The sound -- called a carotid bruit (pronounced brew-ee) -- is caused by turbulent blood flow due to buildup of fatty deposits in one of the two arteries that carry blood to the front and middle part of the brain. It is usually regarded as a possible indicator of increased risk of stroke.

Now an analysis of 22 studies finds that people with carotid bruits are more than twice as likely to have heart attacks or to die of cardiovascular disease. "The presence of a carotid bruit should heighten clinician concern for coronary heart disease," said the report by physicians at Walter Reed Army Medical Center in Washington, D.C.

The studies included 17,295 people who were followed for an average of four years. "In the four studies in which direct comparison of patients with and without bruits were possible, the odds ratio for myocardial infarction [heart attack] was 2.15 and for cardiovascular death 2.27," the report said.

The findings are published in the May 10 issue of The Lancet.

Using the presence of a bruit as an indicator of cardiovascular risk could be helpful, but "there are some unresolved questions about the usefulness of carotid bruit and prognosis," said Dr. Victor Aboyans, a cardiologist at Dupuytren University Hospital in Limoges, France, and co-author of an accompanying editorial in the journal.

"First, many of the patients who were studied already had cardiovascular disease, so what is the additional value of carotid bruit in such a case?" Aboyans asked. "The second issue is that some patients who don't have carotid bruit may have other evidence of cardiovascular disease."

Several studies have shown that starting preventive measures for stroke on the basis of screening for carotid bruit aren't useful, Aboyans said. Nevertheless, presence of carotid bruit could prompt physicians to be more aggressive in recommending measures to reduce the risk of cardiovascular disease, such as cholesterol reduction, he said.

Dr. Deepak Bhatt, associate director of the Cleveland Clinic Cardiovascular Coordinating Center, said, "The [study authors'] recommendation that they be even more aggressive with risk modification, that is good clinical judgment."

Physicians routinely listen for possible carotid bruits when doing a physical examination of people who are middle-aged or older, Bhatt noted.

Studies have shown that there's a link between the risk of stroke and of coronary heart disease, Bhatt said. "The core knowledge already exists," he said. "This study helps put a number on how high the risk is."

But the study raises some practical issues, Bhatt added. "One is whether, if a carotid bruit is found, to go ahead and do an ultrasound examination," he said. "I would say yes, but it is controversial. The U.S. Preventive Task Force recommends against routine ultrasound in general."

More information

Learn what a carotid bruit is and what it might mean from the American Heart Association.

Intrauterine growth retardation (IUGR), which causes low birth weight in newborns, has been linked to the development of type 2 diabetes and other diseases when a child grows up.

And decreased activity of the Pdx1 gene during fetal development has been linked to susceptibility for type 2 diabetes later on. The gene plays an important role in the development and function of pancreatic beta cells, which produce the hormone insulin. Insulin is necessary to transport sugar from the blood stream to the body's cells for energy. People with diabetes either don't produce enough insulin or aren't sensitive enough to the insulin that is produced.

The Pdx1 gene, however, had no mutation in animals with IUGR, presenting a mystery to scientists: If there is no mutation, why is the gene permanently altered?

"What happens in the intra-uterine environment? Why does that lead to the development of diabetes later in life?" asked Dr. Rebecca A. Simmons, senior author of a paper published in the May issue of the Journal of Clinical Investigation.

"What in intra-uterine life makes that beta cell not work properly even after you've been born into a normal environment?" added Simmons, an associate professor of pediatrics at the University of Pennsylvania School of Medicine.

Using a rodent model of IUGR, the researchers found that "epigenetic" changes were responsible for the lowered activity -- the gene was not totally silenced but was "markedly reduced," Simmons said. Epigenetic changes are basically changes in the structure of the DNA that occur when the cell divides and the DNA is replicated. These changes interfere with the ability of DNA to be transcribed, or send messages out to the rest of the body, she said.

Researchers were previously able to normalize the activity of the Pdx1 gene in both newborn and adult animals with diabetes, using the drug Byetta (Exendin-4). It's not clear yet if the drug can also reverse epigenetic changes. The drug comes from Gila monster saliva, Simmons said.

But investigators face a huge technical hurdle trying to confirm these findings in humans.

"We do know this process [gene silencing] occurs in humans, particularly in cancer with tumor suppressor genes," Simmons explained. "What we don't know is if this process is responsible, in humans, for changes that we see in growth-retarded babies growing up."

"We'd like to think this is the case [that the same process is at work in humans], but we have no way right now to determine that," Simmons continued.

If the same mechanism is at work in humans, the Pdx1 gene may present a good target for drug therapy to prevent the development of type 2 diabetes, she said.

More information

Visit the American Diabetes Association for more on type 2 diabetes.

They said their findings could lead to the development of new, genetically targeted therapies to treat and prevent fatal arrhythmias. The study was published online Thursday in The Journal of Clinical Investigation.

"We are still struggling to understand why arrhythmia causes sudden cardiac death in some patients, but not others, and what underlying molecular mechanisms or abnormalities may be at play," study senior author Dr. Gideon Koren, director of the cardiovascular research center at Rhode Island Hospital and a professor of medicine at Brown University's medical school, said in a prepared statement.

He and his team developed animal models of long QT syndrome (LQTS) -- a disorder of the heart's electrical system that causes fast, chaotic heartbeats -- to study the various mechanisms that cause arrhythmia. The animal models included the two most common genetic forms of LQTS in humans -- LQT1 and LQT2.

In both forms, faulty genes lead to production of abnormal ion channels, the proteins responsible for moving potassium in and out of heart cells so they can contract. In LQT1, the mutation is in the KvLQT1 gene, while in LQT2, the mutation is in the HERG gene.

The animals with LQT2 exhibited spontaneous arrhythmias, and some of them died suddenly, while there was no spontaneous arrhythmia or sudden death among the animals with LQT1.

The researchers believe that the electrical cause for the deadly arrhythmias in the LQT2 group is increased spatial dispersion of repolarization across the front of the outside layers of cardiac muscle. The LQT1 group did not have increased dispersion.

Koren and his team also believe that HERG and KvLQT1 may interact, and that a mutation of either one of these genes could affect the other.

"While results from animal models are not always applicable to humans, we believe our findings are a first step toward gaining a better understanding of how and why arrhythmias cause sudden cardiac death. However, there is much more that we still don't know," Koren said.

More information

The American Academy of Family Physicians has more about arrhythmia.

That's the suggestion of a new study that posed the question: Is it better to give food to some hungry children while others go hungry? Or is it better that every child get a share, albeit a smaller one?

"People prefer equity, when all things are equal, to efficiency," said study lead researcher Ming Hsu, a fellow at the University of Illinois Beckman Institute for Advanced Science and Technology.

And different regions of the brain are involved when making decisions involving fairness or efficiency, he said.

"In terms of the brain, we find areas of the insular cortex are activated when people were choosing the equitable allocation of food," Hsu said. "Given the involvement of the insular cortex in emotions and fairness judgments, we conclude that emotions are underlying equity judgments."

Other areas of the brain are activated when people are making judgments about efficiency, he said.

But, not everyone is sensitive to equity, Hsu noted. "Some people care less about equity, and that's associated with a lower sensitivity in their insula," he said. "When these people are confronted with inequitable situations, their insula is activated less."

The study, by researchers at the University of Illinois and the California Institute of Technology, was published in the May 8 issue of Science.

For the study, the volunteers were hypothetically asked to distribute food to children in an orphanage in Uganda. The children would be given the cash equivalent of 24 meals, a "gift" from the research team to the orphanage.

But, a number of meals would have to be cut for some of the children. So, the volunteers were given two options to deal with the problem.

In one option, 15 meals could be taken from one child, or 13 from another child, or five from yet another child, for instance. Choosing this option, the total number of meals lost would be less, but one child would suffer from all cuts. Efficiency would be maintained at the expense of equity.

The second option reduced efficiency, but promoted equity. In this option, all the children would be fed, but they'd share fewer meals.

The researchers found that the study participants overwhelmingly chose the second option. This finding echoed other studies that showed that most people are intolerant of inequity, Hsu said.

During the experiment, the volunteers underwent functional magnetic resonance imaging. This allowed the researchers to determine which parts of the brain were most affected during decision-making.

The researchers found that regions of the brain called the insula, putamen and caudate were activated differently, and at different times, during the experiment. The insula responded to changes in equity, while the putamen responded to changes in efficiency. The caudate appeared to blend both equity and efficiency, Hsu said.

The insights involving the insula, which plays a key role in emotions, supports the idea that emotion rather than reason is at the base of people's attitudes about inequality, Hsu said. Also, studies had found that the insula is involved in deciding fairness. But, the putamen and the caudate are activated during reward-related learning, the researchers noted.

"These results support the idea that people care about equity at a very deep level," Hsu said.

Brian Knutson, an assistant professor of psychology and neuroscience at Stanford University, said the findings illustrate just how much emotion is involved in decision-making.

"We are finding that similar brain regions seem to be involved in individual economic well-being and also the well-being of others," he said.

Because the areas of the brain involved in such decisions are located deep inside the brain, it suggests they have a role in evolutionary survival function, Knutson said. "They are serving some sort of survival and emotional function," he said.

Knutson noted that many economic theories assume that people use reason to make decisions, but the areas of the brain involved in equity and efficiency are really areas activated by emotion.

"When people see an unfair offer, they actually have a negative emotional reaction to it," Knutson said. "They have a visceral reaction to unfairness."

More information

To learn more about the human brain, visit the National Institute of Neurological Disorders and Stroke.

When stroke patients are too weak to walk on their own, physical therapists fit the patients in a harness, put them on a treadmill and help them move. Because this can be physically demanding, robotic devices have been developed as an alternative.

"We wanted to know whether using a robotic device that guides the limb in a symmetrical walking pattern would facilitate greater improvements in walking speed and symmetry than more traditional walking interventions with a physical therapist," study author T. George Hornby, an assistant professor in the physical therapy department, said in a prepared statement.

The study included 48 people who'd suffered strokes at least six months earlier and still had moderate to severe trouble walking due to weakness on one side of the body. The patients were randomly assigned to receive physical therapist-assisted or robotic-assisted locomotor therapy. All the patients received a dozen 30-minute therapy sessions during the four to five weeks of the study.

"We found that stroke patients improved their walking whether they had the robotic device or the therapist helping them. However, the amount of improvement was greater in the therapist-assisted group," Hornby said.

Patients in the therapist-assisted group showed greater improvements in walking speed and in the amount of time spent on the weak leg during therapy. Among patients who had severe walking deficits, those in the therapist-assisted group -- but not those in the robotic-assisted group -- felt their quality of life improved after therapy because they had fewer physical limitations.

The fact that therapist-assisted training allows for patient error, while the robotic device controls movement and minimizes errors, may explain the differences between the two groups.

"When learning to walk again, if people can make mistakes and realize their errors and change their behavior based on those errors, they may learn better," Hornby said. "We also think that patients work harder and therefore improve more with therapists because the robotic device moved patients' legs for them throughout the therapy. Therapists only help as needed."

The study appears in the current issue of Stroke.

Hornby and colleagues suggested that robotic-assisted therapy may be best for stroke patients who have no ability to walk on their own, while therapist-assisted training is best for those who can walk independently, even at very slow speeds.

More information

The U.S. National Institute of Neurological Disorders and Stroke has more about stroke rehabilitation.