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Biomedical subjects

B Lunenfeld

Publications and source records attributed to B Lunenfeld.

At least 55 records · Page 3Linked to original sources
PubMed1993

Sexual behavior, contraception and the risk of contracting HIV.

Recently, concern has been expressed on a possible association between the use of oral contraceptive pills (OCs) and an increased risk of contracting the HIV infection. As a consequence it has been postulated that a low prevalence of condom use due to widespread utilization of oral contraceptive pills would result in an acceleration of the spread of AIDS. The International Committee for Research in Reproduction (ICRR) a group of eleven experts in the field of gynecology, endocrinology and contraception, wishes to comment on the concerns raised about OC use and AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed1993

Polycystic ovaries in non-obese and obese patients: possible pathophysiological mechanism based on new interpretation of facts and findings.

This study was designed to investigate the basic concentrations of different hormones in obese and non-obese patients with polycystic ovarian disease (PCOD). Eight women with PCOD, of whom four were obese with body mass index (BMI, kg/m2) of > 25 and four were non-obese with BMI < 25, volunteered to participate in this study. Serum samples were taken every 20 min over an 8 h period, starting at 2300 h, on day 5 of a spontaneous or gestagen-induced cycle. Basic insulin concentration was found to be significantly higher in the obese women compared with their non-obese counterparts (P < 0.0001). Serum concentrations of insulin-like growth factor binding protein (IGFBP-I) and sex hormone binding globulin (SHBG) were found to be significantly lower (P < 0.001 for both hormones) in the obese compared with the non-obese women. Serum concentrations of insulin-like growth factor I (IGF-I) did not differ between the two groups. The non-obese women had significantly higher serum concentrations of luteinizing hormone (LH) (P < 0.001) and of growth hormone (GH) (P < 0.002) than their obese counterparts. Based on these results, two models of the development of PCOD were suggested. In obese women, hyperinsulinaemia causes an excessive production of androgens through the enhancement of IGF-I receptors which, in synergism with LH, causes increased activity of cytochrome P-450c 17a. In non-obese patients, relative increase of GH concentration stimulates excessive ovarian IGF-I production. At this point synergism with LH results in excessive production of androgens by the same mechanism as in obese patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Follicular development and its control.

The female reproductive cycle is based on a co-ordinated function of several regulatory elements and signalling systems. Of the approximately 7 million oocytes present in the human fetal ovary, only 475 will eventually ovulate. In the human, the development of a primordial follicle into a dominant one takes about 10 weeks. Approximately 300 follicles are recruited initially for growth and development, 30 of them are likely to become gonadotropin-dependent and enter competition for dominance and, finally, only one will achieve ovulation. The mechanisms by which follicle stimulating hormone, luteinizing hormone, growth factors and steroids may promote or disrupt follicular development are discussed in detail. Possible implications of these new facts on diagnosis and treatment of ovulatory disturbances are described.

Female↗
PubMed1993

[Ovarian stimulation: a new approach based on recent physiological and clinical data. Future perspectives].

Taking into account the experience gained in medically assisted conception and ovulation induction, the pregnancy rate and more particularly the baby home rate after ovarian stimulation protocols remain stable. Today, could we expect to improve our results from our recent knowledge on the role of the different factors involved in the follicular maturation process and ovulation? The improvement of our results means to mimic or to amplify the ovarian physiology, taking into account the FSH actions, the key hormone for follicular maturation. At the beginning of the menstrual cycle, FSH is responsible of the "rescue" of one or more follicles selected for ovulation, of their growth and their differentiation allowing the evolution of an androgen intrafollicular environment toward an estrogen intrafollicular environment which is necessary for a good quality. In late follicular phase, whereas FSH is acting continuously on the multiplication and differentiation of granulosa cells, in particularly on the stimulation of the aromatase activity, small quantities of LH (included between 1 and 6-8* IU/L) allow final follicular maturation (androgen production, synergic action with FSH and antagonist action on FSH action). If, low dose of LH complements FSH action in final follicular maturation process, high levels (> 6-8 IU*/l) are deleterious for follicle or oocyte quality. Numerous studies demonstrate a significant correlation between high levels of LH and the lack of pregnancy either the follicle is submitted to high concentrations at the beginning, at mid or at the end of follicular phase.(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical Protocols↗
PubMed1992

Serum and insulin inhibit cell death induced by cycloheximide in the human breast cancer cell line MCF-7.

Continuous exposure of cells to cycloheximide (CHM) terminates in cell death. This may result from CHM's inhibition of protein synthesis. In the present study we investigated the effect of serum and insulin on cell death induced by CHM in the human breast cancer cell line MCF-7, and correlated this effect to the inhibition of protein synthesis. Cell death was evaluated by measuring either dead cells by the trypan blue dye exclusion test or by the release of lactic dehydrogenase into the culture medium. CHM (0.1 to 50 micrograms/ml) was shown to induce cell death in a time- and concentration-dependent manner. Including either fetal bovine serum or insulin in the culture medium inhibited this cell death in a concentration-dependent manner. Protein synthesis as measured by [3H]leucine incorporation was inhibited by the increasing concentration of CHM. However, fetal bovine serum and insulin did not alter the protein synthesis inhibition rate induced by CHM. These results indicate that inhibition of protein synthesis is not enough for cell death to proceed. Insulin or factors present in serum may stabilize some crucial cell proteins (key enzymes, cytoskeletal or membrane components) which are vital for cell life.

Blood Proteins↗
PubMed1992

Tamoxifen increases plasma estrogen-binding equivalents and has an estradiol agonistic effect on histologically normal premenopausal and postmenopausal endometrium.

OBJECTIVE: To determine the effects of single dose tamoxifen on plasma estrogen (E)-binding equivalents and endometrial estradiol (E2) and progesterone (P) receptors. DESIGN: Controlled clinical study. SETTING: Normal human volunteers were studied in an academic research environment. PATIENTS: Premenopausal and postmenopausal women with histologically normal endometrium undergoing curettage or hysterectomy were selected. INTERVENTIONS: Tamoxifen was administered orally; blood and endometrial samples were collected 4 to 96 hours after tamoxifen administration. MAIN OUTCOME MEASURES: Plasma E-binding equivalents, endometrial cytosolic and nuclear E2 and P receptors. RESULTS: (1) Plasma E-binding equivalents increased eightfold at 4 to 24 hours of tamoxifen administration and declined exponentially thereafter, reaching control levels at 73 to 96 hours. Plasma E-binding equivalents were not affected by endogenous E2 levels. (2) Endometrial total E2 and P receptor levels increased in all women 2.9 to 19.2-fold after tamoxifen. (3) Tamoxifen resulted in an increase in the fraction of the E2 receptor measured in the nuclear extract 2.1 to 7.5-fold in midcycle, secretory, and menopausal endometria but not in proliferative endometrium. CONCLUSIONS: (1) Tamoxifen has an E2 agonistic effect on histologically normal human endometrium. (2) Irrespective of the total level of the endometrial E2 receptor, the nuclear capacity of that receptor in vivo is limited (approximately 75% to 80% of the total level).

Adult↗
PubMed1992

The role of insulin-like growth factor-1 (IGF-1) and IGF binding protein-1 (IGFBP-1) in the pathogenesis of polycystic ovary syndrome.

The objective of this study was to elucidate the relationship and role of insulin-like growth factor-1 (IGF-1), IGF binding protein-1 (IGFBP-1), insulin and luteinizing hormone (LH) in the pathogenesis of polycystic ovary syndrome (PCOS). In a pilot study, serum concentrations of IGF-1 were determined in women with PCOS (n = 10), hypopituitarism (n = 12) and normal controls (n = 10). In the main study, serum concentrations of IGF-1, IGFBP-1, insulin and LH in women with anovulation associated (n = 23) and not associated (n = 47) with PCOS were determined. Serum concentrations of IGF-1 were not different in women with PCOS, anovulatory non-PCOS and healthy women but were low in those with hypopituitarism. Mean serum IGFBP-1 in PCOS (33.8 +/- 21.2 micrograms/l) was decreased compared with anovulatory non-PCOS (60.0 +/- 22 micrograms/l) (P = 0.0001), and correlated negatively with insulin concentrations (r = -0.67, P = 0.0006). Patients with PCOS could be separated into those with high LH and those with high insulin levels. It was concluded that women with PCOS have normal serum IGF-1 concentrations but IGFBP-1 levels, regulated by insulin, are low. Hyperinsulinaemia and raised LH are independently capable of stimulating ovarian androgen production. Growth factors may have an important role in the pathogenesis of PCOS.

Adult↗
PubMed1992

Insulin-like growth factor-I (IGF-I) may not be essential for ovarian follicular development: evidence from IGF-I deficiency.

Insulin-like growth factor-I (IGF-I) stimulates growth and differentiation in follicular granulosa cells (GC). To examine whether this effect is prerequisite to human folliculogenesis, a patient with Laron-type dwarfism (IGF-I deficiency secondary to GH receptor abnormality) was examined while undergoing in vitro fertilization treatment. Despite low levels of IGF-I in serum and follicular fluid (less than 3 and less than 2 nmol/L) and very high levels of IGF-I-binding protein, the patient developed normal ovarian follicles. After the administration of GnRH analog (GnRHa) and human menopausal gonadotropin in a dose similar to that used in normovulatory women, estradiol (E2) levels reached above 5000 pmol/L on the day of hCG administration, and mature fertilizable oocytes were retrieved during ovum pickup. The patient's GC E2 production, tested in a primary culture, did not respond to IGF-I after 4 days of incubation, while control cultures showed a significant increase. Only after a priming period of 7 days did IGF-I have a significant effect on E2 production, as observed in the patient's GC culture. This delayed response suggests that the patient's GC were not exposed in vivo to IGF-I. Our data support the view that IGF-I is not required for normal follicular development, but is, rather, a nonessential modulator of FSH action.

Adult↗
PubMed1992

Insulin-like growth factor-I and follicle-stimulating hormone suppress insulin-like growth factor binding protein-1 secretion by human granulosa-luteal cells.

Local regulation of insulin-like growth factor binding protein-1 (IGFBP-1) production in the human ovarian follicle was investigated using cultured human granulosa-luteal cells. Both insulin-like growth factor-I (IGF-I) and follicle-stimulating hormone (FSH) exerted a dual effect on granulosa cells: while estradiol (E2) production was increased by both stimulants, the addition of either of the two hormones led to a reduction in IGFBP-1 secretion by more than 50%. Inhibition of IGFBP-1 production in response to IGF-I was dose-dependent,with the highest effect observed at 5 nM IGF-I. A significant correlation was found between the increase in E2 and inhibition of IGFBP-1 secretion in response to IGF-I. These observations may suggest a novel mechanism, at the follicular level, by which FSH and IGF-I amplify the IGF-I effect in the ovarian follicular cells.

Carrier Proteins↗
PubMed1992

The effect of castration on the synthesis and secretion of proteins in 7,12-dimethylbenz(a)anthracene-induced rat mammary tumors.

UNLABELLED: The effect of castration on the incorporation of [35S]methionine into secreted proteins in 7,12-dimethylbenz(a)anthracene (DMBA)-induced rat mammary tumors, was investigated. Biopsy specimens were obtained from 19 tumors, 0, 24, 48, 72, and 96 h after castration. In 14 tumors, castration induced an increase in the incorporation (mean of 5-fold), reaching the maximal level after 24 h (3 tumors), 48 h (7 tumors), 72 h (3 tumors), and after 96 h (1 tumor). In three tumors castration did not alter the incorporation rate, while in two tumors incorporation declined immediately after castration. One-dimensional sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) analysis of the labeled secreted protein showed that castration did not decrease or increase significantly the incorporation of [35S]methionine into any of the major labeled proteins. CONCLUSION: tumor regression following hormonal deprivation is apparently preceded by an increased synthesis of secreted proteins. However, no qualitative differences in any major labeled proteins could be observed.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1992

Comparison of ovarian response in the same women with the same or different lots of human menopausal gonadotropin.

A variation in the bioactivity of different production lots of human menopausal gonadotropin (hMG) has been suggested. Therefore, we evaluated ovarian response to hMG in 14 women during three separate IVF cycles. The first two cycles were performed with the same lot (#03310027; Cycles A1 and A2); the third cycle utilized different lots of hMG (Cycle B). In all cycles, hMG was administered 3 ampules/day beginning cycle Day 3 and continued for at least 6 days. Estradiol and ultrasound evaluations were performed on Day 3, and then daily, beginning on cycle Day 8. Fourteen women completed all three cycles. There were no significant differences in baseline estradiol and ultrasound. Estradiol levels on Day 8 (A1, 754 +/- 130; A2, 700 +/- 107; B, 520 +/- 80 pg/ml, analysis of variance p greater than 0.5) and on Day 9 (A1, 1051 +/- 144; A2, 1140 +/- 155; B, 840 +/- 124 pg/ml, p greater than 0.05) were similar as well. The number of small (1.0-1.4 cm) follicles, large (greater than or equal to 1.5 cm) follicles, and total follicles (Day 8: total A1, 5.5 +/- 0.9; A2, 4.0 +/- 0.7; B, 4.5 +/- 0.9, p greater than 0.05; Day 9: total A1, 6.7 +/- 0.9; A2, 6.9 +/- 0.8; B, 6.9 +/- 0.9, p greater than 0.05) in all three cycles were also similar.(ABSTRACT TRUNCATED AT 250 WORDS)

Estradiol↗
PubMed1991

Pathophysiology of polycystic ovarian disease: new insights.

The incidence of polycystic ovarian disease (PCOD) varies from 0.6 to 92%, depending on the parameters analysed, PCOD has been reported to appear in association with Cushing's Syndrome, adrenal hyperplasia, hypothyroidism, adrenal and ovarian tumours and some genetic abnormalities. The controversy regarding the pathophysiological mechanism underlying the disease still persists. Critical evaluation of old data, assessment of new findings concerning the possible role of insulin, growth factors and their binding proteins, and extrapolation of neuroendocrinological experiments enabled the construction of a concise hypothesis of the pathophysiology of PCOD. According to this hypothesis, PCOD is a multifactorial disease. The sequence of events finally leading to clinical manifestation of the disease (hyperandrogenism, abnormal luteinizing hormone pulsatility pattern and ovulation disturbances) may originate in different organs or be triggered by different mechanisms. It may stem from the adrenals, the hypothalamus or higher central nervous system centres, or from the ovary itself; it may originate from excess of fat tissue usually combined with hyperinsulinism; or may be the result of a net increase in active growth factors. Each of the above disturbances probably appears early in life, much before the clinical signs of the disease are evident. Predisposing factors such as gestational diabetes of the mother, childhood obesity, borderline adrenal hyperplasia and late menarche have to be looked for as early as possible in order to prevent the late consequences of the disease, such as increased risk of infertility, endometrial and breast cancer and cardiovascular disease.

Female↗