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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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Pregnancy Timeline by SemestersDevelopmental TimelineFertilizationFirst TrimesterSecond TrimesterThird TrimesterFirst Thin Layer of Skin AppearsEnd of Embryonic PeriodEnd of Embryonic PeriodFemale Reproductive SystemBeginning Cerebral HemispheresA Four Chambered HeartFirst Detectable Brain WavesThe Appearance of SomitesBasic Brain Structure in PlaceHeartbeat can be detectedHeartbeat can be detectedFinger and toe prints appearFinger and toe prints appearFetal sexual organs visibleBrown fat surrounds lymphatic systemBone marrow starts making blood cellsBone marrow starts making blood cellsInner Ear Bones HardenSensory brain waves begin to activateSensory brain waves begin to activateFetal liver is producing blood cellsBrain convolutions beginBrain convolutions beginImmune system beginningWhite fat begins to be madeHead may position into pelvisWhite fat begins to be madePeriod of rapid brain growthFull TermHead may position into pelvisImmune system beginningLungs begin to produce surfactant
CLICK ON weeks 0 - 40 and follow along every 2 weeks of fetal development


A hormone to break the obesity cycle?

While obesity rates for pregnant women continue to climb, scientists have discovered they can increase a specific hormone during pregnancy and reduce, or possibly, eliminate the chances the babies born will become obese as well.

Obese pregnant women often give birth to babies at risk for diabetes. "In the U.S., nearly two-thirds of women enter pregnancy either overweight or obese," explains study senior author Thomas Jansson, MD, PhD a professor at the University of Colorado Anschutz Medical Campus. "That makes them susceptible to gestational diabetes, preterm labor and preeclampsia. At the same time, the baby is often born larger with more fat than normal."

These infants often become obese adults too, setting up a vicious cycle that drives the obesity epidemic.  So Jansson and his research team set out to break the cycle. They focused on the hormone Adiponectin which makes people sensitive to insulin.

High levels of Adiponectin guard against obesity and diabetes — low levels put people at risk.

Adiponectin acts as a brake to the amount of nutrients passed through the placenta of a pregnant woman. Low levels of adiponectin allow more nutrients to flow through, resulting in a larger than normal baby with more body fat.

Scientists tested the affects of Adiponectin by infusing it into obese and pregnant mice during the last four days of their normal 20-day gestational period — about equal to the last trimester of human pregnancy. The increase normalized the hormone balance in the mom mice.

"It completely reversed all the negative effects on the placenta. The pups of the obese mice had completely normal weights. Their glucose levels were also normal. We were able to pre-empt all the usual negative consequences of these kinds of pregnancies. This hormone or a similar agent could feasibly do the same thing for humans that it did for mice."

Thomas Jansson, MD, PhD a professor at the University of Colorado Anschutz Medical Campus

More work needs to be done to track the long-term effects of this hormone treatment over the life of a mouse, "But we have laid the foundation for what we believe might ultimately help break the cycle of obesity that has approached epidemic proportions in our society," Jansson adds.

Another group of researchers have developed a compound similar to Adiponectin that can be taken orally, and are now in clinical trials.

This study is published in the Proceedings of the National Academy of Sciences or PNAS.

Obesity and metabolic syndrome may, in part, originate in fetal life. In particular, babies of mothers with obesity and/or gestational diabetes mellitus (GDM) are often large at birth and have increased adiposity, which predisposes them to the development of metabolic disease later in life. Maternal obesity and GDM are typically associated with low circulating levels of adiponectin (ADN), and we found that ADN supplementation to pregnant obese mice completely normalized the changes in placental function and prevented fetal overgrowth caused by maternal obesity. These findings suggest that strategies to increase ADN levels in maternal obesity and GDM may alleviate the adverse effects of these pregnancy complications on the fetus.

Mothers with obesity or gestational diabetes mellitus have low circulating levels of adiponectin (ADN) and frequently deliver large babies with increased fat mass, who are susceptible to perinatal complications and to development of metabolic syndrome later in life. It is currently unknown if the inverse correlation between maternal ADN and fetal growth reflects a cause-and-effect relationship. We tested the hypothesis that ADN supplementation in obese pregnant dams improves maternal insulin sensitivity, restores normal placental insulin/mechanistic target of rapamycin complex 1 (mTORC1) signaling and nutrient transport, and prevents fetal overgrowth. Compared with dams on a control diet, female C57BL/6J mice fed an obesogenic diet before mating and throughout gestation had increased fasting serum leptin, insulin, and C-peptide, and reduced high-molecular-weight ADN at embryonic day (E) 18.5. Placental insulin and mTORC1 signaling was activated, peroxisome proliferator-activated receptor-α (PPARα) phosphorylation was reduced, placental transport of glucose and amino acids in vivo was increased, and fetal weights were 29% higher in obese dams. Maternal ADN infusion in obese dams from E14.5 to E18.5 normalized maternal insulin sensitivity, placental insulin/mTORC1 and PPARα signaling, nutrient transport, and fetal growth without affecting maternal fat mass. Using a mouse model with striking similarities to obese pregnant women, we demonstrate that ADN functions as an endocrine link between maternal adipose tissue and fetal growth by regulating placental function. Importantly, maternal ADN supplementation reversed the adverse effects of maternal obesity on placental function and fetal growth. Improving maternal ADN levels may serve as an effective intervention strategy to prevent fetal overgrowth caused by maternal obesity.

The study was published Monday in the Proceedings of the National Academy of Sciences. The co-authors include, Fredrick J. Rosario, PhD, instructor at CU Anschutz, Professor Theresa Powell, PhD, of CU Anschutz and Irving L. M. Aye of Cambridge University in England.

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Oct 1, 2015   Fetal Timeline   Maternal Timeline   News   News Archive   

The placental blood system regulates molecular substances between mother and fetus.
Adiponectin acts as a brake to the amount of nutrients passing through the placenta.

Image Credit: Wright State University











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