Nucleoside incorporation as a function of hormone levels during the early phases of estrogen-induced genesis of medullary bone in the Japanese quail,Coturnix coturnix

Summary The sequence of changes in RNA synthesis during the early phases of genesis of medullary bone induced in male Japanese quail by estrogen treatment was studied by ³H-uridine uptake. Analyses of plasma estrogen and testosterone were done by radioimmunoassay at 12, 24, 38 and 61 h. A dose of 5 mg kg^-1 estradiol-17 was found to stimulate the same ³H-uridine uptake 15 h after hormone treatment as a dose of 20 mg kg^-1 of estradiol valerate. The uptake of ³H-uridine rose as the dose of estradiol-17 increased. Plasma estrogen levels, which were highest 12 h after injection, declined sharply during the next 12 h, returning to control levels between 38 and 61 h. Testosterone levels declined after estrogen administration and remained below control values at all time points. Following estrogen administration, ³H-uridine uptake declined from control values for the first 8 h. Twelve hours after hormone administration control levels were again reached, with maximum ³H-uridine uptake occurring 16 h after hormone treatment. The 16-h maximum was followed by a steady decline to below control levels at 20, 24 and 28 h, the time at which the experiment was discontinued. Maximum ³H-uridine up-take following estrogen stimulation is similar to that observed for the stimulated immature rat uterus.     

Comparison of serum ethinyl estradiol, sex-hormone-binding globulin, corticoid-binding globulin and cortisol levels in women using two low-dose combined oral contraceptives

The study included 69 women taking a desogestrel (n = 30)- or gestodene (n = 39)-containing low-dose combined oral contraceptive for at least 3 months. Group size was calculated to detect a difference in mean values of 80% of 1 standard deviation (alpha = 0.05, beta = 0.1). Seven serum samples were obtained up to 4 h, and 1 sample 24 h, after drug intake on 1 day between the 10th and the 21st day of the cycle. The concentrations of sex-hormone-binding globulin (SHBG), corticoid-binding globulin (CBG) and cortisol were measured in a 0- to 4-hour serum pool by radioimmunoassay. Ethinyl estradiol (EE2) levels were analyzed in single and pooled samples using anti-EE2-6 beta-carboxymethyloxime-bovine serum albumin antiserum. The area under the curves (AUC) up to 4 and 24 h and Cmax and tmax were evaluated. Statistical analysis (analysis of covariance) did not reveal a dependence of values on duration of treatment or day of cycle. Both treatments resulted in almost identical values for all parameters evaluated. The mean levels of SHBG, CBG and cortisol were in the range of 186-226 nmol/l, 89-93 mg/l and 280-281 micrograms/l, respectively. Mean maximum EE2 levels of 106-129 pg/ml were found 1.6-1.8 h after pill intake and AUC0-4 h accounted for 329-374 pg.h.ml-1. The recently reported differences in serum EE2 and CBG levels between two groups of 11 women each treated with desogestrel- and gestodene-containing pills, respectively, could not be confirmed.     

Hormone treatment of the adult transsexual patient

Hormonal reassignment has two aims: (1) to reduce the hormonally induced secondary sex characteristics of the original sex and (2) to induce the secondary sex characteristics of the new sex. In Europe, cyproterone acetate is generally used to inhibit androgens in male-to-female transsexuals. Medroxyprogesterone acetate is an acceptable, though less effective, alternative. To induce feminization there is a wide range of oestrogens. Oral ethinyloestradiol is a potent and inexpensive oestrogen, but it may cause venous thrombosis. Oral 17beta-oestradiol valerate or transdermal 17beta-oestradiol is the treatment of choice. The goal of treatment in female-to-male transsexuals is to induce virilization, including a male pattern of sexual hair, a male voice and male physical contours, and to stop menses. The principal hormonal treatment is a testosterone preparation. Hormone-dependent tumours have been encountered and surveillance is necessary.     

Early events in the steroidal regulation of alpha2mu globulin in rat liver. Evidence for both androgenic and estrogenic induction.

1. A double-antibody radioimmunoassay for alpha2mu globulin has been developed. With the help of this highly sensitive radoimmunoassay the early effects of both androgen and estrogen treatments on the hepatic synthesis of alpha2mu globulin in the rat have been investigated. 2. Results show that the earlier observation of the long lag period in the androgenic induction of alpha2mu globulin is more apparent than real. 3. Single injections of either 5alpha-dihydrotestosterone(5alpha-dihydro-17beta-hydroxy-4-androsten-3-one) or its physiological antagonist estradiol-17beta (1,3,5(10)-estratriene-3,17beta-idol) to castrated female rats resulted in the induction of alphamu globulin reaching maximum hepatic level of the protein between 6--9 h after the hormone administration. Administration of cycloheximide 15 prior to hormone treatment blocked both androgenic andestrogenic induction of alpha2mu globulin. 4. Daily pretreatments with 5alphamu-dihydrotestosterone increased the sensitivity of subsequent androgenic response to alpha2muglobulin synthesis. On the other hand, daily pretreatments with estradiol 17beta decreased and ultimately abolished the estrogenic induction of alpha2mu globulin. 5. The possible mechanism of both androgenic and estrogenic induction of alpha2mu globulin in rat liver mediated through a sex-hormone-binding protein with dual affinity for both dihydrotestosterone and estradiol has been suggested.     

The effects of postmenopausal hormone replacement therapy and oral contraceptives on the endogenous estradiol metabolism.

The estradiol metabolism may be of clinical relevance in the pathophysiology of various diseases; the increase in D-ring metabolites over A-ring metabolites in breast cancer patients is of special interest. Since estrogen therapy has been blamed for increasing the risk of breast cancer, the effects of hormonal replacement therapy (HRT) and oral contraception were investigated on the ratio of the main D-ring metabolite, 16alpha-hydroxyestrone (16-OHE1), to the main A-ring metabolite, 2-hydroxyestrone (2-OHE1). In our study, hormone replacement therapy (HRT) in postmenopausal women consisted of administration of estradiol valerate either with or without addition of the progestin dienogest. In the second part of the study, women of reproductive age received ethinylestradiol plus dienogest or ethinylestradiol plus norethisterone acetate as oral contraceptives (OC). 2-OHE1 and 16-OHE1 were measured by enzyme immunoassay in 8 h night-urine collected before and after 3 months of hormone administration. With HRT, that is, estradiol valerate or estradiol valerate plus dienogest, the ratios before treatment were 0.47 and 0.60; after 3 months, they were 0.54 and 0.52, respectively. There were no significant differences. With oral contraception, that is, ethinylestradiol plus dienogest or norethisterone acetate, the ratios before administration were 0.62 and 0.68, vs. 0.31 and 0.54 after 3 months, respectively. The ratio after ethinylestradiol and dienogest was significantly lower after treatment. HRT and OC in the estrogen-progestin combinations tested did not impose any negative effects on estradiol metabolism--they did not elicit a higher D-ring metabolism, which is considered to increase breast cancer risk.     

Superovulation in the cow using estradiol 17beta or GnRH in conjunction with FSH-P

A study was designed to evaluate the superovulatory response in the cow when either estradiol 17beta or gonadotrophin releasing hormone (GnRH) was used in a superovulatory regimen with follicle stimulating hormone (FSH-P). Fifty-four cyclic crossbred females were superovulated in replicates between Days 8 and 12 of their cycle. All animals were treated with 28 mg of FSH-P in twice-daily decreasing doses, each receiving 500 mug cloprostenol (PGF) 48 h after initiation of treatment. Group 1 served as FSH-P controls, Group 2 received FSH-P and 400 mug of estradiol 17beta 36 h after PGF, and Group 3 received FSH-P and 250 mug GnRH 48 h after PGF. Inseminations with one vial of frozen semen were done at 12, 24 and 36 h after the onset of estrus. Ova/embryos were collected nonsurgically at Day 7 postestrus. Numbers of corpora lutea (CL) were recorded after palpation per rectum and the recovered ova and embryos were evaluated. All females were bled for endocrine examination. There were no differences in ovarian response among these treatments. Mean total ova/embryos collected in Group 3 was significantly higher than in Groups 1 or 2 (P < 0.05); however, no significant difference existed between groups in the mean numbers of fertilized or transferable embryos. Similarly, no significant differences existed between groups for recovery rate, fertilization rate, or percentage of transferable embryos. Serum estradiol levels were significantly higher at the expected end of ovulation in Group 2, and this tended to be associated with higher fertilization and transferable embryo rates. Furthermore, a significant positive correlation was found to exist between CL numbers and each of the ova/embryo parameters and the estradiol levels at estrus.     

Chronic estradiol treatment increases CA1 cell survival but does not improve visual or spatial recognition memory after global ischemia in middle-aged female rats

Transient global ischemia induces selective, delayed neuronal death in the hippocampal CA1 and cognitive deficits. Physiological levels of 17β-estradiol ameliorate ischemia-induced neuronal death and cognitive impairments in young animals. In view of concerns regarding hormone therapy in postmenopausal women, we investigated whether chronic estradiol treatment initiated 14 days prior to ischemia attenuates ischemia-induced CA1 cell loss and impairments in visual and spatial memory, in ovariohysterectomized (OVX), middle-aged (9-11 months) female rats. To determine whether the duration of hormone withdrawal affects the efficacy of estradiol treatment, hormone treatment was initiated immediately (0 week), 1 week, or 8 weeks after OVX. Age-matched, OVX and gonadally intact females were studied at each OVX interval. Ischemia was induced 1 week after animals were pretested on a variety of behavioral tasks. Global ischemia produced significant neuronal loss in the CA1 and impaired performance on visual and spatial recognition. Chronic estradiol modestly but significantly increased the number of surviving CA1 neurons in animals at all OVX durations. However, in contrast with previous results in young females, estradiol did not preserve visual or spatial memory performance in middle-aged females. All animals displayed normal locomotion, spontaneous alternation and social preference, indicating the absence of global behavioral impairments. Therefore, the neuroprotective effects of estradiol are different in middle-aged than in young rats. These findings highlight the importance of using older animals in studies assessing potential treatments for focal and global ischemia.     

The role of aberrant hypothalamic opiatergic function in generating polycystic ovaries in the rat

Treatment of adult female rats with estradiol valerate produces an intractable hypothalamic impairment that ultimately results in anovulatory acyclicity and polycystic ovaries. Evidence from our laboratory suggests that the hypothalamic impairment compromises regulation of the endogenous opioid system engendering a persistent opiatergic suppression of gonadotropin-releasing hormone secretion, which is subsequently reflected in a chronically low pituitary content of gonadotropin-releasing hormone receptors. If such is the case, inhibition of opiatergic transmission should improve the gonadotropin-releasing hormone pattern resulting in an improvement in the pituitary content of gonadotropin-releasing hormone receptors, and in an amelioration of the polycystic condition. We, therefore, treated rats with the polycystic ovarian condition, with daily injections of naltrexone. Within 1 week, there was a significant increase in the pituitary content of gonadotropin-releasing hormone receptors and a marked improvement in ovarian morphology, indicating that the hypothalamic opiatergic system is chronically active, and contributes significantly to the polycystic ovarian condition.     

Luteinizing hormone concentrations in anestrous ewes administered various estrogens

Twenty four anestrous ewes were evenly assigned to one of six groups and administered either sesame oil, estradiol-17β, estradiol-17α, estrone, estradiol benzoate or estradiol valerate. All estrogen treated ewes received 50 μg of the respective estrogen. Blood plasma was collected for 28 hours post-treatment and quantified for luteinizing hormone (LH) by radioimmunoassay. An estrogen induced LH surge was detected in at least three of the four ewes administered either estradiol-17β, estrone, estradiol benzoate or estradiol valerate whereas only one of the four estradiol-17α treated ewes and none of the ewes administered sesame oil had an LH surge. The interval from treatment to peak LH was similar for estradiol-17β (17.3±2.7 hours), estrone (18.5±1.0 hours) and estradiol benzoate (19.0±0.6 hours) treated ewes but delayed 7 to 9 hours for ewes administered estradiol valerate (26.0±1.2 hours).     

Synchronization of estrus following 7 or 9 day treatment with chlormadinone acetate (CAP)

Synchronization of estrus and fertility were determined in a series of 8 trials. Various levels of chlormadinone acetate (CAP) were fed for either 7 or 9 days. An injection of 5 mg of estradiol valerate and CAP was given at the start of the feeding period. In some trials estradiol 17β was injected near the end of the feeding period. In trial 1, 98% of the CAP-treated heifers were in estrus in a 5-day period, but only 46% conceived at first service compared to 80% in the non-synchronized heifers (P<.01).In trials 2 through 6, 0.25 mg estradiol 17β injected either 60 or 72 hours after the last CAP feeding reduced the interval to ovulation in heifers that ovulated. However, use of estradiol 17β reduced the number of heifers ovulating in most trials.In trials 7 and 8, estrus was effectively synchronized with either 7- or 9-day feeding of 7.5 or 10 mg of CAP daily followed by .5 mg estradiol 17β, 72 hours after the last CAP feeding. Pregnancy rates at first service varied from 21 to 45% in heifers in the synchronized groups, compared to 58% in the controls in trial 7 (P<.05). In trial 8 pregnancy rates at 1st service varied from 29 to 47% in treated heifers compared to 72% in controls (P<.01).In this series of trials, fertility was reduced from 24 to 43% with the use of CAP and estradiol valerate. Conception rates at first service were not improved by varying the length of feeding (7 or 9 days), level of CAP (7.5 or 10 mg) or by attempting to reduce the variation in ovulation time with estradiol 17β. None of the combinations of these three drugs used increased fertility in these trials.     

Evidence for a rapid in vivo effect on estradiol-17 beta on prolactin secretion in ovariectomized rats.

Repeated intraarterial injections of synthetic thryrotropin releasing hormone (TRH, 1 microgram/rat) increased plasma prolactin levels 4 hours after a single subcutaneous injection of 10 micrograms estradiol-17 beta (E2-17 beta) in rats ovariectomized 1, 2 or 4 weeks and at 2 hours after E2-17 beta injection in rats ovariectomized for 6 weeks. The effect of TRH was still present at 24 but not 48 hours after estradiol treatment. TRH-induced increases in plasma prolactin were similar in groups of rats treated with 10 micrograms E2-17 beta (s.c.) or implanted with 0.5 cm Silastic capsules of crystalline E2-17 beta (s.c.) whereas smaller, yet significant, TRH-induced increases in plasma prolactin were observed in rats injected s.c. with 1.0 microgram E2-17 beta. Single intraarterial injections of TRH at 4 or 8 hours after E2-17 beta treatment induced increases in plasma prolactin similar in magnitude to those observed at the same times after E2-17 beta in rats given repeated TRH injections. No effect of TRH was observed in ovariectomized rats given sesame oil and E2-17 beta treatment did not influence plasma prolactin in rats given saline instead of TRH. Intraarterial administration of serotonin creatinine sulfate (5-HT, 10 mg/kg body weight) induced marked increases in plasma prolactin in rats ovariectomized for 4 weeks which were potentiated at 2 and 6 hours after E2-17 beta (10 micrograms) treatment. The data show that estradiol has a fairly rapid stimulatory effect on plasma levels of prolactin induced by two different secretagogues but the exact site and mechanism of action remain unresolved.     

Steroid hormone feedback on LH in prepubertal Holstein heifers

A significant dose-response relationship between gonadotropin-releasing hormone (GnRH) and time to luteinizing hormone (LH) peak, peak serum LH and total serum LH was obtained in prepubertal Holstein heifers (28 weeks of age) (Experiment 1). For the second experiment, the effect of steroid feedback on the anterior pituitary was determined. A steady infusion of saline, estradiol-17 beta or progesterone was maintained for 24 h while GnRH, in various schemes, was administered 8 h after the beginning of steroid infusion. Estradiol-17 beta infusion (2.08 micrograms/h), although it did not affect peripheral concentrations of estrogen, caused an LH release 24 to 30 h later in 37.5% of the heifers. This amount of exogenous estrogen did not affect the LH response to a single GnRH (4 micrograms) challenge. When the same GnRH dosage (4 micrograms) was administered 6 times at hourly intervals, the heifers infused with estradiol had a lower response after the first 2 injections of GnRH and a greater response after the last 4 injections than heifers infused with saline. When GnRH was infused (4 micrograms/h) for 6 h, beginning 8 h after steroid infusion, estradiol infusion caused a significantly higher peak LH and total LH release than an infusion of either saline or progesterone (7.3 micrograms/h). The progesterone infusion had no effect on the GnRH-stimulated LH release. We conclude that prepubertal dairy heifers have an anterior pituitary capable of responding to the feedback effect of estrogen in a positive manner.     

Steroid sulfates in testis tissue of prostatic cancer patients treated for six months with the gonadotropin releasing hormone agonist buserelin

In order to assess the extent of inhibition of testicular steroidogenesis during long-term treatment of prostatic cancer with GnRH agonist, we measured the intratesticular levels of 5 steroid sulfate conjugates in human testis tissue removed from patients after 6 months of intranasal treatment with buserelin. The most pronounced decreases were found in testosterone and pregnenolone sulfates, to 1.6 and 7.1%, respectively, of concentrations measured in testis tissue from primarily orchiectomized prostatic cancer patients. In contrast, clearly smaller decreases were found in three other steroid sulfates measured, those of dehydroepiandrosterone (to 26%), 17-hydroxyprogesterone (to 27%) and 5-androstene-3 beta, 17 beta-diol (to 62%). These results are in keeping with our previous analyses of unconjugated steroids in similar tissue samples, and indicate that testicular steroidogenesis per se is not totally blocked by long-term intranasal treatment with GnRH agonist. Testicular steroid sulfate conjugation may be specifically suppressed since the total concentration of these conjugates decreased more than free steroid levels in our earlier measurements.     

The effect of cyproterone acetate alone and in combination with ethinylestradiol on the hypothalamic pituitary adrenal axis, prolactin and growth hormone release in male-to-female transsexuals

This study investigated the effects of long-term cyproterone-acetate (CA) treatment on the hypothalamus-pituitary-adrenal axis and further on the release of prolactin and growth hormone. Thirty-one male-to-female transsexuals, treated at least 3 months either with 100 mg CA alone or in combination with 50 micrograms ethinyloestradiol (EO)/day, were studied. In all of them the cortisol response to 250 micrograms Synacthen administration was comparable to that measured in controls. Six subjects treated with CA alone (group I) and six subjects treated with CA + EO (group II) underwent an insulin-hypoglycemia test. Seven eugonadal men served as controls. Compared with control values: in two subjects of group I and one subject of group II a low cortisol response was found. The mean growth hormone response was found to be lower in both groups, whereas the mean prolactin response was lower in group I.     

Hormone replacement therapy: one-year follow up of DNA damage

Although hormone replacement therapy (HRT) may offer considerable benefits for menopausal women, the potential cancer risk may limit its use. This work aimed at assessing whether HRT is able to induce DNA damage in postmenopausal women monitored by the micronucleus (MN) test, which provides a reliable biomarker of genotoxicity and cancer risk assessment. A group of 16 healthy women (non-smokers) in spontaneous menopause were given oral estradiol (2 mg oral micronized 17-beta estradiol daily) for 1 month, followed by a 30-day wash-out period and a transdermal treatment with 17-beta estradiol (1.5 mg gel daily) during 1 month. Oral intake of dihydrogesterone (10 mg/day for 12 days/month) was cyclically combined with oral or transdermal estradiol during the next 9 months. Venous blood samples were collected before the treatment, and after 1, 3, 6 and 12 months of therapy. Slides were scored blind and MN frequency was evaluated as number of micronuclei per 1000 binucleated cells. The baseline plasma levels of follicle-stimulating hormone (FSH), luteinizing hormone (LH) and estradiol (E2) were simultaneously measured. The means of MN frequency were 18.2+/-1.6, 18.6+/-2.1, 14.8+/-1.5, 15.9+/-1.0 and 17.7+/-1.3 for samples collected before and at 1, 3, 6 and 12 months, respectively. The MN frequencies at every sampling time did not statistically differ from the basal values. In addition, no statistically significant associations between MN values and hormone levels of E2 and FSH were observed throughout the entire study. This study shows the absence of any significant increase of MN frequencies in women undergoing oral and/or transdermal HRT, sequentially monitored for up to 12 months of therapy.     

Effects of orchidectomy and different modes of high dose estrogen treatment on circulating "free" and total 1,25-dihydroxyvitamin D in patients with prostatic cancer

Serum levels of total 1,25-dihydroxyvitamin D (1,25(OH)2D), vitamin D binding protein (DBP), sex hormone binding globulin (SHBG), testosterone, estradiol 17 beta (E2) and the "free" 1,25(OH)2D index were measured before and during treatment in prostatic cancer patients treated by orchidectomy (n = 15), with combined i.m. polyestradiol phosphate (PEP) + oral ethinyl estradiol (EE) (n = 10) and with i.m. PEP only for 3 months, followed by addition of oral EE (n = 9). Total concentrations of 1,25(OH)2D and DBP were unaffected by orchidectomy and treatment with i.m. PEP only, but were significantly elevated during treatment including oral EE. SHBG levels were unaffected by orchidectomy, slightly increased by i.m. PEP only and greatly increased by oral EE. The free 1,25(OH)2D index was slightly elevated by treatment including oral EE. Evidence was obtained that the increase in 1,25(OH)2D levels observed during oral estrogen treatment was secondary to the estrogen-augmented increase in DBP and not a result of an estrogen-stimulated synthesis of 1,25(OH)2D. Furthermore, the stimulatory effect of estrogen on DBP concentrations seemed to be dependent on the route of administration of the hormone.     

雌二醇联合乳酸菌阴道胶囊治疗老年性阴道炎的临床效果研究

目的:研究雌二醇联合乳酸菌阴道胶囊治疗老年性阴道炎的临床效果,为临床治疗老年性阴道炎提供参考依据。方法:选择2016年1月~2017年5月在我院进行诊治的老年性阴道炎患者94例,随机分为观察组与对照组,每组各47例。对照组给予阴道放置乳酸菌阴道胶囊治疗,每日睡前放置1粒,连续使用一周;观察组联合采用阴道放置戊酸雌二醇治疗,每日睡前放置1片(0.5 mg),连续使用一周。比较两组的临床治疗效果,检测两组患者治疗前后血清孕酮、雌二醇、促黄体生成激素以及促卵泡生成激素水平,并且于治疗后随访观察1年,观察两组的复发率。结果:治疗后,观察组的有效率为95.74%(45/47),明显高于对照组[82.98%(39/47)](P0.05)。两组治疗前后的血清孕酮、雌二醇、促黄体生成激素以及促卵泡生成激素水平比较差异均无统计学意义(P0.05)。治疗后6个月,观察组的复发率为4.25%(2/47),明显低于对照组[14.89%(7/47)](P0.05);观察组治疗后1年的复发率为8.51%(2/47),明显低于对照组[23.40%(11/47)](P0.05)。结论:雌二醇联合乳酸菌阴道胶囊治疗老年性阴道炎的临床效果明显优于单纯使用乳酸菌阴道胶囊治疗,且不会对机体内的激素水平造成影响,并可有效降低其复发率。     

Anisomycin inhibition of estradiol-induced and progesterone-facilitated luteinizing hormone surges in the immature rat

These studies were designed to examine the effect of anisomycin, a potent and reversible inhibitor of protein synthesis with low systemic toxicity in rodents, on induction of luteinizing hormone (LH) surges by estradiol and their facilitation by progesterone. Immature female rats that received estradiol implants at 0900 h on Day 28 had LH surges approximately 32 h later (1700 h on Day 29). Insertion of progesterone capsules 24 h after estradiol led to premature (by 1400 h) and enhanced LH secretion. Protein synthesis was inhibited by 97%, 95%, 47%, and 16% in the hypothalamus-preoptic area (HPOA) and by 98%, 87%, 35%, and 0% in the pituitary at 30 min, 2 h, 4 h, and 6 h after s.c. injection of anisomycin (10 mg/kg BW), respectively. A single injection of anisomycin at 0, 3, 6, 9, 12, 24, 27, or 30 h after estradiol treatment significantly lowered serum LH levels at 32 h. The effect of injecting anisomycin at 0, 24, or 27 h was overridden by progesterone treatment at 24 h, but LH secretion was delayed serum LH levels were basal (10-30 ng/ml) at 1400 h but elevated (500-800 ng/ml) at 1700 h. Complete suppression of LH surges in estradiol-plus-progesterone-treated rats was achieved with 2 injections of anisomycin on Day 29 at 0900 h and again at 1200 h or 1400 h. Further experiments were designed to examine proteins that might be involved in anisomycin blockade of progesterone-facilitated LH surges. Intrapituitary LH concentrations at 1700 h on Day 29 were 70-80% higher (102 +/- 12.5 micrograms/pituitary) in rats that received 2 injections of anisomycin than in vehicle-treated controls (58.5 +/- 7.7 micrograms/pituitary). There were no significant effects of anisomycin on cytosol progestin receptors in the HPOA (7.1 +/- 1.5 fmol/tissue, anisomycin; 7.2 +/- 0.3, vehicle) or pituitary (8.3 +/- 1.3 fmol/tissue, anisomycin; 11.7 +/- 2.9, vehicle) at this time. The concentration of pituitary gonadotropin-releasing hormone receptors (GnRH-R), however, was significantly lower after anisomycin (265 +/- 30 vs. 365 +/- 37 fmol/mg protein) treatment. These results suggest that both estradiol-induced and progesterone-facilitated LH surges involve protein synthetic steps extending over many hours. Blockade of progesterone-facilitated LH surges by anisomycin appears to be due primarily to an effect on release of LH to which lowering of GnRH-R levels may contribute.     

Use of leuprolide to treat endometriosis in a rhesus macaque.

Endometriosis was diagnosed in an aged dysmenorrheic rhesus monkey (Macaca mulatta) after biopsy of a 7 cm abdominal mass which could not be completely resected due to extensive adhesions. A 6-month course of treatment with leuprolide, a gonadotropin-releasing hormone agonist, resulted in cessation of menstrual cycles and marked clinical improvement. Dysmenorrhea and hypovolemic shock occurred 2 months after therapy was completed. Despite supportive treatment and resumption of leuprolide, the primate's clinical deterioration and abdominal mass enlargement necessitated euthanasia. To our knowledge, this is the first report of a case of endometriosis in a rhesus macaque treated with a gonadotropin-releasing hormone agonist. Although prolonged leuprolide therapy was clinically effective, its cost and the difficulty in early diagnosis of endometriosis may limit its use in nonhuman primate medicine.     

Augmentation mammaplasty in male-to-female transsexuals

Hormonal therapy and gender-confirming surgery are the treatments of choice in appropriately selected male-to-female transsexuals. Penectomy and vaginoplasty are the paramount surgical requests of the male transsexual, but breast enlargement greatly increases subjective feelings of femininity. There are only limited reports on augmentation mammaplasty in male transsexuals, and hardly any attention has been paid to the differences between the female mammary anatomy and its male counterpart. The basic anatomic and surgical considerations of augmentation mammaplasty for 201 male-to-female transsexuals who were operated on from 1979 to 1997 are reviewed and discussed. They include the differences between male and female anatomy and how to feminize the male chest, the results of hormonal therapy and the proper timing of surgery, the choice of implant size and surgical approach, the results that may be expected after surgery, and the implications of all mentioned on the long-term outcome and follow-up after augmentation mammaplasty. Because the referring doctor may not check on the breasts or may not be trained to examine augmented breasts for pathologic conditions, the mammaplastic surgeon has an obligation to ensure the proper follow-up of these patients.