Hines Lange (icicledavid7)

The renin-angiotensin system (ARS) is a hormonal cascade that regulates blood pressure, electrolytes and water balance. AngiotensinII (AII) exerts its effects through the AT1 and AT2 receptors. AT1 is found in the syncytiotrophoblast, AT2 predominates during foetal development and its stimulation inhibits cell growth, increases apoptosis, causes vasodilation and regulates the development of foetal tissue. There is also an SRA in the placenta. The local generation of AII is responsible for the activation of AT1 receptors in the trophoblast. In normal pregnancy, concomitantly with reduction of blood pressure the circulating RAS increases, but blood pressure does not rise due to AII refractoriness, which does not occur in preeclampsia. We review the role of the SRA in normal pregnancy and preeclampsia. Cytidine mw Fish are frequently exposed to harmful algal blooms (HAB) and to related toxins. However, the biological effects of okadaic acid (OA), the most abundant and frequent HAB-toxin in Europe, South America and Asia, have been poorly investigated. In this study, fish swimming performance and metabolic rates were investigated in juveniles of Zebra seabream (Diplodus cervinus) exposed to OA-group toxins via dietary route, during three days. Fish fed on contaminated food accumulated up to 455.5 μg OA equiv. Kg-1. Significant lower mean critical swimming speed (Ucrit) were observed in fish orally exposed to OA (and its related isomer dinophysistoxin-1, DTX-1) than fish feeding on non-toxic diet. A tendency to higher demands of oxygen consumption was also recorded in OA-exposed fish at higher current velocities. This study indicates that fish may not be affected by OA-group toxins under basal conditions, but suggests a decrease in fitness linked to a reduction in swimming performance of fish exposed to OA under increased stimulus. OA and related toxins are suggested to have a cryptic effect on swimming performance that may be enhanced when fish deals with multiple stressors. Considering that a reduction in swimming performance may have impact on critical activities, such as foraging and escaping from predators, this study highlights the ecological risk associated with dinoflagellate toxic blooms, biotoxins food web transfer and fish contamination. Evidence from human, animal and cellular studies suggests that high plasma total cysteine (tCys) is causally linked to human obesity, but determinants of population tCys variability are unknown. We hypothesized that tCys elevation in obesity may be mediated by an altered tCys response to intake of its precursor, methionine. We investigated whether BMI influences the change in plasma tCys, total homocysteine (tHcy) and total cysteinylglycine (tCysGly) 6h following a 100 mg/kg oral methionine load in 800 healthy subjects and 750 cardiovascular disease (CVD) cases. Methionine loading decreased tCys from mean 275 (95% CI, 273, 277) μmol/L to 253 (251,255) μmol/L. The decline in tCys was less in overweight (-8%) and obese (-6%) compared to normal weight (-9%) subjects, adjusting for age, gender and CVD (P-ANOVA = 0.006). Compared to normal weight subjects, individuals with obesity had a 2.8-fold likelihood (95% CI, 1.52, 5.01) of experiencing a rise (rather than decline), in tCys postload, after multiple adjustments. tCysGly also decreased postload, and the decline was similarly smaller in overweight (-18%) and obese (-15%) compared to normal weight (-21%) individuals (P-ANOVA less then 0.001). The tHcy response was modified by CVD status, with an increase in tHcy postload being BMI-dependent in controls (P-ANOVA less then 0.001) but not in CVD cases (P-interaction = 0.07). Although the methionine dose used was supraphysiologic, these data suggest that an altered tCys response to ingested methionine occurs in obesity, whereby tCys might rise in response to dietary methionine. This may contribute to explaining why human obesity is consistently associated with