Sunday, January 10, 2010

SEEING WITHOUT LOOKING

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Like a spotlight that illuminates an otherwise dark scene, attention brings to mind specific details of our environment while shutting others out. A new study by researchers at the Salk Institute for Biological Studies shows that the superior colliculus, a brain structure that primarily had been known for its role in the control of eye and head movements, is crucial for moving the mind's spotlight.

Their findings, published in the Dec. 20, 2009, issue of the journal Nature Neuroscience, add new insight to our understanding of how attention is controlled by the brain. The results are closely related to a neurological disorder known as the neglect syndrome, and they may also shed light on the origins of other disorders associated with chronic attention problems, such as autism or attention deficit disorder.

"Our ability to survive in the world depends critically on our ability to respond to relevant pieces of information and ignore others," explains graduate student and first author Lee Lovejoy, who conducted the study together with Richard Krauzlis, Ph.D., an associate professor in the Salk's Systems Neurobiology Laboratory. "Our work shows that the superior colliculus is involved in the selection of things we will respond to, either by looking at them or by thinking about them."

As we focus on specific details in our environment, we usually shift our gaze along with our attention. "We often look directly at attended objects and the superior colliculus is a major component of the motor circuits that control how we orient our eyes and head toward something seen or heard," says Krauzlis.

But humans and other primates are particularly adept at looking at one thing while paying attention to another. As social beings, they very often have to process visual information without looking directly at each other, which could be interpreted as a threat. This requires the ability to attend covertly.

It had been known that the superior colliculus plays a role in deciding how to orient the eyes and head to interesting objects in the environment. But it was not clear whether it also had a say in covert attention.

In their current study, the Salk researchers specifically asked whether the superior colliculus is necessary for covert attention. To tease out the superior colliculus' role in covert attention, they designed a motion discrimination task that distinguished between control of gaze and control of attention.

The superior colliculus contains a topographic map of the visual space around us, just as conventional maps mirror geographical areas. Lovejoy and Krauzlis exploited this property to temporarily inactivate the part of the superior colliculus corresponding to the location of the cued stimulus on the computer screen. No longer aware of the relevant information right in front of them the subjects instead based all of their decision about the stimulus' movement on irrelevant information found elsewhere on the screen.

"The result is very similar to what happens in patients with neglect syndrome," explains Lovejoy, who is also a student in the Medical Scientist Training Program at UC San Diego. "Up to a half of acute right-hemisphere stroke patients demonstrate signs of spatial neglect, failing to be aware of objects or people to their left in extra-personal space."

"Our results show that deciding what to attend to and what to ignore is not just accomplished with the neocortex and thalamus, but also depends on phylogenetically older structures in the brainstem," says Krauzlis. "Understanding how these newer and older parts of the circuit interact may be crucial for understanding what goes wrong in disorders of attention."

(Photo: Lee Lovejoy, Salk Institute for Biological Studies)

Salk Institute for Biological Studies

LADDER-WALKING LOCUSTS SHOW BIG BRAINS AREN'T ALWAYS BEST

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Scientists have shown for the first time that insects, like mammals, use vision rather than touch to find footholds. They made the discovery thanks to high-speed video cameras – technology the BBC uses to capture its stunning wildlife footage – that they used to film desert locusts stepping along the rungs of a miniature ladder.

The study sheds new light on insects' ability to perform complex tasks, such as visually-guided limb control, usually associated with mammals.

According to lead author Dr Jeremy Niven of the University of Cambridge: "This is another example of insects performing a behaviour we previously thought was restricted to relatively big-brained animals with sophisticated motor control such as humans, monkeys or octopuses."

Because insects such as bees and flies spend a lot of time flying, most research has concentrated on how insects use vision during flight. Many insects that spend a lot of time walking, such as stick insects, crickets and cockroaches have relatively small eyes and use long antennae to 'feel' their way through the environment.

Locusts spend time both walking and flying, and have short antennae and large eyes, which made Niven wonder whether they used vision to find footholds.

To answer this question, the team built a miniature locust-sized ladder and filmed the locusts walking along it. They counted the number of times the locusts missed steps, comparing the number of mistakes they made in different situations.

"By combining all these different experiments, we showed that locusts use vision to place their legs. We showed that when locusts can't see one front leg they stop using that leg to reach to the next ladder rung, favouring the leg they can see," Niven explains.

"Big-brained mammals have more neurons in their visual systems than a locust has in its entire nervous system, so our results show that small brains can perform complex tasks. Insects show us how different animals have evolved totally different strategies for doing similar tasks," he says.

As well as illustrating how insects can achieve similar results to mammals by using simpler mechanisms, the findings deepen our understanding of locusts' neural circuits.

This is important because locusts have been a model organism for studying limb control for the past 40 years. Insects such as the locust have been crucial to many breakthroughs in neuroscience, and insects are often the inspiration for limb control in robotics.

(Photo: U. Cambridge)

University of Cambridge

NEW TOOL IN THE FIGHT AGAINST MOSQUITO-BORNE DISEASE: A MICROBIAL 'MOSQUITO NET'

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Earlier this year, researchers showed that they could cut the lives of disease-carrying mosquitoes in half by infecting them with a bacterium they took from fruit flies. Now, a new report in the December 24th issue of Cell, a Cell Press publication, suggests that their strategy might do one better: The Wolbachia bacteria also makes the mosquitoes more resistant to infection by viruses that are a growing threat to humans, including those responsible for dengue fever and Chikungunya.

Once infected with Wolbachia, Aedes aegypti mosquitoes also become less suitable as hosts for a form of malaria parasite that infects birds, said Scott O'Neill of The University of Queensland. (The mosquitoes under study aren't natural carriers of human malaria.)

"This might be very powerful in reducing pathogen transmission by Aedes aegypti to humans, particularly for dengue and Chikungunya," O'Neill said. "Together with the previously described life-shortening effects, the results suggest we might be able to have a major impact on disease." That's if it can be shown that the Wolbachia infection can invade natural mosquito populations, he added, a question his team is working on right now.

There is no vaccine or cure for dengue fever, which is a painful and debilitating disease suffered by some 50 million people worldwide every year. Dengue haemorrhagic fever, the more severe form of the disease, kills more than 40,000 people annually. Chikungunya usually isn't fatal, but can cause symptoms similar to dengue. Human epidemics of Chikungunya have been cited in Africa, Asia and more recently in Europe, according to the CDC.

Wolbachia is already rampant in nature; the bacterium is estimated to infect up to 60 percent of all insect species. They are passed from mother insect to daughter or son through the insect egg and readily spread to high frequency in many species of mosquito. The species that are the major carriers of human disease don't normally carry them, but that's something O'Neill aims to change.

"We are currently conducting a series of experiments in contained outdoor greenhouse settings that are examining the ability of the Wolbachia infection to spread into natural mosquito populations," he said. "If these prove successful, we hope to move to open field testing within the next one to two years."

The idea would be to seed the natural mosquito population with Wolbachia by releasing mosquitoes that had been purposefully infected in the laboratory. Wolbachia bacteria have a good 'trick' to help ensure their spread, O'Neill explained. They are responsible for a developmental defect that makes the would-be offspring of pairings between infected male mosquitoes and uninfected females inviable. Since the bacteria is passed from mothers to their offspring, that means that infected females can actually have a reproductive advantage over uninfected ones, encouraging Wolbachia's spread from one generation to the next.

O'Neill said his team is working on computational models to determine just how many infected mosquitoes would need to be released for the infection to take hold in the wild.

The researchers don't yet know exactly how Wolbachia protects the insects from human disease-causing viruses. They have some evidence to suggest that the bacterial symbiont primes the insects' immune system. Wolbachia may also outcompete the virus by limiting resources such as fatty acids inside the mosquitoes.

Even if the strategy works in a natural setting, there's a chance the mosquitoes or the viruses could become resistant to Wolbachia's influence over time.

“We can predict from evolutionary theory that selection will push the system in the direction of resistance, but we do not know the speed with which this might occur," O'Neill said. "Even if it was effective for a few decades it might have a major impact on human disease."

Cell Press

VITAMIN D AND WEIGHT LOSS

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The world of weight-loss is rife with exercise gizmos and magic pills. But a person’s level of vitamin D may actually be a predictor of his or her ability to lose fat, according to Shalamar Sibley, a researcher in the University of Minnesota Medical School.

In a clinical study of 38 people, Sibley found that higher baseline levels of vitamin D predicted fat loss, especially in the abdominal area.

“What is suggested here is that if you start out with an inadequate vitamin D level, it’s possible that this might inhibit or impede your ability to lose weight on a reduced caloric diet,” she says.

She is quick to point out that hers was an observational study, and there is no definitive causal relationship between vitamin D and weight loss. The next step is to design a follow-up study where vitamin D is administered in a controlled fashion and studied as an addition to standard weight-loss regimens in people who are vitamin D inadequate.

Sibley, who studies metabolic syndrome and obesity, took a special interest in vitamin D about six years ago. The fact that her recent study yielded a potential breakthrough finding on weight loss and vitamin D is a stroke of serendipity.

“One day I ran across a publication by some other researchers showing that a particular hormone pathway—which when overactive can contribute to obesity-related problems such as high blood pressure—was inhibited by the active form of vitamin D,” Sibley says. “Interestingly, this same pathway (the renin-angiotensin system) also affects fat cell development and metabolism. I happened to be doing a weight loss study in which our only intervention was a reduced calorie diet, and came up with the question, 'Is there any possibility that where someone starts with their baseline vitamin D level will predict their ability to lose weight?’

“What’s interesting about our study is we did not recruit people to be vitamin D inadequate; we recruited people who were overweight or obese for our weight-loss study. And they happened, on average, to have inadequate vitamin D levels, so it tells you how prevalent the problem is.”

Indeed, Sibley notes that “vitamin D deficiency is its own epidemic,” and the numbers bear that out. According to one estimate, 36 percent of otherwise healthy young adults in the United States are lacking in vitamin D, and that number jumps to near 57 percent for general medicine inpatients. Increasingly, a deficiency in vitamin D is being linked to a host of health conditions, including higher blood pressure, cardiovascular problems, kidney disease, and a higher risk of certain cancers, including breast and prostate.

More recently, research at the U found that in a group of 150 patients showing chronic musculoskeletal pain, a whopping 93 percent were vitamin D deficient.

Vitamin D can be obtained through sources like fatty fish—herring, salmon, catfish, and tuna are examples—as well as fish liver oils and fortified milk, cereal, yogurt, and bread.

In addition, our bodies naturally produce vitamin D through exposure to the sun. Unfortunately, those of us in northern climes can be left out in the cold; vitamin D is only synthesized from UV radiation between April and early autumn, and while it remains in our bodies for a time, there may not be enough to last all winter.

That makes Minnesotans naturally more susceptible to vitamin D deficiency. “But some of it is also modern lifestyle,” Sibley notes. “People work indoors all day. They like to use sunscreen and they should, because they don’t want skin cancer. That’s fine, but we still need to find a way to have adequate vitamin D levels.”

Sibley says that supplements make sense for people who know or suspect that they’re lacking in vitamin D. “In an adult, 1,000-2,000 IUs (international units) as a supplement is a very reasonable thing to do for maintenance,” she says. “If people are vitamin D inadequate, they’re going to need a higher dose for a short period of time to build up their levels.”

But she cautions against going overboard with vitamin D—there are levels where it can become toxic in the system—and reiterates that there is still no definitive link to weight loss.

“Our results are not saying that everyone should go out there and take extra vitamin D to lose weight,” she says. “But if someone is vitamin D inadequate, then supplementing vitamin D to achieve normal levels might, in fact, help augment his or her weight loss success, [coupled] with standard approaches.”

(Photo: U. Minnesota)

University of Minnesota Medical School

STUDY REDEFINES PLACEBO EFFECT AS PART OF EFFECTIVE TREATMENT

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Researchers used the placebo effect to successfully treat psoriasis patients with one quarter to one half of their usual dose of a widely used steroid medication, according to an early study published online in the journal Psychosomatic Medicine. Early results in human patients suggest that the new technique could improve treatment for several chronic diseases that involve mental state or the immune system, including asthma, multiple sclerosis and chronic pain.

By designing treatment regimens that mix active drug and placebo, researchers at the University of Rochester Medical Center hope to maximize drug benefits, reduce side effects, increase the number of patients who take their medicine and extend the use of drugs otherwise limited by addiction risk or toxicity. Using a fraction of the usual drug dose to get the same effect could also make possible a dramatic and timely reduction in healthcare costs, according to the authors.

The publication is a product of decades of research in the emerging field of “psychoneuro-immunology,” which holds that the ability of the human immune system to fight disease is closely linked with a person’s mind. Thoughts and moods are captured in neurochemicals that cause the release of hormones which interact with disease-fighting cells.

The current research team chose psoriasis for their first human experiments because it is chronic, gets worse when patients feel stress and involves the immune system. The condition causes pain and disability in four million Americans as inherited traits and irritants cause the immune system to trigger the too fast production of skin cells, resulting in red, scaly patches of dead skin.

“Our study provides evidence that the placebo effect can make possible the treatment of psoriasis with an amount of drug that should be too small to work,” said Robert Ader, Ph.D., M.D. (hc), distinguished university professor in the University of Rochester School of Medicine & Dentistry. “While these results are preliminary, we believe the medical establishment needs to recognize the mind’s reaction to medication as a powerful part of many drug effects, and start taking advantage of it,” said Ader, professor of Psychiatry and principal investigator of the study. The placebo effect, obviously, cannot help unconscious patients, or replace substances that the body itself is unable to produce, he added. In the absence of functioning islet cells, for example, placebos cannot stimulate the release of insulin in a Type l diabetic.

A description of the current findings requires expanding the definition of placebo effects to include phenomena that are not fully understood by modern medicine, Ader said. Although placebos, “dummy pills” that have no therapeutic effect by themselves, are prescribed by many physicians today, their use still carries a stigma. It’s as if the effect of a pill containing no medication is not “real,” part magic and part deception.

To accurately define and study the placebo effect, Ader and colleagues chose to frame it as an example of a well established psychological phenomenon: the conditioned response. Nineteenth century Russian physiologist Ivan Pavlov was the first to study the phenomenon of conditioning. By ringing a bell (a conditioned stimulus) each day before giving his dogs food (an unconditioned stimulus), Pavlov found that the dogs would eventually salivate (a conditioned response) at the sound of the bell alone.

In the current study, Ader and colleagues sought to determine if a drug’s therapeutic effect could be triggered by qualities associated with the drug, like its shape, color, smell and packaging, as well as by its administration by an authority figure in a white lab coat. These repeated associations, Ader argues, create conditioned responses, drug-like therapeutic effects of treatment caused, not by a drug’s ingredients alone, but elicited by stimuli associated with the effects of active drug treatment. The results provide the first evidence that conditioned responses might be harnessed to influence the design of drug regimens in humans.

Research teams at the University of Rochester Medical Center and Stanford University conducted an 11 to 14-week, doubleblind, randomized clinical trial in 46 patients with mild-to-moderate psoriasis. Patients were on no other medications during the study, and had signed consent forms after being informed they might receive a reduced dose of topical steroid.

At the start of the study, researchers randomly selected two “target” psoriatic lesions or sores on each patient. Twice each day during a three-week baseline period, all patients spread a lotion containing a full dose of steroid medication (0.1% Aristocort A, triamcinolone acetonide) onto one of their two study lesions. The second lesion was coated with a moisturizing cream. Medicated and unmedicated creams were distributed in coded syringes to make them indistinguishable.

Nearly all past drug studies divided patients into two groups only. One would get the full dose of the drug all of the time (a 100 percent reinforcement schedule). The other would get zero drug all of the time (zero percent reinforcement). The current study asks for the first time: what if we treat patients with something in between drug and placebo? After the three-week baseline period, patients were randomly assigned to one of three groups.

The first continued to receive 100 percent of the treatment drug at each administration for the rest of the study on his or her study lesion. A second, the partial reinforcement group, also continued to receive a full dose, but only 25 or 50 percent of the time, and a steroid-free emollient the rest of the time. The study was designed so that this second group could benefit from exposure to cues they had previously associated with active drug treatment (a conditioned therapeutic effect). A third group, the “dose control group,” received active drug at every administration, but at 25 or 50 percent of the full dose used in the first and second groups. Thus, the partial reinforcement and “dose control” groups received the same total amount of active medication, but in different patterns.

Results were measured in two ways. First, a “blinded” dermatologist measured the severity of a patient’s psoriasis lesions weekly using the Psoriasis Severity Scale (PSS), a standard tool used to track the redness, hardening and thickening of skin. The second measure was whether a patient experienced a “relapse” in lesion severity, defined arbitrarily as a return to a PSS score within two units of a patient’s initial score.

In terms of the overall PSS severity scores, results were mixed. The Stanford study site found no group differences in PSS scores that could be attributed to the different treatment regimens. Ader believes that elevated baseline PSS scores in the randomly selected Dose Control subjects at Stanford might have obscured the differences between the dose control and partial reinforcement groups. For instance, results could have been influenced by differences in the amount of sun patients were exposed to in Upstate New York and California (ultraviolet light is an established treatment for psoriasis).

In Rochester, there were no differences between the PSS values of the Partial Reinforcement and Dose Control groups at the point in the study where experimental treatment began. In this case, partial reinforcement brought about a greater reduction in lesion severity during the experimental period than continuous reinforcement (dose control) with the same cumulative amount of drug.

The relapse results were clearer. Four of 18 patients (22.2 percent) in the 100 percent reinforcement group (full dose all the time) relapsed within the eight-week experimental period. Among patients treated with a full dose of drug, but one half or one quarter of the time (50 or 25 percent reinforcement schedule), four of 15 patients (26.7 percent) relapsed. Thus, the incidence of relapse did not differ substantially between patients receiving a full dose of drug all the time and those treated under the partial reinforcement schedules, researchers said. In contrast, eight of the 13 patients (61.5 percent) in the dose control group who received active drug each time, but not the full does, relapsed in the same period of time.

Thus, the incidence of relapse in the partial reinforcement group (26.7 percent) was significantly less than in dose control patients (61.5 percent) that received the same cumulative amount of drug. Further studies are underway, and others are planned, to confirm the effect, answer the questions raised and explore the effect in other autoimmune diseases.

(Photo: URMC)

University of Rochester Medical Center

COULD ACETAMINOPHEN EASE PSYCHOLOGICAL PAIN?

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A research team led by psychologist C. Nathan DeWall of the University of Kentucky College of Arts and Sciences Department of Psychology has uncovered evidence indicating that acetaminophen (the active ingredient in Tylenol) may blunt social pain.

“The idea—that a drug designed to alleviate physical pain should reduce the pain of social rejection—seemed simple and straightforward based on what we know about neural overlap between social and physical pain systems. To my surprise, I couldn’t find anyone who had ever tested this idea,” DeWall said.

According to a study due to be published in the journal Psychological Science, DeWall and colleagues were correct. Physical and social pain appear to overlap in the brain, relying on some of the same behavioral and neural mechanisms.

DeWall and colleagues investigated this connection through two experiments. In the first experiment, 62 healthy volunteers took 1,000 milligrams daily of either acetaminophen or a placebo. Each evening, participants reported how much they experienced social pain using a version of the “Hurt Feelings Scale” - a measurement tool widely accepted by psychologists as a valid measure of social pain. Hurt feelings and social pain decreased over time in those taking acetaminophen, while no change was observed in subjects taking the placebo. Levels of positive emotions remained stable, with no significant changes observed in either group. These results indicate that acetaminophen use may decrease self-reported social pain over time, by impacting emotions linked to hurt feelings.

“We were very excited about these initial findings,” DeWall said. “The next step was to identify the neural mechanisms underlying the findings.”

In the second experiment, 25 healthy volunteers took 2,000 milligrams daily of either acetaminophen or a placebo. After three weeks of taking the pills, subjects participated in a computer game rigged to create feelings of social rejection. Functional magnetic resonance imaging (fMRI) employed during the game revealed that acetaminophen reduced neural responses to social rejection in brain regions associated with the distress of social pain and the affective component of physical pain (the dorsal anterior cingulate cortex and anterior insula). In other words, the parts of the brain associated with physical lit up in the placebo subjects when they were rejected, while the acetaminophen group displayed significantly less activity in these brain areas in response to rejection.

According to the academic paper detailing the experiments: "...findings suggest that at least temporary mitigation of social pain-related distress may be achieved by means of an over-the-counter painkiller that is normally used for physical aches and pains. Furthermore, many studies have shown that being rejected can trigger aggressive and antisocial behavior, which could lead to further complications in social life... If acetaminophen reduces the distress of rejection, the antisocial behavioral consequences of rejection may be reduced as well.”

Researchers caution that readers should not immediately stock up on acetaminophen to ease social pain and anxiety, noting “[t]o be sure, our findings do not constitute a call for widespread use of acetaminophen to cope with all types of personal problems. Future research is needed to verify the potential benefits of acetaminophen on reducing emotional and antisocial responses to social rejection.” Long-term use of acetaminophen has also been linked to serious liver damage, so it is important for patients to follow all package directions and consult their physicians if they are contemplating taking any medication for an off-label use.

“This research has the potential to change how scientists and laypersons understand physical and social pain. Social pain, such as chronic loneliness, damages health as much as smoking and obesity. We hope our findings can pave the way for interventions designed to reduce the pain of social rejection,” DeWall said.

Psychological Science

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