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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 Nov 26, 2013

 

The Mid-fetal frontal cortex, is a brain region critical to cognition, language, and complex motor behaviors. It is also a molecular crossroads shared by nine genes conclusively linked to autism — and therefore may become an area under observation for developmental autism.

Image Credit: Cell magazine/Yale University.







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Yale team finds clues to origin of autism

Finding major new clues to the origins of autism, a Yale-led team of researchers has pinpointed which cell types and regions of the developing human brain are affected by gene mutations linked to autism.

They report their findings in the Nov. 21 issue of the journal Cell.

Analyzing massive amounts of gene expression data generated by the BrainSpan project, the team identified common neural circuits affected by autism-risk genes and when, where, and in what cell types those genes exert their effects on the developing human brain and lead to autism spectrum disorders.


Although other genes and neural circuits that contribute to autism spectrum still remain to be found, the new findings suggest new targeted treatments for autism may be possible, said Nenad Sestan, professor of neurobiology, investigator for Kavli Institute for Neuroscience at Yale, and co-senior author of the paper.


"We know now that we may not have to treat the whole brain, that changes related to mutations in autism-risk genes may affect particular neural circuits at specific places at specific times," Sestan said.

The genetic causes of autism, like other complex diseases such as schizophrenia, have proved daunting to study. Several hundred genes have already been linked to autism spectrum disorders, but no single gene seems to account for the symptoms of the disorders. The task of searching for a cause for the disorder is the scientific equivalent of trying to reach an unknown town in Maine knowing only that you started from a street in San Diego.

The Yale team led by Sestan and Matthew State, now at the University of California-San Francisco, together with James Noonan of Yale School of Medicine, Bernie Devlin of the University of Pittsburgh, and Kathryn Roeder of Carnegie-Mellon University tackled the difficulty by searching for molecular crossroads shared by nine genes conclusively linked to autism.


An analysis of when and where nine of those autism genes are most co-activated identified at least two such molecular crossroads.

The first influence a specific cell type — excitatory projection neurons — and their neural circuits, which form and become active about three to five months after conception.

The second implicates the mid-fetal frontal cortex, a brain region critical for cognition, language, and complex motor behaviors.


It is unclear exactly how these mechanisms might lead to symptoms of autism, the authors noted. It could be that several developmental changes could influence how the disorders develop in the same way that hypertension contributes to both heart attack and stroke, they said.

Sestan also notes the same approach might be used to find causes of other complex psychiatric and neurological disorders, in which many genes contribute to a wide variety of symptoms that characterize the disease.

"The brain is extraordinarily complicated, but this approach gives us a way to pinpoint some of the mechanisms that contribute to a host of complex brain disorders," Sestan said.

Abstract Highlights
Exome sequencing identifies a novel ASD gene, Ankyrin 2, neuronal (ANK2)
Data from developing human brain are used for coexpression analyses of nine ASD genes
ASD genes converge in midfetal frontal cortex deep projection neurons
Approach clarifies when, where, and in what cell type to study specific ASD mutations

Summary
Autism spectrum disorder (ASD) is a complex developmental syndrome of unknown etiology. Recent studies employing exome- and genome-wide sequencing have identified nine high-confidence ASD (hcASD) genes. Working from the hypothesis that ASD-associated mutations in these biologically pleiotropic genes will disrupt intersecting developmental processes to contribute to a common phenotype, we have attempted to identify time periods, brain regions, and cell types in which these genes converge. We have constructed coexpression networks based on the hcASD “seed” genes, leveraging a rich expression data set encompassing multiple human brain regions across human development and into adulthood. By assessing enrichment of an independent set of probable ASD (pASD) genes, derived from the same sequencing studies, we demonstrate a key point of convergence in midfetal layer 5/6 cortical projection neurons. This approach informs when, where, and in what cell types mutations in these specific genes may be productively studied to clarify ASD pathophysiology.

Authors
A. Jeremy Willsey, Stephan J. Sanders, Mingfeng Li, Shan Dong, Andrew T. Tebbenkamp, Rebecca A. Muhle, Steven K. Reilly, Leon Lin, Sofia Fertuzinhos, Jeremy A. Miller, Michael T. Murtha, Candace Bichsel, Wei Niu, Justin Cotney, A. Gulhan Ercan-Sencicek, Jake Gockley, Abha R. Gupta, Wenqi Han, Xin He, Ellen J. Hoffman, Lambertus Klei, Jing Lei, Wenzhong Liu, Li Liu, Cong Lu, Xuming Xu, Ying Zhu, Shrikant M. Mane, Ed S. Lein, Liping Wei, James P. Noonan, Kathryn Roeder, Bernie Devlinsend email, Nenad Sestansend email, Matthew W. Statesend