Painless laser device could spot early signs of disease

Researchers say that the technique could become widely available in about five years.

The method, called Raman spectroscopy, could help spot the early signs of breast cancer, tooth decay and osteoporosis.

Scientists believe that the technology would make the diagnosis of illnesses faster, cheaper and more accurate.

Raman spectroscopy is the measurement of the intensity and wavelength of scattered light from molecules.

It is already being used in the chemical and pharmaceutical industries. For instance, Raman lasers are used to measure flame characteristics. By studying how fuels burn, pollution from the products of combustion can be minimised.

Michael Morris, a chemistry professor at the University of Michigan, US, has been using Raman for the past few years to study human bones.

So far, he has been working on cadavers, but he says that Raman could prove effective in living patients.

"You can replace a lot of procedures, a lot of diagnostics that are out there right now. The big advantage is that it's non-invasive, pretty fast - much faster than classical procedures - and more accurate," he told BBC News.

When a person is sick, or about to become sick, the chemical mix in the tissue is quite different from that in healthy tissue, scientists say. So the Raman spectrum changes depending on the tissue it analyses, Professor Morris explained.

"Raman gives you a molecular fingerprint, a composition of whatever it is you're measuring," he said.

"In diseased states, the chemical composition is either slightly abnormal or very markedly abnormal, depending upon the diseases."

Non-invasive

The diagnoses could be carried out in a matter of minutes and without need for an X-ray.

"A patient simply puts his or her wrist on a table and then we have the optical fibres delivering laser light... connected to a holder, a sort of a bracelet made out of silicon, that is strapped to the patient's wrist," explained Professor Morris.

"We turn on the laser and after we've collected enough signal in a few minutes, we turn it off. In principle, it will take a couple of seconds to interpret the results."

Besides bone diseases, the tool could prove effective in detecting early tooth decay, say researchers.

And drawing blood might become unnecessary in some cases. For instance, to determine the levels of cholesterol, one would simply have to point the laser "where you would be looking to draw a blood sample at the crook of the arm, where the blood vessels are very close to the skin," said Professor Morris.

New applications

Another application could be using Raman as a non-invasive alternative to a typical mammography - a process that uses low-dose X-rays to screen patients for signs of breast cancer.

The laser would "look" into the tissue and generate different spectra - a distribution of colours reflecting differences in the properties of the tissue. This could reveal benign or malignant tumours, depending on characteristic changes in the protein structure and in the relative amounts of protein, lipids and nucleic acids in the tissue.

British researchers at the Rutherford Appleton Laboratory in Didcot and at the Gloucestershire Royal Hospital have been using Raman to analyse calcifications in breast tissue that might be early signs of cancer.

"We could target those calcifications and make a decision about whether they're benign or malignant," Nicholas Stone, head of the biophotonics research unit at the Gloucestershire Royal Hospital told the magazine Chemical and Engineering News.

"If they're malignant, or look like they are, you would come back for a biopsy. If they're benign, which is 80 to 90% of the cases, you would not come back for a biopsy."

"In the UK alone, that would save about 80,000 patients from having secondary procedures."

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How Injured Nerves Grow Themselves Back

Unlike nerves of the spinal cord, the peripheral nerves that connect our limbs and organs to the central nervous system have an astonishing ability to regenerate themselves after injury. Now, a new report in the October 1st issue of Cell, a Cell Press publication, offers new insight into how that healing process works.

"We know a lot about how various cell types differentiate during development, but after a serious injury like an amputation, nerves must re-grow," said Allison Lloyd of University College London. "They need a new mechanism to do that because the developmental signals aren't there."

That kind of regrowth isn't easy to pull off. Peripheral nerves are long cells; their nucleus is in the spinal cord and the axons that extend from them and relay nerve messages can reach all the way down a leg. "When a nerve gets cut, all the axons downstream degenerate," Lloyd said. Regrowth requires that the two ends somehow find their way back to each other through damaged tissue.

Scientists knew that Schwann cells were important to that process. Those cells are found wrapped around axons, where under normal circumstances they are rather "quiet" cells. All of that changes when an injury occurs; those Schwann cells de-differentiate back to a stem-cell-like state and play an important role in bridging the gap to repair damaged neurons.

"Schwann cells could sit on a nerve for years and then, at any point, switch states," Lloyd said. "They are quite unusual cells." (There are other examples of cells that can return to a stem-cell-like state, she said. For instance, cells in the liver and the endothelial cells that line blood vessels.)

But, the new study shows, the Schwann cells need help to repair the nerves properly. That help comes from a well-studied cell type known to play a role in wound healing: fibroblasts.

"This is a new role for fibroblasts," Lloyd said, an exciting find given that the cells are the type that grows when you place animal tissue in cell culture and have been very well studied as a result. "There is lots known about them, and they are always present at wounds. This shows that they act in a completely new way."

The fibroblasts send a signal to the Schwann cells, causing them to sort themselves into clumps, or cords, that make their way out of the nerve stump as a group. Those cords guide the regrowth of axons across the wound. Lloyd's team found that the response to the so-called ephrin-B signal issued by the fibroblasts depends on a factor called Sox2, best known for its central role in embryonic stem cells. Sox2 is also one of a handful of ingredients that can help reprogram adult cells to behave like embryonic stem cells.

Without the ephrin-B signal, Schwann cells fail to migrate in an organized fashion and the axons don't grow back properly.

Lloyd said the new findings might lead to ways to improve the repair of peripheral nerves, noting that the natural process isn't all that efficient. "It's not perfect, but if a hand is cut off and sewn back on, you can get some movement," Lloyd said. Her team is actively exploring ways to improve upon the natural nerve-healing mechanism now.

The researchers also have plans to investigate whether similar mechanisms might be involved in the movement and spread of cancers of the peripheral nervous system. "We don't know yet, but it wouldn't be surprising if this is relevant to the movement of other cells," Lloyd said.

The researchers include Simona Parrinello, MRC Laboratory for Molecular Cell Biology and the UCL Cancer Institute, University College London, London, UK; Ilaria Napoli, MRC Laboratory for Molecular Cell Biology and the UCL Cancer Institute, University College London, London, UK; Sara Ribeiro, MRC Laboratory for Molecular Cell Biology and the UCL Cancer Institute, University College London, London, UK; Patrick Wingfield Digby, MRC Laboratory for Molecular Cell Biology and the UCL Cancer Institute, University College London, London, UK; Marina Fedorova, MRC Laboratory for Molecular Cell Biology and the UCL Cancer Institute, University College London, London, UK; David B. Parkinson, University of Plymouth, Plymouth, UK; Robin D.S. Doddrell, University of Plymouth, Plymouth, UK; Masanori Nakayama, University of Munster, Munster, Germany; Ralf H. Adams, University of Munster, Munster, Germany; and Alison C. Lloyd, MRC Laboratory for Molecular Cell Biology and the UCL Cancer Institute, University College London, London, UK.

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Faulty Gene Causes Common Migraines

A new study led by researchers from Canada and the UK suggests that a faulty gene causes common migraines: when the gene is not switched on, it inhibits a protein that regulates the threshold of sensitivity of pain centres in the brain.

You can read how the study, led by researchers from the University of Montreal and the University of Oxford, with contributions from other members in the UK and Canada and also Portugal and Australia, arrived at this result in the 26 September online issue of the journal Nature Medicine.

Migraine headaches are a debilitating condition that affect one in five women and one in ten men worldwide; the World Health Organization rates it as a leading cause of disability worldwide and it is also thought to be the most costly neurological disorder in Europe.

The headaches are severe and long-lasting and usually start as a throbbing pain on one side or the front of the head. Sometimes the pain is preceded by a visual disturbance called an "aura", often experienced as blind spots, zigzag lines, flashing lights, visual hallucinations, or tingling in an arm or leg.

The headache itself can also be accompanied by other symptoms such as sensitivity to light and smells, as well as nausea and occasional vomiting.

While previous studies have linked certain parts of human DNA to increased risk of migraines in the general population, none has yet, before this study, found genes directly responsible for common migraines.

In this latest study, the researchers found that a mutation in the KCNK18 gene inhibits the function of a protein called TRESK, which plays an important part in nerve cell communication: it helps to regulate the sensitivity threshold of pain centres in the brain.

The team compared the DNA of people who suffer from migraines with that of people who do not. They found that one large family of sufferers of migraine with aura carried the mutation.

Lead author Ron Lafreniere, Associate Director of the Centre of Excellence in Neuromics of the Université de Montréal (CENUM), said in a statement that:

"We found a mutation in the KCNK18 gene that interrupts TRESK function in one large family suffering from migraine with aura."

"When we tested everyone in the family, all those who suffered from migraine also had the mutation," he added.

Before this study, genes for migraine have only been found in a rare form of the disorder that is accompanied by limb weakness on one side of the body.

"We focused on the more common types of migraine, without this muscle weakness, in our study, and looked at genes controlling brain excitability," explained Lafreniere.

Co-author Dr Zameel Cader, from the MRC Functional Genomics Unit at Oxford, told the press that:

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