Action of natural estrogens on the vessel wall: molecular mechanisms and clinical implications

Myocardial infarction is the major cause of death in the Western world. Men are more prone to develop coronary artery disease than women, who rarely develop coronary disease before menopause. Although epidemiological data has long been available showing a protective effect of estrogen on the vascular system, the underlying mechanisms have been investigated more thoroughly only in recent years. Meta-analysis studies have revealed that only half of the protective effect on estrogen replacement therapy is due to its positive effects on the lipid profile and that a large part of this protection is caused by mechanisms distinct from lipid metabolism. It is now known that estrogens also exert effects on vascular function and structure of the vessel wall involving numerous cellular and molecular mechanisms. Here we review actions of natural estrogens on human vascular cells and arteries. Estrogens can modulate vascular function by increasing nitric oxide production via stimulation of endothelial nitric oxide synthase (eNOS) and decreasing endothelin-1 levels in vivo. Furthermore, 17 beta-estradiol is an inhibitor of vascular smooth muscle cell proliferation and migration, phenomena that play a major role in atherosclerotic vascular disease and in the remodelling process. 17 beta-estradiol can also acutely affect vascular tone in human arteries and attenuates constriction induced by contractile agonists. Finally, clinical studies have shown that 17 beta-estradiol can acutely and chronically ameliorate vascular function in women with and without vascular disease. In conclusion, results from clinical and in vitro studies confirm the positive effects of natural estrogens on vascular function and protection from coronary heart disease. Thus, primary prevention of coronary heart disease by estrogen replacement therapy after the menopause appears to be a new and straightforward approach by which cardiovascular mortality in women can be reduced.     

Testing the potential of sodium fluoride to affect spermatogenesis: a morphometric study

This study provides quantitative information on the effect of sodium fluoride (NaF) on the testes of F1 generation male rats exposed in utero and during lactation to NaF at one of four concentrations (25, 100, 175, 250 ppm). At weaning, the F1 generation males were exposed to NaF in their drinking water for 14 weeks, after which time testicular tissues were perfusion-fixed with glutaraldehyde and observed after being embedded in plastic. The seminiferous tubules comprised 89%, 87%, 88%, 88% and 88% of the total testis volume while the interstitial space occupied 9.3%, 11.2%, 10.2%, 9.8% and 9.9% of the total testis volume for the 0, 25, 100, 175 and 250 ppm NaF treatment groups, respectively. Statistically significant differences between control and NaF-treated rats were not observed with respect to absolute volume of the seminiferous tubules, interstitial space, Leydig cells, blood vessels boundary layer, lymphatic space, macrophages, tubular lumen or absolute tubular length and absolute tubular surface area, mean Sertoli cell nucleoli number per tubular cross-section, mean seminiferous tubule diameter and the mean height of the seminiferous epithelium. A statistically significant decrease in the absolute volume and volume percent of the lymphatic endothelium was observed in the 175 and 250 ppm NaF-treated groups and in the testicular capsule in the 100 ppm NaF-treated groups. The significance of this finding is unknown at the present time. Overall, the quantitative information obtained suggests that exposure to NaF at the doses used in the present study does not adversely affect testis structure or spermatogenesis in the rat.     

Workplace smoking policies in the United States: results from a national survey of more than 100,000 workers

To investigate the activity of cortical regions in the control of movement, we studied event-related desynchronization/synchronization (ERD/ERS), event-related coherence (ERC), and phase coherence in 29-channel EEGs from 9 subjects performing self-paced movements of the right index finger. Movement preparation and execution produced ERD over the sensorimotor areas at 10 Hz and 20 Hz, followed by ERS. ERD corresponded spatiotemporally to an increase in coherence over the frontocentral areas. For both frequency bands, ERD began over the left sensorimotor areas and became bilateral at the time of movement onset. The coherence increase with frontal areas began in the left central areas and became symmetrical after EMG onset. The ERD and coherence increase was longer at 10 Hz than at 20 Hz. Phase coherence at 10 Hz showed a lead of anterior regions to posterior regions throughout the time period, and at 20 Hz showed a tendency toward zero phase delay corresponding with the movement. EEG desynchronization parallels functional coupling over sensorimotor and frontal areas. Event-related coherence and phase coherence findings implicate the frontal lobes in control of movement planning and execution. The involvement of different frequency bands with different timings may represent parallel changes in the cortical network.