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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 Jan 6, 2014

 

Because human embryonic stem cells are different from our own body's cells,
or "allogenic," our immune system will attack these foreign cells.
One way to reduce the body's "allogenic immune response" is to
suppress the immune system with immunosuppressant drugs — or, create
a mouse model of the human immune system to study drug responses.







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Strategy for limiting human stem cell rejection

Biologists at UC San Diego have discovered an effective strategy to prevent the human immune system from rejecting grafts made from human embryonic stem cells, a major problem limiting development of human stem cell therapy.

Their discovery may also help scientists better understand how tumors evade our immune system when they spread through the body.

The achievement is published in a paper in this week's early online edition of Cell Stem Cell, in collaboration with scientists from China. The research was enabled by the development of "humanized" laboratory mice. These mice contain a functional human immune system capable of mounting a vigorous immune rejection of foreign cells derived from human embryonic stem cells.


Because human embryonic stem cells are different from our own body's cells, or are "allogenic," a normally functioning human immune system will attack these foreign cells.

One way to reduce the body's "allogenic immune response" is to suppress the immune system with immunosuppressant drugs.


"For organ transplantation to save patients with terminal diseases [immunosuppressant drugs] have been quite successful. But for stem cell therapies, the long term use of toxic immunosuppressant drugs for chronic diseases like Parkinson's or diabetes, pose serious health problems." says Yang Xu, a professor of biology who headed the team of researchers that included Ananda Goldrath, an associate biology professor at UC San Diego.

Researchers had been looking a long time for a model animal to help them develop safe strategies for implanting allogenic cells made from embryonic stem cells. "The problem was that we only had data from the mouse immune system which is not usually translatable in humans, because human and mouse immune systems are quite different," explains Xu. "What we decided to do was optimize the humanized mouse to carry a functional human immune system."

To do so, biologists grafted into immune deficient laboratory mice, human fetal thymus tissue and hematopoietic stem cells derived from the same donor. "That created in these mice a normally functioning human immune system that effectively rejects cells derived from 'other' human embryonic stem cells," says Xu. With these "humanized" mouse models, the biologists were abe to test a variety of immune suppressing molecules alone or in combination — and discovered one combination that worked perfectly to protect cells derived from human embryonic stem cells from immune rejection.


The working combination of two molecules, CTLA4-lg, (an FDA-approved drug for treating rheumatoid arthritis that suppresses T-cells responsible for immune rejection), and a protein called PD-L1 (known to be important for inducing immune tolerance in tumors), allows allogeneic cells to survive in humanized mice without triggering an immune rejection.


"If we express both molecules in cells derived from human embryonic cells, we can protect these cells from the allogenic immune rejection," says Xu. "If you have only one such molecule expressed, there is absolutely no impact. We still don't know exactly how these pathways work together to suppress immune rejection, but now we've got an ideal system to study."


Xu and his team believe their discovery — along with the development of the humanized mouse — will also be effective in activating an immune response to tumors. These same two molecules are known to be important in allowing tumors to evade the human immune system.


"You're dealing with the same exact pathways that protect tumors from our immune system," says Xu. "If we can develop strategies to disrupt or silence these pathways in tumors, we might be able to activate immunity to tumors. The humanized mouse system is really a powerful model with which to study human tumor immunity."

Highlights
Optimized BAC-based strategy for high efficiency gene targeting in human ESCs
Generated homozygous mutant human ESCs deficient in ATM or p53
ATM−/− hESCs and their derivatives recapitulate the cellular defects seen in patients
p53 is important for maintaining genomic stability in human ESCs

Summary
Although mouse models have been valuable for studying human disease, the cellular and physiological differences between mouse and human have made it increasingly important to develop more relevant human disease models for mechanistic studies and drug discovery. Human embryonic stem cells (hESCs), which can undergo unlimited self-renewal and retain the potential to differentiate into all cell types, present a possible solution. To improve the efficiency of genetic manipulation of hESCs, we have developed bacterial artificial chromosome (BAC) based approach that enables high efficiency homologous recombination. By sequentially disrupting both alleles of ATM or p53 with BAC targeting vectors, we have established ATM−/− and p53−/− hESCs as models for two major human genetic instability syndromes and used the generated cells to reveal the importance of p53 in maintaining genome stability of hESCs. Our findings suggest that it will be feasible to develop genetically modified hESCs as relevant human disease models.

Other researchers involved in the study, besides Xu and Goldrath, were Zhili Rong, Meiyan Wang, Martin Stradner and Huijuan Kong of UC San Diego; Zheng Hu, Huanfa Yi and Yong-Guang Yang of China's Jilin University; Shengyun Zhu and Xuemei Fu of Shenzhen Children's Hospital in China. The study was financed by grants from the California Institute for Regenerative Medicine, the National Institutes of Health (AI-064569 and AI-045897), the Chinese Ministry of Science and Technology, and the Natural Sciences Foundation of China.