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Biomedical subjects

M Finkelstein

Publications and source records attributed to M Finkelstein.

At least 55 records · Page 3Linked to original sources
PubMed1977

A case of adrenogenital syndrome with aberrant 11beta-hydroxylation.

A 17 year old female patient with hypertension, amenorrhoea and hirsutism was found to have subnormal levels of plasma and urinary cortisol, significant plasma levels of Reichstein's compound S and 21-deoxycortisol, high urinary levels of THS and pregnanetriolone as well as elevated levels of plasma and urinary testosterone. Treatment with 0.5 mg/day of dexamethasone or 25 mg/day cortisone reduced her hypertension and restored her menstrual cycles, but also resulted in the development of moon face, body striae and a gain in weight. Lower doses of cortisone were without effect. The deficient cortisol production coupled with the presence of unusual intermediates such as Reichstein's compound S and 21-deoxycortisol can be explained by a shift in the substrate specificity of 11beta-hydroxylase from C-21-hydroxylated substrates (i.e. compound S) to C-21-deoxy substrates (i.e. 17-hydroxyprogesterone).

17-Ketosteroids↗
PubMed1976

Subependymal and intraventricular hemorrhage in neonates. Early diagnosis by computed tomography.

Computed tomography was used to evaluate subependymal and intraventricular hemorrhage in 11 formalin-fixed brains obtained at autopsy from newborn infants from a population with a known high incidence of cerebral hemorrhage. After scanning, the brains were step-sectioned at levels corresponding to those of the scans. Subependymal and/or intraventricular hemorrhage was demonstrated in 6 of the 11 brains. There was a very close correlation between the scan images and the gross pathological findings in the affected brains. The authors conclude that computed tomography is an accurate method for the diagnosis of neonatal cerebral hemorrhage.

Evaluation Studies as Topic↗
PubMed1976

Ovarian enzymatic divergence in patients with polycystic ovary syndrome excreting urinary pregnanetriolone.

When ovarian mitochondria from patients with polycystic ovary syndrome (POS) were incubated with [7-3H]17alpha-hydroxypregnenolone and [4-14C]-17alpha-hydroxyprogesterone, 11beta-hydroxylated metabolites were obtained. The mitochondria, prepared from pooled, frozen, polycystic ovarian tissue of 5 patients, converted [7-3H]17alpha-hydroxypregnenolone to 3beta, 11beta, 17alpha--trihydroxy-5-pregnen-20-one (yield 0.065%) and to 3beta, 17alpha-dihydroxy-5-pregnene-11,20-dione (0.22%), while [4-14C]17alpha-hydroxyprogesterone was converted to 21-deoxycortisol (0.1%). Incubation of mitochondria, prepared from 4 pooled samples of frozen, normal ovarian tissue, yielded no evidence of 11beta-hydroxylation of either of the substrates. Mitochondria obtained from fresh, polycystic ovarian tissue of a single patient with POS converted [7-3H]17alpha-hydroxypregnenolone to 3beta,17alpha-dihydroxy-5-pregnene-11,20-dione (2.1%) and [4-14C]17alpha-hydroxyprogesterone to 21-deoxycortisol (0.1%). When the same mitochondrial preparation was incubated simultaneously with [7-3H]17alpha-hydroxypregnenolone and [4-14C]11-deoxycortisol, it converted 17alpha-hydroxypregnenolone to 3beta,17alpha-dihydroxy-5-pregnene-11,20-dione (1.9%), but no 11beta-hydroxylated derivatives of 11-deoxycortisol were found. These results demonstrate that ovaries of patients with POS contain an 11beta-hydroxylase active towards C-21-deoxysteroids but inert to C-21-hydroxysteroids such as 11-deoxycortisol.

17-alpha-Hydroxypregnenolone↗
PubMed1975

Effect of testosterone and estradiol-17beta on synthesis of DNA, RNA and protein in human breast in organ culture.

Effects of testosterone (T) and estradiol-17beta (E-2) on the synthesis of DNA, RNA and protein were studied in explants of the following types of malignant and non-malignant human female breast grown in organ culture: cystic mastitis (7 cases), fibroadenoma (8), carcinoma (17) and uninvolved tissue from cancer-bearing breast (8). In cultures of systic mastitis T uniformly inhibited the incorporation of thymidine-3H into DNA, uridine-3H into RNA and L-amino acids-14C (AA-14C) into protein. E-2 inhibited the incorporation of thymidine-3H, but had a variable effect on the incorporation of uridine-3H and AA-14C. Cultures of fibroadenoma, with no steroid added, were highly proliferative especially at the outer surface, but the incorporation of thymidine-3H, uridine-3H and AA-14C was much lower than in cystic mastitis. Whereas in fibroadenoma T uniformly inhibited the synthesis of DNA, RNA and protein, the effect of E-2 was variable: in most cases it inhibited the synthesis of DNA,but in one it stimulated it appreciably; in the majority of cases E-2 stimulated RNA and protein synthesis. In cultures of cancerous tissue T depressed, in most cases, the incorporation of thymidine-3H, uridine-3H and AA-14C, but it stimulated it in 4 out of 17. E-2 inhibited the synthesis of DNA, RNA and protein in 6 cases (2 of them were inhibited by T), stimulated them in 9 (one stimulated by T) and had no clear effect in 2. The effect of the steroids on the explants of uninvolved tissue was variable and did not always parallel their effect on the cancerous tissue from the respective patients.

Adenofibroma↗
PubMed1975

Steroidogenesis in a virilizing ovarian tumour.

A metabolic study with tissue from a virilizing arrhenoblastoma, using as precursors [7-3H]pregnenolone, [7-3H]17alpha-hydroxypregnenolone,[4-14C]17alpha-hydroxyprogesterone and [4-14C]testosterone, revealed that in spite of a deficient activity of 3beta-hydroxysteroid dehydrogenase-5-isomerase the overall production of testosterone was compensated by an increased activity of a lyase converting [4-14C]17alpha-hydroxyprogesterone to testosterone (via androstenedione) and was comparable to the production obtained by normal ovarian tissue. The masculinizing effects of the tumour in vivo were most probably caused by accumulation of testosterone due to deficiencies in enzymes catabolizing testosterone to 17-ketosteroids and its aromatization to oestrogen. The unique property of the arrhenoblastoma to convert [4-14C]17alpha-hydroxyprogesterone to [4-14C]11-deoxycortisol (Reichstein's compound S) suggests an adrenal origin of the tumour which may explain its limited capacity to aromatize testosterone.

17-alpha-Hydroxypregnenolone↗
PubMed1975

11 beta-Hydroxylase with affinity to C-21-Deoxysteroids from ovaries of patients with polycystic ovary syndrome.

When ovarian mitochondria from a patient with polycystic ovary syndrome (POS) were incubated with [7-3H]17alpha-hydroxypregnenolone and [4-14C]17alpha-hydroxyprogesterone, 11beta-hydroxylated metabolites were obtained. When the same mitochondrial preparation was incubated with [7-3H]17alpha-hydroxypregnenolone and [4-14C]11-deoxycortisol no 11beta-hydroxylated derivatives of 11-deoxycortisol were found. These results are compatible with and support the conclusion that the ovary of POS patients who excrete pregnanetriolone contains an 11beta-hydroxylase capable of hydroxylating C-21-deoxysteroids but not C-21-hydroxysteroids.

17-alpha-Hydroxypregnenolone↗