Posts tagged science

Posts tagged science
Can Meditation Make You a More Compassionate Person?
Scientists have mostly focused on the benefits of meditation for the brain and the body, but a recent study by Northeastern University’s David DeSteno, published in Psychological Science, takes a look at what impacts meditation has on interpersonal harmony and compassion.
Several religious traditions have suggested that mediation does just that, but there has been no scientific proof—until now.
In this study, a team of researchers from Northeastern University and Harvard University examined the effects meditation would have on compassion and virtuous behavior, and the results were fascinating.
THE STUDY
This study—funded by the Mind and Life Institute—invited participants to complete eight-week trainings in two types of meditation. After the sessions, they were put to the test.
Sitting in a staged waiting room with three chairs were two actors. With one empty chair left, the participant sat down and waited to be called. Another actor using crutches and appearing to be in great physical pain, would then enter the room. As she did, the actors in the chair would ignore her by fiddling with their phones or opening a book.
The question DeSteno and Paul Condon – a graduate student in DeSteno’s lab who led the study – and their team wanted to answer was whether the subjects who took part in the meditation classes would be more likely to come to the aid of the person in pain, even in the face of everyone else ignoring her. “We know meditation improves a person’s own physical and psychological wellbeing,” said Condon. “We wanted to know whether it actually increases compassionate behavior.”
MEDITATION WORKS
Among the non-meditating participants, only about 15 percent of people acted to help. But among the participants who were in the meditation sessions “we were able to boost that up to 50 percent,” said DeSteno. This result was true for both meditation groups thereby showing the effect to be consistent across different forms of meditation. “The truly surprising aspect of this finding is that meditation made people willing to act virtuous – to help another who was suffering – even in the face of a norm not to do so,” DeSteno said, “The fact that the other actors were ignoring the pain creates as ‘bystander-effect’ that normally tends to reduce helping. People often wonder ‘Why should I help someone if no one else is?’”
These results appear to prove what the Buddhist theologians have long believed—that meditation is supposed to lead you to experience more compassion and love for all sentient beings. But even for non-Buddhists, the findings offer scientific proof for meditation techniques to alter the calculus of the moral mind.

Brain Cancer Treatment Using Genetic Material from Bone Marrow Cells
In a first-of-its-kind experiment using microvesicles generated from mesenchymal bone marrow cells (MSCs) to treat cancer, neurological researchers at Henry Ford Hospital have discovered a novel approach for treatment of tumors.
Specifically, the research team found that introducing genetic material produced by MSCs significantly reduced a particularly resistant form of malignant brain tumor in living lab rats.
“This is the first foray of its type in experimental cancer therapy, and it represents a highly novel and potentially effective treatment,” says Michael Chopp, Ph.D., scientific director of the Henry Ford Neuroscience Institute and vice chairman of the Department of Neurology at Henry Ford Hospital.
The research is published in the current issue Cancer Letters.
“I think this is an important and very novel approach for the treatment of cancers, and in this particular case the treatment of glioma,” says Dr. Chopp. “We have been at the forefront of developing microRNAs as a means to treat disease, such as cancer and neurological injury.
“This study shows it is effective in the living brain, and may even lend itself to specific cancer therapy, customized for the individual patient,” Chopp adds.
Chopp and his colleagues focused their efforts on glioma, by far the most common type of malignant brain tumor and one with a notably poor prognosis for survival.
Tumor cells were surgically implanted in the brains of anesthetized male lab rats and allowed to grow for five days.
The tumors then were injected with exosomes containing molecules of a microRNA called miR-146b – found in earlier Henry Ford research to have a strong effect on glioma cells.
Exosomes are microscopic “lipid bubbles” that once were thought to carry and get rid of “old” proteins that were no longer needed by the body. After they were more recently found to also carry RNA, whole new fields of study were suggested, including groundbreaking work by Henry Ford researchers.
In the rat study, Dr. Chopp and his colleagues used MSC bone marrow cells to produce the exosomes containing the miR-146b they injected into the cancerous tumors.
Five days after this treatment, the rats were euthanized and their brains were removed, prepared for study and examined. Tumor size was measured using computer software.
“We found that one injection of exosomes containing miR-146b five days after tumor implantation led to a significant reduction in tumor volume at 10 days after implant,” Chopp says. “Our data suggest that miR-146b elicits an anti-tumor effect in the rat brain, and that MSCs can be used as a ‘factory’ to generate exosomes genetically altered to contain miR-146b to effectively treat tumor.”
(Image: iStock)

Personalized Brain Mapping Technique Preserves Function Following Brain Tumor Surgery
Neurosurgeons can visualize important pathways in the brain using an imaging technique called diffusion tensor imaging (DTI), to better adapt brain tumor surgeries and preserve language, visual and motor function while removing cancerous tissue. In the latest issue of Neurosurgical Focus, researchers from the Perelman School of Medicine at the University of Pennsylvania review research showing that this ability to visualize relevant white matter tracts during glioma resection surgeries can improve accuracy and, in some groups, significantly extend survival (median survival of 21.2 months) compared to cases where DTI was not used (median survival of 14 months).
"We can view the brain from the inside out now, with 3D images detailing connectivity within the brain, making a virtual intraoperative map," said senior author Steven Brem, MD, professor of Neurosurgery, chief of the Division of Neurosurgical Oncology and co-director of the Penn Brain Tumor Center. "Penn is at the forefront of a major shift in the field - we now have such detail about each individual’s brain tumor - combining diffusion tensor imaging and advanced imaging with the entire personalized diagnostics analysis available for all brain tumor patients at Penn Medicine."
Diffusion tensor imaging (DTI) provides a rendering of axon pathways, by tracking water molecules in the brain as they travel in a direction parallel to axonal fibers, in a 3D model known as “the diffusion tensor.” The diffusion tensor directly represents the direction of water and indirectly represents the orientation of white matter fibers. The colorful images, captured as part of an 8 minute sequence during an MRI, show representations of clusters of axon fibers, where each color indicates a direction of travel, and offer a glimpse of the interwoven communication superhighways of the brain.
"The DTI images can be overlaid with structural and functional MRI images, providing a hybrid map showing topography layered with a road map," said Neurosurgery resident Kalil Abdullah, MD, lead author of the paper. "This rendering gives us increased clarity to visualize important white matter tracts in the brain and adapt our surgical approaches to each person’s case. Rather than focusing on solely taking the tumor out, we can avoid damage to healthy tissue and preserve important pathways responsible for speech, vision and motor function."
Relying heavily on the expertise of radiologists who process and analyze the DTI images, including Ronald L. Wolf, MD, PhD, associate professor of Radiology at Penn, the research on DTI is being translated into clinical practice to guide surgical procedures. Further research efforts are targeted at defining language deficits before surgery and following-up post-operatively to determine any changes or improvements following treatment based on the use of DTI.
Working collaboratively with colleagues in Penn’s departments of Neurosurgery, Neurology, Radiology, Radiation Oncology, Nursing, Pathology and Laboratory Medicine and the Abramson Cancer Center, the Penn Brain Tumor Center combines the latest imaging, biomarker and genetic tumor testing to provide a personalized treatment plan for all types of brain cancers. Brain tumors are among the first areas of interest for Penn’s Center for Personalized Diagnostics (CPD), a joint initiative by Penn Medicine’s Department of Pathology and Laboratory Medicine and the Abramson Cancer Center, which integrates Molecular Genetics, Pathology Informatics, and Genomic Pathology for individualized patient diagnoses and to elucidate cancer treatment options for physicians.
(Image: Swedish Research)
Risk prediction tools that estimate future risk of heart disease and stroke may be more useful predictors of future decline in cognitive abilities, or memory and thinking, than a dementia risk test, according to a new study published in the April 2, 2013, print issue of Neurology®, the medical journal of the American Academy of Neurology.
“This is the first study that compares these risk scores with a dementia risk score to study decline in cognitive abilities 10 years later,” said Sara Kaffashian, PhD, with the French National Institute of Health and Medical Research (INSERM) in Paris, France.
The study involved 7,830 men and women with an average age of 55. Risk of heart disease and stroke (cardiovascular disease) and risk of dementia were calculated for each participant at the beginning of the study. The heart disease risk score included the following risk factors: age, blood pressure, treatment for high blood pressure, high density lipoprotein (HDL) cholesterol, total cholesterol, smoking, and diabetes. The stroke risk score included age, blood pressure, treatment for high blood pressure, diabetes, smoking, history of heart disease, and presence of cardiac arrhythmia (irregular heart beat).
The dementia risk score included age, education, blood pressure, body mass index (BMI), total cholesterol, exercise, and whether a person had the APOE ?4 gene, a gene associated with dementia.
Memory and thinking abilities were measured three times over 10 years.
The study found that all three risk scores predicted 10-year decline in multiple cognitive tests. However, heart disease risk scores showed stronger links with cognitive decline than a dementia risk score. Both heart and stroke risk were associated with decline in all cognitive tests except memory; dementia risk was not linked with decline in memory and verbal fluency.
“Although the dementia and cardiovascular risk scores all predict cognitive decline starting in late middle age, cardiovascular risk scores may have an advantage over the dementia risk score for use in prevention and for targeting changeable risk factors since they are already used by many physicians. The findings also emphasize the importance of risk factors for cardiovascular disease such as high cholesterol and high blood pressure in not only increasing risk of heart disease and stroke but also having a negative impact on cognitive abilities,” said Kaffashian.
Study examines change in cognitive function following physical, mental activity in older adults
A randomized controlled trial finds that 12 weeks of physical plus mental activity in inactive older adults with cognitive complaints was associated with significant improvement in cognitive function but there was no difference between intervention and control groups, according to a report published Online First by JAMA Internal Medicine, a JAMA Network publication.
An epidemic of dementia worldwide is anticipated during the next 40 years because of longer life expectancies and demographic changes. Behavioral interventions are a potential strategy to prevent or delay dementia in asymptomatic individuals, but few randomized controlled trials have studied the effects of physical and mental activity together, according to the study background.
"We found that cognitive scores improved significantly over the course of 12 weeks, but there were no significant differences between the intervention and active control groups. These results may suggest that in this study population, the amount of activity is more important than the type of activity, because all groups participated in both mental activity and exercise for [60 minutes/per day, three days/per week] for 12 weeks. Alternatively, the cognitive improvements observed may be due to practice effects," the authors note.
The study by Deborah E. Barnes, Ph.D., M.P.H., of the University of California, San Francisco, and colleagues included 126 inactive, community-dwelling older adults with cognitive complaints. All the individuals engaged in home-based mental activity (1 hour/per day, 3 days/per week) plus class-based physical activity (1 hour/per day, 3 days/per week) for 12 weeks and were assigned to either mental activity intervention (MA-I, intensive computer work); or mental activity control (MA-C, educational DVDs) plus exercise intervention (EX-1, aerobic) or exercise control (EX-C, stretching and toning). The study design meant there were four groups: MA-I/EX-I, MA-I/EX-C, MA-C/EX-1 and MA-C/EX-C.
Global cognitive scores improved significantly over time but did not differ between groups in the comparison between MA-I and MA-C (ignoring exercise), the comparison between EX-I and EX-C (ignoring mental activity), or across all four randomization groups, according to the study results.
"The prevalence of cognitive impairment and dementia are projected to rise dramatically during the next 40 years, and strategies for maintaining cognitive function with age are critically needed. Physical or mental activity alone result in small, domain-specific improvements in cognitive function in older adults; combined interventions may have more global effects," the study concludes.
(Image: Getty Images)
A team of researchers at The New York Stem Cell Foundation Research Institute led by Scott Noggle, PhD, Director of the NYSCF Laboratory and the NYSCF – Charles Evans Senior Research Fellow for Alzheimer’s Disease, and Michael W. Nestor, PhD, a NYSCF Postdoctoral Research Fellow, has developed a technique to produce three-dimensional cultures of induced pluripotent stem (iPS) cells called embryoid bodies, amenable to live cell imaging and to electrical activity measurement. As reported in their Stem Cell Research study, these cell aggregates enable scientists to both model and to study diseases such as Alzheimer’s and Parkinson’s disease.
The NYSCF Alzheimer’s disease research team aims to better understand and to find treatments to this disease through stem cell research. For such disorders in which neurons misfire or degenerate, the NYSCF team creates “disease in a dish” models by reprogramming patients’ skin and or blood samples into induced pluripotent stem (iPS) cells that can become neurons and the other brain cells affected in the diseases.
The cells in our body form three-dimensional networks, essential to tissue function and overall health; however, previous techniques to form complex brain tissue resulted in structures that, while similar in form to naturally occurring neurons, undermined imaging or electrical recording attempts.
In the current study, the Noggle and Nestor with NYSCF scientists specially adapted two-dimensional culture methods to grow three-dimensional neuron structures from iPS cells. The resultant neurons were “thinned-out,” enabling calcium-imaging studies, which measure the electrical activity of cells like neurons.
"Combining the advantages of iPS cells grown in a 3D environment with those of a 2D system, our technique produces cells that can be used to observe electrical activity of putative networks of biologically active neurons, while simultaneously imaging them," said Nestor. "This is key to modeling and studying neurodegenerative diseases."
Neural networks, thought to underlie learning and memory, become disrupted in Alzheimer’s disease. By generating aggregates from iPS cells and comparing these to an actual patient’s brain tissue, scientists may uncover how disease interferes with these cell-to-cell interactions and understand how to intervene to slow or stop Alzheimer’s disease.
"This critical new tool developed by our Alzheimer’s team will accelerate Alzheimer’s research, enabling more accurate manipulation of cells to find a cure to this disease," said Susan L. Solomon, CEO of NYSCF.
(Source: eurekalert.org)
Clumps of proteins that accumulate in brain cells are a hallmark of neurological diseases such as dementia, Parkinson’s disease and Alzheimer’s disease. Over the past several years, there has been much controversy over the structure of one of those proteins, known as alpha synuclein.

MIT computational scientists have now modeled the structure of that protein, most commonly associated with Parkinson’s, and found that it can take on either of two proposed states — floppy or rigid. The findings suggest that forcing the protein to switch to the rigid structure, which does not aggregate, could offer a new way to treat Parkinson’s, says Collin Stultz, an associate professor of electrical engineering and computer science at MIT.
“If alpha synuclein can really adopt this ordered structure that does not aggregate, you could imagine a drug-design strategy that stabilizes these ordered structures to prevent them from aggregating,” says Stultz, who is the senior author of a paper describing the findings in a recent issue of the Journal of the American Chemical Society.
For decades, scientists have believed that alpha synuclein, which forms clumps known as Lewy bodies in brain cells and other neurons, is inherently disordered and floppy. However, in 2011 Harvard University neurologist Dennis Selkoe and colleagues reported that after carefully extracting alpha synuclein from cells, they found it to have a very well-defined, folded structure.
That surprising finding set off a scientific controversy. Some tried and failed to replicate the finding, but scientists at Brandeis University, led by Thomas Pochapsky and Gregory Petsko, also found folded (or ordered) structures in the alpha synuclein protein.
Stultz and his group decided to jump into the fray, working with Pochapsky’s lab, and developed a computer-modeling approach to predict what kind of structures the protein might take. Working with the structural data obtained by the Brandeis researchers, Stultz created a model that calculates the probabilities of many different possible structures, to determine what set of structures would best explain the experimental data.
The calculations suggest that the protein can rapidly switch among many different conformations. At any given time, about 70 percent of individual proteins will be in one of the many possible disordered states, which exist as single molecules of the alpha synuclein protein. When three or four of the proteins join together, they can assume a mix of possible rigid structures, including helices and beta strands (protein chains that can link together to form sheets).
“On the one hand, the people who say it’s disordered are right, because a majority of the protein is disordered,” Stultz says. “And the people who would say that it’s ordered are not wrong; it’s just a very small fraction of the protein that is ordered.”
“This paper seems to bridge the gap” between the two camps, says Trevor Creamer, an associate professor of molecular and cellular biochemistry at the University of Kentucky who was not involved in this research. Also important is the model’s prediction of new structures for the protein that experimental biologists can now look for, Creamer adds.
The MIT researchers also found that when alpha synuclein adopts an ordered structure, similar to that described by Selkoe and co-workers, the portions of the protein that tend to aggregate with other molecules are buried deep within the structure, explaining why those ordered forms do not clump together.
Stultz is now working to figure out what controls the protein’s configuration. There is some evidence that other molecules in the cell can modify alpha synuclein, forcing it to assume one conformation or another.
“If this structure really does exist, we have a new way now of potentially designing drugs that will prevent aggregation of alpha synuclein,” he says.
(Source: web.mit.edu)

Shedding Light on Early Parkinson’s Disease Pathology
In a mouse model of early Parkinson’s disease (PD), animals displayed movement deficits, loss of tyrosine-hydroxylase (TH)-positive fibers in the striatum, and astro-gliosis and micro-gliosis in the substantia nigra (SN), without the loss of nigral dopaminergic neurons. These findings, which may cast light on the molecular processes involved in the initial stages of PD, are available in the current issue of Restorative Neurology and Neuroscience.
“The most intriguing finding of our study was the lack of a significant decrease of TH levels in the SN of the low-dose MPTP-treated mice, suggesting that this treatment does not induce a direct loss of nigral dopaminergic neurons,” says Joost Verhaagen PhD, lead investigator of the study. “These findings appear to support the ‘dying back’ hypothesis of PD, which proposes that the TH-positive terminal loss in the striatum is the first neurodegenerative event in PD, which later induces neuronal degeneration in the SN.” Dr. Verhaagen is Head of the Workgroup on Neuroregeneration at the Netherlands Institute for Neuroscience and Professor at the Free University in Amsterdam.
The neurotoxin MPTP (1-methyl-4-phenyl 1,2,3,6-tetrahydropyridine) was used to induce the degenerative changes. Chronic 5 week administration of 25 mg/kg MPTP combined with probenecid (250 mg/kg), which inhibits MPTP clearance and promotes its crossing of the blood-brain barrier, is known to cause dopaminergic neuron degeneration in the SN and decrease striatal dopaminergic nerve terminals. In the current study, 7 mice were treated with 25 mg/kg MPTP plus probenecid, 6 mice received a lower dose of MPTP (15 mg/kg) plus probenecid, and 8 control mice received saline plus probenecid. A grid test, known to be sensitive to striatal dopaminergic input, was used to detect motor deficits.
Immunohistochemical analysis using TH fluorescence revealed that only the higher dose of MPTP produced significant dopaminergic neuronal cell loss in the SN (65% fluorescence loss, p<0.001). The 15 mg/kg dose produced an 18% decline in fluorescence which was not significantly different than control.
Both dose levels significantly reduced TH immunoreactivity of the striatum. The authors believe that the motor deficits seen at both MPTP dose levels relate to the striatal dopamine depletion.
The study is also the first to report that low-dose MPTP produces astrogliosis and microgliosis in the SN and formation of α-synuclein positive inclusions. “The data suggests that gliosis in the substantia nigra plays a prominent initiating role in the introduction of dopaminergic deficits after MPTP treatment, and may be sufficient to significantly reduce TH levels in the striatum,” says Dr. Korecka, first author and principal investigator of the study and a post-doctoral fellow at the Netherlands Institute for Neuroscience in Amsterdam.
“We are the first to report that this early PD model provides an interesting window of opportunity to study the mechanisms that underlie the early neurodegenerative events that initiate the cellular death of dopaminergic neurons,” write the authors. They suggest that the model can be used to develop potential treatment strategies to counteract early PD cellular changes.
(Image: iStock)
Our internal clocks can become ticking time bombs for diabetes and obesity
New research in The FASEB Journal using mice suggests that disrupting our internal clocks can lead to a complete absence of 24-hour bodily rhythms and an immediate gain in body weight
If you’re pulling and all-nighter to finish a term paper, a new parent up all night with a fussy baby, or simply can’t sleep like you once could, then you may be snoozing on good health. That’s because new research published in The FASEB Journal used mice to show that proper sleep patterns are critical for healthy metabolic function, and even mild impairment in our circadian rhythms can lead to serious health consequences, including diabetes and obesity.
"We should acknowledge the unforeseen importance of our 24-hour rhythms for health," said Claudia Coomans, Ph.D., a researcher involved in the work from the Department of Molecular Cell Biology in the Laboratory of Neurophysiology at Leiden University Medical Center in Leiden, Netherlands. "To quote Seneca ‘We should live according to nature (secundum naturam vivere).’"
To make this discovery, Coomans and colleagues exposed mice to constant light, which disturbed their normal internal clock function, and observed a gradual degradation of their bodies’ internal clocks until it reached a level that normally occurs when aging. Eventually the mice lost their 24-hour rhythm in energy metabolism and insulin sensitivity, indicating that relatively mild impairment of clock function had severe metabolic consequences.
"The good news is that some of us can ‘sleep it off’ to avoid obesity and diabetes," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. "The bad news is that we can all get the metabolic doldrums when our normal day/night cycle is disrupted."

Engineer helping unravel mystery of traumatic brain injury
The American Academy of Neurology issued new guidelines last week for assessing school-aged athletes with head injuries on the field. The message: if in doubt, sit out.
With more than 3 million sports-related concussions occurring in the U.S. each year, from school children to professional athletes, the issue is a burgeoning health crisis.
While concussions may not be difficult to diagnose initially, the longer one waits, the more difficult treatment can be.
The efforts of a researcher and his colleagues at Washington University in St. Louis’ School of Engineering & Applied Science are helping to unravel the many mysteries of traumatic brain injury.
“There’s and urgent need to understand the problem of traumatic brain injuries, for the sake of athletes, military personnel and accident victims,” says Philip Bayly, PhD, the Lilyan and E. Lisle Hughes Professor of Mechanical Engineering.
“Anyone who has met someone who’s had a head injury knows how scary it is, and how frustrating it is that we know so little about the causal pathways, and thus the best therapeutic opportunities,” he says.
Bayly, chair of the Department of Mechanical Engineering & Materials Science, researches the mechanics of brain injury. He recently received a $2.25 million grant from the National Institutes of Health to better understand traumatic brain injuries.
Head injuries, concussions and the resulting trauma have been in public discussion recently as the National Football League (NFL) deals with a lawsuit regarding head injuries by about one-third of living former NFL players. The league is accused of not providing information connecting football-related head injuries to brain damage, memory loss and other long-term health issues.
Bayly’s team is working on ways to measure 3-D relative motion between in the brain and skull and estimate strain during mild head acceleration. Bayly hopes computer simulation can teach researchers about the basic physics of brain injury and ways to develop new approaches to prevention and therapy.
“Our studies provide experimental data on how the brain actually responds mechanically in response to mild external loads,” Bayly says. “This is especially critical to developing useful computer simulations, to make sure they reflect reality.
These simulations will in turn be used to design new equipment, evaluate rule changes in sports and determine exposure thresholds or diagnostic tests.”
Computer simulation is important in creating animal models that can be used to develop diagnostic and therapeutic approaches, he says.
“Understanding mechanical deformation in traumatic brain injury is also essential to anyone studying brain trauma by exposing cultured brain cells to mechanical stress,” Bayly says. “We need to understand how much stress to apply and in what directions.”
How can athletes minimize their risks?
“From a mechanical standpoint, they should avoid repeated high head accelerations,” Bayly says. “Head-to-head collisions and collisions with head-to-ground are clearly to be avoided.”
Bayly says to truly protect athletes, new rules need to be instated.
“I would actually advocate for eliminating sports like boxing, in which injury-level accelerations are known to occur routinely. More research is needed on sports where the threshold is less clear.”
There is where Bayly and his colleagues come in.
“We need to do the research to find out what kinds of repeated accelerations are responsible for producing the degeneration seen in chronic traumatic encephalopathy,” he says.
(Image: Jupiterimages / Getty Images)