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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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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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August 26, 2011--------News Archive


A Question of Gene Silencing
Researchers have found a new way to selectively turn off genes that don't code for proteins which will help identify each gene's function, and perhaps identify cancers.

Scented Products Emit Hazardous Chemicals
Chemical sleuthing has uncovered that fragrance in consumer laundry products contains hazardous chemicals. Some which are even carcinogens.

August 25, 2011--------News Archive

Human Stem Cells Made From Amnionic Fluid
Human epithelial cells transplanted from human amnionic fluid reduce pulmonary fibrosis, and even stimulate lung regeneration in mice.

Scale Models Rule
Body patterns stay in sync with size as an embryo grows into an adult. Observed in the wing of the fruit fly, these patterns most likely exist in all organisms.

Chronic Disease Caused by Fat Cells?
Fat cells in people with metabolic syndrome have biomarkers for insulin resistance and chronic inflammation, conditions in diabetes and cardiovascular disease.

August 24, 2011--------News Archive

In the Early Life of An Embryo, Chaos Lurks
A calcium wave sparks embryonic cell division, doubling as a synchronizer of all further cell division in order for chaos to be reined in and ordered growth to persist.

Smoking Affects Fetal Infant Brain Worse than Feared
Researchers pin-point smoking specifically and find a 40% increase in damage to the fetus.

August 23, 2011--------News Archive

Boys Reach Sexual Maturity Younger and Younger
The phase between being physically but not socially adult is getting longer.

When Cell Fishing Games Go Wrong
Trial-and-error "fishing" for DNA in the nucleus may be the most important cause of female infertility.

A Sticky Egg Captures The Sperm
A sugar molecule makes the outer coat of a human egg 'sticky', which is vital for enabling the sperm and egg to bind together.

At Last, Reason Why Stress Damages DNA
Adreneline produced by chronic stress, degrades the protein p53 which is considered a tumor suppressor protein and "guardian of the genome."

August 22, 2011--------News Archive

The Basis for Head and Sex Organ Deformities
Data reveals a possible therapy using vitamin B2 to reverse enzyme defects is specific areas of fetal development.

Mother’s BMI Linked to Fatter Babies
Babies of mothers with a higher pre-pregnancy body mass index (BMI) are fatter and have more fat in their liver, a study has found.

Celiac Disease May Explain Some Women's Infertility
A recent study found increased rates of celiac disease in women who present with unexplained infertility.

WHO Child Growth Charts

For years, researchers have published papers that associate chronic stress with chromosomal damage.

Now researchers at Duke University Medical Center have discovered a mechanism that helps to explain the stress response in terms of DNA damage.

"We believe this paper is the first to propose a specific mechanism through which a hallmark of chronic stress, elevated adrenaline, could eventually cause DNA damage that is detectable," said senior author Robert J. Lefkowitz, M.D., James B. Duke Professor of Medicine and Biochemistry and a Howard Hughes Medical Institute (HHMI) investigator at Duke University Medical Center.

The paper was published in the Aug. 21 online issue of Nature.

In the study, mice were infused with an adrenaline-like compound that works through a receptor called the beta adrenergic receptor that Lefkowitz has studied for many years. The scientists found that this model of chronic stress triggered certain biological pathways that ultimately resulted in accumulation of DNA damage.

"This could give us a plausible explanation of how chronic stress may lead to a variety of human conditions and disorders, which range from merely cosmetic, like graying hair, to life-threatening disorders like malignancies," Lefkowitz said.

P53 is a tumor suppressor protein and is considered a "guardian of the genome" – one that prevents genomic abnormalities.

"The study showed that chronic stress leads to prolonged lowering of p53 levels," said Makoto Hara, Ph.D., a postdoctoral fellow in the Lefkowitz laboratory. "We hypothesize that this is the reason for the chromosomal irregularities we found in these chronically stressed mice."

Lefkowitz earlier had proved the existence of isolated, and characterized the G-protein-coupled receptors (GPCRs) such as the beta adrenergic receptor. These receptors, which are located on the surface of the membranes that surround cells, are the targets of almost half of the drugs on the market today, including beta blockers for heart disease, antihistamines and ulcer medications.

Now he is continuing studies along another pathway,stemming from the GPCRs, that was discovered in his lab, which is known as the beta-arrestin pathway. At first, the theory was that beta-arrestin proteins turned off or desensitized the G-protein pathways, but evidence is accumulating that these proteins are also responsible for causing certain biochemical activities in their own right.

In the current study, the scientists found a molecular mechanism through which adrenaline-like compounds acted through both G-protein and the beta-arrestin pathways to trigger DNA damage.

The Nature publication showed that the infusion of an adrenaline-like compound for four weeks in the mice caused degradation of p53, which was present in lower levels over time.

The study also showed that the DNA damage was prevented in mice lacking beta-arrestin 1. Loss of beta-arrestin 1 stabilized cellular levels of p53 both in the thymus, an organ that strongly responds to acute or chronic stress, and in the testes, where paternal stress might affect an offspring's genome.

Future studies planned by the Lefkowitz laboratory include studying mice that are placed under stress (restrained), thus creating their own adrenaline or stress reaction to learn whether the physical reactions of stress, rather than an influx of adrenaline in the lab as was done in the current study, also leads to accumulation of DNA damage.

Other authors include Jeffrey J. Kovacs, Erin J. Whalen, Sudarshan Rajagopal, Ryan T. Strachan, Seungkirl Ahn, Barbara Williams, Christopher M. Lam, Kunhong Xiao, and Sudha K. Shenoy, all of the Duke Department of Medicine; Aaron J. Towers and Simon G. Gregory of the Department of Medicine and the Center for Human Genetics at Duke; and Wayne Grant and Derek R. Duckett of the Translational Research Institute, The Scripps Research Institute, Jupiter, Fla..

The study was supported by the Howard Hughes Medical Institute.

Original article:
http://www.eurekalert.org/pub_releases/2011-08/dumc-dmn081911.php