The DNA sequencing technology unlocks secrets stored in human DNA that pinpoints exactly how specific chemicals impact the DNA of individuals on a cellular level.

Companies facing class-action suits are immediate beneficiaries of the technology.

WHERE: Dr. Gillis will present at the International Congress of Toxicology in Montreal Tuesday, July 17, 2007 from 12:00 to 2:00 p.m.

The conference is hosted by the Society of Toxicology of Canada and will be held at the Palais des congres de Montreal, Montreal, Canada, July 15 - 19, 2007.

DETAILS: msds1(TM), pioneered by Dr. Bruce Gillis of The Cytokine Institute and the faculty and staff of the University of Illinois' College of Medicine, can now determine how human cells and their individual DNA respond when exposed to a chemical and its metabolites.

By analyzing gene expression and how 36,000 parameters of an individual's DNA are affected by specific chemical exposures -- such as benzene or asbestos -- this technology can determine with 99.9% certainty if a person was injuriously exposed to a particular toxin, thereby offering an impartial methodology for providing scientifically-based evidence. Dr. Gillis will also discuss the technology's potential ramifications on the fields of healthcare, workers compensation claims, insurance and mass-tort litigation.

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Our study provides a model of how natural selection, exerted by the human immune system, can generate hypervirulent bacterial variants with an increased risk of producing invasive infections, said lead author Mark Walker, Ph.D. a Professor of Biological Sciences at the University of Wollongong. In the case of the invasive strep clone, a bacteriophage provided the bacterium a genetic advantage that turned a relatively benign pathogen into a potential deadly disease agent.

A gene present on the bacteriophage acquired by the M1T1 strep encodes an enzyme that allows the bacteria to escape being trapped and killed by neutrophils “ white blood cells that play a front line role in human's immune defense by pathogenic microbes. The same genetic mutation that allows the strep bacteria to acquire plasminogen and activate it throughout the body also increases production of the bacteriophage-encoded enzyme that blocks neutrophil killing. When neutrophils of the immune system are summoned to clear a simple strep infection, they apply a natural selective pressure favoring the genetic mutation.

The mutation allows the bacteria not only to survive neutrophil killing, but to spread and destroy tissues, as is seen in necrotizing fasciitis and other severe forms of strep infection, said Walker.

The research team used genetically engineered mice expressing human plasminogen and infected them with M1T1 strep clone, discovering that the bacteria routinely mutated to the invasive form, then spread throughout the body to produce a fatal infection. When the researchers eliminated the single bacteriophage gene encoding the neutrophil resistance factor, the M1T1 strep strain lost its ability to undergo the dangerous mutation and could no longer spread to produce severe infection. Ancestral strains of the M1T1 strep, isolated before the acquisition of the bacteriophage, also failed to undergo the mutation to produce serious disease.

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