{"id":{"repo_id":"uiuc","oai_identifier":"oai:www.ideals.illinois.edu:2142/87620"},"canonical_url":"https://search.dev.ndltd.org/etd/uiuc/oai:www.ideals.illinois.edu:2142/87620","repository":{"repo_id":"uiuc","name":"University of Illinois - Urbana-Champaign","base_url":"https://www.ideals.illinois.edu/oai-pmh"},"display":{"title":"Molecular Responses to Desialylation in a Rat Model of Induced Glomerulopathy","abstract":"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. 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