[A case of idiopathic parkinsonism with many Lewy bodies in the cerebral cortex (author's transl)].
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Biomedical subjects
Publications and source records attributed to T Yoshimura.
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The effect of the nephrotoxic substance, N-(3,5-dichlorophenyl)succinimide, on the histological pattern and incidence of kidney tumors induced by streptozotocin in rats was studied. In groups administered streptozotocin alone or in combination with nicotinamide, the histological pattern and the incidence of kidney tumors in rats were similar; renal cell tumors developed in 1 of 9 rats (11.1%) and in 2 of 17 rats (11.8%), respectively. However, post-treatment with N-(3,5-dichlorophenyl)succinimide increased the induction of epithelial tumors by streptozotocin, and embryonal cell tumors were also induced nearly as frequently. Administration of nicotinamide alone did not result in the development of kidney tumors.
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Tumorigenic effect of a diet containing quinoline on the liver of various animals and the synergistic or antagonistic effect by other chemicals on quinoline hepatocarcinogenesis in rats were examined. It was concluded that 4,4'-diaminodiphenylmethane (0.1%) and 3-methylcholanthrene (0.0067%) had a significant inhibitory effect on liver carcinogenesis due to quinoline in rats, but 1-naphthyl isothiocyanate (0.06%) and p-hydroxypropiophenone (1.0%) had no inhibitory effect in the present observations. Transmission electron-microscopic study demonstrated the fine structure of vascular tumors induced by quinoline. On the other hand, it was found that quinoline induced liver tumors in both sexes of mice and rats but not in hamsters or guinea pigs. Male rats were more susceptible than females to the tumorigenic action of quinoline, and mice showed the least susceptibility. Histological changes in the liver of rats or mice induced by quinoline were clasified as hemangioendotheliomas or hemangiosarcomas and hepatocellular carcinomas. Several rats treated with quinoline had hemangiosarcomatous metastatic foci in the lung.
A 28-year-old male of progressive myoclonus epilepsy was reported, who had showed a gradual progression in myoclonus, mental retardation and cerebellar symptoms, and had been treated with a large dosage of diphenylhydantoin. Neuropathologically, slight degenerative changes of the cerebrl cortex, especially in the IV layer, the external pallidum, and the dentate and olivary nuclei were observed. The most obvious change was diffuse reduction of Purkinje's and granular cells in the cerebellum. A congenital cyst was found with surrounding gliosis in the central tegmental tract of the pons. A significant relationship between myoclonus and the cyst was proposed, and furthermore, influences of diphenylhydantoin intoxication on the clinicopathological development of myoclonus epilepsy were emphasized.
1 N-(3'-4'-dimethoxycinnamoyl) anthranilic acid (N-5') exhibited a dose-dependent, potent inhibition of the passive cutaneous anaphylaxis (PCA) mediated by homocytotropic antibodies (HTA), which was hardly affected by anti-inflammatory agents such as phenylbutazone, indomethacin and prednisolone at any dose used. The HTA-induced PCA was significantly inhibited by combined treatment with diphenydramine and cyproheptadine. 2 Doses of N-5' which potently inhibited HTA-induced PCA inhibited only slightly the heterologous PCA produced by anti-bovine serum albumin (BSA) rabbit serum. This heterologous PCA was clearly inhibited by phenylbutazone, indomethacin and prednisolone. Diphenydramine and cyproheptadine, singly or combined inhibited the heterologous PCA only slightly. 3 The increased vascular permeability caused by histamine and 5-hydroxytryptamine was significantly inhibited by diphenyldramine or cyproheptadine, but not by N-5' and the anti-inflammatory agents used. 4 N-5' 150 mg/kg orally inhibited rat paw oedema induced by carrageenin by about 26% while phenylbutazone, indomethacin and prednisolone produced significant inhibition. 5 N-5' at concentrations of 100 and 1000 muM significantly inhibited (by about 52% and 95%, respectively) the histamine release from rat peritoneal cells induced by HTA; 10 muM N-5' had little effect. Histamine release was inhibited by phenylbutazone or indomethacin at 1000 muM but not at 100 muM. Prednisolone had no effect on histamine release at any of the concentrations used. 6 These findings suggest that the inhibition of the HTA-induced PCA by N-5' may be due to inhibition of histamine release and is clearly different from the actions of anti-inflammatory agents such as phenylbutazone, indomethacin and prednisolone.
Clonazepam, an antiepileptic benzodiazepine derivative was administered into 30 patients mainly with incurable type epilepsy. Results were as summarized below: (1) Clonazepam was effective in 44.4% of 36 cases of seizures. The initial effect was noticed in 55.6%. (2) Clonazepam was proved to have a broad spectrum in its efficacy. It showed the highest rate of effectiveness, 71.4%, on psychomotor seizures. (3) Clonazepam was effective in all 4 cases of the photogenic epilepsy which shows the photosensitivity in the EEG. With the exception of 1 case, the sensitivity in the EEG also disappeared responding to clonazepam. (4) The Jacksonian type of the partial motor seizure disappeared in 2 cases after the administration with clonazepam. (5) The effects of clonazepam of EEG were examined in 24 patients. The abnormality of the basic activity, the diffuse epileptic discharge and the focal epileptic discharge were improved in 29.2%, 61.5% and 66.7%, respectively. In addition, the rate of the clinical effectiveness was high in the cases with the centrencephalic discharge. (6) Side effects were observed to have appeared in 38.9% of the patients. They were mostly drowsiness and ataxia. (7) Based on the above-mentioned results, it can be claimed that clonazepam is effective on psychomotor seizures, photogenic epilepsy and the secondary type of generalized convulsion (Jacksonian).
Significant elevations of plasma triglyceride and free fatty acids levels were shown in 107 gouty patients, but no significant difference was found in plasma cholesterol and phospholipid levels as compared with control subjects. A positive correlation was found between plasma triglyceride and free fatty acids levels (r = 0.249, P less than 0.05) in gouty patients. The heavy drinkers with gout (15.9% of the patients) had significantly higher plasma triglyceride, free fatty acids and gamma-glutamyltranspeptidase levels than the moderate or non-drinking gouty subjects. These results suggested that excessive intake of alcohol may play an important role in inducing hyperlipidaemia in gout.
1. Erythrocyte adenosine deaminase (EC 3.5.4.4) and purine nucleoside (inosine) phosphorylase (EC 2.4.1.1) were measured in 33 healthy controls and 43 primary gouty subjects. Adenosine deaminase activity in controls and gouty subjects was 0.373 plus or minus 0.108 and 0.457 plus or minus 0.140 A unit per 5-10-3 ml packed red cells per h, respectively. The difference was statistically significant (P less than 0.01). Mean adenosine deaminase: inosine phosphorylase (X10) in primary gout was also significantly higher than in controls (P less than 0.05). Inosine phosphorylase activities in the two groups were not significantly different. 2. When gouty patients were divided into two groups according to weight, normal weight gouty subjects had a higher adenosine deaminase activity and an increased ration of adenosine deaminase to inosine phosphorylase when compared with overweight patients (P less than 0.10). In two control groups divided according to the percentage overweight, such differences were not found. In the case of two gouty groups divided according to the existence of gouty heredity, tophi or renal impairment, adenosine deaminase and inosine phosphorylase activity in the two groups were not significantly different. The possible biochemical role of adenosine deaminase activity in primary gout is discussed.
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