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        <datestamp>2023-07-11</datestamp>
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          <dc:contributor>Vimr, Eric R.</dc:contributor>
          <dc:creator>Ringenberg, Michael Alan</dc:creator>
          <dc:date>2015-09-28T16:21:35Z</dc:date>
          <dc:date>2015-09-28T16:21:35Z</dc:date>
          <dc:date>10000-01-01</dc:date>
          <dc:date>2002</dc:date>
          <dc:date>2002</dc:date>
          <dc:description>In this study, adaptation of a previously described in vivo model of neuraminidase-induced glomerular injury is described in the rat. Information derived from the initial pilot studies has been used to formulate the hypothesis that loss of glomerular sialic acid, concomitant with functional glomerular damage, results in a re-sialylation event associated with sequentially increased levels of glomerular linkage-specific sialyltransferase transcript levels and activity. The results of these experiments provide insight into specific molecular responses of podocytes to injury, in addition to demonstrating the versatility of this animal model for descriptive and mechanistic studies regarding podocyte sialobiology.</dc:description>
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  Previous issue date: 2002</dc:description>
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Lift date: Forever
Reason: Restricted to the U of I community idenfinitely during batch ingest of legacy ETDs</dc:description>
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          <dc:identifier>(MiAaPQ)AAI3044208</dc:identifier>
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          <dc:subject>Biology, Animal Physiology</dc:subject>
          <dc:title>Molecular Responses to Desialylation in a Rat Model of Induced Glomerulopathy</dc:title>
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            <department>Veterinary Pathobiology</department>
            <discipline>Veterinary Pathobiology</discipline>
            <grantor>University of Illinois at Urbana-Champaign</grantor>
            <level>Dissertation</level>
            <name>Ph.D.</name>
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