[Evaluation of ST elevation in ECG following the repair of atrial septal defect (ASD) secundum--the influence factors before and during the operative procedure].
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Biomedical subjects
Publications and source records attributed to N Inoue.
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To evaluate right ventricular (RV) function in severe left ventricular (LV) failure, we measured RV and LV ejection fractions (EF) in 18 patients with old myocardial infarction (OMI) and in 18 with dilated cardiomyopathy (DCM) using cardiac blood pool scintigraphy. In patients with OMI, RVEF was significantly greater in stage II LV failure than in stage III (functional class of the New York Heart Association, 47 +/- 8% and 28 +/- 12%, respectively: p less than 0.01), and this correlated well with exercise tolerance by bicycle ergometer and mean pulmonary artery pressure (r = 0.83 and r = -0.71, respectively). In patients with DCM, however, there was no correlation between RVEF and these indexes. After the oral administration of denopamine (beta 1 effector), both RVEF and LVEF increased in patients with OMI (35 +/- 13% to 45 +/- 12%, and 27 +/- 9% to 30 +/- 10%: p less than 0.01), but they did not change significantly in patients with DCM. These results indicate that RVEF in patients with OMI correlates well with subjective symptoms, exercise tolerance and RV afterload, but these correlations were not apparent in patients with DCM. We concluded that RV function in cases of severe LV failure has a different meaning between OMI and DCM.
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The same iron pot in which their father had boiled lead with mercury (from a glass thermometer) for the purpose of alchemy, was also used for cooking in the kitchen. Although his wife had died of mercury poisoning, and his 14-year-old and 11-year-old daughters were found to excrete 322 and 455 micrograms/l mercury in the urine, respectively, (1-10 micrograms/l in controls), he stubbornly refused to give permission for them to be examined further. Nine months later, the daughters were permitted to be sent to our clinical ward. While the blood level of mercury had already come down to near normal, its excessive deposition in hair, kidneys and other parts of the body as well as its excessive urinary excretion, were still persistent (beyond tenfold the normal). According to our measurement values, mercury ranged from 14 to 49 micrograms/g in every 1-cm-piece of 10 cm hair of the elder sister, and ranged from 21 to 85 micrograms/g in 14 cm hair from the younger sister. About a 75% decrease in mercury deposition was estimated during these 9 months, based on the speculation of 1.5 cm/month hair-lengthening.
Calcineurin is the calcium (divalent cations)-dependent calmodulin-stimulated phosphoprotein phosphatase which is capable of dephosphorylating various substrate proteins. The subcellular and regional distribution of calcineurin in the rat brain has been studied by light and electron microscopic immunohistochemistry using antiserum against calcineurin. Immunoreactivity was observed in many neurons but was not detected in glial cells, such as astrocytes, oligodendrocytes and ependymal cells by the PAP method. Light microscopy demonstrates strong immunoreactivity in neuronal somata and neurites. By electron microscopy, calcineurin immunoreactivity was found to be present in dendrites including postsynaptic densities, somata, spines, axons and terminals. Calcineurin immunoreactivity was present in neurons throughout the brain, but a marked regional variation in strength of the immunoreactivity was observed. The caudatoputamen, hippocampal formation, and substantia nigra were strongly stained. Cerebral and cerebellar neocortex showed moderate immunoreactivity. In substantia nigra and globus pallidus, only neurites were stained, but neuronal somata not. The staining of the substantia nigra was thought to be due to that of the nerve terminals originating from the caudatoputamen, in view of the findings by cerebral hemitransection and electron microscopic immunohistochemistry. We developed an enzyme-immunoassay (EIA) for calcineurin. The sensitivity of the EIA was 1 ng (13 fmol) of calcineurin. We determined the level of calcineurin in various regions of the rat brain. The caudate nucleus, putamen and hippocampal formation showed a high concentration of calcineurin. The results are consistent with those obtained by immunohistochemistry.
A vapor generator for propylene oxide which has a high vapor pressure (boiling point: 33.9 degrees C, vapor pressure: 442 mmHg at 20 degrees C) was developed. For inhalation toxicity studies, until now, there have been few generators capable of producing a low concentration of vapor from a liquid with high vapor pressure. In this study, the vapor was generated from the surface of a sintered sphere of glass beads filled with propylene oxide. The sphere was hung in a glass column which was installed in a Dewar vessel chilled with ice. The liquid of propylene oxide was automatically supplied from a reservoir to the sphere by capillary suction pressure caused by the evaporation of the liquid from the surface. The concentration of the generated vapor was able to be kept constant over a long period by using a carrier gas dried by a silica gel column, and could be regulated by the flow rate of carrier and dilution gas, and the sphere diameter. This generator is useful for the investigation of health effects of propylene oxide in inhalation toxicity studies.
Calcineurin is one of the calmodulin binding proteins and a Ca2+-dependent and calmodulin-stimulated phosphoprotein phosphatase. We used antisera to the calcineurin as a cell-type-specific marker in order to identify neuronal cells in the rat brain and human neoplasms. In normal rat brain slices, basal ganglia were stained macroscopically, and other areas such as cerebral cortex, corpus callosum, cerebellar cortex, granular layer and pyramidal tract of the spinal cord were lightly identified as well. Under the light microscope, it was found that only the neuronal cells were stained, and astrocytes, oligodendrocytes, ependymal cells and vessels were not. Intracellular distribution of the staining showed various patterns and staining intensity of varying degree. Using the PAP method, localization of the calcineurin in formalin-fixed, paraffin-embedded tissues were studied in 65 human intracranial neoplasms, and in 11 human extracranial neoplasms. The neuronal elements of neuroblastoma, ganglioglioma, ganglioneuroma and retinoblastoma were clearly stained. In contrast, glioblastoma, astrocytoma, oligodendroglioma, ependymoma, meningioma, neurinoma, pituitary adenoma, craniopharyngioma, hemangioblastoma, hamartoma, lymphoma and mesenchymal tumor were all negative. Two cases out of 5 medulloblastomas were stained, but others were not. Although positive tumors disclosed various staining patterns and intensities, these results indicated that calcineurin could be a new neuronal marker in human brain tumors.
Calcineurin immunoreactivity has been successfully detected in formalin-fixed paraffin-embedded postmortem human brain tissue using the peroxidase-antiperoxidase method. We have examined two autopsy cases with Huntington's disease (HD), three cases with Parkinson's disease, and two senile patients as controls. In the controls, calcineurin immunoreactivity was present in neuronal cells only and highly concentrated in the caudate nucleus, putamen, globus pallidus (striato-pallidal pathway), substantia nigra (striato-nigral pathway) and hippocampal formation. These localizations were similar to those identified in rat brain. There was a marked depletion of neurons containing calcineurin in the caudate nucleus and putamen, and a marked reduction of calcineurin-immunoreactive nerve fibers in the globus pallidus and substantia nigra were found in the cases with HD, but not in those with Parkinson's disease. These findings suggest that calcineurin can be a useful and specific index of neuronal degeneration in the caudato-putamen resulting from extrapyramidal disease, and that the calcineurin-immunostaining method can be a valuable tool for clarifying the anatomy of the human extrapyramidal system.
A calmodulin-dependent protein kinase from canine myocardial cytosol was purified 1150-fold to apparent homogeneity with a 1.5% yield. The purified enzyme had a Mr of 550,000 with a sedimentation coefficient of 16.6 S, and showed a single protein band with a Mr of 55,000 (55K protein), determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The purified enzyme had a specific activity of 1.6 mumol/mg protein/min, and Ka values of 67 nM and 1.1 microM for calmodulin and Ca2+, respectively, using chicken gizzard myosin light chain as substrate. Calmodulin bound to the 55K protein. The purified enzyme had a broad substrate specificity. Endogenous proteins including glycogen synthase, phospholamban, and troponin I from the canine heart were phosphorylated by the enzyme. These results suggest that the purified enzyme works as a multifunctional protein kinase in the Ca2+, calmodulin-dependent cellular functions of the canine myocardium, and that the enzyme resembles enzymes detected in the brain, liver, and skeletal muscle.
In Wistar rats subjected to a 6-h exposure to ethylene oxide at the concentration of 250 parts per million once, 5 times a week for 9 months, histopathologic studies of myelinated fibers of the proximal sural, distal sural and peroneal nerves and of the fasciculus gracilis at the 5th thoracic and 3rd cervical segments of the spinal cord were performed to observe whether ethylene oxide of such a concentration would lead to degeneration of primary sensory neurons. Throughout the study, no definite abnormality of the gait or posture was observed in both control and test rats. Qualitative histologic studies disclosed preferential distal axonal degeneration of myelinated fibers in both sural nerves and gracile fascicles in the test rats, although the extent of the distribution and the severity of the degenerative findings were variable. Such findings are consistent with mild axonal degeneration found among patients suffering from ethylene oxide toxicity. Therefore, in rats, exposure to 250 ppm ethylene oxide produces central-peripheral distal axonal degeneration of primary sensory neurons.
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Based on the assumption that middle molecules that induce hepatic coma occur in the plasma of patients with fulminant hepatic failure (FHF), the authors have developed a hemodiafiltration (HDF) method using a large-pore poly(methylmethacrylate) (PMMA) membrane that allows proteins to pass through. PMMA HDF resulted in complete recovery of deep coma and long-term survival in a patient with severe FHF. Although a large-scale controlled trial is needed, PMMA HDF is believed to be promising as a future artificial liver support.