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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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April 22, 2011--------News Archive

Placental Seratonin Critical For Brain Development
For the first time, the human placenta is found to synthesize serotonin - critical to brain development, in a process that could be affected by the mother's nutrition.

Plant Hormone Reveals Molecule Critical To Embryo
The mechanism regulating embryonic development in plants displays similarities to a signalling pathway in embryonic stem cells in mammals.


April 21, 2011--------News Archive

Insecticide Linked to Decrease In Cognitive Function
Columbia Center for Children's Environmental Health at the Mailman School of Public Health report evidence of a link between prenatal exposure to the insecticide chlorpyrifos and deficits in IQ and working memory by age seven.

The ‘Core Pathway’ of Aging
Scientists find root molecular path in the declining aging cell.

April 20, 2011--------News Archive

'Thirdhand Smoke' Poses Danger to Unborn Lungs
Stepping outside to smoke a cigarette may not be enough to protect the lungs and life of a pregnant woman's unborn child.

A Way To Predict Premature Birth?
A new study suggests that more than 80 percent of pre-term births can be spotted in advance with a blood test taken during the second trimester of a pregnancy.


April 19, 2011--------News Archive

Ovarian Cancer May Originate in Fallopian Tube
High-grade serous ovarian cancer is thought by many scientists to often be a fallopian tube malignancy masquerading as an ovarian one.

Parents Like Genetic Testing for Their Kids
Parents offered genetic testing to predict their risks of common, adult-onset health conditions say they would also test their children.


April 18, 2011--------News Archive

Interventions Don't Always Net Healthy Newborn
High rates of induction, primary C-Section, do not always improve infant outcomes in low-risk women at community hospitals.

New Approach to Treating MLL Leukemia In Babies
A Loyola University Health System study points to a promising new approach to treating an aggressive and usually fatal leukemia in babies.

WHO Child Growth Charts

Scientists at the Harvard-affiliated Dana-Farber Cancer Institute say they have identified the root molecular cause of a variety of ills brought on by advanced age, including waning energy, failure of the heart and other organs, and metabolic disorders such as diabetes.

“What we have found is the core pathway of aging connecting several age-related biological processes previously viewed as independent of each other,” said Ronald A. DePinho, senior author of a report posted online by the journal Nature. The first author, Ergun Sahin, is a member of the DePinho Lab and an instructor in medicine at Harvard Medical School (HMS).

DePinho, who is the director of Dana-Farber’s Belfer Institute for Applied Cancer Science and also a professor of medicine at HMS, said that although the studies were conducted in mice, “The findings bear strong relevance to human aging, as this core pathway can be directly linked to virtually all known genes involved in aging, as well as current targeted therapies designed to mitigate the toll of aging on health.”

The scientists found that the basic cause of age-related health decline is malfunctioning telomeres - the end caps on cells’ chromosomes that protect them against DNA damage. As cells reach their predetermined limit of times that they can divide, the telomeres become shortened and frayed, making the chromosomal ends vulnerable to increased rates of unrepaired DNA damage.

Faced with this increasing reservoir of injured DNA, cells activate a gene, p53, that sounds an alarm and shuts down the cells’ normal growth and division cycle, ordering them to rest until the damage can be repaired or, if not, to self-destruct.

Scientists previously had blamed this emergency shutdown and cell death for age-related deterioration of organs whose cells divide rapidly and are rejuvenated by reserves of adult stem cells. Such tissues include skin, intestinal lining, and blood cells, among others, which generate trillions of new cells each day of life.

However, left unanswered is how cells with less cell division, such as the heart or the liver, sustain equivalent levels of aging. The scientists felt if they could solve this mystery, they might gain new insights into how DNA damage could lead to age-related decline across all organs.

The new findings demonstrate that the telomere dysfunction and activation of p53 also trigger a wave of cellular and tissue degeneration that links telomeres to well-known mechanisms of aging that are not simply related to rapid growth and division. In other words, telomere dysfunction is not just one culprit in the declining health of advanced age. It’s the kingpin, according to DePinho and his colleagues.

DePinho published a study in Nature in January 2011 that demonstrated it was possible to reverse the symptoms of extreme aging in mice by increasing their levels of telomerase, the enzyme that maintains the health of the telomeres.

In this new, larger role, the telomere dysfunction also sets off an array of reactions leading to diminished health and longevity. For example, muscles suffer a loss of mitochondria, a cell’s chemical power plant, causing waning vitality and failure of the heart and other organs. Risks of metabolic disorders such as diabetes are increased.

In addition, the process weakens the body’s antioxidant defenses against the damaging molecules known as reactive oxygen species, or “free radicals,” that accumulate with age and exposure to stress. Until now, some researchers had labeled the decline in mitochondria or the buildup of free radicals as the primary causes of age-related ills. The new work integrates these seemingly disparate mechanisms into one unified theory of aging.

Telomere dysfunction causes this wave of metabolic and organ failure, the scientists found, because when the p53 gene is activated, it represses the functions of two master regulators of metabolism, PGC1-alpha and PGC1-beta. This dialing down of the regulators diminishes metabolic processes needed to provide energy and resist stress. In the mouse experiments, the scientists showed that “knocking out” p53 in mice released the brakes on PGC1-alpha and PGC1-beta.

“This is the first study that directly links telomere dysfunction to regulators of the mitochondria and antioxidant defense via p53,” DePinho said. “The discovery of this new pathway of aging integrates a lot of different ideas people have had and gives us a better understanding of the aging process.”

By unifying several major pathways of aging under the umbrella of telomere dysfunction, he said, the findings may yield new targets for therapies. The discoveries also may underlie the relatively sudden and rapid failure of the body leading to the end of life.

“Because telomere dysfunction weakens defenses against damage by free radicals, or reactive oxygen species,” DePinho said, “we think this exposes telomeres to an accelerated rate of damage which cannot be repaired and thereby results in even more organ deterioration. In effect, it sets in motion a death spiral.”

In addition to DePinho and Sahin, the paper’s other authors include faculty members from Dana-Farber, the Belfer Institute for Applied Cancer Science at Dana-Farber; Harvard University; Harvard Medical School; the Boston University School of Medicine; Brigham and Women’s Hospital; the University of Massachusetts, Worcester; and St. Vincent’s Hospital, University of Melbourne, Australia.

The research was funded in part by the National Cancer Institute and the Robert A. and Renee E. Belfer Foundation.

Orginal article: http://news.harvard.edu/gazette/story/2011/02/the-‘core-pathway’-of-aging/