[Serum creatine phosphokinase levels of rural and urban subjects in Japan].
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Biomedical subjects
Publications and source records attributed to Y Tabuchi.
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Pregnancy complicated by hypertension is commonly associated with placental insufficiency, thereby resulting in fetal growth retardation. Furthermore, reduced utero-placental blood flow has been recognized in cases of severe preeclampsia with hypertension. Thus, it must be assumed that histological as well as ultrastructural findings in hypertensive placentas are due to the occlusion or narrowing of the uteroplacental vasculature as well as placental ischemia. Microscopically, these placental changes include infarcts, increased syncytial knots, hypovascularity of the villi, cytotrophoblastic proliferation, thickening of the trophoblastic basement membrane, obliterative enlarged endothelial cells in the fetal capillaries and atherosis of the spiral arteries in the placental bed. In addition, ultrastructural features are characterized by a decreased number of syncytial microvilli, proliferation of cytotrophoblastic cells, focal syncytial necrosis, thickening of trophoblastic basement membrane and narrowing of the fetal capillaries, as a number of studies have demonstrated. These placental abnormalities can be seen not only in human toxemia, but also in animals with experimentally induced toxemia or with spontaneous toxemia.
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An in vivo stathmokinetic technique was used to analyze the mitotic activity of cancer cells from 47 gastric cancer patients. The effect of cellular reaction in cancer tissues and regional lymph nodes on the mitotic activity of cancer cells was examined. Based on the main kind of infiltrating cells in cancer tissues, the cellular reaction was classified into agranulocyte (lymphoid leukocyte) type and granulocyte type. Agranulocyte type was found in 40 cases. The mitotic activity of cancer cells was examined in relation to the degree of agranulocyte infiltration: the average mitotic index in cancer cells 16 hr aft a single dose (0.02 mg/kg body weight) of vincristine sulfate was 91.5% in 22 cases of trace and slight infiltration, 81.3% in 12 cases of moderate infiltration and 53.2% in 6 cases of marked infiltration. The 3 values of mitotic index were significantly different from one another. The relationship between the average mitotic index of cancer cells in primary cancer lesions and the 4 groups of regional lymph node reaction was examined. However, statistically significant results were not obtained. These results suggest that the infiltration of agranulocytes in cancer tissues affects the mitotic activity of cancer cells, and that moderate and marked degrees of infiltration suppress the mitotic activity. It was also suggested that the reaction of regional lymph nodes does not affect the mitotic activity of cancer cells in primary cancer lesions.
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In an autopsy case of the sporadic juvenile ALS (a 17-year-old girl) intracytoplasmic inclusions are found in the upper and lower motor neurons and in nerve cells of the dentate nucleus, pontine nucleus, brain stem reticular formation, substantia nigra, thalamus, globus pallidus and others. Histochemically they contain RNA-Protein compounds. Electron microscopically, they consist of randomly interwoven tubules with granular endoplasmic reticulums and free ribosomes in the margin. Each tubule measures 90--150 A in diameter and shows no distinct periodic constiction. Amorphous substances as well as ribosome granules are scattered and associated with those tubules. The inclusion-bearing cells are usually swollen and chromatolytic and have a large hydropic nucleus, suggesting a close relation between the development of the inclusion and chromatolysis. Clinically, a rapid progress of the symptoms (total duration: about 12 months) and conspicuous disturbances of the autonomic nerve, such as sinus tachycardia and bladder sphincter dysfunction, should be noticed.
The heterotopic urinary bladder with a communicating reservoir is a potentially useful model for bladder carcinogenesis studies. As a test of whether such bladders will develop transitional cell carcinomas after chronic carcinogenic stimuli, two carcinogens, N-methyl-N-nitrosourea and N-butyl-N-(3-carboxypropyl)nitrosamine, were instilled repeatedly into the reservoir connected with the heterotopic bladder. Transitional cell carcinomas developed in 25 of 33 heterotopic bladders exposed to cumulative doses of 1.5, 3.0, or 6.0 mg of N-methyl-N-nitrosourea for between 20 and 30 weeks, while heterotopic bladders exposed to cumulative doses of 150 or 300 mg of N-butyl-N-(3-carboxypropyl)nitrosamine failed to develop tumors. However, 11 of 27 rats with heterotopic bladders that were exposed to N-butyl-N-(3-carboxypropyl)nitrosamine for over 20 weeks developed tumors in their homotopic or natural bladders. N-Methyl-N-Nitrosourea probably acted directly on the bladder epithelial cells to induce neoplastic change. The reason(s) for the development of tumors in homotopic but not heterotopic bladders when N-butyl-N-(3-carboxypropyl)nitrosamine was administered directly into the heterotopic bladders could not be ascertained from these studies.
The process of erosion formation in the glandular stomach of the rat given single and multiple intragastric doses of 100 mg N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)/kg body weight, was studied histologically, histochemically, and ultramicroscopically and compared with erosion induced by other gastric carcinogens and erosion-forming chemicals. The acute effect of several nongastric carcinogens on the glandular mucosa was also studied. The earliest degenerative transformation, fatty change, was found in the surface mucous cells within 1 hour a one-pulse intragastric dose of 100 mg MNNG/kg body weight; the change gradually progressed into deeper glandular cells and after three successive doses, erosion was complete in every rat. Ultrastructurally, four main glandular cells showed essentially similar degenerative alterations. Fatty change was also induced by other gastric caricnogens such as 4-nitroquinoline-1-oxide, methylnitrosocyanamide, methylnitrosourea, N-2-fluorenylacetamide, and iodacetamide, a noncarcinogenic alkylating agent. Mucosal damage induced by acetylsalicylic acid and thermal burn did not show fatty change. Nongastric carcinogens failed to induce mucosal damage. The relationship of the carcinogen-induced fatty change and mucosal damage to carcinogenesis was discussed.
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