Menopause and colorectal cancer

Post-menopausal women who have never used hormone replacement therapy have a higher risk of colon, but not rectal, cancer than do premenopausal women of the same age, socio-cultural class and dietary habits. Such risk increase seems to last about 10 years and to be restricted to lean women, a group who have lower levels of oestradiol after ovarian function ceases after menopause. © 2000 Cancer Research Campaig

Epostane in nonpregnant females: effects on progesterone, 17 alpha-hydroxyprogesterone, and 17 beta-estradiol of two dose levels given for one month

So far, the use of epostane, a relatively new inhibitor of 3 beta-hydroxysteroid dehydrogenase/delta 5-delta 4 isomerase enzyme system (3 beta-HSD), has been confined to short-term interference with luteal and placental function. This study explored whether epostane treatment from the beginning of the cycle for approximately 1 month would also inhibit ovarian follicular function. Twenty females with regular cycles received epostane 150 mg/day (ten healthy volunteers) or 600 mg/day (ten patients with endometriosis). Blood samples were drawn three times per week during control and treatment cycles. At 150 mg/day the mean total area under the serum concentration curve (AUC) of estradiol (E2) was somewhat higher than during the control cycles, despite apparently lower preovulatory E2 surges. During medication the highest value of E2 was found during the luteal phase. The mean AUC of progesterone (P) and 17 alpha-hydroxyprogesterone (17-OHP) during the luteal surge was decreased by approximately 45% each. At 600 mg/day all evaluable patients had lower AUC of E2 than during the control cycle. The mean decrease in AUC of P and 17-OHP was much more pronounced than in the lower dose group. Six of the ten patients showed no hormonal signs of follicular development and, consequently, anovulation. The capacity of epostane to modulate or inhibit, depending on the dose, ovarian follicular steroidogenesis and ovulation may prove valuable in a variety of clinical conditions

Seminal vesicle-secreted proteins and their reactions during gelation and liquefaction of human semen.

The comparison of measurements of fibronectin and lactoferrin in ejaculates from vasectomized men, subjects with functional deficiency or aplasia of the seminal vesicles, and reference subjects provided evidence that both the fibronectin and the lactoferrin in human seminal fluid originate from the seminal vesicles and the ampullae. The fibronectin is incorporated in the framework of the seminal gel formed during the immediate postejaculatory phase, whereas the lactoferrin remains in solution. In the seminal gel fibronectin is linked to its predominant structural protein, a high molecular weight seminal vesicle protein (semenogelin). Both the gel-bound fibronectin and semenogelin are progressively fragmented and solubilized by the abundant prostatic kallikrein-like protease (prostate-specific antigen) during and after seminal gel liquefaction. Lactoferrin remains essentially unaffected by the seminal proteases