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Genetic risks for nicotine dependence span a range of traits and diseases

Tags » Some people casually smoke cigarettes for a while and then stop without a problem, while others develop long-term, several packs-per-day habits. A complex mix of environmental, behavioral and genetic factors appear to raise this risk for nicotine dependence.  Studies of groups of twins suggest that 40 to 70 percent of the risk factors are heritable. Until recently, however, studies have only explained about 1 percent of the observed variation in liability to nicotine dependence, using a genetic score based on how many cigarettes a person smokes per day.  A study led by psychologists at Emory University offers a new model for examining this genetic risk. It leveraged genome wide association studies for a range of different traits and disorders correlated with nicotine dependence and explained 3.6 percent of the variation in nicotine dependence. 

New USask research has potential to make fava beans a new favourite from farm to fork

In research just published in the journal Nature Plants, an international team of researchers including USask plant scientists have identified a key step in how the plant also known as the faba bean or broad bean produces the compounds vicine and convicine. In four per cent of the world’s population who carry a specific gene, digesting fava beans can trigger the blood disorder, known as favism. “Fava bean has been a neglected crop because of the favism issue,” said Dr. Albert Vandenberg (PhD), USask plant breeder and geneticist, and co-author of the research. “Now, we can reduce 99 per cent of the vicine and convicine, and using sequencing and genomics, we should be able to zero in, to shut it down, 100 per cent.”

Cell-type-specific insight into the function of risk factors in coronary artery disease

 E-Mail IMAGE: The researchers analysed the contribution of the five main cell types involved in coronary artery disease. view more  Credit: UEF/Raija Törrönen Using single cell technology, a new study sheds light on the significance of genetic risk factors for, and the diversity of cells involved in, the development of coronary artery disease. The researchers analysed human atherosclerotic lesions to map the chromatin accessibility of more than 7,000 cells. The chromatin accessibility is known to reflect active regions and genes in the genome. The findings were published in Circulation Research. Genome-wide association studies of the human genome have identified over 200 loci associated with coronary artery disease. More than 90% of them are located outside protein-coding genes, in so called cis-regulatory elements, whose significance in the pathogenesis of coronary artery disease remains unclear.

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