Posts tagged science

May 14th, 2012

Using tiny solar-panel-like cells surgically placed underneath the retina, scientists at the Stanford University School of Medicine have devised a system that may someday restore sight to people who have lost vision because of certain types of degenerative eye diseases.

This device — a new type of retinal prosthesis — involves a specially designed pair of goggles, which are equipped with a miniature camera and a pocket PC that is designed to process the visual data stream. The resulting images would be displayed on a liquid crystal microdisplay embedded in the goggles, similar to what’s used in video goggles for gaming. Unlike the regular video goggles, though, the images would be beamed from the LCD using laser pulses of near-infrared light to a photovoltaic silicon chip — one-third as thin as a strand of hair — implanted beneath the retina.

Electric currents from the photodiodes on the chip would then trigger signals in the retina, which then flow to the brain, enabling a patient to regain vision.

A study, to be published online May 13 in Nature Photonics, discusses how scientists tested the photovoltaic stimulation using the prosthetic device’s diode arrays in rat retinas in vitro and how they elicited electric responses, which are widely accepted indicators of visual activity, from retinal cells . The scientists are now testing the system in live rats, taking both physiological and behavioral measurements, and are hoping to find a sponsor to support tests in humans.

“It works like the solar panels on your roof, converting light into electric current,” said Daniel Palanker, PhD, associate professor of ophthalmology and one of the paper’s senior authors. “But instead of the current flowing to your refrigerator, it flows into your retina.” Palanker is also a member of the Hansen Experimental Physics Laboratory at Stanford and of the interdisciplinary Stanford research program, Bio-X. The study’s other senior author is Alexander Sher, PhD, of the Santa Cruz Institute of Particle Physics at UC Santa Cruz; its co-first authors are Keith Mathieson, PhD, a visiting scholar in Palanker’s lab, and James Loudin, PhD, a postdoctoral scholar. Palanker and Loudin jointly conceived and designed the prosthesis system and the photovoltaic arrays.

This pinpoint-sized photovoltaic chip (upper right corner) is implanted under the retina in a blind rat to restore sight. The center image shows how the chip is comprised of an array of photodiodes, which can be activated by pulsed near-infrared light to stimulate neural signals in the eye that propagate then to the brain. A higher magnification view (lower left corner) shows a single pixel of the implant, which has three diodes around the perimeter and an electrode in the center. The diodes turn light into an electric current which flows from the chip into the inner layer of retinal cells. Adapted from Stanford image courtesy of the Daniel Palanker lab.

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May 14, 2012

What goes bump in the night? In many U.S. households: people. That’s according to new Stanford University School of Medicine research, which found that about 3.6 percent of U.S. adults are prone to sleepwalking. The work also showed an association between nocturnal wanderings and certain psychiatric disorders, such as depression and anxiety.

The study, the researchers noted, “underscores the fact that sleepwalking is much more prevalent in adults than previously appreciated.”

Maurice Ohayon, MD, DSc, PhD, professor of psychiatry and behavioral sciences, is the lead author of the paper, which will appear in the May 15 issue of Neurology, the medical journal of the American Academy of Neurology.

Sleepwalking is a disorder “of arousal from non-REM sleep.” While wandering around at night can be harmless and is often played for laughs — anyone remember the Simpsons episode where Homer began wandering around and doing silly things in his sleep? — sleepwalking can have serious consequences. Episodes can result in injuries to the wanderer or others and lead to impaired psychosocial functioning.

It is thought that medication use and certain psychological and psychiatric conditions can trigger sleepwalking, but the exact causes are unknown. Also unclear to experts in the field is the prevalence.

"Apart from a study we did 10 years ago in the European general population, where we reported a prevalence of 2 percent of sleepwalking," the researchers wrote in their paper, "there are nearly no data regarding the prevalence of nocturnal wanderings in the adult general population. In the United States, the only prevalence rate was published 30 years ago."

For this study, the first to use a large, representative sample of the U.S. general population to demonstrate the number of sleepwalkers, the researchers also aimed to evaluate the importance of medication use and mental disorders associated with sleepwalking. Ohayon and his colleagues secured a sample of 19,136 individuals from 15 states and then used phone surveys to gather information on participants’ mental health, medical history and medication use.

Participants were asked specific questions related to sleepwalking, including frequency of episodes during sleep, duration of the sleep disorder and any inappropriate or potentially dangerous behaviors during sleep. Those who didn’t report any episodes in the last year were asked if they had sleepwalked during their childhood. Participants were also queried about whether there was a family history of sleepwalking and whether they had other parasomnia symptoms, such as sleep terrors and violent behaviors during sleep.

The researchers determined that as many as 3.6 percent of the sample reported at least one episode of sleepwalking in the previous year, with 1 percent saying they had two or more episodes in a month. Because of the number of respondents who reported having episodes during childhood or adolescence, lifetime prevalence of sleepwalking was found to be 29.2 percent.

The study also showed that people with depression were 3.5 times more likely to sleepwalk than those without, and people with alcohol abuse/dependence or obsessive-compulsive disorder were also significantly more likely to have sleepwalking episodes. In addition, individuals taking SSRI antidepressants were three times more likely to sleepwalk twice a month or more than those who didn’t.

"There is no doubt an association between nocturnal wanderings and certain conditions, but we don’t know the direction of the causality," said Ohayon. "Are the medical conditions provoking sleepwalking, or is it vice versa? Or perhaps it’s the treatment that is responsible."

Although more research is needed, the work could help raise awareness of this association among primary care physicians. “We’re not expecting them to diagnose sleepwalking, but they might detect symptoms that could be indices of sleepwalking,” said Ohayon.

Among the researchers’ other findings:

• The duration of sleepwalking was mostly chronic, with just over 80 percent of those who have sleepwalked reporting they’ve done so for more than five years.
• Sleepwalking was not associated with gender and seemed to decrease with age.
• Nearly one-third of individuals with nocturnal wandering had a family history of the disorder.
• People using over-the-counter sleeping pills had a higher likelihood of reporting sleepwalking episodes at least two times per month. (Indeed, a sleeping pill was the trigger for Homer Simpson’s middle-of-the-night shenanigans.)

D. Le’ger, MD, PhD, from the Universite Paris Descartes in France, was senior author of the study. Researchers from the University of Minnesota Medical School, the Hopital Gui-de-Chauliac in Montpellier, France, and Duke University School of Medicine were also involved.

Provided by Stanford University Medical Center

Source: medicalxpress.com

May 14, 2012

Why does one person become anorexic and another obese? A study recently published by a University of Colorado School of Medicine researcher shows that reward circuits in the brain are sensitized in anorexic women and desensitized in obese women. The findings also suggest that eating behavior is related to brain dopamine pathways involved in addictions.

Guido Frank, MD, assistant professor director of the Developmental Brain Research Program at the CU School of Medicine and his colleagues used functional magnetic resonance imaging (fMRI) to examine brain activity in 63 women who were either anorexic or obese. Scientists compared them to women considered “normal” weight. The participants were visually conditioned to associate certain shapes with either a sweet or a non-sweet solution and then received the taste solutions expectedly or unexpectedly. This task has been associated with brain dopamine function in the past.

The authors found that during these fMRI sessions, an unexpected sweet-tasting solution resulted in increased neural activation of reward systems in the anorexic patients and diminished activation in obese individuals. In rodents, food restriction and weight loss have been associated with greater dopamine-related reward responses in the brain.

"It is clear that in humans the brain’s reward system helps to regulate food intake" said Frank. "The specific role of these networks in eating disorders such as anorexia nervosa and, conversely, obesity, remains unclear.”

Scientists agree that more research is needed in this area. The study was published in Neuropsychopharmacology.

Provided by University of Colorado Denver

Source: medicalxpress.com

May 14, 2012

Following a stroke, factors as varied as blood sugar, body temperature and position in bed can affect patient outcomes, Loyola University Medical Center researchers report.

In a review article in the journal MedLink Neurology, first author Murray Flaster, MD, PhD and colleagues summarize the latest research on caring for ischemic stroke patients. (Most strokes are ischemic, meaning they are caused by blood clots.)

"The period immediately following an acute ischemic stroke is a time of significant risk,” the Loyola neurologists write. “Meticulous attention to the care of the stroke patient during this time can prevent further neurologic injury and minimize common complications, optimizing the chance of functional recovery.”

Stroke care has two main objectives – minimizing injury to brain tissue and preventing and treating the many neurologic and medical complications that can occur just after a stroke.

The authors discuss the many complex factors that affect outcomes. For example, there is considerable evidence of a link between hyperglycemia (high blood sugar) and poor outcomes after stroke. The authors recommend strict blood sugar control, using frequent finger-stick glucose checks and aggressive insulin treatment.

For each 1 degree C increase in the body temperature of stroke patients, the risk of death or severe disability more than doubles. Therapeutic cooling has been shown to help cardiac arrest patients, and clinical trials are underway to determine whether such cooling could also help stroke patients. Until those trials are completed, the goal should be to keep normal temperatures (between 95.9 and 99.5 degrees F).

Position in bed also is important, because sitting upright decreases blood flow in the brain. A common practice is to keep the patient lying flat for 24 hours. If a patient has orthopnea (difficulty breathing while lying flat), the head of the bed should be kept at the lowest elevation the patient can tolerate.

The authors discuss many other issues in stroke care, including blood pressure management; blood volume; statin therapy; management of complications such as pneumonia and sepsis; heart attack and other cardiac problems; blood clots; infection; malnutrition and aspiration; brain swelling; seizures; recurrent stroke; and brain hemorrhages.

Studies have shown that hospital units that specialize in stroke care decrease mortality, increase the likelihood of being discharged to home and improve functional status and quality of life.

All patients should receive supportive care — including those who suffer major strokes and the elderly. “Even in these populations, the majority of patients will survive their stroke,” the authors write. “The degree of functional recovery, however, may be dramatically impacted by the intensity and appropriateness of supportive care.”

Provided by Loyola University Health System

Source: medicalxpress.com

May 14, 2012

(Medical Xpress) — It has long been suspected that humans do not experience the world continuously, but rather in rapid snapshots.

Now, researchers at the University of Glasgow have demonstrated this is indeed the case. Just as the body goes through a 24-hour sleep-wake cycle controlled by a circadian clock, brain function undergoes such cyclic activity – albeit at a much faster rate.

Professor Gregor Thut of the Institute of Neuroscience and Psychology, said: “Rhythms are intrinsic to biological systems. The circadian rhythm, with its very slow periodicity of sleep and wake cycles every 24 hours has an obvious, periodic effect on bodily functions.

“Brain oscillations – the recurrent neural activity that we see in the brain – also show periodicity but cycle at much faster speeds. What we wanted to know was whether brain function was affected in a cyclic manner by these rapid oscillations.”

The researchers studied a prominent brain rhythm associated with visual cortex functioning that cycles at a rate of 10 times per second (10Hz).

They used a ‘simple trick’ to affect the oscillations of this rhythm which involved presenting a brief sound to ‘reset’ the oscillation.

Testing subsequent visual perception, by using transcranial magnetic stimulation of the visual cortex, revealed a cyclic pattern at the very rapid rate of brain oscillations, in time with the underlying brainwaves.

Prof Thut said: “Rhythmicity therefore is indeed omnipresent not only in brain activity but also brain function. For perception, this means that despite experiencing the world as a continuum, we do not sample our world continuously but in discrete snapshots determined by the cycles of brain rhythms.”

The research, ‘Sounds reset rhythms of visual cortex and corresponding human visual perception’ is published in the journal Current Biology.

Provided by University of Glasgow

Source: medicalxpress.com

May 14, 2012 By Sandy Evangelista

(Medical Xpress) — Swiss scientists have proven that light intensity influences our cognitive performance and how alert we feel, and that these positive effects last until early evening.

Credit: 2012 EPFL

Tests conducted in EPFL’s Solar Energy and Building Physics Laboratory (LESO) have confirmed the hypothesis that light influences our subjective feeling of sleepiness. The research team, led by Mirjam Münch, also showed that the effects of light exposure last until the early evening, and that light intensity has an impact on cognitive mechanisms. The results of this research were recently published in the journal Behavioral Neuroscience.

Light synchronizes our biological clocks. It is collected in the eye by photoreceptors that use photopigments (pigments that change when exposed to light), known as melanopsin. These cells, which differ from rods and cones, are considered a third class of photoreceptors in the retina and were discovered just ten years ago. They’re not there to form an image, but to perceive and absorb photons in the visible light spectrum. In addition, they are stimulated by blue light.

Exploring office lighting

Münch and her team wanted to know how our circadian rhythm could be influenced by our perception of light during the daytime. They created realistic office lighting conditions and recruited 29 young participants. “For this study, we took into account the intensity of natural and artificial light without specifically evaluating their spectra.”

From daytime to dusk

To synchronize their internal biological clocks, the volunteers had to maintain a regular sleep schedule during the seven days leading up to the test. They wore bracelets equipped with light sensors and accelerometers, so that the scientists could monitor their movements.

The study itself took place over two eight-hour sessions. The participants spent the first six hours in an experiment room, first in well-lighted conditions (1000-2000 lux, more or less equivalent to natural light in a room). In the second session, the light intensity was about 170 lux, which is what the eye perceives in a room without a window, lit with artificial light. For this experiment, light intensity was measured at eye-level. Every 30 minutes, the subjects were asked to assess how alert or sleepy they felt.

Finally, at the end of each session, the participants underwent two hours of supplemental memory tests in a darkened room – less than 6 lux. During these last two hours, the researchers took saliva samples in order to measure cortisol and melatonin concentrations. These two hormones are produced in a in a 24-hour cycle by the human body.

Boosted by the light

The volunteers who were subjected to higher light intensity during the afternoon were more alert all the way into the early evening. When they were subjected to light intensity ten times weaker, however, they showed signs of sleepiness and obtained lower scores on the memory tests.

These results were observed even in the absence of changes in cortisol and melatonin concentrations in their saliva. “With this study, we have discovered that light intensity has a direct effect on the subjective feeling of sleepiness as well as on objective cognitive performance, and that the benefits of more intense light during the daytime last long past the time of exposure,” concludes Münch.

Provided by Ecole Polytechnique Federale de Lausanne

Source: medicalxpress.com

ScienceDaily (May 13, 2012) — Scientists at Weill Cornell Medical College have discovered that the single protein — alpha 2 delta — exerts a spigot-like function, controlling the volume of neurotransmitters and other chemicals that flow between the synapses of brain neurons. The study, published online in Nature, shows how brain cells talk to each other through these signals, relaying thoughts, feelings and action, and this powerful molecule plays a crucial role in regulating effective communication.

In the study, the investigators also suggest how the widely used pain drug Lyrica might work. The alpha 2 delta protein is the target of this drug and the new work suggests an approach to how other drugs could be developed that effectively twist particular neurotransmitter spigots on and off to treat neurological disorders. The research findings surprised the research team, which includes scientists from University College London.

"We are amazed that any single protein has such power," says the study’s lead investigator Dr. Timothy A. Ryan, professor of Biochemistry and associate professor of Biochemistry in Anesthesiology at Weill Cornell Medical College. "It is indeed rare to identify a biological molecule’s function that is so potent, that seems to be controlling the effectiveness of neurotransmission."

The researchers found that alpha 2 delta determines how many calcium channels will be present at the synaptic junction between neurons. The transmission of chemical signals is triggered at the synapse by the entry of calcium into these channels, so the volume and speed of neurotransmission depends on the availability of these channels.

Researchers discovered that taking away alpha 2 delta from brain cells prevented calcium channels from getting to the synapse. “But if you add more alpha 2 delta, you can triple the number of channels at synapses,” Dr. Ryan says. “This change in abundance was tightly linked to how well synapses carry out their function, which is to release neurotransmitters.”

Before this study, it was known that Lyrica, which is used for neuropathic pain, seizures and fibromyalgia, binds to alpha 2 delta, but little was understood about how this protein works to control synapses.

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ScienceDaily (May 11, 2012) — Neuroscientist Patrik Verstreken, associated with VIB and KU Leuven, succeeded in undoing the effect of one of the genetic defects that leads to Parkinson’s using vitamin K2. His discovery gives hope to Parkinson’s patients.

Male fruit fly (Drosophila Melanogaster). Scientists have succeeded in undoing the effect of one of the genetic defects that leads to Parkinson’s using vitamin K2. The research was done in fruit flies. (Credit: © Studiotouch / Fotolia)

This research was done in collaboration with colleagues from Northern Illinois University (US) and was recently published in the journal Science.

"It appears from our research that administering vitamin K2 could possibly help patients with Parkinson’s. However, more work needs to be done to understand this better," says Patrik Verstreken.

Malfunctioning power plants are at the basis of Parkinson’s.

If we looked at cells as small factories, then mitochondria would be the power plants responsible for supplying the energy for their operation. They generate this energy by transporting electrons. In Parkinson’s patients, the activity of mitochondria and the transport of electrons have been disrupted, resulting in the mitochondria no longer producing sufficient energy for the cell. This has major consequences as the cells in certain parts of the brain will start dying off, disrupting communication between neurons. The results are the typical symptoms of Parkinson’s: lack of movement (akinesia), tremors and muscle stiffness.

The exact cause of this neurodegenerative disease is not known. In recent years, however, scientists have been able to describe several genetic defects (mutations) found in Parkinson’s patients, including the so-called PINK1 and Parkin mutations, which both lead to reduced mitochondrial activity. By studying these mutations, scientists hope to unravel the mechanisms underlying the disease process.

Paralyzed fruit flies

Fruit flies (Drosophila) are frequently used in lab experiments because of their short life spans and breeding cycles, among other things. Within two weeks of her emergence, every female is able to produce hundreds of offspring. By genetically modifying fruitflies, scientists can study the function of certain genes and proteins. Patrik Verstreken and his team used fruitflies with a genetic defect in PINK1 or Parkin that is similar to the one associated with Parkinson’s. They found that the flies with a PINK1 or Parkin mutation lost their ability to fly.

Upon closer examination, they discovered that the mitochondria in these flies were defective, just as in Parkinson’s patients. Because of this they generated less intracellular energy — energy the insects needed to fly. When the flies were given vitamin K2, the energy production in their mitochondria was restored and the insects’ ability to fly improved. The researchers were also able to determine that the energy production was restored because the vitamin K2 had improved electron transport in the mitochondria. This in turn led to improved energy production.

Conclusion

Vitamin K2 plays a role in the energy production of defective mitochondria. Because defective mitochondria are also found in Parkinson’s patients with a PINK1 or Parkin mutation, vitamin K2 potentially offers hope for a new treatment for Parkinson’s.

Source: Science Daily

May 11, 2012

Regenerating sensory hair cells, which produce electrical signals in response to vibrations within the inner ear, could form the basis for treating age- or trauma-related hearing loss. One way to do this could be with gene therapy that drives new sensory hair cells to grow.

Researchers at Emory University School of Medicine have shown that introducing a gene called Atoh1 into the cochleae of young mice can induce the formation of extra sensory hair cells.

Their results show the potential of a gene therapy approach, but also demonstrate its current limitations. The extra hair cells produce electrical signals like normal hair cells and connect with neurons. However, after the mice are two weeks old, which is before puberty, inducing Atoh1 has little effect. This suggests that an analogous treatment in adult humans would also not be effective by itself.

The findings were published May 9 in the Journal of Neuroscience.

"We’ve shown that hair cell regeneration is possible in principle," says Ping Chen, PhD, associate professor of cell biology at Emory University School of Medicine. “In this paper, we have identified which cells are capable of becoming hair cells under the influence of Atoh1, and we show that there are strong age-dependent limitations on the effects of Atoh1 by itself.”

The first author of the paper, Michael Kelly, now a postdoctoral fellow at the National Institute on Deafness and Other Communication Disorders, was a graduate student in Emory’s Neuroscience program.

Kelly and his coworkers engineered mice to turn on the Atoh1 gene in the inner ear in response to the antibiotic doxycycline. Previous experimenters had used a virus to introduce Atoh1 into the cochleae of animals. This approach resembles gene therapy, but has the disadvantage of being slightly different each time, Chen says. In contrast, the mice have the Atoh1 gene turned on in specific cells along the lining of the inner ear, called the cochlear epithelium, but only when fed doxycycline.

Young mice given doxycycline for two days had extra sensory hair cells, in parts of the cochlea where developing hair cells usually appear, and also additional locations (see accompanying image).

The extra hair cells could generate electrical signals, although those signals weren’t as strong as mature hair cells. Also, the extra hair cells appeared to attract neuronal fibers, which suggests that those signals could connect to the rest of the nervous system.

"They can generate electrical signals, but we don’t know if they can really function in the context of hearing.” Chen says. “For that to happen, the hair cells’ signals need to be coordinated and integrated.”

Although doxycycline could turn on Atoh1 all over the surface of the cochlea, extra sensory hair cells did not appear everywhere. When they removed cochleae from the mice and grew them in culture dishes, her team was able to provoke even more hair cells to grow when they added a drug that inhibits the Notch pathway.

Manipulating the Notch pathway affects several aspects of embryonic development and in some contexts appears to cause cancer, so the approach needs to be refined further. Chen says that it may be possible to unlock the age-related limits on hair cell regeneration by supplying additional genes or drugs in combination with Atoh1, and the results with the Notch drug provide an example.

"Our future goals are to develop approaches to stimulate hair cell formation in older animals, and to examine functional recovery after Atoh1 induction," she says.

Provided by Emory University

Source: medicalxpress.com

May 11, 2012

A brain study in infant rats demonstrates that the anti-epilepsy drug phenobarbital stunts neuronal growth, which could prompt new questions about using the first-line drug to treat epilepsy in human newborns.

In Annals of Neurology EarlyView posted online May 11, researchers at Georgetown University Medical Center (GUMC) report that the anti-epilepsy drug phenobarbital given to rat pups about a week old changed the way the animals’ brains were wired, causing cognitive abnormalities later in life.

The researchers say it has been known that some of the drugs used to treat epilepsy increase the amount of neurons that die shortly after birth in the rat brain, but, until this study, no one had shown whether this action had any adverse impact on subsequent brain development.

"Our study is the first to show that the exposure to these drugs — and just a single exposure — can prevent brain circuits from developing their normal connectivity, meaning they may not be wired correctly, which can have long-lasting effects on brain function,” says the study’s senior investigator, Karen Gale, Ph.D., a professor of pharmacology at GUMC. “These findings suggest that in the growing brain, these drugs are not as benign as one would like to believe.”

For their study, the Georgetown researchers studied four agents including phenobarbital.

"The good news is not all anti-epilepsy drugs have this disruptive effect in the animal studies," Gale says.

The researchers found that the anti-epilepsy drug levetiracetam did not stunt synaptic growth. Animals treated with a third drug, lamotrigine, showed neural maturation, but it was delayed. An additional finding involved melatonin. When added to phenobarbital, it appeared to prevent the persistent adverse neural effects in the rat pups. Melatonin has been used clinically to protect cells from injury in humans.

"Many clinicians have been advocating for a reexamination of the use of these drugs in infants, and our findings provide experimental data to support that need," says the study’s co-lead investigator, Patrick A. Forcelli, Ph.D., a postdoctoral fellow in the department of pharmacology and physiology at GUMC. "Phenobarbital has been used to treat seizures for over 100 years — well before a Food and Drug Administration approval process was established— and for more than 50 years, it has been the first drug of choice in the treatment of seizures in neonates."

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