The difference in endocrine functions in right and left segmental pancreas autografts in dogs.
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Biomedical subjects
Publications and source records attributed to M Gotoh.
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The influence of neuropeptides on hypothalamic regulation of plasma glucose and pancreatic hormone secretion was studied in anesthetized rats. Neuropeptides were injected directly into the ventromedial hypothalamus (VMH) and the lateral hypothalamic area (LHA) and changes in hepatic venous plasma glucose, insulin, and glucagon concentrations were studied. Injection of bombesin into the VMH resulted in a marked and sustained hyperglycemia in the hepatic venous plasma, which was also observed after injection into the LHA. Microinjection of SRIF into the VMH or LHA caused a decrease in hepatic venous plasma glucose concentration. Injection of neurotensin into the VMH or LHA resulted in a transient release of insulin in the 10-min postinjection samples. In 30- and 60-min postinjection samples, significant increases in glucagon concentrations were observed after substance P injection into the VMH or LHA. No major difference in the plasma glucose, insulin, or glucagon concentrations was observed when VMH and LHA stimulation was compared. These data suggest that glucoregulatory neuropeptides may act on the VMH and LHA, which do not necessarily follow the currently recognized anatomical boundaries.
In low-renin hypertensive patients, the acute effect of the angiotensin I-converting enzyme inhibitor, captopril, was evaluated in relation to the response of plasma bradykinin (PBK) levels as a parameter of its inhibitory effect on kininase II. Captopril significantly lowered the blood pressure and increased PBK levels. While there was no significant relationship between the reduction of blood pressure and pretreatment plasma renin activity, a significant correlation was observed between the antihypertensive effect of captopril and changes in PBK (r = -0.834, p less than 0.01, n = 10). Furthermore, in a patient with primary aldosteronism and, also, in a patient with glucocorticoid responsive hyperaldosteronism, captopril increased plasma PBK with reduction of the blood pressure. It is likely, therefore, that in low-renin hypertension, the vasodepressor effect of acute converting enzyme inhibition is due mainly to kinin accumulation rather than inhibition of angiotensin II formation.
Captopril, an orally active angiotensin-converting enzyme inhibitor, was administered to 15 patients with essential hypertension. The serum lipid peroxides level, aldosterone concentration in plasma and blood pressure decreased rapidly after administration, while plasma renin activity was not significantly changed. It is suggested that inhibition of angiotensin-converting enzyme by captopril offers a possible therapeutic approach to the treatment of atherosclerosis complicated with hypertension.
We report 4 cases of double cancer, combined sarcoma and carcinoma. Case 1 was a 50-year-old woman, had a malignant fibrous histiocytoma in the leg and an advanced gastric carcinoma. The soft tissue sarcoma was resected and the gastric carcinoma was treated with chemotherapy. She died from pulmonary metastasis from the sarcoma. Case 2 was a 72-year-old woman with a liposarcoma in the leg and a thyroid carcinoma. Both tumors were resected, however, she died from pulmonary metastasis from the carcinoma. Case 3 was a 65-year-old man with a liposarcoma in the buttock and lung carcinoma. Both tumors were resected and he is alive and disease-free. Case 4 was a 47-year-old man with spindle cell sarcoma of the tibia and a rectal carcinoma. Both tumors were treated surgically, but he died from pulmonary metastasis from the sarcoma. We suggest that the combination of sarcoma and carcinoma is very rare and that the prognosis in these cases is very poor.
A morphological study of the Leydig's cells in the testes of cryptorchid patients was made by light and electron microscopy. Seventy four unilateral and bilateral cryptorchids (aged 2 to 37 years) were selected for light microscopic observation, and 28 of these specimens were also examined by electron microscopy. In 5 cases of pre-pubertal and pubertal cryptorchids, tissue specimens were biopsied after 20,000 units of HCG had been given and examined similarly. In addition, Leydig's cell density was evaluated quantitatively in the undescended and contralateral scrotal testes of 12 post-pubertal patients. This was based on the determination of the total number of Leydig's cells, Leydig's cell clusters and seminiferous tubules in the entire histologic section of each biopsy and the calculation of the following indices; mean number of Leydig's cells per tubule, mean number of Leydig's cell clusters per tubule and mean number of Leydig's cells per cluster. In addition, the number of Sertoli's cells was counted, and the ratio of Leydig's cells to Sertoli's cells was also calculated. In the undescended testes, almost no mature Leydig's cells were found by light or electron microscopy during pre-pubertal periods; and, even in puberty they were few, while immature precursor Leydig's cells were abundant. In the 5 cases treated preoperatively with HCG, even at 5 years, mature Leydig's cells were observed by light and electron microscopy. On the contrary, after puberty, not only the undescended but also the contralateral scrotal testes of the cryptorchids had more mature Leydig's cells than the normal controls. This Leydig's cell hyperplasia was also confirmed by the quantitative analysis of Leydig's cell density. In the mature Leydig's cells of the undescended testes, however, the electron microscopic observation showed marked regressive changes, in cytology especially prominent depletion of the smooth endoplasmic reticulum and frequent occurrence of specific cytoplasmic inclusion bodies. Such regressive changes as found in the cells of the undescended testes were not observed in the cells of the contralateral scrotal testes. Thus, the morphological alteration of Leydig's cells observed here suggest that the cells are in a dysfunctional condition and that the androgen production is consequently decreased in the undescended testes of cryptorchid patients.
Morphological changes in the wall of the seminiferous tubules in the cryptorchid testes were studied using light and electron microscopy. Seventy four unilateral and bilateral cryptorchids (aged 2 to 37 years) were selected, and biopsied specimens were stained with H-E, Azan and Weigert for light microscopic observation. Twenty eight of these specimens were also examined by electron microscopy. In the undescended testes, light microscopy showed irregularity and thickening of the wall (tunica propria), and the thickened wall strongly reacted to the Azan stain. This thickening of the tunica propria was observed to begin at puberty, but was not found in the contralateral scrotal testes of the cryptorchids or in the normal testes. The wall of the normal adult testes was well stained by the Weigert stain, suggesting the presence of elastin. In the undescended testes, however, the wall was not stained in prepubertal or pubertal patients, and even after puberty the wall was stained much less than that in the contralateral scrotal testes and the normal controls. On electron microscopic observation, various ultrastructural changes were noticed in each component of the tubular wall; basement membrane, fibrous layer and cellular layer. In the undescended testes, the lamina densa of the basement membrane consisted of one layer with a serrated outer margin throughout the pre-pubertal and pubertal periods, while after puberty the lamina densa underwent marked multiple lamella formation and increased in thickness. In the fibrous layer was already noticed in the undescended testes of 5-year-old cryptorchids. The development of myoid cells in the cellular layer during puberty was observed to be delayed. The morphological changes occurring in the seminiferous tubular wall of the cryptorchid testes were believed to be related to the impaired spermatogenesis often found in cryptorchidism.
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Pest control operators usually spray pesticides in small areas such as a kitchen in a restaurant and are exposed to various pesticides, especially those of the organophosphorus (OP) type. In order to evaluate their occupational exposure to OP pesticides during the work, OP pesticides in blood and alkyl phosphate metabolites in urine of these operators were analyzed and the relationship between pesticide exposure and analytical results were studied. OP pesticides in blood were analyzed by gas chromatography with flame photometric detector (FPD-GC) after separation of phospholipid in blood with silicagel column chromatography. OP pesticides were not detected in any blood samples (the limit of detection was 1 ng/ml). Dimethylphosphate (DMP) and dimethylthiophosphate (DMTP), being urinary metabolites of OP pesticides, were analyzed by FPD-GC after benzyl derivatization. This method eliminated interfering peaks in gas chromatograms. The ratio of two isomeric derivatives of DMTP was found to be constant. Both DMP and DMTP of the exposed group were significantly higher than those of the non-exposed group, DMP being higher than DMTP. The ratio of DMP to DMTP in the fenitrothion-dichlorvos-exposed group was significantly higher than that in the fenitrothion-exposed group. It was considered that the ratio might reflect a result of pesticide exposure. The urinary metabolites of OP pesticides tended to become lower with the lapse of time since the last exposure. However, small amounts were detected in a few samples even 5 days after the last exposure.
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Two cases of inverted papilloma of the urinary bladder are reported. The patients were a 39-year-old male with macrohematuria and a 36-year-old female with interrupted urination. In both of the patients, tumors were resected transurethrally, and histologic examination revealed them to be typical inverted papilloma.
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In order to clarify the role of the kallikrein-kinin system in the hypotensive mechanisms of converting-enzyme inhibition, captopril was administered in a single oral dose of 50 mg to 17 hypertensive patients, of whom 14 had essential hypertension, one had chronic renal failure, one had primary aldosteronism, and one had glucocorticoid responsive hyperaldosteronism. Captopril lowered blood pressure remarkably in either low-renin or normal-, and high-renin hypertensives, however, there was no significant relationship between the fall in blood pressure and pretreatment levels of plasma renin activity (PRA) in any of the patients any time after the administration. PRA was significantly increased in normal- and high-renin hypertensives but not in low-renin patients. Plasma aldosterone concentration (PAC) was decreased significantly in normal- and high-renin patients, while no significant change in PAC was observed in patients with low-renin activity. Captopril elevated plasma bradykinin concentration (PBK) from a control value of 12.5 +/- 4.1 (mean +/- s.d.) to 20.3 +/- 7.7 pg/ml (p less than 0.001) at 30 min, and there was a significant correlation between changes in PBK and changes in mean blood pressure 120 min after the administration in all the patients (r = 0.741, p less than 0.01, n = 17). In one patient with primary aldosteronism, PBK increased from a baseline of 10.0 to a maximum value of 19.0 pg/ml, corresponding to the rapid fall in blood pressure. Also, in one patient with glucocorticoid responsive hyperaldosteronism, captopril increased PBK from a control of 14.1 to 27.9 pg/ml at 30 min, corresponding to the marked fall in blood pressure from 170/106 to 136/90 mmHg. From these findings, it is suggested that the accumulation of kinins following captopril administration plays a major role in the short-term reduction of blood pressure in hypertensive patients, especially in those with low renin-angiotensin activity.
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