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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.

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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
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Home | Pregnancy Timeline | News Alerts |News Archive Dec 17, 2014

A complex interaction between bacteria, the gut, and immune system could be a prerequisite
for the development of metabolic diseases. Image Credit: APS Physiology

 






 

 

Intestinal tract helps control weight

Scientists have identified an unexpected intestinal bacterial interaction potentially affecting the human development of obesity and diabetes type 2.

The team at Louvain Drug Research Institute, Université Catholique de Louvain (UCL) led by Patrice D. Cani PhD, discovered how the intestinal immune system helps control energy metabolism. It found that inactivation of a protein called MyD88 in the cells lining the intestinal track of diabetic mice, allowed those mice to gain more energy from their food.


Disabling the protein MyD88 slowed down development of diabetes by limiting the development of adipose (fat) tissue.

Reducing the harmful inflammation of obesity strengthened the function of the intestine as a barrier to limit inappropriate transit of bacteria through the intestines and into the mouse.

Specifically, the team found inactivation of MyD88 seems to strengthen the intestinal barrier and limit much of the transit of bacteria from our intestines into our body.


Researchers also found they could transfer (by grafting) intestinal cells with MyD88 protein into the intestines of mice with the MyD88 deletion — making it possible for those mice to lose weight even when they were already obese and diabetic.

The observation was made that during consumption of a fatty diet, the intestinal immune system played an important role in regulating fat storage by modifications to intestinal bacteria.

The discovery is published in the scientific journal Nature Communications, and confirms the involvement of intestinal bacteria in the development of obesity. More importantly, the work provides new therapeutic possibilities for treating obesity and type 2 diabetes.

Abstract
Obesity is associated with a cluster of metabolic disorders, low-grade inflammation and altered gut microbiota. Whether host metabolism is controlled by intestinal innate immune system and the gut microbiota is unknown. Here we report that inducible intestinal epithelial cell-specific deletion of ?MyD88 partially protects against diet-induced obesity, diabetes and inflammation. This is associated with increased energy expenditure, an improved ?glucose homeostasis, reduced hepatic steatosis, fat mass and inflammation. Protection is transferred following gut microbiota transplantation to germ-free recipients. We also demonstrate that intestinal epithelial ?MyD88 deletion increases anti-inflammatory endocannabinoids, restores antimicrobial peptides production and increases intestinal regulatory T cells during diet-induced obesity. Targeting ?MyD88 after the onset of obesity reduces fat mass and inflammation. Our work thus identifies intestinal epithelial ?MyD88 as a sensor changing host metabolism according to the nutritional status and we show that targeting intestinal epithelial ?MyD88 constitutes a putative therapeutic target for obesity and related disorders.

Everard A et al. Intestinal epithelial MyD88 is a sensor switching host metabolism towards obesity according to nutritional status. Nature Communications. 5:5648, DOI: 10.1038/ncomms6648.

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