Welcome to The Visible Embryo

 

 

Home-- -History-- -Bibliography- -Pregnancy Timeline- --Prescription Drugs in Pregnancy- -- Pregnancy Calculator- --Female Reproductive System- -Contact
 

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!



Home

History

Bibliography

Pregnancy Timeline

Prescription Drug Effects on Pregnancy

Pregnancy Calculator

Female Reproductive System

Contact The Visible Embryo

News Alerts Archive

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.
Content protected under a Creative Commons License.

No dirivative works may be made or used for commercial purposes.

 

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
Google Search artcles published since 2007
 
 

Home | Pregnancy Timeline | News Alerts |News Archive Oct 23, 2013

 

Green fluorescent protein (green) labeled cells in the mouse brain are assayed for mTOR activity using phospho-S6 immunostaining (red).

Image Credit: Nathaniel Hartman, co-author of this study








WHO Child Growth Charts

 

 

 

Possible treatment for rare brain disorder?

Scientists are working to determine how neurons are generated, vital to providing treatment for neurological disorders such as Tuberous Sclerosis Complex (TSC), a rare genetic disease causing tumors in the brain and other vital organs. The research may reveal how autism, epilepsy and cognitive impairment arise from abnormal generation of neurons.

“Current medicine is directed at inhibiting the mammalian target of rapamycin (mTOR), a common feature within these tumors that have abnormally high activity,” said David M. Feliciano, assistant professor of biological sciences, Clemson University. “However, current treatments have severe side effects, likely due to mTOR’s many functions including playing an important role in cell survival, growth and migration.”

Feliciano and colleagues published their findings in journal Cell Reports.

“Neural stem cells generate the primary communicating cells of the brain called neurons through the process of neurogenesis, yet how this is orchestrated is unknown,” said Feliciano.

Stem cells lie at the core of brain development and repair, and alterations in these cells’ self-renewal and differentiation can have major consequences for brain function at any stage of life.

To better understand the process of neurogenesis, the researchers used a genetic approach known as neonatal electroporation to deliver pieces of DNA into neural stem cells in young mice, which allowed them to express and control specific components of the mTOR pathway.


The researchers found that when they increased activity in the mTOR pathway, neural stem cells made neurons at the expense of making more stem cells.

They also found this phenomenon is linked to a specific mTOR target known as 4E-BP2, which regulates the production of proteins.

Ultimately, this study points to a possible new treatment, 4E-BP2, for neurodevelopmental disorders like TSC— and may have fewer side effects.


Future experiments are aimed at identifying which proteins are synthesized due to this pathway in neurological disorders.

Abstract Highlights
mTORC1 loss of function limits NSC differentiation and neuron production
mTORC1 gain of function induces NSC differentiation at the expense of self-renewal
4E-BP2, but not S6K1/S6K2, mediates mTORC1-induced NSC differentiation
Differential 4E-BP2 and S6K1/S6K2 roles in NSC self-renewal and growth
Summary

The mammalian target of rapamycin complex 1 (mTORC1) integrates signals important for cell growth, and its dysregulation in neural stem cells (NSCs) is implicated in several neurological disorders associated with abnormal neurogenesis and brain size. However, the function of mTORC1 on NSC self-renewal and the downstream regulatory mechanisms are ill defined. Here, we found that genetically decreasing mTORC1 activity in neonatal NSCs prevented their differentiation, resulting in reduced lineage expansion and aborted neuron production. Constitutive activation of the translational repressor 4E-BP1, which blocked cap-dependent translation, had similar effects and prevented hyperactive mTORC1 induction of NSC differentiation and promoted self-renewal. Although 4E-BP2 knockdown promoted NSC differentiation, p70 S6 kinase 1 and 2 (S6K1/S6K2) knockdown did not affect NSC differentiation but reduced NSC soma size and prevented hyperactive mTORC1-induced increase in soma size. These data demonstrate a crucial role of mTORC1 and 4E-BP for switching on and off cap-dependent translation in NSC differentiation.

Clemson University
Ranked No. 21 among national public universities, Clemson University is a major, land-grant, science- and engineering-oriented research university that maintains a strong commitment to teaching and student success. Clemson is an inclusive, student-centered community characterized by high academic standards, a culture of collaboration, school spirit and a competitive drive to excel.

This material is based upon work supported by the National Institutes of Health under Grant No. 10668225 and the Connecticut Stem Cell Research Program. Any opinions, findings and conclusions or recommendations expressed in this material are those of the authors and do not necessarily reflect the views of the National Institutes of Health.

Original press releas:http://media-relations.www.clemson.edu/5186