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Biomedical subjects

H Beppu

Publications and source records attributed to H Beppu.

At least 55 records · Page 3Linked to original sources
PubMed1984

Analysis of cerebellar motor disorders by visually guided elbow tracking movement.

Motor control was analysed by a visuomotor tracking movement using elbow flexion both in patients with cerebellar ataxia and in normal controls. A TV screen was divided into upper and lower halves, in each of which a vertical strip was displayed. The upper strip (T, target) was moved horizontally from the centre of the screen to the left or right by ramp voltage. The lower strip (D, displacement of the handle) was moved in proportion to angular displacement of the handle by a potentiometer coupled to the handle axis. The subject, while sitting in front of the TV screen, had to make D match the movement of T by controlling the handle with his right arm. The range of T movement was 30 deg in terms of the handle's angular movement. T velocity was 7.5, 15 or 30 deg/s. The subjects were told the direction and velocity of T in advance. The process of tracking was divided into three phases (initial catch-up phase, middle pursuit phase, and terminal phase), in each of which the performance of cerebellar ataxia patients differed from that of the controls. The characteristic features of the ataxic cases were (1) prolongation of the reaction time, mainly due to the increase of premotor time; (2) difficulty in selecting an appropriate amplitude of initial peak velocity in proportion to the target velocity in the initial catch-up phase; (3) disruption of smooth continuous movement, namely, the saccadic pattern in the middle pursuit phase; (4) delay in the initiation of deceleration in the terminal phase; (5) difficulty in corrective adjustment in reaching the final target point; and (6) irregular EMG activity in the agonist muscles and/or cocontraction of the antagonistic muscles. Quantitative treatment of the second and third features, as exemplified in the relationship between initial error and initial peak velocity and in the ratio of the movement arrest period, respectively, was found to be helpful in the evaluation of disease severity. The significance of these findings is discussed and the role of the cerebellar system in the control of slow voluntary movement is stressed.

Adult↗
PubMed1984

Mitochondrial encephalomyopathy: fluctuating symptoms and CT.

We describe a 29-year-old man with mitochondrial encephalomyopathy. The patient's disorder was characterized by lactic acidosis, hemiparesis, seizures, aphasia, and hemianopia. CT revealed low-density areas that corresponded to the symptoms. His 56-year-old mother is also involved subclinically, demonstrating that muscle biopsy is an important requisite in the final determination of a familial inheritance pattern in mitochondrial myopathy. Neuronal mitochondrial disorders are suggested as the pathogenesis of his neurologic symptoms.

Adult↗
PubMed1983

Concanavalin A binding sites on the erythrocytes of normal and genetically dystrophic chickens.

Red blood cells (RBCs) were obtained from genetically dystrophic chickens (Dy) and age-matched controls (C). Dy-RBCs had a lower titer of agglutination to concanavalin A (Con A) compared to C-RBCs. In order to ascertain the difference in agglutination, Con A binding on RBCs was studied, using 125I-labeled Con A ([125I]Con A) and ferritin conjugate to Con A (Fer-Con A). Kinetic analysis of [125I]Con A binding to Dy-RBCs showed a reduction of major binding sites of Con A. There was no difference in the apparent association constant for the major binding sites of Con A between Dy-RBCs and C-RBCs. Quantitative analysis of Con A binding site distribution on RBCs using Fer-Con A showed a remarkable diminution of ferritin particles tagged on the surface of Dy-RBCs. There was no significant difference in the distribution pattern of ferritin particles between Dy-RBCs and C-RBCs.

Agglutination Tests↗
PubMed1981

beta-Galactosidase-neuraminidase deficiency in adults: deficiency of a freeze-labile neuraminidase in leukocytes and fibroblasts.

4-methylumbelliferyl neuraminidase activity was studied in fibroblasts, leukocytes, and frozen tissues from adult patients with beta-galactosidase-neuraminidase deficiency and specific clinical manifestations. This enzyme was almost completely deficient in fibroblasts, but the residual activity was relatively high (20% of the control mean) in the leukocytes from the patients. The frozen liver from one patient showed the enzyme activity as high as controls. This enzyme consisted of two components, freeze-labile and freeze-stable, and it was demonstrated that only the labile enzyme was deficient in fibroblasts and leukocytes. The apparently normal activity of neuraminidase in frozen autopsy tissues of a patient may be explained by the loss of the labile component in control tissues after a long-term freezing. The neuraminidase activity was variable in parents and no definite conclusion was drawn on the hereditary nature of the disease.

Brain↗