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

Hydrodynamics Transform Embryonic Cells Into Us
H
ydrodynamics can contribute to our understanding of how a cluster of embryonic cells can transform into an animal.

New Data on Adenine, a Crucial Building Block of Life
The five nucleic acids making up DNA are some of the few that can withstand ultraviolet light. But adenine turns out to have an extensive range of respones.


August 18, 2011--------News Archive

Pluripotent Stem Cells Developmentally Immature
Researchers have discovered that though similar, induced pluripotent stem cells are similar to embryonic stem cells, but are much more developmentally immature.

Change the Environment, Not the Child
National study finds equal benefit for children with cerebral palsy.


August 17, 2011--------News Archive

Molecular Delivery Serves Gene Therapy Cocktail
Scientists have devised a gene therapy cocktail that has the potential to treat some inherited diseases associated with "misfolded" proteins.

Children of Depressed Mothers Have a Different Brain
MRI scans show their children have an enlarged amygdala.

Discovery Likely to Spur Medicine and Human Health
Scientists have gained new insight into the relationship between two proteins that, out of balance, can prevent normal development of stem cells in the heart.


August 16, 2011--------News Archive

Study Finds New Role for Protein in Hearing
A protein involved in sound sensing in the inner ear may also play a role in transmitting sound information to the brain.

Retinoblastoma Made of Hybrid Cells
Scientists settle a century-old debate about retinoblastoma's beginnings and identify new targets for treating the childhood eye tumor.

Can Oral Care for Babies Prevent Future Cavities?
A recent study confirms the presence of bacteria associated with early childhood caries (ECC) in infant saliva.


August 15, 2011--------News Archive

Slowing the Allergic March
Researchers identify a target that could combat allergies of early childhood.

Gene Clue in the Development of Rheumatoid Arthritis
Findings will help lead to personalized therapies for common, complex illnesses characterized by abnormal immune responses.

Sight Re-Constructs Moving Objects: One by One
Our visual system groups areas of the world with similar characteristics, such as color, shape, or motion.

WHO Child Growth Charts

In a kind of molecular gymnastics, scientists at the University of North Carolina at Chapel Hill School of Medicine have devised a gene therapy cocktail that has the potential to treat some inherited diseases associated with "misfolded" proteins.

Like strings of beads attached end-to-end on a chain, a given sequence of a protein's amino acids usually folds into a characteristic, three-dimensional structure. When "misfolded," a mutant protein's natural biological role may be compromised, sometimes with implications for disease development.

This is one of the challenging research arenas chosen by R. Jude Samulski, PhD, director of the UNC Gene Therapy Center and a professor of pharmacology.

"Among the roughly 5,000 genetic disorders for which the majority of genes have been mapped, there's a subset in which the mutant or misfolded protein by itself can cause disease symptoms – this is in addition to the lack of a normal gene," he says. "And that has added another layer of complication faced by the clinical research community when trying to develop and test new treatment approaches to disorders that result from toxicity associated with cellular accumulation of misfolded proteins."

Among these disorders are cystic fibrosis, Huntington disease, amyotrophic lateral sclerosis (ALS, or Lou Gehrig's disease), and Alzheimer's disease.

The report published in the on-line Early Edition of the Proceedings of the National Academy of Sciences during the week of August 15, 2011, reveals that the Samulski lab has focused a gene therapy approach on a protein deficiency that causes serious lung and liver disease in children and adults: alpha-1 antitrypsin (AAT) deficiency, or alpha-1.

This inherited condition is caused by an abnormal AAT protein that is mainly produced by the liver. An estimated 1 out every 2,500 people in the U.S. have the condition, which is often misdiagnosed as asthma or smoking-related emphysema. (See http://www.alpha1.org/). Scarring of healthy liver tissue (cirrhosis) also may affect infants as well as adults diagnosed with the condition.

Studies suggest that a build-up in liver cells of "misfolded" abnormal AAT is responsible for alpha-1. It is thought that the misfolded protein builds up in the cellular endoplasmic reticulum, the part of the cell that manufactures proteins, and is unable to move out of the liver and into the bloodstream.

"Alpha-1 antitrypsin plays a very important role in the health of the lungs, preventing fluid build-up, protecting against infections," Samulski said. "But in some individuals, the protein mutation they've acquired actually creates additional toxicity in the liver. And so, there's a liver pathology in addition to the lung damage. You have two complications going on, and not just one involving a lack of alpha-1 antitrypsin's protective role in the airway."

In the study, first- and co-corresponding author with Samulski, Chengwen Li, PhD, research assistant professor of pediatrics, conducted a series of gene therapy experiments using a mouse model of alpha-1 disorder. All involved the adeno-associated virus (AAV) vector as a molecular delivery truck.

Samulski, also a member of the UNC Lineberger Comprehensive Cancer Center, has long pioneered methodologies for using viruses to deliver genes effectively and safely to various targets in the body, including the brain, lungs, heart and muscle. As a graduate student at the University of Florida in the early 1980s, his thesis project was understanding and developing AAV as a vector for therapeutic genes. This work eventually led to development of AAV type-2 as a viral vector, which has been used for gene therapy trials in cystic fibrosis, hemophilia, Parkinson's disease, retinal disorders and in several other settings, including the first clinical trial of gene therapy for muscular dystrophy in the United States.

"In essence, we engineered this sophisticated molecular Fed-Ex truck that delivers two payloads simultaneously. One payload involves a genetic approach that disables the mutant protein so that it no longer causes toxicity, and the other payload provides a new gene to replace the protein activity that is missing," Samulski said.

"In this way, Chengwen packaged both strategies into the same vector, a single therapeutic approach that would resolve both problems."

The researchers delivered the gene therapy cocktail via the bloodstream, and targeted it to the liver. Once there, the replacement gene payload and the other payload for disabling the misfolded protein acted independently, and successfully. The authors observed "over 90 percent knockdown of the mutant AAT along with a 13- to 30-fold increase" of therapeutic AAT in the blood circulation.

"I believe we've validated a path to go forward and test this cocktail cassette approach in a clinical trial," Samulski said. "This general approach has potential application to other diseases associated with misfolded proteins, such as Huntington's disease and ALS, among others."

Other UNC coauthors are Pingjie Xiao, Steven James Gray, and Marc Scott Weinberg. The research was supported by grants from the National Institutes of Health.

Original article: http://news.unchealthcare.org/news/2011/august/molecular-delivery-truck-serves-gene-therapy-cocktail