By observing the skin of mice at the cellular level over a whole year, they have turned previous thinking about skin renewal on its head. Their research is published today on Nature Online.

Previously, it was thought that two types of cells were needed to regenerate skin: adult stem cells and short lived cells that soon stopped dividing. New research led by the MRC Cancer Cell Unit in Cambridge found that what actually happens is very different. The adult stem cells don't seem to do anything in normal skin. Their role is to help repair and replace injured skin. The MRC scientists found that the skin is actually regenerated by non stem cells behaving in a very surprising way. Most cells expand by doubling, producing 2, 4, 8, etc, daughter cells as they grow.

Dr Philip Jones who led the research explained: "Using a fluorescent genetic marker and 3D imaging, we found that the cells followed a 1, 2, 3, 4, 5 growth model, where one of the daughter cells stops growing after cell division while the other carries on. This means that regular, healthy skin maintains itself on its own without the skin adult stem cell population being involved. One of the implications of this is that these progenitor skin cells can also potentially go bad and cause skin cancer if they linger long enough."

Being able to track these cells in the actual animals at the cellular level over a year has allowed the scientists to develop mathematical models for predicting confidently what happens to skin long-term for the first time. These models may help to understand what genes do and inform our understanding of how cancer develops. They could also allow us to refine our drug testing procedures. This has led the team to patent this new mathematical tool for predicting skin growth.

"Our ultimate goal though is to be able to model the evolution of cancer from the single cell stage onwards so we can find better ways to tackling the disease. By using the right gene to label the cells, this might just be possible." said Dr Jones.

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Cortisol belongs to a class of human hormones known as glucocorticoids that have been shown to kill hippocampal cells in animals; a reduction in hippocampal size can make it more difficult for a child to process and deal with traumatic events, which in turn may raise both stress and cortisol levels that cause even more damage; all in all a vicious cycle.

Carrion says everyday levels of stress are necessary to stimulate normal brain development, but excess levels can be harmful.

Carrion says a common treatment for PTSD is to encourage a sufferer to develop a narrative of the traumatic experience, however if the stress of the event is affecting areas of the brain responsible for processing information and incorporating it into a story, that treatment may not be as effective.

Carrion and his team are now using an imaging technique known as functional MRI, in order to visualize whether and how the children's brains differ when performing emotional and cognitive tasks.

Carrion says they know that PTSD is chronic and pervasive but hopefully with further research more effective, targeted interventions will be developed to help such children.

Experts are already aware of the importance genes and environment play, and they say that there is increasing evidence that adversity in early life can have long-lasting results on subsequent mental and physical health, and that at least some of these associations are the result of changes in the secretion of cortisol.

The major question remains - is the smaller hippocampus a predictor of PTSD or a consequence?

The study was funded by the National Institutes of Health, the National Alliance for Research on Schizophrenia and Depression, the American Foundation for Suicide Prevention and the Aloha Foundation.

The study is published in the March issue of Pediatrics.