Women's Health; HIV/AIDS and the Workplace in South Africa

This work explores the connections between gender inequality; HIV/AIDS and women's health in the world of work in South Africa. These connections are located within a context of significant reversals in development; specifically declining life expectancy and premature mortality for South Africans - particularly for women. By relying on the existing literature and interviews with 33 key informants; the paper examines the extent to which South African workplaces are recognising women's social and biological vulnerability to HIV. In particular; the paper considers the potential role of the workplace in responding to growing evidence that links gender and health by establishing targeted HIV/AIDS interventions. The findings suggest that the vast majority of company representatives do not recognise women's social and biological vulnerability and related social norms vis-a-vis HIV and AIDS. Importantly; most workplaces are not initiating programmes that specifically address women's or men's health. The author briefly identifies factors that may help explain the current state of knowledge and practice in the realm of HIV and women's health in the workplace; and puts forward suggestions for future research

An in vivo animal model to study chronic adriamycin cardiotoxicity: a P-31 nuclear magnetic resonance spectroscopy investigation.

The mechanism responsible for adriamycin induced cardiotoxicity is unknown. We have developed an in vivo rabbit model for use with P-31 nuclear magnetic resonance spectroscopy which allows serial investigations of the drug's effects on myocardial metabolism. Eleven animals were studied over a 10 week period and changes in intracellular pH and phosphate metabolites were observed. The magnitude of changes in pH and inorganic phosphate were the best indicators of the severity of the cardiomyopathy. The results are consistent with an adriamycin induced degeneration of myofibrils rather than a severe metabolic impairment.

Modulation by cortisol of adrenocorticotropin-induced activation of adrenal function in fetal sheep.

We examined the hypothesis that cortisol (F) modulates the activation of adrenal function induced by treating fetal sheep in vivo with pulsatile ACTH (P-ACTH). Chronically catheterized sheep fetuses were infused in utero for 100 h between day 127 and day 131 of pregnancy with P-ACTH; P-ACTH plus metopirone; P-ACTH plus metopirone plus F; P-ACTH plus metopirone plus dexamethasone, or saline (controls). After 100 h, basal and ACTH-stimulated output of 11-desoxycortisol (S), F, and progesterone from collagenase-dispersed fetal adrenal cells was measured. Adrenal cells from fetuses treated with P-ACTH in vivo had significantly greater basal and stimulated (delta) outputs of F and S in vitro than controls. These effects were attenuated in fetuses pretreated with P-ACTH plus metopirone. Concurrent in vivo treatment with ACTH plus metopirone plus F restored basal and delta outputs of F and S to values that were not significantly different from those after P-ACTH alone. In vivo treatment with dexamethasone in addition to P-ACTH plus metopirone significantly raised basal outputs of F and S, but the cells were unresponsive to ACTH in vitro. Basal output of progesterone was significantly greater after in vivo P-ACTH plus metopirone plus dexamethasone, but no treatment raised delta progesterone output over controls. These results support a role for glucocorticoids in modulating ACTH-induced activation of adrenal function in late gestation fetal sheep.

Wrist driven flexor hinge orthosis: linkage design improvements.

Wrist driven flexor hinge orthosis (WDFHO) linkage movements were analyzed graphically for existing kit form orthoses and modified orthoses. The graphical analysis indicated improved function by increased torque and resultant pinch force in modified orthoses. A geometric solution to pivot point location which will allow clinicians and orthotists to properly locate the linkage pivot points for WDFHOs was developed. Improved function was documented in 5 orthoses converted from kit form linkages to modified linkages.

Activation of ovine fetal adrenal function by pulsatile or continuous administration of adrenocorticotropin-(1-24). I. Effects on fetal plasma corticosteroids.

ACTH given as a continuous infusion to fetal sheep causes an increase in plasma cortisol concentrations and premature labor. However, the effects on fetal adrenal responsiveness in vivo and the mode of ACTH administration on plasma corticosteroids are unknown. We examined the effects on plasma corticosteroids of giving the same total amount of ACTH to fetal sheep in utero either as pulses (P-ACTH; 66.7 ng/min for 15 min every 2 h) or continuously (C-ACTH; 0.5 micrograms/h) for 72 h. We determined the changes in vivo in fetal adrenal responsiveness during P-ACTH treatment, and we examined the ability of continued P-ACTH administration to induce premature labor. Both modes of ACTH administration led to a significant (P less than 0.05) increase in the fetal plasma cortisol (F) concentration compared with that in saline-treated controls, but C-ACTH resulted in significantly higher (P less than 0.05) F values than P-ACTH treatment. There was a small increase in the F-binding capacity of fetal plasma during both P-ACTH and C-ACTH, but there was no difference in the cortisol-binding capacity between the two treatments. Twenty minutes from the start of P-ACTH, there was an acute elevation in plasma F to values similar to those found with C-ACTH administration. The magnitude of this response rose significantly (P less than 0.05) between days 1-4 of P-ACTH treatment. There was no significant change in fetal plasma corticosterone during either P-ACTH or C-ACTH, resulting in a 4- to 6-fold increase in the plasma F to corticosterone ratio of both groups. In animals in which P-ACTH treatment was continued beyond 72 h, fetal plasma F continued to rise, and premature labor occurred after 99.0 +/- 4.1 (+/- SE) h. Fetal adrenal weights were not significantly different between P-ACTH for 72 or 100 h or C-ACTH for 72 h, although in each of these groups, the glands were heavier than those in control fetuses. We conclude that activation of fetal adrenal function is demonstrable in vivo during P-ACTH administration. This is reflected by selective F hypersecretion and may lead to premature delivery.

Relation between diurnal changes in peripheral plasma progesterone, cortisol, and estriol in normal women at 30-31, 34-35, and 38-39 weeks of gestation.

To determine the relation of diurnal changes in plasma progesterone to those in cortisol and estriol we measured the concentrations of progesterone, cortisol and estriol in samples of plasma taken at 30- to 60-min intervals throughout 24 h from women at 30-31, 34-35, and 38-39 weeks of gestation. Plasma progesterone showed a significant diurnal rhythm at 30-31 and at 34-35 weeks of pregnancy, with troughs at 04.30-10.00 h. Major peaks occurred between 15.30 and 02.30 h. There was no diurnal rhythm in progesterone at 38-39 weeks. Plasma progesterone showed a significant negative correlation with plasma cortisol at 30-31 and 34-35 but not at 38-39 weeks. Plasma progesterone showed a significant positive correlation with estriol at 34-35 and at 38-39 weeks. We suggest that daily fluctuations in plasma progesterone may be related to the concentration of plasma cortisol, either directly by competition for binding sites on transcortin, or indirectly after modulation of fetal pituitary-adrenal function by maternally derived glucocorticoid.

Dominance of the senescent phenotype in heterokaryons between replicative and post-replicative human fibroblast-like cells.

In heterokaryons between senescent and young diploid fibroblast-like cells, dominance of the former with respect to nuclear DNA synthesis (incorporation of [(3)H]thymidine) was demonstrated. For identification of the respective partners, double-layer autoradiography was used after the old cells were labeled with [(3)H]methionine and the young cells were labeled with [(14)C]thymidine. Synchrony of nuclear labeling (i.e., all nuclei in a cell labeled with [(3)H]thymidine) was observed in the majority of di- and polykaryons during the second and third of three 24-hr periods of labeling with [(3)H]thymidine. The results are compatible with either terminal differentiation or error theories of clonal senescence.

Clonal selection, attenuation and differentiation in an in vitro model of hyperplasia.

Observations of the growth kinetics and morphologies of clones and subclones of diploid human skin fibroblast cultures lead to the working hypothesis that these cells, presumably like their counterparts in healing wounds, constitute a differentiating system. There is attenuation of the growth of serial clones, with continual selection for more vigorous stem cells. The latter segregate daughter cells of varying growth potential, including a class of cells which may be regarded as terminally differentiating; we propose that such cells may be histiocytes or macrophages. These studies a) demonstrate extensive epigenetic heterogeneity in fibroblast cultures, b) suggest that hyperplastic foci may be monoclonal or oligoclonal, c) rule out a simple biologic clock mechanism as an explanation of clonal senescence, d) suggest a new approach to the analysis of various inborn errors of metabolism, such as Werner's Syndrome.