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Full-Text Articles in Medicine and Health Sciences

Gout, Lorrie Listebarger Jul 2015

Gout, Lorrie Listebarger

Nursing Student Class Projects (Formerly MSN)

Gout is a syndrome caused by an inflammatory response creating an over production of uric acid increasing uric acid levels in the blood and body fluids. Gout is defined as a disorder resulting from tissue deposition of MSU crystals (in joints, bursae, bone, and certain other soft tissues, such as ligaments, tendons and occasionally, skin) and/or crystallization of uric acid within the renal collecting system (tubules and renal pelvis) that typically occurs in acid urine” (Terkeltaub & Edwards, 2013, p. 20). Gout is among the oldest diseases affecting approximately 3.9% of adults in America (Terkeltaub & Edwards, 2013, p. xv). …


Timp3 Regulation Of Macrophage Activation And Apoptosis, Michael S. Brock Apr 2015

Timp3 Regulation Of Macrophage Activation And Apoptosis, Michael S. Brock

Electronic Thesis and Dissertation Repository

Acute respiratory distress syndrome (ARDS) is a lung disease involving profound inflammation. Origins of persistent inflammation in select cases of ARDS are poorly understood, and we propose persistent inflammatory macrophages may be one of its mechanisms. Macrophages polarize to either promote inflammation, or suppress inflammation. Tissue inhibitor of metalloproteinases 3 (TIMP3) reduces the pro-inflammatory polarization in macrophages. Additionally, studies have shown TIMP3 promotes apoptosis, and its absence delays recovery from bleomycin-induced lung injury.

We hypothesize that TIMP3 promotes apoptosis of murine macrophages through inhibition of metalloproteinase activity and stabilization of FAS on the cell surface. Pro-inflammatory Timp3-/- bone marrow-derived …


Neuroinflammatory Alterations Via Cd-36 In Traumatic Brain Injury, Diana G. Hernandez-Ontiveros Jan 2015

Neuroinflammatory Alterations Via Cd-36 In Traumatic Brain Injury, Diana G. Hernandez-Ontiveros

USF Tampa Graduate Theses and Dissertations

Traumatic brain injury (TBI) has become an increasingly unmet clinical need due to intense military conflicts worldwide. Directly impacted brain cells suffer massive death, with neighboring cells succumbing to progressive neurodegeneration accompanied by inflammatory and other secondary cell death events. Subsequent neurodegenerative events may extend to normal areas beyond the core of injury, thereby exacerbating the central nervous system’s inflammatory response to TBI. Recently CD-36 (cluster of differentiation 36/fatty acid translocase (FAT), a class B scavenger receptor of modified low-density lipoproteins (mLDLs) in macrophages, has been implicated in lipid metabolism, atherosclerosis, oxidative stress, and tissue injury in cerebral ischemia, and …


The Role Of C-Reactive Protein In Acute Kidney Injury, Melissa A. Pegues Jan 2015

The Role Of C-Reactive Protein In Acute Kidney Injury, Melissa A. Pegues

All ETDs from UAB

Acute kidney injury (AKI), which manifests as an abrupt decline in renal function, occurs in ~1% of all hospitalization. Ischemia reperfusion injury (IRI), a common cause of AKI, can occur in any situation where blood flow to the kidney is significantly reduced such as hypertensive crisis, cardiovascular surgery, and inevitably during renal transplantation. Mortality from AKI is up to 80% due to incomplete knowledge of the pathogenesis of IRI and the lack of an effective therapy. It is thought that cellular damage as a result of hypoxia signals the release of proinflammatory cytokines that lead to a systemic inflammatory response. …


Tumor Necrosis Factor Alpha Converting Enzyme Inhibition During Acute Colitis In Mice: A Regional Analysis, Brian Maddox Jan 2015

Tumor Necrosis Factor Alpha Converting Enzyme Inhibition During Acute Colitis In Mice: A Regional Analysis, Brian Maddox

MSU Graduate Theses

Tumor Necrosis Factor-a Converting Enzyme (TACE) induces active TNFa and may contribute to the development of colitis in humans. I hypothesized that pharmacological blockade of TNFa production would improve colitis scoring through decreased expression of inflammatory biomarkers. Acute colitis was induced in wild type BALB/c mice using 5% dextran sulfate sodium (DSS) in drinking water for 7 days. TACE inhibition was accomplished through twice daily intraperitoneal injection of DPC- 333 (10mg/kg; BSM Inc.) To determine the effects of TACE blockade during colitis, the following experimental groups (n=6-7/group) were tested: 1) vehicle; 2) DPC-333; 3) 5% DSS and vehicle; and 4) …