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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.

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!



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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.
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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
Google Search artcles published since 2007
 
 

Home | Pregnancy Timeline | News Alerts |News Archive Feb 25, 2014

 

Image D shows representative heart images from non-transgenic (NTG)
and transgenic (TG) whole-heart lysated mice [lysis is a process used
to break open cells but avoid degrading sensitive proteins and DNA].

Image Credit: J Am Heart Assoc. 2013 December.






WHO Child Growth Charts

 

 

 

Improving a genetic heart defect

By suppressing a faulty protein, researchers reduced the thickness of a mouse’s heart muscles and improved it's cardiac functioning.

Congenital heart disease is the most common form of birth defect, affecting one out of every 125 babies, according to the National Institutes of Health.

Researchers from the University of Missouri (MU) recently found success using a drug to treat laboratory mice with one form of congenital heart disease, hypertrophic cardiomyopathy — a weakening of the heart caused by abnormally thick muscle.

Maike Krenz, MD, has been studying hypertrophic cardiomyopathy for nearly 10 years, soon after a gene was discovered in 2001 that linked the disease to the genetic conditions Noonan syndrome and LEOPARD syndrome.


In Noonan and LEOPARD syndromes*, the thickened heart muscle of hypertrophic cardiomyopathy is caused by a defective Shp2 protein, created by a mutation in the gene PTPN11.


“Previously, not much has been known about the biochemistry behind Shp2 and hypertrophic cardiomyopathy,” said Krenz, assistant professor of medical pharmacology and physiology at the MU School of Medicine, and a researcher at MU’s Dalton Cardiovascular Research Center. “We know the thickened heart muscle is sick and doesn’t work properly, and we know a defective Shp2 protein can cause heart muscle to thicken. However, to create an effective treatment, we needed to know what Shp2 is doing inside the heart to cause the defect.”


To test whether they could interrupt the heart’s hypersensitivity to growth signals, the researchers gave a chemical compound, PHPS1, to mice with a mutated gene that produces the defective Shp2 protein.


“Not only did the compound reduce the thickness of the heart muscle to the size of normal heart muscle, but it also improved the cardiac pumping of the heart,” Krenz said. “That’s important because people with hypertrophic cardiomyopathy have an increased risk of sudden cardiac death. If we could develop an effective treatment for the disease and improve patients’ heart function, we could save many people’s lives.”

Because of the role Shp2 plays in signaling heart growth, Krenz believes the research could be translated in the future into improved treatments for other types of heart disease, such as damage caused by heart attack.

The work was published in the Journal of the American Heart Association in December of 2013.

Abstract
Background
The enzyme hexokinase-2 (HK2) phosphorylates glucose, which is the initiating step in virtually all glucose utilization pathways. Cardiac hypertrophy is associated with a switch towards increased glucose metabolism and decreased fatty acid metabolism. Recent evidence suggests that the increased glucose utilization is compensatory to the down-regulated fatty acid metabolism during hypertrophy and is, in fact, beneficial. Therefore, we hypothesized that increasing glucose utilization by HK2 overexpression would decrease cardiac hypertrophy.

Methods and Results
Mice with cardiac-specific HK2 overexpression displayed decreased hypertrophy in response to isoproterenol. Neonatal rat ventricular myocytes (NRVMs) infected with an HK2 adenovirus similarly displayed decreased hypertrophy in response to phenylephrine. Hypertrophy increased reactive oxygen species (ROS) levels, which were attenuated by HK2 overexpression, thereby decreasing NRVM hypertrophy and death. HK2 appears to modulate ROS via the pentose phosphate pathway, as inhibition of glucose-6-phosphate dehydrogenase with dehydroepiandrosterone decreased the ability of HK2 to diminish ROS and hypertrophy.

Conclusions
These results suggest that HK2 attenuates cardiac hypertrophy by decreasing ROS accumulation via increased pentose phosphate pathway flux.

Krenz presented the research findings, “Inhibition of Shp2’s Phosphatase Activity Ameliorates Cardiac Hypertrophy in LEOPARD Syndrome Models,” at the American Heart Association’s Scientific Sessions conference in November 2013, where it received the Outstanding Research Award in Pediatric Cardiology.

*LEOPARD syndrome is related to Noonan syndrome and receives its name from an acronym for multiple errors in development, including: electrocardio conduction abnormalities, abnormally increased distance between the eyes (ocular hypertelorism), obstruction of flow from the right ventricle of the heart to the pulmonary artery (pulmonic stenosis), abnormal genitalia, retardation of growth and deafness.