Welcome to The Visible Embryo

Home-- -History-- -Bibliography- -Pregnancy Timeline- --Prescription Drugs in Pregnancy- -- Pregnancy Calculator- --Female Reproductive System- -Contact

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!



Home

History

Bibliography

Pregnancy Timeline

Prescription Drug Effects on Pregnancy

Pregnancy Calculator

Female Reproductive System

Contact The Visible Embryo

News Alerts Archive

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.
Content protected under a Creative Commons License.

No dirivative works may be made or used for commercial purposes.

Return To Top Of Page
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
Google Search artcles published since 2007
 
April 4 - 8, 2011--------News Archive

Simple Treatment Prevents Premature Births
Treating high-risk pregnant women with the hormone progesterone cut their rate of early delivery by 45 % and helped lower the risk of breathing complications in their babies.

Babies Are Born Early Near Busy Road Intersections
Babies are born earlier when their mothers live near a concentration of freeways and main roads, reports a study of 970 mothers and their newborn babies in Logan City, a town south of Brisbane, Australia.

New Gene Found Increases Risk For Epilepsy
Vanderbilt University researchers have identified a new gene that can influence a person's risk for developing epilepsy.

Gene Linked To Autism's Social Dysfunction
With the help of two sets of brothers with autism, Johns Hopkins scientists have identified a gene associated with autism that appears to be linked very specifically to the severity of social interaction deficits.

Study Reveals How Eye Is Formed
Scientists at King’s College London have discovered specific cells responsible for ensuring that different parts of the eye come together during development.

WHO Child Growth Charts

The gene, GRIP1 (glutamate receptor interacting protein 1) acts as a blueprint, directing proteins at synapses - the specialized contact points between brain cells across which chemical signals flow.

It was identified more than a decade ago by Richard L. Huganir, Ph.D., professor and director of the Solomon H. Snyder Department of Neuroscience at the Johns

Hopkins University School of Medicine, and a Howard Hughes Medical Institute investigator.

The new study tracked two versions of GRIP1 in the genomes of 480 people with autism, and was published March 22 in the Proceedings of the National Academy of Sciences, and lends support to a prevailing theory that autism spectrum disorders (ASD), molecularly speaking, reflect an imbalance between inhibitory and excitatory signaling at synapses.

“The GRIP1 variants we studied are not sufficient to cause autism by themselves, but appear to be contributing factors that can modify the severity of the disease,” says Tao Wang, M.D., Ph.D., assistant professor, McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine. “GRIP1 mutations seem to contribute to social interaction deficits in the patients we studied.”

The Johns Hopkins researchers examined a part of the genomes of 480 patients with autism and compared these with 480 people of similar ethnicity without the disorder. They analyzed about 50 genes known to make proteins involved in a brain-signaling pathway, ultimately focusing their investigation on GRIP1, a protein found at both inhibitory and excitatory synapses, according to Wang.

Initially, looking under a microscope at normal mouse neurons and neurons with a mutant version of GRIP1, the investigators marked the receptor proteins with green fluorescence, added a chemical that promotes their “disappearance” deep inside a cell and timed the rates at which they disappeared — leaving a cell unable to respond to signals from other cells. They also timed the reemergence of the protein back to the cell surface. With the GRIP1 mutant neurons, the receptors recycled to the surface twice as fast as in the normal neurons.

“If the receptors are recycling faster, the number of receptors on the surface is greater, so the cells are more sensitive to glutamate,” Huganir explains. “The quicker the recycling, the more receptors on the surface and the stronger the excitatory transmission.”

Even if just the excitatory synapses are affected, and the inhibitory ones don’t change, that alone affects the relative balance of signaling, Huganir says.

Next, using 10 mice genetically engineered to lack both normal and mutant GRIP proteins, researchers watched what happened when each animal was put into a box where it could choose between spending time with a mouse it hadn’t encountered before, or an inanimate object. They compared the behaviors of these mice with 10 normal mice put into the same social situation. Mice lacking both GRIP1 and GRIP2 spent twice as much time as wild-type (normal) mice interacting with other mice as they did with inanimate objects.

“These results support a role for GRIP1 in social behavior and implicate its variants in modulating autistic behavior,” says Wang.

Finally, the team looked at the behavioral analyses of individuals in two families, each with two autistic brothers, and correlated their scores on standard diagnostic tests that assessed social interaction with their genotypes for GRIP1 variants.

In one family, the brother with two copies of the GRIP1 mutant variety scored lower on social interaction tests than his brother who had only one copy of the GRIP1 variant. The boys’ mother, although not diagnosed as autistic, had a history of restricted interests, poor eye contact and repetitive behavior. Tests showed she also carried one copy of the variant.

In a second family, the autistic brother with one copy of the GRIP1 variant had lower social interaction scores than his autistic sibling without a GRIP1 variant.

Because the GRIP1 gene resides in synapses where other genes also implicated in autism have been found, this location is potentially important in terms of clinical relevance, says Huganir. The team plans to sequence hundreds more synaptic proteins in autistic patients to look for mutations and then follow up with functional analyses.

This study was supported in part by research grants from Autism Speaks Foundation and the National Institute of Child Health and Human Development.

Authors on the paper from Johns Hopkins, in addition to Huganir and Wang, are Rebeca Mejias, Abby Adamczyk, Victor Anggono, Tejasvi Niranjan, Gareth M. Thomas, Kamal Sharma, M. Daniele Fallin, Walter E. Kaufmann, Mikhail Pletnikov and David Valle.

Cindy Skinner, Charles E. Schwartz and Roger Stevenson, all of the Greenwood Genetic Center, are also authors on the paper.