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D Gal

Publications and source records attributed to D Gal.

At least 73 records · Page 4Linked to original sources
PubMed1986

Hormonal therapy for lesions of the endometrium.

Megestrol acetate, 20 to 40 mg/d, was given continuously to 70 postmenopausal women with a variety of endometrial hyperplastic changes. All patients were followed up with periodic endometrial biopsies. The study was conducted for 14 years with mean patient follow-up of more than 5 years. In 65 patients (93%), surgery was avoided due to this protocol. No patient developed endometrial carcinoma, and there were no major side effects. This regimen proved to be most effective in preventing hysterectomy in postmenopausal patients who presented with surgical risk factors and endometrial hyperplasia.

Body Weight↗
PubMed1985

The demethylation of guaiacol by a new bacterial cytochrome P-450.

Spectroscopic studies were carried with a cytochrome P-450 in Moraxella sp., strain GU2, that could grow on guaiacol or 2-ethoxyphenol as the sole source of carbon and energy. The dissociation constant of the guaiacol-cytochrome complex was estimated to 0.15 microM, as determined in vivo or using the cell soluble extract. Cytochrome P-450 could also bind 2-ethoxyphenol, 2-propoxyphenol, and 2-butoxyphenol, and the dissociation constants have been determined in each case. Metyrapone depressed the degradation of guaiacol by whole bacteria, and was bound competitively to guaiacol with a constant of about 0.8 mM. Some catechol was excreted by the bacteria when growing on either guaiacol or 2-ethoxyphenol. Catechol and the other product of guaiacol demethylation, formaldehyde, were further oxidized by the bacteria. All the data available so far are consistent with cytochrome P-450 in Moraxella GU2 as a hydroxylase for the guaiacol side chain, behaving as a nonspecific O-dealkylase with broad specificity for guaiacol and homologous compounds with a longer carbon part in the side chain.

Catechols↗
PubMed1984

The role of laparoscopy in the diagnosis of ectopic pregnancy: a plea for conservative management.

This report evaluates the role of laparoscopy in patients admitted with the diagnosis of "Rule Out Ectopic". There were 186 patients admitted to the Brookdale Hospital Medical Center in the 6-year period 1974-1979 inclusive with a diagnosis of "Rule Out Ectopic" or "Possible Unruptured Ectopic". These patients were all laparoscoped. There were 157 satisfactory and 27 unsatisfactory laparoscopies. There were 71 ectopic pregnancies: 42 ruptured, 25 unruptured. Thirty-six cysts were diagnosed. The value of early laparoscopy is clearly established. Particular emphasis is placed on the diagnosis of the unruptured ectopic so that appropriate conservative management of the tube can be instituted in order to preserve potential reproductive capacity.

Female↗
PubMed1984

Effect of radiation on prostaglandin production by human bowel in vitro.

The effect of gamma irradiation on the production of prostaglandins by human colon was investigated. Squares of tissue in organ culture dishes were irradiated with 500, 1000, or 2500 rad in single applications. Tissues that were not irradiated served as controls. After treatment the tissues were superfused and prostaglandin concentrations in the effluent fluid were determined. The rates of production of prostaglandins E2 and F2 alpha by irradiated tissues were significantly lower (p less than 0.05) than those of nonirradiated tissues. Neither the release of lactate dehydrogenase nor the rate of production of 13,14-dihydro-15-keto-prostaglandin F2 alpha were increased in the irradiated samples, suggesting that neither decreased cell viability nor increased prostaglandin metabolism accounted for the decreased prostaglandin production rates. We conclude that irradiation of the human colon in vitro results in an acute inhibition of prostaglandin synthesis. The cytoprotective nature of prostaglandins is discussed with regard to the possible pathophysiological significance of these findings.

6-Ketoprostaglandin F1 alpha↗
PubMed1983

Long-term effect of megestrol acetate in the treatment of endometrial hyperplasia.

Fifty-two postmenopausal women who were poor surgical risks and had histologically proved adenomatous hyperplasia, atypical hyperplasia, or adenocarcinoma in situ of the endometrium were treated with megestrol acetate, 40 mg per day, continuously for 9 to 104 months (mean, 42 months). More than 90% of these women had complete remissions of the hyperplasia. Three women with carcinoma in situ were followed up for 57, 65, and 104 months, without recurrence of the disease. Four women required hysterectomy; none had invasive adenocarcinoma. No adverse side effects of the drug were observed. Thus, we conclude that the continuous use of megestrol acetate is an effective, safe, alternative form of therapy for endometrial hyperplasia in postmenopausal women.

Adenocarcinoma↗
PubMed1983

A cinefluoroscopic study of ureteral function following radical hysterectomy.

Twenty patients were studied with static and cinefluoroscopic intravenous pyelograms to quantitate the morphologic and physiologic ureteral alterations following radical hysterectomy and pelvic lymphadenectomy. More than 87% of the patients in the 48-hour study had ureteral dilatation, which persisted for 7 days in most patients, proximal to the site of pelvic dissection. By 6 weeks after surgery, the dilatation had regressed and pyelograms returned to normal. Transit time from renal pelvis to bladder was doubled at 7 days. An alteration in the character of peristalsis was noted on the cinefluoroscopic studies at 48 hours and at 7 days. The distal ureter appeared as a rigid conduit, and the peristaltic activity was replaced by bolus emptying.

Adult↗
PubMed1982

Defective internalization of low density lipoprotein in epidermoid cervical cancer cells.

Cells of an epidermoid cancer cell line of human uterine cervix, which possessed a high-affinity, specific receptor for low density lipoprotein (LDL), internalized and degraded [125I]iodo-LDL at a very low rate. In these cells, LDL did not stimulate cholesteryl ester synthesis, nor did it suppress 3-hydroxy-3-methylglutaryl coenzyme A reductase to the same extent as in the control cells. The binding of [125I]iodo-LDL by these cells was not decreased by preincubation of the cells in medium containing LDL. Using ferritin-labeled LDL (F-LDL) and electron microscopy, it was determined that at 4 degrees C the cells bound F-LDL in the same way as other cancer cell lines that did not have a defect in internalization. When these cells were warmed to 37 degrees C the F-LDL remained on the surface, whereas in cells from control cancer cell lines the F-LDL was internalized and was no longer observed on the cell surface. On the basis of the results of these studies it is concluded that cells of this epidermoid cancer cell line have a defective ability to internalize LDL.

Binding Sites↗
PubMed1982

Mesenchyme-epithelial interactions in human endometrium. Prostaglandin synthesis in separated cell types.

Glandular epithelium and stromal cells of human endometrium were separated and maintained in monolayer culture. At the time the cells became confluent, cell suspensions were prepared and incubated with [14C]arachidonic acid. Radiolabeled prostaglandin E2 and, to a lesser extent, prostaglandin F2 alpha and metabolites of these prostaglandins, were formed principally in stromal cells. There was considerably less prostaglandin formation in endometrial glands either after maintenance in monolayer culture or in freshly separated glands. In stromal cells of endometrium prostaglandin formation was linear with time of incubation for 2.5 min and with [14C]arachidonic acid concentrations up to 8 microM. When stromal cells and epithelial cells were combined, all prostaglandin formation could be accounted for by that produced in stromal cells. Little or no prostaglandin formation was detected in stromal cells from human adipose tissue or in fibroblasts from human genital or abdominal skin or human fallopian tube.

Arachidonic Acid↗
PubMed1981

Cholesterol metabolism in cancer cells in monolayer culture. III. Low-density lipoprotein metabolism.

The metabolism of low-density lipoprotein (LDL) was studied in neoplastic and non-neoplastic cells of human gynecological origin, in monolayer cultures. The neoplastic cells were derived from epidermoid vaginal carcinoma, epidermoid cervical carcinoma and endometrial adenocarcinoma, in various degrees of differentiation. The non-neoplastic cells were cervical fibroblasts and epithelial cells from proliferative endometrial glands. Both neoplastic and non-neoplastic cells assimilated and degraded LDL in a similar fashion to other human cells (e.g. skin fibroblasts). However, the neoplastic cells metabolized LDL at a higher rate than the non-neoplastic cell (e.g. epidermoid cervical cancer cells metabolized LDL at a 20 times higher rate than did cervical fibroblasts). Such a high rate of LDL metabolism probably enables continuously replicating cancer cells to obtain the large amounts of cholesterol required for cell membrane synthesis. If a high rate of LDL metabolism proves to be a general property of cancer cells, such a property could prove useful for tumor chemotherapy, providing cytotoxic chemicals could be incorporated within the LDL molecule.

Adenocarcinoma↗
PubMed1981

Low-density lipoprotein as a potential vehicle for chemotherapeutic agents and radionucleotides in the management of gynecologic neoplasms.

Cholesterol metabolism was studied in cells from two established gynecologic cancer cell lines which were maintained in monolayer cultures. The cell lines were derived and established from poorly differentiated epidermoid cervical carcinoma (EC-50) and endometrial adenocarcinoma (AC-258). The specific activity of 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase, the rate-limiting enzyme of cholesterol de novo synthesis, in AC-258 cells (1,700 pmoles x mg-1 microsomal protein x min-1) was three times higher than that found in EC-50 cells (550 pmoles x mg-1 microsomal protein x min-1). However, epidermoid cervical cancer cells (EC-50) metabolized low-density lipoprotein (LDL), the major transport vehicle for cholesterol in plasma, at a very high rate (14,000 ng x mg-1 cell protein x 6 hours). This rate is fifteen times greater than the rate observed in fetal adrenal tissue and fifty times greater than the rate observed in nonneoplastic gynecologic tissue, each in organ culture. Both cancer cells (EC-50 and AC-258) in monolayer culture were shown to have specific receptors for LDL. These cancer cells demonstrate no defect in LDL metabolism, and lysosomal degradation of LDL was blocked by chloroquine. From the results of studies of specific binding of LDL in tissues obtained from nude mice it was demonstrated that membrane fractions prepared from EC-50 cells, after propagation in the mice, contained fifteen to thirty times more specific binding capacity for [125I]iodo-LDL than vital organs of the mouse, such as the liver, heart, lung, kidney, or brain. The results of these studies are suggestive that certain tumor cells might have a higher affinity for LDL than normal tissues and cytotoxic drugs or radionucleotides ligated to the LDL macromolecule may be utilized for the specific delivery of these agents.

Adenocarcinoma↗
PubMed1981

Failure of contraceptive steroids to modify human chorionic gonadotrophin secretion by hydatidiform mole tissue and choriocarcinoma cells in culture.

The effect of steroids contained in oral contraceptives, namely ethinylestradiol:17 alpha-ethinyl-1,3,5,(10)-estratriene-3, 17-diol (E) and norethindrone acetate:17 beta-acetoxy-17-ethinyl-4-estren-3-one (N), on cell replication and human chorionic gonadotropin (hCG) secretion by choriocarcinoma cells in monolayer culture and by hydatidiform mole tissue maintained in organ culture were studied. The steroids were added to the culture medium individually or in combination to achieve a range of concentrations (10-10 to 10-4), within and beyond the presumed concentration of these substances in the blood of women taking oral contraceptives. The effect of luteinizing hormone releasing hormone (LHRH) on hCG secretion by choriocarcinoma cells in monolayer culture also was investigated. The rate of hCG production by either choriocarcinoma cells in monolayer culture or by hydatidiform mole tissue maintained in organ culture was not affected by the hormones used in this study; indeed hCG secretion remained reasonably unchanged even with high concentrations of steroids (up to 10-4 M) or LHRH (up to 10-4 mg x ml-1). Cell replication, as measured by increase in amount of cellular protein and DNA, was not stimulated by either of these compounds.

Cell Division↗
PubMed1981

Cholesterol metabolism in human cancer cells in monolayer culture. V. The effect of progesterone on the regulation of 3-hydroxy-3-methylglutaryl coenzyme A reductase activity by low density lipoprotein.

The effect of progesterone on the regulation of 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase activity by low density lipoprotein (LDL) was studied in eight gynecological cancer cell lines maintained in monolayer culture. In the absence of LDL and progesterone, the specific activity of HMG CoA reductase varied widely from one cell line to another (range, 200-2500 pmol mg microsomal protein-1 min-1). As in noncancerous cells, LDL suppressed the activity of HMG CoA reductase in all cell lines. Progesterone (40 microM) attenuated or abolished the decrease in specific enzyme activity normally brought about by LDL. Progesterone, in the absence of LDL, stimulated HMG CoA reductase activity in some of these cell lines. Other steroids (cortisol and estradiol) had no effect on the specific activity of HMG CoA reductase. The mechanism by which progesterone stimulates HMG CoA reductase activity is not clear, but since progesterone receptors were not detectable in these cells a mechanism independent of the classic hormone receptor-mediated phenomenon is likely to be involved.

Cells, Cultured↗
PubMed1981

Nicotinamide adenine dinucleotide-dependent 15-hydroxyprostaglandin dehydrogenase activity in hydatidiform mole tissue and choriocarcinoma cells.

Prostaglandins may occupy an important role in viral and chemical carcinogen-induced neoplasia. To evaluate the possible role of prostaglandin catabolism in neoplastic cells, we measured nicotinamide adenine dinucleotide-dependent 15-hydroxyprostaglandin dehydrogenase activity in hydatidiform mole tissue and in choriocarcinoma cells maintained in monolayer culture. The specific activity of nicotinamide adenine dinucleotide-dependent 15-hydroxyprostaglandin dehydrogenase in hydatidiform mole tissue (0 to 1.2 nmol 15-ketoprostaglandin E2 formed x min-1 x mg-1 cytosolic protein) and in choriocarcinoma cells (1.0 nmol 15-ketoprostaglandin E2 x min-1 x mg-1 protein) was strikingly less than that found in normal placental tissue [11.4 +/- 2.3 (S.E.) nmol 15-ketoprostaglandin x min-1 x mg-1 protein].

Cells, Cultured↗
PubMed1981

Effect of cell density and confluency on cholesterol metabolism in cancer cells in monolayer culture.

Cholesterol metabolism in four gynecological cancer cell lines in monolayer culture was evaluated as a function of cell density. The rate of uptake and degradation of [125I]iodinated low-density lipoprotein increased during the first 24 to 48 hr of culture, but decreased thereafter. Once the cells became confluent, the rate of metabolism of [125I]iodinated low-density lipoprotein was only one-tenth that in cells which were in the preconfluent state. The specific activity of 3-hydroxy-3-methylglutaryl coenzyme reductase increased during the first 24 to 48 hr of culture and subsequently declined, reaching a nadir after confluency was attained. The rate of incorporation of [14C]oleate into cholesteryl esters was low when the cells were in the log-exponential phase of replication but increased gradually as cell density increased. The highest specific activity of acylcoenzyme A: cholesterol acyltransferase was attained after the cells became confluent. Generally speaking, there was an inverse relationship between the specific activity of 3-hydroxy-3-methylglutaryl coenzyme A reductase, on the one hand, and the rate of [125I]iodinated low-density lipoprotein metabolism and cholesteryl ester synthesis, on the other. It is concluded that cholesterol metabolism in cancer cells in monolayer culture is regulated, in part, by the rate of cell division. In the cancer cells utilized in this study, it is apparent that cholesterol metabolism was subject to the same regulatory mechanisms as are present in nonneoplastic cells.

Adenocarcinoma↗