University of British Columbia

About: University of British Columbia is a education organization based out in Vancouver, British Columbia, Canada. It is known for research contribution in the topics: Population & Health care. The organization has 89939 authors who have published 209679 publications receiving 9226862 citations. The organization is also known as: UBC & The University of British Columbia.

Psychopathy as a clinical and empirical construct.

Abstract: In this review, we focus on two major influences on current conceptualizations of psychopathy: one clinical, with its origins largely in the early case studies of Cleckley, and the other empirical, the result of widespread use of the Hare Psychopathy Checklist-Revised (PCL-R) for assessment purposes. Some investigators assert that the PCL-R, ostensibly based on Cleckley’s work, has “drifted” from the construct described in his Clinical Profile. We evaluate this profile, note its basis in an unrepresentative sample of patients, and suggest that its literal and uncritical acceptance by the research community has become problematical. We also argue that the idea of construct “drift” is irrelevant to current conceptualizations of psychopathy, which are better informed by the extensive empirical research on the integration of structural, genetic, developmental, personality, and neurobiological research findings than by rigid adherence to early clinical formulations. We offer some suggestions for future research on psychopathy.

Divergent selection and heterogeneous genomic divergence.

Abstract: Levels of genetic differentiation between populations can be highly variable across the genome, with divergent selection contributing to such heterogeneous genomic divergence. For example, loci under divergent selection and those tightly physically linked to them may exhibit stronger differentiation than neutral regions with weak or no linkage to such loci. Divergent selection can also increase genome-wide neutral differentiation by reducing gene flow (e.g. by causing ecological speciation), thus promoting divergence via the stochastic effects of genetic drift. These consequences of divergent selection are being reported in recently accumulating studies that identify: (i) ‘outlier loci’ with higher levels of divergence than expected under neutrality, and (ii) a positive association between the degree of adaptive phenotypic divergence and levels of molecular genetic differentiation across population pairs [‘isolation by adaptation’ (IBA)]. The latter pattern arises because as adaptive divergence increases, gene flow is reduced (thereby promoting drift) and genetic hitchhiking increased. Here, we review and integrate these previously disconnected concepts and literatures. We find that studies generally report 5–10% of loci to be outliers. These selected regions were often dispersed across the genome, commonly exhibited replicated divergence across different population pairs, and could sometimes be associated with specific ecological variables. IBA was not infrequently observed, even at neutral loci putatively unlinked to those under divergent selection. Overall, we conclude that divergent selection makes diverse contributions to heterogeneous genomic divergence. Nonetheless, the number, size, and distribution of genomic regions affected by selection varied substantially among studies, leading us to discuss the potential role of divergent selection in the growth of regions of differentiation (i.e. genomic islands of divergence), a topic in need of future investigation.

Degradation of glucose-dependent insulinotropic polypeptide and truncated glucagon-like peptide 1 in vitro and in vivo by dipeptidyl peptidase IV

Abstract: The combined actions of glucose-dependent insulinotropic polypeptide (GIP) and truncated glucagon-like peptide-1 (tGLP-1) may fully account for the incretin effect. These hormones are released from the small intestine in response to oral glucose and stimulate insulin release. Recently, evidence has been provided demonstrating the degradation of GIP-(1-42) and GLP-1-(7-36)NH2 by the serum enzyme dipeptidyl peptidase IV (DPP IV) into the biologically inactive products GIP-(3-42) and GLP-1-(9-36)NH2. The objective of the current investigation was to develop a method to monitor the degradation of these hormones in vivo. Synthetic peptides were radiolabeled and purified by HPLC. Subsequent degradation of the peptides under various conditions was then monitored by further HPLC analysis. Incubation of [125I]GIP-(1-42) or [125I]GLP-1-(7-36)NH2 with Wistar rat serum or purified DPP IV resulted in the major N-terminal-truncated products [125I]GIP-(3-42) and [125I]GLP-1-(9-36)NH2. These products were significantly r...