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Pregnancy Timeline by SemestersFemale Reproductive SystemFertilizationThe Appearance of SomitesFirst TrimesterSecond TrimesterThird TrimesterFetal 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 HemispheresEnd of Embryonic PeriodEnd of Embryonic PeriodFirst Thin Layer of Skin AppearsThird TrimesterDevelopmental Timeline
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June 27, 2012--------News Archive Return to: News Alerts


The heart tube takes on an S-shape establishing the asymetry of the heart.
As the S-shape forms, cardiac muscle contraction begins.

WHO Child Growth Charts

       

New Mouse Helps Explain Congenital Heart Disease

Scientists now have clues to how a gene mutation discovered in families affected with congenital heart disease leads to underdevelopment of the walls that separate the heart into four chambers

When babies are born with a hole in their heart (either between the upper or lower chambers), they have a septal defect, the most common form of congenital heart disease. Although it's not clear what causes all septal defects, genetic studies primarily utilizing large families have led to the discovery of several causative genes.

A Nationwide Children's Hospital study appearing in PLoS Genetics suggests that abnormal development of heart cells during embryogenesis may be to blame.


A single nucleotide change in the GATA4 gene in humans causes atrial and ventricular septal defects along with pulmonary valve stenosis.


Vidu Garg, MD, the study's lead author, previously reported that a single nucleotide change in the GATA4 gene in humans causes atrial and ventricular septal defects along with pulmonary valve stenosis. In mice, the GATA4 gene has been shown to be necessary for normal heart development and its deletion leads to abnormal heart development.

"While GATA4 has been shown to be important for several critical processes during early heart formation, the mechanism for the heart malformations found in humans with the mutation we previously reported is not well understood," said Dr. Garg, a pediatric cardiologist in The Heart Center and principal investigator in the Center for Cardiovascular and Pulmonary Research at The Research Institute at Nationwide Children's Hospital.

To better characterize the mutation, Dr. Garg and colleagues generated a mouse model harboring the same human disease-causing mutation. They saw heart abnormalities in the mice that were consistent with those seen in humans with GATA4 mutations.


Upon further examination, they found that the mutant protein leads to functional deficits in the ability for heart cells to increase in number during embryonic development.


"Our findings suggest that cardiomyocyte proliferation deficits could be a mechanism for the septal defects seen in this mouse model and may contribute to septal defects in humans with mutations in GATA4," said Dr. Garg, also a faculty member at The Ohio State University College of Medicine.

"This mouse model will be valuable in studying how septation and heart valve defects arise and serve as a useful tool to study the impact of environmental factors on GATA4 functions during heart development."

Original article: http://www.eurekalert.org/pub_releases/2012-06/nch-nmm062612.php