Infection with HIV, the virus that causes AIDS, can increase the risk of heart failure even in patients who don't have a prior history of heart disease, a U.S. study said.

And as the HIV virus replicates, the risk increases, added the study, published in Archives of Internal Medicine.

"Health care providers traditionally think of HIV and its therapies increasing the risk of atherosclerotic heart disease," said lead author Adreel Butt, at the University of Pittsburgh School of Medicine in Pennsylvania.

"The surprising finding from our study was the association of HIV with heart failure in the absence of prior coronary heart disease."

The study involved nearly 8,500 adults, with a median age of 48 years in both HIV infected subjects and controls.

The HIV group was more likely to also be infected with Hepatitis C, 31 percent to 11 percent, and to abuse cocaine -- 22 percent to 16 percent.

They were also more likely to be smokers but less likely to have hypertension or diabetes.

During a median follow-up of 7.3 years, 286 people developed heart failure. Rates of heart failure per 1,000 person-years, adjusted for age as well as race and ethnicity, were 7.12 for HIV patients and 4.82 for the controls.

After accounting for traditional risk factors, the hazard ratio for heart failure with HIV was 1.81.

In addition, ongoing replication of the virus led to a significantly higher risk of heart failure.

"On the other hand, if HIV replication is well controlled, then the risk of heart failure is closer to that seen among HIV-uninfected persons," Butt said.

The exact mechanism by which HIV infection is linked to heart failure remains unclear, but possible explanations include the direct effects of the HIV infection, antiretroviral treatment that leads to an increased risk of coronary heart disease, and nutritional deficiencies.

"Our results suggest that HIV itself is playing an important and independent role," Butt and her colleagues wrote.

The message for HIV care providers is clear, though.

"Be on the lookout for early signs of heart failure in HIV-infected persons, even if there is no history of preceding coronary heart disease," Butt told Reuters Health.

"Controlling HIV well may reduce the risk of heart failure."

Jason Huang, M.D., and colleagues undertook the study after noticing that patients with brain injuries who had been prescribed anti-depressants were doing better in unexpected ways than their counterparts who were not taking such medications. Not only did their depression ease; their memory also seemed improved compared to patients not on the medication.

"We saw these patients improving in multiple ways -- their depression was improved, but so were their memory and cognitive functioning. We wanted to look at the issue more, so we went back to the laboratory to investigate it further," said Huang, associate professor of Neurosurgery and chief of Neurosurgery at Highland Hospital, an affiliate of the University of Rochester Medical Center.

The team's findings were published online recently in the Journal of Neurotrauma.

Huang said many patients who have a traumatic brain injury also experience depression -- by some estimates, half of such patients are depressed. Doctors aren't sure whether the depression is a byproduct of the sudden, unfortunate change in circumstances that patients find themselves in, or whether the depression is a direct consequence of brain damage.

Previous research by other groups indicated that anti-depressants help generate new brain cells and keep them healthy in healthy animals. That, together with the experience of his patients, led Huang to study the effects of the anti-depressant imipramine (also known as Tofranil) on mice that had injuries to their brains.

Scientists found that imipramine boosted the number of neurons in the hippocampus, the part of the brain primarily responsible for memory. By one measure, mice treated with imipramine had approximately 70 percent more neurons after four weeks than mice that did not receive the medication.

That change was borne out on behavioral tests as well. The team tested mice by using what scientists call a novel object recognition test. Like human infants, mice tend to spend more time sizing up objects that they haven't encountered before -- or don't remember encountering -- than they do objects that they've seen before. This gives scientists a way to measure a mouse's memory.

The team found that mice that had been treated with imipramine had a better memory. They were more likely to remember objects they had seen previously and so spent more time exploring truly novel objects, compared to mice that did not receive the compound.

The benefits did not extend to the motor skills of the mice -- a finding that parallels what neurosurgeons like Huang have seen in their patients on anti-depressants, who don't show improved mobility after use of the medications.

Scientists aren't sure whether the drug helps spur the creation of more new neurons, or whether it helps newly created neurons survive -- or both. Some of the team's evidence indicates that the drug helps immature stems evolve into useful cells such as neurons and astrocytes, and to travel to the exact areas of the brain where they're needed.

In addition to sorting out those questions, investigators will try to identify the molecular pathway that prompts the brain to create more neurons in response to anti-depressants. The team suspects that a molecule known as BDNF or brain-derived neurotrophic factor may play a role.

Huang notes that one of his mentors, co-author Douglas H. Smith, M.D., of the University of Pennsylvania, has found that a brain injury itself also seems to prompt the brain to create more brain cells, perhaps as a way to compensate for injury.

"The brain has an intrinsic mechanism to repair itself to a certain extent," said Huang. "Our goal is to learn more about that mechanism and improve it, to help patients recover even more brain function than they can now, even with extensive work and rehabilitation."

Some of Huang's work is based on his experiences treating soldiers and civilians while working for four months as a neurosurgeon with the U.S. Army Reserve in Iraq, as well as more than a decade of experience treating patients affected by incidents like motor vehicle accidents.

He said that traumatic brain injury -- an injury experienced by approximately 1.4 million Americans each year -- must be treated aggressively. Often this involves surgery to relieve pressure on the brain, other procedures to protect the brain against immediate further injury, and then rehabilitation for months or years.

"It's exciting that the study involves a drug that is already safe and approved by FDA and is used clinically. If we could add a medication to the treatment regimen -- even a slight improvement would be a big gain for these patients. It's our hope that the work will ultimately make a difference in patient care," added Huang, who is also a scientist in the Center for Neural Development and Disease.

In addition to Huang, other authors at Rochester include post-doctoral associates Xiaodi Han, M.D., Ph.D., Jing Tong, M.D., and Jiankai Yang, M.D.; neurosurgery resident Arash Farahvar, M.D.,; and undergraduate Ernest Wang. Other authors include Jun Zhang, M.D., of the Chinese PLA General Hospital in Beijing; Uzma Samadani, M.D., Ph.D., of New York University; and Douglas H. Smith, M.D., of the University of Pennsylvania.

In a major breakthrough in the battle against multiple sclerosis (MS), scientists claim to have identified a chemical that triggers the devastating disease and also found a way to stop it in its tracks.

Researchers at the University of Zurich, Switzerland, found that an immune system chemical,
called GM-CSF, is the "driving force" behind the debilitating condition that affects over 2.5 million people worldwide.

MS is an autoimmune disease that affects the brain and spinal cord, or the central nervous system. The condition, which can cause blindness and paralysis, has no cure at present and drugs are not suitable for all.

But the Swiss researchers claimed that an antibody, which they tested on mice with a MS-like condition, was found to be very effective in countering GM-CSF and improved their health, the Daily Mail reported.

Although the experiments were on mice, the researchers said they were "quietly optimistic" that a similar approach would help people with MS. The first trials on patients are planned for later this year.

In the healthy body, the researchers said, GM-CSF is part of the defence against disease, attacking viruses and other invaders. But in MS, it triggers a series of reactions that culminate in "scavenger cells" destroying myelin -- the fatty protective sheath around nerve fibres in the brain and spinal cord -- which disrupts the transmission of messages from the brain.

Professor Burk-hard Becher, who led the study, said: "It is relatively easy to stop mice from getting the disease, so we waited until they had the disease and were pretty sick.

"This is similar to the clinical situation -- patients don't go to the doctor because they think they might get MS, they go when they have MS."

The drug was also given to mice whose disease was similar to the most common form of MS, in which relapses are followed by periods of remission. Mopping up the GM-CSF prevented any further relapses, the researchers reported in the journal Nature Immunology.

Prof Becher said: "We are extremely hopeful but whether this form of therapy will actually help MS patients remains to be seen. Quiet optimism is the way to go.

"I am not sure this is going to work in patients but, based on the mouse data, I believe GM-CSF is a good thing to target." Another study on MS, from Thomas Jefferson University in Philadelphia, also pointed the finger at GM-CSF.

Although the chemical was known to play a role in MS, its pivotal contribution was not understood until now. Dr Doug Brown, of the MS Society, said: "This is a very interesting development in research for a condition where there are limited treatment options and no cure.

Bacterial Meningitis can befatal. It can cause severe brain damage and, if untreated, can even lead to death. The disease is more common among children who inhabit crowded areas with poor sanitation and hygiene.

The good news is that Karnataka is one of the first four states where Haemophilus influenza Type B vaccine has been made mandatory. Talks are on and, shortly, the Union government is going to make Haemophilus influenza Type B vaccine compulsory under the National Immunisation Schedule, all over the country.

"This vaccine has about 80% efficacy. It is required to be given in four doses, with the first three at a gap of one-and-a-half to two months each and the fourth dose at the age of one-and-a-half years," said Dr Preethi Galagali, consultant pediatrician, Chord Road Hospital.

"Roughly, around 2% of children suffer from some form of meningitis. Though Haemophilus influenza Type B vaccine has been there for the last 18 years, it is only over the last five years that there has been an awareness about this vaccine, leading to reduction in the incidence of meningitis," said Dr Kishore Kumar, CEO and MD, Cloudnine and member of the Indian Academy of Pediatrics.

As many people age they complain about not being able to remember things - and rather than thinking the cause could be anything as sinister as the first signs of dementia, say they have simply accumulated too much in their minds over the decades.

Now scientists say there is evidence that their explanation is more than an excuse.

New research indicates older people are less able to process information - including remembering things - because their memories tend to be cluttered with masses of information.

Mervin Blair, a PhD student at Concordia University in Montreal, Canada, led a study comparing how well people in their 20s and 60s recalled information.

He said: "Basically, older adults are less able to keep irrelevant information out of their consciousness, which then impacts on other mental abilities."

He and colleagues asked the two groups, each of about 30 people, to perform what he called a "working memory task".

This involved reading sentences and recalling parts of them accurately, including the last word in each.

"Overall, we showed that our older participants had reduced working memory compared to our younger participants," said Blair.

The two groups were also asked to memorise the order of a series of images and then tell researchers what that order was, while simultaneously being shown the images in a random order.

This "sequential memory task" was to examine how well participants could jettison irrelevant information and concentrate on the task at hand - technically called "inhibition deletion".

Blair said: "Older adults had poor inhibition, repeatedly responding to previously relevant images."

He suggested older people worried about mild memory lapses could improve their performance by "reducing clutter" through the use of "relaxation exercises".

He warned: "Reduce clutter, if you don't, you may not get anything done."

Karen Li, professor of psychology at Concordia, and the senior author of the study, commented: "Our study was novel because we looked at how the ability to recall and process information at the same time changes as people get older."

Gordon Wilcock, professor of geratology at Oxford University, and an expert on memory and ageing, welcomed the study for "suggesting mechanisms for phenomenae that trouble people".

He described it as "an interesting hypothesis", but added: "It doesn't fit will with other hypotheses that we have."

He also questioned whether the differences in results were truly explained by age.

Younger people might be better at this sort of memory retrieval because their brains had been primed to do so by early exposure to computer technology, he said, while members of the older group could have been on drugs for health conditions. The two groups should also be matched for IQ, he said.