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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 Nov 19, 2013

 

Inhibition of myostatin (MSTN) and activin signalling.
Image Credit: Lee and Glass Skeletal Muscle 2011 1:2 doi:10.1186/2044-5040-1-2.







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New pathway to genetic muscular diseases

Scientists find key gene that activates muscle growth to help improve treatment.

For decades, scientists have searched for treatments for myopathies — genetic muscular diseases such as muscular dystrophy and ALS, or 'Lou Gehrig's disease.'

Now, an interdisciplinary team of researchers from Arizona State, Stanford University and the University of Arizona, has discovered a new avenue to search for treatment possibilities.

Their findings are featured in an article in this week's early online edition of the journal Proceedings of the National Academy of Sciences (PNAS).


Under healthy circumstances, individual muscles grow or atrophy based on the demands placed on them.

However, in cases of trauma or myopathies, acute muscle loss requires a rapid increase in muscle growth. Such rapid increases are controlled through the activation of an adult stem cell population known as satellite cells.

Researchers believe understanding this process is a necessary step toward developing effective therapies for muscle repair.


Jeanne Wilson-Rawls, associate professor in the School of Life Sciences, and her colleagues have examined what role Numb — a gene known to regulate the degradation of proteins —plays in promoting muscle growth.

"Based on the proteins it targets, we believed that Numb sat at the 'decision point' where satellite cells either retained their stemness or became muscle fibers," said Wilson-Rawls. "Now we know that in mice, where the Numb gene was mutated, there was another role for the gene."


The researchers found that the gene 'Numb' suppressed Myostatin, a gene that limits muscle growth and can cause muscle atrophy.


"This makes the gene an ideal target for developing drugs aimed at the therapeutic treatments of muscle loss," added Wilson-Rawls. "Our finding demonstrates the linked nature of the two opposing processes of growth and atrophy and opens new avenues to pursue treatments of muscle diseases," said Wilson-Rawls.

"We also need to consider parallel efforts to suppress the atrophy signaling pathways, while promoting muscle growth in patients with muscular dystrophy," said Alan Rawls, associate professor with the School of Life Sciences and co-author of the paper.

Significance
This study discloses a role for Numb in the activation and proliferation of adult muscle satellite cells and a unique function in the regulation of the muscle mass determinant Myostatin. Using two different genetic approaches to ablate Numb, one that ablated Numb in the myogenic lineage developmentally leading to reduced muscle mass. We determined that, in Numb-deficient muscle, regeneration was impaired, there was reduced stem cell proliferation, and there was an up-regulation of Myostatin. Overexpression of Numb suppressed Myostatin expression, and Myostatin-specific siRNA rescued the proliferation defect. These studies increase our knowledge of the signaling pathways involved in stem cell function and raise the possibility of regulating the Numb/Myostatin balance as a therapeutic approach to enhance muscle regeneration.

Abstract
The adaptor protein Numb has been implicated in the switch between cell proliferation and differentiation made by satellite cells during muscle repair. Using two genetic approaches to ablate Numb, we determined that, in its absence, muscle regeneration in response to injury was impaired. Single myofiber cultures demonstrated a lack of satellite cell proliferation in the absence of Numb, and the proliferation defect was confirmed in satellite cell cultures. Quantitative RT-PCR from Numb-deficient satellite cells demonstrated highly up-regulated expression of p21 and Myostatin, both inhibitors of myoblast proliferation. Transfection with Myostatin-specific siRNA rescued the proliferation defect of Numb-deficient satellite cells. Furthermore, overexpression of Numb in satellite cells inhibited Myostatin expression. These data indicate a unique function for Numb during the initial activation and proliferation of satellite cells in response to muscle injury.

myogenesis stem cell skeletal muscle conditional mutation
Footnotes
1R.M.G. and S.B. contributed equally to this work.

2To whom correspondence may be addressed. E-mail: Jeanne.Wilson-Rawls@asu.edu or rando@stanford.edu.
Author contributions: S.B., R.E.A., A.R., T.A.R., and J.W.-R. designed research; R.M.G., S.B., B.J.B., E.R., A.K.M., and J.W.-R. performed research; R.M.G., S.B., R.E.A., A.R., T.A.R., and J.W.-R. analyzed data; and R.M.G., S.B., A.R., T.A.R., and J.W.-R. wrote the paper.

The authors declare no conflict of interest.

*This Direct Submission article had a prearranged editor.

This article contains supporting information online at www.pnas.org/lookup/suppl/doi:10.1073/pnas.1311628110/-/DCSupplemental.

Author Affiliations
Edited* by Eric N. Olson, University of Texas Southwestern Medical Center, Dallas, TX, and approved September 30, 2013 (received for review June 21, 2013)


In addition to Wilson-Rawls and Rawls, the research team included ASU's Rajani George, Brian Beres, Erik Rogers and Amanda Mulia; Stanford's Stefano Biressi, and Thomas A. Rando; and University of Arizona's Ron Allen. The research was funded by grants from the Muscular Dystrophy Association; Glenn Foundation for Medical Research; National Institutes of Health Director's Pioneer Award; the Department of Veterans Affairs; and American Heart Association.

The School of Life Sciences is an academic unit of ASU's College of Liberal Arts and Sciences.