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Biomedical subjects

M Inokawa

Publications and source records attributed to M Inokawa.

7 recordsLinked to original sources
PubMed1999

Role of somatosensory feedback from tools in realizing movements by patients with ideomotor apraxia.

In order to investigate the underlying mechanism of ideomotor apraxia, we studied 9 patients who could not mime using tools despite the ability to manipulate actual tools normally. In all the mime tasks, visually presented tools or model gestures by examiners were fundamentally ineffectual in improving the patients' performances. Even the remarkable improvement demonstrated when using actual tools disappeared immediately after the subjects took their hands off them. In a further experiment, 4 of the 9 patients were required to pretend to use tools while holding a stick, resulting in significant improvements or normal miming. These findings suggest that the somatosensory feedback continuously supplied from a handheld tool is a crucial component in enabling patients with ideomotor apraxia to actually use tools.

Acoustic Stimulation↗
PubMed1998

Amnesia after a discrete basal forebrain lesion.

Destructive lesions of the basal forebrain are often associated with memory impairment and this structure is thought to contribute to memory function by providing a cholinergic input to critical structures associated with memory such as the hippocampus and amygdala. In previously reported cases of amnesia associated with damage in the basal forebrain, multiple neuroanatomical regions were damaged, and the critical lesion responsible for amnesia has not been identified clearly. We report a patient who developed primarily anterograde amnesia after clipping of an unruptured anterior communicating artery aneurysm. Postoperative magnetic resonance imaging showed a discrete lesion, centering in the right diagonal band of Broca and including the anterior hypothalamus, septal nucleus, lamina terminalis, and paraterminal gyrus, and an indiscrete patchy lesion in the corresponding area on the opposite side. The nucleus basalis of Meynert was minimally affected and the diencephalon was not damaged. Single photon emission computed tomography showed marked hypoperfusion in the midline frontobasal region corresponding to the MRI lesion and hypoperfusion in the hippocampus bilaterally. It is concluded that disconnection of the pathway between the diagonal band of Broca and the hippocampus contributed to memory impairment.

Amnesia↗
PubMed1988

Effects of 3-methyl-1-(5-oxohexyl)-7-propylxanthine on the in vivo release of monoamines studied by intracerebral dialysis.

The effect of a xanthine derivative, 3-methyl-1-(5-oxohexyl)-7-propylxanthine (HWA 285, 10 mg/kg i.p.), on the release of endogenous monoamines and their metabolites from the rat striatum and hippocampus are examined in vivo by intracerebral dialysis technique. Using this method, which is based on the dialysis principle, a small-calibered (0.5 mm) dialysis tube is inserted into the striatum or hippocampus transversally and is perfused with Ringer solution. The amounts of dopamine, 3,4-dihydroxyphenylacetic acid, homovanillic acid, 5-hydroxytryptamine and 5-hydroxyindoleacetic acid in the perfusates are measured by high performance liquid chromatography system with electrochemical detection. HWA 285 (10 mg/kg) decreased monoamine levels in hippocampal perfusates after its i.p. administration. However, there were no consistent changes in monoamine release in striatal perfusates after the drug administration. These findings suggest that HWA 285 exerts an inhibitory influence on hippocampal dopaminergic and serotonergic systems.

Animals↗
PubMed1984

Effects of methylmercury and some metal ions on microtubule networks in mouse glioma cells and in vitro tubulin polymerization.

Mercury compounds and some other metal ions were investigated with respect to their effect on in vitro tubulin polymerization and on cellular microtubules in mouse glioma. In vitro tubulin polymerization was completely inhibited by 2.5 X 10(-5) M Hg2+, 5 X 10(-5) M CH3Hg+, 2 X 10(-4) M Cr3+, 2.5 X 10(-4) M Cu2+, and 5 X 10(-4) M Cd2+. Zn2+ did not affect the polymerization up to 5 X 10(-4) M. Indirect immunofluorescence study with rabbit antiporcine tubulin antibody revealed that methylmercury disrupted the microtubule network at an early stage of growth inhibition. On the other hand, in the presence of Cd2+, Cu2+, and Cr3+ at their growth inhibitory concentrations, no effects on microtubule networks were observed for the first 1 hr. These results indicate that only methylmercury affects cellular microtubules, while other ions seem to interfere with other sites in the cells, although these ions showed the ability to depress in vitro tubulin polymerization.

Animals↗
PubMed1983

Studies on biological actions of dimethyl sulfoxide in familial amyloidosis.

DMSO was therapeutically administered to patients with FAP and in about half of the patients there was some clinical improvement. Urinary proteins were analyzed biochemically and immunochemically before and after DMSO administration in seven cases of amyloidosis. As the results, increased excretion of various proteins of different molecular weights in the urine was observed depending on cases and examined organs. The in vitro effects of DMSO on amyloid proteins were examined. DMSO-degraded amyloid proteins showed void-volume materials and lower molecular weight components on Sephadex G column elution profiles as did guanidine-degraded amyloid protein. Among various denaturating or reducing agents, DMSO is the least potent in dissolving amyloid fibrils into prealbumin-related proteins.

Adult↗
PubMed1980

Mechanism of methylmercury cytotoxicity: by biochemical and morphological experiments using cultured cells.

Effects of methylmercury on the cell growth of mouse glioma in vitro were studied in relation to the microtubules as a possible target. The electron microscopic observation revealed that methylmercury added in culture medium specifically attacked microtubules in the cells at growth inhibitory concentration, while mercuric mercury injured microtubules to the same extent as other cell organelles. However the latter showed a little stronger depressing effect on tubulin polymerization in vitro than the former. Further, 3 other inorganic metal ions (Cd2+, Cu2+ and Cr3+), which were reported to suppress tubulin polymerization in vitro, did not disturb the microtubule networks even at their cell growth inhibitory concentrations. Therefore, of these metal compounds tested, when they were added in the culture medium, methylmercury seemed to specifically interact with microtubules and cause inhibition of cell growth.

Animals↗