69, 95% CI 5.61-24.34, p < 0.001), the presence of emergent vegetation (OR 2.83, 95% CI 1.35-5.95, p = 0.006), and algae (at borderline significance; OR 1.87, 95% CI 0.96-3.618, p = 0.065). The density of larvae was reduced in sites that were larger than 100 m in perimeter (OR 0.151; 95% CI 0.060-0.381, p < 0.001), where water was tidal (OR 0.232; 95% CI 0.101-0.533, p = 0.001), vegetation shaded over 25% of the habitat (OR 0.352; 95% CI 0.136-0.911, p = 0.031) and water conductivity was above 2,000 mu S/cm (OR 0.458; 95% CI 0.220-0.990,

p = 0.048). Pools produced the highest numbers of Anopheles gambiae adults compared with rice fields, floodwater areas close to the edge of the floodplain or close to the river, and stream click here fringes. Pools were characterized by high water temperature and turbidity, low conductivity, increased presence of algae, and absence of tidal water.

Conclusion: There are few breeding sites that produce a high number of adult this website vectors in the middle reaches of the river in The Gambia, whereas those with low productivity are larger in area and can be found throughout the rainy season. Even though risk factors could be identified for the presence and density of larvae and productivity of habitats, the results indicate that anti-larval interventions

in this area of The Gambia cannot be targeted in space or time during the rainy season.”
“Polycyclic aromatic hydrocarbons (PAHs) are widespread environmental pollutants produced in the combustion of organic matter. Exposure to PAHs raises the risk of lung cancer and inflammatory and allergic disorders such as asthma. DNA microarray technologies have been applied to research on toxicogenomics in the recent years. To evaluate the Crenolanib mutagenicity of PAHs and constituents of environmental

pollutants in lung tissue, including metabolic activation, human alveolar epithelial type II cells (A549) were treated with nonmutagenic PAH pyrene and with the mutagenic PAHs benzo-[a]-pyrene, 1-nitropyrene, or 1,8-dinitropyrene. Comparison of genome-wide microarray expression profiles between a nonmutagenic and a mutagenic PAH-treated group revealed that xenobiotic response genes such as CYP1B1 were commonly upregulated in two groups and that DNA damage induced genes, especially p53-downstream genes such as p21 (CDKN1A) were upregulated only in the mutagenic PAH-treated group. Pretreatment with cytochrome P450 inhibitor -naphthoflavone or p53 inhibitor pifithrin- inhibited the benzo-[a]-pyrene-induced p21 expression. These data suggest that when PAHs enter the cells, lung epithelium induces PAH metabolic activating enzymes, and then the DNA damages-recognition signal is converged with p53 downstream genes. This metabolic activation and DNA damage is induced in lung epithelium, and the mutagenicity of PAHs can be classified by DNA microarray expression profiles. (c) 2011 Wiley Periodicals, Inc.