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Biomedical subjects

T Miyatake

Publications and source records attributed to T Miyatake.

At least 127 records · Page 7Linked to original sources
PubMed1993

Activation of human lysosomal sialidase.

An acid sialidase [EC 3.2.1.18], partially purified from human placenta by Con A-Sepharose adsorption and p-aminophenyl thio-beta-D-galactoside-CH-Sepharose (PATG-Sepharose) affinity chromatographies, was activated by incubation at 37 degrees C. This activation showed both time and temperature dependencies, with the most effective activation observed at 37 degrees C in the pH range between 4.3 and 5.2. The influence of various protease inhibitors on its activation was investigated. Among the protease inhibitors tested, amastatin, an inhibitor of aminopeptidase A, significantly inhibited activation. The partially purified enzyme preparation contained aminopeptidase activity, which was inhibited by amastatin. Zinc ions inhibited either the activation of sialidase or the aminopeptidase activity in the enzyme preparation. These results suggest the possibility of participation of aminopeptidase function in the activation process of sialidase.

Aminopeptidases↗
PubMed1993

Fucosyl-GM1 in human sensory nervous tissue is a target antigen in patients with autoimmune neuropathies.

Several gangliosides of human nervous tissues have been reported to be potential target antigens in autoimmune neuropathies. To explain the diversity of clinical symptoms in patients with antiganglioside antibodies, we have searched for ganglioside antigens that are specific to individual nervous tissues such as motoneurons, peripheral motor nerves, and sensory nerves. Although the major ganglioside compositions were not different among human peripheral motor and sensory nerves, fucosyl-GM1 was found to be expressed in sensory nervous tissue but not in spinal cord, motor nerve, and sympathetic ganglia. Sera from several patients with sensory nerve involvement also reacted with fucosyl-GM1 as well as GM1. Thus, fucosyl-GM1 may be a responsible target antigen for developing sensory symptoms in some patients with autoimmune neuropathies.

Animals↗
PubMed1993

Subarachnoid haemorrhage in the elderly: a necropsy study of the association with cerebral amyloid angiopathy.

To clarify the contribution of cerebral amyloid angiopathy (CAA) to subarachnoid haemorrhage (SAH) in the elderly, relationships between SAH and CAA were investigated in 997 necropsy cases aged 60 years or older. Primary SAH (bleeding from subarachnoid vessels) was found in 15 cases (1.5%). There was no case in which primary SAH was clearly attributed to CAA. Secondary SAH [secondary rupture of intracerebral haemorrhage (ICH) through the cortex to the subarachnoid space] was found in 23 patients (2.3%). In 11 (48%) of them, ICH with secondary SAH was associated with CAA. The results indicated that primary SAH is rarely related to CAA, however, CAA is the most frequent cause of ICH accompanying secondary SAH in the elderly.

Aged↗
PubMed1993

Circulating autoantibody to mature neurons and astrocytes of humans and some mammals present in a demented patient with autoimmune disorder.

Circulating autoantibody to a 48-kD nuclear protein in neurons and astrocytes of the human and bovine cerebrum were present in the serum of a demented patient with an autoimmune disorder. Other human visceral organs, dorsal root ganglion cells, neuroblastoma and glioblastoma cell lines, and rat cerebrum did not react with the patient's serum. No sera from age-matched controls, including those with Alzheimer's disease, reacted with the 48-kD protein. Only the mature neurons and astrocytes of humans and some mammals express the 48-kD protein. This antibody may be responsible for the patient's demented condition.

Aged↗
PubMed1993

Isolation of 353 NotI-linking clones and 62 DNA markers (DXS607-DXS668) from human chromosome Xq24-->qter.

Through restriction enzyme digestion of 1,784 cosmid DNAs derived from human chromosome region Xq24-->qter, we identified 353 NotI-linking cosmids (11 individual groups of overlapping NotI-linking cosmids at Xq24-->q25.6 groups at Xq26-->q27, and 19 groups at Xq28). Sixty-two of the 353 clones (DXS607-DXS668) contained multiple rare-cutter sites, including multiple SacII sites within a 2-kb region, as well as one to six sites for BssHII, MluI, NotI, or NruI.

Cosmids↗
PubMed1993

Computer-assisted three-dimensional image analysis of cerebral amyloid angiopathy.

BACKGROUND AND PURPOSE: Microaneurysms and fibrinoid necrosis of cerebral cortical arteries have been reported to be related to the pathogenesis of intracerebral hemorrhage associated with cerebral amyloid angiopathy. To elucidate the pathogenesis of such vascular lesions, we conducted the present study. METHODS: Five hundred serial sections from brain tissue of a patient with severe amyloid angiopathy and intracerebral hemorrhage were analyzed histologically and immunohistochemically. Three-dimensional reconstructions of the vascular lesions were performed using a computer-assisted image analysis system. RESULTS: The microaneurysms were found to develop in small cortical arteries with diameters of about 40 to 50 microns. They were spindle-shaped dilatations, with a maximum diameter of about 200 microns, and appeared within vascular segments bearing severe amyloid deposition. In the walls of the aneurysms, the intima was thickened, and the media and adventitia showed thinning and disruption. Fibrinoid necrosis was found in the vascular walls of the most dilated, middle portions of the aneurysm. The vascular walls undergoing fibrinoid necrosis did not show any beta/A4 or cystatin C but presented with fibrinogen-like immunoreactivities, indicating invasion of plasma components. CONCLUSIONS: These results suggested the following sequential events for the pathogenesis of the cerebral amyloid angiopathy-associated vascular lesions leading to hemorrhage: (1) damage of the media and adventitia due to severe amyloid deposition results in dilatation of the cortical arteries, (2) the vascular dilatation progresses and is accompanied by thickening of the intima and disruption of the media and adventitia (microaneurysm formation), (3) plasma components invade to the vascular wall (fibrinoid necrosis), and (4) finally, hemorrhage develops.

Aged↗
PubMed1993

Frequent presence of anti-GQ1b antibody in Fisher's syndrome.

We used the enzyme-linked immunosorbent assay to investigate autoantibodies against the gangliosides GM1, GD1a, GD1b, GT1b, GD2, and GQ1b in sera from 16 patients with Fisher's syndrome. We found high anti-GQ1b antibody titers, mainly those of the IgG class, in the sera of 13 of these patients. The titers decreased with the clinical course of the illness. Moreover, anti-GQ1b antibody-positive patients had more severe ataxia of cerebellar type than the antibody-negative patients.

Adult↗
PubMed1993

The generation of macrophages from precursor cells incubated with brain endothelial cells--a release of CSF-1 like factor from endothelial cells.

The perivascular macrophages in the brain are thought to be derived from bone marrow precursor cells. Results presented here demonstrate that immature macrophages obtained from nonadherent spleen cell populations can adhere to cerebrovascular endothelial cell (EC) monolayers and proliferate. The proliferation of these cells can be stimulated by either purified murine granulocyte-macrophage colony-stimulating factor (GM-CSF) or EC conditioned medium but not by IL-3. No proliferation of the GM-CSF- or IL-3-dependent murine cell line IC-2 was observed in the presence of EC conditioned medium. Macrophage-like cells could also be derived from murine bone marrow cells but inhibited by anti-macrophage-CSF (M-CSF or CSF-1). The capacity of EC conditioned medium to induce the proliferation of macrophage-like cells from the spleen is therefore not due to the release of GM-CSF but CSF-1. In concomitant experiments using mature macrophages incubated on EC monolayers, no proliferation was observed. These findings suggest that the growth of perivascular macrophages in the brain may be stimulated by cerebrovascular EC.

Animals↗
PubMed1993

Shy-Drager syndrome with abnormal circadian rhythm of plasma antidiuretic hormone secretion and urinary excretion.

A 67-year-old patient with Shy-Drager syndrome (SDS), exhibited nocturnal polyuria associated with abnormal circadian rhythm of antidiuretic hormone (ADH) secretion and nocturnal polyuria. The patient excreted a larger volume of urine during the nighttime compared to that in the daytime. The specific gravity of urine at night was lower than that during the day. In contrast to normal circadian rhythm of ADH, the patient's plasma concentration of ADH was increased in the daytime. The present study raised the possibility that an altered circadian rhythm of plasma ADH secretion might be considered a result of the neurodegenerative changes involving the hypothalamus.

Aged↗
PubMed1993

Hereditary lipo-muscular atrophy with joint contracture, skin eruptions and hyper-gamma-globulinemia: a new syndrome.

We previously reported two siblings with decreased subcutaneous adipose tissue, muscular atrophy, joint contractures, recurrent skin eruptions, hyper-gamma-globulinemia, and reduced natural killer cell activity. Some of their clinical features are similar to those of partial lipodystrophy, but they are distinct in that muscular atrophy, joint contractures and recurrent skin eruptions are not found in patients with partial lipodystrophy. Thirteen other Japanese patients with similar clinical manifestations have been reported. We propose that such cases should be considered a distinct clinical entity.

Contracture↗
PubMed1993

[Distribution of nitric oxide synthase activity in rat brain--analysis by high performance liquid chromatography].

As a basic study to investigate the involvement of nitric oxide in the pathogenesis of central nervous system diseases, we have established an assay system to measure nitric oxide synthase (NOS) activity by a high performance liquid chromatography monitoring conversion of arginine into citrulline. NOS activity in the rat brain was calcium-dependent and inhibited by L-nitro-arginine, a specific NOS inhibitor. The activities in the discrete brain regions were in the order cerebellum > olfactory bulb > striatum > hippocampus > cerebral cortex > midbrain > hypothalamus > pons.

Amino Acid Oxidoreductases↗
PubMed1993

[Immunobiological approach to spinocerebellar degeneration--anti-Purkinje cell antibodies in paraneoplastic cerebellar degeneration].

We analyzed the antibodies against cerebellum in five patients with paraneoplastic cerebellar degeneration (PCD). Four patients were found to have autoantibodies against rat brain, first one to cerebral 250 kd and 110 kd and cerebellar 110 kd proteins, second one to cerebral and cerebellar 98 kd and 68 kd proteins, third one to cerebellar 58 kd protein and fourth one to 58 kd protein especially in the cytoplasm and nucleus of Purkinje cells. We isolated a cDNA clone from a human cerebellar library to identify the target antigen for fourth antibody. Homology searches revealed a similarity with the zinc finger proteins. Zinc finger proteins are considered to regulate gene expression. Therefore, degeneration of this protein by its antibody may affect the synthesis of proteins in Purkinje cell and may cause cerebellar degeneration.

Aged↗
PubMed1993

[Sudomotor dysfunction in Parkinson's disease].

Sudomotor function was evaluated by using the sympathetic skin response (SSR) and the sweat response to intradermal acetylcholine (ACh) injection in 69 patients with Parkinson's diseases (PD). The incidence of SSR abnormality (34.8%) was as high as that of orthostatic hypotension (30.4%) and increased with the severity of the illness. Anticholinergic drug did not influence the incidence of SSR abnormality. Therefore, the SSR is useful in evaluating sudomotor efferent pathway in PD patients. Moreover, in all patients, sweat response to ACh showed a reduced number of excitable sweat glands and a low volume of sweat. In a patient in whom sweat response to ACh was markedly impaired, however, the density of acetylcholinesterase-positive unmyelinated fibers in biopsied sural nerve was in normal range. Therefore, this is considered to indicate functional disturbance of the postganglionic sympathetic fibers in PD patients, without morphological changes.

Aged↗
PubMed1993

[Proximal lower motor neuron syndrome associated with serum antibodies to asialo-GM1, GM1 and LM1].

A 31-year-old man had noticed slowly progressive weakness in his right upper limb girdle. On admission at age 32, fasciculation and muscle atrophy were observed in the right pectoralis major muscle. There was mild muscle weakness in the right triceps brachii muscle. The deep tendon reflexes were normal and the pathologic reflexes were absent. Sensory and autonomic nerve functions were intact. Needle EMG showed fibrillation potentials and positive sharp waves in the right pectoralis major, infraspinatus, extensor carpi radialis, extensor digitorum muscles, the bilateral sternocleidomastoideus and triceps brachii muscles. Motor nerve conduction studies revealed normal conduction velocities and distal latencies as well as no evidence of conduction block or abnormal temporal dispersion. Serum immunoelectrophoresis failed to detect an M protein. Thin-layer chromatography with immunostaining revealed that the serum contained auto antibodies which reacted with asialo-GM1, GM1 and LM1. This case must belong to "proximal lower motor neuron syndrome" proposed by Pestronk et al.

Adult↗