{"id":{"repo_id":"bu","oai_identifier":"oai:open.bu.edu:2144/32698"},"canonical_url":"https://search.dev.ndltd.org/etd/bu/oai:open.bu.edu:2144/32698","repository":{"repo_id":"bu","name":"Boston University","base_url":"https://open.bu.edu/oai/request"},"display":{"title":"Resolvin E1 actions on polymorphonuclear neutrophils in diabetes","abstract":"Diabetes and periodontal disease exhibit a bidirectional relationship centered on an enhanced inflammatory response manifested both locally and systemically. The observation that hyperglycemia by itself, in the absence of additional inflammatory signals, promotes a proinflammatory environment indicates that diabetes is an independent risk factor for periodontal disease. Leukocyte pre-activation or priming in diabetes has been demonstrated. Excessive ROS release by leukocytes, upregulation of pro-inflammatory mediators and adhesion molecules are characteristic to T2DM-associated low-grade inflammation. However, the mechanisms by which chronic hyperglycemia leads to leukocyte activation are not fully understood. [TRUNCATED]","abstract_html":"Diabetes and periodontal disease exhibit a bidirectional relationship centered on an enhanced inflammatory response manifested both locally and systemically. The observation that hyperglycemia by itself, in the absence of additional inflammatory signals, promotes a proinflammatory environment indicates that diabetes is an independent risk factor for periodontal disease. Leukocyte pre-activation or priming in diabetes has been demonstrated. Excessive ROS release by leukocytes, upregulation of pro-inflammatory mediators and adhesion molecules are characteristic to T2DM-associated low-grade inflammation. However, the mechanisms by which chronic hyperglycemia leads to leukocyte activation are not fully understood. 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Excessive ROS release by leukocytes, upregulation of pro-inflammatory mediators and adhesion molecules are characteristic to T2DM-associated low-grade inflammation. However, the mechanisms by which chronic hyperglycemia leads to leukocyte activation are not fully understood. [TRUNCATED]"]},{"key":"dc:title","label":"Title","values":["Resolvin E1 actions on polymorphonuclear neutrophils in diabetes"]}]}],"canonical_facts":{"dc:creator":["Sima, Corneliu"],"dc:date.accessioned":["2018-11-27T16:25:08Z"],"dc:date.available":["2018-11-27T16:25:08Z"],"dc:date.issued":["2010"],"dc:description":["Dissertation (DScD) -- Boston University, Henry M. Goldman School of Dental Medicine, 2010 (Department of Periodontology and Oral Biology)."],"dc:description.abstract":["Diabetes and periodontal disease exhibit a bidirectional relationship centered on an enhanced inflammatory response manifested both locally and systemically. The observation that hyperglycemia by itself, in the absence of additional inflammatory signals, promotes a proinflammatory environment indicates that diabetes is an independent risk factor for periodontal disease. Leukocyte pre-activation or priming in diabetes has been demonstrated. Excessive ROS release by leukocytes, upregulation of pro-inflammatory mediators and adhesion molecules are characteristic to T2DM-associated low-grade inflammation. However, the mechanisms by which chronic hyperglycemia leads to leukocyte activation are not fully understood. [TRUNCATED]"],"dc:identifier.uri":["https://hdl.handle.net/2144/32698"],"dc:language.iso":["en_US"],"dc:publisher":["Boston University"],"dc:rights":["This work is being made available in OpenBU by permission of its author, and is available for research purposes only. 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