Posts tagged science
Articles and news from the latest research reports.
Mirror, mirror on the wall - who has the fairest ORGANS of them all? Smart surface reveals ‘your’ insides
Mirrors have existed for thousands of years but the looking glass has just been given a 21st century makeover.
A new digital mirror gives people X-ray vision to let them see their insides – complete with bones, organs and muscle on show.
The 3D art installation, called the ‘Primary Intimacy of Being,’ recreates what a body looks like inside and eerily tracks a person’s movements as if they are seeing themselves.
Brain ‘Stones’ Found in Man with Celiac Disease
A young man in Brazil who suffered from throbbing headaches and vision problems for 10 years turned out to have stonelike buildups of calcium in his brain.
The stones were likely a rare complication of the man’s celiac disease, a digestive condition that the man didn’t know he had, according to a new report of his case.
Because of his recurring headaches and vision problems, the man had been treated for migraines, but he hadn’t improved. When doctors did a CT scan, they found patches of calcification in the back of the man’s brain, in the areas that handle vision.
Lab tests showed that although the fluid circulating in the man’s brain was normal, it had higher levels of the antibodies linked to celiac disease, according to the report published in the New England Journal of Medicine.
Smoking’s toll on mentally ill analyzed
Those in the United States with a mental illness diagnosis are much more likely to smoke cigarettes and smoke more heavily, and are less likely to quit smoking than those without mental illness, regardless of their specific diagnosis, a new study by researchers from the Yale School of Medicine shows.
They also found variations in smoking rates and likelihood of quitting among different diagnoses of mental illness. The results are reported in the April issue of the journal Tobacco Control.
Thirty-nine percent of adults with a psychiatric diagnosis smoked compared to 16% without a diagnosis, according to data from the National Epidemiologic Survey on Alcohol and Related Conditions analyzed by researchers. Two out of every three people with drug use disorder smoke, compared to one out of three with social phobia.
“We know that smokers with mental illness are more susceptible to smoking-related disease, and those with mental illness die 25 years earlier than adults without mental illness,” said Sherry McKee, associate professor of psychiatry, and senior author on the study. “Effective smoking cessation treatments are available and we know that smokers with mental illness can quit smoking. We need to address why smokers with mental illness are not being treated for their smoking.”
Over the three-year study period, 22% of smokers with no psychiatric disorders were able to quit smoking, whereas rates of quitting among those with psychiatric disorders were 25% lower. Rates of quitting were lowest among those with dysthymia (10%), agoraphobia (13%), and social phobia (13%). “We also found that individuals with multiple diagnoses had the lowest quit rates,” added Philip Smith, lead author on the study.
This study adds to evidence that smokers with mental illness consume nearly half of all cigarettes in the United States, despite making up a substantially smaller proportion of the population.
Researchers and policymakers are increasingly calling attention to this important public health issue, and this study helps point to a need for interventions and policy that directly help individuals with mental illness quit smoking.
Discovery Could Lead to Novel Therapies for Fragile X Syndrome
Scientists studying the most common form of inherited mental disability—a genetic disease called “Fragile X syndrome”—have uncovered new details about the cellular processes responsible for the condition that could lead to the development of therapies to restore some of the capabilities lost in affected individuals.
In a paper that will be published in the May 8 Molecular Cell, but is being made available this week in the early online edition of the journal, the researchers show how the fragile X mental retardation protein, or FMRP, which is in short supply in individuals with Fragile X, affects the protein-making structures of cells in the brain to cause the disease.
Researchers previously knew that in the absence of FMRP, protein-synthesizing structures called ribosomes translated some of the genetic instructions to produce proteins in the brain incorrectly, but exactly how this translation went awry was a mystery.
“The precise mechanism used by FMRP to regulate translation was not known,” said Simpson Joseph, a professor of chemistry and biochemistry at UC San Diego and a senior author of the study, which also involved scientists at the State University of New York at Albany and the New York State Department of Health. “Our study shows that FMRP can bind directly to the ribosome to regulate its function.”
More precisely, the researchers found that the protein binds to a region of the ribosome—between two ribosomal subunits—likely to be critical for the proper production of many proteins in the brain responsible for normal cognitive function. Using laboratory fruit flies, which have FMRP and ribosomes similar to those in humans, the scientists mapped the primary binding site of FMRP on the ribosome. With that information, medical researchers might be able to identify potential drugs that target those areas of the ribosome to help restore normal protein production in individuals with Fragile X.
“Similar to FMRP, it is possible that there are other proteins in the cell that bind directly to the ribosome as well to regulate gene expression,” said Joseph.
Low Tolerance for Pain? The Reason May Be In Your Genes
Researchers may have identified key genes linked to why some people have a higher tolerance for pain than others, according to a study released today that will be presented at the American Academy of Neurology’s 66th Annual Meeting in Philadelphia, April 26 to May 3, 2014.
“Our study is quite significant because it provides an objective way to understand pain and why different individuals have different pain tolerance levels,” said study author Tobore Onojjighofia, MD, MPH, with Proove Biosciences and a member of the American Academy of Neurology. “Identifying whether a person has these four genes could help doctors better understand a patient’s perception of pain.”
Researchers evaluated 2,721 people diagnosed with chronic pain for certain genes. Participants were taking prescription opioid pain medications. The genes involved were COMT, DRD2, DRD1 and OPRK1. The participants also rated their perception of pain on a scale from zero to 10. People who rated their pain as zero were not included in the study. Low pain perception was defined as a score of one, two or three; moderate pain perception was a score of four, five or six; and high pain perception was a score of seven, eight, nine or 10.
Nine percent of the participants had low pain perception, 46 percent had moderate pain perception and 45 percent had high pain perception.
The researchers found that the DRD1 gene variant was 33 percent more prevalent in the low pain group than in the high pain group. Among people with a moderate pain perception, the COMT and OPRK variants were 25 percent and 19 percent more often found than in those with a high pain perception. The DRD2 variant was 25 percent more common among those with a high pain perception compared to people with moderate pain.
“Chronic pain can affect every other part of life,” said Onojjighofia. “Finding genes that may be play a role in pain perception could provide a target for developing new therapies and help physicians better understand their patients’ perceptions of pain.”
(Source: newswise.com)
Common links between neurodegenerative diseases identified
Diseases of the central nervous system are a big burden to society. According to estimates, they cost €800 billion per year in Europe. And for most of them, there is no definitive cure. This is true, for example, for Parkinson disease. Although good treatments exist to manage its symptoms, they become more and more ineffective as the disease progresses. Now, the EU-funded REPLACES project, completed in 2013, which associated scientists with clinicians, has shed light on the abnormal working of a particular brain circuitry related to Parkinson’s disease. The results of the project suggest that these same circuits are implicated in different forms of pathologies. And this gives important insights into the possible common links between neurodegenerative diseases such as Parkinson and intellective disabilities or autism.
Existing treatments for Parkinson are very effective at the beginning. When the disease progresses, however, drugs, such as levodopa and so-called dopamine agonists, produce side effects that are sometimes even worse than the initial symptoms of the condition. In particular, they cause a complication called dyskinesia, characterised by abnormal involuntary movements. Therapies are therefore sought that allow better management of symptoms.
The project focused on the study of a highly plastic brain circuitry, which connects regions of the cerebral cortex with the basal ganglia. It is involved in very important functions such as learning and memory. “This system, based onglutamate as a mean of signalling between neurons, has also been discovered to be damaged in Parkinson disease,” says Monica Di Luca, professor of neuropharmacology at the University of Milan, Italy, and the project coordinator. She adds: “Parkinson’s more well-known and characteristic trait is the selective loss of cells producers of neurotransmitter dopamine.”
Researchers involved into the project studied the function and plasticity of this circuit in different animal models of Parkinson disease, from mice to non-human primates. They found that exactly the same alterations were present and conserved. This makes it an interesting and alternative target for trying to re-establish the correct functioning and reverse the symptoms of the disease.
One expert agrees with the need to target alternative target systems. “What researchers are trying to do is to intervene to modulate other systems that do not involve dopamine and obtain a better symptoms management,” explains Erwan Bezard, a researcher at the Neurodenerative Diseases Institute at the University of Bordeaux, in France. He also works on alternative targets in Parkinson disease. In monkeys, compounds that target glutamate receptors, used in combination with traditional drugs, have previously shown to improve some deficits in voluntary motor control.
But the research has also shed some light into apparently unrelated diseases. It is becoming more and more obvious that the same alterations in the working of the communication systems among neurons are shared among different diseases. “This is why we speak about ‘synaptopathies’: there are common players among Parkinson disease, autism and other forms of intellectual disabilities and even schizophrenia. Several of the mutated genes are the same, and affect the signalling systems through common molecules,” says Claudia Bagni, who works on synaptic plasticity in the context of intellectual disabilities at the University of Leuven, in Belgium and University of Rome Tor Vergata, in Italy. “For example, the glutamatergic system is also affected in the X-fragile syndrome, the most common form of inherited intellectual disability.”
Progress is in sight thanks to a much better understanding of the working of the abnormal synapses in Parkinson disease, and experiments performed in monkeys showing encouraging results. Indeed, “the team studied human primates, the model system closest to humans, and therefore their findings are relevant to human health.” says Bagni. Project researchers hope the door is now opened for the first clinical trials in humans. “We have identified a potential new target for treatment, and tested a couple of molecules in animals,” says Di Luca, the “next step would be to find a partnership with pharmaceutical industries interested in pursuing this research.”
Harvard neuroscientists have made a discovery that turns 160 years of neuroanatomy on its head.
Myelin, the electrical insulating material in the body long known to be essential for the fast transmission of impulses along the axons of nerve cells, is not as ubiquitous as thought, according to new work led by Professor Paola Arlotta of the Harvard Stem Cell Institute (HSCI) and the University’s Department of Stem Cell and Regenerative Biology, in collaboration with Professor Jeff Lichtman of Harvard’s Department of Molecular and Cellular Biology.
“Myelin is a relatively recent invention during evolution,” says Arlotta. “It’s thought that myelin allowed the brain to communicate really fast to the far reaches of the body, and that it has endowed the brain with the capacity to compute higher-level functions.”
In fact, loss of myelin is a feature in a number of devastating diseases, including multiple sclerosis and schizophrenia.
But the new research shows that despite myelin’s essential roles in the brain, “some of the most evolved, most complex neurons of the nervous system have less myelin than older, more ancestral ones,” said Arlotta, co-director of the HSCI neuroscience program.
What this means, she said, is that the higher one looks in the cerebral cortex — closer to the top of the brain, which is its most evolved part — the less myelin one finds. Not only that, but “neurons in this part of the brain display a brand-new way of positioning myelin along their axons that has not been previously seen. They have ‘intermittent myelin’ with long axon tracts that lack myelin interspersed among myelin-rich segments.”
“Contrary to the common assumptions that neurons use a universal profile of myelin distribution on their axons, the work indicates that different neurons choose to myelinate their axons differently,” Arlotta said. “In classic neurobiology textbooks, myelin is represented on axons as a sequence of myelinated segments separated by very short nodes that lack myelin. This distribution of myelin was tacitly assumed to be always the same, on every neuron, from the beginning to the end of the axon. This new work finds this not to be the case.”
The results of the research by Arlotta and postdoctoral fellow Giulio Srubek Tomassy, the first author on the report, are published in the latest edition of the journal Science.
The paper is accompanied by a “perspective” by R. Douglas Fields of the Eunice Kennedy Shriver National Institute of Child Health and Human Development at the National Institutes of Health, who said that Arlotta and Tomassy’s findings raise important questions about the purpose of myelin, and “are likely to spark new concepts about how information is transmitted and integrated in the brain.”
Arlotta and Tomassy collaborated closely on the new work with postdoctoral fellow Daniel Berger of the Lichtman lab, which generated one of the two massive electron microscopy databases that made the work possible.
“The fact that it is the most evolved neurons, the ones that have expanded dramatically in humans, suggest that what we’re seeing might be the ‘future.’ As neuronal diversity increases and the brain needs to process more and more complex information, neurons change the way they use myelin to achieve more,” said Arlotta.
Tomassy said it is possible that these profiles of myelination “may be giving neurons an opportunity to branch out and ‘talk’ to neighboring neurons.” For example, because axons cannot make synaptic contacts when they are myelinated, one possibility is that these long myelin gaps may be needed to increase neuronal communication and synchronize responses across different neurons. He and Arlotta postulate that the intermittent myelin may be intended to fine-tune the electrical impulses traveling along the axons, in order to allow the emergence of highly complex neuronal behaviors.
In Old Age, Lack of Emotion and Interest May Signal Your Brain Is Shrinking
Older people who have apathy but not depression may have smaller brain volumes than those without apathy, according to a new study published in the April 16, 2014, online issue of Neurology®, the medical journal of the American Academy of Neurology. Apathy is a lack of interest or emotion.
“Just as signs of memory loss may signal brain changes related to brain disease, apathy may indicate underlying changes,” said Lenore J. Launer, PhD, with the National Institute on Aging at the National Institutes of Health (NIH) in Bethesda, MD, and a member of the American Academy of Neurology. “Apathy symptoms are common in older people without dementia. And the fact that participants in our study had apathy without depression should turn our attention to how apathy alone could indicate brain disease.”
Launer’s team used brain volume as a measure of accelerated brain aging. Brain volume losses occur during normal aging, but in this study, larger amounts of brain volume loss could indicate brain diseases.
For the study, 4,354 people without dementia and with an average age of 76 underwent an MRI scan. They were also asked questions that measure apathy symptoms, which include lack of interest, lack of emotion, dropping activities and interests, preferring to stay at home and having a lack of energy.
The study found that people with two or more apathy symptoms had 1.4 percent smaller gray matter volume and 1.6 percent less white matter volume compared to those who had less than two symptoms of apathy. Excluding people with depression symptoms did not change the results.
Gray matter is where learning takes place and memories are stored in the brain. White matter acts as the communication cables that connect different parts of the brain.
“If these findings are confirmed, identifying people with apathy earlier may be one way to target an at-risk group,” Launer said.
Researchers Find Boosting Depression-Causing Mechanisms in the Brain Increases Resilience, Surprisingly
A new study points to a conceptually novel therapeutic strategy for treating depression. Instead of dampening neuron firing found with stress-induced depression, researchers demonstrated for the first time that further activating these neurons opens a new avenue to mimic and promote natural resilience. The findings were so surprising that the research team thinks it may lead to novel targets for naturally acting antidepressants. Results from the study are published online April 18 in the journal Science.
Researchers from the Icahn School of Medicine at Mount Sinai point out that in mice resilient to social defeat stress (a source of constant stress brought about by losing a dispute or from a hostile interaction), their cation channel currents, which pass positive ions in dopamine neurons, are paradoxically elevated to a much greater extent than those of depressed mice and control mice. This led researchers to experimentally increase the current of cation channels with drugs in susceptible mice, those prone to depression, to see whether it would enhance coping and resilience. They found that such boosting of cation channels in dopamine neurons caused the mice to tolerate the increased stress without succumbing to depression-related symptoms, and unexpectedly the hyperactivity of the dopamine neurons was normalized.
Allyson K. Friedman, PhD, Postdoctoral Fellow in Pharmacology and Systems Therapeutics at the Icahn School of Medicine at Mount Sinai, and the study’s lead author said: “To achieve resiliency when under social stress, the brain must perform a complex balancing act in which negative stress-related changes in the brain actively trigger positive changes. But that can only happen once the negative changes reach a tipping point.”
The research team used optogenetics, a combination of laser optics and gene virus transfer, to control firing activity of the dopamine neurons. When light activation or the drug lamotrigine is given to these neurons, it drives the current and neuron firing higher. But at a certain point, it triggers compensatory mechanisms, normalizes neuron firing, and achieves a kind of homeostatic (or balanced) resilience.
"To our surprise, we found that resilient mice, instead of avoiding deleterious changes in the brain, experience further deleterious changes in response to stress, and use them beneficially," said Ming-Hu Han, PhD, at Icahn School of Medicine at Mount Sinai, who leads the study team as senior author.
Drs. Friedman and Han see this counterintuitive finding as stimulating research in a conceptually novel antidepressant strategy. If a drug could enhance coping and resilience by pushing depressed (or susceptible) individuals past the tipping point, it potentially might have fewer side effects, and work as a more naturally acting antidepressant.
Eric Nestler, MD, PhD, at the Icahn School of Medicine at Mount Sinai praised the study. “In this elegant study, Drs. Friedman and Han and their colleagues reveal a highly novel mechanism that controls an individual’s susceptibility or resilience to chronic social stress. The discoveries have important implications for the development of new treatments for depression and other stress-related disorders.”
(Source: mountsinai.org)
Beating the clock for sufferers of ischemic stroke
A ground-breaking computer technology raises hope for people struck by ischemic stroke (缺乏血性中風), which is a very common kind of stroke accounting for over 80 per cent of overall stroke cases. Developed by research experts at The Hong Kong Polytechnic University (PolyU), this novel application that expertly analyses brain scans could save lives by helping doctors determine if a patient has the life-threatening condition.
The CAD stroke technology is capable of detecting signs of stroke from computed tomography (CT) scans. A CT scan uses X-rays to take pictures of the brain in slices. When blood flow to the brain is blocked, an area of the brain turns softer or decreases in density due to insufficient blood flow, pointing to an ischemic stroke.
As demonstrated by Dr Fuk-hay Tang from the Department of Health Technology and Informatics at PolyU, CT scans are fed into the CAD stroke computer, which will make sophisticated calculations and comparisons to locate areas suspected of insufficient blood flow. In 10 minutes, scans with highlighted areas of abnormality will come out for doctors’ review. Early changes including loss of insular ribbon, loss of sulcus and dense MCA signs can be identified, helping doctors determine if blood clots are present.
Ischemic stroke occurs when an artery to the brain is blocked, cutting off oxygen and essential nutrients being sent to the brain, and brain cells will die in just a few minutes. Clot-busting drugs are effective in minimising brain damage but they should be administered within 3 hours from the onset. Immediate diagnosis and treatment are therefore absolutely essential.
In that sense, a diagnostic tool that can expedite the process will be greatly helpful in saving lives. As Dr Tang shared with us, “The clock is ticking for stroke patients. Medications taken in three hours from the onset of stroke are deemed most effective. Chances of recovery decrease with every minute passing by. It usually takes half an hour for the ambulance to arrive at the hospital, at best. Then, another 45 minutes to 1 hour are needed for CT or MRI scans after the patient has been checked and dispatched for the test, which means some waiting and time will slip by. Afterwards, the brain scan will take another 10 to 15 minutes. If our tool can help doctors arrive at a diagnosis in 10 minutes, the shorter response time will make meeting the target more achievable.”
“It might come in handy for physicians with less experience in stroke,” added Dr Tang, “and patient care can be maintained in hospitals where human and other vital resources are already stretched to the limit.”
The life-saving application can also detect subtle and minute changes in the brain that would escape the eye of even an experienced specialist, slashing the chances of missed diagnosis. False-positive and false-negative cases, and other less serious conditions that mimic a stroke can also be ruled out, allowing a fully-informed decision to be made.
Furthermore, equipped with the built-in artificial intelligence feature, the CAD stroke technology would learn by experience. With every scan passing through, along with feedback from stroke specialists, the application will improve on its accuracy over time.
“It is important to identify stroke patients and help them get the urgent treatment they need,” said Dr Tang. “Prompt and accurate diagnosis is in the forefront of our minds when designing the medical application. Healthcare professionals should focus on what they do best and let us take care of the rest.”