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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.


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Pregnancy Timeline by SemestersFemale Reproductive SystemFertilizationThe Appearance of SomitesFirst TrimesterSecond TrimesterThird TrimesterFetal 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 HemispheresEnd of Embryonic PeriodEnd of Embryonic PeriodFirst Thin Layer of Skin AppearsThird TrimesterDevelopmental Timeline
Click weeks 0 - 40 and follow fetal growth
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November 25, 2011--------News Archive

Women at Low Risk Can Safely Choose Birth Style
Women with low risk pregnancies should be able to choose where they give birth, concludes The Birthplace in England national prospective cohort study.

Finger (Mal)formation Function of Desert DNA
Explaining the diversity of leg shapes in the animal kingdom and hereditary defects in finger formation.

Key Molecular Switch for Telomere Extension Found
For the first time, a key target for DNA damage is found that must be chemically modified to enable an enzyme thought to play a key role in cancer and aging.

New Role for Gene in Maintaining Steady Weight
Findings may help combat obesity and diabetes.

November 24, 2011--------News Archive

New Facts About Stuttering
Some forms of persistent stuttering are caused by mutations in a gene governing the recycling of old cell parts - not speech.

Preventing Preemie Brain Injury
New advances could eventually help reduce the number of premature babies who develop cerebral palsy, epilepsy or behavioral disorders such as ADHD.

Short Stature May Be Due To a 'Shortage' of Genes
Research suggests that uncommon genetic deletions are associated with short stature.

November 23, 2011--------News Archive

Intestinal Disorder, Preemies and AB Blood Type
Preemies with the AB blood type who develop NEC are nearly three times as likely to die from it as preemies with other blood types.

Babies Fed Fish Before 9 Months Wheeze Less
But pre-natal pain and fever antibiotics taken by mom in pregnancy, or by the baby in the first-week of life, increase risk of "pre-school wheeze."

Physical Activity Improves Quality Of Sleep
People sleep significantly better and feel more alert during the day if they get at least 150 minutes of exercise a week, a new study concludes.

November 22, 2011--------News Archive

Critical Molecules For Hearing/Balance Discovered
Gene-therapy trial will attempt to restore hearing in deaf mice.

Tweaking One Gene Makes Muscles Twice As Strong
Salk scientists and their collaborators find new avenue for treating muscle degeneration in people who can't exercise.

Fruit Fly Intestine Holds Secret to Fountain of Youth
Long-lived fruit flies offer Salk scientists clues to slowing human aging and fighting disease.

November 21, 2011--------News Archive

Nerve Cells Key to making Sense of All of Our Senses
Scientists have unraveled how the brain manages to process complex, rapidly changing, and often conflicting sensory signals and make sense of our world.

Discovery of A New Muscle Repair Gene
Thanks to next-generation DNA sequencing, an international team of scientists have discovered more about the function of muscle stem cells.

Immune System Governs Stem Cell Regeneration
Controlling a stem cell transplant recipient’s immune response may be major key to successful bone regeneration.

WHO Child Growth Charts

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Researchers at Washington University School of Medicine in St. Louis have obtained new evidence that at least some persistent stuttering is caused by mutations in a gene governing not speech, but a metabolic pathway involved in recycling old cell parts.

Beyond a simple association, the study provides the first evidence that mutations affecting cellular recycling centers called lysosomes actually play a role in causing some people to stutter.

“This was extremely unexpected,” says senior author Stuart A. Kornfeld, MD, the David C. and Betty Farrell Professor of Medicine. “Why would impairment in a lysosomal pathway lead to stuttering? We don’t know the answer to that. Partly because we don’t know very much about the mechanisms of speech, including which neurons in the brain are involved. So we can’t fully explain stuttering, but now we have clues.”

The research is available online in the Journal of Biological Chemistry

Genetic clues to stuttering were first identified in a paper published in the New England Journal of Medicine in February 2010. In it, Dennis Drayna, PhD, a senior investigator with the National Institute on Deafness and Other Communication Disorders and a co-author on the current study, and his colleagues reported results of genetic studies on members of a large Pakistani family, many of whom stutter.

Among most of the stuttering family members, they found mutations in three genes involved in directing proteins to the lysosome. These same mutations were present in many unrelated individuals in Pakistan, North America and Europe who stutter, but not in those with normal speech.

“They found mutations in three genes that encode a pathway for directing newly made lysosomal enzymes to the lysosomes,” Kornfeld says. “And it turned out to be a pathway we discovered years ago. So this is a nice collaboration.”

Until now, one of the three genes, NAGPA, had not been implicated in any human disorder. This is where Kornfeld and Wang-Sik Lee, PhD, research instructor in medicine at Washington University, began their in-depth biochemical investigation of the mutations that Drayna’s group identified.

NAGPA encodes an enzyme responsible for the last step in “addressing” proteins to the lysosome. Drayna’s work identified three separate mutations in NAGPA in individuals who stutter. And according to Lee’s biochemical analysis, all three of the mutations impaired the enzyme, but each did so in a different way. In general, mutations in a gene often cause the resulting protein to be folded into the wrong shape. Cells are very good at recognizing misfolded proteins and destroying them.

In this case, Lee’s biochemical analysis shows that two mutations appear to trap the proteins in the cell’s protein manufacturing center, though some get out before being destroyed.

“It’s not an all-or-nothing thing,” Kornfeld says. “Of the material that does get out, its activity is normal.”

But the third mutation causes a larger folding problem and the protein is destroyed just minutes after being made.

Such findings offer a glimpse at possible future therapies for stuttering. For two of the mutations at least, the problem is not that the protein can’t function, but rather that it can’t get out of the cell’s protein manufacturing center and go to the intracellular site where it acts to direct proteins to lysosomes. If some compound can be found that helps the protein escape, Lee’s work suggests that it would function normally. But Kornfeld cautions that this type of therapy for stuttering is a long way off.

“There are billions of neurons in the brain, and we have very little idea which neurons are involved in speech,” he says. “Our main finding is that these three mutations in NAGPA in people with persistent stuttering all have harmful effects. This is biochemical evidence that these mutations are meaningful, and not just markers of some other genetic change that is the real cause.”

Having described the three harmful mutations in NAGPA, Kornfeld’s group is now performing biochemical analyses on the other two mutated genes Drayna’s group identified: GNPTAB and GNPTG. Drayna and his colleagues estimate that these three mutated genes account for only about 10 percent of people who stutter with a family history. As such, they are continuing the search for additional genes responsible for stuttering.

Lee WS, Kang C, Drayna D, Kornfeld S. Analysis of mannose 6-phosphate uncovering enzyme mutations associated with persistent stuttering. Journal of Biological Chemistry. Nov. 18, 2011.

Kang C, Riazuddin S, Mundorff J, Krasnewich D, Friedman P, Mullikin JC, Drayna D. Mutations in the lysosomal enzyme-targeting pathway and persistent stuttering. The New England Journal of Medicine. February 2010.

This work was supported by grants from the National Institutes of Health (NIH) and from the National Institute on Deafness and Other Communication Disorders, which is a part of the NIH.

Washington University School of Medicine’s 2,100 employed and volunteer faculty physicians also are the medical staff of Barnes-Jewish and St. Louis Children’s hospitals. The School of Medicine is one of the leading medical research, teaching and patient care institutions in the nation, currently ranked fourth in the nation by U.S. News & World Report. Through its affiliations with Barnes-Jewish and St. Louis Children’s hospitals, the School of Medicine is linked to BJC HealthCare.

Original article: http://news.wustl.edu/news/Pages/23026.aspx