Posts tagged science
Articles and news from the latest research reports.
Disney researchers add sense of touch to augmented reality applications
Technology developed by Disney Research, Pittsburgh, makes it possible to change the feel of real-world surfaces and objects, including touch-screens, walls, furniture, wooden or plastic objects, without requiring users to wear special gloves or use force-feedback devices. Surfaces are not altered with actuators and require little if any instrumentation.
Instead, Disney researchers employ a newly discovered physical phenomenon called reverse electrovibration to create the illusion of changing textures as the user’s fingers sweep across a surface. A weak electrical signal, which can be applied imperceptibly anywhere on the user’s body, creates an oscillating electrical field around the user’s fingers that is responsible for the tactile feedback.
The technology, called REVEL, could be used to create “please touch” museum displays, add haptic feedback to games, apply texture to projected images on surfaces of any size and shape, provide customized directions on walls for people with visual disabilities and enhance other applications of augmented reality.
3D-printed sugar network to help grow artificial liver
Researchers have moved a step closer to creating a synthetic liver, after a US team created a template for blood vessels to grow into, using sugar.
Scientists have long been experimenting with the 3D printing of cells and blood vessels, building up tissue structure layer by layer with artificial cells. But the synthetically engineered cells often die before the tissue is formed. The technology, in which a 3D printer uses sugar as its building material, could one day be used for transplants. The study appears in the journal Nature Materials.
Study examines effects of growth hormone-releasing hormone on cognitive function
6-Aug-2012
Treatment with growth hormone-releasing hormone appears to be associated with favorable cognitive effects among both adults with mild cognitive impairment and healthy older adults, according to a randomized clinical trial published Online First by Archives of Neurology, a JAMA Network publication.
"Growth hormone-releasing hormone (GHRH), growth hormone and insulinlike growth factor 1 have potent effects on brain function, their levels decrease with advancing age, and they likely play a role in the pathogenesis of Alzheimer disease," the authors write as background information in the study.
To examine the effects of GHRH on cognitive function in healthy older adults and in adults with mild cognitive impairment (MCI), Laura D. Baker, Ph.D., of the University of Washington School of Medicine and Veterans Affairs Puget Sound Health Care System, Seattle, and colleagues, conducted a randomized, double-blind, placebo-controlled trial in which participants self-administered daily injections of a form of human GHRH (tesamorelin), or placebo.
The authors enrolled 152 adults ranging in age from 55 to 87 years (average age, 68 years) and 137 participants (76 healthy patients and 61 patients with MCI) successfully completed the study. At baseline, at 10 and 20 weeks of treatment, and after a 10-week washout (30 weeks total), the authors collected blood samples and administered parallel versions of cognitive tests.
Among the original 152 patients enrolled in the study, analysis indicated a favorable effect of GHRH on cognition, which was comparable in adults with MCI and healthy older adults. Analysis among the 137 patients who successfully completed the trial also showed that treatment with GHRH had a favorable effect on cognition among both groups of patients. Although the healthy adults outperformed those with MCI overall, the cognitive benefits relative to placebo was comparable among both groups.
Treatment with GHRH also increased insulin like growth factor 1 levels by 117 percent, which remained within the physiological range, and increased fasting insulin levels within the normal range by 35 percent in adults with MCI but not in healthy adults.
"Our results replicate and expand our earlier positive findings, demonstrating that GHRH administration has favorable effects on cognitive function not only in healthy older adults but also in adults at increased risk of cognitive decline and dementia," the authors conclude. "Larger and longer-duration treatment trials are needed to firmly establish the therapeutic potential of GHRH administration to promote brain health in normal aging and ‘pathological aging.’"
Source: EurekAlert!
Scientists peek at the early evolution of sex chromosomes
Two new studies offer insight into sex chromosome evolution by focusing on papaya, a multimillion dollar crop plant with a sexual problem (as far as growers are concerned) and a complicated past.
The research reveals that the papaya sex chromosomes have undergone dramatic changes in their short evolutionary histories (they are about 7 million years old; by comparison, human sex chromosomes began their evolution more than 167 million years ago). One of the two studies compares the papaya X chromosome with that of a closely related non-sex chromosome (called an autosome) in a sister species. The other looks at differences between the X and Y chromosomes.
Pupil Dilation Reveals Sexual Orientation
There is a popular belief that sexual orientation can be revealed by pupil dilation to attractive people, yet until now there was no scientific evidence. For the first time, researchers at Cornell University used a specialized infrared lens to measure pupillary changes to participants watching erotic videos. Pupils were highly telling: they widened most to videos of people who participants found attractive, thereby revealing where they were on the sexual spectrum from heterosexual to homosexual.
The findings were published August 3 in the scientific journal PLoS ONE.
Brain signal ID’s responders to fast-acting antidepressant
August 3, 2012
Scientists have discovered a biological marker that may help to identify which depressed patients will respond to an experimental, rapid-acting antidepressant. The brain signal, detectable by noninvasive imaging, also holds clues to the agent’s underlying mechanism, which are vital for drug development, say National Institutes of Health researchers.
Dr. Zarate views subject in MEG scanner from scanner control room.
The signal is among the latest of several such markers, including factors detectable in blood, genetic markers, and a sleep-specific brain wave, recently uncovered by the NIH team and grantee collaborators. They illuminate the workings of the agent, called ketamine, and may hold promise for more personalized treatment.
"These clues help focus the search for the molecular targets of a future generation of medications that will lift depression within hours instead of weeks," explained Carlos Zarate, M.D., of the NIH’s National Institute of Mental Health (NIMH). "The more precisely we understand how this mechanism works, the more narrowly treatment can be targeted to achieve rapid antidepressant effects and avoid undesirable side effects."
Zarate, Brian Cornwell, Ph.D., and NIMH colleagues report on their brain imaging study online in the journal Biological Psychiatry.
Previous research had shown that ketamine can lift symptoms of depression within hours in many patients. But side effects hamper its use as a first-line medication. So researchers are studying its mechanism of action in hopes of developing a safer agent that works similarly.
Ketamine works through a different brain chemical system than conventional antidepressants. It initially blocks a protein on brain neurons, called the NMDA receptor, to which the chemical messenger glutamate binds. However, it is not known if the drug’s rapid antidepressant effects are a direct result of this blockage or of downstream effects triggered by the blockage, as suggested by animal studies.
To tease apart ketamine’s workings, the NIMH team imaged depressed patients’ brain electrical activity with magnetoencephalography (MEG). They monitored spontaneous activity while subjects were at rest, and activity evoked by gentle stimulation of a finger, before and 6.5 hours after an infusion of ketamine.
It was known that by blocking NMDA receptors, ketamine causes an increase in spontaneous electrical signals, or waves, in a particular frequency range in the brain’s cortex, or outer mantle. Hours after ketamine administration— in the timeframe in which ketamine relieves depression — spontaneous electrical activity in people at rest was the same whether or not the drug lifted their depression.
Electrical activity evoked by stimulating a finger, however, was different in the two groups. MEG imaging made it possible to monitor excitability of the somatosensory cortex, the part of the cortex that registers sensory stimulation. Those who responded to ketamine showed an increased response to the finger stimulation, a greater excitability of the neurons in this part of the cortex.
Such a change in excitability is likely to result, not from the immediate effects of blocking the receptor, but from other processes downstream, in the cascade of effects set in motion by NMDA blockade, say the researchers. Evidence points to changes in another type of glutamate receptor, the AMPA receptor, raising questions about whether the blocking of NMDA receptors is even necessary for ketamine’s antidepressant effect. If NMDA blockade is just a trigger, then targeting AMPA receptors may prove a more direct way to effect a lifting of depression.
While antipsychotic drugs alleviate the symptoms of many people with schizophrenia, around a third of patients resist such treatments. A new study, led by Javier Gonzalez-Maeso of the Mount Sinai School of Medicine, suggests that this frustrating intractability depends on how DNA is packaged.
Gonzalez-Maeso and his colleagues found that antipsychotic drugs can suppress the expression of glutamate receptors in the brain, stunting their effectiveness as treatments for schizophrenia. But the researchers also found a way of boosting the effects of antipsychotics—by pairing them with drugs that block the gene suppression pathway.
Schizophrenia
Credit: JOHN BAVOSI/SCIENCE PHOTO LIBRARY
Caption: Schizophrenia. Artwork of a man hearing non- existent women’s voices. Auditory hallucinations are one of the most common symptoms of schizophrenia. One explanation for this disease is known as the dopamine hypothesis. Dopamine (the molecules at lower left & right) is a type of neurotransmitter. This chemical (tiny red spheres) is released from the ends (synapses) of nerve cells (neurons, upper left & right) when they pass on nerve impulses to other neurons. In schizophr- enia, however, the dopamine-producing neurons of the brain are overactive. This causes the sufferer to lose contact with reality, suffering from confused thoughts and emotional responses.
Guinea pig hearts beat with human cells
Damaged skin and liver can often repair themselves, but the heart rarely heals well and heart disease is the world’s leading cause of death. Research published today raises hopes for cell therapies, showing that heart muscle cells differentiated from human embryonic stem cells can integrate into existing heart muscle.
“What we have done is prove that these cells do what working heart muscles do, which is beat in sync with the rest of the heart,” says Chuck Murry, a cardiovascular biologist at the University of Washington in Seattle, who co-led the research.
It’s a longstanding question in biology: How do cells know when to progress through the cell cycle? In simple organisms such as yeast, cells divide once they reach a specific size. However, determining if this holds true for mammalian cells has been difficult, in part because there has been no good way to measure mammalian cell growth over time.
A team of MIT and Harvard Medical School (HMS) researchers has precisely measured the growth rates of single cells, allowing them to answer that fundamental question. In the Aug. 5 online edition of Nature Methods, the researchers report that mammalian cells divide not when they reach a critical size, but when their growth rate hits a specific threshold.