Comparison of Emission of Dioxins and Furans from Gasohol- and Ethanol-Powered Vehicles

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)The exhaust emissions of 17 polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans (PCDD/Fs) were investigated in two spark-ignition light-duty vehicles, one gasohol-fueled and a flexible-fuel one fueled with hydrated ethanol. Gasohol is a mixture of gasoline and 22% ethanol. The influence of fuel type and quality, lubricant oil type, and use of fuel additives on the formation of these compounds was tested using standardized U.S. Federal Test Procedure (FTP)-75 cycle tests. The sampling of the PCDD/Fs followed the recommendations of a modified U.S. Environmental Protection Agency (EPA) Method 23 ( A:www.epa.gov/ttn/emc/promgate/m-23.pdf) and the analysis basically followed the U.S. EPA Method 8290 (http://www.epa.gov/osw/hazard/testmethods/sw846/pdfs/8290a.pdf). Results showed that emission factors of PCDD/Fs for the gasohol vehicle varied from undetected to 0.068 pg international toxic equivalency (I-TEQ) km(-1) (average of 0.0294 pg I-TEQ km-1), whereas in the ethanol vehicle they varied from 0.004 to 0.157 pg (I-TEQ) km(-1) (average of 0.031 pg I-TEQ km(-1)). In the gasohol-powered vehicle, the use of fuel additive diminished the emission of Octachlorodibenzo-p-dioxin (OCDD) significantly, whereas in the ethanol vehicle no significant associations were observed between the investigated variables and the emissions.611213441352Sao Paulo FoundationFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)FAPESP [2004/02623-6

Genomic analysis of two phlebotomine sand fly vectors of leishmania from the new and old World.

Phlebotomine sand flies are of global significance as important vectors of human disease, transmitting bacterial, viral, and protozoan pathogens, including the kinetoplastid parasites of the genus Leishmania, the causative agents of devastating diseases collectively termed leishmaniasis. More than 40 pathogenic Leishmania species are transmitted to humans by approximately 35 sand fly species in 98 countries with hundreds of millions of people at risk around the world. No approved efficacious vaccine exists for leishmaniasis and available therapeutic drugs are either toxic and/or expensive, or the parasites are becoming resistant to the more recently developed drugs. Therefore, sand fly and/or reservoir control are currently the most effective strategies to break transmission. To better understand the biology of sand flies, including the mechanisms involved in their vectorial capacity, insecticide resistance, and population structures we sequenced the genomes of two geographically widespread and important sand fly vector species: Phlebotomus papatasi, a vector of Leishmania parasites that cause cutaneous leishmaniasis, (distributed in Europe, the Middle East and North Africa) and Lutzomyia longipalpis, a vector of Leishmania parasites that cause visceral leishmaniasis (distributed across Central and South America). We categorized and curated genes involved in processes important to their roles as disease vectors, including chemosensation, blood feeding, circadian rhythm, immunity, and detoxification, as well as mobile genetic elements. We also defined gene orthology and observed micro-synteny among the genomes. Finally, we present the genetic diversity and population structure of these species in their respective geographical areas. These genomes will be a foundation on which to base future efforts to prevent vector-borne transmission of Leishmania parasites

New opportunities for managing acute and chronic lung infections

Lung diseases caused by microbial infections affect hundreds of millions of children and adults throughout the world. In Western populations, the treatment of lung infections is a primary driver of antibiotic resistance. Traditional therapeutic strategies have been based on the premise that the healthy lung is sterile and that infections grow in a pristine environment. As a consequence, rapid advances in our understanding of the composition of the microbiota of the skin and bowel have not yet been matched by studies of the respiratory tree. The recognition that the lungs are as populated with microorganisms as other mucosal surfaces provides the opportunity to reconsider the mechanisms and management of lung infections. Molecular analyses of the lung microbiota are revealing profound adverse responses to widespread antibiotic use, urbanization and globalization. This Opinion article proposes how technologies and concepts flowing from the Human Microbiome Project can transform the diagnosis and treatment of common lung diseases.</p