Scientists have found that people with diabetes who sleep poorly have higher insulin resistance, and a harder time controlling the disease.

The result suggests that poor sleep may contribute to worse outcomes in people with diabetes.

"Poor sleep quality in people with diabetes was associated with worse control of their blood glucose levels," said Kristen Knutson, assistant professor of medicine and lead author of the study.

"People who have a hard time controlling their blood glucose levels have a greater risk of complications. They have a reduced quality of life. And, they have a reduced life expectancy," said Knutson.

For the study, the researchers monitored the sleep of 40 people with diabetes for six nights.

The subjects wore activity monitors on their wrists at night, which measure their wrist movements throughout the night.

Poor sleep, or insomnia, was determined by both poor sleep quality based on the activity monitors and the subject telling the researchers that they often had a hard time falling asleep or woke up during the night.

Among the diabetics, poor sleepers had 23% higher blood glucose levels in the morning, and 48% higher blood insulin levels.

Using these numbers to estimate a person's insulin resistance, the researchers found that poor sleepers with diabetes had 82% higher insulin resistance than normal sleepers with diabetes.

The findings were published in the June issue of Diabetes Care.

Psychologists found that people who watched an eight minute clip from a scary movie suffered more symptoms associated with post traumatic stress if they were left handed than if they were right handed.

When asked to recall events from the film clip, taken from near the tense climax of thriller Silence of the Lambs, left handed volunteers gave more fragmented accounts filled with more repetition than their right handed counterparts.

This effect is common in people suffering from Post Traumatic Stress Disorder.

The scientists now believe their results could provide new insights into how people develop post traumatic stress and the way the brain deals with fear.

Dr Carolyn Choudhary, who led the research at Queen Margaret University in Edinburgh, said: "The prevalence of post traumatic stress disorder is almost double in left handers compared to right handers.

"We used a portion of film from Silence of the Lambs that we know elicits fear, so we could check the recalled account against the film. People who were left handed showed significantly more fragmentation in their memories and more repetition.

"It seems that after experiencing a fearful event, even on film, people who are left handed had subtle behaviours that were like people suffering from post traumatic stress disorder."

Silence of the Lambs, starring Anthony Hopkins as serial killer Hannibal Lector and Jodie Foster as FBI agent Clarice Starling, is widely regarded as one of the most tense thrillers ever made.

Participants who were left handed showed more signs of symptoms found in patients suffering from post traumatic stress disorder after watching the eight minute clip from the movie.

Dr Choudhary, who will present her findings at the annual conference of the British Psychology Society this week, added: "The mistakes they made were subtle errors in verbal recall.

"It appears these are tied to the way the brain makes memories during fearful experiences.

"It is apparent the two sides of the brain have different roles in PTSD and the right hand-side of the brain seems to be involved in fear. In people who are left handed, the right hand side of their brain is dominant, so it may have something to do with that.

"We need to do more experiments to understand what exactly is going on here."

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.