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 ' million visitors each month.


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.

Return To Top Of Page
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 weeks 0 - 40 and follow fetal growth
Google Search artcles published since 2007
 
April 4 - 8, 2011--------News Archive

Simple Treatment Prevents Premature Births
Treating high-risk pregnant women with the hormone progesterone cut their rate of early delivery by 45 % and helped lower the risk of breathing complications in their babies.

Babies Are Born Early Near Busy Road Intersections
Babies are born earlier when their mothers live near a concentration of freeways and main roads, reports a study of 970 mothers and their newborn babies in Logan City, a town south of Brisbane, Australia.

New Gene Found Increases Risk For Epilepsy
Vanderbilt University researchers have identified a new gene that can influence a person's risk for developing epilepsy.

Gene Linked To Autism's Social Dysfunction
With the help of two sets of brothers with autism, Johns Hopkins scientists have identified a gene associated with autism that appears to be linked very specifically to the severity of social interaction deficits.

Study Reveals How Eye Is Formed
Scientists at King’s College London have discovered specific cells responsible for ensuring that different parts of the eye come together during development.

WHO Child Growth Charts

The findings, reported in the March 29 Proceedings of the National Academy of Sciences, could improve molecular diagnostic tools and point to novel therapeutic targets for epilepsy.

The gene, KCNV2, codes for a unique type of potassium channel, a protein that participates in the electrical activity of nerve cells. Disturbed electrical activity in the brain – and resulting

seizures – are hallmarks of epilepsy, a group of disorders that affects about 1 percent of the world's population.

A number of genetic mutations that cause inherited epilepsies have been identified. But the clinical severity of inherited epilepsies varies widely – from mild childhood seizures that resolve with age to severe lifelong seizures – even in individuals who have the same single-gene mutation, said Jennifer Kearney, Ph.D., assistant professor of Medicine in the Division of Genetic Medicine.

The gene, KCNV2, codes for a unique type of potassium channel, a protein that participates in the electrical activity of nerve cells. Disturbed electrical activity in the brain – and resulting seizures – are hallmarks of epilepsy, a group of disorders that affects about 1 percent of the world's population.

A number of genetic mutations that cause inherited epilepsies have been identified. But the clinical severity of inherited epilepsies varies widely – from mild childhood seizures that resolve with age to severe lifelong seizures – even in individuals who have the same single-gene mutation, said Jennifer Kearney, Ph.D., assistant professor of Medicine in the Division of Genetic Medicine.

The range of clinical severity "tells us that there are other factors that contribute," she said. "We think that susceptibility and resistance genes that are inherited in addition to the primary mutation are probably a major factor."

Identifying susceptibility and resistance genes may suggest new targets for drugs that fine-tune neuronal excitability, rather than dampening it completely as many current antiepileptic drugs do, Kearney said.

The investigators began to look for these types of "modifier" genes after they made a curious observation in a mouse model of epilepsy – that epilepsy severity depended on the genetic background strain of the mice.

They were studying mice with an epilepsy-causing gene mutation in a sodium channel, a protein that is important for neuronal excitability. The mice had spontaneous, progressive seizures and a reduced lifespan. But when the researchers "moved" the gene mutation into mice with a different genetic background (using breeding strategies), the epilepsy became less severe: the mice developed seizures later and had improved survival.

Using genetic strategies, the investigators zeroed in on two chromosome regions that influenced the difference in epilepsy severity in the two mouse strains. In one of these regions, the mouse Kcnv2 gene (the mouse equivalent of the human KCNV2 gene) appeared to be the strongest candidate gene, based on its potential for altering electrical activity in neurons.

The current report demonstrates that increased expression of the mouse Kcnv2 gene – not changes in its coding sequence – is associated with more severe epilepsy in the susceptible mouse strain. Increasing Kcnv2 expression in the resistant mouse strain caused these mice to develop more severe symptoms, supporting the gene's contribution as an epilepsy modifier.

The investigators then screened 209 pediatric epilepsy patients for variations in KCNV2 and found two different variations in two unrelated patients.

Colleagues in the laboratory of Alfred George Jr., M.D., director of the Division of Genetic Medicine, conducted electrophysiology studies in cells to examine how the two variations affected the function of the potassium channel. They found that both variations suppressed a type of potassium current that normally dampens excitability in neurons.

"The mutations make a neuron more excitable, so you could have longer periods of excitation and also repetitive excitation (that leads to seizures)," says Kearney.

The team plans to screen additional patients with epilepsy to assess the incidence of variations in KCNV2. They are also collaborating with Dave Weaver, Ph.D., director of the Vanderbilt High-Throughput Screening Facility, to find compounds that target the potassium channel and may be useful therapeutics for epilepsy.

Kearney said that understanding how genes such as KCNV2 modify the clinical severity of epilepsy is important for molecular diagnostics and genetic counseling. Patients may currently learn that they have an epilepsy-causing gene mutation, but because clinical severity varies, their prognosis may not be clear.

"We need to understand how all of these different gene interactions impact the final clinical disorder to improve risk assessment and disease management in epilepsy," Kearney said.

The National Institutes of Health supported the research.

http://www.eurekalert.org/pub_releases/2011-04/wfu-fps040411.php