Posts tagged science
Articles and news from the latest research reports.
The BCMI-MIdAS (Brain-Computer Music Interface for Monitoring and Inducing Affective States) project
The central purpose of the project is to develop technology for building innovative intelligent systems that can monitor our affective state, and induce specific affective states through music, automatically and adaptively. This is a highly interdisciplinary project, which will address several technical challenges at the interface between science, technology and performing arts/music (incorporating computer-generated music and machine learning).
Research questions
- How can music change affective states and what are the specific musical traits (i.e., the parameters of a piece of music) that elicit such states?
- How can we control such traits in a piece of music in order to induce specific affective states in a participant?
- How can we effectively detect information about affective states induced by music in the EEG signal, going beyond EEG asymmetry and characterising information contained in synchronisation patterns?
- How can we use the EEG to monitor the affective state induced by music on-line (i.e., in “real-time”)?
- How can we produce a generative music system capable of generating music embodying musical traits aimed at inducing specific affective states, observable in the EEG of the participant?
- How can we build an intelligent adaptive system for monitoring and inducing affective states through music on-line?
(Source: cmr.soc.plymouth.ac.uk)
The zebrafish is a major player in the study of vertebrate biology and human disease. Its transparent, externally fertilized eggs, short reproductive cycle and fast growth mean that its embryonic development can be studied closely while the animal is alive, and the fish is a useful model for studying gene behaviour and function.
Now, researchers led by Stephen Ekker, a molecular biologist at the Mayo Clinic in Rochester, Minnesota, have for the first time made custom changes to parts of the zebrafish (Danio rerio) genome, using artificial enzymes to cut portions of DNA out of targeted positions in a gene sequence, and replace them with synthetic DNA.
Sleep Oscillations in the Thalamocortical System Induce Long-Term Neuronal Plasticity
Long-term plasticity contributes to memory formation and sleep plays a critical role in memory consolidation. However, it is unclear whether sleep slow oscillation by itself induces long-term plasticity that contributes to memory retention. Using in vivo prethalamic electrical stimulation at 1 Hz, which itself does not induce immediate potentiation of evoked responses, we investigated how the cortical evoked response was modulated by different states of vigilance. We found that somatosensory evoked potentials during wake were enhanced after a slow-wave sleep episode (with or without stimulation during sleep) as compared to a previous wake episode. In vitro, we determined that this enhancement has a postsynaptic mechanism that is calcium dependent, requires hyperpolarization periods (slow waves), and requires a coactivation of both AMPA and NMDA receptors. Our results suggest that long-term potentiation occurs during slow-wave sleep, supporting its contribution to memory.
Naked mole-rats evolved to thrive in an acidic environment that other mammals, including humans, would find intolerable. Researchers at the University of Illinois at Chicago report new findings as to how these rodents adapted, which may offer clues to relieving pain in other animals and humans.
Dark matter DNA active in brain during day — night cycle
NIH study of rats shows DNA regions thought inactive highly involved in body’s clock
Long stretches of DNA once considered inert dark matter appear to be uniquely active in a part of the brain known to control the body’s 24-hour cycle, according to researchers at the National Institutes of Health.
Working with material from rat brains, the researchers found some expanses of DNA contained the information that generate biologically active molecules. The levels of these molecules rose and fell, in synchrony with 24-hour cycles of light and darkness. Activity of some of the molecules peaked at night and diminished during the day, while the remainder peaked during the day and diminished during the night.
How does electrical stimulation affect the brain? A project by Aalto University and the University of Helsinki, launched in early 2012, studies the impact mechanism of deep brain stimulation and develops electrochemical sensors for more effective measuring of neurotransmitters in the brain. The long-term goals of the research are more specific treatment for Parkinson’s disease and many other diseases of the nervous system.
Giving lithium to those who need it
Lithium is a ‘gold standard’ drug for treating bipolar disorder, however not everyone responds in the same way. New research published in BioMed Central’s open access journal Biology of Mood & Anxiety Disorders finds that this is true at the levels of gene activation, especially in the activation or repression of genes which alter the level the apoptosis (programmed cell death). Most notably BCL2, known to be important for the therapeutic effects of lithium, did not increase in non-responders. This can be tested in the blood of patients within four weeks of treatment.
A research team from Yale University School of Medicine measured the changing levels of gene activity in the blood of twenty depressed adult subjects with bipolar disorder before treatment, and then fortnightly once treatment with lithium carbonate had begun.
Over the eight weeks of treatment there were definite differences in the levels of gene expression between those who responded to lithium (measured using the Hamilton Depression Rating Scale) and those who failed to respond. Dr Robert Beech who led this study explained, “We found 127 genes that had different patterns of activity (turned up or down) and the most affected cellular signalling pathway was that controlled programmed cell death (apoptosis).”
For people who responded to lithium the genes which protect against apoptosis, including Bcl2 and IRS2, were up regulated, while those which promote apoptosis were down regulated, including BAD and BAK1.
The protein coded by BAK1 can open an anion channel in mitochondrial walls which leads to leakage of mitochondrial contents and activation of cell death pathways. Damage similar to this has been seen within the prefrontal cortex of the brain of patients with bipolar disorder. BAD protein is thought to promote BAK1 activity, while Bcl2 binds to BAK1 and prevents its ability to bind to the channel.
Dr Beech continued, “This positive swing in regulation of apoptosis for lithium responders was measurable as early as four weeks after the start of treatment, while in non-responders there was a measureable shift in the opposite direction. It seems then, that increased expression of BCL2 and related genes is necessary for the therapeutic effects of lithium. Understanding these differences in genes expression may lead towards personalized treatment for bipolar disorder in the future.”
(Source: biomedcentral.com)
The promise of stem cells seems limitless. If they can be coaxed into rebuilding organs, repairing damaged spinal cords and restoring ravaged immune systems, these malleable cells would revolutionize medical treatment. But stem cell research is still in its infancy, as scientists seek to better understand the role of these cells in normal human development and disease.
On Friday, September 14, the Ruth L. and David S. Gottesman Institute for Stem Cell and Regenerative Medicine Research at Albert Einstein College of Medicine of Yeshiva University offered the Einstein community and invited guests an opportunity to hear from leading stem cell scientists investigating the dynamic field. The 2012 Einstein Stem Cell Institute Symposium featured speakers from around the globe presenting the latest research on induced pluripotent stem cells (iPS cells), cell reprogramming, as well as cancer and hematopoietic (blood-forming) stem cells.
"This symposium was an important milestone for stem cell research at Einstein and confirms our intent to contribute to advances in stem cell biology," said the event’s host and organizer, Paul Frenette, M.D., director and chair of Einstein’s Stem Cell Institute and professor of medicine and of cell biology.
A University of Arizona professor is overseeing the manufacture of an experimental drug that could help reduce brain damage after a stroke.
The drug, known as 3K3A-APC, currently is undergoing clinical trials in Europe to determine its safety in humans after proving effective in animal models at reducing brain damage and improving motor skills after a stroke when given in combination with another commonly used stroke therapy.
Thomas Davis, professor of pharmacology in the UA College of Medicine, was chosen to direct the manufacture of the drug for human trials after co-authoring a recent paper in the journal Stroke that pointed to the drug’s effectiveness in rats and mice when used in conjunction with a clot-busting therapy known as tissue plasminogen activator, or tPA.
While tPA is commonly given to sufferers of ischemic stroke, which results from an obstruction in a blood vessel supplying blood to the brain, the therapy poses significant challenges when administered alone, including a limited treatment window, Davis said.
"It has to be given within the first three to four and a half hours of the stroke," Davis said. "It only works in 10 percent of the patients, and it causes bleeding, so tPA alone isn’t that effective."
Neurodegenerative diseases such as Alzheimer’s or Parkinson’s are characterised by the loss of nerve cells and the deposition of proteins in the brain tissue. A group of researchers led by Gabor G. Kovacs from the Clinical Institute of Neurology at the MedUni Vienna has now demonstrated that Alzheimer’s disease does not just – as previously believed – involve the proteins that are attributed to Alzheimer’s, but instead the condition can involve a mixture of interacting proteins from different neurodegenerative diseases.
“As a result, Alzheimer’s should not be treated in isolation. According to these latest findings, pure, classical Alzheimer’s disease, which involves only the attributed proteins tau and amyloid beta, appears not to be the norm,” says Kovacs. There is also a varied regional distribution of nerve cell loss and protein deposits between patients which, taken together, have clinical prognostic significance. As a consequence of this, differentiated strategies need to be developed for personalised therapy that takes account of all the interacting factors.
The new treatment concepts which are currently being developed by the MedUni Vienna’s neuropathologists, neurobiologists, neurologists, psychiatrists and neuroimaging experts will divide the patients into “sub-groups”. Says Kovacs: “The aim is to define these groups very precisely in future in order to be able to offer them personalised treatment.”
Dementia diseases: a growing trend
Around 100,000 Austrians are currently suffering from a dementia-related illness, according to statistics from the Austrian Alzheimer Society. According to estimates, this figure will rise to around 280,000 by 2050 as a result of the increasing age of the general population. Alzheimer’s disease is responsible for 60 to 80 per cent of these conditions.The global Alzheimer’s report by “Alzheimer’s Disease International” reckons that the prevalence of dementia doubles every 20 years. There are currently around 35 million people worldwide suffering a dementia-related illness. By 2030, their number will rise to 65.7 million and reach as many as 115.4 million by 2050.