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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 ' 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!



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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 weeks 0 - 40 and follow fetal growth
Google Search artcles published since 2007
 
September 9, 2011--------News Archive

Pregnancy Diet Influences Baby's Allergies
A possible link between what a mother eats during pregnancy and the risk of her child developing allergies has been identified.

When Do Infants Gain the Capacity for Pain?
The evidence suggests that developing brain networks become mature enough to identify pain as distinct from touch fairly late in development.

Early Motor Skill Training Jump Starts Infants
Study indicates infants at risk for autism could benefit from motor training.

September 8, 2011--------News Archive

Clue Found to Cause of Childhood Hydrocephalus
When it comes to the circuits that make up the olfactory system, it seems that sleep eliminates some smell receptors. Perhaps sleepless parenting of newborns preserves intense smell receptivity!

Sleep Controls Survival of "Smell" Neurons in Adults
When it comes to neurons that make up the olfactory system, it seems that sleep eliminates some smells. Perhaps sleepless parents are preserving intense smells!

Improving Treatment of Craniosynostosis
Craniosynostosis is a condition that causes the bone plates in the skull to fuse too soon.

September 7, 2011--------News Archive

In Socially Engaged Mice, White Fat Turns to Brown
Given an engaging place to live with greater opportunities for social stimulation, some energy-storing white fat is transformed to energy-burning brown fat.

Lifetime 'Dose' of Excess Weight Linked to Diabetes
Degree and duration of obesity in adolescents and young adults are important for type 2 diabetes risk, especially for Hispanics and blacks.

Mom's Use of Oxycodone Not Safe for Breastfeeding
Doctors have been prescribing codeine for postpartum pain management for many years. Until recently, it was considered safe to breastfeed while taking.

September 6, 2011--------News Archive

Missing Genes Separate Coach Potato from Action
You may think your lack of resolve to get off the couch to exercise is because you're lazy, but research has discovered it may be you are missing key genes.

Phthalates and Decrease In Mental-Motor Growth
Phthalates are endocrine-disrupting chemicals widely present in the environment, and are linked to increased behavioral problems at age 3.

Missing Genes Separate Coach Potato from Action
You may think your lack of resolve to get off the couch to exercise is because you're lazy, but research has discovered it may be you are missing key genes.

September 5, 2011--------News Archive

Found, Gene Defect Predisposing You to Leukemia
Those at risk because of family history may soon obtain tests to detect the genetic error before symptoms emerge.

New Blood Sugar Control for Diabetes
Study finds inflammation may be part of the solution, not the problem.

WHO Child Growth Charts

Aclose-up of a bone marrow by Daniel E. Sabath, University of Washington (UW) professor of laboratory medicine.

A new genetic defect that predisposes people to acute myeloid leukemia and myelodysplasia has been discovered. The mutations were found in the GATA2 gene. Among its several regulatory roles, the gene acts as a master control during the transition of primitive blood-forming cells into white blood cells.

The researchers started by studying four unrelated families who, over generations, have had several relatives with acute myeloid leukemia, a type of blood cancer. Their disease onset occurred from the teens to the early 40s. The course is rapid.

The findings will be reported Sept. 4 in Nature Genetics. The results come from an international collaboration of scientists and the participation of families from Australia, Canada, and the United States.

The genetic mutation was first discovered in a patient from central Washington. The research participant had been successfully treated for leukemia in 1992 through a bone marrow transplant at UW Medical Center. At that time, Horwitz decided to seek a possible genetic reason after learning his patient had several family members with myelodysplastic syndrome, myeloid leukemia, and intractable mycobacteria infections.

Myelodysplastic syndrome is a difficulty in producing certain kinds of blood cells. The problem originates in the bone marrow with a decline in the number and quality of blood-forming cells. Patients often have severe anemia and need frequent blood transfusions. The disease generally worsens due to bone marrow failure and low blood counts. About one- third of those with the syndrome soon develop acute myeloid leukemia, in which abnormal white cells build up in the bone marrow and interfere with normal blood production.

Horwitz's Australian colleagues had described a family with a similarly inherited blood disorder. Eighteen years later, after rifling through many candidate genes, the researchers on both continents were relieved finally to have hit upon the mutated gene responsible for the leukemia that affect these families. They have gone on to identify abnormal GATA2 genes in more than 20 families and individuals.

"It's likely that this inherited error is more common than we had thought," the researchers noted.

In some families with a GATA2 mutation, the over-riding concern has been leukemia, while others suffer dangerous infections from bacteria, viruses and fungi because of a lack of white blood cells to fight off germs.

The lab of Dr. Dennis Hickstein, formerly of the UW School of Medicine and the Puget Sound Veterans Affairs Health System and now at the National Institute of Health, in collaboration with NIH colleague Dr. Steven Holland, associated the mutation with mycobacteria infections. Those results were reported in separate study appearing in the journal Blood.

Another paper appearing Sept. 4 in Nature Genetics from a London group found similar mutations of GATA2 in leukemia patients with lymphedema and, in some cases, deafnesss. By blocking the vessels that drain fluid from the body's tissues, lympedema causes swelling of the arms or legs.

Ongoing work in Seattle and Adelaide has identified a congenital syndrome associated with developmental delay and a risk of myelodysplasia. This syndrome results from chromosomal loss of GATA2 and adjacent genes.

Comparable GATA2 mutations also have been found in people with the more common, non-inherited leukemias.

Scientists are trying to figure out why apparently similar gene mutations in GATA 2 cause such assorted health problems. Also perplexing is how hard it has been to find genetic errors underlying blood cancers, compared with other cancers.

"While several genes have been discovered and linked to solid, malignant tumors such as breast cancer in families susceptible to those types of cancer, so far very few inherited mutations have been uncovered for blood cancers," Horwitz said.

Previously, other scientists linked mutations in two other genes -- RUNX1 and CEBPA – to injerited forms of myelodysplastic syndrome and acute myeloid leukemia. These genes bind to DNA and control the copying of information encoded in this molecule.

Keeping this in mind, researchers looked for mutations in similar genes in families who did not have the RUNX1 and CEBPA mutations and who had no other explanations for their inherited blood cancer. In so doing, the researchers identified the GATA2 mutations. They also observed that these mutations relate to loss of function by making the gene unable to perform the molecular duties necessary to manufacture healthy white blood cells.

According to Horwitz, the GATA2 mutations in DNA occur adjacent to an amino acid mutated in some patients with terminal chronic myeloid leukemia. This proximity suggests a common pathway may be critical for several types of myeloid malignancies, he said.

People at risk because of their pedigree eventually may obtain tests to detect this genetic error before symptoms emerge. Learning that they have the gene mutation might help patients and their doctors decide on appropriate follow-up for early diagnosis and treatment of problems that might arise.

Additional knowledge about how the GATA2 gene and its mutations operate may foster the development of new therapeutic agents.

In collaboration with Dr. Hamish Scott and Dr. Richard J. D'Andrea at the Centre for Cancer Biology, University of Australia, Adelaide, the U.S. portion of the study was conducted by Dr. Marshall Horwitz, University of Washington (UW) professor of pathology. Horwitz practices genetic medicine at UW Medical Center and the UW Center for Human Development and Disability, both in Seattle.

A clinical trial under way in the United States may point to specific treatment recommendations for persons with a GATA2 genetic mutation.

The research for "Heritable GATA2 Mutations Associated with Familial Myelodysplastic Syndrome and Acute Myeloid Leukemia," was supported by grants from the National Health and Medical Research Council of Australia, a Dora Lush Postgraduate Award, Leukaemia Foundation of Australia, the Cancer Council of South Australia, MedVet Pty Ltd., and the U.S. National Institutes of Health.

The researchers extend their gratitude to the families and individuals who participated in this project.

Horwitz has been invited to speak on the role of GATA2 in myelodysplastic syndromes at a National Institutes of Health conference Sept. 7-8 in Bethesda, Md.

Original article: http://www.eurekalert.org/pub_releases/2011-09/uow-gdt090211.php