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Home > Divisions > Dysmorphology-Teratology > Research Activities
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Our research group has been involved in a number of areas of investigation. The group’s primary focus is to better understand the etiology and developmental pathogenesis of birth defects. A major research theme is based on the premise that a substantial number of birth defects which presently have an unknown etiology are the result of drugs, chemicals and/or environmental agents to which the fetus is exposed. Follow-up through systematic post-marketing surveillance of prenatally exposed infants whose mothers were ascertained through the California Teratogen Information Service and Clinical Research Program provide a wealth of research material. In addition, our group is the coordinating center for research studies conducted through the Organization of Teratology Information Services (OTIS), a group of 18 services throughout North America. We provide the infrastructure that allows for proper study design, subject ascertainment, follow-up, collection of data, statistical analysis and interpretation of data for a number of large collaborative studies that are being performed by OTIS. A second major research theme relates to the prenatal effects of alcohol. One study sponsored by the National Institute on Alcohol Abuse and Alcoholism (NIAAA) examines a variety of risk factors for fetal alcohol spectrum disorders in the Moscow region of Russia and in Ukraine. A second study, also funded by NIAAA compares the dysmorphologic features of children exposed to alcohol across cultures. A third research theme is based on the theory that intrauterine vascular accidents play a major role in the etiology of birth defects which previously have defied a rationale embryologic explanation. We are particularly involved at the present time in attempting to better understand the etiology of gastroschisis, which we strongly believe has a vascular etiology. An additional theme that we have recently been pursuing is based on the premise that a certain portion of birth defects are the result of chronic or acute alterations in embryonic and/or fetal nutrition.