Blood tests for cancer and other diseases could be carried out in minutes using a revolutionary microchip detector.

Scientists have successfully tested the technology for the first time to detect biomarkers for prostate and breast cancer.

The device uses arrays of tiny "nanosensors" that catch specific proteins in blood.

It could be developed to test for numerous conditions ranging from cancers to heart disease at the same time.

"Doctors could have these small, portable devices in their offices and get nearly instant readings," said Dr Tarek Fahmy, a member of the US development team at Yale University.

"They could also carry them into the field and test patients on site."

At present blood tests involve taking a sample, sending it to a laboratory, and subjecting it to chemical analysis.

Often patients have to wait several days to get their results. The new microchip can deliver biomarker readings in a matter of minutes.

The device is also much more precise than existing technologies so that results are less dependent on human interpretation.

The chip is embedded with microscopic nanowires sensitive to certain "antigen" proteins which act as markers for different diseases. The research is reported in the journal Nature Nanotechnology.

Scientists have discovered five genetic variants that are associated with the health of the human lung. The research by an international consortium of 96 scientists from 63 centres in Europe and Australia sheds new light on the molecular basis of lung diseases.

The new findings provide hope for better treatment for lung diseases like Chronic Obstructive Pulmonary Disease (COPD) and asthma. In the past it has been difficult to develop new treatments because the molecular pathways that affect the health of the lung are not completely understood. It's hoped the new pathways discovered could in the future be targeted by drugs.

The ground-breaking research involved a genetic study of 2.5 million sites across the human genome involving samples from 20,000 people across the world. The consortium was led by Dr Martin Tobin from the University of Leicester and Professor Ian Hall from The University of Nottingham.

The research, part-funded by the Medical Research Council (MRC) and Asthma UK, is published today in Nature Genetics. It represents a significant advance because it is the first time that these five common genetic variations have been definitely linked with lung function.

The scientists said: "This work is important because until now we have known very little about the genetic factors that determine an individual's lung function. By identifying the genes important in determining lung function, we can start to unravel the underlying mechanisms which control both lung development and lung damage. This will lead to a better understanding of diseases such as chronic obstructive pulmonary disease (COPD) and asthma. Crucially, it could open up new opportunities to manage and treat patients with lung conditions".

The authors added: "A large reduction in lung function occurs in chronic obstructive pulmonary disease (COPD), which affects around 1 in 10 adults above the age of 40 and is thought to be the fourth most common cause of death worldwide. Smoking is the major risk factor for development of COPD. Lung function and COPD cluster within families, indicating that variations in genes also predispose individuals to reduced lung function.

"The scientists of the SpiroMeta consortium compared genetic variants at each of 2.5 million sites across the human genome in over 20,000 individuals of European ancestry with their lung function measures. In five different locations in the human genome, genetic variants resulted in alterations in lung function. The scientists showed that these were real findings by checking the effects of the same variants in over 33,000 additional individuals. They also compared their results to those of a second consortium, CHARGE, which has published a paper in the same issue of the journal.

The scientists emphasise that they do not expect these findings to lead to immediately to genetic tests to predict who will develop lung disease. What is more important, they say, is that the findings will help understand the underlying causes of lung diseases and thus may indicate new ways of treating the condition.

Blood vessel blockage, a common condition in old age or diabetes, leads to low blood flow and results in low oxygen, which can kill cells and tissues. Such blockages can require amputation resulting in loss of limbs. Now, using mice as their model, researchers at Johns Hopkins have developed therapies that increase blood flow, improve movement and decrease tissue death and the need for amputation. The findings, published online last week in the early edition of the Proceedings of the National Academy of Sciences, hold promise for developing clinical therapies.

"In a young, healthy individual, hypoxia low oxygen levels triggers the body to make factors that help coordinate the growth of new blood vessels but this process doesn't work as well as we age," says Gregg Semenza, M.D., Ph.D., professor of pediatrics and genetic medicine and director of the vascular biology program at the Johns Hopkins Institute for Cell Engineering. "Now, with the help of gene therapy and stem cells we can help reactivate the body's response to hypoxia and save limbs."

Previously, Semenza's team generated a virus that carries the gene encoding an active form of the HIF-1 protein, which turns on genes necessary for building new blood vessels. When injected into the hind legs of otherwise healthy mice and rabbits that had been treated to reduce blood flow, the HIF-1 virus treatment partially restored blood flow.

People with diabetes have a 40 times higher risk of losing a limb to amputation, says Semenza. To find out if HIF-1 gene therapy could improve blood flow in a diabetic animal, the team then tested the same virus in diabetic and non-diabetic mice that had blood flow cut off to one hind leg. Twenty-one days after treatment, the HIF-1 virus-treated mice had 85 percent recovery of blood flow compared with 24 percent in the mock-treated mice. And, treated, diabetic mice had much less tissue damage compared to the untreated diabetic mice. These results were reported in the Nov. 3 issue of the Proceedings of the National Academy of Sciences.

In the current study, the team asked if the same gene therapy treatment could improve reduced blood flow associated with advanced age. Comparing 13 month old mice to 3 month old mice, blocking the femoral artery in the hind leg causes all older mice to lose their legs while only about a third of younger mice have to lose their legs. The research team treated young and old mice with the HIF-1 virus and examined blood flow and tissue health. They found that while treatment improved young mice, it did not make a noticeable difference in the older mice.

But, it was known that when HIF-1 normally activates signals in the body to build new vessels, one of the many types of cells recruited to the site of new vessel growth is a population of stem cells from the bone marrow, which are called bone marrow-derived angiogenic cells. So the team isolated these cells from mice and grew them under special conditions that would turn on HIF-1 in these cells.

When the researchers treated the mice with both the HIF-1 virus and simultaneously injected bone marrow-derived angiogenic cells, treated, older mice were less likely to lose their legs compared to their untreated counterparts.

Further study of these mice showed that activating HIF-1 in the cells appeared to turn on a number of genes that help these cells not only home to the ischemic limb, but to stay there once they arrive. To figure out how the cells stay where they're needed, the research team built a tiny microfluidic chamber and tested the cells' ability to stay stuck with fluid flowing around them at rates mimicking the flow of blood through vessels in the body. They found that cells under low oxygen conditions were better able to stay stuck only if those same cells had HIF-1 turned on.

"Our results are promising because they show that a combination of gene and cell therapy can improve the outcome in the case of critical limb ischemia associated with aging or diabetes," says Semenza. "And that's critical for bringing such treatment to the clinic."

Fifteen minutes of treatment with high flow oxygen significantly eased cluster headaches, according to a new study.

Cluster headache attacks, characterised by bouts of excruciating pain usually near the eye or temple, typically last for 15 minutes to three hours if untreated and have a frequency of up to eight attacks a day on alternate days.

High flow oxygen is given at a rate of six to seven litres per minute for 10 to 20 minutes at the start of a cluster headache.

Attacks usually occur in bouts, or clusters, lasting for weeks or months, separated by remissions lasting months or years, according to the study.

The current treatment for acute attacks of cluster headache is injection with the drug sumatriptan, but frequent dosing is not recommended because of adverse effects.

Another treatment option is the inhalation of high-dose, high-flow oxygen, but its use may be limited because of the lack of a good quality controlled trial.

Anna S. Cohen, of the National Hospital for Neurology and Neurosurgery, and colleagues conducted a randomised, placebo-controlled trial of high-flow oxygen for the treatment of acute attacks of cluster headache.

The study included 109 adults (aged 18-70 years). Patients treated four cluster headache episodes alternately with high-flow oxygen (inhaled oxygen at 100 percent, or 12 litres per minute, delivered by face mask, for 15 minutes at the start of an attack) or placebo (high-flow air).

Patients were recruited and followed up between 2002 and 2007. The final analysis included 57 patients with episodic cluster headache and 19 with chronic cluster headache.

The researchers found that 78 percent of the patients who received oxygen reported being pain-free or to have adequate relief within 15 minutes of treatment, compared to 20 percent of patients who received air.

For other outcomes, such as being pain-free at 30 minutes or a reduction in pain up to 60 minutes, treatment with oxygen was superior to air. There were no serious adverse events related to the treatments, says a National Hospital release.

"To our knowledge, this is the first adequately powered trial of high-flow oxygen compared with placebo, and it confirms clinical experience and current guidelines that inhaled oxygen can be used as an acute attack therapy for episodic and chronic cluster headache," the authors write.

The study appeared in the Wednesday issue of JAMA.

'Live' pictures of spreading breast cancer cells have highlighted a biological pathway that scientists hope will lead to new treatments.

Researchers tagged cancer cells in laboratory mice with a protein that glowed blue when the tumour-spreading process was active.

The cells were driven from the main tumour into the blood by a biological 'control switch' called transforming growth factor beta (TGFb).

Once in the blood stream, they could easily travel to other parts of the body. Cancer spread to organs such as the brain or liver, known as metastasis, is what kills most patients with the disease.

The research opens up new avenues for developing drugs that prevent or reduce metastasis.

Study leader Dr Erik Sahai, from the charity Cancer Research UK, said: "The results helped us to find the set of genes that are behind the spread of breast cancer - and that the genes need to be first turned on and then off in order for single cancer cells to be able to 'relocate'."

The findings were published in the journal Nature Cell Biology and also presented at the annual meeting of the American Society for Cell Biology in San Diego, California.

Previous research had shown that TGFb can regulate normal cell growth and movement.

In the new study, cells were observed as one-by-one they broke away and entered the blood circulation.

The blue tag protein showed when the TGFb control system was active. Metastasis occurred when TGFb first turned on certain messenger genes in the cancer cells and then turned them off.