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Biomedical subjects

Y Tabuchi

Publications and source records attributed to Y Tabuchi.

At least 145 records · Page 8Linked to original sources

Effect of captopril on renal vascular resistance, renin, prostaglandins and kinin in the isolated perfused kidney.

Vasodilatory and natriuretic effects of captopril were studied in the isolated hog kidney perfused with modified Krebs-Ringer solution. Renal arterial infusion of captopril caused increases in releases of renin, prostaglandins (PGE2, 6-keto-PGF1 alpha and PGF2 alpha) and kinin, and was accompanied by a decrease in the renal vascular resistance and an increase in urinary sodium excretion. Indomethacin administered with captopril diminished the saluretic effect of captopril and evoked an increase in kinin, but was associated with a marked decrease in prostaglandin and renin releases, while renal vascular resistance remained decreased. Indomethacin alone did not alter vascular resistance and kinin; however, renin and prostaglandin releases were decreased. Aprotinin administered with captopril showed a decrease in releases of prostaglandins, renin and kinin without any change in vascular resistance. These results suggest that increased release of kinin induced by captopril contributes to a reduction in renal vascular resistance. Increased prostaglandin release after captopril administration may be caused by an increase in kinin without direct involvement of captopril in prostaglandin synthesis. Renal prostaglandins may enhance sodium excretion and mediate renin secretion in captopril perfusion.

Animals↗

The diagnostic significance of large action potentials in myopathy.

Electromyographic and histopathological studies were performed on 112 skeletal muscles in 101 subjects with myopathy. The diagnostic significance of large action potentials (LAPs) in myopathy was studied. LAPs were defined as those action potentials with a duration of over 13 ms and an amplitude of over 3 mV (peak to peak). The following results were obtained: Most muscles with LAPs showed the grouped atrophy of small fibers of neuropathic change in addition to myopathic findings. Even in myopathy most LAPs reflected neuropathic change, except in thyrotoxic myopathy. LAPs were not related to an increase of connective tissue increasing the impedance in volume conduction of the action potentials. LAPs were frequently seen in: progressive muscular dystrophy of limb-girdle type; scapuloperoneal dystrophy; distal myopathy; oculopharyngeal dystrophy; myotonic dystrophy; polymyositis; and thyrotoxic myopathy. Other types of myopathy had few LAPs. There were two types of progressive muscular dystrophy. One had LAPs frequently and the other, rarely. In myotonic dystrophy the muscles with LAPs showed scattered small angular fibers, possibly indicating neurogenic changes. Interstitial myositis had LAPs more frequently than parenchymatous polymyositis. The chronic phase of polymyositis had LAPs more frequently than the acute or subacute phases. In thyrotoxic myopathy the muscles with LAPs rarely showed definite neuropathic change histopathologically. Therefore, LAPs in thyrotoxic myopathy may not indicate denervation.

Action Potentials↗

Morphologic changes in the hypertensive placenta.

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.

Adult↗

Effect of cellular reaction in gastric cancer tissue and in regional lymph nodes on the mitotic activity of cancer cells.

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.

Adenocarcinoma↗

A sporadic juvenile case of the amyotrophic lateral sclerosis with neuronal intracytoplasmic inclusions.

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.

Adolescent↗

Induction of tumors in heterotopic bladder by topical application of N-methyl-N-nitrosourea and N-butyl-N-(3-carboxypropyl)nitrosamine.

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.

Animals↗