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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
Google Search artcles published since 2007
 
 

Home | Pregnancy Timeline | News Alerts |News Archive March 27, 2014

 

Human fossils show that at least twice in our evolutionary history our brains grew in size.
Scientists have been studying the human genome for a long time and found the gene SRGAP2
plays a role in brain cell growth by slowing the maturation of specific brain cells, triggering
the development of denser neuronal structures called spines. Spines help form connections
between brain cells. DUF1220 has also duplicated in humans more rapidly than any
other protein-coding region of the genome. DUF1220 is part of a gene family
in which individual genes carry 5 to 50 copies. Overall, humans have more
than 250 copies of DUF1220. Other great apes have 90 to 125,
monkeys about 30, and non-primates fewer than 10.

Image Credit: The Simons Foundation 02 January 2014 https://www.simonsfoundation.org/quanta/20140102-
a-missing-genetic-link-in-human-evolution/






WHO Child Growth Charts

 

 

 

Brain evolution gene linked to autism

The same gene family that may have helped the human brain become larger and more complex also is linked to the severity of autism, according to new research from the University of Colorado Anschutz Medical Campus.

This brain gene family is made up of over 270 copies of a segment of DNA called DUF1220. The DUF1220 gene family codes for a protein domain – a specific segment within a protein. The more copies of a DUF1220 subtype a person with autism has, the more severe their symptoms, according to a paper just published in PLoS Genetics.

This association of increasing copy number (or dosage) of a gene-coding segment of DNA with increasing severity of autism is a first, and suggests a focus for future research into the condition called Autism Spectrum Disorder (ASD). ASD is a common behaviorally defined condition whose symptoms can vary widely – which is why the word "spectrum" is part of the name. One federal study showed that ASD affects one in 88 children.

"Previously, we linked increasing DUF1220 dosage with the evolutionary expansion of the human brain," says James Sikela, PhD, a professor in the Department of Biochemistry and Molecular Genetics, University of Colorado School of Medicine. Sikela is the corresponding author of the study just published.

"One of the most well-established characteristics of autism is an abnormally rapid brain growth that occurs over the first few years of life. That feature fits very well with our previous work linking more copies of DUF1220 with increasing brain size. This suggests that more copies of DUF1220 may be helpful in certain situations but harmful in others."


The research team found that not only was DUF1220 linked to severity of autism overall, they found that as DUF1220 copy number increased, the severity of each of three main symptoms of the disorder — social deficits, communicative impairments and repetitive behaviors — became progressively worse.


In 2012, Sikela was the lead scientist of a multi-university team whose research established the link between DUF1220 and the rapid evolutionary expansion of the human brain. The work also implicated DUF1220 copy number in brain size both in normal populations as well as in microcephaly (small brain size) and macrocephaly (large brain size) — both abnormalities.

The first author of the autism study, Jack Davis, PhD, who contributed to the project while a postdoctoral fellow in the Sikela lab, has a son with autism and thus had a very personal motivation to seek out the genetic factors that cause autism.

The research by Davis, Sikela and colleagues at the Anschutz campus in Aurora, Colo., focused on the presence of DUF1220 in 170 people with autism.


Strikingly, DUF1220 is as common in people who do not have ASD as in people who do.

"Something else is at work here, a contributing factor that is needed for ASD to manifest itself.

"We were only able to look at one of the six different subtypes of DUF1220 in this study, so we are eager to look at whether the other subtypes are playing a role in ASD."


Jack Davis, PhD, formerly in James Sikela lab.


Because of the high number of copies of DUF1220 in the human genome, the domain has been difficult to measure.

As Sikela says, "To our knowledge DUF1220 copy number has not been directly examined in previous studies of the genetics of autism and other complex human diseases .So the linking of DUF1220 with ASD is also confirmation that there are key parts of the human genome that are still unexamined but are important to human disease."

Abstract
One of the three most frequently documented copy number variations associated with autism spectrum disorder (ASD) is a 1q21.1 duplication that encompasses sequences encoding DUF1220 protein domains, the dosage of which we previously implicated in increased human brain size. Further, individuals with ASD frequently display accelerated brain growth and a larger brain size that is also associated with increased symptom severity. Given these findings, we investigated the relationship between DUF1220 copy number and ASD severity, and here show that in individuals with ASD (n = 170), the copy number (dosage) of DUF1220 subtype CON1 is highly variable, ranging from 56 to 88 copies following a Gaussian distribution. More remarkably, in individuals with ASD CON1 copy number is also linearly associated, in a dose-response manner, with increased severity of each of the three primary symptoms of ASD: social deficits (p = 0.021), communicative impairments (p = 0.030), and repetitive behaviors (p = 0.047). These data indicate that DUF1220 protein domain (CON1) dosage has an ASD-wide effect and, as such, is likely to be a key component of a major pathway underlying ASD severity. Finally, these findings, by implicating the dosage of a previously unexamined, copy number polymorphic and brain evolution-related gene coding sequence in ASD severity, provide an important new direction for further research into the genetic factors underlying ASD.