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    <title>Cannon, Barbara (Physiology (Wenner-Gren Institute))</title>
    <link>http://su.avedas.com/converis/ws/public/feed/simple/rss/Person/469/Contract</link>
    <description>Cannon, Barbara (Physiology (Wenner-Gren Institute))</description>
    <pubDate>Thu, 16 May 2013 02:03:13 GMT</pubDate>
    <dc:date>2013-05-16T02:03:13Z</dc:date>
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      <title>Adipokines as Drug Targets to Combat Adverse Effects of Excess Adipose Tissue</title>
      <link>http://su.avedas.com/converis/contract/267</link>
      <description>Obesity represents the major risk factor for the cardiometabolic syndrome, which is an epidemic disease that generates a severe global socio-economic burden for the public health systems. Enhanced production of proinflammatory adipocytokines by expanded adipose tissue is now considered as a key event in the pathogenesis of this syndrome. This process involves i) the systemic release of adipokines, preferentially by visceral abdominal fat and ii) the paracrine, adipokine-mediated crosstalk between periorganic fat and different organs including skeletal and cardiac muscle. Members of the ADAPT consortium have pioneered this novel view of adipose tissue as an active endocrine organ. However, there is very limited knowledge if adipokines and their downstream signalling pathways may represent &amp;ldquo;drugable&amp;rdquo; targets potentially opening new avenues to combat the devastating complications linked to obesity and the cardiometabolic syndrome. Therefore, the major goal of this project is to identify novel or existing adipocytokines as drug targets that could be used to reverse obesity-associated inflammation and adverse reactions related to excess fat, as outlined in the work programme. For this purpose the mustidisciplinary ADAPT consortium has been formed which integrates basic and clinical science, bioinformatics, in silico drug design and the specific expertise of a large pharmaceutical company. To reach the objectives, a stepwise strategy will be used including i) the identification of novel adipocytokines and the cellular sources and regulation of adipokine production ii) the analysis of intraorgan crosstalk within adipose tissue which plays a pivotal role in adipose tissue inflammation iii) the assessment of interorgan crosstalk with a focus on skeletal and cardiac muscle and the role of brown fat and iv) the pharmacological and clinical evaluation of adipokines as drug targets and potential biomarkers.</description>
      <pubDate>Tue, 08 Dec 2009 14:49:29 GMT</pubDate>
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      <dc:creator>Barbara Cannon</dc:creator>
      <dc:date>2009-12-08T14:49:29Z</dc:date>
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    <item>
      <title>The physiology of thermogenesis: acute and adaptive processes in brown adipose tissue</title>
      <link>http://su.avedas.com/converis/contract/3013</link>
      <description>Brown adipose tissue is an organ unique to mammals, and is responsible for nonshivering thermogenesis. Central to an understanding of thermogenesis is an understanding of the mitochondrial uncoupling protein UCP1; regulation of its activity will be examined in-vitro and in knock-in mice with mutations in reintroduced UCP1. We have characterized the developmental determination of brown versus white adipocytes by microarray analyses and shown that brown preadipocytes unexpectedly express myogenic transcription factors, showing for the first time that the cells constitute separate lineages. These analyses also indicate a role for hitherto uncharacterised proteins in the control of cell differentiation. We have identified a novel isoform of the transcription factor PPARg, associated with the occurrence of the brown phenotype and its the function will be investigated. The physiological significance of brown adipose tissue will be determined using several animal models (e.g. UCP1-ablated mice); the phenomena analysed will include UCP1-dependent and -independent NE-induced thermogenesis, stress fever and classical fever. Particularly, the role of the tissue in the control of energy balance will be analysed; such investigations have special interest as evidence is accumulating that brown adipose tissue, in addition to being important for survival of smaller mammals (including human newborns) exposed to cold, may also be active in adult humans and thus affect their energy balance.</description>
      <pubDate>Sat, 22 May 2010 02:02:40 GMT</pubDate>
      <guid isPermaLink="false">http://su.avedas.com/converis/contract/3013</guid>
      <dc:creator>Barbara Cannon</dc:creator>
      <dc:date>2010-05-22T02:02:40Z</dc:date>
    </item>
    <item>
      <title>Brown adipose tissue and human obesity</title>
      <link>http://su.avedas.com/converis/contract/3595</link>
      <pubDate>Sun, 29 Aug 2010 02:00:50 GMT</pubDate>
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      <dc:creator>Barbara Cannon</dc:creator>
      <dc:date>2010-08-29T02:00:50Z</dc:date>
    </item>
    <item>
      <title>Recruitment and activation of brown adipocytes as preventive and curative therapy for type 2 diabetes</title>
      <link>http://su.avedas.com/converis/contract/4805</link>
      <description>The DIABAT project will employ knowledge of the function, dysfunction and physiological regulation of brown adipocytes to develop innovative therapeutic and preventive strategies for type 2 diabetes. Brown adipose tissue (BAT) is currently a worldwide recognized target to combat obesity and diabetes due to last year's re-discovery of functional BAT in adult humans by several of the members of the DIABAT network (van Marken LIchtenbelt et al., N. Engl. J. Med. 360, 1500, 2009; Virtanen, Enerback &amp;amp; Nuutila, N. Engl. J. Med. 360, 1518, 2009) along with sharp rise in insight in cellular, genetic, and regulatory mechanisms from animal studies. Therefore, the DIABAT project aims at recruiting and re-activating endogenous energy-dissipating BAT as a preventive and/or remedial measure for weight and blood sugar control in obesity-related type 2 diabetes (diabesity), thereby halting or preventing destruction and facilitating recovery of pancreatic beta-cells under diabetic conditions.</description>
      <pubDate>Sun, 04 Dec 2011 03:29:14 GMT</pubDate>
      <guid isPermaLink="false">http://su.avedas.com/converis/contract/4805</guid>
      <dc:creator>Barbara Cannon</dc:creator>
      <dc:date>2011-12-04T03:29:14Z</dc:date>
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