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 in 1993 as a first generation internet teaching tool consolidating human embryology teaching for first year medical students.

Today, The Visible Embryo is linked to over 600 educational institutions and is viewed by more than 1 million visitors each month. The field of early embryology has grown to include the identification of the stem cell as not only critical to organogenesis in the embryo, but equally critical to organ function and repair in the adult human.

The identification and understanding of genetic malfunction, inflammatory responses, and the progression in chronic disease, begins with a grounding in primary cellular and systemic functions manifested in the study of the early embryo.

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Did evolution give us inflammatory disease?

Researchers demonstrate that some variants in our genes that could put a person at risk for inflammatory diseases such as multiple sclerosis, Crohn's disease or rheumatoid arthritis, might have been the result of natural selection over the course of human history.

In new research from Brigham and Women's Hospital (BWH), looked at genome-wide association studies along with protein-protein interaction networks, as well as other data and found 21 places in the genome that bear a 'signature' for both inflammatory disease susceptibility and natural selection.

The results are published in the April 4, 2013 issue of The American Journal of Human Genetics. Towfique Raj, PhD, BWH Department of Neurology, is the lead author on this study, which was led by Philip De Jager, MD, PhD, BWH Department of Neurology, and Barbara Stranger, PhD, University of Chicago

The findings suggest that in the past these 21 variants rose in frequency in the human population to help protect us against viruses, bacteria and other pathogens. But now in our modern world, the environment and exposure to pathogens has changed, and the genetic variants that were originally meant to protect us, now make an autoimmune reaction more likely.

These results are consistent with the hygiene hypothesis in which our cleaner environment is thought to contribute to the increasing prevalence of inflammatory diseases.

Abstract

Genome-wide association studies (GWASs) have identified hundreds of loci harboring genetic variation influencing inflammatory-disease susceptibility in humans.

It has been hypothesized that present day inflammatory diseases may have arisen, in part, due to pleiotropic effects of host resistance to pathogens over the course of human history, with significant selective pressures acting to increase host resistance to pathogens. The extent to which genetic factors underlying inflammatory-disease susceptibility has been influenced by selective processes can now be quantified more comprehensively than previously possible.

To understand the evolutionary forces that have shaped inflammatory-disease susceptibility and to elucidate functional pathways affected by selection, we performed a systems-based analysis to integrate (1) published GWASs for inflammatory diseases, (2) a genome-wide scan for signatures of positive selection in a population of European ancestry, (3) functional genomics data comprised of protein-protein interaction networks, and (4) a genome-wide expression quantitative trait locus (eQTL) mapping study in peripheral blood mononuclear cells (PBMCs).

We demonstrate that loci for inflammatory-disease susceptibility are enriched for genomic signatures of recent positive natural selection, with selected loci forming a highly interconnected protein-protein interaction network. Further, we identify 21 loci for inflammatory-disease susceptibility that display signatures of recent positive selection, of which 13 also show evidence of cis-regulatory effects on genes within the associated locus. Thus, our integrated analyses highlight a set of susceptibility loci that might subserve a shared molecular function and has experienced selective pressure over the course of human history; today, these loci play a key role in influencing susceptibility to multiple different inflammatory diseases, in part through alterations of gene expression in immune cells.

This research was supported by the National Institutes of Health (RC2 GM093080, R01 NS067305 and F32 AG043267).

Full manuscript can be found at: http://www.cell.com/AJHG/abstract/S0002-9297(13)00109-2

Original article: