Test Report for the INL Sunlution Photovoltaic Module Ground Clip Test

Sunlution, LLC asked the Idaho National Laboratory (INL) for a small proof test of their proposed solar panel grounding clip. This report documents the results of that test

DEVELOPMENT OF A VALIDATED MODEL FOR USE IN MINIMIZING NOx EMISSIONS AND MAXIMIZING CARBON UTILIZATION WHEN CO-FIRING BIOMASS WITH COAL

In full-scale boilers, the effect of biomass cofiring on NO{sub x} and unburned carbon (UBC) emissions has been found to be site-specific. Few sets of field data are comparable and no consistent database of information exists upon which cofiring fuel choice or injection system design can be based to assure that NOX emissions will be minimized and UBC be reduced. This report presents the results of a comprehensive project that generated an extensive set of pilot-scale test data that were used to validate a new predictive model for the cofiring of biomass and coal. All testing was performed at the 3.6 MMBtu/hr (1.75 MW{sub t}) Southern Company Services/Southern Research Institute Combustion Research Facility where a variety of burner configurations, coals, biomasses, and biomass injection schemes were utilized to generate a database of consistent, scalable, experimental results (422 separate test conditions). This database was then used to validate a new model for predicting NO{sub x} and UBC emissions from the cofiring of biomass and coal. This model is based on an Advanced Post-Processing (APP) technique that generates an equivalent network of idealized reactor elements from a conventional CFD simulation. The APP reactor network is a computational environment that allows for the incorporation of all relevant chemical reaction mechanisms and provides a new tool to quantify NOx and UBC emissions for any cofired combination of coal and biomass

Pediatric pacemaker infections: Twenty years of experience

AbstractObjective: We sought to evaluate possible predictors of early and late pacemaker infections in children. Methods: A review was performed of all pacemakers implanted in children at The Children's Hospital of Philadelphia between 1982 and 2001. Infections were classified as superficial cellulitus, deep pacemaker pocket infection necessitating removal, or positive blood culture without an identifiable source. Results: A total of 385 pacemakers (224 epicardial and 161 endocardial) were implanted in 267 patients at 8.4 ± 6.2 years. All 2141 outpatient visits were reviewed (median follow-up, 29.4 months; range, 2-232 months). There were 30 (7.8%) pacemaker infections: 19 (4.9%) superficial infections; 9 (2.3%) pocket infections; and 2 (0.5%) isolated positive blood cultures. All superficial infections resolved with intravenous antibiotics. The median time from implantation to infection was 16 days (range, 2 days-5 years). Only 1 deep infection occurred after primary pacemaker implantation. Six patients with deep infections were pacemaker dependent and were successfully managed with intravenous antibiotics, followed by lead-generator removal and implantation of a new pacemaker in a remote location. In univariate analyses trisomy 21 (relative risk, 3.9; P <.01), pacemaker revisions (relative risk, 2.5; P <.01), and single-chamber devices (relative risk, 2.4; P <.05) were identified as predictors of infection. However, in multivariate analyses only trisomy 21 and pacemaker revisions were predictors. Conclusions: The incidences of superficial and deep pacemaker infections were 4.9% and 2.3%, respectively. Trisomy 21 and pacemaker revisions were significant risk factors in the development of infection after pacemaker implantation. For primary pacemaker implantation, the risk of infection requiring system removal is low (0.3%).J Thorac Cardiovasc Surg 2002;124:821-

Lanthanum staining of coronary microvascular endothelium: Effects of ischemia reperfusion, propranolol, and atenolol

Cat isolated hearts were perfused via the aorta with normothermic arterial blood from donor cats. After 1 hr of equilibration, dl-propranolol (1.9 mg/kg), atenolol (1.65 mg/kg), or physiological saline solution was infused via the aortic cannula. The hearts were made globally ischemic for 1 hr and reperfused for 1 hr. Hearts given saline but not made ischemic, and hearts from blood-donor cats served as controls. The hearts were flushed with physiological saline for 2 min, then perfused with cacodylate-buffered glutaraldehyde containing 1% LaCl3. Samples of left ventricle were postfixed in osmium and prepared for electron microscopy. Microvessels in nonischemic tissues had heavy La3+ staining on luminal surfaces of endothelial cells. Many plasmalemmal vesicles along luminal surfaces of endothelial cells were filled with La3+. Several vesicles appeared to open onto both surfaces thus forming channels through the endothelium. Lanthanum penetrated into, and occasionally through, interendothelial junctions. Endothelial cells lining vessels in ischemic myocardium were swollen, had pale cytoplasm, and showed little La3+ on the luminal surfaces. Few plasmalemmal vesicles were present and the mitochondria contained deposits of La3+. Extravascular spaces were distended but interendothelial junctions seemed to be intact. Lanthanum staining and morphology of endothelial cells in hearts treated with propranolol or atenolol were very similar to nonischemic myocardium. The data suggest that the [beta]-blocking agents, propranolol and atenolol, maintain the integrity of coronary vascular endothelium during ischemia.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/24387/1/0000657.pd

Time-dependent changes in canine cardiac mitochondrial function and ultrastructure resulting from coronary occlusion and reperfusion

Time-dependent changes in mitochondrial function and structure resulting from 1 hr of left circumflex coronary artery occlusion followed by 2 to 24 hrs of reperfusion were examined. These changes were correlated with changes in myocardial ultrastructure, tissue water content, infarct size and mitochondrial calcium content. The heart was removed after different periods of reperfusion, and mitochondria were isolated from ischemic and nonischemic regions of the left ventricle. Tissue samples from ischemic and nonischemic myocardium also were taken for electron microscopy and tissue water content determinations. Infarct size was measured by the nitroblue tetrazolium staining method. Oxygen consumption by mitochondria isolated from ischemic and nonischemic myocardium was measured in vitro . Mitochondria from ischemic myocardium showed time-dependent decreases in rates of oxygen consumption and tightness of coupling. Electron microscopy revealed progressive ultrastructural deterioration in ischemic myocardium, including accumulation of calcium deposits within mitochondria, a finding corroborated by elevated concentrations of calcium in mitochondria isolated from the same area. Tissue wet-to-dry weight ratios were increased significantly in ischemic myocardium. A small, but significant, decrease in respiratory function was observed in mitochondria isolated from nonischemic myocardium several hrs after reperfusion; however, nomal respiration was observed 24 hrs after release of occlusion. This latter observation indicates that the nonischemic zone also is affected by regional ischemia. The results obtained indicate that temporary left circumflex artery occlusion and reperfusion result in progressively decreasing mitochondrial function and structure within the ischemic myocardium, and that these changes are accompanied by cellular electrolyte alterations. Untersucht wurden zeitabhängige Veränderungen in Struktur und Funktion der Mitochondrien, die durch einstündigen Verschluß und 2- bis 24stündige Reperfusion des Ramus circumflexus der linken Koronararterie erzeugt wurden. Diese Veränderungen wurden mit Veränderungen der myokardialen Ultrastruktur, dem Wassergehalt des Gewebes, der Infarktgröße und dem mitochondrialen Calciumgehalt korreliert. Das Herz wurde nach verschiedenen Reperfusionszeiten entnommen und die Mitochondrien aus ischämischen und nichtischämischen Gebieten des linken Ventrikels isoliert. Ebenso wurden Gewebeproben von ischämischem und nichtischämischem Myokard für Elektronenmikroskopie und Bestimmung des Wassergehaltes des Gewebes entnommen. Die Infarktgröße wurde durch die Anfärbung mit Nitroblau-Tetrazolium bestimmt. Der Sauerstoffverbrauch der Mitochondrien aus ischämischem und nichtischämischem Myokard wurde in vitro gemessen. Mitochondrien aus ischämischem Myokard zeigten eine zeitabhängige Abnahme des Sauerstoffverbrauchs und seiner Bindung an die Phosphorylierung von ADP. Die Elektronenmikroskopie zeigte eine fortschreitende Zerstörung der Ultrastruktur im ischämischen Myokard, einschließlich einer Zunahme der Calciumablagerungen in Mitochondrien, was mit erhöhten Calciumkonzentrationen in Mitochondrien aus dem gleichen Gebiet übereinstimmte. Im ischämischen Myokard war die Relation Feuchtgewicht/Trockengewicht signifikant erhöht. Eine geringe, aber signifikante Abnahme der Atmung wurde in Mitochondrien, die nach einigen Stunden Reperfusion aus nichtischämischem Myokard isoliert worden waren, beobachtet; aber nach 24 h Reperfusion fand sich normale Atmung. Letzteres weist darauf hin, daß auch das nichtischämische Gebiet von der regionalen Ischämie betroffen ist. Die Ergebnisse zeigen, daß vorübergehender Verschluß des Ramus circumflexus der linken Koronararterie und Reperfusion zu fortschreitender Zerstörung mitochondrialer Funktion und Struktur führen und daß diese Veränderungen von Änderungen des Electrolytstatus der Zelle begleitet werden.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/41744/1/395_2005_Article_BF01907837.pd