291 research outputs found

    Movement and habitat use of two aquatic turtles (\u3cem\u3eGraptemys geographic\u3c/em\u3e and \u3cem\u3eTrachemys scripta\u3c/em\u3e) in an urban landscape

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    Our study focuses on the spatial ecology and seasonal habitat use of two aquatic turtles in order to understand the manner in which upland habitat use by humans shapes the aquatic activity, movement, and habitat selection of these species in an urban setting. We used radiotelemetry to follow 15 female Graptemys geographica (common map turtle) and each of ten male and female Trachemys scripta (red-eared slider) living in a man-made canal within a highly urbanized region of Indianapolis, IN, USA. During the active season (between May and September) of 2002, we located 33 of the 35 individuals a total of 934 times and determined the total range of activity, mean movement, and daily movement for each individuals. We also analyzed turtle locations relative to the upland habitat types (commercial, residential, river, road, woodlot, and open) surrounding the canal and determined that the turtles spent a disproportionate amount of time in woodland and commercial habitats and avoided the road-associated portions of the canal. We also located 21 of the turtles during hibernation (February 2003), and determined that an even greater proportion of individuals hibernated in woodland-bordered portions of the canal. Our results clearly indicate that turtle habitat selection is influenced by human activities; sound conservation and management of turtle populations in urban habitats will require the incorporation of spatial ecology and habitat use data

    Bigger is not always better : viability selection on body mass varies across life stages in a hibernating mammal

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    ACKNOWLEDGEMENTS: We would like to express our thanks to all the hard-working marmoteers, across the course of the study, that helped to collect the annual field data. In addition, we would like to specifically thank Kenneth B. Armitage for starting the project and access to the long-term body mass data. This work 431 was supported by an EASTBIO PhD studentship from the Biotechnology and Biological Sciences Research Council (BBSRC) and the University of Aberdeen, which was awarded to A.H.M.J. D.T.B was supported by the National Geographic Society, UCLA (Faculty Senate and the Division of Life Sciences), a Rocky Mountain Biological Laboratory research fellowship, and NSF-IDBR-0754247, DEB435 1119660 and 1557130 (to DTB); and NSF-DBI 0242960, 0731346, and 1262713 (to the RMBL).Peer reviewedPublisher PD

    Predictive control methods to improve energy efficiency and reduce demand in buildings

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    Abstract This paper presents an overview of results and future challenges on temperature control and cost optimization in building energy systems. Control and economic optimization issues are discussed and illustrated through sophisticated simulation examples. The paper concludes with effective results from model predictive control solutions and identification of important directions for future work

    Parameters of Reserpine Analogs That Induce MSH2/MSH6-Dependent Cytotoxic Response

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    Mismatch repair proteins modulate the cytotoxicity of several chemotherapeutic agents. We have recently proposed a “death conformation” of the MutS homologous proteins that is distinguishable from their “repair conformation.” This conformation can be induced by a small molecule, reserpine, leading to DNA-independent cell death. We investigated the parameters for a small reserpine-like molecule that are required to interact with MSH2/MSH6 to induce MSH2/MSH6-dependent cytotoxic response. A multidisciplinary approach involving structural modeling, chemical synthesis, and cell biology analyzed reserpine analogs and modifications. We demonstrate that the parameters controlling the induction of MSH2/MSH6-dependent cytotoxicity for reserpine-analogous molecules reside in the specific requirements for methoxy groups, the size of the molecule, and the orientation of molecules within the protein-binding pocket. Reserpine analog rescinnamine showed improved MSH2-dependent cytotoxicity. These results have important implications for the identification of compounds that require functional MMR proteins to exhibit their full cytotoxicity, which will avoid resistance in MMR-deficient cells

    Bone Marrow Transplantation Augments the Effect of Brain- and Spinal Cord-Directed Adeno-Associated Virus 2/5 Gene Therapy by Altering Inflammation in the Murine Model of Globoid-Cell Leukodystrophy

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    Globoid-cell leukodystrophy (GLD) is an inherited demyelinating disease caused by the deficiency of the lysosomal enzyme galactosylceramidase (GALC). A previous study in the murine model of GLD (twitcher) demonstrated a dramatic synergy between CNS-directed adeno-associated virus 2/5 (AAV2/5) gene therapy and myeloreductive bone marrow transplantation (BMT). However, the mechanism by which these two disparate therapeutic approaches synergize is not clear. In addition, the therapeutic efficacy may have been limited since the CNS-directed gene therapy was restricted to the forebrain and thalamus. In the current study, intrathecal and intracerebellar injections were added to the therapeutic regimen and the mechanism of synergy between BMT and gene therapy was determined. Although AAV2/5 alone provided supraphysiological levels of GALC activity and reduced psychosine levels in both the brain and spinal cord, it significantly increased CNS inflammation. Bone marrow transplantation alone provided essentially no GALC activity to the CNS and did not reduce psychosine levels. When AAV2/5 is combined with BMT, there are sustained improvements in motor function and the median life span is increased to 123 d (range, 92–282 d) compared with 41 d in the untreated twitcher mice. Interestingly, addition of BMT virtually eliminates both the disease and AAV2/5-associated inflammatory response. These data suggest that the efficacy of AAV2/5-mediated gene therapy is limited by the associated inflammatory response and BMT synergizes with AAV2/5 by modulating inflammation
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