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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 SemestersLungs begin to produce surfactantImmune system beginningHead may position into pelvisFull TermPeriod of rapid brain growthWhite fat begins to be madeHead may position into pelvisWhite fat begins to be madeImmune system beginningBrain convolutions beginBrain convolutions beginFetal liver is producing blood cellsSensory 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 Apr 20, 2015

Normal aging causes breast tissue to lose the ability to develop new cells or repair old ones.
Scientists found genetically eliminating TIMP1 and TIMP3 from breast cell tissue expanded
the pool of stem cells — which then remained functional throughout mice lifetimes.

 

 


 

 

Breast cancer and the fountain of youth

The Fountain of Youth has been discovered and it's not in Florida as Ponce de Leon claimed. Instead, it is in the mammary glands of genetically modified mice.

A research team led by Professor Rama Khokha has found that when two factors that control tissue development are removed, you can avoid the impact of aging.

Ttissue is constantly under renovation and "metalloproteinases" are constantly working to demolish as well as reconstruct tissue. "Tissue inhibitors of metalloproteinases" — or TIMPs reign in and direct the metalloproteinases. However, when the metalloproteinases and TIMPs don't communicate well, the result can lead to cancer.

To understand how metalloproteinases and TIMPs interact, medical researchers breed mice with one or more of the four different types of TIMPs genetically removed. Khokha's team examined the different combinations and found that when TIMP1 and TIMP3 were removed, breast tissue stayed young, even in aged mice. The results are presented in Nature Cell Biology.

Normal aging causes tissues to lose their ability to develop new cells or repair old ones as fast as when young. That's because stem cells decline with age. However, the UT team found with TIMP1 and TIMP3 missing, the pool of stem cells expanded and remained functional throughout the lifetime of these mice.

"Normally in mice these pools of stem cells reach their peak at six months, then start to decline. As a result, mammary glands start to degenerate, increasing the risk for breast cancer," explains Rama Khokha. "However, we found that in these particular mice the stem cells remained consistently high when we measured them at every stage." The team also found that despite larger numbers of stem cells, there was no increased risk of cancer. Khokha: "It's generally assumed that the presence of a large number of stem cells can lead to an increased cancer risk. However, these mice had no greater predisposition to cancers." 

"Breast tissue goes through cycles of change in the adult female. New structures appear and regress. It is therefore a good system to explore in order to understand tissue maintenance and epithelial cell turnover - those cells that underlie carcinomas and are in the most frequent types of cancer."

Rama Khokha, Professor Departments of Medical Biophysics and Laboratory Medicine and Pathobiology, senior scientist at the Princess Margaret Cancer Centre, Toronto, Canada.

Abstract
Cancer-associated fibroblasts (CAFs) drive tumour progression, but the emergence of this cell state is poorly understood. A broad spectrum of metalloproteinases, controlled by the Timp gene family, influence the tumour microenvironment in human cancers. Here, we generate quadruple TIMP knockout (TIMPless) fibroblasts to unleash metalloproteinase activity within the tumour-stromal compartment and show that complete Timp loss is sufficient for the acquisition of hallmark CAF functions. Exosomes produced by TIMPless fibroblasts induce cancer cell motility and cancer stem cell markers. The proteome of these exosomes is enriched in extracellular matrix proteins and the metalloproteinase ?ADAM10. Exosomal ?ADAM10 increases aldehyde dehydrogenase expression in breast cancer cells through Notch receptor activation and enhances motility through the GTPase ?RhoA. Moreover, ?ADAM10 knockdown in TIMPless fibroblasts abrogates their CAF function. Importantly, human CAFs secrete ?ADAM10-rich exosomes that promote cell motility and activate ?RhoA and Notch signalling in cancer cells. Thus, Timps suppress cancer stroma where activated-fibroblast-secreted exosomes impact tumour progression.

This work is supported by the Canadian Breast Cancer Foundation and the Canadian Cancer Society Research Institute.

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