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Deaeration units of a commercial multi-stage flash (MSF) cogeneration facility underwent venting modifications to increase system distillate productivity without increasing energy consumption or elevating top brine temperatures. Three MSF units were investigated after oxygen levels of deaerators spiked above design limits (20 ppb). The investigation found a significant biotic presence in the deaerator unit's MSF heat rejection sections that included algae, bacteria, bivalves, and bivalve larvae. The bivalve taxa consists of Barbatia parva, Diodora funiculata, Pinctada margaritifera, Amiantis umbonella, and Acrostergma assimile. Galvanic corrosion exacerbated by biofilm was also observed in heat rejection sections. While attesting to the tenacity and adaptability of marine life, the presence of biological communities is symptomatic of the abnormally high oxygen levels in deaerator units. Elevated oxygen levels contribute to systems performance declines resulting from biological fouling of deaerator packing materials, partially responsible for inefficiencies in reducing the gas solubilities of MSF process feed waters and elevated concertation ratios [1,2]. Several thermal desalination units presented similar process issues, but one was selected for detailed inspection and evaluation. [ABSTRACT FROM AUTHOR]

Affirmative action is a divisive issue in society today. Attitudes toward affirmative action vary both between and within ethnic and racial groups, with Whites exhibiting the majority of negative attitudes. Researchers have suggested a variety of psychological explanations for differences in attitudes toward affirmative action (e.g., racism, self-interest, fairness). The current study investigates whether motivation to control prejudice acts as a mediator of ethnic/racial identity and Whites' attitudes toward affirmative action. Support was found for the mediating role of motivation to control prejudice for several aspects of ethnic and racial identity and affirmative action attitudes. Limitations of the study are discussed, as are topics for future research.

Fibroblast growth factor 23 (FGF23) is a hormone released primarily by osteocytes that regulates phosphate and vitamin D metabolism. Recent observational studies in humans suggest that circulating FGF23 is independently associated with cardiac hypertrophy and increased mortality, but it is unknown whether FGF23 can directly alter cardiac function. We found that FGF23 significantly increased cardiomyocyte cell size in vitro, the expression of gene markers of cardiac hypertrophy, and total protein content of cardiac muscle. In addition, FGFR1 and FGFR3 mRNA were the most abundantly expressed FGF receptors in cardiomyocytes, and the coreceptor α-klotho was expressed at very low levels. We tested an animal model of chronic kidney disease (Col4a3(-/-) mice) that has elevated serum FGF23. We found elevations in common hypertrophy gene markers in Col4a3(-/-) hearts compared with wild type but did not observe changes in wall thickness or cell size by week 10. However, the Col4a3(-/-) hearts did show reduced fractional shortening (-17%) and ejection fraction (-11%). Acute exposure of primary cardiomyocytes to FGF23 resulted in elevated intracellular Ca(2+) ([Ca(2+)](i); F/F(o) + 86%) which was blocked by verapamil pretreatment. FGF23 also increased ventricular muscle strip contractility (67%), which was inhibited by FGF receptor antagonism. We hypothesize that although FGF23 can acutely increase [Ca(2+)](i), chronically this may lead to decreases in contractile function or stimulate cardiac hypertrophy, as observed with other stress hormones. In conclusion, FGF23 is a novel bone/heart endocrine factor and may be an important mediator of cardiac Ca(2+) regulation and contractile function during chronic kidney disease.