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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 33333333333333333333333
Google Search artcles published since 2007
May 27, 2011--------News Archive

Predicting Diabetes 7 Years Before Pregnancy
A woman's risk of developing diabetes during pregnancy can be identified up to seven years before she is pregnant based on routine blood sugar and weight.

Caffeine Can Reduce Fertility In Women
Caffeine reduces muscle activity in the fallopian tubes which should move eggs from a woman's ovaries into her womb.

May 26, 2011--------News Archive

Take Prenatal Vitamins Early And Reduce Autism
Women who reported not taking daily prenatal vitamins immediately before and during the first month of pregnancy, were nearly twice as likely to have a child with an autism spectrum disorder.

High-Fat Pregnancy Diet Programs Child for Diabetes
A high-fat diet during pregnancy can program a woman's baby for future diabetes, even if she herself is not obese or diabetic.

May 25, 2011--------News Archive

New Insight Into Obesity and Metabolic Disorders
Focussing on endoplasmic reticulum reverses Type 2 diabetes in mice.

New Drug Stops Aggressive Childhood Leukemia
Investigators have been able to overcome a form of leukemia through targeted therapy, completly eradicating the cancer in cell and animal studies.

May 24, 2011--------News Archive

New Genetic Testing Technology for IVF Embryos
Johns Hopkins School of Medicine has devised a technique to help couples have in vitro fertilized babies free of genetic disease and chromosomal abnormalities.

A New Program for Neural Stem Cells
Max Planck Institute scientists have just produced central nervous system cells from neural stem cells taken from the peripheral nervous system.

May 23, 2011--------News Archive

The Mosh Pit of Cell Movement
Physical forces that guide how cells migrate - how they get from place to place inside the living body - are a mess.

Understanding and Treating Brittle Bones
Hope for developing new treatment of bone density mutations leading to such conditions as osteoporosis in adults and osteogenesis imperfecta in children.

Anesthesiologists' Affect On Maternal Fetal Outcome
A first-of-its-kind study exploring how anesthesiologists are perceived by labor and delivery colleagues.

Understanding How Retinas Develop
Using inbred mice, scientists have identified where genes contribute to cone photoreceptor development.

WHO Child Growth Charts

by Ellen Barlow, edited by Carmen Arbona

Building on a decade of discoveries concerning obesity’s role in Type 2 diabetes and related metabolic disorders, researchers at the Harvard School of Public Health have uncovered surprising roles for lipid and calcium-processing abnormalities in the liver.

By correcting these problems in a mouse model, the team reversed high blood-glucose levels, insulin resistance and other metabolic hallmarks of Type 2 diabetes.

As the related epidemics of obesity and diabetes escalate around the world, “the discovery of a faulty metabolic mechanism in fatty liver tissue opens new opportunities to consider for therapeutics,” said Gökhan Hotamisligil, J.S. Simmons Professor of Genetics and Metabolism and chair of the Department of Genetics and Complex Diseases at HSPH. His team reported their findings in the May 2 issue of Nature.

The chain of molecular events by which obesity disrupts metabolism causes a domino effect of damage: 1) high blood pressure, 2) cholesterol abnormalities and 3) resistance to insulin, a prelude to diabetes in which cells are unresponsive to the hormone and cannot efficiently make energy from blood sugar. In addition to diabetes, obesity has been linked to cardiovascular, liver and neurodegenerative diseases and certain cancers.

Stressed Out

The Hotamisligil lab established chronic inflammation as a prime cause of metabolic disruption by obesity, implicating the organelle known as the endoplasmic reticulum (ER) and tracing insulin resistance and Type 2 diabetes to ER overload, or ER stress, as obesity develops. His group and others observed similar ER-stress-related problems in human obesity.

Until the Hotamisligil lab explained ER’s role in regulating metabolism, the organelle was known mainly for manufacturing and trafficking proteins. Why the endoplasmic reticulum fails in obesity was a mystery for the lab to solve.

HSPH Research Associate Suneng Fu, first author on the Nature paper, began by comparing the endoplasmic reticulum found in fat and lean liver tissues. Instead of looking at one possible mechanism at a time, he extensively mapped all the organelle’s functions.

Fu developed a method to purify the ER from lean and obese tissues, then isolated and identified each of the endoplasmic reticulum proteins and lipids in each.

The researchers had anticipated that in obesity, the primary driver of endoplasmic reticulum stress was flooding of the ER factory by proteins. But in what Hotamisligil called a “shocking surprise,” they found that obese samples had fewer proteins and more lipids than did lean samples.

“Obesity was spurring a switch in the ER from synthesizing proteins to synthesizing lipids,” Hotamisligil said.

Lipid Changes

Looking closely at lipid changes in the fatty tissue, the researchers noted that two lipids critical to the structure of the endoplasmic reticulum membrane, phosphatidylcholine (PC) and phosphatidylethanolamine (PE) were the most altered. If the membrane were affected, they reasoned, perhaps its tubular channels which transport calcium, are affected as well.

Hotamisligil likens ER and its channels to a 12-cylinder Formula One race car, one that runs on calcium for fuel. The endoplasmic reticulum needs calcium to make and fold proteins. While searching the literature on channel function, the team uncovered a 25-year-old paper describing how a precise ratio of PC to PE is necessary for the function of proteins critical to channeling calcium. Interestingly, this ratio precisely resembled liver ER in normal, lean mice. In fatty tissue, on the other hand, the ratio was high - perhaps explaining why calcium escapes through endoplasmic reticulum membranes in an obese liver.

To fix the leak, the researchers used two strategies. Through genetic manipulation they blocked the effect of an enzyme, PEMT, and corrected the PC/PE ratio. They also used a virus to deliver the SERCA protein (known to be responsible for pumping calcium into ER) into the fatty livers of lab mice.

Both maneuvers led to the same result: a reversal of metabolic problems in the mice.

“ER stress went away, blood glucose levels fell back to normal, insulin sensitivity was restored and fatty liver was resolved,” said Hotamisligil.

In obesity an increased synthesis of lipids, not of proteins, disrupts endoplasmic reticulum function and leads to stress, the researchers conclude. Looking ahead to potential drug therapies, it might be possible to restore lipid metabolism and calcium homeostasis knowing the actual processes involved. I may also mean that dietary solutions are possible.

The liver isn’t the only site where obesity disrupts metabolism and ignites metabolic disease. ER stress has been observed in adipose tissue and in the pancreas and brain. In these tissues, too, he said, “we’re working to decode the ER landscape.”

Original article: http://www.focushms.com/features/new-insight-into-obesity-and-metabolic-disorders/