Eugenia Rosemberg was a charter member of the American Society of Andrology (ASA) and Program Chair for the First Annual Meeting on March 31 to April 2, 1976 in Worcester, Mass. She was also an important scientist responsible for the beginnings of the American Society of Andrology. Dr Rosemberg served as a member of the Executive Council from 1976–1980 and was the first chair of the Publications Committee (1975–1980). As such, she was instrumental in the negotiations and formation of the Journal of Andrology. In 1982, Dr Rosemberg was the recipient of the Distinguished Andrologist Award, the highest honor given by the ASA to a member with lifetime achievements in the field of Andrology. Originally, her family—active in radio and television communications—escaped Russia for Argentina. Dr Rosemberg's education began in Argentina where she received her Bachelor's of Arts from the Liceo Nacional de Senoritas in Buenos Aires in 1936. This was followed with Medical School at the University of Buenos Aires, graduating in 1944. She remained at the university as Anatomy Instructor (1940–1946), Pediatric Instructor, and Associate Professor (1946–1948). Dr Rosemberg left Argentina in 1948, coming to Johns Hopkins University under the auspices of the Mead Johnson Fellowship and the Society for Pediatric Research. She subsequently stayed on in the Endocrinology Department at the Harriet Lane Home, Johns Hopkins University under the direction of Lawson Wilkins. In 1951, she joined the Endocrinology Section of the National Institute for Arthritis and Metabolic Diseases, National Institutes of Health (NIH) as a research fellow. Two years later, she joined the staff at the Worcester Foundation for Experimental Biology in Shrewsbury, Mass. Dr Rosemberg returned to NIH in 1970 as Chief of the Contraceptive Development Branch. Dr Rosemberg was an active member of many scientific societies, including: American Association for the Advancement of Science, American Fertility Society, American Heart Association, American Medical Women's Association, the Argentine Endocrine Society, the Argentine Pediatric Society, and the Argentine Sterility Society. While a scientist at the Medical Research Institute of Worcester, she was one of the leaders that made the American Society of Andrology so successful. Not only was she an active founding member of the American Society of Andrology, but also she was instrumental in securing funding for our meetings and symposia for the first meeting on March 31, 1976. For those of us who were present and active at the initiation of our Society, it is clear that her persuasive energy in promoting the first Annual Meeting in 1976 in Worcester was critical in creating a viable Society. She marshaled space, obtained financial support from industry, invited world-class speakers, and gathered key charter members from multiple disciplines resulting in a large attendance, all by the shear dynamism and infectious enthusiasm for which she was known. This was a woman who was strong to begin with and achieved recognition at a time when women were not recognized. She had a great talent for contacting friends throughout the world and arranging numerous meetings. Many ASA members remember her not only for her scientific expertise but her flair as a person. Upon her death, Dr Rosemberg bequeathed a substantial sum of money to the American Society of Andrology with a written request that it be “used to establish an annual award to be presented at the time of the Annual Meeting of the American Society of Andrology in consideration of the candidate's original contributions to the field of Andrology.” Subsequently, the Eugenia Rosemberg Endowment Fund was established and, with ASA Council approval, the investment income will be used in perpetuity to sponsor the annual ASA Distinguished Andrologist Award. The first sponsored award will be given at the 2006 Annual Meeting in Chicago to Dr Norman Hecht. We thank Eugenia Rosemberg for her vision, dedication, and generosity to the American Society of Andrology. Special thanks to C. A. Paulsen.
In Brief Objective To evaluate the clinical outcome of in vitro fertilization (IVF) treatment cycles from individual oocyte donors who underwent multiple sequential donations. Methods We reviewed clinical outcome data from sequential anonymous oocyte donation cycles using donors who underwent multiple IVF stimulations. Donors were grouped by the interval between cycles and the cycle number (rank). The primary outcome measure was delivery rate by individual donor per retrieval from the combined derivative fresh and frozen embryo transfers. Results Duration and amount of gonadotropin therapy and the fertilization rates did not correlate significantly with the interval between cycles or cycle rank. Cumulative delivered pregnancy rates for cycles 1–6 were 51.5%, 54.6%, 50.5%, 51.5%, 51.1%, and 57.6%, respectively. Delivered pregnancy rates did not vary by interval between cycles. Conclusion Young healthy presumed or proven fertile women can reliably donate oocytes for at least six cycles with the expectation of consistently high pregnancy rates. Individual oocyte donors undergoing multiple sequential in vitro fertilization cycles maintain high delivered pregnancy rates in recipients.
Mice injected with a rabbit antiserum to Ehrlich's ascites tumor developed hemorrhagic edematous lungs with a markedly increased serotonin content. Such lung findings were not seen in mouse anaphylaxis.
The hypothesis that increased estradiol production may be the cause of impaired spermatogenesis in infertile men with idiopathic oligozoospermia was tested by administering the aromatase inhibitor, testolactone, and by assessing its effects on sperm output and fertility. Our study was a randomized, placebo‐controlled doubleblind crossover trial. Subjects (n = 25) with infertility due to unexplained oligozoospermia were given testolactone (2 g/day) or placebo for 8 months followed by crossover to the other treatment for an additional 8 months. Total estradiol and testosterone levels during testolactone exposure did not change from basal and placebo values. However, sex hormone‐binding globulin binding capacity consistently decreased (30%, p < 0.01) and free testosterone levels increased (36%, p < 0.01). Free estradiol values increased but not significantly. Additionally, LH and FSH serum levels increased by 15% and 20%, respectively (p < 0.05), and 17α‐hydroxyprogesterone values increased by 90% (p < 0.05) during drug administration. Sperm output and semen quality remained unchanged during either testolactone or placebo treatment, and no pregnancies occurred during the 16‐month study. These data suggest that chronic administration of testolactone at this dose fails to maintain aromatase inhibition despite depression of 17,20‐desmolase activity with elevated 17α‐hydroxyprogesterone and depressed SHBG binding capacity with elevation of free testosterone. Testolactone is not efficacious in the treatment of idiopathic oligozoospermic infertility.
We studied the neurologic abnormalities in 41 men with isolated hypogonadotropic hypogonadism. Findings included anosmia, hyposmia, mirror movements, ocular motor abnormalities, cerebellar dysfunction, and pes cavus foot deformity. One-third of the subjects had a family history of delayed sexual maturation. Patients with a family history of delayed sexual maturation had a significantly higher incidence of olfactory dysfunction, mirror movements, and pes cavus foot deformity. Our data suggest that isolated hypogonadotropic hypogonadism and its accompanying neurologic abnormalities may arise from a genetically linked developmental abnormality of CNS structures.
The effect of sex steroids on plasma concentrations of FSH and LH was studied in 18 men. Steroids were administered by constant infusion for 96 hr at twice the estimated daily production rate of normal men to obtain stable levels in peripheral blood. Testosterone, 15 mg daily, increased plasma testosterone and estradiol levels 2-fold and suppressed FSH and LH approximately 40% during the 3rd and 4th days of infusion. Infusion of estradiol, 90 μg daily, caused similar suppression of FSH and LH (approximately 30%), and addition of 17α-hydroxyprogesterone, 4.5 mg daily, to the estradiol, 90 μg daily, had no additive effect. Dihydrotesterone, in pharmacologic dosage (7.5 mg daily) produced no detectible changes in plasma FSH or LH. There was no evidence for a selective effect of any of the steroids on FSH secretion. This study supports our previous concept that although there is a specific seminiferous tubular factor regulating FSH secretion, testicular steroids also modulate FSH secretion.
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