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BACKGROUND In dynamic cardiomyoplasty electro-stimulation achieves full transformation of the latissimus dorsi (LD); therefore, its slowness limits the systolic support. Daily activity-rest could maintain partial transformation of the LD. METHODS Sheep LD were burst-stimulated either 10 or 24 hours/day. Before and 2, 4, 6, and 12 months after stimulation,(More)
We found that LPL enhances the binding to HepG2 cells and fibroblasts of both VLDL and apoE free LDL. In the presence of 1.7 micrograms/ml of purified bovine LPL, the binding of LDL and VLDL was up to 60 fold increased as compared to the control binding. In addition, LPL enhances the binding in LDL-receptor negative fibroblasts to the same extent as it does(More)
It has previously been shown that lipoprotein lipase (LPL) enhances the binding of low density lipoproteins (LDL) and very low density lipoproteins (VLDL) to HepG2 cells and fibroblasts, up to 80-fold. This increase in binding is LDL receptor-independent and is due to a bridging of LPL between extracellular heparan sulfate proteoglycans (HSPG) and the(More)
OBJECTIVES Near-infrared spectroscopy monitors cerebral oxygen saturation. This parameter parallels jugular venous oxygen saturation and reflects the balance between cerebral oxygen supply and demand. Experience with near-infrared spectroscopy in univentricular physiology is limited. This study explores the relationship between cerebral oxygen saturation,(More)
FCE 24304 (6-methylenandrosta-1,4-diene-3,17-dione), a new irreversible aromatase inhibitor, has been identified and characterized in vitro and in vivo. The compound caused time-dependent inactivation of human placental aromatase with a t1/2 of 13.9 min and ki of 26 nM. When tested in PMSG-treated rats, ovarian aromatase activity was reduced 24 h after(More)
Familial hypercholesterolemia (FH) results from mutations in the low density lipoprotein receptor (LDLR) gene. We applied denaturing gradient gel electrophoresis (DGGE) to screen for sequence variations in the coding and splice site consensus sequences of the LDLR gene. For amplification of each exon by the polymerase chain reaction (PCR), optimal pairs of(More)
Familial hypercholesterolemia (FH) is a genetic disease caused by mutations in the low-density lipoprotein receptor gene. Among the more than 200 mutations so far identified, the T705I substitution in exon 15, designated FH-Paris 9, has been previously described as an FH-causing mutation. During the course of denaturing gradient gel electrophoretic(More)
The history of direct myocardial revascularization without cardiopulmonary bypass dates to 1961 in the dawn of coronary artery surgery. With the introduction and development of techniques of extracorporeal circulation around the same time, beating heart surgery was largely abandoned. Over the subsequent decades, cardiopulmonary bypass and electromechanical(More)
BACKGROUND In single-ventricle physiology, cerebral blood flow and oxygen (O2) delivery may be inadequate. This study tests the hypotheses that in acute univentricular physiology (1) cerebral blood flow increases inadequately to maintain O2 delivery, (2) the brain is incapable of increasing O2 extraction due to hypoxemia, and (3) cerebral O2 delivery(More)
Familial hypercholesterolemia (FH) is an autosomal semi-dominant disorder caused by defects in the low density lipoprotein receptor (LDLR) gene and is a well-documented risk factor for developing cardiovascular disease. The LDLR genes of five Swedish children with FH were examined in this study. Initial mutation screening was performed by denaturing(More)