Biomedical subjects
Publications and source records attributed to T Shimazu.
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Electrical stimulation of the vagus nerve in intact or pancreatectomized rabbits resulted in a marked increase, within 5 minutes of the onset of stimulation, in the total activity of liver glycogen synthetase. The effect was completely counteracted by simultaneous stimulation of the splanchnic nerve, although stimulation of the splanchnic nerve alone had little effect on the enzyme. Injection of insulin caused an increase in both the total activity of glycogen synthetase and the activity that was independent of glucose-6-phosphate. The response of the enzyme to vagal stimulation was much faster than to administration of insulin.
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Electrical stimulation of the splanchnic nerve of rabbits caused a marked increase, within 30 seconds after the onset of stimulation, in liver-glycogen phosphorylase and glucose-6-phosphatase activities. The increased activity of liver phosphorylase after splanchnic-nerve stimulation was likewise observed in adrenalectomized and pancreatectomized rabbits. Glycogen content of the liver decreased only slightly after 5-minute stimulation.
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Various mutations of PO, PASII/PMP22 and connexin 32 genes were recently reported in hereditary neuropathies, such as Charcot-Marie-Tooth disease (CMT) and Dejerine Sottas disease (DS). However, physiological roles of the proteins in PNS are not well understood. To address the functions of the proteins, we examined their localization in PNS comparatively by immunohistochemical methods. In Western blotting, a polyclonal antibody against the carboxyl terminal peptide of PASII/PMP22 reacted to 20-24 kD bands of PASII/PMP22 in mammalian PNS myelin, but produced no reaction in either mammalian or carp CNS myelin proteins. Monoclonal anti-connexin 32 antibody recognised connexin 32 of a dimer or monomer form in rat and human PNS myelin. By histological examination, PASII/PMP22 expressed dominantly in rat PNS compact myelins, while connexin 32 localized exclusively in the nodes of Ranvier, but not in compact myelins. In cell culture, axonal contact induced a remarkable increase of PASII/PMP22 in the Schwann cell in contrast to faint staining in immature Schwann cells. While localization of connexin 32 is quite different from that of PASII/PMP22, the mutations of the two proteins often induce similar phenotypes of hereditary neuropathies.
To clarify the role of the ventromedial hypothalamus (VMH)-sympathetic nervous system in insulin-independent glucose uptake in peripheral tissues, tissue glucose uptake was assessed in vivo by the 2-[3H]deoxyglucose method during electrical stimulation of the VMH in anesthetized rats. VMH stimulation significantly increased the rate constant of glucose uptake in brown adipose tissue (BAT), heart and skeletal muscles, but not in white adipose tissue and brain. The effect of VMH stimulation on glucose uptake in BAT was abolished by local sympathetic denervation, indicating that the increase in glucose uptake is mediated by the sympathetic nerves. Electrical stimulation of the lateral hypothalamus, on the other hand, had no appreciable effects on 2-[3H]deoxyglucose uptake in any tissues. Changes in glucose transporters after VMH stimulation were also examined by the [3H]cytochalasin B binding method using sarcolemmal membranes isolated from heart muscle. Scatchard analysis of cytochalasin B binding indicated that VMH stimulation did not alter both the number and affinity (dissociation constant) of glucose transporters in the heart sarcolemmal membranes, whereas insulin administration increased the number of transporters in the membranes. These results suggest that the mechanism by which VMH stimulation increases glucose uptake in muscle is different from that of insulin.
We investigated how patients were evacuated and transported from affected hospitals in the disaster area to backup hospitals following the 1995 catastrophic Hanshin-Awaji earthquake. A retrospective review was conducted of medical records of 6107 patients hospitalized during the first 15 days after the earthquake, collected from 48 affected hospitals in the disaster area and 47 backup hospitals in the surrounding area. Of the 6107 patients, a total of 2290 (38%) were transferred to backup hospitals, consisting of 187 patients (50%) with crush syndrome, 702 (26%) with other traumas, and 1401 (41%) with illness. Of those 2290 patients, 1741 (76%) were transferred from affected hospitals to backup hospitals, while 549 patients (24%) were evacuated directly to backup hospitals. The peak in transport came during the first 4 days. The family car was the most frequently used means of transport; ambulance was used in only 26% of cases, and helicopters were used minimally. There was no notable difference in the percentage of intensive care patients and nonintensive care patients transferred to backup hospitals. The mortality rate for patients with trauma and crush syndrome was significantly higher in the affected hospitals. These results suggest that the existing emergency medical service system was not adequate for this urban earthquake. From our vantage point, we are keenly aware of the need for improved communications between hospitals, a well equipped patient transport system, and a well coordinated disaster response mechanism.
We report the reversible MR findings in a 7-year-old girl with hemolytic uremic syndrome and mild encephalopathy. The splenium of the corpus callosum showed isointense to low signal intensity on T1-weighted images and high signal intensity on T2-weighted images, representing local edema. These findings returned to near normal on MR images obtained 1 week later. The patient recovered without CNS impairment.