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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 one million visitors each month.

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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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 ON weeks 0 - 40 and follow along every 2 weeks of fetal development
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Home | Pregnancy Timeline | News Alerts |News Archive Dec 27, 2013

 

Small DNA errors, or variants, work together to negatively affect the 1 - 2% of genes
that actually lead to the production of proteins. The cumulative affect of these protein
errors leads to autoimmune diseases including rheumatoid arthritis, Crohn’s
disease, celiac disease, multiple sclerosis, lupus and colitis.







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Common disorders: not the genes, but how controlled

Many rare disorders are caused by gene mutation, like sickle cell anemia. However, the underlying genetic cause of more common conditions – for example, rheumatoid arthritis – has evaded scientists for years.

New research from Case Western Reserve University School of Medicine published in the journal Genome Research finds that six common diseases arise from DNA changes located outside of the genes associated with these diseases.

The study from the laboratory of Peter Scacheri, PhD, shows that multiple DNA changes, or variants, work in concert affecting protein producing genes, and ultimately give rise to autoimmune diseases including rheumatoid arthritis, Crohn’s disease, celiac disease, multiple sclerosis, lupus and colitis. Specifically, for each of these diseases genes were manipulated by small differences in DNA that either increased or decreased protein production.


“We’ve known that rare diseases are due to one change within one gene with major effects. The key take away from this research is that common diseases are due to many small changes in a handful of genes.”

Peter Scacheri, associate professor of genetics and genome sciences, Case Western Reserve University School of Medicine


The human genome includes 3 billion letters of DNA — of which only 1 to 2 percent are useful as blueprints for making proteins — the body’s building blocks. Scacheri’s team is part of group of scientists investigating the remaining 98 percent — the regions between genes — for where, and why, DNA may go awry.


The regions between genes contain thousands of gene switches controlling gene production. This is a new finding.

In some common diseases, it appears the fine-tuning of these switches is incorrect and expression [creation] of key genes is negatively affected.

“This is a paradigm shift for the field with respect to pinpointing the genetic causes of common disease susceptibility.”

Peter Scacheri, PhD


The Scacheri lab is providing a new model for understanding how genetic variation in common, complex diseases such as rheumatoid arthritis and colitis, occurs. The effect of one variant may be of little consequence, but coupled with many variants, manifests in a much greater effect.

“This model may also help explain why genetic studies of these and other common diseases have so far fallen short of providing a satisfactory explanation of the genetic pathways important in the development of these disorders," says Anthony Wynshaw-Boris, MD, PhD, chair of the Department of Genetics and Genome Sciences at Case Western Reserve University School of Medicine and University Hospitals Case Medical Center, and the James H. Jewell MD '34 Professor of Genetics at the School of Medicine.


“This is vital information for creating therapies to target these disorders. For example, if an individual has a gene that is aberrantly high, he or she will need medication to dial it back down.

"Scientists can’t begin to develop a drug to do this without first knowing the gene target and how it can be manipulated to either be increased or decreased."

Olivia Corradin, School of Medicine PhD candidate, lead author of the study.


Now that the Corradin and Scacheri team know the identity of genes affecting six autoimmune diseases and understand how the genes are disrupted, their next step is to help identify therapies to restore these genes to normal levels, so that these diseases can be treated or prevented.

In addition, the researchers hope their discovery can lead to improved diagnostic testing for other common diseases in addition to these six.

Abstract
DNA variants (SNPs) that predispose to common traits often localize within noncoding regulatory elements such as enhancers. Moreover, loci identified by genome-wide association studies (GWAS) often contain multiple SNPs in linkage disequilibrium (LD), any of which may be causal. Thus, determining the effect of these multiple variant SNPs on target transcript levels has been a major challenge. Here, we provide evidence that for six common autoimmune disorders (rheumatoid arthritis, Crohn's disease, celiac disease, multiple sclerosis, lupus, and ulcerative colitis), the GWAS association arises from multiple polymorphisms in LD that map to clusters of enhancer elements active in the same cell type. This finding suggests a “multiple enhancer variant” hypothesis for common traits, where several variants in LD impact multiple enhancers and cooperatively affect gene expression. Using a novel method to delineate enhancer–gene interactions, we show that multiple enhancer variants within a given locus typically target the same gene. Using available data from HapMap and B lymphoblasts as a model system, we provide evidence at numerous loci that multiple enhancer variants cooperatively contribute to altered expression of their gene targets. The effects on target transcript levels tend to be modest and can be either gain- or loss-of-function. Additionally, the genes associated with multiple enhancer variants encode proteins that are often functionally related and enriched in common pathways. Overall, the multiple enhancer variant hypothesis offers a new paradigm by which noncoding variants can confer susceptibility to common traits.

Authors
Olivia Corradin, Alina Saiakhova, Batool Akhtar-Zaidi, Lois Myeroff, Joseph Willis, Richard Cowper-Sal·lari, Mathieu Lupien, Sanford Markowitz and Peter C. Scacheri


This study was supported by grants from the National Institutes of Health: R01CA160356 and 5T32GM008056-29.

About Case Western Reserve University School of Medicine
Founded in 1843, Case Western Reserve University School of Medicine is the largest medical research institution in Ohio and is among the nation's top medical schools for research funding from the National Institutes of Health. The School of Medicine is recognized throughout the international medical community for outstanding achievements in teaching. The School's innovative and pioneering Western Reserve2 curriculum interweaves four themes--research and scholarship, clinical mastery, leadership, and civic professionalism--to prepare students for the practice of evidence-based medicine in the rapidly changing health care environment of the 21st century. Eleven Nobel Laureates have been affiliated with the school.

Annually, the School of Medicine trains more than 800 M.D. and M.D./Ph.D. students and ranks in the top 25 among U.S. research-oriented medical schools as designated by U.S. News & World Report's "Guide to Graduate Education."

The School of Medicine's primary affiliate is University Hospitals Case Medical Center and is additionally affiliated with MetroHealth Medical Center, the Louis Stokes Cleveland Department of Veterans Affairs Medical Center, and the Cleveland Clinic, with which it established the Cleveland Clinic Lerner College of Medicine of Case Western Reserve University in 2002.