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METHOD: To test the hypothesis that psychosocial symptomatology differs by country of origin and acculturation among Hispanic women, we examined 419 women, aged 42-52 years at baseline, enrolled in the New Jersey site of the Study of Women's Health Across the Nation (SWAN). Women were categorized into six groups: Central (CA, n = 29) or South American (SA, n = 106), Puerto Rican (PR, n = 56), Dominican (D, n = 42), Cuban (Cu, n = 44) and non-Hispanic Caucasian (NHC, n = 142). Acculturation, depressive symptoms, hostility/cynicism, mistreatment/discrimination, sleep quality, social support, and perceived stress were assessed at baseline. Physical functioning, trait anxiety and anger were assessed at the fourth annual follow-up. Comparisons between Hispanic and non-Hispanic Caucasians used χ², t test or non-parametric alternatives; ANOVA or Kruskal-Wallis testing examined differences among the five Hispanic sub-groups. Multivariable regression models used PR women as the reference group. RESULTS: Hispanic women were overall less educated, less acculturated (p < 0.001 for both) and reported more depressive symptoms, cynicism, perceived stress, and less mistreatment/discrimination than NHCs. Along with D women, PR women reported worse sleep than Cu women (p < 0.01) and more trait anxiety than SA and Cu women (p < 0.01). Yet, PR women were most acculturated (21.4% highly acculturated vs. CA (0.0%), D (4.8%), SA (4.8%) and Cu (2.3%) women; p < 0.001). In regression models, PR women reported depressive symptoms more frequently than D, Cu, or SA women, and reported trait anxiety more frequently than Cu or SA women. Greater acculturation was associated with more favorable psychosocial status, but PR ethnicity was negatively related to psychosocial status. CONCLUSION: Psychosocial symptomatology among Hispanic women differs by country of origin and the relatively adverse profile of Puerto Rican women is not explained by acculturation.

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OBJECTIVE: A possible association of endometriosis with decreased bone mineral density in women has been proposed. It has been reported that cortical and trabecular bone mass of the distal portion of the radius is decreased in patients with endometriosis. The objective of this study was to investigate the relationship between endometriosis and bone mineral density with the use of a rat model. STUDY DESIGN: Cycling female Sprague-Dawley rats (180 days old) were randomly assigned to 1 of 2 groups. The treatment group (n = 16) underwent surgical induction of endometriosis. Female rats (n = 17) with surgically transplanted abdominal muscle served as control animals. Dual-energy x-ray absorptiometry measurements were obtained before surgery and after 90 days with a Lunar DPX-MD+ (GE Lunar, GE Medical Systems, Milwaukee, Wis) bone densitometer, with software standardized for small animal research. RESULTS: Experimental animals had grossly visible endometriotic disease at necropsy (90 days). The mean net change in total bone mineral density from baseline to 90 days in the control group was +0.019 +/- 0.002 g/cm2, whereas the mean net change in total bone mineral density for the experimental group was +0.013 +/- 0.002 g/cm2. The experimental group gained less bone than the control group (P = .02). CONCLUSION: The age-appropriate increase in bone mineral density known to occur in this animal model is attenuated by surgically induced endometriosis. This finding supports the idea that endometriosis might be associated with decreased bone mineral density.

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Angiotensin II type 2 (AT(2)) receptor is highly expressed in the fetal tissues and decreases rapidly after birth. AT(2) receptor is re-expressed in the adult atretic ovarian follicles. Recently, it has been reported that AT(2) receptor mediates apoptosis. Primarily, we have cloned human AT(2) receptor cDNA and mapped it to the X-chromosome. To further analyze the organization and function of the AT(2) receptor gene, in this study we cloned the human AT(2) receptor genomic DNA. Human AT(2) receptor gene is composed of three exons and two introns. Primer extension analysis revealed a putative transcription initiation site at 24 bp downstream from TATA box. Furthermore, we identified a polymorphism (C-A) in 3' untranslated region of exon 3, which may be a useful genetic marker for genetic analysis of human X-linked inherited disease. In this study, we postulated that the patients with premature ovarian failure, which has been reported to be linked with X-chromosome abnormality, have AT(2) receptor mutation that may contribute to the early onset of atresia. We examined the entire coding sequence of this receptor in two different families of sisters with premature ovarian failure (POF) but found no changes in nucleotide sequences.

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Pendred's syndrome is manifested by congenital sensorineural deafness in association with familial goiter due to defective organic binding of iodine in the thyroid gland. The majority of patients with Pendred's syndrome are euthyroid. We report on an unusual case of a patient with Pendred's syndrome presenting with amenorrhea and late-onset hypothyroidism.

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To determine whether cortisol has an effect on hypothalamic-pituitary-gonadal function, we studied 11 eumenorrheic women in the early follicular phase of consecutive menstrual cycles by performing daytime 10-min blood sampling, one before and one during hydrocortisone administration. Daily blood sampling for gonadotropins and sex steroids was also performed. LH pulsations were determined by modification of a widely used threshold method and compared by paired t-testing. The LH interpulse interval was significantly prolonged (95 +/- 5 to 119 +/- 14 min; p = 0.001), and the mean LH pulse amplitude remained unchanged (1.3 +/- 0.1 and 1.5 +/- 0.2 mIU/ml) with glucocorticoid exposure. Mean estradiol was not altered (46 +/- 5 and 43 +/- 3 pg/ml), but mean LH and FSH from pooled serum aliquots were slightly but significantly reduced (2.6 +/- 0.2 to 2.2 +/- 0.2, 5.5 +/- 0.4 to 4.5 +/- 0.3 mIU/ml; p = 0.004, 0.012, respectively). Mean progesterone levels were also decreased (0.8 +/- 0.3 to 0.5 +/- 0.2 ng/ml; p = 0.011) in the presence of exogenous glucocorticoid. Twenty-four-hour urinary free cortisol levels confirmed a substantial increase in free cortisol excretion (74 +/- 10 to 305 +/- 50 micrograms/day; p = 0.001). These results demonstrate that cortisol can slow LH pulse frequency and, by inference, hypothalamic GnRH secretion, in a manner that appears independent of corticotropin releasing factor. Excess cortisol alone may therefore play a role in the development of stress-associated menstrual disturbances.

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The use of pulsatile gonadotropin-releasing hormone is an effective means of inducing ovulation, but requires prolonged intravenous (IV) or subcutaneous administration. We hypothesized that the use of self-contained infusion pumps using fluids maintained in a closed system would permit safe peripheral IV administration of gonadotropin-releasing hormone, and possibly other hormones, over prolonged intervals. Thirty-eight female patients undergoing pulsatile IV gonadotropin-releasing hormone therapy were followed for 1958 catheter days (230 catheters). Catheters were removed for signs of local inflammation, at the completion of a treatment episode or, initially, at routine intervals of 7-10 days. There were no episodes of fever (temperature over 37.5C) and three episodes of local inflammation. The incidence of significant catheter-tip cultures was 11%, and none were associated with local inflammation. There were four positive blood cultures (2%), none associated with local or systemic signs of infection. We conclude that the use of a closed system of prolonged peripheral IV cannulation is relatively safe when combined with fastidious care of the catheter site and careful outpatient monitoring for long-term administration of pulsatile gonadotropin-releasing hormone.

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To examine gonadotropin secretory frequency as a component of the disordered neuroendocrine regulation of gonadotropin secretion in women with polycystic ovarian disease (PCOD), we measured serum gonadotropin concentrations in 12 women with PCOD at 10-min intervals for periods of 12-24 h. The patterns of LH and FSH release in these patients were compared to the findings of 24 studies in 21 age-matched normal women during the early, mid- and late follicular phases (EFP, MFP and LFP) of their cycles. Serum sex steroid levels during the 12-24 h of study in the women with PCOD were compared to those in normal women studied during the follicular phase. The mean serum estradiol (E2) level in the women with PCOD was similar to that in normal women studied in the EFP, but lower than those in normal women in the MFP (P less than 0.05) and LFP (P less than 0.01). Mean serum estrone, however, was significantly higher in women with PCOD than in women in the EFP and MFP (P less than 0.05 and P less than 0.02, respectively), but lower than that in women in the LFP (P less than 0.02). Total and unbound testosterone (T) levels were significantly elevated in women with PCOD compared to those in normal women at all stages of the follicular phase (P less than 0.001). The mean serum LH concentration and LH pulse amplitude were markedly elevated in the women with PCOD compared to normal women at all three stages of the follicular phase (P less than 0.05 or less). In addition, LH pulse frequency was faster in women with PCOD [24.8 +/- 0.9 ( +/- SE) pulses/24 h] than that in women in the EFP (15.6 +/- 0.7; P less than 0.01), MFP (22.2 +/- 1.1; P less than 0.05) and LFP (20.8 +/- 1.2; P less than 0.01). This increased LH pulse frequency in women with PCOD correlated with ambient serum E2 levels on the day of study (r = 0.84; P less than 0.001), but not with serum estrone, T, or unbound T. Repeat studies in four women with PCOD demonstrated a similarly abnormal gonadotropin secretory pattern in each. We conclude that 1) women with PCOD have an increase in both the amplitude and frequency of LH secretion compared to those in normally cycling women throughout the follicular phase; 2) the defect in women with PCOD is reproducible.(ABSTRACT TRUNCATED AT 400 WORDS)

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Human uterine luminal fluids contain over two dozen proteins distinct from those of serum as detected by two dimensional gel electrophoresis and silver-type protein staining. Eighty-one percent of these uterine fluid proteins can be detected in vitro by radiolabeled methionine incorporation studies and the vast majority of these products are epithelial in origin. The major recognizable menstrual cycle phase-dependent change in the protein pattern in these gels was the appearance of a protein group (number 27) of approximately 25,000 mw and pI of 5.8 - 6.3. This group of proteins was found in nearly all mid- and all late secretory phase fluids or culture media and in none obtained earlier in the cycle. As yet, however, it has not been possible to induce these proteins in proliferative specimens in vitro by the addition of estrogens and/or progestins, though studies along these lines are continuing. Although we cannot be certain, it appears as though protein group number 27 is distinct from, but similar in several respects to, other proteins of human endometrium reported in the literature.

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By combining two-dimensional gel electrophoresis, protein staining and a sensitive computer-assisted gel scanning system, it was possible to examine human uterine fluid (n = 56) qualitatively and quantitatively for the presence of endometrial proteins. The protein concentration of uterine fluids ranged from 0.1 to 12.0 mg/ml with early secretory phase samples (n = 15) having significantly less protein (0.72 +/- 0.2 SEM mg/ml p less than or equal to 0.05) than the proliferative phase (n = 57) samples (1.58 +/- .29 SEM mg/ml). Whole blood contamination of uterine fluid, as measured by hemoglobin content, averaged 6.2 +/- 0.88% throughout the menstrual cycle. Human uterine fluids collected throughout the menstrual cycle were found to contain serum and up to 24 other proteins in addition to those previously described (MacLaughlin and Richardson, 1983). These proteins represent approximately 1% of the total protein in the gels and exhibit isoelectric points from 4.5 to 7.0 and molecular weights in the 26,000 to 60,000 range. These proteins are absent from human serum, which exhibits an identical pattern whether obtained in the proliferative or secretory phase of the menstrual cycle. These secreted endometrial proteins now become the standard against which to compare proteins identified in vitro using organ, gland and cell culture techniques and to characterize proteins that are regulated by steroid hormones in vivo.

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