New defense mechanism against viruses discovered

 

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When it comes to defense against viruses, the immune system has an arsenal of weapons at its disposal including killer cells, antibodies and messenger molecules, to name just a few. When a pathogen attacks the body, the immune system usually activates the appropriate mechanisms. However, some of the mechanisms do not have to be triggered; they are continuously active as a standing army. Researchers from ETH Zurich, in collaboration with scientists from the University of Bern, have now discovered a new form of this so-called innate immune defense. They have shown that it acts against particular viruses with a genome in the form of single-stranded, positive-sense RNA. Many known pathogens, such as hepatitis C, tick-borne encephalitis, polio, SARS, yellow fever and dengue fever viruses belong to this group, as well as potyviruses, a group of plant viruses that can cause severe damage to economically important crops.

Researchers led by Ari Helenius, Professor of Biochemistry at ETH Zurich, discovered the mechanism during their research with human cells in cell culture and a model virus that is frequently used in basic research, the Semliki Forest virus. In an extensive screening process, the scientists turned off individual genes inside host cells; they discovered that the cells were more susceptible to infection by the virus if the genes of a cellular quality control and regulatory system for RNA, known as NMD (nonsense-mediated mRNA decay), were turned off.

Viruses identified as incorrect cellular RNA

In a parallel large-scale screening effort, Olivier Voinnet, Professor of RNA Biology at ETH Zurich, and his colleagues realised that this mechanism is also acting against viruses in plants. They used the model plant Arabidopsis thaliana and potato virus X for their investigation. Helenius and Voinnet's groups have published their two research papers on human cells and plants in the latest edition of the journal Cell Host & Microbe -- the former in collaboration with the group of Oliver Mühlemann, a professor at the University of Bern, who has dealt intensively with the NMD system in recent years.

The NMD system has been known for some time in biology as a quality control and regulatory mechanism that eliminates incorrectly fabricated and non-functional messenger RNA molecules in cells. However, the new studies show that this system also serves a second function: It ensures that the genome of certain RNA viruses is broken down, thereby preventing them from replicating in host cells. "The RNA genome of these viruses bears certain similarities to incorrect messenger RNA molecules in human, animal and plant cells and is identified as such by the NMD system," explains Giuseppe Balistreri, post-doctoral fellow and lead author of one of the two studies.

Oldest defense mechanism

The researchers believe that the NMD system provides a first line of defense against infection by this class of viruses. "The mechanism attacks the viral genome directly before it can multiply in the host cell," say both Helenius and Voinnet. The ETH scientists also believe that this is one of the oldest defense mechanisms against viruses in evolutionary history, as the NMD system is so fundamental that it is found in all higher organisms; i.e. people, animals, plants and fungi.

However, the mechanism is not 100 per cent efficient. "If it were, then RNA viruses wouldn't exist at all," says Helenius. Instead, the viruses have evolved ways to avoid or actively suppress the NMD system, as both ETH research groups suggest in their respective studies. "Viruses and their hosts are engaged in an endless battle, of which the NMD system is a previously unsuspected yet significant component," says Voinnet. "In this battle, the NMD mechanism likely contributed to shape the genomes of RNA viruses as we see them today."

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Story Source:

The above story is based on materials provided by ETH Zurich. Note: Materials may be edited for content and length.

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Journal References:

1. Damien Garcia, Shahinez Garcia, Olivier Voinnet. Nonsense-Mediated Decay Serves as a General Viral Restriction Mechanism in Plants. Cell Host & Microbe, 2014; DOI: 10.1016/j.chom.2014.08.001
2. Giuseppe Balistreri, Peter Horvath, Christoph Schweingruber, David Zünd, Gerald McInerney, Andres Merits, Oliver Mühlemann, Claus Azzalin, Ari Helenius. The Host Nonsense-Mediated mRNA Decay Pathway Restricts Mammalian RNA Virus Replication. Cell Host & Microbe, 2014; 16 (3): 403 DOI: 10.1016/j.chom.2014.08.007

The quantum revolution is a step closer: New way to run a quantum algorithm

 

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Dr Austin Lund (left) and Dr Anthony Laing, co-authors of the research.

Theories show how computing devices that operate according to quantum mechanics can solve problems that conventional (classical) computers, including super computers, can never solve. These theories have been experimentally tested for small-scale quantum systems, but the world is waiting for the first definitive demonstration of a quantum device that beats a classical computer.

Now, researchers from the Centre for Quantum Photonics (CQP) at the University of Bristol together with collaborators from the University of Queensland (UQ) and Imperial College London have increased the likelihood of such a demonstration in the near term by discovering a new way to run a quantum algorithm with much simpler methods than previously thought.

The first definitive defeat for a classical computer could be achieved with a quantum device that runs an algorithm known as Boson Sampling, recently developed by researchers at MIT.

Boson Sampling uses single photons of light and optical circuits to take samples from an exponentially large probability distribution, which has been proven to be extremely difficult for classical computers.

Unlike other quantum algorithms, Boson Sampling has the benefit of being practical for near-term implementations, with the only experimental drawback being the difficulty of generating the dozens of single photons required for the important quantum victory.

However, the Bristol-UQ-Imperial researchers have found that the Boson Sampling algorithm can still be proven to be hard for classical computers when using standard probabilistic methods to generate single photons.

Dr Anthony Laing who led the CQP elements of the research said: "We realised we could chain together many standard two-photon sources in such a way as to give a dramatic boost to the number of photons generated."

Dr Austin Lund from UQ and currently on sabbatical in CQP added: "Once we had the idea for the boosted source, we needed to prove that it could solve a version of the Boson Sampling algorithm. We hope that the last major experimental hurdle has now been overcome."

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Story Source:

The above story is based on materials provided by University of Bristol. Note: Materials may be edited for content and length.

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Journal Reference:

1. A. P. Lund, A. Laing, S. Rahimi-Keshari, T. Rudolph, J. L. O’Brien, T. C. Ralph. Boson Sampling from a Gaussian State. Physical Review Letters, 2014; 113 (10) DOI: 10.1103/PhysRevLett.113.100502

New genetic targets discovered in fight against muscle-wasting disease

 

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Dr. Sue Shackleton (standing) and post-doctoral researcher Dr. Farhana Haque (seated) are studying fluorescence microscope images of muscle cells obtained from a patient with Emery-Dreifuss muscular.

Scientists have pinpointed for the first time the genetic cause in some people of an incurable muscle-wasting disease, Emery-Dreifuss muscular dystrophy (EDMD).

The international research team led by the University of Leicester say the finding of two target genes opens the possibility of developing drugs to tackle the disease in these patients. Their work has been published today in the journal PLOS Genetics.

The research was funded by The Wellcome Trust and was only possible by the University of Leicester team collaborating with groups in Germany (University of Greifswald), Italy (Institute of Molecular Genetics, Bologna, Italy) and the USA (Columbia University).

To date, only six genes have been linked to EDMD. Despite rigorous screening, at least 50% of patients with EDMD have no detectable mutation in the 6 known genes.

Now the breakthrough study has discovered two more genes linked to the disease.

Lead researcher at Leicester, Dr Sue Shackleton, senior lecturer in Biochemistry, said:

"We are really excited to have identified mutations in two new genes -- SUN1 and SUN2 -- that are responsible for causing some cases of the muscle wasting disease Emery-Dreifuss muscular dystrophy.

"Emery-Dreifuss muscular dystrophy (EDMD) is an inherited condition that affects around 1,000 people in the UK. It involves muscle wasting and stiffening of the joints. These symptoms usually begin in early childhood and worsen over time, so that many patients have significantly reduced mobility later in life.

"By adulthood, most individuals also develop heart problems that result in an abnormal heartbeat and a high risk of sudden cardiac arrest -- the main treatment for this is insertion of a pacemaker. At the moment there is no cure for this disease and no effective treatment for the muscle wasting and joint stiffening."

Dr Shackleton said that in some individuals, EDMD is caused by mutations in one of several genes that are responsible for producing proteins that form a structural support network, or "scaffold," for each cell's nucleus -- the compartment that contains the DNA. The reason why mutations in these genes cause this disease is not fully understood, but one theory proposes that the mutations weaken the scaffold structure, leading to damage and death of muscle cells as they continually contract and relax.

However, in up to 50% of individuals with EDMD, no mutation has been identified in any these genes.

Dr Shackleton said: "Our research has identified two new genes, SUN1 and SUN2, that are responsible for causing EDMD in some of these individuals. The proteins produced by these genes also form part of the structural scaffold of the nucleus.

Importantly, we have identified a novel way in which these mutations act in muscle cells.

"Our research has shown that the mutated SUN1 and SUN2 proteins interfere with connections between the nucleus and the rest of the cell and that this results in abnormal positioning of the nuclei within the muscle cells. The nuclei are normally anchored at the edges of muscle cells, probably so that they do not get in the way of the main structures of the cell that are involved in muscle contraction. Incorrect positioning could further damage the nuclei and could also impair muscle contraction, leading to the muscle wasting and weakness seen in EDMD sufferers.

"We therefore believe that incorrect positioning of muscle nuclei may contribute to causing the symptoms of EDMD. Further research is now needed to investigate this new potential disease mechanism and to increase our understanding of how nuclei are positioned in normal muscle cells, but our findings offer the possibility for a novel drug target for the treatment of this disease in the future."

Dr Marita Pohlschmidt, Director of Research at the Muscular Dystrophy Campaign, said:

"We welcome the encouraging results of this study, which has identified two new genes which can cause Emery-Dreifuss muscular dystrophy. In the future, this will give more people an accurate genetic diagnosis, helping them to understand the risk of passing it on to their children and to make informed choices with regards to planning for a family.

An accurate genetic diagnosis also means that patients will receive more precise information about the prognosis of the condition. Most importantly, a better understanding of the condition is crucial for the development of treatments for this complex and devastating condition."

Emily Beale, whose son Tayler (11) has Emery-Dreifuss muscular dystrophy, said:

"Tayler's condition affects the muscles in his legs, arms and neck. He falls regularly because of the weakness in his calf muscles which causes his feet to droop and general instability in his legs. This year he lost the ability to run, he was never very fast, but he misses the ability to try and keep up. In the last year, Tayler's elbows have started to contract meaning he cannot stretch his arms out straight. He finds carrying heavy objects difficult, and struggles to hold things for long periods of time with his hands.

"We are thrilled that someone is researching Emery-Dreifuss muscular dystrophy and we hope that Tayler will see a treatment within his lifetime."

Simple method turns human skin cells into immune strengthening white blood cells

 

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Red blood cells surrounding a white blood cell (stock illustration).

For the first time, scientists have turned human skin cells into transplantable white blood cells, soldiers of the immune system that fight infections and invaders. The work, done at the Salk Institute, could let researchers create therapies that introduce into the body new white blood cells capable of attacking diseased or cancerous cells or augmenting immune responses against other disorders.

The work, as detailed in the journal Stem Cells, shows that only a bit of creative manipulation is needed to turn skin cells into human white blood cells.

"The process is quick and safe in mice," says senior author Juan Carlos Izpisua Belmonte, holder of Salk's Roger Guillemin Chair. "It circumvents long-standing obstacles that have plagued the reprogramming of human cells for therapeutic and regenerative purposes."

Those problems includes the long time -- at least two months -- and tedious laboratory work it takes to produce, characterize and differentiate induced pluripotent stem (iPS) cells, a method commonly used to grow new types of cells. Blood cells derived from iPS cells also have other obstacles: an inability to engraft into organs or bone marrow and a likelihood of developing tumors.

The new method takes just two weeks, does not produce tumors, and engrafts well.

"We tell skin cells to forget what they are and become what we tell them to be -- in this case, white blood cells," says one of the first authors and Salk researcher Ignacio Sancho-Martinez. "Only two biological molecules are needed to induce such cellular memory loss and to direct a new cell fate."

Belmonte's team developed the faster technique (called indirect lineage conversion) and previously demonstrated that these approaches could be used to produce human vascular cells, the ones that line blood vessels. Rather than reversing cells all the way back to a stem cell state before prompting them to turn into something else, such as in the case of iPS cells, the researchers "rewind" skin cells just enough to instruct them to form the more than 200 cell types that constitute the human body.

The technique demonstrated in this study uses a molecule called SOX2 to become somewhat plastic -- the stage of losing their "memory" of being a specific cell type. Then, researchers use a genetic factor called miRNA125b that tells the cells that they are actually white blood cells.

The researchers are now conducting toxicology studies and cell transplantation proof-of-concept studies in advance of potential preclinical and clinical studies.

"It is fair to say that the promise of stem cell transplantation is now closer to realization," Sancho-Martinez says.

Study co-authors include investigators from the Center of Regenerative Medicine in Barcelona, Spain, and the Centro de Investigacion Biomedica en Red de Enfermedades Raras in Madrid, Spain.

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Story Source:

The above story is based on materials provided by Salk Institute for Biological Studies. Note: Materials may be edited for content and length.

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Journal Reference:

1. Julian Pulecio, Emmanuel Nivet, Ignacio Sancho-Martinez, Marianna Vitaloni, Guillermo Guenechea, Yun Xia, Leo Kurian, Ilir Dubova, Juan Bueren, Leopoldo Laricchia-Robbio, Juan Carlos Izpisua Belmonte. Conversion of Human Fibroblasts into Monocyte-Like Progenitor Cells. Stem Cells, 2014; DOI: 10.1002/stem.1800

Long-term use of pills for anxiety and sleep problems may be linked to Alzheimer's

 

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Taking benzodiazepines -- widely prescribed drugs to treat anxiety and insomnia -- is associated with an increased risk of developing Alzheimer's disease, particularly for long-term users, suggests a new study.

The researchers warn that unwarranted long-term use should be considered a public health concern. Dementia currently affects about 36 million people worldwide and this number is expected to double every 20 years, reaching 115 million by 2015. Although a increased risk of dementia has been identified in benzodiazepine users, the nature of this association, whether causal or not, remains unclear.

So a team of researchers based in France and Canada set out to investigate the relationship between the risk of Alzheimer's disease and benzodiazepine exposure over a several years, as well as a potential dose-response relationship.

Using data from the Quebec health insurance program database (RAMQ), they tracked the development of Alzheimer's disease in a sample of elderly residents living in Quebec, Canada who had been prescribed benzodiazepines.

Over a period of at least six years, they identified 1,796 cases of Alzheimer's disease. They then compared each case with 7,184 healthy people matched for age, sex, and duration of follow-up.

Results show that past use of benzodiazepines for three months or more was associated with an increased risk (up to 51%) of Alzheimer's disease. The strength of association increased with longer exposure and with use of long-acting benzodiazepines rather than short-acting ones.

Further adjustment for symptoms that might indicate the start of dementia, such as anxiety, depression or sleep disorders, did not meaningfully alter the results.

In this large case-control study, benzodiazepine use was associated with an increased risk of Alzheimer's disease, say the authors. They emphasise that the nature of the link is still not definitive, but say the stronger association seen with long-term exposures "reinforces the suspicion of a possible direct association, even if benzodiazepine use might also be an early marker of a condition associated with an increased risk of dementia."

Benzodiazepines are "indisputably valuable tools for managing anxiety disorders and transient insomnia" they write, but warn that treatments "should be of short duration and not exceed three months."

They conclude that their findings are of "major importance for public health, especially considering the prevalence and chronicity of benzodiazepine use in elderly populations and the high and increasing incidence of dementia in developed countries."

In view of the evidence, they conclude that "it is now crucial to encourage physicians to carefully balance the benefits and risks when initiating or renewing a treatment with benzodiazepines and related products in elderly patients."

In an accompanying editorial, Professor Kristine Yaffe of the University of California at San Francisco and Professor Malaz Boustani of the Indiana University Center for Aging Research, point out that in 2012 the American Geriatrics Society updated its list of inappropriate drugs for older adults to include benzodiazepines, precisely because of their unwanted cognitive side effects.

Yet almost 50% of older adults continue to use these drugs, they say. And without any formal monitoring system, the potential long term consequences on brain health are likely to be missed, adding to the growing prevalence of cognitive impairment among older people, they suggest.

Given the expanding numbers of older people likely to be treated with several drugs at a time, and/or who are at risk of Alzheimer's disease, this gap needs to be plugged, they say.

Sugar should be regulated like alcohol, tobacco, commentary says

 

 

 

(CBS) Should the government regulate sugar, just like it regulates alcohol and tobacco?

A new commentary published online in the Feb. 1 issue of Nature says sugar is just as "toxic" for people as the other two, so the government should step in to curb its consumption.

The United Nations announced in September that chronic diseases like heart disease, cancer, and diabetes contribute to 35 million deaths worldwide each year, according to the commentary. The U.N. pegged tobacco, alcohol, and diet as big risk factors that contributed to this death rate.

Two of those are regulated by governments, "leaving one of the primary culprits behind this worldwide health crisis unchecked," the authors, Robert H. Lustig, Laura A. Schmidt and Claire D. Brindis, argued.

They said that over the past 50 years, sugar consumption has tripled worldwide. That's also helped contribute to the obesity epidemic - so much so that there are 30 percent more obese people in this world than there are malnourished people.

But how does sugar compare to alcohol?

Sugar meets the same criteria for regulation as alcohol, the authors wrote, because it's unavoidable, there's potential for abuse, it's toxic, and it negatively impacts society. They write that sugar is added to so many processed foods that it's everywhere, and people eat up to 500 calories per day in added sugar alone. Sugar acts on the same areas of the brain as alcohol and tobacco to encourage subsequent intake, they wrote, and it's toxic because research shows that sugar increases disease risk from factors other than added calories, such as when it disrupts metabolism.

"Many people think that obesity is the root cause of these diseases," they wrote. But 40 percent of normal-weight people are developing diseases like diabetes, hypertension, lipid problems, heart and liver disease. "Obesity is not the cause; rather, it is a marker."

That's why it's time that the government steps in and regulates sugar in ways similar to tobacco and alcohol, the authors wrote. That includes taxes, age restrictions and other policies to control the distribution of sugar.

"We are now seeing the toxic downside," co-author and sugar researcher Lustig, a professor of clinical pediatrics at the UCSF Center for Obesity Assessment, Study, and Treatment, told WebMD. "There has to be some sort of societal intervention. We cannot do it on our own because sugar is addictive. Personal intervention is necessary, but not sufficient."

Dr. Marion Nestle, professor of nutrition, food studies, and public health at New York University, told HealthPop that she agrees that it's time for policy changes, since many Americans take in roughly 25 percent of their daily calorie intake through sugar.

"I don't think people have any idea how many calories they take in when they take in soft drinks - particularly because they are consumed in such large quantities," Nestle said. She thinks regulation could eventually be possible, since many local governments are already enacting policies to curb sugar in schools or tax sodas.

"If you have enough of those, the federal government can step in."

Industry groups disagreed with the science and implications of the commentary.

The Sugar Association said it  disputes some of the statistics presented - namely the tripled sugar consumption rates, which it said were based on "incomplete science" in a statement emailed to HealthPop.

"We are confident that the American people are perfectly capable of choosing what foods to eat without stark regulations and unreasonable bans imposed upon them," read a prepared statement from the Sugar Association.

The American Beverage Association added in a separate statement, "Moreover, an isolated focus on a single ingredient such as sugar or fructose to address health issues noted by the World Health Organization to be caused by multiple factors, including tobacco use, harmful alcohol use, an unhealthy diet and lack of physical activity, is an oversimplification"

Worldwide study demonstrates accuracy of genetic analyses

 

Physicians envision a future in which genomic data from patients is heavily used to manage care—but experts have questioned the accuracy and reliability of these analyses. Now, a study by 150 researchers in 12 countries finds real strength and agreement across RNA genomic sequencing techniques and laboratories—as well as ways to improve what little variability exists to set a new high standard.

The results of the study were published in Nature Biotechnology in three separate research articles.

These results should provide assurance to patients, clinicians and the research community that genomic sequencing is accurate, says E. Aubrey Thompson, Ph.D., a professor of cancer biology at Mayo Clinic in Florida, one of three institutions that led the study. Dr. Thompson is a study co-author and member of the project leadership.

"It seems very likely that decisions about patient care are going to be influenced by genomic data, derived from sequencing both RNA and DNA from patient samples, and we now know the extent to which these sequence-based analyses can be relied upon within a given laboratory or from laboratory to laboratory," he says.

"That means that results of a patient's sample, from which clinical management decisions will likely be made, will be accurate worldwide," says Dr. Thompson.

RNA sequencing is being used with increasing frequency to characterize a growing array of conditions—everything from prenatal birth defects to disorders of the elderly.

The other institutions involved in the study are the Beijing Genomic Institute and Weill Cornell Medical School. All three institutions have extensive experience in sequencing RNA and have helped develop novel analytical tools for interpreting the data.

The U.S. Food and Drug Administration (FDA) funded the research, given its need to understand the accuracy of such data submitted in applications for approval of new drugs, clinical applications and genomic diagnostic procedures, Dr. Thompson says.

The purpose of this project, known as Sequence Quality Control (SEQC), was to rigorously define both the scope and the sources of variation in RNA sequencing data.

Laboratory groups at the three leading institutions sequenced the same two RNA samples multiple times.

More than 1 billion nucleotides of sequencing data were generated by each site. The data were then analyzed under the direction of the FDA with the assistance of a large group of academic and industrial statisticians. The researchers also examined the current technologies and major biochemical methods of 30 RNA-sequencing labs and hundreds of researchers. The researchers also found that RNA can be accurately extracted and analyzed from severely degraded genetic samples, such as from tissue samples that have been stored for many years.

"It was determined that there is very strong agreement between the sequence data generated by experienced sequencing laboratories," Dr. Thompson says. "The studies now establish the best practice for all laboratories to use, so that results are reliable and reproducible across laboratories."

More information: Nature Biotechnology, www.nature.com/nbt/journal/v32… 9/full/nbt.3025.html

Home sensors enable seniors to live independently

Home sensors enable seniors to live independently People are living longer and they desire to live as independently as possible in their senior years. But independent lifestyles come with risks, such as debilitating falls and deteriorating health resulting from inadequate care. But what if there were new sensors and high speed networks that could detect falls or health issues? Researchers are developing "smart home" technologies to enhance the safety of residents and monitor their health conditions using sensors and other devices. The research could have a positive impact on health care and quality of life for older adults.

10 Things Happy Couples Do

 

Fireworks are great, but that's not what keeps love strong for years.

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  Real-Life Secrets

  Here's the movie version of what happy couples do: They always laugh at each other's jokes, cook dinner together, fly off to romantic getaways, and have lots of great sex (they never do laundry). The real-life version looks a lot different but creates stronger, richer marriages in the long run. The happiest partners aren't constantly chasing fireworks and bliss. The secret to their success is much simpler, say researchers: Real-life happy couples do 10 things to keep their love strong.



 

• Let Love Build

  If you think the heart-pounding rapture of a new relationship is what long-term love is like, you're in for a big surprise. Couples who start out thinking the fiery intensity of new romance will last forever lose 50% of their passion for each other after just 18 months, according to Harvard psychologist Robert Epstein, PhD. The couples who grow happier over time are the ones who understand that love evolves, becoming calmer, deeper, richer, and more powerful.

• Play Nice

  The happiest couples do something other couples often don't: They're kind to each another. It's not about nightly back rubs and offers to do the dishes, either (although those never hurt). Happy partners simply don't get mean or nasty with each other, even during arguments. "Happy couples treat each other like best friends," says David Penner, PhD, assistant clinical director of the Gottman Relationship Institute. "They're nice to each other across the board. That's what builds loving feelings.

• Do This in Bed

  Surprise: Fooling around -- aka, sex -- is not tops on the list of the most important things happy couples do in bed. What is? Talking. Spending a few minutes chatting every night before sleep lets you catch up, make plans, and discuss problems in a quiet, tender setting, explains University of Minnesota family social science professor Paul Rosenblatt, PhD, author of Two in a Bed: The Social System of Couple Bed Sharing.

• Double Date

  Dinners for two are cozy, but dinners for four are just as important in a relationship. Bonding with other couples actually strengthens your own relationship, according to a 2010 study at Wayne State University. Having open, intimate conversations with other twosomes reinforces your own sense of togetherness. Being close to them makes you feel closer to each other.

• Face Your Differences

  Most couples have their differences, and the more you have, the greater the seeming threat to your relationship, according to Dr. Epstein. But it's how you handle them that really matters. Happy couples bring their differences out into the open rather than denying or dismissing them. "Put issues on the table, and look for ways you can work around them," he says. "The process of examination and renewal makes the threats diminish."

• Skip Some of the Small Talk

  Couples who have deep conversations are far likelier to be happy than couples who always keep it light, according to a 2010 study in the journal Psychological Science. Researchers report that the happiest couples have twice as many substantive discussions -- and far fewer superficial ones -- as the unhappiest couples.

• Be Equally Committed

  If you're both pretty lazy when it comes to working out your problems, you can be just as happy as partners who put in a lot of effort. What matters is that you both feel you devote the same amount of care and effort -- a lot or a little -- to keeping your relationship strong, according to a 2011 study in Psychological Science. Happiness doesn't necessarily depend on how intense your level of commitment is, but on how mutual it is.

• Soften Up

  It's impossible to avoid arguments entirely. In fact, they happen frequently. But the happiest couples keep conflicts from becoming confrontations. They soften their approach when bringing up tough issues. And neither feels as if one of them always gets his or her way. Each occasionally yields to the other.

• Accentuate the Positive

  Happy couples make at least five times as many positive statements to and about each other as negative ones, even when they are arguing, says Dr. Penner. Yes, you're right, it's not always easy to be nice (you did read slide 3, didn't you?), but it pays off by solidifying the bond between you.

• Hang In There

  Up to 80% of those who are most committed to marriage contemplate divorce at some point, says Dr. Epstein. But slogging through bad times can make both of you happier than ever. "If you can do that and get to the other side, it makes the relationship stronger," he adds. "It strengthens love."

The beautiful brain cells you don't know about

Hint: They're not neurons

Glia in a mouse brain.
Credit and Larger Version

June 3, 2014

The number of nerve cells in the human brain sounds impressive: 100 billion. And it is.

But neurons may make up as little as 15 percent of cells in the brain. The other cells are called glial cells, or glia.

Glia are the rising stars of the neuroscience universe. Once delegated to simply a supporting role for neurons, these cells are now thought to play an important part in early brain development, learning and memory.

A 2013 workshop funded by the National Science Foundation (NSF) enabled researchers who study learning and memory to get together (many for the first time) and reconsider glia's function.

"It was paradigm-shifting," said R. Douglas Fields, a neurobiologist at the National Institutes of Health and meeting organizer. "Everyone left enthused about the enormous potential for understanding brain function, especially learning and memory by studying how all the cells in the brain work together, rather than focusing exclusively on neurons."

In fact, Fields and other brain researchers who specialize in glia have since called for a greater focus on non-neuronal cells as part of the BRAIN Initiative, a collaborative research project announced by the Obama administration in April 2013.

When you learn something, how to catch a ball or use an equation, information is transmitted along the spindly arms of neurons via electrical signals. At the same time, glia called oligodendrocytes work to insulate these particular arms with a fatty substance called myelin so the information flows more efficiently.

Some studies show that glial cells known as astrocytes may have an even more active role in learning. Astrocytes may release chemicals that strengthen newly formed connections between neurons, making it more likely you'll be able to remember a new face, or the name of your co-worker's beloved golden retriever.

Understanding how we learn requires that scientists and engineers take a holistic approach to brain research.

NSF-funded research centers such as the Center of Excellence for Learning in Education, Science and Technology and the Temporal Dynamics of Learning Center integrate experimentation, modeling and technical application to help us understand what's really going on inside the brain. And to use that knowledge to educate students and to build intelligent technologies.

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Sarah Bates, NSF (703) 292-7738 sabates@nsf.gov

Investigators
Earl Miller
Beth Stevens
Heather Ames
Ennio Mingolla
Frank Guenther
Richard Fields
Robert Sekuler
Michael Hasselmo
Garrison Cottrell
Barbara Shinn-Cunningham

Related Institutions/Organizations
Trustees of Boston University
Children's Hospital Corporation
University of California-San Diego

Related Programs
Science of Learning Centers
Office of Multidisciplinary Activities

Related Awards
#1005256 REU Site: The Temporal Dynamics of Learning
#0835976 CELEST: A Center of Excellence for Learning in Education, Science, and Technology
#1258562 Glial Biology of Learning and Cognition, to be held in Arlington, Virginia, February, 2013

 

Related Websites
Understanding the Brain: www.nsf.gov/brain
Brain power: Bright ideas and smart tools for neuroengineering: www.nsf.gov/brainpower