The sensor, which has been successfully tested by researchers in Switzerland, could also be used by emergency room doctors to determine whether a patient has developed diabetic ketoacidosis, a potentially serious complication that happens when diabetics do not take enough insulin.

Even diabetics could use the technology someday in their own homes, to determine whether they need more insulin.

Professor Sotiris E. Pratsinis and colleagues at ETH Zurich in Switzerland explain that everyone has a little bit of acetone in their breath.

But people with Type I diabetes release unusually high levels of the chemical when they exhale.

If they have diabetic ketoacidosis, a dangerous buildup of acetone in the blood, they exhale even-larger amounts of acetone.

The researchers built an extremely sensitive acetone detector by directly depositing from a flame plume a thin film of semiconducting, mixed ceramic nanoparticles between a set of gold electrodes.

The device acts like an electrical resistor. When it gets hit with a puff of acetone-filled air, its resistance drops, allowing more electricity to pass between the electrodes.

If a diabetic were to breathe on the sensor, its resistance would suddenly drop.

When a healthy person exhales onto the nanoparticles, their resistance will not change very much.

The scientists found this new sensor can detect acetone in extremely moist air, an attribute that is critical for any breath test.

It is sensitive enough to detect acetone at 20 parts per billion, a concentration that is 90 times lower than the level at which it can be found in the breath of diabetic patients.

The study has been published in ACS’ Analytical Chemistry, a semi-monthly journal. (ANI)

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Researchers transcribed the complete genetic blueprints for a pair of identical twins, looking for differences that might explain why one has multiple sclerosis and the other does not. No trace of what caused the discrepancy appeared in the twins’ DNA. And scientists found no smoking gun when they compared levels of gene activity between the sick and well twin. The results appear in a report published April 29 in Nature.

“We looked under a lot of rocks and we found no differences that we could replicate,” says Stephen Kingsmore, a geneticist at the National Center for Genome Resources in Santa Fe, N.M., and leader of the new study. The finding “points to some novel environmental trigger that must be very important to the disease. We don’t know what it is.”

But the new study is small; it examines only three pairs of twins and one type of immune cell known to be involved in multiple sclerosis. A telling difference between sickness and health might be found in other types of cells, such as immune cells called B cells or in oligodendrocytes, which are cells that make the nerve cell insulation called myelin, says Esteban Ballestar of the Bellvitge Biomedical Research Institute in Barcelona, Spain. “They are closing a door here, but I think, perhaps, the door should be open,” he says.

In multiple sclerosis the immune system attacks and damages the myelin sheath that helps speed electrical communication between nerves, the equivalent of scraping the coating away from an electrical wire. The damage results in pain and symptoms such as loss of coordination and vision.

In the new study, Kingsmore and his colleagues determined the entire genetic makeup of immune cells called T cells from a pair of female twins. One of the women developed multiple sclerosis at age 30 while her twin remained healthy. The twins are now old enough that the healthy one is not likely to develop the disease.

Identical twins share the same genetic makeup, and the researchers confirmed that both women carried variants of genes already known to increase the risk of getting multiple sclerosis. Scientists had thought that maybe the sick twin had developed an additional mutation in her DNA that finally triggered the disease. But the team found no such mutations.

Another way to rev up the immune system and induce it to attack the body is to increase the activity of certain genes. Upping gene activity doesn’t necessarily involve changing the genes themselves, but can be done by altering chemical tags on the DNA. In two pairs of twins, the team examined more than 2 million DNA locations that had been tagged with a common label, known as a methyl group, that keeps gene activity in check.

In a previous study, Ballestar’s group found lower levels of methylated DNA when they compared people with lupus (SN: 1/16/2010, p.13) to their healthy identical twins. But Kingsmore and his colleagues found no similar differences that could account for just one twin developing MS.

The team also measured gene activity in three sets of identical twins, including the sisters who had their genomes sequenced. The researchers did find some minor differences, but none could explain why one twin got sick and the other didn’t.

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Researchers found a compound from a New Zealand blackcurrant may reduce lung inflammation with a multi-action assault in allergy-induced asthma. The compound was found in laboratory experiments to enhance the natural defence mechanisms in lung tissue by both suppressing inflammation-causing reactions and minimising inflammation.

The findings are published in the journal Molecular Nutrition and Food Research.

Fruit consumption has been shown to reduce symptoms in allergy-induced asthma yet this research is the first to give insights into the mechanism by which this may occur. The researchers identified that the component, epigallocatechin, reduced inflammation in lung tissue. Epigallocatechin is a known antioxidant and a major component of proanthocyanidins found in blackcurrants.

In the Plant & Food Research study, led by Dr Roger Hurst, cells from lung tissue were used to test the effects on the immune system of a proanthocyanidin rich extract, from blackcurrant cultivars grown in New Zealand.

When the lungs are exposed to allergens, the body’s natural response is to attack the perceived foreign body which in some individuals results in long-term inflammation. Selective compounds found in fruit and vegetables may work together with the body’s own natural defence mechanism to suppress long-term lung inflammation.

This study shows that epigallocatechin, from blackcurrants, works in conjunction with other natural immune responses that occur at the same time to reduce inflammation. These actions are distinct from the inflammation-reducing activity of another group of compounds, anthocycanins, which are also rich in blackcurrants. Anthocyanins are known for their antioxidant properties and, interestingly, have been shown by Dr Hurst’s research group to also influence inflammatory mechanisms and complement the body’s own natural immune responses. The research shows some compounds in fruit thought to promote health with their antioxidant activity are keeping us well by other means.

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