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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 SemestersFemale Reproductive SystemFertilizationThe Appearance of SomitesFirst TrimesterSecond TrimesterThird TrimesterFetal 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 HemispheresEnd of Embryonic PeriodEnd of Embryonic PeriodFirst Thin Layer of Skin AppearsThird TrimesterDevelopmental Timeline
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September 26, 2012--------News Archive Return to: News Alerts

Lindsay, age 18 months. Photo courtesy of the Progeria Research Foundation

Human cell nucleus. The nucleolus is contained within the cell nucleus.

Structure and function of the nuclear lamina:
The nuclear lamina lies on the inner surface of the inner nuclear membrane (INM),
where it serves to maintain nuclear stability, organize chromatin and bind nuclear
pore complexes (NPCs) to a steadily growing list of nuclear
envelope proteins (purple) and transcription factors (pink)

Images: Wikipedia

WHO Child Growth Charts


Treatment for 'Untreatable' Progeria has Roots in Basic Cell Research

Clinical trial reports significant slowing of rare rapid aging disorder, progeria, in children

The good news being widely reported, is of positive results from a clinical drug trial at Boston Children's Hospital. The previously "untreatable" rapid aging disorder in children known as progeria is rooted in basic biology discoveries made in recent years.

In the two and a half year since the clinical trial began, physicians at Boston Children's have given Lonafarnib to 26 children with progeria.

The use of farnesyl transferase inhibitors (FTI)
significantly slows the progress of progeria,
a rare and – until now "untreatable"–
lethal genetic disorder.

Known as Hutchinson-Gilford Progeria Syndrome
(HGPS), progeria has been described as out-of-control
rapid aging in children. A ""normal"" baby born
with HGPS will stop growing by 16-18 months
and quickly develop signs of old age including
hair loss, thin skin, osteoporosis and, progressive
arteriosclerosis. By 10 years of age
progeria children appear to be 80.

The work published in the Proceedings of the National Academy of Sciences (PNAS) paper shows a significant slowing of bone loss and blood vessel blockage in children with progeria. The clinical trial grew out of the identification of the defective progeria gene, LMNA, in 2003 by the Human Genome Project and the laboratory of current NIH Director, Francis Collins.

But the link to defective proteins – called lamins – that make up the envelope surrounding the cell nucleus came about through "untargeted" basic cell biology research.

Veteran lamin researchers remember having
their grant applications dismissed by
review panels as "boring" and irrelevant.

But basic work by Robert Goldman of
Northwestern University School of Medicine
and other nuclear lamin researchers around the world
revealed that a greasy tag molecule called farnesyl
accumulates on defective Lamin A proteins.

The Lamin A protein burdened with farnesyl molecules,
eventually warps the structure of the entire nuclear
envelope, disrupting the orderly dispersion of gene
messages to direct normal growth within the nucleus.

The identification of the defective LMNA gene transformed progeria into a "laminopathy," a now growing class of diseases caused by problems with the once-irrelevant nuclear lamins. "Normal" aging is thought to involve many of the same processes as do laminopathies.

With the discovery of the lamin link, clinical researchers were suddenly looking for farnesyl transferase inhibitors (FTI) to treat progeria. They zeroed in on Lonafarnib, an FTI drug developed by Merck. It had been extensively tested and found safe for use in adults and children, but ineffective against its initial brain cancer targets.

The American Society for Cell Biology has been reporting on progeria since 2006. In 2008, the ASCB Newsletter published a report on the proposed clinical drug trial. The ASCB has pulled together a file of these earlier reports for reporters and the general public interested in the deeper scientific background of progeria at: http://www.ascb.org/progeria-background.html

The PNAS paper was published online before print September 24, 2012, doi: 10.1073/pnas.1202529109 PNAS September 24, 2012 Gordon, Leslie B. et al, Clinical trial of a farnesyltransferase inhibitor in children with Hutchinson–Gilford progeria syndrome

Reporters: For further information, contact ASCB Science Writer John Fleischman, jfleischman@ascb.org or 513-706-0212.

Original article: http://www.ascb.org/index.php?option=com_content&view