No abstract available.
HIV* ; Humans*

No abstract available.
Arsenic* ; Keratosis*

No abstract available.
Aged* ; Femur* ; Humans ; Osteoporosis*

No abstract available.
Congenital Abnormalities* ; Knee* ; Osteoarthritis* ; Osteotomy*

No abstract available.
Child* ; Humans

No abstract available.
Shoulder Fractures*

BACKGROUND: To evaluate the role of free fatty acids on the ischemic myocardium, influences of various free fatty acids upon transmembrane action potential and ATP-sensitive K+(KATP) channel activity were examined in the ventricular myocardium and single cardiac myocytes. METHODS: KATP channel activities were measured in the enzymatically (collagenase) isolated single rat ventricular cardiac myocytes by the method of the excised inside-out and the cell-attached patch clamp, and transmembrane action potentials were recorded using the conventional 3M-KCl microelectode techniques in the rat ventricular myocardium. RESULTS: Free fatty acids [FFAs; arachidonic acid (AA), linoleic acid (LA) and lysophosphatidylcholine (LPC)] reduced the KATP channel activity in a dose-dependent manner in the inside-out patch, and 50%-inhibition concentrations (IC50) were 88 +/- 11.2, 49 +/- 12.5, and 188 +/- 17.4 M respectively. Both frequency of channel opening and the mean open-burst duration were markedly decreased, but the amplitude of single channel currents were not changed by the FFAs. AA (50 micrometer) and LPC (50 micrometer) did not affect the dinitrophenol (DNP, 50 micrometer)-induced KATP channel activity, whereas LA (50 micrometer) had a tendency to reduce the activity. The channel inhibition effects by 10 micrometer AA in the inside-out patch were significantly augmented by diclofenac (10 micrometer), but was not changed by nordihydroguaiaretic acid. FFAs never stimulated KATP channel activity, even in the inside-out patch where KATP channel activity reduced in the presence of internal ATP (100 micrometer). Time for 90% repolarization (APD90) significantly increased during superfusion of the FFAs, to 22 (50 micrometer AA), 24 (50 micrometer LA), and 18 (50 micrometer LPC) % from those of the contol at the time of 10 min superfusion, but the other action potential characteristics were not changed by the FFAs. AA (10 micrometer) attenuated cromakalim (10 micrometer)-induced APD90 shortening effects. CONCLUSION: It was inferred that FFAs inhibit the KATP channel activity directly by themselves and/or indirectly by their metabolites in the rat ventricular cardiomyocytes, and therefore, duration of action potential lengthens to be a burden over the ischemic myocardium accounting for the injury of myocardium at the late stage of ischemia.
Action Potentials* ; Adenosine Triphosphate ; Animals ; Arachidonic Acid ; Cromakalim ; Diclofenac ; Fatty Acids, Nonesterified* ; Ischemia ; Linoleic Acid ; Lysophosphatidylcholines ; Masoprocol ; Myocardium* ; Myocytes, Cardiac ; Potassium Channels* ; Potassium* ; Rats*

No abstract available.
Catheters* ; Renal Dialysis*

No abstract available.

Abrupt reoxygenation (or reperfusion) after anoxia (or ischemia)-induced injury resulted in the loss of contractile property, destruction of cell organelles, and ultimately, cell death in cardiac myocytes. This phenomenon has been called 'oxygen paradox' or 'reperfusion injury'. The purpose of this study was to investigate the changes of fine structures and enzyme activities associated with oxygen paradox during 60 min. of anoxia, followed by a 30 min. of reoxygenation. Cardiac myocytes were dissociated from neonatal rat ventricles and cultured for three days. While they were exposed to anoxia and reoxygenation, the cardiac myocytes were investigated through beating counts, enzyme cytochemistry, immunofluorescence, electron microscopy for morphological study. Activity staining and Western blot for Cu, Zn-SOD, NADPH-diaphorase stain and nitrite concentration mesurement for nitric oxide synthase, and catalase activity measurement were performed. After 60 min. of anoxia, the beating rate increased remarkably. Swollen mitochondria with amorphous dense clumps, mild contracture of myofibrils and retraction of cytoplasmic processes were observed in cardiac myocytes. Under confocal microscope, weak reaction of Mn-SOD and myosin were observed, whereas reaction of Cu, Zn-SOD was enhanced in perinuclear region. Cu, Zn-SOD and catalase activity in cardiac myocytes increased markedly. Nitric oxide synthase activity increased gradually with time. After 30 min. of reoxygenation following 60 min anoxia, structural changes of myocardial cells was more pronounced than in the cells of anoxic group. Beating rate was variable but decreased gradually. Myocardial cells showed evidence of severe structural alterations, including marginal clumping of chromatids, varying-sized bleb formation, many vacuoles, mitochondrial matrix exposed to cytoplasm and fragmen-tation of cristae, myofibrillar hypercontracture. Decline of immunocytochemical reaction of Mn-SOD, myosin and Cu, Zn-SOD were observed under confocal microscope. The declines of activity and quantity of Cu, Zn-SOD were severe compared to control. In contrast, nitric oxide synthase activity significantly increased. Catalase activity was lower than in anoxic group, but still higher than in control activity. These results suggested that there were two possible mechanisms for the drastic morphological changes induced by anoxia-reoxygenation; 1) direct effect of oxygen free radicals, and 2) reaction of nitric oxide with superoxide radicals, which resulted in generation of toxic metabolites of nitric oxide, exacerbated myocardial cellular damages.
Animals ; Anoxia ; Blister ; Blotting, Western ; Catalase ; Cell Death ; Chromatids ; Contracture ; Cytoplasm ; Fluorescent Antibody Technique ; Free Radicals ; Histocytochemistry ; Microscopy, Electron ; Mitochondria ; Myocytes, Cardiac* ; Myofibrils ; Myosins ; Nitric Oxide ; Nitric Oxide Synthase ; Organelles ; Oxygen ; Rats ; Superoxide Dismutase ; Superoxides ; Vacuoles