University of Louisville

About: University of Louisville is a education organization based out in Louisville, Kentucky, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 24600 authors who have published 49248 publications receiving 1573346 citations. The organization is also known as: UofL.

Data-Mining Concepts

Abstract: This chapter contains sections titled: Introduction Data-Mining Roots Data-Mining Process Large Data Sets Data Warehouses for Data Mining Business Aspects of Data Mining: Why a Data-Mining Project Fails Organization of This Book Review Questions and Problems References for Further Study ]]>

Intracoronary infusion of bone marrow-derived selected CD34+CXCR4+ cells and non-selected mononuclear cells in patients with acute STEMI and reduced left ventricular ejection fraction: results of randomized, multicentre Myocardial Regeneration by Intracoronary Infusion of Selected Population of Stem Cells in Acute Myocardial Infarction (REGENT) Trial.

Abstract: Aims Comparison of intracoronary infusion of bone marrow (BM)-derived unselected mononuclear cells (UNSEL) and selected CD34+CXCR4+ cells (SEL) in patients with acute myocardial infarction (AMI) and reduced <40% left ventricular ejection fraction (LVEF). Methods and results Two hundred patients were randomized to intracoronary infusion of UNSEL ( n = 80) or SEL ( n = 80) BM cells or to the control (CTRL) group without BM cell treatment. Primary endpoint: change of LVEF and volumes measured by magnetic resonance imaging before and 6 months after the procedure. After 6 months, LVEF increased by 3% ( P = 0.01) in patients treated with UNSEL, 3% in patients receiving SEL ( P = 0.04) and remained unchanged in CTRL group ( P = 0.73). There were no significant differences in absolute changes of LVEF between the groups. Absolute changes of left ventricular end-systolic volume and left ventricular end-diastolic volume were not significantly different in all groups. Significant increase of LVEF was observed only in patients treated with BM cells who had baseline LVEF < median (37%). Baseline LVEF < median and time from the onset of symptoms to primary percutaneous coronary intervention ≥ median were predictors of LVEF improvement in patients receiving BM cells. There were no differences in major cardiovascular event (death, re-infarction, stroke, target vessel revascularization) between groups. Conclusion In patients with AMI and impaired LVEF, treatment with BM cells does not lead to a significant improvement of LVEF or volumes. There was however a trend in favour of cell therapy in patients with most severely impaired LVEF and longer delay between the symptoms and revascularization.

Polysomnographic characteristics in normal preschool and early school-aged children

Abstract: OBJECTIVE. The objective of this study was to describe overnight polysomnographic measures in normal children aged 3 to 7 years. We conducted a retrospective analysis of normal polysomnographic evaluations from participants in 2 large community-based studies of sleep-disordered breathing among preschoolers and early school-aged children at Kosair Children’s Hospital Sleep Medicine Research Center at the University of Louisville. Participants included 542 healthy children with ages ranging from 3.2 to 8.6 years. RESULTS. Subjects were excluded from analysis if they had documented snoring during polysomnography, an obstructive apnea-hypopnea index of ≥1.0, or a periodic leg-movement index of ≥5.0. Because the greatest differences in polysomnography occurred between ages 5 and 6 years, analyses were performed for children 3 to 5 years and for ages ≥6. Sleep cyclicity was distinct between age groups, with both showing an initial brief rapid-eye-movement period, which lengthened across the night, but only the older group showing a decrease in cycle length across the night. Average obstructive apnea indices were 0.03 per hour of total sleep time (TST) for 3- to 5-year-old children and 0.05 per hour of TST for ≥6-year-old children, whereas central apnea indices were 0.82 and 0.45 per hour of TST, respectively. Older children spent a greater percentage of sleep time supine, and the apnea-hypopnea index differed according to body position. Twenty percent of all subjects had end tidal carbon dioxide values of >45 mm Hg, and 2.2% had recorded values >50 mm Hg during ≥50% TST. High variance was present on all measures. CONCLUSIONS. Developmental changes occur in several polysomnographic measures among normal children from 3 to 7 years of age, particularly during transition from preschool to early school age. Our findings in a large number of healthy community children comprise the most extensive compilation of normative reference values for laboratory-based pediatric polysomnography to date.

Protein Kinase Cε Interacts With and Inhibits the Permeability Transition Pore in Cardiac Mitochondria

Abstract: Although functional coupling between protein kinase Ce (PKCe) and mitochondria has been implicated in the genesis of cardioprotection, the signal transduction mechanisms that enable this link and the identities of the mitochondrial proteins modulated by PKCe remain unknown. Based on recent evidence that the mitochondrial permeability transition pore may be involved in ischemia/reperfusion injury, we hypothesized that protein-protein interactions between PKCe and mitochondrial pore components may serve as a signaling mechanism to modulate pore function and thus engender cardioprotection. Coimmunoprecipitation and GST-based affinity pull-down from mouse cardiac mitochondria revealed interaction of PKCe with components of the pore, namely voltage-dependent anion channel (VDAC), adenine nucleotide translocase (ANT), and hexokinase II (HKII). VDAC1, ANT1, and HKII were present in the PKCe complex at ≈2%, ≈0.2%, and ≈1% of their total expression, respectively. Moreover, in vitro studies demonstrated that PKCe can directly bind and phosphorylate VDAC1. Incubation of isolated cardiac mitochondria with recombinant PKCe resulted in a significant inhibition of Ca2+-induced mitochondrial swelling, an index of pore opening. Furthermore, cardiac-specific expression of active PKCe in mice, which is cardioprotective, greatly increased interaction of PKCe with the pore components and inhibited Ca2+-induced pore opening. In contrast, cardiac expression of kinase-inactive PKCe did not affect pore opening. Finally, administration of the pore opener atractyloside significantly attenuated the infarct-sparing effect of PKCe transgenesis. Collectively, these data demonstrate that PKCe forms physical interactions with components of the cardiac mitochondrial pore. This in turn inhibits the pathological function of the pore and contributes to PKCe-induced cardioprotection.