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dc.contributor.authorSima, Corneliuen_US
dc.date.accessioned2018-11-27T16:25:08Z
dc.date.available2018-11-27T16:25:08Z
dc.date.issued2010
dc.identifier.urihttps://hdl.handle.net/2144/32698
dc.descriptionDissertation (DScD) -- Boston University, Henry M. Goldman School of Dental Medicine, 2010 (Department of Periodontology and Oral Biology).en_US
dc.description.abstractDiabetes 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]en_US
dc.language.isoen_US
dc.publisherBoston Universityen_US
dc.rightsThis work is being made available in OpenBU by permission of its author, and is available for research purposes only. All rights are reserved to the author.en_US
dc.subjectEicosapentaenoic aciden_US
dc.subjectPeriodontal diseasesen_US
dc.subjectNeutrophilsen_US
dc.subjectHyperglycemiaen_US
dc.subjectMiceen_US
dc.titleResolvin E1 actions on polymorphonuclear neutrophils in diabetesen_US
dc.typeThesis/Dissertationen_US
etd.degree.nameDoctor of Science in Dentistryen_US
etd.degree.leveldoctoralen_US
etd.degree.disciplinePeriodontology and Oral Biologyen_US
etd.degree.grantorBoston Universityen_US
dc.identifier.mmsid99186225230001161


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