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Biomedical subjects

H Mizusawa

Publications and source records attributed to H Mizusawa.

At least 55 records · Page 3Linked to original sources
PubMed2001

Differentiating between progressive supranuclear palsy and corticobasal degeneration by brain perfusion SPET.

The purpose of this study was to evaluate the usefulness of brain perfusion single photon emission computed tomography (SPET) to differentiate between progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD). Twelve patients with PSP and 12 with CBD were examined by brain perfusion SPET using 99Tc(m)-ethyl cysteinate dimer (99Tc(m)-ECD). The regions of interest (ROIs) were five cortical regions, the basal ganglia, the thalamus, the cerebellar cortex and the brain stem. The mean regional cerebral blood flow (CBF) and the mean right/left asymmetry index in each ROI were calculated. The asymmetry index of the regional CBF was significantly higher in CBD patients compared with PSP patients in all of the cortical regions and in the basal ganglia. The greatest differences in asymmetry were in the parietal cortex (P<0.001), high frontal cortex (P<0.001), frontal cortex (P<0.005), temporal cortex (P<0.01) and basal ganglia (P<0.01). Significant asymmetry was also detected in the occipital cortex (P < 0.05). No significant difference in asymmetry was found in the thalamus or the cerebellum. There were no significant differences between the two groups in any of the regional CBF values. In conclusion, brain perfusion SPET with 99Tc(m)-ECD is useful in detecting the significantly higher perfusion asymmetry in CBD patients compared with PSP patients in all cortical regions and in the basal ganglia. SPET may be a useful tool for differentiating between PSP and CBD.

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PubMed2001

Presynaptic inhibition of cerebellar GABAergic transmission by glutamate decarboxylase autoantibodies in progressive cerebellar ataxia.

Autoantibodies against glutamic acid decarboxylase (GAD) have been found in stiff-man syndrome, insulin dependent diabetes mellitus, and progressive cerebellar ataxia. A patient with progressive cerebellar ataxia is described who was positive for GAD autoantibodies, and had Sjögren's syndrome. Immunohistochemical studies using CSF and serum samples from the patient showed immunoreactivities in axon terminals of cerebellar GABAergic neurons. A whole cell patch clamp technique recording from rat cerebellar slices showed that the CSF, presumably through GAD autoantibodies, presynaptically inhibited GABAergic transmission. Intravenous administration of immunoglobulin failed to improve clinical symptoms and immunoreactivities examined after therapy. The findings suggest that GAD autoantibodies play a pathogenic part in reducing GABA release in in vitro slices.

Aged↗
PubMed2001

Preferential recruitment of ataxin-3 independent of expanded polyglutamine: an immunohistochemical study on Marinesco bodies.

In an immunohistochemical study of Marinesco bodies--a neuronal intranuclear inclusion often seen in neurons of the substantia nigra of patients with hepatic encephalopathy--it was shown that one of the polyglutamine proteins, ataxin-3, is preferentially recruited into this inclusion, whereas other polyglutamine proteins (ataxin-2 and TATA box-binding protein) are not. This suggests that recruitment of each of the polyglutamine proteins may be differently regulated. Because this nuclear inclusion is thought to be formed in response to cellular stress, as occurs in hepatic encephalopathy, even in the absence of an expanded CAG/polyglutamine repeat, recruitment of ataxin-3 and ubiquitin into Marinesco bodies may represent a cellular response to noxious external stimuli unrelated to expanded CAG/polyglutamine.

Aged↗
PubMed2001

Immunohistochemical diagnosis of Cryptococcus neoformans var. gattii infection in chronic meningoencephalitis: the first case in Japan.

Cryptococcus neoformans (C. neoformans) var. gattii infection usually occurs in tropical and subtropical areas, and rarely in the northern hemisphere. We report the first Japanese with cryptococcal meningoencephalitis caused by C. neoformans var. gattii infection that occurred during a trip to Australia. This agent was identified in a cerebellar biopsy specimen by immunohistochemical technique with serotype-specific anti-sera. Because the meningitis caused by it did not respond well to conventional therapy, we used an aggressive therapeutic regimen to successfully treat the patient. Even in areas where C. neoformans var. gattii does not exist, this infection should be considered possible as a travel-related infection.

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PubMed2001

[Japanese guidelines on research use of human materials and disease information].

Demand on the use of human materials and personal disease information for research and development comes on the stage of action. International competition in biomedical and pharmaceutical research pushed the government and related societies about to release guidelines on the issue to ensure the protection of direct and indirect research participants. To work on human materials and information now requires ethical and scientific review by the research ethical committee and the guidelines set the stage of reviewing process. We should aware of the overall view of situation around and of the guidelines before planning the experiments and analyses on human materials and personal information. In this review we summarized the related guidelines and put comments on them to help researchers to understand the situation.

Embryo, Mammalian↗
PubMed2001

[Spinocerebellar ataxia type 6].

Spinocerebellar ataxia type 6 (SCA6) is an autosomal dominant cerebellar ataxia caused by a CAG repeat expansion in the human alpha1A-calcium channel gene. In this section, recent advances regarding pathogenic mechanism underlying in SCA6 is presented. When human alpha1A-calcium channel gene with expanded CAG repeat is transfected into HEK cells, the voltage dependence of inactivation shifting negatively 6 to 11 mV was observed, indicating that calcium influx across plasma membrane is reduced. When alpha1A-calcium channel protein and polyglutamine stretch are examined in SCA6 brain by immunohistochemistry, formations of aggregations within the cytoplasm of SCA6 Purkinje cells were seen. These findings may indicate that both alteration of calcium channel function and formation of protein aggregation are involved in the pathogenic mechanism of SCA6.

English Abstract↗
PubMed2001

[Episodic ataxia type 2].

Episodic ataxia type 2 is an autosomal dominant paroxysmal cerebellar ataxia characterized by acetazolamide-responsive recurrent attacks with interictal nystagmus. This disease is caused by mutations (mainly truncating mutation) within the alpha1(A) subunit of P/Q type voltage-dependent calcium channel gene, CACNA1A. Further researches would establish the genotype/phenotype correlation and clarify the mechanism of this disorder.

English Abstract↗