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1999
Award Recipients |
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The feasibility
of investigating the role of environmental and genetic
factors, and H.pylori in gastrointestinal diseases.
Myles Cockburn, Ph.D., DPH, post-doctoral fellow,
Department of Preventive Medicine, USC |
| Abstract:
The environmental and genetic risk factors for the
acquisition, clearance and pathogenicity of H. pylori
are largely unknown. H. pylori causes a majority
of gastric and duodenal ulcers (GU/DU), and its
role in gastric cancer remains equivocal, due to
the lack of an acceptable method of detecting the
bacterium in epidemiological studies. No environmental
reservoirs for the bacterium have yet been discovered,
and its mode of transmission remains a mystery,
hampering primary prevention efforts aimed at the
control of gastrointestinal disease. This study
is a pilot to determine the feasibility of self-administered
Urea Breath Test (UBT) for H. pylori infection.
UBT is the most accurate non-invasive method of
determining infection, and it has recently become
a cost-effective method to use on a large scale.
It’s potential as a tool in the investigation
of complex gene-environment interactions in the
acquisition, clearance and pathogenicity of H. pylori
are investigated here in a sample of 120 California
native-born twins, in whom it will later be used
in large-scale studies should it prove feasible.
Self-administered UBT will be compared to supervised
UBT, to determine the test’s utility in epidemiological
studies. |
Progress report:
The study population has been identified, and a
database set up for keeping track of participants.
A project manager has been identified, but not employed.
The IRB approved the study on 8/25/99 (#996042).
At present the investigators are waiting for the
University of Southern California to come to some
agreement with the University of Texas, El Paso,
regarding the distribution of overhead costs for
approximately $4,000 of work to be carried out by
a co-investigator, Dr. Thomas Redlinger. The sum
covers the cost of the UBT kits themselves, and
a nominal fee for laboratory processing. As soon
as this issue is resolved, the study will start,
and they expect to be able to recruit roughly 15-20
subjects per week until all 120 are enrolled.
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Fine mapping the
murine cdm gene via a C57BL/6 and DBA/2 strain intercross.
Mike Collins, Ph.D., Environmental Health Sciences,
Toxicology, UCLA |
Abstract:
This project has been initiated with the long-term
goal of isolating and cloning a murine gene, cdm,
which causes resistance to cadmium-induced testicular
toxicity. Murine strains are either homozygous carriers
or homozygous non-carriers. The gene was mapped
to the 64.7 cM region of chromosome 3 in the 1970s
using recombinant inbred strains. Because this gene
confers resistance as a single Mendalian recessive
trait, it is considered an ideal candidate for isolation
and cloning. The cdm gene that causes resistance
to testicular toxicity, also causes an increase
sensitivity to cadmium-induced acute toxicity (lethality)
and cadmium-induced teratology. The project has
been initiated to fine map the cdm gene by a standard
cross between C57BL/6 and DBA/2 mice. The C57BL/6
strain was determined to be a homozygous carrier
of the gene (cdm/cdm), whereas the DBA/2 strain
was homozygous for lack of the gene (+/+). A doctoral
student has been hired (Ms. Lisa Martin), and she
is using microsatellite markers to detect crossovers
in a 2.1 cM region of chromosome 3 which contains
the cdm gene. Hundreds of mice are tested for crossovers,
but only a few of each hundred have a crossover
in the 2.1 cM region. A number of mice with crossovers
in the 2.1 cM region have been injected with cadmium
to phenotypically classify the murine testes as
either sensitive or resistant. Only one of every
four mice with crossovers in the region should be
homozygous for the cdm gene and thus display resistance
to testicular toxicity caused by cadmium injection.
To date, they have 3 mice that have crossovers in
the 2.1 cM region and are resistant to cadmium-induced
testicular toxicity.
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Pesticide exposure
modeling based on historical use reporting in California
to investigate long-term health effects.
Beate Ritz, M.D., Ph.D., Department of Epidemiology,
UCLA |
| Abstract:
The goal of this pilot project is to develop an
exposure assessment methodology and generate preliminary
data for a study of pesticide-exposure related occurrence
of Parkinson’s disease. Geographic information
system tools will be used to create a long-term
pesticide exposure model for California residents
based on a historical database of pesticide use
in California (PUR), interviews with agricultural
commissioners and other experts for the period not
covered by the state-wide reporting system, crop
patterns identified on land-use surveys, and aerial
and satellite photography. |
Publications:
Ritz B, Yu F. Parkinson’s Disease Mortality
and Pesticide Exposure in California 1984-1994.
Accepted for publication by IJE, 1999.
Ritz B, Yu F. Parkinson’s Disease Mortality
and Pesticide Use in California. J Clin Epidemiology,
1998; 51 (Suppl.1): S24
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Effects of cigarette
smoking cessation on male germ cell quality
Naureen G. Tareen, MPH, Doctoral student under Dr.
W. Robbins, Dept. of Environmental Health Sciences,
UCLA |
| Abstract:
Cigarette smoking has been associated with poor
semen quality including decreased sperm density
and reduced motility. Recent evidence has demonstrated
that smoking also increases the risk of genetic
abnormalities in male germ cells, specifically aneuploidy
and DNA strand breaks. Germ cell abnormalities such
as numerical and structural DNA damage pose an increased
risk for offspring born with congenital defects
or mutations. The studies conducted to date have
been cross sectional in design. This study is the
first which seeks to follow smokers enrolled in
smoking cessation programs over time as they quit
smoking in order to investigate whether smoking
cessation can lead to an improvement in semen quality,
specifically in DNA fragmentation and aneuploidy
load. Semen samples will be collected along with
self-administered health questionnaires at three
different time points in order to determine baseline
effects and effects after smoking cessation. Seminal
fluid cotinine measurements will be used as a biomarker
verifying smoking status. Multicolor florescence
in situ hybridization (FISH) techniques will be
used to measure aneuploidy for the sex chromosomes
X and Y and for autosomes 18 and 21. The Comet (single
gel electrophoresis) and TUNEL (terminal uridine
nick-labelling) assays will be used to measure DNA
fragmentation. |
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