Browsing by Subject "Vascular Diseases"
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Item Abnormal vasoactive states(1967-01-26) Smiley, J. DonaldItem The cutaneous and visceral manifestations of systemic necrotizing vasculitis(1976-09-09) Gilliam, James N.Item Donald W. Seldin, M.D., Research Symposium finalist presentations(2023-05-05) Eleazu, Ijeoma; Ramos, Lisandro Maya; Salcedo Betancourt, Juan; Singh, Sumitabh; Smith, AaronThis edition of the UT Southwestern Internal Medicine Grand Rounds features presentations by the six Foster Fellows selected as finalists from the Eighth Annual Donald W. Seldin, M.D. Research Symposium, which was held on April 28, 2023. These Foster Fellows presented work that spanned the breadth and depth of scholarly activity across the department, and at the close of Grand Rounds, one will be selected as the 2023 Seldin Scholar, in honor of Dr. Donald W. Seldin. The Grand Rounds presentation includes additional award presentations recognizing Clinical Vignettes, as well as the Award for Research in Quality of Care and Education at Parkland Hospital, the Social Impact Award, and the Award for Basic Science (non-GME).Item The link between homocysteine and vascular disease(1996-04-18) Hobbs, Helen H.Item Molecular Basis of HDL-Mediated Endothelial Cell Migration and Reendothelialization(2005-12-20) Seetharam, Divya; Shaul, Philip W.Vascular disease risk is inversely related to circulating levels of high density lipoprotein (HDL) cholesterol. The atheroprotective nature of HDL is attributed mainly to its role in reverse cholesterol transport (RCT). However, recent reports of human and animal studies have suggested that the atheroprotective nature of HDL is not sufficiently explained by RCT. Therefore, the mechanisms by which HDL provides vascular protection are unclear. The disruption of endothelial monolayer integrity is an important contributing factor in multiple vascular disorders, and vascular lesion severity is tempered by enhanced endothelial repair. In these studies we show that HDL stimulates endothelial cell migration in vitro in a nitric oxide-independent manner via scavenger receptor B type I (SR-BI)-mediated activation of Rac GTPase. This process does not require HDL cargo molecules, and it is dependent on the activation of Src kinases, phosphatidylinositol 3-kinase, and p44/42 mitogen-activated protein kinases. Rapid initial stimulation of lamellipodia formation by HDL via SR-BI, Src kinases and Rac is also demonstrable. Paralleling the in vitro findings, carotid artery reendothelialization following perivascular electric injury is blunted in apolipoprotein A-I null (apoA-I-/-) mice, and reconstitution of apoA-I expression rescues normal reendothelialization. Furthermore, reendothelialization is impaired in SR-BI-/- mice. Thus, HDL stimulates endothelial cell migration via SR-BI-initiated activation of Rac GTPase, and HDL and SR-BI promote reendothelialization in vivo, revealing that signaling by the HDL-SR-BI tandem has a potent beneficial impact on the cardiovascular system.Item [News](1988-05-21) Rutherford, SusanItem Peripheral vascular disease: missed opportunity for cardiovascular intervention(2012-01-27) Banerjee, SubhashItem Systemic allergic vasculitis(1971-11-04) Smiley, J. DonaldItem [UT Southwestern Medical Center News](2010-06-23) Shear, Kristen HollandItem Vascular occlusion in sickle cell disease: patho-physiology and management(1995-02-23) Rutherford, Cynthia J.