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Analysis now indicates that polluting of the environment has a part to play in atherosclerosis.

Findings published in the open access journal, Genome Biology, display how the body fat that clog arteries work with polluting of the environment particles together, triggering the genes behind inflammation. A research group drawn from medical and environmental engineering disciplines at the Universities of California, Los Angeles, investigated the partnership between oxidized phospholipids found in the reduced density lipoprotein particles, the bad fat that clog arteries, and diesel exhaust contaminants. They uncovered cells that line human blood vessels to both exhaust particles and oxidised phospholipids, and measured the result on genes by using microarray expression profiling. This allowed the identification of gene modules containing a higher number of co-expressed genes.In the grouped family members in our study, two members passed away from a fungal disease and a third presumably passed away from an identical cause. Further studies may clarify whether human CARD9 deficiency accounts only for recurrent mucosal infections or also makes up about an increased susceptibility to serious invasive fungal attacks. In this consanguineous family members, we cannot exclude the chance that a second genetic defect may possess contributed to a more serious phenotype in the deceased family. Unfortunately, we were not able to study viable cells from the grouped family members in vitro due to logistical constraints.