FEAT DAILY NEWSLETTER
Sacramento, California http://www.feat.org
November 8, 2001
News Morgue Search www.feat.org/search/news.asp
·
Scientists Announce Creation for Autism
·
Researchers To Use Genomic Tech On Toxins/Disease
Susceptibility Link
ABSTRACTS (non-IMFAR)
·
Aminoglycoside Antibiotics And Autism: A Speculative
Hypothesis
·
EEG Finding with Autism
http://www.eurekalert.org/pub_releases/2001-11/uocd-sac110801.php
San Diego, Calif. – Autism experts around the world will
reportedly establish the first and only scientific organization dedicated to researching
autism spectrum disorders, marking perhaps one of the most significant steps in
the quest to unravel this puzzling disorder. The society will be organized at
the inaugural International Meeting for Autism Research (IMFAR) conference
being held Nov. 9 and 10 at the San Diego Convention Center.
The scientific community’s newest society, the
International Society for Autism Research (ISAR) will formalize its charter and
elect its first president during the two-day autism research conference being
held Nov. 9 and 10. Organizers of the society foresee ISAR as a major stimulus
in attaining the highest quality interdisciplinary research on autism spectrum disorders
by fostering collaboration among scientists and healthcare professionals.
“Those of us who have focused our research efforts on
autism spectrum disorders have not had the benefit of sharing and discussing
our findings with each other in a forum dedicated to this disorder,” said Sally
Rogers, an autism expert and a psychologist at the University of Colorado
School of Medicine’s Department of Psychiatry who is one of the founders of
ISAR. “We absolutely must have a dialog to keep research, not only moving
forward, but also to a much higher level.”
The new society will support international research
through the sharing of information, findings and new ideas. Organizers
anticipated that once the society is formalized this weekend, members will
immediately work to establish a scientific journal for publication of
peer-reviewed research as well as an annual scientific meeting and a regular
newsletter. Pending a vote of the founding members, membership will likely be
limited to scientists and researchers who hold graduate degrees from accredited
universities and who have either authored a peer-reviewed journal article related
to autism, have extramural funding to carry out research related to autism or
have other scientific credentials that can be submitted to the membership
committee for review.
“The formation of this new society signals a new era of
cooperation and communication in the multidisciplinary research of autism,”
said David G. Amaral, research director at the UC Davis M.I.N.D. Institute and professor
of psychiatry at UC Davis School of Medicine. “This is an extremely complicated
neurodevelopmental disorder which will only be understood through the dedicated
effort of the various types of researchers and clinicians who will be attending
ISAR. I think this day will be a landmark in the treatment of patients with
autism.” More information about the IMFAR conference can be viewed at IMFAR’s
virtual newsroom at www.newswise.com/vpr/mtg2001.ucm.html.
The International Meeting for Autism Research (IMFAR) is
being promoted as the first-ever scientific research conference specifically devoted
to the topic of autism. The conference is underwritten collaboratively by the
Cure Autism Now Foundation, the UC Davis M.I.N.D.
Institute and the National Alliance for Autism Research
(NAAR). Its mission
is to provide a unique opportunity for researchers,
advocates, health care
professionals, service providers and others affected by
autism to discuss
and promote new research into the condition. www.imfar.org
In order to reach
the IMFAR virtual newsroom, please log onto
http://www.newswise.com/vpr/mtg2001.ucm.html
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* * *
Researchers To Use Genomic Technology On Toxins/Disease
Susceptibility Link
Hutchinson Center, University Of Washington join in $37
Million national
effort to study health impact of toxic substances
[They intend to study mercury, which is specifically
included in this
announcement.
However, not specifically mentioned with the “disease
susceptibility” factor is the immune system component. How would they
otherwise be able to control for the effects of immune
weakening viral
infections? Along with the efforts of the new researcher’s
organization ISAR
(see above article), these developments represent ever more
new hope for
finding the cause of autism soon. -LS]
http://www.fhcrc.org/news/science/2001/11/05/Toxico.htm
The Fred Hutchinson Cancer Research Center, in
collaboration with the University of Washington, has been selected to
participate in a federally funded, $37 million research consortium to study how
individual genetic makeup affects one’s response to various environmental
agents, from asbestos to tobacco smoke. Such research will help answer puzzling
questions such as why some people who have never smoked a cigarette develop
lung cancer, while others who have smoked heavily for years never show signs of
the disease.
The Hutchinson Center/UW Toxicogenomics Consortium, part
of a research collective involving a handful of academic institutions nationwide,
will receive more than $7 million in funding over five years from the National Institute
of Environmental Health Sciences, or NIEHS, headquartered in Research Triangle
Park, N.C.
Each member of the NIEHS Toxicogenomics Research
Consortium brings its own area of expertise, but collectively the group will
use the tools of genomics to obtain a fundamental understanding, on a
genome-wide scale, of the mechanisms of environmentally induced disease
processes. Researchers will attempt to better understand how disease occurs;
how to identify potential environmental hazards; how to predict potential
disease; how to identify exposed individuals; and how to prevent disease.
The long-range goal of the Hutchinson Center/UW
partnership is to shed light on genetic differences that make some people more
sensitive than others to various environmental exposures.
The Seattle-based consortium will exploit the combined
strengths of the Hutchinson Center and University of Washington in
DNA-microarray technology – the use of so called “gene chips” to monitor the
expression of thousands of genes at once – and the UW’s long-standing expertise
in toxicology and environmental-health sciences.
The principal investigator of the Seattle consortium, an
expert in both environmental sciences and DNA-array technology, is Helmut
Zarbl, Ph.D., member of the Hutchinson Center’s Human Biology and Public Health
Sciences divisions. His work focuses on using DNA-array technology to determine
whether particular genes are sensitive to the actions of chemical toxicants and
how these genes are involved in cancer development. Genes that are sensitive to
a particular toxic substance can be identified by an increase or decrease in
their expression level after exposure.
“The ultimate goal is to predict an individual’s risk of
cancer based on their genetic profile and environmental exposures,” said Zarbl,
also an associate professor of pathology and toxicology at UW.
“If a person carries a combination of genes that puts them
at higher risk with a particular environmental exposure, then we may be able to
develop methods of intervention such as dietary modifications, chemopreventive
agents or drugs to counter the effects of exposure,” he said. “Or, among
individuals we identify as highly susceptible, we may give them information on
the types of occupations they should avoid, for example, or the types of
exposures to which they may be particularly sensitive.”
Co-principal investigator of the consortium is David
Eaton, Ph.D., director of the NIEHS-funded UW Center for Ecogenetics and
Environmental Health.
“Many chronic diseases – such as most cancers, Parkinson’s
disease and Alzheimer’s disease – are caused by complex interactions between
genetics and the exposures to factors in our environment,” said Eaton, a
professor of environmental health and associate dean for research in the UW
School of Public Health and Community Medicine.
“For example, recent research has shown that genetic
factors alone account for only 20 to 40 percent of our risks for developing
some form of cancer. Factors in our environment, such as diet, smoking and
chemical pollutants, interact with our genetics to account for the other 60 to
80 percent of risk.
“The work of the Hutchinson Center/UW Toxicogenomics
Consortium can help us better understand genetic differences that make some
people more sensitive to environmental exposures.”
The consortium’s four laboratory-based projects will focus
on the effects of various toxic substances on breast-cancer development, how exposures
to certain pesticides may affect behavior in children, environmental factors
that may harm the developing nervous system, and the development of laboratory
tests that can replace animal testing.
Below are brief descriptions of each project:
Project 1: Many environmental factors can harm the
development of the nervous system in infants before and after birth. These
factors can include exposure to metals such as methyl mercury, nutritional
changes, and physical factors such as hyperthermia (exposure to excessive heat,
which can occur if a pregnant woman experiences a high fever). Adverse
neurodevelopmental effects of exposures can range from behavioral changes to
major birth defects such as spina bifida. The goal of this project is to use
genomic approaches to improve the understanding of how environmental factors
can damage the developing nervous system and so improve our ability to identify
and prevent birth defects. (Project leaders: Elaine Faustman, Ph.D., professor
of environmental health, UW; Philip Mirkes, Ph.D., research professor of
pediatrics, UW.)
Project 2: The goal of this project is to gain a better
understanding of how exposures to certain pesticides can affect the behavior of
children. The researchers are focusing
on the HDL-associated plasma enzyme paraoxonase, which provides protection from
the effects of exposures to some organophosphates, a group of chemicals that
includes the pesticides chlorpyrifos and diazinon. Children produce very little
paraoxonase enzyme until they are about a year old, and so are extremely
vulnerable to these chemical exposures. (Project leaders: Clement Furlong,
Ph.D., research professor of medical genetics, UW; Lucio Costa, Ph.D.,
professor of environmental health, UW.)
Project 3: This project aims to develop tests for toxic
exposure and stress responses using liver cells cultured in the laboratory.
Because the liver processes nearly all chemicals that enter the body, the
expression of genes in liver cells could predict how a given exposure would
affect one’s health. To see if their cell-culture systems accurately model the
toxic effects of chemical exposures, the researchers will compare the results
of tests using cultured cells to those using rodents. One of their ultimate goals
is to develop laboratory tests that can replace animal testing. (Project leader: Curtis Omiecinski, Ph.D.,
professor of environmental health, UW.)
Project 4: This project will use DNA-microarray technology
to map and identify genes that influence susceptibility to environmental toxins
that cause breast cancer. Relatively few women diagnosed with breast cancer –between
5 percent and 10 percent – carry BRCA1 and BRCA2, the so-called “breast-cancer
genes” that have been linked to an inherited form of the disease. However, up
to half of all women are believed to carry genetic mutations that may make them
susceptible to various environmental exposures linked with breast-cancer
growth. Researchers hope that by identifying such genes in rats – and
ultimately, humans – they’ll better understand how to identify sensitivity to
environmental breast-cancer risk factors in the majority of women. (Project
leader: Helmut Zarbl, Ph.D., member of the Hutchinson Center’s Human Biology
and Public Health Sciences divisions and principal investigator of the
Hutchinson Center/UW Toxicogenomics Consortium.)
Each research project is supported by an infrastructure of
technology cores that will provide a range of materials and services. A tissue-acquisition
core, directed by UW pathology professor Peter Rabinovitch, M.D., Ph.D., will provide
access to genetically defined tissues and cell cultures. A DNA-expression array
core, led by Zarbl, will compare the molecular fingerprints of cells exposed to
different doses of environmental agents.
Another important strength of the consortium is the
combined Hutchinson Center/UW expertise in bioinformatics and statistics, which
will be key in analyzing data that ultimately will contribute to a national microarray
gene-expression database. The consortium’s bioinformatics core will be co-directed
by Steven Self, Ph.D., member of the Hutchinson Center’s Public Health Sciences
Division; and Roger Bumgarner, Ph.D., director of the UW Center for Expression
Arrays and research assistant professor in the Department of Microbiology.
A toxicology core, directed by Terry Kavanagh, Ph.D.,
associate professor of environmental health at UW, will coordinate the
development of standardized methodologies in expression-array analysis to be
used across the national consortium’s participating universities as well as the
NIEHS.
Other academic institutions participating in the NIEHS
Toxicogenomics Research Consortium are the University of North Carolina at
Chapel Hill;
Oregon Health and Science University in Portland; Duke
University in Durham, N.C.; and the Massachusetts Institute of Technology in
Cambridge.
“We know that we can stretch the research dollar by having
scientists at NIEHS and grantees at universities work in concert,” said Kenneth
Olden, Ph.D., director of NIEHS. “But perhaps more important, we know that
bringing ideas together in science increases the advances we achieve.”
* * *
Aminoglycoside Antibiotics And Autism: A Speculative
Hypothesis.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ui
ds=11696245&dopt=Abstract <-- address ends here. Manev R, Manev H. Department of Psychiatry, The Psychiatric Institute The University
of Illinois at Chicago, Chicago, IL 60612, USA.
Background: Recently, it has been suspected that there is
a relationship between therapy with some antibiotics and the onset of autism; but
even more curious, some children benefited transiently from a subsequent treatment
with a different antibiotic. Here, we speculate how aminoglycoside antibiotics
might be associated with autism.
Presentation: We hypothesize that aminoglycoside
antibiotics could a) trigger the autism syndrome in susceptible infants by
causing the stop codon read through, i.e., a misreading of the genetic code of
a hypothetical critical gene, and/or b) improve autism symptoms by correcting
the premature stop codon mutation in a hypothetical polymorphic gene linked to
autism.
Testing: Investigate, retrospectively, whether a link
exists between aminoglycoside use (which is not extensive in children) and the
onset of autism symptoms (hypothesis “a”), or between aminoglycoside use and improvement
of these symptoms (hypothesis “b”). Whereas a prospective study to test
hypothesis “a” is not ethically justifiable, a study could be designed to test
hypothesis “b”.
Implications: It should be stressed that at this stage no
direct evide nce supports our speculative hypothesis and that its main purpose
is to initiate development of new ideas that, eventually, would improve our understanding
of the pathobiology of autism.
PMID: 11696245 [PubMed - as supplied by publisher]
* * *
EEG Finding with Autism
Paroxysmal discharges on EEG in young autistic patients are
frequent in
frontal regions
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11694957&dopt=Abstract Hashimoto T, Sasaki M, Sugai K, Hanaoka S,
Fukumizu M, Kato T. Department of
Education for Handicapped Children, Naruto University of Education, 748
Nakashima, Takashima, Naruto-cho, Naruto-city, Tokushima 772-8502, Japan.
EEGs were recorded in 86 autistic patients during sleep.
Epileptic discharges were observed in 37 cases (43%). Twenty-seven (73%) of
these 37 cases had localized spikes, 8 had multiple spike foci, one had
generalized spikes, and one had both multiple spike foci and generalized
spikes. Forty-seven epileptic discharge
foci were registered in 36 cases, the exception being one with generalized
spikes.
Thirty-six (76.6%) of the
registered 47 epileptic discharge foci were in the frontal region, one (2.1%)
in the temporal region, 7 (14.1%) in the centro-parietal region, and 3 (6.4%)
in the occipital region. Twenty (55.6%) of the 36 frontal spikes were at
midline (11 at Fz and 9 at Cz), 8 on the left side, and 8 on the right side.
The dipole of midline spikes was in the deep midline frontal region. These
results suggest that frontal dysfunctions are important in the mechanism of
symptoms in autism.
Lenny Schafer, Editor Catherine Johnson PhD
Ron Sleith Kay Stammers
Editor@feat.org Edward Decelie CALENDAR: Michelle Guppy events@feat.org
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