[Suggestions to the requirements of future midwives].
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Biomedical subjects
Publications and source records attributed to Y Shindo.
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We report a 24-year-old male patient with sarcoidosis who developed subcutaneous nodules on his thighs and buttocks at the sites of repeated intramuscular injections. Histologically, there were extensive areas of caseation necrosis surrounded by typical sarcoidal granuloma. The nodules regressed spontaneously over a period of 4 months, concurrently, both his bilateral hilar adenopathy and the results of immunological tests, returned to normal. We think that these lesions developed at the sites of subcutaneous scar tissue induced by frequent injections in childhood. We believe the pathomechanism to be similar to that for scar sarcoidosis, and that the extensive caseation necrosis reflected a regressing stage of the disease.
To study transforming potential as well as growth stimulating activity of the fos genes on primary cells, we have developed avian retrovirus vectors by constructing derivatives of Rous sarcoma virus DNA in which the v-src gene was replaced by either the v-fos gene of FBJ-MuSV or the mouse c-fos gene. After each derivative was introduced into chicken embryo fibroblasts by transfection, replication-competent viruses that carry the v-fos gene (FJ2) or the c-fos gene (FM4) were recovered. FM4 and FJ2 introduced the fos genes into almost all chicken embryo fibroblasts within 3 days after infection, expressed their gene products, and induced morphological transformation and colony formation in soft agar. Results show that overproduction of the c-fos gene product is enough for cellular transformation not only of rat established fibroblasts as reported previously but also of avian primary fibroblasts. Using this vector system, we have further shown that the c-fos gene and the v-fos gene have biological activities that induce cellular proliferation of chicken neuroretinal cells, which normally stay in the resting stage of growth in monolayer culture.
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We conducted a prospective evaluation of the effects of chronic captopril therapy on glucose tolerance in 8 nondiabetic, hypertensive patients and 6 hypertensive patients with impaired glucose tolerance, including 3 diabetic patients. Captopril was well tolerated by all patients, and no untoward effects were observed. Chronic captopril therapy produced a significant decrease in blood pressure in all patients. No patients with normal glucose tolerance developed diabetes mellitus. Neither fasting nor post-glucose-load venous plasma glucose deteriorated in any patients during chronic captopril therapy. There were no significant changes in the insulinogenic index (delta IRI/delta BS at 30 min post-glucose load) in patients with either normal or impaired glucose tolerance. These results suggest that, in addition to its antihypertensive effect, chronic captopril therapy does not compromise glucose metabolism in hypertensive patients. Thus, captopril may have a clinical advantage in that it apparently can be given safely to hypertensive patients with either normal or impaired glucose metabolism.
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The acute effect on the renin-angiotensin system and the pharmacokinetic properties of delapril, a new angiotensin converting enzyme inhibitor and its active diacid metabolites (delapril diacid and 5-hydroxy delapril diacid) arising from delapril in vivo were investigated in 4 hypertensive patients with chronic renal failure (CRF: 4 males, average age 49.5 (37-64) years, mean Ccr 22.2 ml/min/1.73 m2) and 9 patients with essential hypertension (EH: 6 males, 3 females, average age 42.8 (28-61) years, mean Ccr 79.3 ml/min/1.73 m2). In CRF, following a single dose of delapril hydrochloride (30 mg), the biological half lives (t1/2) of delapril diacid and 5-OH-delapril diacid were 4.69, 12.88 hours, the maximum serum concentration (Cmax) and the area under the plasma concentration-time curve ([AUC]24(0)) of delapril and its diacid metabolites were 414, 797 and 435 ng/ml, and 658, 6400 and 5068 ng X h/ml, respectively. In EH, the t1/2 of delapril diacid and 5-OH-delapril diacid were 1.21, 1.40 hours and the Cmax and [AUC]24(0) of delapril and its diacid metabolites were 489, 635 and 229 ng/ml, and 572, 1859 and 948 ng X h/ml, respectively. The [AUC]24(0) in CRF were significantly increased as compared with those in EH. The cumulative urinary excretions were significantly lower in CRF than in EH. The serum angiotensin converting enzyme (ACE) was markedly inhibited in both groups up to 24 hours. The plasma concentration of angiotensin II decreased in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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