Although a large number of genes have been associated with tobacco smoking, only a very limited number of genetic variants are considered to be causative. How to find these functional variants and then characterize them remains challenging in the field of human genetics.

In the traditional genetic dogma, DNA codes for RNA and RNA codes for protein. But what about the leftover bits of RNA that do not seem to code for proteins? One type of RNA 'leftovers' is the microRNAs. These small pieces of RNA do not code for proteins. Instead, they influence the extent to which other genes are expressed, i.e., the rate or extent of conversion of DNA to RNA. To date, there have been relatively few examples of the direct involvement of microRNAs in psychiatric disorders.

However, a study scheduled for publication in the April 15th issue of Biological Psychiatry (elsevier/locate/biopsychiat), published by Elsevier, has now provided new insights into how variation in the dopamine D1 receptor gene (DRD1) may be linked to the risk for nicotine dependence through microRNA action.

Huang and Li, researchers at the University of Virginia, previously showed that the DRD1 gene, one of the major receptors in the brain that mediate the actions of the neurotransmitter dopamine, is associated with tobacco dependence, and that two alleles of a variant within this gene are differentially expressed. "In the current study, we demonstrated that such differential expression of DRD1 is regulated by microRNA miR-504," explains Dr. Li.

In other words, this microRNA seems to directly influence how these genetic variations are expressed within the DRD1 gene, thereby influencing ones risk to developing nicotine dependence. John Krystal, M.D., Editor of Biological Psychiatry , comments: "This study provides an interesting example of how variation in a gene that contributes to the risk of smoking may do so by throwing a 'micro switch' and thereby increasing the expression of the dopamine 1 receptor gene."

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Scientists also infected human cells with the DENV-2 virus and found 82 of the mosquito genes had analogous genes in humans and about half that number turned out to be Dengue-specific host factors important in human infection.

Dr. Garcia-Blanco says each one of these newly identified host factors is a potential therapeutic target that could be used to block or slow Dengue infection and as there are currently no vaccines to prevent the disease, new ways to fight the disease are important.

Dr. Garcia-Blanco says there are already a couple of Dengue vaccine candidates in development.

The scientists say the study which was funded by the National Institute of Allergy and Infectious Diseases, a part of the National Institutes of Health, reflects the value of the growing research partnership between Duke University Medical Center and the two-year old Duke-NUS Graduate Medical School in Singapore.

Queensland Health has also turned to Singapore experts in preventing Dengue becoming endemic, with international experts attending a special summit in Cairns to help Queensland Health adDr.ess the problem of eradicating the virus before the next wet season.

Dr. Scott Ritchie from the Tropical Population Health says more cases could re-emerge in May following rain over Easter - of the 963 cases in the current outbreak in North Queensland, 890 have been recorded in the Far North and for the first time, all four strains of Dengue fever were circulating simultaneously in North Queensland.

The research appears in the April 23 issue of the journal Nature.