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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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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 Sep 23, 2013

 



In the study, researchers used animal models to examine the interactions between two cell receptors: EGFRvIII and RIP1. Both are used to activate NFκB, a family of proteins important to the growth of cancerous tumor cells.






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Switch controls most aggressive brain tumor cells

Scientists have identified a cellular switch that potentially can be turned off and on to slow down, and eventually inhibit the growth of the most commonly diagnosed and aggressive malignant brain tumors.

Findings of researchers at UT Southwestern Medical Center show that the protein RIP1 acts as a mediator of brain tumor cell survival, either protecting or destroying cells. Researchers believe that the protein, found in most glioblastomas, can be targeted to develop a drug treatment for these highly malignant brain tumors. The study was published online Aug. 22 in Cell Reports.


"Our study identifies a new mechanism involving RIP1that regulates cell division and death in glioblastomas. For individuals with glioblastomas, this finding identified a target for the development of a drug treatment option that currently does not exist."

Dr. Amyn Habib, senior author associate professor of neurology and neurotherapeutics, UT Southwestern, and staff neurologist at VA North Texas Health Care System.


In the study, researchers used animal models to examine the interactions of the cell receptor EGFRvIII and RIP1. Both are used to activate NFκB, a family of proteins that is important to the growth of cancerous tumor cells.


When RIP1 is switched off in the experimental model, NFκB and the signaling that promotes tumor growth is also inhibited.

Furthermore, the findings show that RIP1 can be activated to divert cancer cells into a death mode so that they self-destruct.


According to the American Cancer Society, about 30 percent of brain tumors are gliomas, a fast-growing, treatment-resistant type of tumor that includes glioblastomas, astrocytomas, oligodendrogliomas, and ependymomas.

In many cases, survival is tied to novel clinical trial treatments and research that will lead to drug development.

Summary
RIP1 is a central mediator of cell death in response to cell stress but can also mediate cell survival by activating NF-κB. Here, we show that RIP1 acts as a switch in EGFR signaling. EGFRvIII is an oncogenic mutant that does not bind ligand and is coexpressed with EGFRWT in glioblastoma multiforme (GBM). EGFRvIII recruits ubiquitin ligases to RIP1, resulting in K63-linked ubiquitination of RIP1. RIP1 binds to TAK1 and NEMO, forming an EGFRvIII-RIP1 signalosome that activates NF-κB. RIP1 is essential for EGFRvIII-mediated oncogenicity and correlates with NF-κB activation in GBM. Surprisingly, activation of EGFRWT with EGF results in a negative regulation of EGFRvIII, with dissociation of the EGFRvIII-RIP1 signalosome, loss of RIP1 ubiquitination and NF-κB activation, and association of RIP1 with FADD and caspase-8. If EGFRWT is overexpressed with EGFRvIII, the addition of EGF leads to a RIP1 kinase-dependent cell death. The EGFRWT-EGFRvIII-RIP1 interplay may regulate oncogenicity and vulnerability to targeted treatment in GBM.

The Department of Neurology and Neurotherapeutics at UT Southwestern is ranked in the top 20 in the nation, according to U.S. News & World Report. UT Southwestern physicians routinely deal with the most difficult neurology cases referred from around the region, state, and nation.

The research was conducted with support from the National Institutes of Health, NASA, and the Cancer Prevention and Research Institute of Texas.

UT Southwestern investigators who participated in the study include former postdoctoral researcher Dr. Vineshkumar Puliyappadamba, senior research associate Dr. Sharmistha Chakraborty, former research assistant Sandili Chauncey, and senior research scientist Dr. Li Li, all from the Department of Neurology and Neurotherapeutics. Dr. Kimmo Hatanpaa, associate professor of pathology; Dr. Bruce Mickey, director of the Annette G. Strauss Center in Neuro-Oncology; Dr. David Boothman, professor of radiation oncology and pharmacology in the Harold C. Simmons Comprehensive Cancer Center; and Dr. Sandeep Burma, associate professor of radiation oncology, also contributed to the research.

About UT Southwestern Medical Center
UT Southwestern, one of the premier academic medical centers in the nation, integrates pioneering biomedical research with exceptional clinical care and education. The institution's faculty includes many distinguished members, including five who have been awarded Nobel Prizes since 1985. Numbering more than 2,700, the faculty is responsible for groundbreaking medical advances and is committed to translating science-driven research quickly to new clinical treatments. UT Southwestern physicians provide medical care in 40 specialties to nearly 90,000 hospitalized patients and oversee more than 1.9 million outpatient visits a year.

Original press releas: http://www.utsouthwestern.edu/home/news/index.html