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 Nov 15, 2013

 



(a) Two views (with a 90° rotation) of the complete apo-IDUA molecule in the P21 crystal form.
The TIM barrel is in slate blue with the central eight strands of the β-barrel in yellow.

Credit: Nature Chemical Biology 20 September 2013







WHO Child Growth Charts

 

 

 

Potential drug target in sight for rare genetic disease

Researchers have discovered the structure of a potential drug target for a MPS I (Mucopolysaccharidosis I), paving the way for an alternative treatment for the condition.

University of Alberta, Faculty of Medicine and Dentistry researcher Michael James and his team recently published their findings about MPS I (Mucopolysaccharidosis I) in the peer-reviewed journal, Nature Chemical Biology.

Children born with a severe form of this disease usually die before they are 10 years old, while those with less severe forms can live well into adulthood. Symptoms can include improperly formed bones and teeth, carpal tunnel syndrome, an enlarged spleen, hearing or vision problems, distinct facial characteristics, heart problems and mental delays. MPS I affects about one in 100,000 people.

The human body continually churns out building blocks that rebuild various parts of the body, such as bone and cartilage. For example, bones in the body are rebuilt every seven years.

"Your body has to have a way of doing this, so that there is a breakdown of bone and then a production of the bone building-blocks," said research associate and team member Jiang Yin. He explained that with MPS I, the body can't complete this process due to a malfunctioning enzyme.

The gene responsible for creating this enzyme and directing its work is mutated in patients who have the disease. In fact, more than 100 mutations in this gene can cause the disease and impact its severity.

In order to better understand MPS I, researchers have been trying to figure out the three-dimensional structure of this important enzyme. James's team was the first to determine the 3-D structures that link specific defects in the enzyme to specific symptoms of the disease and specific genetic mutations.


"Now that we know how this enzyme functions and where the mutations are, the sites of the mutations can now be related to the disease symptoms.

"We've identified a drug target. There won't be a cure yet, but hopefully we can develop drugs to treat the less severe forms of the disease."
Michael James, PhD, researcher, University of Alberta, Faculty of Medicine and Dentistry

Research associate and team member Jiang Yin adds:
If we can treat people in the early stages of the disease, we may be able to lessen the severity of the disease and the mental delays."


James said this paves the way for the possibility of an alternative to enzyme replacement therapy, which involves weekly injections of a needle between a protective membrane and the spinal cord. The treatment is both painful and expensive, costing about $450,000 a year per patient.

"We're very excited about this discovery," said James. "We've all worked very hard."


Approximately 70 diseases relate to improperly functioning enzymes and collectively affect 1 in 5,000 people around the world.

These diseases are caused by a deficiency in lysosomal enzymes which are responsible for breaking down large molecules – such as those in bone, cartilage and fat.


The University of Alberta team has been collaborating with researchers from Simon Fraser University and the University of British Columbia on their work. Haiying Bie, a post-doctoral fellow from the U of A, was also a key member of the team.

Abstract
Mucopolysaccharidosis type I (MPS I), caused by mutations in the gene encoding α-L-iduronidase (IDUA), is one of approximately 70 genetic disorders collectively known as the lysosomal storage diseases. To gain insight into the basis for MPS I, we crystallized human IDUA produced in an Arabidopsis thaliana cgl mutant. IDUA consists of a TIM barrel domain containing the catalytic site, a β-sandwich domain and a fibronectin-like domain. Structures of IDUA bound to iduronate analogs illustrate the Michaelis complex and reveal a 2,5B conformation in the glycosyl-enzyme intermediate, which suggest a retaining double displacement reaction involving the nucleophilic Glu299 and the general acid/base Glu182. Unexpectedly, the N-glycan attached to Asn372 interacts with iduronate analogs in the active site and is required for enzymatic activity. Finally, these IDUA structures and biochemical analysis of the disease-relevant P533R mutation have enabled us to correlate the effects of mutations in IDUA to clinical phenotypes.

Original press release: http://www.uphs.upenn.edu/news/News_Releases/2013/11/bale/