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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 Sept 16, 2014

Normal muscle (left) and muscle from Muscular Dystrophy patient (right)

 






WHO Child Growth Charts

 

 

 

Key to making new muscles

Researchers have developed a new technique to promote tissue repair in damaged muscles. The technique also creates a pool of muscle stem cells to support multiple rounds of muscle repair.

The study, published on September 7 in Nature Medicine, provides promise for a new therapeutic approach to treating the millions of people suffering from muscle diseases, including those with muscular dystrophies and muscle wasting associated with cancer and aging.


There are two important processes that need to happen to maintain skeletal-muscle health.

First, when muscle is damaged by injury or degenerative disease such as muscular dystrophy, muscle stem cells—or satellite cells—need to differentiate into mature muscle cells to repair injured muscles.

Second, a pool of satellite cells needs to be replenished so there is a supply to repair muscle in case of future injuries.


In the case of muscular dystrophy, the chronic cycles of muscle regeneration and degeneration involving satellite-cell activation exhausts the muscle stem-cell pool to the point of no return.


“Our study found that by introducing an inhibitor of the STAT3 protein in repeated cycles, we could alternately replenish the pool of satellite cells and promote their differentiation into muscle fibers.

“Our results are important because the process works in mice and in human muscle cells.”

Alessandra Sacco PhD, assistant professor, Development, Aging, and Regeneration Program, Sanford-Burnham Medical Research Institute.


“Our next step is to see how long we can extend the cycling pattern, and test some of the STAT3 inhibitors currently in clinical trials for other indications such as cancer, as this could accelerate testing in humans,” added Sacco.

“These findings are very encouraging. Currently, there is no cure to stop or reverse any form of muscle-wasting disorders—only medication and therapy that can slow the process,”
said Vittorio Sartorelli, M.D., chief of the Laboratory of Muscle Stem Cells and Gene Regulation and deputy scientific director at the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS).

“A treatment approach consisting of cyclic bursts of STAT3 inhibitors could potentially restore muscle mass and function in patients, and this would be a very significant breakthrough.”

STAT3 (signal transducer and activator of transcription 3) is a protein that activates the transcription of genes in response to IL-6, a signaling protein released by cells in response to injury and inflammation. Prior to the study, scientists knew that STAT3 played a complex role in skeletal muscle, promoting tissue repair in some instances and hindering it in others. But the precise mechanism of how STAT3 worked was a mystery.

The research team first used normally aged mice and mice models with a form of muscular dystrophy that resembles the human disease, to see what would happen if they were given a drug to inhibit STAT3. They found that the STAT3 inhibitor initially promoted satellite-cell replication, followed by differentiation of the satellite cells into muscle fibers.

When they injected the STAT3 inhibitor every seven days for 28 days, they found an overall improvement in skeletal-muscle repair, and an increase in the size of muscle fibers.


“We were pleased to find that we achieved similar results when we performed the experiments in human muscle cells.

“We have discovered that by timing the inhibition of STAT3—like an “on/off” light switch—we can transiently expand the satellite-cell population followed by their differentiation into mature muscle cells.”

Alessandra Sacco PhD


Abstract
The progressive loss of muscle regenerative capacity with age or disease results in part from a decline in the number and function of satellite cells, the direct cellular contributors to muscle repair1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11. However, little is known about the molecular effectors underlying satellite cell impairment and depletion. Elevated levels of inflammatory cytokines, including interleukin-6 (IL-6), are associated with both age-related and muscle-wasting conditions12, 13, 14, 15. The levels of STAT3, a downstream effector of IL-6, are also elevated with muscle wasting16, 17, and STAT3 has been implicated in the regulation of self-renewal and stem cell fate in several tissues18, 19, 20, 21. Here we show that IL-6–activated Stat3 signaling regulates satellite cell behavior, promoting myogenic lineage progression through myogenic differentiation 1 (Myod1) regulation. Conditional ablation of Stat3 in Pax7-expressing satellite cells resulted in their increased expansion during regeneration, but compromised myogenic differentiation prevented the contribution of these cells to regenerating myofibers. In contrast, transient Stat3 inhibition promoted satellite cell expansion and enhanced tissue repair in both aged and dystrophic muscle. The effects of STAT3 inhibition on cell fate and proliferation were conserved in human myoblasts. The results of this study indicate that pharmacological manipulation of STAT3 activity can be used to counteract the functional exhaustion of satellite cells in pathological conditions, thereby maintaining the endogenous regenerative response and ameliorating muscle-wasting diseases.

See more at: http://beaker.sanfordburnham.org/2014/09/researchers-discover-a-key-to-making-new-muscles/#sthash.KAD6f7TL.dpuf

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