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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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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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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 April 15, 2014

 

Abnormally high levels of lipid [energy storage] molecules in the brain can affect the interaction
between two key pathways in prenatal brain development, triggering autism.
Environmental causes also affect levels of these lipids.






WHO Child Growth Charts

 

 

 

Prenatal lipid levels impact autism

Groundbreaking work finds that abnormally high levels of lipid - energy storing - molecules in the brain will affect the prenatal brain, triggering autism. Environmental causes such as exposure to chemicals in some cosmetics and common over-the-counter medication — also change lipid levels.


“We found that the abnormal level of a lipid molecule called Prostaglandin E2 in the brain can affect the function of Wnt proteins. This is important because Wnt proteins affect the course of early embryonic development,”

Dorota Crawford, professor, faculty of health, member of the York Autism Alliance Research Group.


This research is the first evidence for cross-talk between PGE2 and Wnt signalling in neuronal stem cells. The study is published in Cell Communication and Signaling.

Autism is considered to be the primary disorder of brain development with symptoms ranging from mild to severe and including repetitive behaviour, deficits in social interaction, and impaired language.

It is four times more prevalent in boys than in girls and the incidence continues to rise. The US Center for Disease Control and Prevention (CDC) data from 2010 estimates that 1 in 68 children now has autism.


“Using real-time imaging microscopy, we determined that higher levels of PGE2 changes Wnt-dependent behaviour of neural stem cells by increasing cell proliferation. As a result, how the brain is organized and wired is affected.

"Moreover, we found that an elevated level of PGE2 can increase expression of the Wnt-regulated genes — Ctnnb1, Ptgs2, Ccnd1, and Mmp9.

“All of these genes have been previously implicated in various autism studies.”

Christine Wong , lead researcher, York University doctoral student


“Statistics are alarming. Autism is 30 per cent higher than a previous estimate of 1 in 88 children from only two years ago. Perhaps we can no longer attribute this rise to better diagnostic tools or awareness,” notes Crawford. “It’s even more apparent in recent literature that the environment might have an even greater impact on vulnerable genes — particularly in pregnancy.

According to Crawford, genes don’t undergo significant changes in evolution, so even though genetic factors are the main cause — environmental factors such as insufficient dietary supplement with fatty acids, exposures to infections, various chemicals or drugs — can change gene expression and contribute to autism.

Abstract (provisional)
Prostaglandin E2 (PGE2) is a natural lipid-derived molecule that is involved in important physiological functions. Abnormal PGE2 signalling has been associated with pathologies of the nervous system. Previous studies provide evidence for the interaction of PGE2 and canonical Wnt signalling pathways in non-neuronal cells. Since the Wnt pathway is crucial in the development and organization of the brain, the main goal of this study is to determine whether collaboration between these pathways exists in neuronal cell types. We report that PGE2 interacts with canonical Wnt signalling through PKA and PI-3K in neuroectodermal (NE-4C) stem cells. We used time-lapse microscopy to determine that PGE2 increases the final distance from origin, path length travelled, and the average speed of migration in Wnt-activated cells. Furthermore, PGE2 alters distinct cellular phenotypes that are characteristic of Wnt-induced NE-4C cells, which corresponds to the modified splitting behaviour of the cells. We also found that in Wnt-induced cells the level of beta-catenin protein was increased and the expression levels of Wnt-target genes (Ctnnb1, Ptgs2, Ccnd1, Mmp9) was significantly upregulated in response to PGE2 treatment. This confirms that PGE2 activated the canonical Wnt signalling pathway. Furthermore, the upregulated genes have been previously associated with ASD. Our findings show, for the first time, evidence for cross-talk between PGE2 and Wnt signalling in neuronal cells, where PKA and PI-3K might act as mediators between the two pathways. Given the importance of PGE2 and Wnt signalling in prenatal development of the nervous system, our study provides insight into how interaction between these two pathways may influence neurodevelopment.

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