Mosquito coil emissions and health implications.

Burning mosquito coils indoors generates smoke that can control mosquitoes effectively. This practice is currently used in numerous households in Asia, Africa, and South America. However, the smoke may contain pollutants of health concern. We conducted the present study to characterize the emissions from four common brands of mosquito coils from China and two common brands from Malaysia. We used mass balance equations to determine emission rates of fine particles (particulate matter < 2.5 microm in diameter; PM(2.5)), polycyclic aromatic hydrocarbons (PAHs), aldehydes, and ketones. Having applied these measured emission rates to predict indoor concentrations under realistic room conditions, we found that pollutant concentrations resulting from burning mosquito coils could substantially exceed health-based air quality standards or guidelines. Under the same combustion conditions, the tested Malaysian mosquito coils generated more measured pollutants than did the tested Chinese mosquito coils. We also identified a large suite of volatile organic compounds, including carcinogens and suspected carcinogens, in the coil smoke. In a set of experiments conducted in a room, we examined the size distribution of particulate matter contained in the coil smoke and found that the particles were ultrafine and fine. The findings from the present study suggest that exposure to the smoke of mosquito coils similar to the tested ones can pose significant acute and chronic health risks. For example, burning one mosquito coil would release the same amount of PM(2.5) mass as burning 75-137 cigarettes. The emission of formaldehyde from burning one coil can be as high as that released from burning 51 cigarettes

Gene expression profiles in rat mesenteric lymph nodes upon supplementation with Conjugated Linoleic Acid during gestation and suckling

Background Diet plays a role on the development of the immune system, and polyunsaturated fatty acids can modulate the expression of a variety of genes. Human milk contains conjugated linoleic acid (CLA), a fatty acid that seems to contribute to immune development. Indeed, recent studies carried out in our group in suckling animals have shown that the immune function is enhanced after feeding them with an 80:20 isomer mix composed of c9,t11 and t10,c12 CLA. However, little work has been done on the effects of CLA on gene expression, and even less regarding immune system development in early life. Results The expression profile of mesenteric lymph nodes from animals supplemented with CLA during gestation and suckling through dam's milk (Group A) or by oral gavage (Group B), supplemented just during suckling (Group C) and control animals (Group D) was determined with the aid of the specific GeneChip® Rat Genome 230 2.0 (Affymettrix). Bioinformatics analyses were performed using the GeneSpring GX software package v10.0.2 and lead to the identification of 89 genes differentially expressed in all three dietary approaches. Generation of a biological association network evidenced several genes, such as connective tissue growth factor (Ctgf), tissue inhibitor of metalloproteinase 1 (Timp1), galanin (Gal), synaptotagmin 1 (Syt1), growth factor receptor bound protein 2 (Grb2), actin gamma 2 (Actg2) and smooth muscle alpha actin (Acta2), as highly interconnected nodes of the resulting network. Gene underexpression was confirmed by Real-Time RT-PCR. Conclusions Ctgf, Timp1, Gal and Syt1, among others, are genes modulated by CLA supplementation that may have a role on mucosal immune responses in early life

Gene expression profiles in rat mesenteric lymph nodes upon supplementation with Conjugated Linoleic Acid during gestation and suckling

Background Diet plays a role on the development of the immune system, and polyunsaturated fatty acids can modulate the expression of a variety of genes. Human milk contains conjugated linoleic acid (CLA), a fatty acid that seems to contribute to immune development. Indeed, recent studies carried out in our group in suckling animals have shown that the immune function is enhanced after feeding them with an 80:20 isomer mix composed of c9,t11 and t10,c12 CLA. However, little work has been done on the effects of CLA on gene expression, and even less regarding immune system development in early life. Results The expression profile of mesenteric lymph nodes from animals supplemented with CLA during gestation and suckling through dam's milk (Group A) or by oral gavage (Group B), supplemented just during suckling (Group C) and control animals (Group D) was determined with the aid of the specific GeneChip® Rat Genome 230 2.0 (Affymettrix). Bioinformatics analyses were performed using the GeneSpring GX software package v10.0.2 and lead to the identification of 89 genes differentially expressed in all three dietary approaches. Generation of a biological association network evidenced several genes, such as connective tissue growth factor (Ctgf), tissue inhibitor of metalloproteinase 1 (Timp1), galanin (Gal), synaptotagmin 1 (Syt1), growth factor receptor bound protein 2 (Grb2), actin gamma 2 (Actg2) and smooth muscle alpha actin (Acta2), as highly interconnected nodes of the resulting network. Gene underexpression was confirmed by Real-Time RT-PCR. Conclusions Ctgf, Timp1, Gal and Syt1, among others, are genes modulated by CLA supplementation that may have a role on mucosal immune responses in early life

Size correction in biology: how reliable are approaches based on (common) principal component analysis?

Morphological traits typically scale with the overall body size of an organism. A meaningful comparison of trait values among individuals or populations that differ in size therefore requires size correction. A frequently applied size correction method involves subjecting the set of n morphological traits of interest to (common) principal component analysis [(C)PCA], and treating the first principal component [(C)PC1] as a latent size variable. The remaining variation (PC2–PCn) is considered size-independent and interpreted biologically. I here analyze simulated data and natural datasets to demonstrate that this (C)PCA-based size correction generates systematic statistical artifacts. Artifacts arise even when all traits are tightly correlated with overall size, and they are particularly strong when the magnitude of variance is heterogeneous among the traits, and when the traits under study are few. (C)PCA-based approaches are therefore inappropriate for size correction and should be abandoned in favor of methods using univariate general linear models with an adequate independent body size metric as covariate. As I demonstrate, (C)PC1 extracted from a subset of traits, not themselves subjected to size correction, can provide such a size metric