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dc.contributor.supervisor McNicol, Archibald (Oral Biology) en
dc.contributor.author Abdulrehman, Ahmed Y.
dc.date.accessioned 2010-12-13T19:31:03Z
dc.date.available 2010-12-13T19:31:03Z
dc.date.issued 2010-12-13T19:31:03Z
dc.identifier.uri http://hdl.handle.net/1993/4300
dc.description.abstract There is increasing evidence suggesting the contribution of bacterial infections in atherothrombotic conditions. Studies have demonstrated that bacteria residing within the oral cavity activate platelets once they enter circulation. S. sanguis 2017-78 is capable of stimulating platelet aggregation in a thromboxane-dependent manner. In the present study, the signaling events associated with S. sanguis have been studied further. S. sanguis 2017-78 caused the phosphorylation of p38 MAP kinase and subsequently cPLA2. The p38 MAP kinase inhibitor, SB203580 inhibited S. sanguis 2017-78-induced platelet aggregation as well as the phosphorylation of both p38 MAP kinase and cPLA2. These data are consistent with cPLA2 as a physiological target of p38. A second component of the study examined the effects of aspirin, a known inhibitor of cyclooxygenase, on these signalling pathways. en
dc.format.extent 1056655 bytes
dc.format.mimetype application/pdf
dc.language.iso en_US
dc.subject platelet en
dc.subject Streptococcus en
dc.subject cell en
dc.subject blood en
dc.title Platelet GPIb and downstream activation by S. sanguis en
dc.degree.discipline Oral Biology en
dc.contributor.examiningcommittee Chelikani, Prashen (Oral Biology) Scott, James Elliott (Oral Biology) Hatch, Grant (Pharmacology/Biochemistry & Medical Genetics) en
dc.degree.level Master of Science (M.Sc.) en
dc.description.note February 2011 en


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