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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 ' million visitors each month.


WHO International Clinical Trials Registry Platform
The World Health Organization (WHO) has created a new Web site to help researchers, doctors and patients obtain reliable information on high-quality clinical trials. Now you can go to one website and search all registers to identify clinical trial research underway around the world!



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Disclaimer: The Visible Embryo web site is provided for your general information only. The information contained on this site should not be treated as a substitute for medical, legal or other professional advice. Neither is The Visible Embryo responsible or liable for the contents of any websites of third parties which are listed on this site.
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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 weeks 0 - 40 and follow fetal growth
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May 20, 2011--------News Archive

New Complexity In Genetic Diversity Of RNA
It turns out
RNA proteins do not precisely match the genes that encode them.

Validating Preschool Programs For Autism
Scientists from the Universities of Miami, North Carolina and Colorado, developed measures to evaluate teaching programs for autistic preschool children.


May 19, 2011--------News Archive

New Technique To 'Lift The Hood’ On Autism
A new study provides compelling evidence that exome-sequencing is an effective way to discover which of the 20,000 and more genes in the human genome are responsible for autism spectrum disorders.

Maternal Smoking Causes Changes In Fetal DNA
Children whose mothers or grandmothers smoked during pregnancy are at increased risk of asthma in childhood. A new study indicates changes in DNA methylation occuring before birth may be the root cause.


May 18, 2011--------News Archive

New Antiepileptic Drugs Don't Increase Birth Defects
Use of newer-generation antiepileptic drugs prescribed for bipolar mood disorders and migraine headaches, during the first trimester of pregnancy, are not associated with an increased risk of major birth defects in the first year of life in Denmark.

Neglect And Deprevation Age a Child's Chromosomes
Study of institutionalized Romanian children finds prematurely shortened telomeres, a mark of cell aging.


May 17, 2011--------News Archive

Older Fathers Linked to Autism In Children
Researchers sequenced protein-coding sections of affected childrens' genomes and their findings support population studies showing that autism is more common among children of older parents, especially older fathers.

Gene Variation Linked to Infertility in Women
A variation in a gene involved in regulating cholesterol also appears to affect progesterone in women, making it a likely culprit in cases of infertility.


May 16, 2011--------News Archive

Genetic Clue to Common Birth Defects Found
Scientists at King’s College London have for the first time uncovered a gene responsible for Adams-Oliver Syndrome, giving valuable insight into the possible genetic causes of common birth defects found in the wider population.

'Master switch' For Obesity and Diabetes Discovered
A gene linked to type 2 diabetes and cholesterol levels is in fact a 'master regulator' gene, which controls other genes found within fat in the body.

Tiny Change in One Gene May Explain Human Brain
The deep fissures and convolutions that increase the surface area and allow for rational and abstract thoughts of the human brain may be due to the LAMC3 gene.

Gene Change Can Get You Cancer Or Normal Growth
The deep fissures and convolutions that increase the surface area and allow for rational and abstract thoughts of the human brain may be due to one gene.


WHO Child Growth Charts

A gene-sequencing study of children with autism, published in Nature Genetics on 15 May, offers a sneak peek at a technique which, combined with other approaches, may explain 40 to 50 percent of the genetic causes of the disorder.

Evan Eichler of the University of Washington in Seattle, the study's lead investigator, proposes the work can be completed within just a few years. The new approach will potentially allow clinicians to "lift the hood on what has gone wrong in each individual child with autism," with the hope of ultimately devising individually-tailored drug therapies.

Autism spectrum disorders manifest in a wide variety of ways, and researchers believe they are highly genetically diverse, involving mutations in any of several hundred genes.

While studies of twins suggest that as much as 90 percent of autism is genetically based, large-scale genetic screens over the last decade that searched for common genetic variants underlying the disorder have been disappointing.

A growing body of evidence suggests that, especially in families with no prior history of the disorder, autism results not from the inheritance of an unfortunate combination of common gene variants, but from rare, spontaneous — or de novo — mutations in the egg or sperm.

Over the past few years, this theory has been supported by numerous microarray studies showing that children with spontaneous autism are more likely than their unaffected siblings to have de novo copy number variants, mutations in which a large chunk of DNA is duplicated or deleted.

Now, in work funded in part by the Simons Foundation, Brian O'Roak, a joint postdoc in Jay Shendure's and Eichler's labs at the University of Washington, has sequenced the exome — the protein-coding regions of the genome — of 20 families consisting of one child with an autism spectrum disorder and unaffected parents and siblings. In contrast to most previous studies, which could detect only large copy number variants, the new study can detect even point mutations, in which just a single DNA nucleotide is affected.

"Our approach has the advantage of taking a snapshot of an individual's protein-coding genome and quickly identifying the one or two new sporadic mutations they carry," O'Roak says.

The families in the study were drawn from the Simons Simplex Collection, a large repository of genetic, phenotypic and biological data from families with just one affected child and unaffected parents and siblings. The collection was created for the express purpose of facilitating the search for rare, de novo autism mutations.

While the 20 children with autism did not have significantly more de novo point mutations than would be expected in the population at large, their mutations were much more disruptive to the proteins they encoded than is typical. What's more, a significant number of the mutations occurred in regions of the genome in which mutations are rarely found, probably because these regions are so crucial to bodily functioning that individuals with defects in those regions usually die without reproducing.

In four children, the researchers identified de novo mutations that are so deleterious that they likely play a causative role in these children's autism. Probably not coincidentally, these four children are among the most severely affected in the study group.

Three of the four mutated genes — FOXP1, GRIN2B and SCN1A — have previously been implicated in autism, and are thought to play roles in speech and language disorders, intellectual disability and epilepsy, respectively.

The fourth gene, LAMC3, has not previously been linked to autism, but is known to be expressed in many areas of the cortex and limbic system. "Finding a LAMC3 mutation will probably set the stage for some new research agendas," Eichler says.

Two of the four children appear to have experienced a genetic double-whammy, having inherited a deleterious mutation from a parent in addition to having a de novo mutation. The child with a FOXP1 mutation also inherited a defective copy of CNTNAP2, another gene that may be involved in language development. "It's like getting hit by lightning twice," Eichler says. That child has severe autism and the greatest language deficit of any individual in the study.

The child with the epilepsy-related SCN1A mutation also inherited from his mother a deletion that increases the risk for epilepsy; and indeed, that child has been diagnosed with epilepsy. The findings support the 'multi-hit' theory of autism, the idea that it may take a combination of mutations in the same pathway to cause severe autism or related disorders.

Studying 20 families is just a start — "a teaser," as Eichler puts it. At the same time, the study offers two important proofs of principle: It provides compelling evidence that de novo point mutations may underlie many cases of autism, and it shows that exome-sequencing is an effective way to discover which of the more than 20,000 genes in the human genome are responsible for autism spectrum disorders.

"It's like having a dartboard with 20,000 candidates — the fact that we could pick off four outstanding candidate genes is a great success," Eichler says. "It's proof on the ground that this technique is fruitful."

As whole-exome and eventually whole-genome sequencing become more accurate and affordable, it won't be long before it will be possible to sequence several thousand families, which should be enough data to provide statistical arguments about which genes are responsible for autism spectrum disorders, Eichler says.

"Within a couple of years, we should have a pretty comprehensive view of the genes that cause autism," he says.

The Simons Foundation is providing funding for Eichler's team and several other groups to do whole-exome sequencing of several hundred families in the Simons Simplex Collection over the next few months.