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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!




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


TUESDAY November 3, 2009---------------------News Archive
The Visible Embryo maintains a searchable database of artcles published since 2007


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Half of US Children Will Use Food Stamps
Nearly half of American children – including 90 percent of black children and 90 percent of children who spend their childhoods in single-parent households – will eat meals paid for by food stamps at some point during childhood, reports a Cornell researcher.

Nearly one-quarter of U.S. children will live in homes that receive food stamps for five or more years. Food stamps are important indicators of poverty and risk of food insecurity, "two of the most detrimental economic conditions affecting a child's health," says Thomas A. Hirschl, Cornell professor of development sociology and co-author of a study published in the November issue of Archives of Pediatrics and Adolescent Medicine (163:11).

The study is based on an analysis of the Panel Study of Income Dynamics, a 32-year study of about 4,800 U.S. households; it builds on the authors' 2004 research that reported that half of all Americans will use food stamps during adulthood.

"Children in poverty are significantly more likely to experience a range of health problems, including low birth weight, lead poisoning, asthma, mental health disorders, delayed immunization, dental problems and accidental death," write Hirschl and co-author Mark R. Rank of Washington University in St. Louis. "Poverty during childhood is also associated with a host of health, economic and social problems later in life."

It also adds some $22 billion per year in additional health care costs, the researchers report.

And the risk of living in homes using food stamps is far from equitably distributed: Ninety percent of children who live with single parents (compared with 37 percent who live in married and other two-parent households), 90 percent of black children (compared with 37 percent of white children) and 62 percent of those whose head of household did not graduate from high school (compared with 31 percent where the head has more than 12 years of school) "encounter spells of food stamp use," the authors find.

Putting those risk factors together, the researchers found that 97 percent of black children living in non-married households where the household head has less than 12 years of education will have received food stamps, compared with 21 percent of white children living in married households whose head of household has 12 or more years of education.

"The situation is likely bad for children," says Hirschl, "because families eligible for food stamps who participate tend to be worse off nutritionally than eligible families who don't participate." Only about 60 percent of families eligible for food stamps actually participate, he said, because of the stigma associated with government help. Although the sample used is representative of the U.S. populations, it does not reflect the immigrant population.


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Slimming Gene Regulates Body Fat
Pregnant women experiencing depression and stress had higher levels of inflammatory markers in their blood than did pregnant women with low depression and stress levels.
Genetic defect inhibits fruit flies from being able to store fat - are there parallels to humans?

Scientists at the University of Bonn have discovered a previously unknown fruit fly gene that controls the metabolism of fat. Larvae in which this gene is defective lose their entire fat reserves. Therefore the researchers called the gene 'schlank' (German for 'slim'). Mammals carry a group of genes that are structurally very similar to 'schlank'. They possibly take on a similar function in the energy metabolism. The scientists therefore have hopes in new medicines with which obesity could be fought. Their research bas been published in 'The EMBO Journal' (doi: 10.1038/emboj.2009.305).

If scientists decipher the function of a gene, they are allowed to name it. With the fruit fly Drosophila there is a rather paradox convention. The names always indicate what the fly looks like if the respective gene is defective. That is also the case with the schlank gene. If it is unimpaired the fly larva can build up fat reserves. It becomes fat. 'Larvae with a mutation of schlank, however, remain slim,' Professor Michael Hoch from the University of Bonn explains. 'In extreme cases the defect can even lead to death.'

Together with Dr. Reinhard Bauer and other employees the development biologist has explored what exactly 'schlank' does. According to their research the gene contains the instructions of what is known as ceramide synthase. Ceramides serve as raw materials for the gauzy membranes that enclose all of the cells in the body. Moreover, schlank also has a regulatory function. It promotes lipid synthesis and at the same time inhibits the mobilisation of fat from the fat reserves.

Mouse Gene Saves Fly Larvae
There is a chance that this is not only the case in fruit flies. Humans also produce ceramide synthases however not just one as Drosophila does but rather as many as six different ones. For this purpose humans rely on a group of genes so-called Lass genes. Ceramide synthases are extremely important for animals. Mutations in the corresponding genes lead to severe metabolic disorders and to malfunctions of organ systems. That is why our Lass genes look surprisingly similar to the schlank gene of fruit flies.

This resemblance is so striking that Lass genes from mice can partially compensate for the defect schlank gene in mutant flies. 'We introduced a mouse Lass gene in mutant Drosophila larvae,' Michael Hoch says. 'Normally the larvae died immediately after hatching. Thanks to the Lass gene they resumed building up body fat and survived until the next development stage.'

Up to now, the Lass genes of mammals have not been connected with the regulation of the lipid metabolism. 'But due to the strong parallels with schlank we think such a function is very probable,' Professor Hoch presumes. 'If this is the case they would be a promising approach for new medications for obesity.'

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