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Articles 1 - 7 of 7
Full-Text Articles in Medicine and Health Sciences
Mdivi-1, A Mitochondrial Division Inhibitor, Exerts Cardioprotective Effects In Myocardial Ischemia/Reperfusion (Mi/R) When Given At Reperfusion, Devon P. Stutzman
Mdivi-1, A Mitochondrial Division Inhibitor, Exerts Cardioprotective Effects In Myocardial Ischemia/Reperfusion (Mi/R) When Given At Reperfusion, Devon P. Stutzman
PCOM Biomedical Studies Student Scholarship
Acute myocardial infarction (MI) remains a leading cause of morbidity and mortality worldwide. Accompanying MI is myocardial ischemia/reperfusion (MI/R) injury, which results in cardiac contractile dysfunction and additional myocardial cell death. MI/R injury is initiated in part by mitochondrial-derived reactive oxygen species due to mitochondrial membrane potential collapse and uncoupling of the electron transport chain, which may be due to mitochondrial fission in MI/R. Mitochondrial fission is in turn associated with shortening/fragmentation of mitochondria, decreased ATP production, and is thought to promote cardiac contractile dysfunction and post-reperfused cardiomyocyte loss, leading to increased infarct size. Therefore, inhibiting mitochondrial fission may be …
Gp91ds-Tat, A Selective Nadph Oxidase Peptide Inhibitor, Increases Blood Nitric Oxide (No) Bioavailability In Bind Limb Ischemia And Reperfusion (I/R), Sydney Walker, Tyler Galbreath, Qian Chen, Robert J. Barsotti, H. Patel, William Chau, Lindon H. Young
Gp91ds-Tat, A Selective Nadph Oxidase Peptide Inhibitor, Increases Blood Nitric Oxide (No) Bioavailability In Bind Limb Ischemia And Reperfusion (I/R), Sydney Walker, Tyler Galbreath, Qian Chen, Robert J. Barsotti, H. Patel, William Chau, Lindon H. Young
Research Day
I/R injury induces cell death and organ dysfunction in part due to a burst of reactive oxygen species that occurs upon the reintroduction of oxygen into the ischemic area, leading to endothelial dysfunction: decreased blood NO and increased hydrogen peroxide (H2O2 ) levels. We’ve previously shown in isolated rat hearts subjected to I/R injury, gp91ds-tat attenuated cardiac contractile dysfunction and reduced infarct size compared to controls presumably by the inhibition of NADPH oxidase induced superoxide release. Superoxide can quench NO via the formation of peroxynitrite and also be converted to H2O2 in blood. We attempted to confirm this hypothesis using …
Mitoquinone (Mitoq) Exerts Antioxidant Effects Independent Of Mitochondrial Targeted Effects In Phorbol-12-Myristate-13-Acetate (Pma) Or N-Formyl-L-Methiony-L-Leucyl-L-Phenylalanine (Fmlp) Stimulated Polymorphonuclear Leukocyte (Pmn) Superoxide (So) Release, Matthew Lepera, D. Pesikan, J. Voeun, Kerry-Anne Perkins, Qian Chen, Robert J. Barsotti, Lindon H. Young
Mitoquinone (Mitoq) Exerts Antioxidant Effects Independent Of Mitochondrial Targeted Effects In Phorbol-12-Myristate-13-Acetate (Pma) Or N-Formyl-L-Methiony-L-Leucyl-L-Phenylalanine (Fmlp) Stimulated Polymorphonuclear Leukocyte (Pmn) Superoxide (So) Release, Matthew Lepera, D. Pesikan, J. Voeun, Kerry-Anne Perkins, Qian Chen, Robert J. Barsotti, Lindon H. Young
Research Day
MitoQ is a mitochondrial-targeted coenzyme Q antioxidant analog that dose-dependently restored cardiac function and reduced infarct size in isolated perfused rat hearts subjected to ischemia reperfusion (I/R). Moreover, mitoQ also dose-dependently attenuated PMA stimulated PMN superoxide (SO) release at the same concentration (10uM) as the cardioprotective dose. NADPH oxidase is the principle source of PMN SO release. We speculate that mitoQ may exert antioxidant effects independent of the mitochondria. Therefore, we hypothesized that inhibition of mitoQ on PMN-SO release will be similar as other coenzyme Q analogs: coenzyme Q1 and decylubiquinone without affecting cell viability. SO release was measured spectrophotometrically …
Cyclic Nucleotide-Dependent Phosphorylation Regulates Bk-Ca Channel Activity In Human Coronary Artery Smooth Muscle Cells, Raeonda Williams
Cyclic Nucleotide-Dependent Phosphorylation Regulates Bk-Ca Channel Activity In Human Coronary Artery Smooth Muscle Cells, Raeonda Williams
PCOM Biomedical Studies Student Scholarship
Cardiovascular diseases (CVD) can induce dysfunction in organ systems by attenuating normal blood flow. Gonadal steroids are vasoactive hormones, but their role in contributing to cardiovascular function remains controversial. We have demonstrated that gonadal steroids can relax coronary arteries by opening the large-conductance, calcium- and voltage-activated potassium (BKca) channel in smooth muscle cells by increasing cyclic nucleotide levels; however, the signaling pathways involved remain to be elucidated. The purpose of this study was to identify how phosphorylation (via cAMP- and cGMP-dependent protein kinases) I dephosphorylation (via phosphoprotein phosphatase 2A, PP2A) regulates BKca channel activity in human coronary artery smooth muscle …
The Effects Of Dihydrobiopterin And Tetrahydrobiopterin On Hydrogen Peroxide And Nitric Oxide Release During Extracorporeal Shockwave Lithotripsy (Eswl), Brittany Deiling
The Effects Of Dihydrobiopterin And Tetrahydrobiopterin On Hydrogen Peroxide And Nitric Oxide Release During Extracorporeal Shockwave Lithotripsy (Eswl), Brittany Deiling
PCOM Biomedical Studies Student Scholarship
ESWL is an effective, non-invasive therapy utilized to fragment stones in the kidney and subsequently be cleared in the urinary tract. Although lithotripsy provides a safer alternative to invasive treatments for removing stones, ESWL may cause vasoconstriction after ESWL treatment, reducing renal blood flow, which can cause kidney damage leading to acute to chronic hypertension clinically. This may be due to kidney vascular endothelial dysfunction, which is characterized as increased oxidative stress and decreased endothelial nitric oxide synthase (eNOS)-derived nitric oxide (NO) bioavailability. We hypothesized that ESWL would decrease NO and increase hydrogen peroxide (H2O2) in …
Autophagy And Apoptotic Genes Implicated In Alzheimer’S Disease Are Modulated Following Infection Of Neuronal Cells With Chlamydia Pneumoniae, Denah M. Appelt, Ian Kohler, Annette K. Slutter, Juliana Zoga, Susan T. Hingley, Brian J. Balin
Autophagy And Apoptotic Genes Implicated In Alzheimer’S Disease Are Modulated Following Infection Of Neuronal Cells With Chlamydia Pneumoniae, Denah M. Appelt, Ian Kohler, Annette K. Slutter, Juliana Zoga, Susan T. Hingley, Brian J. Balin
Scholarly Posters
Background: The focus of the current studies was to determine the relationship between the molecular mechanisms interconnecting autophagy and apoptosis following Chlamydia pneumoniae infection in neuronal cells. Dysfunctions in apoptosis and autophagy have been implicated in the neurodegeneration associated with Alzheimer’s disease (AD). Autophagy in AD pathogenesis has been shown to play a role in amyloid processing through the endosomal-lysosomal system. Apoptosis may contribute to the neuronal cell loss observed in AD; however, there is limited evidence of the apoptotic process proceeding to terminal completion. Although Aβ1-42 has been shown to induce apoptosis in neurons and may be an early …
Characterization Of A Hyperthermophilic Redox Protein, Rubredoxin, As A Potential Targeted Cancer Therapeutic, Siri Lakshmi Chirumamilla
Characterization Of A Hyperthermophilic Redox Protein, Rubredoxin, As A Potential Targeted Cancer Therapeutic, Siri Lakshmi Chirumamilla
PCOM Biomedical Studies Student Scholarship
Cancer is an elusive neoplastic disease that claims the lives of many people around the world every year. Though treatments have become more specific to the different types of cancer, the need remains for antineoplastic drugs that target cancer cells and leave normal cells unharmed, with little to no systemic toxicity. The search for a targeted cancer therapeutic is necessary and urgent, and Pyrococcus furiosus rubredoxin might be such a tool. Rubredoxin is a small (53 amino acids), water soluble, non-heme iron electron transfer protein that contains an iron atom cofactor bound by the sulfurs of four cysteine residues, which …