University of Kansas

About: University of Kansas is a education organization based out in Lawrence, Kansas, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 38183 authors who have published 81381 publications receiving 2986312 citations. The organization is also known as: KU & Univ of Kansas.

Uses and requirements of ecological niche models and related distributional models

Abstract: Modeling approaches that relate known occurrences of species to landscape features to discover ecological properties and predict geographic occurrences have seen extensive recent application in ecology, systematics, and conservation. A key component in this process is estimation or characterization of species' distributions in ecological space, which can then be useful in understanding their potential distributions in geographic space. Hence, this process is often termed ecological niche modeling or (less boldly) species distribution modeling. Applications of this approach vary widely in their aims, products, and requirements; this variety is reviewed herein, examples are provided, and differences in data needs and possible interpretations are discussed.

Rebels with a Cause: Group Identification as a Response to Perceived Discrimination from the Mainstream

Abstract: Two studies involving people with body piercings tested the hypothesis that perceived discrimination increases group identification. In Study 1, group identification mediated the positive relationship between perceived discrimination and attempts to differentiate the ingroup from the mainstream. In Study 2, perceived discrimination against people with body piercings was manipulated and was found to increase group identification. Support was found for the prediction that group identification mediates the relation-ship between perceptions of discrimination and collective self-esteem. Results demonstrate the importance of group identification for both the meaning of group membership and its consequences for well-being among members of disadvantaged groups.

Viral and therapeutic control of IFN-β promoter stimulator 1 during hepatitis C virus infection

Abstract: Viral signaling through retinoic acid-inducible gene-I (RIG-I) and its adaptor protein, IFN promoter-stimulator 1 (IPS-1), activates IFN regulatory factor-3 (IRF-3) and the host IFN-α/β response that limits virus infection. The hepatitis C virus (HCV) NS3/4A protease cleaves IPS-1 to block RIG-I signaling, but how this regulation controls the host response to HCV is not known. Moreover, endogenous IPS-1 cleavage has not been demonstrated in the context of HCV infection in vitro or in vivo. Here, we show that HCV infection transiently induces RIG-I- and IPS-1-dependent IRF-3 activation. This host response limits HCV production and constrains cellular permissiveness to infection. However, HCV disrupts this response early in infection by NS3/4A cleavage of IPS-1 at C508, releasing IPS-1 from the mitochondrial membrane. Cleavage results in subcellular redistribution of IPS-1 and loss of interaction with RIG-I, thereby preventing downstream activation of IRF-3 and IFN-β induction. Liver tissues from chronically infected patients similarly demonstrate subcellular redistribution of IPS-1 in infected hepatocytes and IPS-1 cleavage associated with a lack of ISG15 expression and conjugation of target proteins in vivo. Importantly, small-molecule inhibitors of NS3/4A prevent cleavage and restore RIG-I signaling of IFN-β induction. Our results suggest a dynamic model in which early activation of IRF-3 and induction of antiviral genes are reversed by IPS-1 proteolysis and abrogation of RIG-I signaling as NS3/4A accumulates in newly infected cells. HCV protease inhibitors effectively prevent IPS-1 proteolysis, suggesting they may be capable of restoring this innate host response in clinical practice.

Endocrine functions of bone in mineral metabolism regulation

Abstract: Given the dramatic increase in skeletal size during growth, the need to preserve skeletal mass during adulthood, and the large capacity of bone to store calcium and phosphate, juxtaposed with the essential role of phosphate in energy metabolism and the adverse effects of hyperphosphatemia, it is not surprising that a complex systems biology has evolved that permits cross-talk between bone and other organs to adjust phosphate balance and bone mineralization in response to changing physiological requirements. This review examines the newly discovered signaling pathways involved in the endocrine functions of bone, such as those mediated by the phosphaturic and 1,25(OH)2D-regulating hormone FGF23, and the broader systemic effects associated with abnormalities of calcium and phosphate homeostasis.