Emission factors are highly dependent on the care and skill of the operator and the resulting combustion; these do not appear to be accurately reproduced in laboratory settings. The single scattering albedo (SSA) of the emissions was very low in both lab and field measurements, averaging about 0.3 for lab tests and around 0.5 for field tests, indicating that the primary particles are climate
warming. Over the course of three summers in Honduras, we measured field emissions from traditional cookstoves, relatively new improved cookstoves, and “broken-in” improved cookstoves. We found that well-designed improved cookstoves can significantly reduce PM and CO emission factors below traditional cookstoves. For improved stoves, the presence of a chimney generally RG7112 resulted in lower emission factors but left the SSA unaffected. Traditional cookstoves had an average PM emission factor of 8.2 g kg(-1) – significantly
larger than previous studies. Particulate emission factors for improved cookstoves without and with chimneys averaged about 6.6 g kg(-1) and 4.5 g kg(-1), respectively. The elemental carbon (EC) fraction of PM varied significantly between individual tests, but averaged about 25% for each of the categories. (C) 2008 Elsevier Ltd. All rights reserved.”
“Studies have reported that Na,K-ATPase interacts with E-cadherin to stabilize (AJs) and regulate the expression of claudins, the main proteins present in the tight junction (TJ) in epithelial cells containing caveolae. However, the role of this ATPase in the regulation Entinostat mw of the AJ and TJ proteins in Torin 2 manufacturer colorectal cancer cells as well as the molecular events underlying this event in a caveolae-independent system remain undefined. In the present study, we used ouabain, a classic drug known to inhibit Na,K-ATPase, and Caco-2 cells, which are a well-established human colorectal cancer model that does not exhibit caveolae. We demonstrated
that ouabain treatment resulted in a reduction of the beta 1 Na,K-ATPase protein and cell redistribution of the AJ proteins E-cadherin and beta-catenin, as well as the alpha 1 Na,K-ATPase subunit. Furthermore, ouabain increased claudin-3 protein levels, impaired the TJ barrier function and increased cell viability and proliferation during the early stages of treatment. Additionally, the observed ouabain-induced events were dependent on the activation of ERK1/2 signaling; but in contrast to previous studies, this signaling cascade was caveolae-independent. In conclusion, our findings strongly suggest that alpha 1 and beta 1 Na,K-ATPase downregulation and ERK1/2 activation induced by ouabain are interlinked events that play an important role during cell-cell adhesion loss, which is an important step during the tumor progression of colorectal carcinomas.