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Biomedical subjects

H Ishida

Publications and source records attributed to H Ishida.

At least 955 records · Page 53Linked to original sources
PubMed1983

Carcinoma in situ of germ cells and subsequent development of an invasive seminoma in a hyperprolactinaemic man.

A 25-year-old man was first seen complaining of impotence and found to have a pituitary tumour and hyperprolactinaemia. Both testes were small and atrophic, but a testicular tumour was not apparent. Biopsy of the right testis was performed, and the pathology report described thickening of the seminiferous tubule walls and impaired spermatogenesis. The patient refused to undergo an operation for his pituitary tumour and was lost to follow-up. 5 years later, the same patient presented with enlargement of his right testis, and this and the pituitary tumour were excised. The testicular tumour was classified as seminoma, and the pituitary tumour as an adenoma with low malignancy. Re-examination of the previous specimen of his right testis revealed foci of carcinoma-in-situ. This is an additional example of the growth of an invasive germ cell tumour from non-invasive carcinoma-in-situ of the testis.

Adenoma↗
PubMed1983

beta-Adrenoceptor alterations coupled with secretory response in rat parotid tissue.

Simultaneous studies on the secretory response of amylase and the neurotransmitter receptors of rat parotid gland, after brief treatment with agonists, showed selective alteration in beta-adrenoceptors with specific change in amylase secretion, suggesting a regulatory role of the receptors in the secretory response. The beta-adrenergic agonist (+/-)-isoprenaline (IPR) stimulated amylase secretion from rat parotid tissues much more than did the same concentration of an alpha-adrenergic or cholinergic agonist. The stimulatory effects of IPR were studied by pre-treating rat parotid tissues with IPR for 10 min and then incubating the tissue in fresh medium for 10 min. Pre-treatment with 10 microM-IPR for 10 min resulted in increased amylase secretion during further incubation with IPR and also in a lower EC50 value of amylase secretion for IPR. This treatment also resulted in selective changes in the number and affinity of beta-adrenoceptors, assessed by measuring binding of [3H]dihydroalprenolol (DHA): the maximal binding sites increased from 286/357 f-mole to mg protein and the IC50 value (the concentration for 50% inhibition of specific [3H]DHA binding) of beta-agonists, not antagonists, decreased significantly. An increase in the period of pre-treatment with IPR to 30 min resulted in a decrease in the maximal binding sites of beta-adrenoceptors and a decrease in amylase secretion during further incubation with IPR. Experiments with other agonists showed that supersensitivity of the secretory response was induced specifically by beta-agonists. Binding studies with [3H]WB-4101 and [3H]quinuclidinyl benzilate showed that alpha-adrenoceptors and muscarinic ACh receptors in rat parotid did not change under the conditions tested. The alteration in beta-adrenoceptors was parallel with a change in amylase secretion after IPR pre-treatment, but not with a change in cyclic AMP content.

Acetylcholine↗
PubMed1983

Plasma antidiuretic hormone levels in patients with normal and low renin essential hypertension, and secondary hypertension.

In order to investigate the antidiuretic hormone (ADH) in essential hypertension and secondary hypertension, plasma ADH levels were measured in normal subjects, in patients with normal and low essential hypertension, and in other patients with various forms of secondary hypertension. Plasma ADH levels were significantly lower in low renin essential hypertension and higher in malignant hypertension than in normal subjects. The plasma ADH levels tended to be lower in renal hypertension and primary aldosteronism, and higher in renovascular hypertension, but these differences were not statistically significant. From these results, it appeared that ADH might play a role in malignant hypertension, but not in the other hypertensive diseases.

Adolescent↗
PubMed1983

Effects of streptozotocin-induced diabetes on circulating levels of vitamin D metabolites.

In order to investigate vitamin D metabolism in insulin-deficient diabetic rats, plasma vitamin D metabolites were measured at various periods after induction of diabetes by iv administration of 60 mg/kg streptozotocin (STZ). After STZ injection, plasma insulin was significantly decreased and plasma urea nitrogen increased with the duration of diabetes, while plasma creatinine remained unchanged. Plasma calcium, 25-dihydroxyvitamin D (25(OH)D), and 24,25-dihydroxyvitamin D (24,25(OH)2D) progressively decreased. On the other hand, plasma 1,25-dihydroxyvitamin D (1,25(OH)2D) did not change at any period, but the ratio of 1,25(OH)2D to 25(OH)D became high in proportion to the severity of hypocalcaemia. Since significantly lower 25(OH)D and 24,25(OH)2D levels were observed at the later stage of diabetes, it is suggested that the altered vitamin D metabolism in diabetes is secondary to the disturbances in metabolic homeostasis derived form the insulin deficiency.

24,25-Dihydroxyvitamin D 3↗
PubMed1982

Investigation of genetic markers in a true hermaphrodite with chi 46,XX/46,XY.

We documented a new case of chi 46,XX/46,XY true hermaphroditism substantiated by the evaluation of chromosomal heteromorphism in banded preparations. The patient, a 12-year-old Japanese boy with ambiguous external genitalia, was seen because of abnormal breast development. Surgical exploration showed the right gonad to be an ovotestis and the left gonad to be an ovary. Cytogenetic studies revealed cell admixtures of 46,XX and 46,XY karyotypes in peripheral lymphocytes, skin fibroblasts, and gonadal fibroblasts. From the pedigree studies, the paternal double genetic contributions were evidenced by the differences of sex chromosomes and the blood group types for the ABO and MNSs systems in the two cell lines of the patient. The maternal double genetic contributions were confirmed by the inheritance of Q-fluorescent markers on chromosomes 13 and 22 and by alleles for the Kidd blood group system.

Blood Grouping and Crossmatching↗