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Welcome to The Visible Embryo, a comprehensive educational resource on human development from conception to birth.

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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 Sept 26, 2014

The protein called neuregulin-4 (NRG4) is present in breast milk but absent in formula.
Research has found that NRG4 protects against the intestinal destruction caused by NEC.


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Breast milk protects infant from intestinal disorder

Growth factor found in breast milk protects against devastating intestinal disorder of newborn infants — necrotizing enterocolitis, or NEC.

Premature infants are at increased risk for the potentially lethal gastrointestinal disease Necrotizing Enterocolitis, or NEC. Research from Children's Hospital Los Angeles demonstrates that a protein called neuregulin-4 (NRG4) — which is present in breast milk but absent in formula— protects against the intestinal destruction caused by NEC.

Human NEC is characterized by a loss of specialized intestinal cells called Paneth cells. Located throughout the small intestine, Paneth cells protect the small intestine from microbial damage. They also sustain intestinal stem cells, required for renewal of intestinal lining. A mouse model of NEC demonstrated NRG4 prevents loss of Paneth cells.

Their results are published in the American Journal of Pathology.

Thirty percent of babies with NEC die from their disease. Survivors can face lifelong consequences that may include removal of part of their intestine and dependence upon intravenous nutrition. Formula feeding is a known risk factor for the disease.

"Our research suggests that without the NRG4 protein found in breast milk, normal protection for the immature gut may be missing. If a baby on formula encounters a NEC trigger — such as intestinal infection or injury — he or she may be at increased risk for a life-threatening condition."

Mark R. Frey, PhD, principal investigator, the Saban Research Institute of Children's Hospital Los Angeles.

Investigators conducted studies with mice, as well as analysis of human breast milk and human infant intestinal tissue. Formula-fed mice developed a condition similar to NEC, but those receiving formula plus NRG4 were protected against intestinal damage. These experiments suggest that NRG4 binds to a receptor found in the intestine — ErbB4 — to block inflammatory damage.

"We're finding a protective protein in breast milk, with its receptor in the intestine. Given that NEC is a significant clinical problem without an effective treatment, we plan to evaluate NRG4 for its therapeutic potential in this disease."

Mark R. Frey, assistant professor of Pediatrics and Biochemistry & Molecular Biology, Keck School of Medicine of the University of Southern California.

Necrotizing enterocolitis (NEC) affects up to 10% of premature infants, has a mortality of 30%, and can leave surviving patients with significant morbidity. Neuregulin-4 (NRG4) is an ErbB4-specific ligand that promotes epithelial cell survival. Thus, this pathway could be protective in diseases such as NEC, in which epithelial cell death is a major pathologic feature. We sought to determine whether NRG4-ErbB4 signaling is protective in experimental NEC. NRG4 was used i) in the newborn rat formula feeding/hypoxia model; ii) in a recently developed model in which 14- to 16-day-old mice are injected with dithizone to induce Paneth cell loss, followed by Klebsiella pneumoniae infection to induce intestinal injury; and iii) in bacterially infected IEC-6 cells in vitro. NRG4 reduced NEC incidence and severity in the formula feed/hypoxia rat model. It also reduced Paneth cell ablation–induced NEC and prevented dithizone-induced Paneth cell loss in mice. In vitro, cultured ErbB4−/− ileal epithelial enteroids had reduced Paneth cell markers and were highly sensitive to inflammatory cytokines. Furthermore, NRG4 blocked, through a Src-dependent pathway, Cronobacter muytjensii–induced IEC-6 cell apoptosis. The potential clinical relevance of these findings was demonstrated by the observation that NRG4 and its receptor ErbB4 are present in human breast milk and developing human intestine, respectively. Thus, NRG4-ErbB4 signaling may be a novel pathway for therapeutic intervention or prevention in NEC.

Additional contributors include first author Steven J. McElroy of the University of Iowa; Shannon L. Castle, Jessica K. Bernard, Dana Almohazey, Brandon A. Bell, Denise Al Alam, Larry Wang, and Henri R. Ford of The Saban Research Institute of Children's Hospital Los Angeles; and Catherine Jane Hunter of the Ann and Robert H. Lurie Children's Hospital, Northwestern University.

Funding for this study was provided by National Institutes of Health grants R01DK095004, K01DK077956, R03DK090295, K08DK0836777, R01AI014032, by a Senior Research Award from the Crohn's and Colitis Foundation of America, and a Research Career Development Award from The Saban Research Institute.

About Children's Hospital Los Angeles
Children's Hospital Los Angeles has been named the best children's hospital on the West Coast and among the top five in the nation for clinical excellence with its selection to the prestigious U.S. News & World Report Honor Roll. Children's Hospital is home to The Saban Research Institute, one of the largest and most productive pediatric research facilities in the United States. Children's Hospital is also one of America's premier teaching hospitals through its affiliation since 1932 with the Keck School of Medicine of the University of Southern California.

For more information, visit CHLA.org and follow us on ResearCHLAblog.org.
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