Posts tagged science
Articles and news from the latest research reports.
Acute Stress Alters Control of Gene Activity: Researchers Examine DNA Methylation
ScienceDaily (Aug. 15, 2012) — Acute stress alters the methylation of the DNA and thus the activity of certain genes. This is reported by researchers at the Ruhr-Universität Bochum together with colleagues from Basel, Trier and London for the first time in the journal Translational Psychiatry. “The results provide evidence how stress could be related to a higher risk of mental or physical illness,” says Prof. Dr. Gunther Meinlschmidt from the Clinic of Psychosomatic Medicine and Psychotherapy at the LWL University Hospital of the RUB. The team looked at gene segments which are relevant to biological stress regulation.
In stressful social situations, the methylation patterns (bright spheres) of the DNA change. (Credit: Illustration: Christoph Unternährer and Christian Horisberger)
Epigenetics — the “second code” — regulates gene activity
Our genetic material, the DNA, provides the construction manual for the proteins that our bodies need. Which proteins a cell produces depends on the cell type and the environment. So-termed epigenetic information determines which genes are read, acting quasi as a biological switch. An example of such a switch is provided by methyl (CH3) groups that attach to specific sections of the DNA and can remain there for a long time — even when the cell divides. Previous studies have shown that stressful experiences and psychological trauma in early life are associated with long-term altered DNA methylation. Whether the DNA methylation also changes after acute psychosocial stress, was, however, previously unknown.
Two genes tested
To clarify this issue, the research group examined two genes in particular: the gene for the oxytocin receptor, i.e. the docking site for the neurotransmitter oxytocin, which has become known as the “trust hormone” or “anti-stress hormone”; and the gene for the nerve growth factor Brain-Derived Neurotrophic Factor (BDNF), which is mainly responsible for the development and cross-linking of brain cells. The researchers tested 76 people who had to participate in a fictitious job interview and solve arithmetic problems under observation — a proven means for inducing acute stress in an experiment. For the analysis of the DNA methylation, they took blood samples from the subjects before the test as well as ten and ninety minutes afterwards.
DNA methylation changes under acute psychosocial stress
Stress had no effect on the methylation of the BDNF gene. In a section of the oxytocin receptor gene, however, methylation already increased within the first ten minutes of the stressful situation. This suggests that the cells formed less oxytocin receptors. Ninety minutes after the stress test, the methylation dropped below the original level before the test. This suggests that the receptor production was excessively stimulated.
Possible link between stress and disease
Stress increases the risk of physical or mental illness. The stress-related costs in Germany alone amount to many billions of Euros every year. In recent years, there have been indications that epigenetic processes are involved in the development of various chronic diseases such as cancer or depression. “Epigenetic changes may well be an important link between stress and chronic diseases” says Prof. Meinlschmidt, Head of the Research Department of Psychobiology, Psychosomatics and Psychotherapy at the LWL University Hospital. “We hope to identify more complex epigenetic stress patterns in future and thus to be able to determine the associated risk of disease. This could provide information on new approaches to treatment and prevention.” The work originated within the framework of an interdisciplinary research consortium with the University of Trier, the University of Basel and King’s College London. The German Research Foundation and the Swiss National Science Foundation supported the study.
Source: Science Daily
In a major breakthrough, an international team of scientists has proven that addiction to morphine and heroin can be blocked, while at the same time increasing pain relief.
The team from the University of Adelaide and University of Colorado has discovered the key mechanism in the body’s immune system that amplifies addiction to opioid drugs. Laboratory studies have shown that the drug (+)-naloxone will selectively block the immune-addiction response. The results - which could eventually lead to new co-formulated drugs that assist patients with severe pain, as well as helping heroin users to kick the habit - will be published in the Journal of Neuroscience.
"Our studies have shown conclusively that we can block addiction via the immune system of the brain, without targeting the brain’s wiring," says the lead author of the study, Dr Mark Hutchinson, ARC Research Fellow in the University of Adelaide’s School of Medical Sciences.
"Both the central nervous system and the immune system play important roles in creating addiction, but our studies have shown we only need to block the immune response in the brain to prevent cravings for opioid drugs."
Watch a video of Dr Mark Hutchinson talking about this study.
Yale researchers studying epileptic seizures have shed new light on the neurological origins of consciousness.
When epileptics lose consciousness during a variety of types of seizures, the signals converge on the same brain structures, but through different pathways, says Dr. Hal Blumenfeld, professor of neurology, neurobiology, and neurosurgery.
“Understanding of these mechanisms could lead to improved treatment strategies to prevent impairment of consciousness and improve the quality of life of people with epilepsy,” he said.
Blumenfeld’s research is described in the current issue of the journal Lancet Neurology.
(Image: The fMRI images are different viewpoints of the brain of a child experiencing an epileptic seizure. Areas in yellow and orange represent increased brain activity compared to its normal state, while areas in blue show decreased activity. These are the areas of the brain needed for normal consciousness.)
The stalked eyes of mantis shrimp species that live in shallow water can have up to 16 kinds of photoreceptor cells, 12 of which are specialized for different colors. People make do with four kinds, three of which pick up colors.
Hanne Thoen of the University of Queensland in Brisbane, Australia, tested the color vision of mantis shrimp by training them to scoot out of their burrows toward a pair of optical fibers and punch at the one glowing a particular color. As she narrowed the color gap between the two fibers, she could tell when the animals no longer discerned a difference.
So far, Thoen has tested her mantis shrimp on six target colors ranging from a 425-nanometer purple to a 628-nanometer red. If the animals perform just as poorly at distinguishing colors in other wavelengths, then mantis shrimp may be using some unknown system of color perception.
People and other animals studied so far distinguish colors through brainpower by interpreting competing activity in different kinds of light-receptor cells. Instead of doing such fancy brainwork, mantis shrimp may just rely on what a particular specialized cell responds to strongly. Wavelengths that tickle the purple-sensitive cells may be just plain purple regardless of whether they’re more toward the blue or the ultraviolet.
So many scientific studies are making incorrect claims that a new service has sprung up to fact-check reported findings by repeating the experiments.
A year-old Palo Alto, California, company, Science Exchange, announced on Tuesday its “Reproducibility Initiative,” aimed at improving the trustworthiness of published papers. Scientists who want to validate their findings will be able to apply to the initiative, which will choose a lab to redo the study and determine whether the results match.
The project sprang from the growing realization that the scientific literature - from social psychology to basic cancer biology - is riddled with false findings and erroneous conclusions, raising questions about whether such studies can be trusted. Not only are erroneous studies a waste of money, often taxpayers’, but they also can cause companies to misspend time and resources as they try to invent drugs based on false discoveries.
Last year, Bayer Healthcare reported that its scientists could not reproduce some 75 percent of published findings in cardiovascular disease, cancer and women’s health. In March, Lee Ellis of M.D. Anderson Cancer Center and C. Glenn Begley, the former head of global cancer research at Amgen, reported that when the company’s scientists tried to replicate 53 prominent studies in basic cancer biology, hoping to build on them for drug discovery, they were able to confirm the results of only six.
The new initiative, said Begley, senior vice president of privately held biotechnology company TetraLogic, “recognizes that the problem of non-reproducibility exists and is taking the right steps to address it.”
The initiative’s 10-member board of prominent scientists will match investigators with a lab qualified to test their results, said Elizabeth Iorns, Science Exchange’s co-founder and chief executive officer. The original lab would pay the second for its work. How much depends on the experiment’s complexity and the cost of study materials, but should not exceed 20 percent of the original research study’s costs. Iorns hopes government and private funding agencies will eventually fund replication to improve the integrity of scientific literature.
Unlocking a major secret of the brain
McGill researchers uncover crucial link between hippocampus and prefrontal cortex
A clue to understanding certain cognitive and mental disorders may involve two parts of the brain which were previously thought to have independent functions, according to a McGill University team of researchers led by Prof. Yogita Chudasama, of the Laboratory of Brain and Behavior, Department of Psychology. The McGill team discovered a critical interaction between two prominent brain areas: the hippocampus, a well-known memory structure made famous by Dr. Brenda Milner’s patient H.M., and the prefrontal cortex, which is involved in decision-making and inhibiting inappropriate behaviours.
“We had always thought that the hippocampus and the prefrontal cortex functioned independently,” says Prof. Chudasama. “Our latest study provides the first indication that that is not the case.”
The team’s finding, just published in the Journal of Neuroscience, reveals a critical interaction between these two brain areas and the control of behavior, and may advance the treatment of some cognitive and mental disorders including schizophrenia, and depression. The interaction between the hippocampus and the prefrontal cortex shows that brain circuits function not just as specific parts of the brain, but are linked together and work as a system.
“Although the prefrontal cortex has long been known to be the driving force that steers our behavior, pushing us to make good decisions and withhold improper actions, it turns out that it can’t do this unless it interacts with the hippocampus,” added Prof. Chudasama. “We found that when we prevented these two structures from communicating with each other, like humans with compulsive disorders, rats persisted with behaviours that were not good for them; they didn’t correct their errant behaviours and could not control their natural urges.
The ability to control impulsive urges or inhibit our actions allows us to interact normally in personal or social situations, and this type of behaviour depends on the normal interaction of the hippocampus and the prefrontal cortex. This result provides a means for understanding the neural basis for social and cognitive deficits in disorders of brain and behaviour, such as those with frontotemporal dementia”, concludes Prof. Chudasama.
To find out how mice use their high-resolution ganglion, a team from Harvard attached a tiny camera to a rat volunteer and then watched to see what sorts of things it focused on. Next, they played the video back directly onto the retinas of several test mice while simultaneously monitoring neural cell activity. In so doing, they found that the high-resolution cells sat mostly quiet, doing nothing.
When silhouettes of birds were projected overhead, the waiting ended as the ganglia sprang into action, interpreting every movement. This shows, the researchers say, that the high-resolution neuron groups in mice retinas serve not as interpreters of everyday life, but as highly specific predator detectors. More specifically they found the nerves reacted when the birds were in their center of view, meaning close and ready to snatch them up. Sadly, they also found that the nerves quit firing once the birds came close enough, indicating the mice were doomed.
Genetics of Obsessive-Compulsive Disorder Narrowed Down
The first genome-wide searches for the genes responsible for Tourette syndrome and obsessive-compulsive disorder have uncovered a few clues to the underpinnings of both disorders.
Tourette syndrome is a neurological disorder characterized by muscle and vocal tics such as eye blinking, throat clearing and uttering taboo words or phrases. Tourette’s often co-occurs with obsessive-compulsive disorder (OCD), a mental illness marked by repetitive behaviors and anxiety-producing intrusive thoughts.
Neither Tourette syndrome nor OCD are simple enough to be traced to a single gene, but two new studies detailed today (Aug. 14) in the journal Molecular Psychiatry find several locations on the human chromosome that may contribute to the conditions.
A DNA molecule.
CREDIT: Giovanni Cancemi | Shutterstock
"Both disorders clearly have a complex underlying genetic architecture, and these two studies lay the foundation for understanding the underlying genetic etiology of Tourette syndrome and OCD," said Jeremiah Scharf, a neurologist at Massachusetts General Hospital in Boston, who worked on both projects.
Genetics of Tourette Syndrome
In the Tourette syndrome study, Scharf and his colleagues compared the genomes of more than 1,200 people with the disorder with the genomes of nearly 5,000 healthy individuals. They conducted what’s called a genome-wide association study, scanning hundreds of thousands of genetic variants from across the genomes to see if any were more common in the people with the disorder.
They found that no single genetic signal was significantly different between the two genomes, meaning that the researchers could not rule out random chance as the reason for any given difference. But among the top genetic variations, the researchers found an unusually high number that influence levels of gene expression in the frontal lobe of the brain — a region important in both Tourette syndrome and OCD, Scharf said.
One intriguing gene that varied the most between Tourette- and non-Tourette genomes was called COL27A1, a gene that encodes a collagen protein found in cartilage. The same gene is also active in the cerebellum, a brain region important for motor control during development. More research will be necessary to find what link, if any, COL27A1 has to Tourette syndrome, Scharf said.
The architecture of OCD
In a separate study, the scientists carried out the same analysis on healthy genomes as well as about 1,500 people with obsessive-compulsive disorder. Again, no one gene rose to the top as a definitive OCD gene, but the results revealed a good candidate near a gene called BTBD3, which is involved in multiple cellular functions. BTBD3 is very active in the brain during childhood and adolescent development, when OCD often first appears. It’s also related to a gene called BTBD9, which has been linked to Tourette syndrome in the past.
This first genome-wide pass is bound to turn up some false positives, Scharf said, so researchers will now need to home in on the intriguing genes in larger samples of people. They are also merging the two studies to look for genetic linkages that might explain why Tourette syndrome and OCD so frequently co-occur.
"The important thing this study does is that it really brings Tourette syndrome and OCD into the company of a number of other psychiatric diseases, which people have studied using genome-wide association," Scharf said, citing autism, schizophrenia and bipolar disorder as examples. “Now that we have these data for Tourette syndrome and OCD, we can work with investigators who are studying those other diseases to try to see what we can learn about what variants are shared between different neurodevelopment disorders.”
Source: Live Science
A young autistic boy has found his outlet in making science videos. Jordan Hilkowitz was diagnosed with autism when he was just 18 months old, he didn’t begin to speak until he was 5. His mother Stacey remembers the heartbreak she experienced as she watched her young son bang his head against the wall out of frustration at not being able to communicate.
It was his babysitter’s idea for Jordan to start making science videos. He’d always had an interest in science, and she felt that this could be an outlet for him to communicate to a larger audience. Larger indeed! Jordan’s channel, Doctor Mad Science, has received over 2.4 million views to date – and he’s become a local celebrity for his scientific knowhow.
(Source: blogs.scientificamerican.com)
Palaeontologists from the University of Zurich have “rediscovered” a skull bone that was thought to have been lost during the course of evolution for many mammals.
Mammals’ skulls are composed of around 20 bones — fewer than those of fish, reptiles and birds. This is because when mammals evolved from reptile-like vertebrates 320 million years ago, the skull structure simplified. Some bones were lost in the process, particularly some of the skull roof bones. The interparietal is one such bone, but it has perplexed researchers since it had survived in some mammals, such as horses and cats (and 2.8 percent of humans) but not in others.
The interparietal is clearly discernible in the embryo, but fuses with other bones beyond recognition shortly afterwards. As a result it’s often been missed. However, new imaging techniques have been able to detect its presence in all mammals.