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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
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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 July 4, 2013

 
Phagocytosis
Macrophage responding to cholesterol crystals and amyloid plaques

It is known tha a macrophage will ingest a pathogen.
However, new research has identified the receptor (CD36) on the outside of a
macrophage which draws soluble cholesterol and protein matter inside of the macrophage
transforming those substances into triggers for inflammation.

a. CD36
b. the pathogens are broken down by enzymes
c. inflammation triggered by substances made from pathogens
Parts:
1. Particulate matter associated with vascular disease, amyloid plaques
2. Phagosome
3. Lysosomes
4. Waste material to be expelled
5. Cytoplasm
6. Cell membrane






WHO Child Growth Charts

 

 

 

Blocking alzheimer’s, atherosclerosis and type-2 diabetes

Findings suggest there may be one therapeutic target for multiple diseases.Researchers at NYU Langone Medical Center have discovered a mechanism that triggers chronic inflammation in Alzheimer’s, atherosclerosis, and type-2 diabetes.

The results, published in Nature Immunology, suggest a common biochemical thread to multiple diseases and points the way to a new class of therapies that could treat chronic inflammation in these non-infectious diseases without crippling the immune system.


Alzheimer’s, atherosclerosis and type-2 diabetes—diseases associated with aging and inflammation—affect more than 100 million Americans.


When the body encounters a pathogen, it unleashes a rush of chemicals known as cytokines that draws immune cells to the site of infection and causes inflammation.

Particulate matter in the body, such as the cholesterol crystals associated with vascular disease and the amyloid plaques that form in the brain in Alzheimer’s disease, can also cause inflammation but the exact mechanism of action remains unclear.

Researchers previously thought that these crystals and plaques accumulate outside of cells, and that macrophages—immune cells that scavenge debris in the body—induce inflammation as they attempt to clear them.

“We’ve discovered that the mechanism causing chronic inflammation in these diseases is actually very different,” says Kathryn J. Moore, PhD, senior author of the study and associate professor of medicine and cell biology, Leon H. Charney Division of Cardiology at NYU Langone Medical Center.


The researchers found that particulate matter does not linger on the outside of cells. Instead, a receptor called CD36 located on macrophages draws the soluble forms of these particles inside the cell where they are transformed into substances that trigger an inflammatory response.


Says Dr. Moore, “What we found is that CD36 binds soluble cholesterol and protein matter associated with these diseases, pulls them inside the cell, and then transforms them. The resulting insoluble crystals and amyloid damage the macrophage and trigger a powerful cytokine, called interleukin-1B, linked to a chronic inflammatory response.”


These findings hold exciting clinical implications.

When the researchers blocked the CD36 receptor in mice with atherosclerosis (in which cholesterol thickens the arteries), the cytokine response declined, fewer cholesterol crystals formed in plaques, and inflammation decreased.

Consequently, atherosclerosis also abated.


Other less-targeted strategies to control inflammation may hamper the immune response, but the CD36 strategy spares certain cytokines to fight off pathogens, while blocking CD36’s ability to trigger interleukin-1B.

“Our findings identify CD36 as a central regulator of the immune response in these conditions and suggest that blocking CD36 might be a common therapeutic option for all three diseases,” says Dr. Moore.

Support for this work comes from The National Institutes of Health and the American Heart Association.

Original press release: http://communications.med.nyu.edu/media-relations/news/researchers-discover-new-way-block-inflammation-alzheimer’s-atherosclerosis-and