HOUSTON -- (June 18, 2008) -- A consortium of autism research institutions, including Baylor College of Medicine in Houston, is seeking the help of children with autism and their families in establishing a genetic database that will foster research into the disorder.

Thirteen institutions are contributing to the database called the Simons Simplex Collection, which will help scientists who are looking for the cause of the disorder. Simplex refers to families with only one child affected with autism.

Future treatment

"This study will be a very important resource for treating autism in the future, and assessing the disorder, both from the standpoint of genetics and observed symptoms," said Dr. Diane Treadwell-Deering, assistant professor of psychiatry and behavioral sciences at BCM and co-chief of the Clinic for Autistic Spectrum Disorders at Texas Children's Hospital. Treadwell-Deering will co-direct the local part of the study with Dr. Arthur Beaudet, chair of molecular and human genetics at BCM.
“This is an important extension of recent discoveries about genetic causes of autism," said Beaudet.

Criteria

To be eligible families must have:

• Only one child with an autism spectrum disorder between the ages of 4 and 18 years.
• One or more other children at least 4 years old who does not have an autism spectrum disorder.
• Both biological parents who are willing to participate.

Researchers will assess the behavior and symptoms of children in the study and ask members of their families for blood samples.

Contribute to research

"This is a wonderful opportunity for families to contribute to research that will have a profound impact on our ability to study autism," said Dr. Robin Goin-Kochel, assistant professor of molecular and human genetics at BCM and co-investigator on the project.

Funding for this study comes from the Simons Foundation, a philanthropic organization based in New York City, which seeks to advance the frontiers of research in the basic sciences and mathematics. For more information about the Simons Foundation, visit http://www.simonsfoundation.org/.

Families interested in enrolling in this study can contact Dr. Goin-Kochel at 832-822-4299 or kochel@bcm.edu

Federal statistics from the national Centers for Disease Control and Prevention indicate that as many as one in 150 children have some form of autism, a developmental disability that causes substantial impairments in social interaction and communication and the presence of unusual behaviors and interests.

HOUSTON -- (June 18, 2008) -- When a person develops a sore or a boil, it erupts, drawing to it immune system cells that fight the infection. Then it resolves and flattens into the skin, often leaving behind a mark or a scar.

A similar scenario plays out in the blood vessels. However, when there is a defect in the resolution response – the ability of blood vessels to recover from inflammation – atherosclerosis or hardening of the arteries can result, said researchers at Baylor College of Medicine in Houston and Harvard Medical School in Boston in a report that appears online today in The Journal of the Federation of American Societies for Experimental Biology. The major factor in this disease is a deficiency in the chemical signals that encourage resolution (pro-resolution signals). These signals are produced in the blood vessel where the inflammation occurs, the researchers said.

Hardening of the arteries

Chronic inflammation of the artery wall can cause atherosclerosis, a major risk factor for heart disease and heart attack. However, said Dr. Lawrence C.B. Chan, professor of medicine and molecular and cellular biology and chief of the division of division of diabetes, endocrinology and metabolism at BCM, in many instances, the lesions or little sores inside the artery arise and then resolve, often from a very young age. The mystery is why some lesions do not heal.

What he and his colleagues from BCM and Harvard found was that genetically increasing the production of the pro-resolution signals would cool down the inflammation and give the “sores” a chance to heal or the atherosclerosis to slow down. However, genetically clamping down on these signals would fan the fire of inflammation and speed up the progression of atherosclerosis.

Two-edged sword

“Inflammation is a two-edged sword. If resolution fails and the response gets out of hand there is a never ending civil war in the body,” said Dr. Aksam J. Merched, assistant professor of molecular and cellular biology at BCM and lead author of the study. “Continued inflammation draws more macrophages (potent immune system cells) to the site of the inflammation. They produce molecules that turn this into a vicious cycle.”

Dr. Charles Serhan of Brigham and Women’s Hospital and Harvard Medical School in Boston, a key collaborator who first discovered many of the chemical mediators, provided special expertise in understanding the role of the mediators as well as performed analyses that allowed us to measure them accurately, said Chan.

“Resolution is not a passive process,” said Chan, who is also the Betty Rutherford Chair for Diabetes Research at BCM. “It is active and produces specific anti-inflammatory mediators that ‘cool down’ the inflammatory process.

Cool down process

Some natural mediators that ‘cool’ this inflammation are derived from omega-3 polyunsaturated fatty acids, which are plentiful in fish and are frequently cited for their beneficial effects on the heart. Another kind of mediator is triggered by the anti-inflammation drug aspirin, said Chan.

“The specific chemical mediators that naturally cool down the inflammatory process identified in this study represent a new drug target for anti-atherosclerosis therapy,” said Merched.

Others who participated in the study include Kerry Ko from BCM and Katherine H. Gotlinger from the Center for Experimental Therapeutics and Reperfusion Injury at Harvard Medical School.

Funding for this work came from the American Heart Association and the National Institutes of Health.

The article is available at http://www.fasebj.org/contents-by-date.0.shtml

HOUSTON -- (June 16, 2008) -- Dr. Nancy Weigel, professor of molecular and cellular biology at Baylor College of Medicine in Houston, has been awarded the 2008 Roy O. Greep Award Lecture at ENDO 08, the 90th Annual Meeting of The Endocrine Society.

This award is presented annually for outstanding contributions to research in endocrinology. Weigel presented a lecture entitled "Dissecting the Interplay between Cell Signaling and Progesterone Receptor."

Her work has focused primarily on the role of cell signaling in steroid receptor action and the activities of nuclear hormone receptors in prostate cancer. Her research has shown that a derivative of the active form of vitamin D can inhibit the growth of prostate cancer cells in mice.

In addition to her work in the lab, Weigel has organized national and international meetings, and served on several journal editorial boards for The Endocrine Society. She is a Searle Scholar and was also awarded the Marc Dresden Award for Excellence in Graduate Education.

"Nancy is widely respected as one of the most thoughtful and definitive scientists in the field of endocrinology, and is well deserving of the high honor that accompanies the Roy O. Greep Award," said Dr. Bert O'Malley, chair of molecular and cellular biology at BCM.

The 90th Annual Meeting of The Endocrine Society took place June 15-18 in San Francisco.

HOUSTON -- (June 11, 2008) -- Children whose immune systems rebound after treatment with potent anti-viral drugs for HIV infection face an increased risk of developing asthma, said a federally funded consortium of researchers led by those from Baylor College of Medicine in a report that appears online in the Journal of Allergy and Clinical Immunology.

"We think this occurs because important immune system components called CD4 cells increase in children treated with highly active antiretroviral therapy," said Dr. William T. Shearer, professor of pediatrics and immunology at BCM in Houston and chief of the allergy and immunology service at Texas Children's Hospital. He is also senior author of the report. CD4 cells are thought to be associated with the inflammation in the lung tissue that accompanies asthma. When CD4 cells decline in children with HIV, their asthma symptoms also decrease.

Shearer and his colleagues evaluated the use of asthma medication among children with HIV who took the anti-HIV drugs and those who did not. They found that about one-third of those on the anti-HIV medications used asthma drugs compared to 11.5 percent of those who did not take anti-HIV drugs.

Shearer said a study that evaluates the lung function of children with HIV on anti-viral therapy would help explain how an increase in the immune system affects the risk of asthma.

"This AIDS model of asthma might help understand at a molecular level what is causing the current epidemic of asthma among children more generally," he said.

Others who took part in the study include Samuel B. Foster and Mary E. Paul of BCM and Texas Children's; Kenneth McIntosh of Harvard Medical School, Bruce Thompson, Ming Lu and Wanrong Yin of Clinical Trials and Surveys Corporation in Baltimore, MD., Kenneth C. Rich of the University of Illinois in Chicago, Hermann Mendez of the State University of New York in Brooklyn, Leslie K. Serchuck of the National Institute of Child Health and Development in Bethesda, MD and Clemente Diaz of the Puerto Rico School of Medicine in San Juan.

Funding for this work came from the National Institutes of Health, the Pediatric Research and Education Fund at Baylor College of Medicine; the David Fund and the Pediatric AIDS Fund and Immunology Research Fund at Texas Children's Hospital.

The abstract is at http://www.jacionline.org/article/S0091-6749(08)00941-X/abstract.

Women who gain more or less than recommended amounts of weight during pregnancy are likely to increase the risk of problems for both themselves and their child, as per a new report by the RTI International-University of North Carolina at Chapel Hill Evidence-based Practice Center.

The report, which was supported by the U.S. Department of Health and Human Services Agency for Healthcare Research and Quality (AHRQ) in partnership with the American Dietetic Association, is based on a systematic review of 150 studies that assessed the short- and long-term effects of maternal weight gain on pregnancy, mothers, fetuses, and children. The studies were published in English between January 1990 and October 2007.

Among the reports key findings is a strong association between high maternal weight gain and increased fetal growth and infant birth weight, which can contribute to complications during labor if a baby is too big, and can lead to long term health effects for the child. High maternal weight gain also is linked to cesarean delivery and weight retention by mothers after childbirth.

The review also confirmed that gaining too little weight during pregnancy can be a problem. Low maternal weight gain is linked to poor fetal growth, lower birth weight, and the chance of a baby being born prematurely.

The report was prompted by several trends, including an increase in the number of American women who are overweight and obese, as well as the number who gain more weight during pregnancy than amounts laid out in the Institute of Medicines 1990 recommendations for maternal weight gain. Public health officials also are concerned about an increase in pregnancy complications such as diabetes and cesarean delivery.

The Institute of Medicine is currently reviewing its pregnancy weight guidelines to see if they need to be revised; it expects to issue a report next summer.

Unfortunately, the existing body of research on maternal weight gain is inadequate to permit a more comprehensive assessment, said Meera Viswanathan, Ph.D., the study director and a senior research analyst at RTI International. Most beneficial would be an analysis that considers the risks and potential benefits of various maternal weight-gain scenarios to all women irrespective of age, race or ethnicity, or their body mass index before they became pregnant. But such an analysis is not possible at this time.

Her research colleague at UNC, Anna Maria Siega-Riz, Ph.D., agreed.

Despite the large body of research, clear clinical recommendations based on this systematic review will be challenging to formulate because of major shortcomings in this research, said Siega-Riz, an associate professor in the UNC School of Public Healths epidemiology and nutrition departments. To fully understand the effects of maternal weight gain on short- and long-term health outcomes for both women and infants, future studies will need to adopt standard measures and consistent definitions of exposures and outcomes.

The scientists said future studies will need to examine multiple outcomes within the same study population to explore fully the trade-offs between the risks and benefits to the mother and to the child.


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