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Two immune system molecules could form the basis of a new test to quickly detect whether tuberculosis is dormant or active and infectious, U.S. researchers said on Sunday.

“A rapid test that could tell the difference between latent and active tuberculosis would be a major step forward,” said Dr. Jason Stout of Duke University Medical Center who presented his findings at the American Thoracic Society meeting in New Orleans.

Doctors could more quickly treat active infections, helping to limit the spread of the disease, Stout said.

Current blood tests can distinguish between people who are infected with TB and those who are not but they cannot tell whether an infection is active or dormant. It takes a culture test that grows the TB bacilli to show if it is active or not, and that can take weeks.

Stout and colleagues collected blood samples from 71 people with active TB, latent TB or no infection at all.

They added a bit of TB bacteria to the blood samples to stimulate an immune response, then measured the activity of 25 immune signaling chemicals called cytokines to try to identify a pattern that could be used as a signature of active TB infection.

“We found that a pattern of two cytokines, called MCP-1 and IL-15, was reasonably good at differentiating between persons sick with TB and persons infected but not sick,” Stout said.

A third cytokine called IP-10 also showed promise at sorting between people who are infected and those who are not.

Stout said other studies have pointed to these three cytokines individually as possible TB markers, but his is the first to put all three together as a possible TB test.

“These findings could lead to earlier diagnosis of active tuberculosis, which could be beneficial for both the sick person and others around her or him who might be spared from infection,” Stout said in a statement.

Tuberculosis killed 1.8 million people in 2008, or nearly 5,000 people a day. It is caused by the Mycobacterium tuberculosis bacteria. More than 2 billion people, or about a third of the world’s population, are thought to be infected.

It is not only a scourge in poor countries but also in the West, where it has flared anew in the last 20 years because of AIDS, which weakens the immune system.

TB can be cured with antibiotics, but they need to be taken daily for months to be effective. Because people often skip doses, multiple drug resistant forms are spreading and the World Health Organization says the hard-to-treat infection is spreading.

(Reporting by Julie Steenhuysen; Editing by Anthony Boadle)

Something in dark chocolate seems to help protect the heart, and now researchers say they have identified the molecular mechanism by which a compound found in cocoa can guard against the damage of a stroke.

The compound, a flavanol called epicatechin, triggers two built-in protective pathways in the brain, according to a report published online last week in the Journal of Cerebral Blood Flow & Metabolism. The research team was led by Sylvain Dore, an associate professor of anesthesiology and critical care medicine and pharmacology and molecular sciences at John Hopkins University School of Medicine in Baltimore.

Animal studies raise the possibility that epicatechin may someday be used to treat strokes in humans, since its protective effect can be seen more than three hours after a stroke. Existing stroke treatments typically have a shorter window of activity.

While the cardioprotective effect of dark chocolate seen in several human studies appears to open the possibility that eating lots of chocolate is healthy, “I prefer to focus on cocoa,” Dore said. “Cocoa is not like chocolate, which is high in saturated fat and calories. Cocoa can be part of a healthy diet, combined with fruits and vegetables.”

It was a study of the cocoa-drinking Kuna Indians, living on islands off the coast of Panama, that led researchers to study epicatechin. An unusually low incidence of stroke and other cardiovascular disease in that population could not be explained by genetic studies, and eventually was attributed to consumption of a very bitter cocoa drink.

Studies by a number of scientists, including Dr. Norman K. Hollenberg of Harvard Medical School, identified epicatechin as the protective ingredient in dark chocolate and cocoa.

The latest research looked at the mechanism of protection in mice who were induced to have strokes. “We gave different doses of epicatechin in mice 90 minutes before a stroke and found that it reduced infarct [stroke damage] size,” Dore explained. “When we gave epicatechin after a stroke, it had a protective effect up to 3.5 hours later, but not after six hours.”

Detailed studies showed that the flavanol activated two well-known pathways that shield nerve cells in the brain from damage, the Nrf2 and heme oxygenase pathways, Dore said. Epicatechin had no protective effect in mice bred to lack those pathways.

The possibility of using epicatechin to limit human stroke damage is distant, Dore said. “We have to be very careful,” he said. “There are a lot of steps before going to human trials, potential risks and side effects. We need more work and more funding.”

Dore’s long-term plan calls for studies of epicatechin metabolites and derivatives, in cardiac disease as well as stroke. “At this point, we are using only the pure compound,” he said.

Dr. Martin Lajous, a doctoral candidate at the Harvard School of Public Health who took part in one study that showed a reduced incidence of stroke in people who ate dark chocolate regularly, agreed with Dore in saying that eating a lot of chocolate is not a healthy dietary move.

Not all chocolate is created equal, Lajous said. “That’s why we did the study in France, where they eat dark chocolate that is rich in flavanols,” he said. “Chocolate comes with a lot of calories. I would talk about small amounts of dark chocolate rather than chocolate in general.”

And the protective mechanism by which chocolate might prevent stroke isn’t yet clear, Lajous added. The main effect appears to be the lowering of blood pressure, he said. “Flavanols are hypothesized to affect relaxation of smooth vascular muscle, such as the endothelial lining of blood vessels,” Lajous said.

SOURCES: Sylvain Dore, Ph.D., associate professor, anesthesiology, critical care medicine, pharmacology and molecular sciences, Johns Hopkins University School of Medicine, Baltimore; Martin Lajous, M.D., doctoral candidate, Harvard School of Public Health, Boston;

Using magnets to stimulate the brain may ease depression in people who have not found relief from antidepressants, new research has found.

“We have settled a fundamental question about [transcranial magnetic stimulation, or TMS] therapy, which is: ‘Does it work?’” said the study’s lead author, Dr. Mark George, a professor of psychiatry, radiology and neuroscience at the Medical University of South Carolina. “The answer is ‘yes.’”

The researchers administered the magnet therapy to half of a group of 190 adults who had been depressed for at least three months, but not longer than five years, and who had taken medication for depression but were not helped. The others were given a sham treatment — simulated magnet therapy that was mostly indistinguishable from the real thing, the researchers said.

After three weeks, about 14 percent of those receiving magnet therapy were no longer depressed, compared with 5 percent who were getting the fake treatment.

The researchers continued the magnet treatment for three more weeks for those who were still depressed and also offered the real treatment to participants who’d gotten the sham treatment.

After that period, about 30 percent were no longer depressed, the researchers said.

“In a rigorous, industry-free multisite trial with a convincing sham, we found unambiguously that TMS worked better than the sham. It’s watershed,” George stated.

The findings are published in the May issue of Archives of General Psychiatry.

Psychiatrists have been interested in the possibilities of treating depression with magnet therapy for more than a decade, the experts said. Magnets are believed to work by creating electrical currents in the nerve cells in the left prefrontal cortex, a region of the brain involved with regulating mood. The current may jump-start the area, which has been shown to be underactive in people who are depressed, George said.

But testing magnet therapy has been difficult. “Double-blind” studies, in which neither the researchers nor participants know who is getting the real treatment and who is getting the fake, have been difficult to carry out.

The current study overcame that by creating an elaborate sham. During magnet therapy, participants were painlessly zapped by a pulsing electromagnetic coil 3,000 times over 37 minutes. The current created a head-tapping sensation that some people said reminded them of a woodpecker, George said.

The coil, which is aimed at the brain area to be stimulated, creates a magnetic field that passes through the skin and skull, inducing an electrical current in the brain.

Participants receiving the sham treatment felt the same head-tapping, but a metal insert below the magnet blocked the magnetic field from entering the brain while electrodes on the scalp delivered the tapping sensation.

Using electrical current to treat brain disorders has been around in some form since the 1940s and 1950s, said Tony Tang, an adjunct professor in the psychology department at Northwestern University. However, electroconvulsive, or electroshock, therapy can induce seizures, and some studies showed it might cause memory loss and brain damage. Though effective in some people, electric shock was viewed with suspicion by the public, and today is used only as a last resort, Tang said.

Magnet therapy is essentially a much gentler, less invasive form of electric shock therapy, Tang said.

“Transcranial magnet therapy is one of the most exciting new developments in our field,” Tang said. “There are new drugs coming out every year, but they are all fairly similar to each other, and we don’t see much difference in efficacy. With TMS, the mechanism is completely different. It’s a very, very safe and gentle, noninvasive way to do electric shock therapy.”

In 2008, the U.S. Food and Drug Administration approved the marketing of a device used for magnet therapy to treat depression that is considered mildly resistant to treatment, according to background information on the study provided by the U.S. National Institute of Mental Health, which funded the study.

The next step, the researchers said, is to fine-tune the treatment to determine if higher levels of magnetic stimulation or changing the location of the magnetic coil might be even more effective or if magnet therapy might work best in conjunction with medications.

In the study, the only significant side effects were headaches and mild discomfort at the stimulation site. Most participants remained depression-free for several months after treatment stopped, according to the study.

SOURCES: Mark George, M.D., professor, psychiatry, radiology and neuroscience, and director, Brain Stimulation Laboratory, Medical University of South Carolina, Charleston, S.C.; Tony Tang, Ph.D., adjunct professor, department of psychology, Northwestern University, Evanston, Ill.

Adding the antiviral drug telaprevir to a second-round treatment for hepatitis cures about half the people who were not helped in the first round, new research shows.

“This is the first large study in patients who had not responded to standard treatment,” said Dr. John G. McHutchison, associate director of the Duke Clinical Research Institute and lead author of a report in the April 8 issue of the New England Journal of Medicine.

The study is one of the last steps in a series of trials designed to get approval for the use of the drug in clinical practice. Approval of the drug will bring encouragement to people whose hepatitis C infection had not been cured by the existing treatments, McHutchison said.

“There has been no alternative for people who have been treated and have not responded,” he added. “So it holds great promise for them, that potentially something will be available in the future that can cure half of them.”

About 4 million Americans are infected with hepatitis C, a virus that is the leading cause of cirrhosis and liver cancer and the most common reason for liver transplantation. It is usually transmitted by infected blood, most often by using a contaminated needle.

Standard treatment for hepatitis C is a 48-week course of two drugs, peginterferon alpha and ribavirin, which cures about 40 percent to 50 percent of patients but is accompanied by side effects, such as a severe rash, that makes many discontinue the treatment. Previous studies have shown a substantial improvement in cure rates when telaprevir is added to the standard therapy.

Until now, the only recourse for those who were not helped by the first round of treatment was a second round of the same therapy. The newly reported trial, sponsored by Vertex Pharmaceuticals, the maker of telaprevir, included 453 people who had not responded to a first round of treatment. All had the most common, and most difficult to treat, form of the virus, genotype 1.

Just over half, 52 percent, of those who had telaprevir added to the two-drug regimen in the second round were virus-free after six months, compared to 14 percent of those who had a second round of the two-drug treatment.

But the therapy was not problem-free, McHutchison noted. “There were also more side effects, rashes and anemia,” he said. “Also, the rate of discontinuation was higher as well.”

Still, the high cure rate speaks for itself, McHutchison added. Data from the various trials probably will be submitted to the U.S. Food and Drug Administration later this year, he said.

Telaprevir is a protease inhibitor, which works by blocking reproduction of the hepatitis C virus. It is not the only protease inhibitor being tested against hepatitis C, McHutchison said. Another such drug, boceprevir, appears to be running close to telaprevir in the race for regulatory approval. It is being developed by Merck, which acquired it when it bought Schering-Plough.

If and when they are approved, both protease inhibitors probably will be used for first-line treatment of hepatitis C, McHutchison said.

“Having more options for the patient is what it is all about,” he explained.

A number of other protease inhibitors now are in various stages of testing, added Dr. Ira Jacobson, a professor of medicine at Weill Cornell Medical College in New York City and a member of the research team that did the telaprevir study. Jacobson has also been involved in development of boceprevir.

A new era in treatment of hepatitis C will begin when a first protease inhibitor is approved, Jacobson said. “The hope in the medical community is that the regulatory agencies will see fit to approve it for all populations,” he added.