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UC Merced Professor Receives Prop. 99 Grant Money to Study Tobacco Effects

June 20, 2005

MERCED - In 1988, California voters approved Proposition 99, an
initiative specifying that five percent of cigarette tax revenue be
appropriated for research on tobacco-related disease. UC Merced
professor Henry Jay Forman is now bringing $420,000 of that money
to Merced to study how human bronchial epithelial cells try to
protect against the toxins found in cigarette smoke.

“The California Tobacco-related Disease Research Program funds
have a reputation for being pretty tough to get, particularly on
the first try,” says Forman, whose experience researching related
topics spans 25 years. “We overcame the odds to bring this research
funding to Merced, and that’s a good thing as this is a challenging
time to obtain research money.”

His research group participated in a competitive
grant-application process to win the funding in the same way that
scientists often compete for grants from organizations like the
National Science Foundation or National Institutes of Health. The
grant will be awarded over three years.

“Professor Forman’s new research project is an example of how
his stellar basic research to understand the response of cells to
damage is now being applied to work on a problem that affects the
lives of many individuals in our community,” says Dean Maria
Pallavicini of the UC Merced School of Natural Sciences.

Forman will use the new funding to investigate byproducts from
smoking-related oxidation of cell membranes that trigger changes in
the DNA of bronchial epithelial cells and how those DNA changes
increase protective enzymes that shield cells from further damage.

So far it has been generally assumed that the genes in the DNA
that regulate production of a group of protective enzymes in the
lung, all work in the same way. Forman’s hypothesis is that there
are important differences among the group that will help him
understand how the protective enzymes are made.

The protective enzymes made by cells in response to
smoking-related toxins do not provide a sufficient shield against
cell damage. If research discovered a way to increase those
enzymes, it could be useful for those already addicted to smoking
or suffering from smoking-related diseases. Still, Forman
emphasizes that even in larger quantities the enzymes would not
provide an absolute barrier to smoking-related injury and would not
provide a license for smoking.

Forman will conduct the research funded by his new grant in his
laboratory at UC Merced’s Castle facility until they move to the
new campus next year. He describes the project as cell-culture work
performed on established bronchial epithelial cell lines as well as
cells obtained form autopsy.

Forman arrived at UC Merced in 2003 as one of the original
faculty members. He was previously chairman of the Department of
Environmental Health Sciences in the School of Public Health at the
University of Alabama, Birmingham.