd

    Zoonotic orthopoxviruses encode a high-affinity antagonist of NKG2D

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    NK and T lymphocytes express both activating and inhibiting receptors for various members of the major histocompatibility complex class I superfamily (MHCISF). To evade immunologic cytotoxicity, many viruses interfere with the function of these receptors, generally by altering the displayed profile of MHCISF proteins on host cells. Using a structurally constrained hidden Markov model, we discovered an orthopoxvirus protein, itself distantly class I–like, that acts as a competitive antagonist of the NKG2D activating receptor. This orthopoxvirus MHC class I–like protein (OMCP) is conserved among cowpox and monkeypox viruses, secreted by infected cells, and bound with high affinity by NKG2D of rodents and humans (KD ∼ 30 and 0.2 nM, respectively). OMCP blocks recognition of host-encoded ligands and inhibits NKG2D-dependent killing by NK cells. This finding represents a novel mechanism for viral interference with NKG2D and sheds light on intercellular recognition events underlying innate immunity against emerging orthopoxviruses

    Internal lee wave closures: Parameter sensitivity and comparison to observations

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    This is the final version. Available from AGU via the DOI in this recordThe SOFine and DIMES data analyzed in this paper can be obtained through the British Oceanographic Data Centre (BODC) by navigating the following links, respectively: http://archive.noc.ac.uk/SOFINE/and http://dimes.ucsd.edu/en/data/This paper examines two internal lee wave closures that have been used together with ocean models to predict the time‐averaged global energy conversion rate into lee waves and dissipation rate associated with lee waves and topographic blocking: the Garner (2005) scheme and the Bell (1975) theory. The closure predictions in two Southern Ocean regions where geostrophic flows dominate over tides are examined and compared to microstructure profiler observations of the turbulent kinetic energy dissipation rate, where the latter are assumed to reflect the dissipation associated with topographic blocking and generated lee wave energy. It is shown that when applied to these Southern Ocean regions, the two closures differ most in their treatment of topographic blocking. For several reasons, pointwise validation of the closures is not possible using existing observations, but horizontally averaged comparisons between closure predictions and observations are made. When anisotropy of the underlying topography is accounted for, the two horizontally averaged closure predictions near the seafloor are approximately equal. The dissipation associated with topographic blocking is predicted by the Garner (2005) scheme to account for the majority of the depth‐integrated dissipation over the bottom 1000 m of the water column, where the horizontally averaged predictions lie well within the spatial variability of the horizontally averaged observations. Simplifications made by the Garner (2005) scheme that are inappropriate for the oceanic context, together with imperfect observational information, can partially account for the prediction‐observation disagreement, particularly in the upper water column.D. S. Trossman and B. K. Arbic gratefully acknowledge support from National Science Foundation (NSF) grant OCE‐0960820 and Office of Naval Research (ONR) grant N00014‐11‐1‐0487. S. Waterman gratefully acknowledges support from the Australian Research Council (grants DE120102927 and CE110001028) and the National Science and Engineering Research Council of Canada (grant 22R23085)

    Internal lee wave closures : parameter sensitivity and comparison to observations

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    Author Posting. © American Geophysical Union, 2015. This article is posted here by permission of American Geophysical Union for personal use, not for redistribution. The definitive version was published in Journal of Geophysical Research: Oceans 120 (2015): 7997–8019, doi:10.1002/2015JC010892.This paper examines two internal lee wave closures that have been used together with ocean models to predict the time-averaged global energy conversion rate into lee waves and dissipation rate associated with lee waves and topographic blocking: the Garner (2005) scheme and the Bell (1975) theory. The closure predictions in two Southern Ocean regions where geostrophic flows dominate over tides are examined and compared to microstructure profiler observations of the turbulent kinetic energy dissipation rate, where the latter are assumed to reflect the dissipation associated with topographic blocking and generated lee wave energy. It is shown that when applied to these Southern Ocean regions, the two closures differ most in their treatment of topographic blocking. For several reasons, pointwise validation of the closures is not possible using existing observations, but horizontally averaged comparisons between closure predictions and observations are made. When anisotropy of the underlying topography is accounted for, the two horizontally averaged closure predictions near the seafloor are approximately equal. The dissipation associated with topographic blocking is predicted by the Garner (2005) scheme to account for the majority of the depth-integrated dissipation over the bottom 1000 m of the water column, where the horizontally averaged predictions lie well within the spatial variability of the horizontally averaged observations. Simplifications made by the Garner (2005) scheme that are inappropriate for the oceanic context, together with imperfect observational information, can partially account for the prediction-observation disagreement, particularly in the upper water column.National Science Foundation Grant Number: OCE-0960820; Office of Naval Research (ONR) Grant Number: N00014-11-1-0487; Australian Research Council Grant Number: (DE120102927 and CE110001028); National Science and Engineering Research Council of Canada Grant Number: (22R23085)2016-06-1
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