[Effect of endothelin on gastric mucosal blood flow in rat].
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Biomedical subjects
Publications and source records attributed to M Kawamura.
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It has been well established that acquired lesions of the corpus callosum such as surgical section bring about disturbances of interhemispheric transfer of visual information. In contrast, patients with callosal agenesis do not display these specific deficits. The mechanisms of this compensation have been postulated as follows; (1) bilateral development of language function, (2) exploitation of extracallosal commissure fibers such as the anterior commissure. Several studies have reported, however, minor disturbances of interhemispheric visual transfer in callosal agenesis, such as less efficient interhemispheric transfer of complex visual stimuli (Gott & Saul, 1978), slower reaction time in interhemispheric comparison of visual stimuli (Sauerwein & Lassonde, 1983), or deficits in spatial localization in the right hemi-field (Martin, 1985). In order to settle these issues, we have administered four kinds of tachistoscopic visual recognition tests on 4 patients with complete agenesis of the corpus callosum confirmed by magnetic resonance imaging (MRI). This technique enabled us to see the mid-sagittal plane of the corpus callosum and diagnose its total absence with much higher certainty and precision than previous studies employing computed tomography (CT) or pneumoencephalography. Case 1: A 41-year-old right-handed man visited us because of recurrent numbness in the four extremities. Neurological examination revealed no abnormalities. MRI has confirmed that the corpus callosum was totally lacking, and that the anterior commissure was normally visualized. Case 2: A 31-year-old right-handed man was referred to us for the treatment of partial complex seizure. Total agenesis and lipoma of the corpus callosum was diagnosed by MRI and reconstructed sagittal view of CT scan.(ABSTRACT TRUNCATED AT 250 WORDS)
Degenerative changes in the retina and the optic nerve were investigated morphologically and immunohistochemically following administration of monosodium-L-glutamate (MSG) in rats. MSG (5mg/g b.w.) was injected subcutaneously every other day for 5 times after birth. The retina and the optic disc was observed ophthalmoscopically at 1, 3 and 6 months after birth. At the same stage, morphological and immunohistochemical changes were also investigated under light microscopy. The neuron of the retinal ganglion cell was identified immunohistochemically with antiserum to neurofilament 200 kD (NF). Glial cells were stained with antisera to glial fibrillary acidic protein (GFAP) and S-100 beta protein, and myelin of oligodendrocytes was also stained with antiserum to myelin basic protein (MBP). Histologically the inner layer of the retina was selectively destroyed, and the optic nerve also showed degeneration, changing into a thin strand. The retinal vessels were narrow and coarse, however, they extended to the peripheral region. Although immunohistochemical staining with NF antiserum was scarcely detected both in the retina and in the optic nerve, glial stainings with GFAP and S-100 beta protein antisera were widely observed in the perivascular space of the retina and in the glial column of the optic nerve. These findings indicated that the ganglion cells and their neurons are significantly affected by MSG, but the retinal vessels and glial cells are rarely affected. Ophthalmoscopically, the optic discs of rats treated with MSG were small and deeply excavated. The vitreous vessels persisted in most cases even at 6th months after birth.(ABSTRACT TRUNCATED AT 250 WORDS)
Changes in the eyeball size were investigated in rats treated with monosodium glutamate (MSG) during the neonatal period. Correlations among ocular size and degenerative changes of the retina and optic nerve were also studied ophthalmoscopically and histologically. Rats received MSG 5 times, 2 times or once. In rats which received MSG 5 times, the administration was made at 1, 3, 5, 7 and 9 days of birth. In rats, which received MSG 2 times, the administration was made on 2 subsequent days (1 and 2, 3 and 4, 5 and 6, 7 and 8, 9 and 10, 12 and 13 or 15 and 16 postnatal days). In the group of rats, which received MSG once, the administration was made on each from the 1st to the 15th postnatal day. Microphthalmos formation was clearly observed only in rats with 5 times and 2 times (9 and 10 days) injection of MSG. In these rats, narrowing of retinal vessels, paleness and excavation of optic disks were observed ophthalmoscopically. Total liquefaction of the vitreous body were seen in the same groups. Histological examinations also revealed degeneration of the inner layers of the retina. These findings indicated that the administration of MSG at critical stages during postnatal development induces disturbances of eyeball growth. It was also suggested that the growth of the eyeball is closely associated with the postnatal development of the retina.
Changes in the transparency and size of lenses in rats were investigated following administration of monosodium-L-glutamate (MSG), MSG (5 mg/g b.w.) was injected subcutaneously on the 9th and 10th days after birth. Morphological changes of the lenses were examined ophthalmoscopically and histologically. Ophthalmoscopically, localized opacity was apparent at the posterior pole of the lens corresponding to the attached portion of hyaloid artery at 1 months of age. The incidence of cataract increased with age, reaching more than 75% at 4 months of age. Morgagni's globules were histologically detected in the opacity of the posterior lens cortex. Degenerative changes of the lens epithelium were observed in the mature cataract. However, the capsules of the lens were well preserved. The size and weight of the lens were smaller than those of controls. Although the pathogenesis of the cataract and small lenses are not clear at the moment, these findings indicate that administration of MSG could be an etiologic factor in cataract formation in the developing rat.
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A cDNA for a chimeric alpha subunit of the (Na,K)ATPase was constructed and expressed in Xenopus oocytes in order to elucidate structural features involved in ouabain sensitivity. A chimeric alpha subunit, in which the N-terminal 165 amino acid sequence of ouabain-resistant rat alpha subunit, including the first two transmembrane segments (M1 and M2), was replaced by a sequence from the corresponding region of ouabain-sensitive Torpedo alpha subunit, was ouabain-sensitive, suggesting that the M1-M2 junction is a site responsible for ouabain sensitivity of the (Na,K)ATPase.
(Na,K)ATPase from Torpedo californica was expressed in Xenopus laevis oocytes in the presence of tunicamycin by injecting mRNAs for the alpha- and beta-subunits derived from the cloned cDNAs into the oocytes. The oligosaccharide-deficient ATPase thus synthesized was transported to the oocyte plasma membrane, where it exhibited virtually the same ATPase activity, ouabain-binding capacity and 86Rb+ transport activity as the fully glycosylated enzyme. We conclude that the oligosaccharide chains on the beta-subunit has no effect on the catalytic activities of (Na,K)ATPase.
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Phenylmethanesulfonyl fluoride (PMSF) enabled vanadate to catalyze the oxidation of NADH. Superoxide dismutase and manganese inhibited the oxidation, suggesting that superoxide anion played a crucial role. Since PMSF is widely used to protect enzymes from proteolytic cleavage when they are purified, attention should be paid when the toxicity of vanadate on the enzyme, whose activities are monitored by the oxidation of NADH, is evaluated or when vanadate dependent NADH oxidase is purified and assayed.
The enzyme renin has been purified and characterized by structural analysis. Pure renin protein was used to produce a specific antibody to renin, which was useful in demonstrating the presence of a specific renin in many tissues other than kidney. Further, in these cells angiotensins I and II and converting enzyme all were found to coexist with renin by immunohistochemical studies, indicating the local production of renin, angiotensinogen and angiotensins in these cells. Angiotensin II produced in the cultured cells was secreted to the outside of the cells. Secretion of angiotensin II from the angiotensin-producing cells was demonstrated with perfused mesenteric artery. The secretion of angiotensin II from the vascular beds was inhibited by converting enzyme inhibitors, and was stimulated by the adrenergic beta-agonist isoproterenol. These studies demonstrate local production and controlled secretion of angiotensin II and define its physiologic role.
A 14-year-old boy had persistent haematuria along with complete C7 deficiency. No significant changes in glomeruli and tubules were found in a renal biopsy specimen by light microscopy and immunofluorescence gave negative results for immune deposits. Electron microscopic examination demonstrated an attenuation of the glomerular capillary basement membrane without lamination and a diagnosis of thin basement membrane disease was made. It would be difficult to conclude that patients with C7 deficiency were predisposed to develop glomerulonephritis caused by immunologic aberrations. A family study failed to provide evidence of an association of C7 deficiency and thin basement membrane disease.
A woman was operated on for pulmonary metastasis four years after a radical resection of the rectum, and four years thereafter a solitary metastasis to the left adrenal was found. An elevated serum carcinoembryonic antigen (CEA) level indicated the lesion. Adrenalectomy was performed and the patient has been well with no further evidence of disease.