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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 Feb 19, 2015

Obese women often require access to fertility treatments. Previous studies have
shown that this difficulty to conceive is partially due to damage to their eggs.

 






 

 

Reversing effects of obesity on female fertility

Scientists were able to increase the fertility of obese mice by reversing some of the obesity-induced changes made to their eggs. This suggests therapeutic approaches could be developed to help overweight women conceive.

The research is published in the scientific journal Development by scientists at the University of Adelaide, Monash University and the Baker IDI Heart and Diabetes Institute, Melbourne, Australia.

Obese women often require access to fertility treatments. Previous studies have shown that this difficulty to conceive is partially due to damage to their eggs.


Cell machinery for folding proteins is negatively affected by overnutrition, leading to various effects downstream. The team led by Rebecca Robker, University of Adelaide, reasoned it might be possible to improve the viability of a woman's eggs by inhibiting these downstream effects.


"Research into how obesity affects other tissues, such as liver and brain, has revealed that a very specific stress response is often involved. We also found that egg cells of both obese mice and obese women are similarly affected by this stress response. Once we identified the type of stress that occurred, we used known agents to alleviate that stress. We were particularly interested in one agent already on trial in diabetic humans to address stress responses," said Dr Rebecca L. Robker, associate professor, Obstetrics and Gynaecology, University of  Adelaide, Australia.


Scientists injected obese mice with compounds that can inhibit the molecular paths involved in egg damage. Eggs were then removed from the obese mice, fertilized and transplanted into surrogate mice mothers. Results showed improvement in the number of viable embryos.


"Similar to what our colleagues in diabetes research had found in muscle, the new agents very potently alleviated the stress in eggs," explained Dr Robker.


"Because eggs provide the building blocks for making an embryo, reversing cellular damage in eggs not only prevents damage to that cell but prevents the damage from being perpetuated into the next generation."

Rebecca L. Robker, Associate Professor, Obstetrics and Gynaecology, University of  Adelaide, Australia.


These results suggest that a similar strategy could be used in the future to help obese women conceive more easily, by therapeutically reducing the damage to their eggs. "More broadly, the work shows that maternal nutritional signals are contained within the eggs and are modifiable even in the days prior to fertilization. This is more key evidence for the importance of women having good nutrition and health before conceiving," added Dr Robker.

Abstract
Over-nutrition in females causes altered fetal growth during pregnancy and permanently programs the metabolism of offspring; however, the temporal and mechanistic origins of these changes, and whether they are reversible, are unknown. We now show that, in obese female mice, cumulus-oocyte complexes exhibit endoplasmic reticulum (ER) stress, high levels of intracellular lipid, spindle abnormalities and reduced PTX3 extracellular matrix protein production. Ovulated oocytes from obese mice contain normal levels of mitochondrial (mt) DNA but have reduced mitochondrial membrane potential and high levels of autophagy compared with oocytes from lean mice. After in vitro fertilization, the oocytes of obese female mice demonstrate reduced developmental potential and form blastocysts with reduced levels of mtDNA. Blastocysts transferred to normal weight surrogates that were then analyzed at E14.5 showed that oocytes from obese mice gave rise to fetuses that were heavier than controls and had reduced liver and kidney mtDNA content per cell, indicating that maternal obesity before conception had altered the transmission of mitochondria to offspring. Treatment of the obese females with the ER stress inhibitor salubrinal or the chaperone inducer BGP-15 before ovulation increased the amount of the mitochondrial replication factors TFAM and DRP1, and mtDNA content in oocytes. Salubrinal and BGP-15 also completely restored oocyte quality, embryo development and the mtDNA content of fetal tissue to levels equivalent to those derived from lean mice. These results demonstrate that obesity before conception imparts a legacy of mitochondrial loss in offspring that is caused by ER stress and is reversible during the final stages of oocyte development and maturation.

Authors:
Wu, L. L., Russell, D. L., Wong, S. L., Chen, M., Tsai, T., St John, J. C., Norman, R. J., Febbraio, M. A., Carroll, J. and Robker, R. L. (2015).

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