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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.

WHO International Clinical Trials Registry Platform

The World Health Organization (WHO) has created a new Web site to help researchers, doctors and
patients obtain reliable information on high-quality clinical trials. Now you can go to one website and search all registers to identify clinical trial research underway around the world!




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Disclaimer: The Visible Embryo web site is provided for your general information only. The information contained on this site should not be treated as a substitute for medical, legal or other professional advice. Neither is The Visible Embryo responsible or liable for the contents of any websites of third parties which are listed on this site.
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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 May 30, 2014


Sox9 OFF Image credit:
The Genetics of Sex Determination: Rethinking Concepts and Theories
Stanford University


WHO Child Growth Charts




Egg and sperm require lifelong protection

The way the sex of an organism is determined may require lifelong maintenance, as retinoic acid signals can reverse a male germ cell to a female germ cell.

Previous work at the University of Minnesota's Department of Genetics, Cell Biology, and Development found sex determination is not permanent. According to a study published in the journal Developmental Cell, sex-specific factors must perform lifelong work to maintain sexual determination and protect against reprogramming cells from one sex to the other.

Using a mouse model, researchers found the sex of gonadal cells – those cells in the ovaries or testes – require maintenance throughout life. Loss of a single transcription factor can result in the transformation of male cells into female cells.

"DMRT1 [1] in the testis and FOXL2 [2] in the ovary have been identified as key factors responsible for maintaining sexual differentiation. What we asked in this study was how the cells maintain sexual differentiation and why their sex determination requires continuous protection," said David Zarkower, Ph.D., principal author and director of the Developmental Biology Center at the University of Minnesota.

Zarkower's research team took a close look at DMRT1 — a human protein encoded by the DMRT1 gene located at the end of the 9th chromosome. Loss of the DMRT1 gene is associated with incomplete germ cell development leading to infertility, abnormal testicular formation, and/or feminization of that individual.

Research determined DMRT1 partners with the male fetal sex gene - Sox9 - to maintain male sexual determination after birth in a mouse. Part of that work includes turning off (silencing) genes normally involved in female fetal sex determination. This discovery indicates that prenatal sex determination is related to maintenance of lifelong sex determination.

Another notable discovery is DMRT1's ability to limit retinoic acid (RA) signals, therefore preventing RA from activating genes normally involved in female sex determination and female organ development.

"While RA [retinoic acid] signaling between cells is absolutely required for sperm production and male fertility, we found that if DMRT1 is not there to guardian maleness, RA can potentially activate genes and drive male-to-female differentiation.

"This shows cell signaling can transform the identities of the very cells that use it from being male to female. We think other cell types may also require mechanisms allowing them to use critical signaling molecules without becoming reprogrammed."

David Zarkower, Ph.D., principal author, Director, Developmental Biology Center, University of Minnesota.

•RA is essential for spermatogenesis but can cause Sertoli cell transdifferentiation
•DMRT1 blocks RA signaling from activating female gonadal genes
•DMRT1 permits cell signaling while protecting from cell fate reprogramming
•Related gene networks control ovary development and transdifferentiation

Mammalian sex determination initiates in the fetal gonad with specification of bipotential precursor cells into male Sertoli cells or female granulosa cells. This choice was long presumed to be irreversible, but genetic analysis in the mouse recently revealed that sexual fates must be maintained throughout life. Somatic cells in the testis or ovary, even in adults, can be induced to transdifferentiate to their opposite-sex equivalents by loss of a single transcription factor, DMRT1 in the testis or FOXL2 in the ovary. Here, we investigate what mechanism DMRT1 prevents from triggering transdifferentiation. We find that DMRT1 blocks testicular retinoic acid (RA) signaling from activating genes normally involved in female sex determination and ovarian development and show that inappropriate activation of these genes can drive sexual transdifferentiation. By preventing activation of potential feminizing genes, DMRT1 allows Sertoli cells to participate in RA signaling, which is essential for reproduction, without being sexually reprogrammed.

Funding for this project was provided by the National Institutes of Health, through grants 5 R01 GM59152 and 1 F32 GM106484, as well as a National Science Foundation pre-doctoral fellowship. Funding was also provided by the Minnesota Medical Foundation and the French Agence Nationale de la Recherche under the program Inestissements d'Avenir labeled ANR-10-LABX-0030-INRT.

The University of Minnesota Medical School, with its two campuses in the Twin Cities and Duluth, is a leading educator of the next generation of physicians. Our graduates and the school's 3,800 faculty physicians and scientists advance patient care, discover biomedical research breakthroughs with more than $180 million in sponsored research annually, and enhance health through world-class patient care for the state of Minnesota and beyond. Visit http://www.med.umn.edu to learn more.
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