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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

Scientists at the University of Washington (UW) Department of Genome Sciences have identified several sporadic or "de novo" genetic mutations in children with autism spectrum disorder.

Published in Nature Genetics, the research applied leading edge molecular biology techniques and massively parallel sequencing to examine all of the protein coding portions of the genome, called the exome.

The study was led by Dr. Brian O'Roak, senior fellow in the UW Department of Genome Sciences, and senior authors Dr. Evan Eichler, UW professor of genome sciences and a Howard Hughes Medical Institute investigator, and Dr. Jay Shendure, UW assistant professor of genome sciences.

O'Roak and colleagues analyzed the exomes of 20 individuals with autism spectrum disorder and their parents, an approach called trio-based exome sequencing. Autism spectrum disorders encompass a range of social impairments in language, communicating and interacting with others, repetitive behaviors, and engrossing fascinations. The condition can be mildly to severely disabling.

They found 21 newly occurring mutations, 11 of which altered proteins. Proteins altered by genetic mutations may hold clues to the biological pathways involved in the development of the disease. The abnormal proteins or the pathways they affect could draw interest as targets in the design of preventive or treatment drugs.

O'Roak's fellowship at the UW, as well as part of the research itself, was supported by American Recovery and Reinvestment Act funding from the U.S. government. O'Roak said, "I came to the UW with the specific plan to use the latest genomic technology to study autism because it affects the lives of so many children, adults and their families."

In four of the 20 families studied, O'Roak and colleagues identified disruptive new mutations that are potentially cause for autism. In examining the clinical data on the child in each of the four families, they learned that these children were among the most severely affected of the study group, both in intellectual disability and in their autistic features.

These findings suggest the mutations could contribute substantially to the underlying mechanisms and severity of autism in perhaps 20 percent of cases where no family history of autism exists. In some cases, the combination of newly appearing mutations and those inherited from the parents may worsen the severity of the disorder.

"The results of the study suggest a multi-hit model as a trend, but this possibility would need to be further explored by comparing a much larger number of affected and unaffected siblings," said Eichler.

Many of the discovered mutations were in areas of the genome which were highly conserved during evolution. These parts of the genome likely play a fundamental role in the biology of many animals, including humans, and tend to have significant repercussions.

"Consistent with the complexity of autism and its symptoms, the new mutations were identified in several different genes," lead author O'Roak said. Moreover, many of these mutated genes have already been associated with other brain disorders, including epilepsy, schizophrenia and intellectual disability -- reflecting a surprising genetic overlap.

Eichler explained that scientists are not sure what the genetic overlap indicates; perhaps a common underlying mechanisms in the development of neurological diseases, or different manifestations originating from similar genetic lesions. Overlap might also be due to environmental triggers or other genes in a person's make-up that influence how and when genes function; whether or not a disease will appear in genetically susceptible individuals, and what type of disease will manifest.

Although the how and why of sporadic mutations is as yet unknown, researchers are uncovering clues about risk factors.

In six of the affected children in this study, scientists were able to trace the original genes in the child back to the father's half of the child's genome, and in one case to the mother's half.

These genetic findings further support population studies showing that autism is more common among children of older parents, especially older fathers. Eichler explained that certain genetic mutations might more likely occur during sperm formation as men age.

The scientists wrote, "The identification of de novo events along with disruptive inherited mutations underlying sporadic cases of autism spectrum disorders has the potential to fundamentally transform our understanding of the genetic basis of autism."

"Our results," Shendure noted, "show that trio-based exome sequencing is a powerful approach for identifying new candidate genes for autism spectrum disorders."

From identifying mutations, researchers hope to learn more about the biology of autism and to understand interacting genetic and environmental factors within the context of families with affected and unaffected members.

In addition to O'Roak, Shendure and Eichler, other researchers on the study included Pelagia Deriziotis from the Wellcome Trust Centre for Human Genetics, University of Oxford, United Kingdom; Choli Lee, Laura Vives, Jerrod J. Schwartz, Santosh Girirajan, Emre Karakoc, Alexandra P. MacKenzie, Sarah B. Ng, Carl Baker, Mark J. Rieder, Deborah A. Nickerson, all from the UW Department of Genome Sciences in Seattle; Raphael Bernier of the UW Department of Psychiatry and Behavioral Sciences; and Simon E. Fisher of the Wellcome Trust Centre for Human Genetics and the Language and Genetics Department of the Max Planck Institute for Psycholinguistics, Nijmegen, Netherlands.

The research was funded by the United States National Institutes of Health, Wellcome Trust, Max Planck Society, the Simons Foundation Autism Research Initiative, and the Howard Hughes Medical Institute. Original article: http://www.eurekalert.org/pub_releases/2011-05/uow-smi051611.php