No description available.

No description available.

No description available.

This investigation was conducted to determine the effect of estrogen replacement therapy (ERT) on vitamin B-6 status of postmenopausal women. Nineteen postmenopausal women served as subjects. Nine (54.7 + 4.7 years) were taking ERT (experimental group); ten (56.8 + 2.3 years) were not (control group). For three consecutive days, subjects recorded their dietary intake and collected their 24-hour urine specimens. On the fourth day, a fasting blood sample was drawn from the subjects. The dietary intake of vitamin B-6, as well as the concentration of total vitamin B-6 in plasma (PB6; and urine (UB6) were measured. PB6 and UB6 were determined by a microbiological method with Saccharomyces uvarum as the assay organism. The mean age, height, hematocrit and hemoglobin values were similar for the two groups. The experimental group was significantly heavier than the control group (p<0.05). The experimental group had a lower mean PB6 than the control group: 47.7 ± 19.7 nmol/L vs. 56.2 + 20.6 nmol/L. These means were not significantly different (p=0.05). PB6 was positively correlated with dietary vitamin B-6 intake (p=0.0001) and vitamin B-6 to protein ratio (p=0.0021). When the means were adjusted for dietary vitamin B-6 and the vitamin B-6 to protein ratio, the mean PB6 of the experimental group (42.7 nmol/L) was significantly lower than that of the control group (60.6 nmol/L) (p<0.05). PB6 was not positively correlated with either age (r=0.20) or the vitamin B-6 dietary history score (r=0.15). UB6 was similar for the two groups. UB6 correlated positively with daily dietary intake of vitamin B-6 (r=0.51, p<0.05) and the ratio of vitamin B-6 to protein (r=0.47, p<0.05), UB6 was not significantly correlated to urine volume (r=0.05). The mean daily intakes of vitamin B-6 and protein were similar for the two groups. One of the 19 subjects had a vitamin B-6 intake that was less than 67 percent of the RDA. Most subjects' (89%) intake of vitamin B-6 was adequate when the ratio of 0.016 mg of vitamin B-6 per g of protein was used as the standard. / Graduation date: 1990

The effectiveness of estrogen replacement therapy in the prevention of postmenopausal osteoporosis has led to its current widespread use throughout the United States and much of Western Europe, and recently, clinical correlations between circulating androgen levels and structural bone integrity have been presented. Nevertheless, the biochemical mechanism through which estrogens and androgens act to protect and maintain bone has remained unclear. One possibility is that these hormones directly modulate the activity of cells responsible for bone formation. Therefore, studies were conducted to examine the effects of sex steroids on human osteoblast-like cells. In the first set of experiments, a finite human cell line was established from trabecular bone explants obtained from a 48 year-old woman. These cells, designated BG688, were characterized as osteoblast-like in phenotype using several independent criteria. In addition to classical osteoblast markers, BG688 cells also possess approximately 2400 high affinity (K(d) = 0.45nM) 17-β estradiol (E₂) binding sites per cell. The binding of E₂ to a subset of these sites was specific. BG688 cells were also shown to respond to a physiological concentration (10nM) of E₂, which elicits pleiotropic changes in several mRNA levels including a 2-fold increase in the steady state concentration of α₁(I)-procollagen mRNA. These results indicate that human osteoblast-like cells respond to E₂ via a receptor mediated mechanism, but that, unlike the reproductive tissues, osteoblasts are a less sensitive target. In the second series of experiments, the effects of androgenic hormones on the osteoblast-like, human osteosarcoma cell line, HOS TE85 were evaluated. Employing radiolabelled dihydrotestosterone (DHT), 2800 saturable, high-affinity (K(d) = 0.66nM) androgen binding sites were detected per HOS TE85 cell. Androgen binding was specific. The expression of androgen receptors in HOS TE85 cells was further substantiated by Northern analysis. Physiological concentrations of DHT and testosterone decreased HOS TE85 cell proliferation. This finding suggests that androgens may also play a role in osteoblast differentiation. In support of this hypothesis, treatment with testosterone enhanced the abundance of both α₁ (I)-procollagen mRNA and transforming growth factor- β mRNA. The non-aromatizable androgen DHT also elicited an increase in the steady state concentration of α₁(I)-procollagen mRNA. The findings presented herein are significant within the field of bone cell biology in that they demonstrate that osteoblasts are a target cell for the action of sex steroids, via their cognate, high-affinity receptors. These results also have important implications within the broader context of bone pathophysiology in that they suggest a direct modulation of bone forming and bone remodeling activity by sex steroids.

This study analyzed the effects of estrogen replacement therapy (ERT), ethnicity, marital status, education level, maternal status and financial security on the perceived life satisfaction of women over fifty. Information was collected from 125 subjects at an independent school district. The instrument was adapted from a life satisfaction scale originally developed by B. Neugarten. Eight demographic items included ERT use, age, menopause status, marital status, educational level, ethnicity and perception of financial security. Statistical analysis consisting of one way analysis of variance, Student Newman-Keuls ad hoc procedure and multiple regression indicated an independent correlation between financial security and education level to life satisfaction scores. Neither ERT nor menopause status was correlated with perceived life satisfaction score of respondents.

No description available.

The effects of exogenous estrogen administration on aspects of memory and cognition in women were examined in two studies. In Study 1, women receiving estrogen replacement therapy were compared to untreated women on four measures of verbal memory. Those receiving estrogen had significantly better scores on a measure of delayed memory for propositional material. In Study 2, women in the early stages of Alzheimer's Disease (AD) were administered either estrogen or placebo on a double-blind basis for six months. Women given estrogen showed improvement on a measure of verbal memory and spatial attention compared to the placebo controls. The combined results of these studies provide evidence that estrogen enhances aspects of verbal memory in both healthy postmenopausal women and in postmenopausal women in the early stages of AD as measured by neuropsychological tests. These effects might be mediated by actions of estrogen on neuronal morphology and physiology in brain areas important for memory and cognition.

Memory function was examined in association with sex hormone levels in women. The results of the first study suggest that self-reports of memory problems were especially prevalent among women attending a menopause clinic compared to a nonpatient sample. In the following investigation, women given placebo after undergoing a bilateral oophorectomy showed decreases in memory performance, specifically on a paired-associate learning task, coincident with declines in estrogen levels. Significant improvements were found in estrogen-treated women pre- to postoperatively in the immediate recall of paragraphs, in association with supraphysiological estrogen levels. A final study on naturally-cycling women found a decline in visual memory performance during the menstrual compared to the luteal phase of the cycle. Visual memory scores were positively correlated with progesterone levels whereas paired-associate recall scores were positively associated with estradiol levels during the luteal phase. These results suggest that certain aspects of memory covary with changes in sex steroid levels in some women.

[Truncated abstract] Our understanding of the actions of oestrogen on the vasculature has recently been questioned following the results of large clinical trials revealing a negative effect of hormone replacement therapy (HRT) on cardiovascular disease (CVD) risk amongst postmenopausal women. It is important to determine how a hormone with numerous positive effects on intermediate pathways of atherosclerosis fails to offer cardioprotection. Further investigation into the actions of oestrogen in the vasculature may add to our current understanding of the pathogenesis of atherosclerosis and oestrogen biology. The primary aim of this thesis was to investigate involvement of the oestrogen receptors (ERs) in atherosclerotic CVD and to provide further insight into the actions of oestrogen on the vasculature by studying the actions of oestrogen on the regulation of an oestrogen-responsive gene within human vascular cells. Following confirmation of ERa and ERß expression at the RNA and protein level in human aorta sections, correlations of receptor expression with age and atherosclerosis were examined. Significantly strong negative relationships of ERa, androgen receptor (AR), and progesterone receptor (PR) with age in both males and females were detected. No trend was detected between ERß expression and age. These findings suggest that the receptor-mediated actions of hormones in the vasculature may change with age. Further, this thesis compared for the first time sex hormone receptor expression in normal and adjacent atherosclerotic aortic tissue providing a critical assessment of receptor differences due to atherosclerosis. Results revealed reductions of all hormone receptors in early atherosclerotic versus normal aorta tissue. ... These results suggest that the 3'-UTR SNPS may have more of an influence on carotid thickening when oestrogen levels are lower, suggesting the importance of both genetic variation of the ERß gene and oestrogen status on carotid thickening. Finally, this was the first study to investigate oestrogen-induced regulation of angiotensinogen (AGT), a candidate gene for CVD, in human vascular cells. Oestrogen influenced AGT transcription in a cell specific manner. The overall influence of oestrogen on AGT transcription in the vasculature is unknown. This thesis adds to the knowledge of oestrogen and atherosclerosis by suggesting the involvement of the sex hormone receptors (ERa, ERß, PR and AR) in atherosclerosis, presenting ERß as a potentially important candidate gene for atherosclerosis, revealing interactions between estrogen status and associations of ERß SNPs with carotid thickening, and demonstrating vascular cell-specific actions of oestrogen on the regulation of a candidate gene for CVD. These factors may have contributed to the lack of cardio-protection following HRT, as revealed by large clinical trials.