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Welcome to The Visible Embryo, a comprehensive educational resource on human development from conception to birth.

The Visible Embryo provides visual references for changes in fetal development throughout pregnancy and can be navigated via fetal development or maternal changes.

The National Institutes of Child Health and Human Development awarded Phase I and Phase II Small Business Innovative Research Grants to develop The Visible Embryo. Initally designed to evaluate the internet as a teaching tool for first year medical students, The Visible Embryo is linked to over 600 educational institutions and is viewed by more than one million visitors each month.

Today, The Visible Embryo is linked to over 600 educational institutions and is viewed by more than 1 million visitors each month. The field of early embryology has grown to include the identification of the stem cell as not only critical to organogenesis in the embryo, but equally critical to organ function and repair in the adult human. The identification and understanding of genetic malfunction, inflammatory responses, and the progression in chronic disease, begins with a grounding in primary cellular and systemic functions manifested in the study of the early embryo.

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Pregnancy Timeline by SemestersFetal liver is producing blood cellsHead may position into pelvisBrain convolutions beginFull TermWhite fat begins to be madeWhite fat begins to be madeHead may position into pelvisImmune system beginningImmune system beginningPeriod of rapid brain growthBrain convolutions beginLungs begin to produce surfactantSensory brain waves begin to activateSensory brain waves begin to activateInner Ear Bones HardenBone marrow starts making blood cellsBone marrow starts making blood cellsBrown fat surrounds lymphatic systemFetal sexual organs visibleFinger and toe prints appearFinger and toe prints appearHeartbeat can be detectedHeartbeat can be detectedBasic Brain Structure in PlaceThe Appearance of SomitesFirst Detectable Brain WavesA Four Chambered HeartBeginning Cerebral HemispheresFemale Reproductive SystemEnd of Embryonic PeriodEnd of Embryonic PeriodFirst Thin Layer of Skin AppearsThird TrimesterSecond TrimesterFirst TrimesterFertilizationDevelopmental Timeline
CLICK ON weeks 0 - 40 and follow along every 2 weeks of fetal development
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Home | Pregnancy Timeline | News Alerts |News Archive Dec 3, 2013

 

Autism spectrum disorder (ASD) is a lifelong neurodevelopmental disability characterized by problems with social interaction, communication and repetitive behaviors.







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Air pollution combined with genetics increases risk for autism

Exposure to air pollution appears to increase the risk for autism among people who carry a genetic disposition for the neurodevelopmental disorder.

according to newly published research led by scientists at the Keck School of Medicine of the University of Southern California (USC).

"Our research shows that children with both the risk genotype and exposure to high air pollutant levels were at increased risk of autism spectrum disorder compared to those without the risk genotype and lower air pollution exposure," said the study's first author, Heather E. Volk, Ph.D., M.P.H., assistant professor of research in preventive medicine and pediatrics at the Keck School of Medicine of USC and principal investigator at The Saban Research Institute of Children's Hospital Los Angeles.

The study, "Autism spectrum disorder: Interaction of air pollution with the MET receptor tyrosine kinase gene," is scheduled to appear in the January 2014 edition of Epidemiology.

Autism spectrum disorder (ASD) is a lifelong neurodevelopmental disability characterized by problems with social interaction, communication and repetitive behaviors. The Centers for Disease Control and Prevention estimates that one in 88 children in the United States has an ASD.


"Although gene-environment interactions are widely believed to contribute to autism risk, this is the first demonstration of a specific interaction between a well-established genetic risk factor and an environmental factor that independently contribute to autism risk.

"The MET gene variant has been associated with autism in multiple studies, controls expression of MET protein in both the brain and the immune system, and predicts altered brain structure and function. It will be important to replicate this finding and to determine the mechanisms by which these genetic and environmental factors interact to increase the risk for autism."

Daniel B. Campbell, Ph.D., assistant professor of psychiatry and behavioral sciences, Keck School of Medicine, USC and study senior author.


Independent studies by Volk and Campbell have previously reported associations between autism and air pollution exposure and between autism and a variant in the MET gene. The current study suggests that air pollution exposure and the genetic variant interact to augment the risk of ASD.

Campbell and Volk's team studied 408 children between 2 and 5 years of age from the Childhood Autism Risks From Genetics and the Environment Study, a population-based, case-control study of preschool children from California. Of those, 252 met the criteria for autism or autism spectrum disorder. Air pollution exposure was determined based on the past residences of the children and their mothers, local traffic-related sources, and regional air quality measures. MET genotype was determined through blood sampling.

Campbell and Volk continue to study the interaction of air pollution exposure and the MET genotype in mothers during pregnancy.

Abstract
Background: Independent studies report association of autism spectrum disorder with air pollution exposure and a functional promoter variant (rs1858830) in the MET receptor tyrosine kinase (MET) gene. Toxicological data find altered brain Met expression in mice after prenatal exposure to a model air pollutant. Our objective was to investigate whether air pollution exposure and MET rs1858830 genotype interact to alter the risk of autism spectrum disorder.

Methods: We studied 252 cases of autism spectrum disorder and 156 typically developing controls from the Childhood Autism Risk from Genetics and the Environment Study. Air pollution exposure was assigned for local traffic-related sources and regional sources (particulate matter, nitrogen dioxide, and ozone). MET genotype was determined by direct resequencing.

Results: Subjects with both MET rs1858830 CC genotype and high air pollutant exposures were at increased risk of autism spectrum disorder compared with subjects who had both the CG/GG genotypes and lower air pollutant exposures. There was evidence of multiplicative interaction between NO2 and MET CC genotype (P= 0.03).

Conclusions: MET rs1858830 CC genotype and air pollutant exposure may interact to increase the risk of autism spectrum disorder.

Co-authors include Tara Kerin and Rob McConnell of USC, Fred Lurmann of Sonoma Technology and Irva Hertz-Picciotto of the University of California, Davis. Their work was supported by grants from the National Institute of Environmental Health Sciences (grant numbers ES019002, ES013578, ES007048, ES11269, ES015359, ES016535, ES011627, EPA Star-R, 823392, 833292), the MIND Institute, and Autism Speaks.