Urinary undiversion--when and how.
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Biomedical subjects
Publications and source records attributed to M Menon.
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Incubation of luteal cells with human, horse and rat sera, but not bovine sera resulted in enhanced basal and hCG-stimulated progesterone accumulation. The stimulatory effect of human or rat sera on basal, hCG- or 8 Br-cyclic AMP-induced progesterone synthesis in luteal cells was evident within 15-30 min after incubation, reaching a maximum after 3-4 h. The stimulatory effects of hCG and/or sera were blocked by inhibitors of RNA and protein synthesis. Similarly, lysosomotropic agents, chloroquine (100 microM) and ammonium chloride (10 mM), partly blocked the steroidogenic response of luteal cells to hCG and/or human or rat sera. Incubation of cells in the presence of 2-deoxyglucose, sodium azide and phenylmethylsulfonyl fluoride resulted in partial inhibition of progesterone secretion in response to hCG or sera. Fractionation of human or rat sera into various lipoprotein fractions demonstrated that LDL and HDL most effectively supported and potentiated the steroidogenic response to hCG. Lipoprotein-deficient serum, however, did not alter gonadotropin-induced steroid production. Incubation of luteal cells with increasing concentrations of h-LDL and h-HDL enhanced both basal and hCG-mediated steroidogenesis in a dose-related manner, although very high concentrations of these lipoproteins were inhibitory. Further, [3H]cholesterol from [3H]cholesteryl linoleate-LDL was incorporated into luteal cell progesterone and the extent of this incorporation was enhanced by hCG. Addition of excess unlabeled h-LDL, h-HDL, as well as r-HDL, drastically reduced the incorporation of radioactive label into progesterone. These studies suggest that (a) serum potentiation of steroidogenesis was due to presence of lipoproteins, mainly LDL and HDL, and (b) the lipoprotein-bound cholesterol is delivered into the luteal cells and utilized for steroidogenesis.
Data on tumorigenicity and mutagenicity of INH show that INH is tumorigenic in mice but not in rats. The metabolic studies on the two species denote that rats are rapid inactivators whereas mice are slow inactivators of INH. Rats are also resistant to the immediate inhibitory effect of INH on DNA biosynthesis. Using Ames test it was observed that INH is mutagenic to salmonella typhimurium strains TA 100 and 1535 and this effect is abolished in presence off 59 mixture. In vivo and in vitro studies on INH interaction with macromolecules reveal that there is a greater interaction with RNA than with DNA and the site of interaction is the cytidine and deoxycytidine, respectively. A preliminary study is undertaken to see if healed TB cases have a higher risk for cancer. It is found that cancer incidence in this group is higher as compared to noncancer patients.
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The capabilities of radiography (mammography film) and ultrasonography (7 MHz. probe) were investigated in cadaver kidneys. Stones of varying size and composition were studied. Clinically, 11 patients then were studied with intraoperative radiography and ultrasonography. Both techniques appeared to localize calculi more than 3 mm. with high consistency in cadaver kidneys and in patients. Real-time B scan ultrasonography is a rapid and accurate technique that has the ability to identify lucent calculi. When used in association with intraoperative radiography, intraoperative ultrasonography can be a great aid in the surgical removal of renal calculi.
Monolayer cultures of anterior pituitary glands from female rats were exposed to 5 X 10(-6) M danazol for 0, 4, 24, 48, and 72 h in Dulbecco's Modified Eagle's Medium supplemented with 10% horse serum and 2.5% fetal calf serum. After this treatment, the cell cultures were rinsed and challenged with 10(-8) M LHRH for 6 h. The media were collected and assayed for LH by a hormone-specific RIA using the double antibody precipitation technique. A control incubation was carried out by exposing cell cultures for the same length of time in the absence of danazol but in the presence of 0.5% ethanol in which danazol was dissolved, then challenging the culture with 10(-8) M LHRH, as was done in the experimental group, and assaying the LH released in the medium. The results showed that exposure of cell cultures to danazol caused a significant decrease in LH release in response to LHRH from 13,800 +/- 500 to 3,500 +/- 200 ng/ml. The inhibition of LH release was dependent on both the duration of danazol exposure and its concentration. Danazol exposure had, however, little effect on basal LH secretion by the pituitaries, which remained at about 600 ng/ml at all time points examined. Under the experimental conditions, danazol exerted no effect on the incorporation of amino acid into protein in the cell culture. These results suggest that one of the mechanisms of the antigonadotropic effect of danazol is inhibition of the responsiveness of the pituitary to LHRH-induced LH release.
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The action of danazol on 125I-human chorionic gonadotropin (hCG) binding, gonadotropin-stimulated adenosine 3',5' cyclic monophosphate (cAMP) accumulation and progesterone production has been investigated in luteinized rat ovaries. Preincubation of luteal cells for short periods of time with increasing concentrations of danazol caused a significant inhibition of gonadotropin-stimulated steroidogenesis. The inhibitory effect of danazol was both concentration and time dependent. Danazol also reduced progesterone production in response to cholera enterotoxin and 8 bromo-adenosine-cAMP, but it had no effect on hCG, luteinizing hormone, and cholera enterotoxin stimulated cAMP formation. Similarly danazol did not affect 125I-hCG binding as assessed by the equilibrium dissociation constant (Kd) and number of hormone-binding sites on the luteal cell surface. These results suggest that in intact luteal cells danazol inhibits steroidogenesis at a point distal to hormone-receptor interaction and cAMP formation.
Sera of patients with prostatic malignancy were assayed for human chorionic gonadotropin-beta (HCG-beta). The levels of HCB-beta are negligible in the patients and in a control group with benign prostatic hypertrophy. Slight increases in HCG-beta found in a small percentage of patients with advanced malignancy are attributed to cross-reacting gonadotropins.
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Radiographic findings of the 2 new cases of oxyphilic renal adenoma, so-called renal oncocytoma, are reported and compared to previous descriptions. Ultrasonography shows no typical findings, but the vascular capsule of this tumor may show enhancement on computed tomography. Angiography contributes the most specific findings, because of the vascularity of these tumors: In the larger lesions a typical 'spoke wheel pattern' can be expected which may not be as prominent in smaller tumors. Notable is the absence of abrupt arterial caliber changes, AV shunting and contrast puddling which sets this tumor apart from the great majority of vascular renal cell carcinomas. The incidence of renal oncocytomas appears to be rising.
Cytosol receptors for progesterone were assayed in human endometrial tissue during the proliferative and secretory phases of the menstrual cycle and in the hyperplastic and carcinomatous endometrium. The assays were performed utilizing a technique involving prior treatment of the cytosol extract with dextran-coated charcoal to remove endogenous progesterone. The results showed that the progesterone receptor activity was higher during the later proliferative and early secretory phases of the menstrual cycle. Hyperplastic and carcinomatous endometrium also contained specific cytosol receptor for progesterone, and the binding activity of the hyperplastic endometria and endometrial polyps was comparable to that found during the later proliferative phase of the menstrual cycle. No apparent correlation between the progesterone receptor level and the morphologic degree of differentiation in Grades 1 and 2 adenocarcinomas of the endometrium was observed.
Sera from patients with carcinoma of the prostate were screened for the presence of blocking factors by measuring the inhibition of phytohemagglutinin-induced blastogenesis of normal lymphocytes. The blastogenic index obtained in cancer sera is not significantly different from that obtained in sera of patients with benign prostatic hypertrophy (control group). Determination of alpha-2-globulins in the cancer sera by cellulose acetate electrophoresis revealed slightly elevated levels in patients with metastatic disease but it did not correlate with the inhibitory blocking activity of the serum.
Sucrose density gradient analysis of the R3327H tumor cytosol demonstrated the presence of both androgen and estrogen binding proteins. Competitive binding analysis with 17 beta-estradiol, 5 alpha-dihydrotestosterone, R1881, cyproterone acetate, and cortisol was consistent with the presence of 2 different binding sites for androgens and estrogens. Scatchard binding analysis was performed in the dorsal-lateral prostate as well as the R3327H tumor from normal Copenhagen rats. High affinity receptors for androgen and estrogen but not progesterone were found. However, in R3327H tumors relapsing following castration, the presence of high affinity receptors for progesterone were readily detectable.