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Biomedical subjects

T Miyatake

Publications and source records attributed to T Miyatake.

At least 271 records · Page 15Linked to original sources
PubMed1987

Antibodies to brain proteins in a patient with subacute cerebellar degeneration and Lambert-Eaton myasthenic syndrome.

The serum IgG of a 50-year-old woman with lung cancer associated with subacute cerebellar degeneration and Lambert-Eaton myasthenic syndrome showed the antibody activity to rat brain proteins. Using an immunoblotting method, the patient serum reacted with 98 kDa neutral cytoplasmic protein and 68 kDa membrane protein. These proteins were different in molecular weight from those we described previously (Tanaka et al. 1986), which suggests that proteins reacting with serum antibody are variable individually among patients with subacute cerebellar degeneration. These proteins from human brain could not be stained by the patient's serum IgG since these antigen proteins needed to be prepared quickly after death under protease inhibitors and were thought to be easily degraded.

Antibodies↗
PubMed1987

[An autopsy case of myoclonus epilepsy associated with ragged-red fibers (Fukuhara disease)].

In 1980, Fukuhara et al. have reported two patients with "myoclonus epilepsy associated with ragged-red fibers" (MERRF), which is at present accepted as a distinctive clinical entity among the mitochondrial encephalomyopathies. We describe here postmortem findings of the case whose clinical findings were reported in detail by Fukuhara et al. (1980) as Case 1. The neuropathological findings were summarized as follows: 1) degeneration of dentate nucleus, red nucleus, globus pallidus, subthalamic nucleus and pontine tegmentum, 2) degeneration of the Clarke's column, spinocerebellar tract, posterior column and corticospinal tract, as well as of the posterior spinal nerve root and sural nerve, and 3) degeneration of substantia nigra, locus ceruleus, cerebellar cortex and inferior olivary nucleus. The lesions were degenerative in nature, and their distribution was different from those of dentato-rubropallidoluysian atrophy, Joseph's disease or Friedreich's ataxia. It was concluded that MERRF is a single disease entity also from pathological point of view.

Adult↗
PubMed1986

Deficiency of subunits in heart mitochondrial NADH-ubiquinone oxidoreductase of a patient with mitochondrial encephalomyopathy and cardiomyopathy.

The heart mitochondria isolated from a patient with hypertrophic cardiomyopathy associated with mitochondrial encephalomyopathy were analyzed by immunoblotting using specific antibody against each of the purified mitochondrial energy transducing complexes from beef heart. Subunits of NADH-ubiquinone oxidoreductase (Complex I) were markedly decreased and those of cytochrome c oxidase (Complex IV) were decreased to some extent, but the deficiency of any of these subunits was only partial. On the other hand, the contents of subunits of ubiquinol-cytochrome c oxidoreductase (Complex III) were normal. These results suggest that the decreased levels of some of the Complex I subunits might be the primary cause of disorder in this patient.

Adolescent↗
PubMed1986

Joseph's disease: clinical and pathological studies in a Japanese family.

Joseph's disease is a hereditary ataxia found among descendants of Portuguese from the Azores Islands. We describe the clinical and pathological features of 4 members of a Japanese family who were diagnosed as having Joseph's disease. The illness began with cerebellar ataxia between the ages of 18 and 45 years. Nystagmus, dysarthria, and pyramidal signs were early manifestations. External ophthalmoplegia, dystonia and/or athetotic movements, and muscular atrophy appeared in the late stages. Neuropathological findings in one patient revealed degeneration of the dentatorubral and pallidoluysian systems, substantia nigra, pontocerebellar system, Clarke's column and spinocerebellar tracts, and anterior horn cells, as well as the cranial nuclei in the brainstem. Neurons in the inferior olivary nuclei, Purkinje's and granule cells, the cerebral cortex, thalamus, and striatum were spared. Involvement of the dentatorubral and pallidoluysian systems seems to be a characteristic feature of this disease in Japan.

Adolescent↗
PubMed1986

31P-NMR studies on an animal model of human defective muscle glycolysis.

Sequential metabolic changes in leg muscles of a model of defective muscle glycolysis that was produced by intraaortic injection of sodium iodoacetate were observed by in vivo 31P-NMR spectroscopy with a surface coil. Spectra obtained from iodoacetate-treated muscles presenting exercise-induced cramp showed decreased levels of phosphocreatinine (PCr) and adenosine triphosphate (ATP) and an accumulation of sugar phosphate. The chemical shift of inorganic phosphate (Pi) resonance, which reflects the intracellular pH of the contracted muscles, showed a milder shift to the acidic condition than those of controls. In vivo 31P-NMR study showed dynamic information on the muscle energetics under defective glycolytic conditions.

Animals↗
PubMed1986

Degradation of myelin basic protein in myelin by protease in cerebrospinal fluid and effects of protease inhibitors.

Neutral protease is shown to be present in cell-free human cerebrospinal fluid. Incubation of heated human myelin with CSF at 25 degrees C resulted in a marked reduction of myelin basic protein (MBP) with time. Degradation products appeared at apparent mol wt 14 KDa and 12 KDa on polyacrylamide gel electrophoresis. Optimal pH of the protease was 7.0. This protease was activated by calcium ion. Degradation of MBP was inhibited by FOY305 (camostat mesilate), Trasylol, and Leupeptin, but not a specific calcium-activated neutral protease inhibitor, E-64-a. FOY305, which is a synthesized specific serine protease inhibitor, was the strongest inhibitor of all. The role of this protease in CSF has not been elucidated. In may be related to the physiological turnover of MBP, and may affect myelin maintenance in pathological conditions such as demyelination.

Humans↗
PubMed1986

Characterization of the antigenic determinant on HSB-2 cells shared with myelin-associated glycoprotein (MAG) using monoclonal antibodies.

The existence of cross-antigenicity between myelin-associated glycoprotein (MAG) and natural killer cells has been reported previously. In this study, we have characterized the antigenic determinant on HSB-2 cells which is shared with MAG using two types of mouse monoclonal anti-MAG antibodies, one recognizing the peptide molecule (IgG-P) and the other recognizing the carbohydrate molecule of MAG (IgM-C). Enzyme-linked immunosorbent assay (ELISA) revealed that IgM-C was absorbed by cell homogenate of HSB-2, and some bands were stained by IgM-C on the immunoblot of HSB-2 cell homogenate, while IgG-P was not absorbed by HSB-2 cell homogenate and no band was stained by IgG-P on the immunoblot of HSB-2 cell homogenate. Therefore it is suggested that the shared antigenic determinant between MAG and HSB-2 cells is not in the peptide molecule but in the carbohydrate molecule.

Antibodies, Monoclonal↗
PubMed1986

Production and characterization of monoclonal antibodies against myelin-associated glycoprotein.

Monoclonal antibodies against myelin-associated glycoprotein were generated by fusing mouse myeloma cells with spleen lymphocytes from BALB/c mice immunized with human myelin-associated glycoprotein purified from CNS myelin. Three groups of antibodies were identified: IgG antibodies recognizing the polypeptide moiety and IgG and IgM antibodies recognizing the carbohydrate moiety of the intact molecule. Properties of these antibodies were examined with sodium dodecyl sulfate-polyacrylamide gel electrophoresis and the immunostaining technique using human CNS and peripheral nerve myelin, and ganglioside fractions isolated from human brain and peripheral nerve, and with immunohistochemical staining of human peripheral nerves. Part of human peripheral blood mononuclear cells was stained with the antibodies against the carbohydrate moiety, but not with IgG antibodies recognizing the polypeptide moiety. Natural killer activity was partially reduced after treatment of human peripheral blood lymphocytes with an IgM antibody and complement in vitro. The possibility that anti-myelin-associated glycoprotein antibodies might play a role in the pathogenesis of demyelinating diseases through modification of natural killer activity is discussed.

Animals↗
PubMed1986

Anti-myelin-associated glycoprotein antibody in sera from patients with demyelinating diseases.

An enzyme-linked immunosorbent assay (ELISA) was developed for quantitating anti-myelin-associated glycoprotein (MAG) IgM antibody in human sera. Absorbance values of anti-MAG antibody were higher than 0.2 at 1:80 of serum dilution in sera from some patients with demyelinating diseases of the central or peripheral nervous systems including multiple sclerosis, subacute sclerosing panencephalitis, Guillain-Barré syndrome, chronic relapsing polyradiculoneuritis and carcinomatous polyneuropathy and also some patients with autoimmune diseases such as collagen diseases and myasthenia gravis. However, absorbance values of anti-MAG antibody in sera from control individuals and patients with some other neurological diseases were less than 0.2 and considered as negative. Because of the reported existence of a cross antigenicity between MAG and lymphocyte, and especially natural killer cells, the possibility of the functional importance of anti-MAG antibody on cellular immunity is discussed with particular reference to the demyelinating diseases.

Autoantibodies↗
PubMed1986

Experimental neuropathy induced by methyl mercury compounds: autoradiographic study of GABA uptake by dorsal root ganglia.

Methyl mercury chloride (MMC, 10 mg/kg body weight/day) was subcutaneously injected into rats for 1 week. Animals were killed at 5 or 14 days (at the onset of clinical symptoms) after injection of MMC. Morphologically, most of the myelinated fibers in peripheral nerves showed axonal degeneration. Ganglion cells showed histopathological changes similar to those in previous reports. The cytoplasm of satellite cells stained dark with toluidine blue and was narrow, and sometimes showed focal disappearance of rough endoplasmic reticula, ribosomes or filaments. Autoradiography in the control rats showed that 3H-GABA was exclusively localized within the satellite cells and Schwann cell cytoplasm of the myelinated fibers and was not revealed within the ganglion cells. The number of silver grains markedly decreased in the satellite cells of the MMC-treated rats. 14C-GABA uptake by dorsal root ganglia also decreased to 75.0% of the control on the 5th day and to 49.2% on the 14th day. Therefore, MMC was found to inhibit greatly the GABA uptake into the satellite cells in the earlier stage of poisoning, and was considered to affect primarily the satellite cells and Schwann cells as well as the ganglion cells.

Animals↗
PubMed1986

Antibodies to brain proteins in paraneoplastic cerebellar degeneration.

A 68-year-old man had subacute cerebellar degeneration and a non-Hodgkin's lymphoma. Using an immunoblotting method, we found serum antibodies to rat cerebral 250-kd and 110-kd and cerebellar 110-kd acidic cytoplasmic proteins. The antibodies did not react unless the antigens were prepared soon after death with protease inhibitors. Two hundred fifty-kd and 110-kd proteins are minor components of soluble cytoplasmic proteins of the brain. The molecular weights differed from other soluble brain-specific proteins already characterized.

Aged↗
PubMed1986

Chronic T cell leukemia with a NK phenotype reacting with anti-myelin-associated glycoprotein (MAG) mouse monoclonal antibody.

We describe a patient demonstrating chronic T cell leukemia with a natural killer (NK) phenotype. The leukemic cells could be stained by OKT 3 (T cells), anti-Leu-7 and anti-myelin-associated glycoprotein (MAG) (NK cells) but not anti-Leu-11 monoclonal mouse antibody (activated NK cells). Fresh mononuclear cells showed a very low NK activity, although this activity returned to normal levels after 18 days incubation with interleukin-2 and some stimulants. It was not known why the NK activity of fresh mononuclear cells was low. This report is the first on leukemia characterized by anti-MAG monoclonal antibody.

Antibodies, Monoclonal↗
PubMed1985

Adrenomyeloneuropathy: report of a family and electron microscopical findings in peripheral nerve.

A family with adrenomyeloneuropathy (AMN) is reported, whose female carriers showed severe neurological and biochemical abnormalities. Cytoplasmic lamellar inclusions were found in endoneurial cells of the biopsied sural nerve of a male patient. In spite of the peripheral nervous system involvement in patients with AMN, there have been few reports of these inclusions in the peripheral nerves of such cases.

Adrenal Gland Diseases↗