THURSDAY, Nov. 6 (HealthDay News) -- Nerve cells in the spinal cord and brain can't be repaired now if they are severed or damaged, but two ways to get them to grow again are being proposed by separate groups of researchers.

The basic idea of both approaches is to interfere with the built-in mechanisms that prevent nerve cell regeneration. One approach attacks it from the outside of nerve cells, the other from the inside.

Zhigang He, an associate professor of neurology at Children's Hospital Boston, a teaching affiliate of Harvard University, compared the two approaches to different ways of starting a stalled auto.

"Their idea is that something is blocking the highway," said He, lead author of one of the two papers in the Nov. 7 issue of Science. "Our mechanism deals with possible engine trouble."

Growth controls are built into the genes of nerve cells, He said. His group has identified two of the key genes that inhibit the major growth pathway in nerve cells. When those two genes are knocked out, cells that are damaged or severed can grow new axons, the pathways that carry messages from cell to cell.

A study in which mice whose optic nerves were damaged showed up to 50 percent of those cells engineered to lack the two growth-inhibiting genes survived, compared to 20 percent of the cells carrying those genes. Significant axon growth was seen in up to 10 percent of the mice lacking the genes.

Genetic engineering is not necessary to achieve that kind of nerve growth, He said. "In the future, we could have small-molecule drugs to activate these pathways," He said. "Other people have studied this pathway already, and there are quite a few possible targets."

He's group has started to work with some candidate compounds. "It's too early to say if these compounds would be effective," he said. "We don't know about toxicity, that sort of thing. We have lots of work to do."

A second paper by researchers at the San Francisco-based biotechnology company Genentech looked at the growth-preventing mechanism built into myelin, the protective sheath that surrounds nerve cells. They have identified a previously unknown receptor for the growth-preventing molecules in myelin. Block that receptor, and growth can be restored, said Marc Tessier-Lavigne, executive vice president of research drug discovery at Genentech.

"This is a mechanism we can try to target," Tessier-Lavigne said. The paper describes a molecule that has blocked the receptor in mice. "Now we are working on a human protein."

Both approaches require more work, said Dr. William D. Snider, director of the University of North Carolina Neurosciences Institute, and co-author of an accompanying editorial.

The idea of blocking growth-preventing genes "is a very clever way of restoring normal levels of proteins," Snider said, but he was cautious, because all the work reported in the paper was done in mice.

"Mice are extremely small animals when you compare their nervous systems to humans," Snider said. "Work in primates might be more relevant. Those of us who have been in the field for a while are extremely cautious about extrapolating from mice."

The Genentech myelin approach is not new, Snider noted. "People have known in general that myelin down-regulates nerve cell growth capacity, although they're not certain why that is true," he said. One belief is that the myelin mechanism is designed to prevent errors at times when there is a major change in the central nervous system. Knowledge of a new receptor that governs nerve cell growth could be of practical value, Snider said.

More information

The workings of nerve cells are explained by the U.S. National Institute of Neurological Disorders and Stroke.

MONDAY, Oct. 27 (HealthDay News) -- People newly diagnosed with rheumatoid arthritis face twice the risk of a heart attack, and those who do suffer a heart attack tend to have more heart-related complications, new research says.

It seems that a condition called diastolic dysfunction, which causes the lower chambers of the heart to become stiff, is the culprit. Diastolic dysfunction impairs the ability of the ventricles to fill with blood and can lead to heart failure, the researchers said.

These are the conclusions of three reports presented at the American College of Rheumatology (ACR) annual scientific meeting, which runs from Oct. 24-29, in San Francisco.

"Rheumatoid arthritis patients not only have more heart attacks and heart failures, but they also have worse prognosis once they have a cardiovascular event," said Dr. Hilal Maradit Kremers, lead researcher on one of the studies and an epidemiologist at the Mayo Clinic in Rochester, Minn.

For the study, Kremers' team followed 38 patients with rheumatoid arthritis who had suffered a heart attack. Then they compared these patients with patients without rheumatoid arthritis who also had a heart attack.

The researchers found that the rheumatoid arthritis patients had a 45 percent greater risk of developing heart failure after a heart attack, compared with the general population, and a 75 percent greater risk of dying.

Kremers said patients with rheumatoid arthritis should take all the usual precautions to reduce their risk of a heart attack, including proper diet, exercise, no smoking and maintaining a healthy weight. "Try to avoid to get that heart attack," she said.

For the second study, Marie Gunnarsson, a doctoral student at the Institute of Environmental Medicine at the Karolinska Institute in Stockholm, Sweden, and colleagues found that the risk of heart attack among newly diagnosed rheumatoid arthritis patients doubled during the first 10 years after diagnosis.

The researchers collected data on 7,954 newly diagnosed rheumatoid arthritis patients and compared that information with 38,913 people from the general Swedish population.

Over 10 years of follow-up, the researchers found that patients diagnosed with rheumatoid arthritis had almost double the risk of a heart attack and dying from a heart attack. The increased risk grew over time, starting five years after diagnosis, the study found.

"This study shows that having rheumatoid arthritis confers an increased risk of having a myocardial infarction [heart attack], and that this risk increase is manifest already early in RA disease progress," Gunnarsson said in an ACR news release.

"The fact that there is no increased risk prior to rheumatoid arthritis diagnosis suggests that there is something in the rheumatoid arthritis disease itself, such as inflammatory processes that lead to this increased risk. Measures to bring down inflammation in rheumatoid arthritis might, thus, be beneficial also from a cardiovascular prevention point of view in this population," she said.

In the last report, a research team led by Dr. Kimberly Liang, an assistant professor at the University of Pittsburgh, found that diastolic dysfunction was more common in patients with rheumatoid arthritis, which could help explain the increased risk for heart problems in these people.

"Diastolic dysfunction occurred in 38.9 percent, compared to 28.8 percent in the non-rheumatoid arthritis group," Liang said. "We also found that patients in the rheumatoid arthritis group had higher average pulmonary arterial pressure, which is high blood pressure in the lungs and the right side of the heart. This is consistent with the impaired filling of the heart seen in diastolic dysfunction."

Wider use of echocardiography in patients with rheumatoid arthritis may reveal heart abnormalities before they are detected clinically, Liang said. An echocardiogram is a test that uses sound waves to create a moving picture of the heart, according to the U.S. National Institutes of Health.

Dr. John Hardin, chief science officer at the Arthritis Foundation, said these new studies highlight the toll that rheumatoid arthritis can take on the cardiovascular system.

"These studies are consistent with the idea that systemic inflammation promotes cardiovascular disease," Hardin said. "Rheumatoid arthritis creates a general state of inflammation within the body."

Hardin also noted that some arthritis drugs can increase the risk of heart problems in rheumatoid arthritis patients who already have damaged hearts. "For example, Enbrel (etanercept) can, in fact, in some people, potentiate heart failure, which can be a complication of myocardial infarction," he said.

To prevent a heart attack, patients with rheumatoid arthritis need to pay particular attention to cholesterol, blood pressure and maintaining a healthy lifestyle, Hardin said. "If you have rheumatoid arthritis, the things you do to protect yourself against cardiovascular disease become doubly important," he said.

Rheumatoid arthritis is a chronic disease that results in pain, stiffness, swelling, and limitation in the motion and function of multiple joints. The disease also can cause inflammation in other organs. An estimated 1.3 million Americans suffer from rheumatoid arthritis, according to the Arthritis Foundation.

More information

To learn more about rheumatoid arthritis, visit the U.S. National Library of Medicine.

THURSDAY, Aug. 7 (HealthDay News) -- B cells may be more responsible for causing autoimmune diseases like lupus or rheumatoid arthritis than initially thought, according to a new study.

The finding, published in the Aug. 7 online issue of the journal Immunity, may give scientists a new path to pursue in finding ways to stop the immune system's chronic attacks on the body's own tissue during these diseases.

B cells, the source of damaging auto-antibodies, have long been thought to remain quiet in autoimmune diseases unless they are given a kick-start by T-cells. Researchers from Yale and Boston universities had found that toll-like receptors recognize and react to "self" molecules, in particular mammalian DNA and RNA. When this occurs, these receptors help activate B cells that make the classical auto-antibodies of lupus.

These signals, like those from T-cells, start the autoimmune process in B cells. In the new study, the researchers theorize that once activated in this way, the B cells can subsequently recruit T-cells. This creates a "vicious cycle" of chronic autoimmune disease in which the two types of cell prod each other into action.

The findings could explain why autoimmune-disease treatments aimed at T-cells have not done as well as those targeting B cells, the researchers said.

More information

The U.S. National Library of Medicine has more about autoimmune diseases.