Culture

It was the most serious release of radioactive material since Fukushima 2011, but the public took little notice of it: In September 2017, a slightly radioactive cloud moved across Europe. Now, a study has been published, analyzing more than 1300 measurements from all over Europe and other regions of the world to find out the cause of this incident. The result: it was not a reactor accident, but an accident in a nuclear reprocessing plant. The exact origin of the radioactivity is difficult to determine, but the data suggests a release site in the southern Urals. This is where the Russian nuclear facility Majak is located. The incident never caused any kind of health risks for the European population.

Among the 70 experts from all over Europe who contributed data and expertise to the current study are Dieter Hainz and Dr. Paul Saey from the Institute of Atomic and Subatomic Physics at TU Wien (Vienna). The data was evaluated by Prof. Georg Steinhauser from the University of Hanover (who is closely associated with the Atomic Institute) together with Dr. Olivier Masson from the Institut de Radioprotection et de Sûreté Nucléaire (IRSN) in France. The team has now published the results of the study in the renowned journal Proceedings of the National Academy of Sciences of the USA (PNAS).

Unusual Ruthenium Release

"We measured radioactive ruthenium-106," says Georg Steinhauser. "The measurements indicate the largest singular release of radioactivity from a civilian reprocessing plant." In autumn of 2017, a cloud of ruthenium-106 was measured in many European countries, with maximum values of 176 millibecquerels per cubic meter of air. The values were up to 100 times higher than the total concentrations measured in Europe after the Fukushima incident. The half-life of the radioactive isotope is 374 days.

This type of release is very unusual. The fact that no radioactive substances other than ruthenium were measured is a clear indication that the source must have been a nuclear reprocessing plant.

The geographic extent of the ruthenium-106 cloud was also remarkable - it was measured in large parts of Central and Eastern Europe, Asia and the Arabian Peninsula. Ruthenium-106 was even found in the Caribbean. The data was compiled by an informal, international network of almost all European measuring stations. In total, 176 measuring stations from 29 countries were involved. In Austria, in addition to TU Wien, the AGES (Austrian Agency for Health and Food Safety) also operates such stations, including the alpine observatory at Sonnblick at 3106m above sea level.

No Health Hazard

As unusual as the release may have been, the concentration of radioactive material has not reached levels that are harmful to human health anywhere in Europe. From the analysis of the data, a total release of about 250 to 400 terabecquerel of ruthenium-106 can be derived. To date, no state has assumed responsibility for this considerable release in the fall of 2017.

The evaluation of the concentration distribution pattern and atmospheric modelling suggests a release site in the southern Urals. This is where the Russian nuclear facility Majak is located. The Russian reprocessing plant had already been the scene of the second-largest nuclear release in history in September 1957 - after Chernobyl and even larger than Fukushima. At that time, a tank containing liquid waste from plutonium production had exploded, causing massive contamination of the area.

Olivier Masson and Georg Steinhauser can date the current release to the time between 25 September 2017, 6 p.m., and 26 September 2017 at noon - almost exactly 60 years after the 1957 accident. "This time, however, it was a pulsed release that was over very quickly," says Professor Steinhauser. In contrast, the releases from Chernobyl or Fukushima lasted for days. "We were able to show that the accident occurred in the reprocessing of spent fuel elements, at a very advanced stage, shortly before the end of the process chain," says Georg Steinhauser. "Even though there is currently no official statement, we have a very good idea of what might have happened."

All over the world, immigration has become a source of social and political conflict. But what are the roots of antipathy toward immigrants, and how might conflict between immigrant and native populations be dampened?

Political scientist Nicholas Sambanis has spent his career considering various forms of inter-group conflict, starting with civil wars and international interventions to help countries transition from war to peace. More recently, he has studied non-violent forms of conflict, including discrimination between individuals of different ethnic or religious background. Understanding why groups come into conflict and how to resolve those conflicts and avoid violent escalations is the mission of the Penn Identity and Conflict (PIC) Lab, which he founded when he arrived at Penn in 2016.

His newest research on identity politics, an experimental approach that explores the causes of discrimination against Muslim immigrants in Germany, was just published in the Proceedings of the National Academy of Sciences.

"Opposition toward immigration can be due to economic reasons because of competition for jobs or due to the perceived cultural threat that immigrants pose to their host country by challenging dominant norms and changing the national identity," he says.

He finds arguments centered on cultural threat more convincing than economic explanations of opposition to immigration, especially in Europe.

"Most previous research is limited to presenting survey-based attitudinal measures of antipathy toward immigrants or refugees and correlating them with socio-economic characteristics of the survey respondents or their political beliefs," Sambanis says. "We wanted to go beyond that and measure actual behavior in the field. We wanted to figure out what particular aspects of refugees or immigrants generate more hostility. Is it racial differences? Ethnic differences? Is it linguistic or religious differences? Is there merit to the idea that discrimination toward immigrants is due to the perception that they do not follow the rules and threaten dominant social norms?"

There's very little experimental research, Sambanis says, on the causes of anti-immigrant bias and even less research on how to reduce it.

Working with University of Pittsburgh assistant professor Donghyun Danny Choi, a former PIC Lab postdoc, and Mathias Poertner, a PIC Lab fellow and postdoc at the University of California, Berkeley, Sambanis designed the experimental study. They targeted Germany because of the high influx of immigrants and refugees and the political salience of immigration issues in recent elections there and because Germans are strongly inclined toward conforming with social norms, especially around keeping order.

Their hypothesis: If it is true that opposition to immigration is driven by the perception that immigrants threaten valued social norms and pose a cultural threat, then in a country that values norm adherence they would see a reduction in discrimination toward immigrants if immigrants show that they respect local social norms and care about their new society.

They staged an intervention against a native male German who littered in a public space, since not littering is a social norm there. A female researcher would approach the person littering, asking him to pick up his trash and dispose of it properly. Bystanders, unaware that they were being studied, observed the interaction. Shortly thereafter, the woman would take a call and while speaking on the phone would drop a bag of groceries, causing oranges to spill out on the floor. The observing researchers recorded whether the bystanders who had witnessed this entire interaction helped the woman pick up her oranges.

In some versions, the woman dropping the oranges would have sanctioned the norm violator, signaling her integration with the German culture. In others, she did not intervene so as to seem indifferent to the littering.

Researchers also used the woman's identity as a variable: In some versions, she was a native German, in others a Muslim immigrant wearing a hijab. Her degree of religiosity, her ethnic background, and her linguistic assimilation to German society were all manipulated as part of the experiment.

This allowed the researchers to measure whether immigrants who are more socially distant than the average German receive less assistance and whether following social norms offsets any bias toward them.

They ran this experiment more than 1,600 times in train stations in 30 cities in both western and eastern Germany using multiple teams of research assistants, with more than 7,000 bystanders unwittingly participating. Then, the researchers measured whether women who wore a hijab received less assistance than native Germans, whether ethno-racial differences between immigrants matters less than religious differences in generating bias, whether immigrants who wore a cross received more help than those who did not wear any outward symbols of religiosity, and whether good citizenship--enforcing anti-littering norms--generated more help from bystanders, eliminating any bias against immigrants.

"We found that bias toward Muslims is too pronounced and is not overcome by good citizenship; immigrant women who wore a hijab always received less assistance relative to German women, even when they followed the rules," Sambanis says.

"But we also found that good citizenship has some benefit, as the degree of discrimination toward Muslims goes down if they signal that they care about the host society. And ethnic or racial differences alone do not cause discrimination in our setup. Nor is religious assimilation--wearing a cross rather than a hijab--necessary to be treated with civility."

On average, women wearing a hijab who did not enforce the norm got help in about 60% of cases, whereas "German" women who did scold the litterer got help in 84% of the cases. The rates of assistance offered to a Muslim who enforced social norms by scolding the litterer were equivalent to those for a German who did not enforce the norm.

"The reason to run such an experiment focusing on everyday interactions is that it gives you a sense of the accumulated impact of discrimination in shaping perceptions of identity and belonging," Sambanis says. "Getting help to pick up something you drop on the floor seems like a small thing. But these small things--and small slights--add up to form lasting impressions of how others perceive you and, in turn, can inform the immigrants' own attitudes and behavior toward the host society."

Now, Sambanis, Choi, and Poertner are extending their research to new questions trying to understand the mechanisms underlying the effects they picked up with their experiments in Germany.

This collaborative effort between Sambanis, Choi, and Poertner will become a book on how conflict between immigrants and native populations can be managed and whether norms can form the basis for the reduction in discrimination. The German experiments will be expanded next year and applied to a different social context in Greece, which also faces an intense political crisis due to unsustainably high levels of immigration and which differs from Germany with respect to the degree of public adherence to laws and rules.

Individuals there are less likely to follow rules and contribute less to the public good. So Sambanis and his co-authors think they may observe even lower effects of the ability of social norms to offset discrimination due to ethno-religious differences. That research will provide a useful comparison to better understand the existing experimental results.

"A key idea in socio-biological theories of inter-group conflict is that there is an almost innate antipathy or suspicion toward members of "out groups" [immigrant], however those groups are defined. But clearly societies can manage sources of tension and avoid conflict escalation since there is very little observed conflict relative to how many different types of inter-group differences exist out there," Sambanis says. "A lot of the literature on immigration has suggested that assimilation is the key to reducing conflict between natives and immigrants: Immigrants must shed their names, change their religion, or hide their customs so they can be more accepted.

"Is this really necessary? Or is it enough for immigrants to just signal credibly that they care about being good citizens as much as everybody else?"

Understanding these types of questions is at the heart of the PIC Lab's mission. A unifying theme of Sambanis' work has been reducing inter-group conflict, particularly inter-ethnic conflict.

His interests were shaped by the wars in Bosnia and Rwanda, which were going on when he was in graduate school and pushed him away from international economics and toward studying peacekeeping. At the PIC Lab, researchers tackle questions both at the larger country level and at the smaller individual and group level, integrating ideas from political science, social psychology, and behavioral economics to understand human behavior and explore the outcomes of different policy interventions to reduce conflict. The lab conducts data-based, mostly quantitative research that can inform policy design but also theory-building in political science, Sambanis says.

"Ethnic differences, religious differences, racial differences--they all matter for politics, but they do not need to produce conflict," he says. "When people are faced with the hard realities of ethnic wars, separatist conflicts, genocides, or hate crimes, they usually assume that these are inevitable outcomes of innate human prejudices or fears and that people just can't get along because of deep differences in their preferences or their customs.

"A lot of the work that I do shows that ethnic conflict is not inevitable. The key is to understand the conditions that make ethnic differences salient and then find ways to defuse or manage conflict."

Editor's Note: This release has been updated since it was originally published by request of the submitting institution. Three paragraphs describing future research plans have been removed.

LA JOLLA, CA--In addition to the four major bases in the DNA alphabet - A, C, G and T - there is also a minor "fifth" base, 5-methylcytosine (5mC), which plays a disproportionately important role in deciding whether genes and other DNA elements are turned on or off. Not surprisingly, defects in cytosine methylation are associated with developmental abnormalities, genetic diseases and cancer.

In their latest study, published in this week's online issue of Proceedings of the National Academy of Sciences, researchers at La Jolla Institute for Immunology (LJI), reveal how the finely tuned balance between DNA methylation and demethylation prevents genomic instability and cancer.

While scientists knew that enzymes known as DNMTs were responsible for putting the 5mC mark on cytosines, how this mark was removed remained a mystery for decades. In an earlier study, Anjana Rao, Ph.D., LJI professor and senior author of the current study, together with former colleagues at Harvard University, Cambridge, and the National Institutes of Health, Bethesda, Maryland, showed that cancer-related proteins known as TETs convert 5mC to a "sixth base", 5hmC, which subsequently reverts to C. Soon thereafter, it became clear that loss of TET function is strongly linked to many types of cancers, both in humans and in mice.

Although DNMTs and TETs are expected to have opposite activities--DNMTs produce 5mC whereas TETs remove it--human blood cancers with mutations in either TET2 or DNMT3A display similar features, including increased levels of DNA damage and genome instability. Moreover, DNMT3A and TET2 are the top two proteins mutated in clonal haematopoiesis, a disease of aging in which certain clones of blood stem cells expand more than others. People with clonal hematopoiesis are at risk for atherosclerosis and for progressive cancers.

The latest findings by the Rao lab provide an explanation why mutations in TETs and DNMTs have similar effects in disease.

When Isaac F. López-Moyado, a graduate student in the Rao lab and the first author of the study, analyzed the methylation patterns in an aggressive lymphoma that arose when TET2 and TET3 were deleted in mouse T cells, he found that DNA methylation increased in large regions of the genome as expected. However, these same cancer samples possessed equally large genomic regions which had lost DNA methylation when compared with normal, non-cancerous T cells.

"This was surprising because the dogma for the last ten years has been that TET mutations lead to increased DNA methylation," said López-Moyado. "While this is correct for certain genomic regions, it is not true for large swaths of the genome known as heterochromatin." Heterochromatin is a form of DNA that is tightly packed, usually inactive and typically resides in the periphery of the nucleus.

A closer look at the distribution of Dnmt3a molecules in TET-deficient cells showed that a portion of Dnmt3a molecules had relocated away from heterochromatin, explaining the seemingly paradoxical loss of methylation in this region of the genome.

Interestingly, a substantial number of leukemia patients bear both TET2 and DNMT3A mutations and mice that carry dual mutations in both TET2 and DNMT3A are known to develop more severe cancers than mice with TET2 or DNMT3A mutations alone. This observation prompted López-Moyado to analyze published data from mouse hematopoietic stem cells--the cells from which blood cancers arise--to establish whether double mutations correlate with changes in the methylation status of heterochromatin.

López-Moyado found that cells with dual TET2 and DNMT3A mutations showed an even more pronounced loss of DNA methylation in heterochromatin than cells with only one of these mutations. In fact, even without mutations in TET or DNMT3A, decreased DNA methylation in heterochromatin is common in cancer, suggesting that loss of TET or DNMT function may be involved.

Heterochromatin constitutes more than half of mammalian genomes, and contains not only the genes that need to be silenced in any particular cell type, but also "parasitic" DNA elements and various "repeat" sequence that long ago invaded the genome. These DNA elements, which include transposons and ancient viruses, need to be stringently repressed in heterochromatin.

"If heterochromatin loses DNA methylation, these elements can become reactivated and can form aberrant structures or jump from one genomic location to another, leading to genome instability and DNA damage, the hallmarks of cancer," explains López-Moyado. Indeed, these features are commonly observed, together with DNA hypomethylation, in many types of hereditary as well as non-hereditary cancers, including cancers with TET and DNMT3A mutations.

Future research will establish if the loss of DNA methylation in heterochromatin that results from mutations in the DNA methylation pathway has a direct role in heterochromatin reactivation and cancer initiation and progression.

Even young children know what typical dogs and fish look like -- and they apply that knowledge when they hear new words, reports a team from the Princeton Baby Lab, where researchers study how babies learn to see, talk and understand the world.

In a series of experiments with children 3 to 5 years old, the researchers found that when children are learning new nouns, they use what they know about these objects -- how typical or unusual they are for their categories (such as fish, dog, bird or flower) -- to help them figure out what these words mean. This type of sophisticated reasoning was thought to only develop later. The researchers' work appears in the current issue of the Journal of Child Language.

"What we're showing is that meaning matters!" said Adele Goldberg, professor of psychology at Princeton University and the senior author on the paper. "Children take the meaning of the objects that they are seeing into account when they learn new words."

The researchers coined this tactic the "blowfish effect." If children see a blowfish (or a greyhound or an unusual tropical flower) and learn a new word to go with it, they will assume it refers to that specific type of object and not the broader category of fish (or dogs or flowers).

"This study helps to solve one of the big puzzles in language development," said Lauren Emberson, assistant professor of psychology and first author on the paper. Many years of studies have shown that when children learn new words, they assume that word means something fairly general: If taught a new word for a goldfish, children assume that it means "fish."

"But children can learn these more specific terms," like blowfish and greyhound, said Emberson, who is also one of the directors of the Princeton Baby Lab. "How do they start to do that? We are showing that they use the objects themselves to do this. If they see an unusual fish and their parent calls it something, they will learn that it refers to that specific fish."

Using a custom designed iPad program, the researchers taught children four new words: fep, zak, lat and galt. Two of these terms were used for typical objects and two for unusual objects. The objects came from four categories that children are familiar with: fish, birds, dogs and flowers.

In each trial, a child saw either one or three examples at the top of the screen, identified by a new word: "This is a fep," or "These are three feps." With the press of an arrow, the child got 12 more images below: two that matched the examples, two that shared the category, and eight unrelated creatures. The experimenter then asked, "Can you find the feps?"

The researchers were curious whether children would decide a "fep" only meant the specific creature in the examples -- a robin, for example, or a Dalmatian -- or if the term was applied more generally to all birds or dogs.

Each child could choose as many images as she wanted to, at her own pace, before proceeding to the next trial by pressing the arrow again. The order of the four categories -- fish, birds, dogs and flowers -- was randomized across participants.

The researchers ran the same experiment with college students; the only differences were that the undergraduates were told that this was an experiment intended for young children, and they were allowed to hold the iPads themselves.

The team found that both children and adults processed the new words in the same way. When any of them saw an unusual dog labeled a "fep," they were more likely to interpret it narrowly -- as meaning that type of dog, not "dogs" more generally. These findings run counter to the idea that children will always assume that new words should be interpreted as general terms.

In addition, the researchers found that the more "typical" an example looks, the more likely children are to assume it's a general term, unless it is repeated: A "zak" was likely to be interpreted as "fish" if it labeled a single salmon -- a fairly typical-looking fish -- but it was interpreted as "salmon" if illustrated by three salmon. But if "zak" labeled even a single odd-looking fish -- like a blowfish -- the children were more likely to decide that the word meant "blowfish" than "fish."

"The finding helps shed light on the mysteries and intricacies of language development," Emberson said.

A genome-wide association study (GWAS) and bioinformatic analysis of more than 165,000 U.S. veterans confirms a genetic vulnerability to post-traumatic stress disorder (PTSD), specifically noting abnormalities in stress hormone response and/or functioning of specific brain regions, report scientists in a paper published July 29, 2019 in Nature Neuroscience.

GWAS are a relatively new scientific tool in which scientists rapidly scan markers across complete sets of DNA or genomes of many people, looking for genetic variations associated with a particular disease. The findings are used to develop better methods to detect, treat and prevent the disease.

In the new paper, a diverse team led by Murray B. Stein, MD, MPH, Distinguished Professor of Psychiatry and Family Medicine and Public Health at University of California San Diego School of Medicine and a psychiatrist at Veterans Affairs San Diego Healthcare System, and Joel Gelernter, MD, professor of psychiatry, genetics and neuroscience at Yale School of Medicine and VA Connecticut Healthcare System, sought to better parse the pathophysiology of PTSD -- its underlying biological mechanisms -- by analyzing genetic data from members of the Million Veteran Program, a national voluntary research effort funded by the Department of Veterans Affairs Office of Research & Development.

The scientists focused on finding genetic links relevant to "intrusive re-experiencing of trauma," the most common symptom of PTSD, which is characterized by unintentional and unwanted recall, emotions and behaviors linked to past traumatic events, such as flashbacks.

The research sample consisted of 146,660 European American veterans and 19,983 African American veterans. In the European American group, the scientists found eight distinct genetic regions with strong associations between PTSD and how the brain responds to stress. It highlighted the role of one specific kind of brain cell: striatal medium spinal neurons, which are prevalent in a region of the brain responsible for, among other things, motivation, reward, reinforcement and aversion.

"The genes implicated in this study point to this region of the brain, and these types of neurons, as potentially involved in PTSD vulnerability," said Stein. "Because we know something about the regulation of these neurons, we can test hypotheses about drugs that might be useful for PTSD, such as drugs that influence dopamine or GABA, both of which are regulatory of these types of neurons."

The researchers found no significant associations among the African American cohort, but Stein suggested the likely reason was the comparatively small size of the sample.

Stein said future research will be needed to replicate the findings, including postmortem PTSD analyses to confirm physiological effects on brain. The findings, he said, may also point to possible drug treatments to be explored.

Influencer marketing is extremely widespread, yet ineffective. Eighty-six percent of companies use it as part of their social media strategy, but effectiveness remains low. For an influencer on Facebook, the average engagement rate per post is 0.37 percent; on Twitter, it is even lower at 0.05 percent.

New research from the University of Notre Dame provides a framework of strategies to help managers yield larger returns on engagement.

"Driving Brand Engagement Through Online Social Influencers: An Empirical Investigation of Sponsored Blogging Campaigns" is forthcoming in the Journal of Marketing from lead author Christian Hughes, assistant professor of marketing in Notre Dame's Mendoza College of Business.

Hughes, along with her co-authors Vanitha Swaminathan of the University of Pittsburgh and Gillian Brooks from the University of Oxford, collected a data set of 57 sponsored blogging campaigns run by companies including AT&T, Walmart, Procter & Gamble, Chick-fil-A, Listerine, OshKosh B'Gosh, Chef Boyardee and Walmart, between 2012 and 2016. The data came from The Motherhood, a social media influencer marketing agency focused on "mommy bloggers," and involved 600 blogs and 1,800 posts. The researchers followed up the data analysis with an experiment to replicate their findings.

They noticed multiple factors affected success in generating online engagement (posting comments, liking a brand), depending on the type of platform, blog post content and the goals of the campaign -- whether trying to generate awareness for a brand or prompt consumer purchase.

"On Facebook, attention-grabbing, creative content is more effective when the campaign goal is to win the purchase versus simply raise awareness," Hughes says. "And interestingly, including giveaways increases engagement on blogs, but the opposite happens on Facebook."

In addition, the research finds that posting on a weekend rather than a weekday results in higher engagement on Facebook, but not on blogs, and the type of content influencers are posting also impacts engagement depending on the platform and goals.

They also focused on the expertise of the blogger, which they determined matters on blogs, but not in higher-distraction environments such as Facebook, Instagram or Twitter.

"The biography of a high-expertise blogger may read something like 'professional marketing and content creator, brand ambassador, social media influencer, freelancer, etc.," Hughes says. "While a low-expertise blogger bio might boast 'loves family, travel, bad jokes and good coffee.' Though both are sponsored bloggers, they portray themselves very differently, and our research shows for a campaign trying to raise awareness on the blog platform, a high-expertise blogger can generate greater engagement."

The findings highlight the critical interplay of platform type, campaign intent, source, campaign incentives and content in driving engagement.

"Running a successful influencer marketing campaign is about more than picking an influencer with the most followers and posting across platforms," Hughes says. It involves designing a cohesive strategy, selecting influencers and encouraging content that is going to have the biggest impact for the company's specific campaign goals."

Hughes teaches social media marketing at Notre Dame and researches in the areas of digital and social media, with a focus on influencer marketing and social influence. She formerly worked as a marketing research analyst for Management Science Associates Inc. and consulted for companies such as Avon, Danone, Georgia-Pacific and R.J. Reynolds.

NASA's newest planet-hunting satellite has discovered a type of planet missing from our own solar system.

Launched in 2018, the Transiting Exoplanet Survey Satellite, or TESS, has found three new worlds around a neighboring star. Stephen Kane, a UC Riverside associate professor of planetary astrophysics, says the new star system, called TESS Object of Interest, or TOI-270, is exactly what the satellite was designed to find.

A paper describing TOI-270 has been published in the journal Nature Astronomy and is now available online. Of the three new exoplanets, meaning they're outside our solar system, one is rocky and slightly larger than Earth, while the two others are gaseous and roughly twice Earth's size.

Not only is the smaller planet in the habitable zone -- the range of distances from a star that are warm enough to allow liquid-water oceans on a planet -- but the TOI-270 star is nearby, making it brighter for viewing. It's also "quiet," meaning it has few flares and allows scientists to observe it and its orbiting planets more easily.

"We've found very few planets like this in the habitable zone, and many fewer around a quiet star, so this is rare," said Kane. "We don't have a planet quite like this in our solar system."

In our own solar system, there are either small, rocky planets like Earth, Mercury, Venus, and Mars, or much larger planets like Saturn, Jupiter, Uranus, and Neptune that are dominated by gasses rather than land. We don't have planets about half the size of Neptune, though these are common around other stars.

"TOI-270 will soon allow us to study this "missing link" between rocky Earth-like planets and gas-dominant mini-Neptunes, because here all of these types formed in the same system," said lead researcher Maximilian Gunther, a Torres Postdoctoral Fellow at the Massachusetts Institute of Technology.

Follow-up observations on the system have been planned for 2021, when the James Webb Space Telescope launches. It will be able to measure the composition of the TOI-270 planets' atmospheres for oxygen, hydrogen, and carbon monoxide.

Kane says these kinds of observations can help determine whether a planet has ever had a liquid water ocean, and whether any of the planets has conditions suitable for life as we know it.

While TOI-270 is far enough away that no one living will likely ever travel there, at 73 light-years away it is still considered close.

"The diameter of our galaxy is 100,000 light years, and our galaxy is just one of millions of galaxies," Kane said. "So, 73 light years means it's one of our neighboring stars."

TESS is a NASA Astrophysics Explorer mission led and operated by MIT and managed by NASA's Goddard Space Flight Center. Additional partners include Northrop Grumman, NASA's Ames Research Center, the Harvard-Smithsonian Center for Astrophysics, MIT's Lincoln Laboratory, and the Space Telescope Science Institute. More than a dozen universities, research institutes, and observatories worldwide are participants in the mission.

Kane, a member of UCR's NASA-funded Alternative Earths Astrobiology Center, is available for media interviews about TESS and his involvement in analyzing its data and observations.

He and the team hope further research will reveal additional planets in the system beyond the three now known. The smaller planet is unlikely to host life because its surface could be too warm for the presence of liquid water. But additional planets at greater distances from the star might be cooler, allowing water to pool on their surfaces.

For respiratory infections in children under 12, physicians are increasingly more likely to recommend antihistamines and less likely to recommend cough and cold medicines, a Rutgers study found.

Antihistamines are widely used over-the-counter to treat various allergic conditions. However, these medicines have little known benefit for children with colds, and some older antihistamines cause sedation and occasionally agitation in children.

The study, in JAMA Pediatrics, found a sharp decline in cough and cold medicine recommendations for children under 2 after 2008, when the Food and Drug Administration recommended against the medicines for that age group due to safety concerns and uncertain benefits. The American Academy of Pediatrics subsequently recommended avoiding cough and cold medicines in children under 6.

"Families often treat their children's respiratory infections with cough and cold medicines, some of which include opioid ingredients, such as codeine or hydrocodone. However, there is little proof that these medications effectively ease the symptoms in young children," said study lead author Daniel Horton, assistant professor of pediatrics, Rutgers Robert Wood Johnson Medical School. "Also, many cough and cold medicines have multiple ingredients, which increases the chance of serious accidental overdose when combined with another product."

The researchers looked at national surveys representing 3.1 billion pediatric ambulatory clinic and emergency department visits in the United States from 2002 to 2015. During that period, physicians ordered approximately 95.7 million cough and cold medications, 12 percent of which contained opioids.

After the FDA's 2008 public health advisory, however, physician recommendations declined by 56 percent for non-opioid cough and cold medicines in children under 2 and by 68 percent for opioid-containing medicines in children under 6. At the same time, researchers saw a 25 percent increase in doctor recommendations for antihistamines to treat respiratory infections in children under 12.

"Sedating antihistamines such as diphenhydramine [Benadryl] may have a small effect on some cold symptoms in adults," said Horton. "However, there is little evidence that antihistamines actually help children with colds feel better or recover faster. We do know that these medicines can make kids sleepy and some kids quite hyper."

"It is nice to see physicians are heeding the advice to avoid cough and cold medications for children, but switching them to antihistamines is not necessarily an improvement," said co-author Brian Strom, chancellor, Rutgers Biomedical and Health Sciences.

The American Academy of Pediatrics has various suggestions for treating children with the cold or flu, including use of over-the-counter medicines for pain or fever, honey to relieve cough in children over 1 year old, and plenty of rest and hydration. For more information and suggestions, visit healthychildren.org's Caring for Your Child's Cold or Flu information page.

In addition to Strom, who is affiliated with Rutgers Center for Pharmacoepidemiology and Treatment Science and the Institute for Health, Health Care Policy and Aging Research, the study was co-authored by Tobias Gerhard, Rutgers Ernest Mario School of Pharmacy.

A new Portland State University study suggests that bullying bosses aren't just bad for employee morale and well-being -- they can also be bad for workplace safety.

Liu-Qin Yang, an associate professor of industrial-organizational psychology in PSU's College of Liberal Arts and Sciences, and her co-authors surveyed airline pilots and manufacturing technicians and found that employees' safety behavior can be worsened when they're treated in ways that detract from their bonds to a work group.

The study was published in the Journal of Applied Psychology.

Yang said that bosses' behaviors can strengthen or weaken employees' sense of belonging to the work group by supporting or undermining their status within the group. Poor treatment from a boss can make employees feel that they're not valued by a group. As a result, they can become more self-centered, leading them to occasionally forget to comply with safety rules or overlook opportunities to promote a safer work environment.

Yang said this was especially true among employees who were more uncertain about their social standing within the group.

"When people are less sure about their strengths and weaknesses and their status within a group, they become more sensitive," she said. "They're more likely to respond negatively to their boss' bullying behaviors."

Yang said workplace safety is a critical issue -- and more so in an environment where one employee's failure to behave safely can create circumstances where other people are likely to be injured.

"Organizations need to understand how important it is to curb leaders' bad behavior and to create positive team dynamics, so that there will be fewer negative safety consequences for employees or customers," she said. "It's really critical to manage such leader behavior, support victimized employees and prevent such issues."

Among the study's recommendations: 

Implement training programs that can improve leaders' skills in interacting with their employees, so as to provide feedback and discipline in ways that are neither offensive nor threatening.

Promote a more civil and engaged work environment that strengthens social bonds between employees and creates a buffer against the negative consequences of their boss' bad behaviors

Implement transparent performance evaluation processes so employees have less uncertainty about their social status in the workplace

Inside the brains of patients with amyotrophic lateral sclerosis, a debilitating neurodegenerative disease, is a telltale sign that marks almost every case: clumps of toxic proteins.

Now, researchers from the Stanford University School of Medicine and their collaborators have pinpointed a key gene behind the formation of one type of these neuron-damaging aggregates. They've also shown how inhibiting the gene's function curbs production of the harmful protein.

"We know that these protein-rich aggregates are a clear hallmark of ALS," said Aaron Gitler, PhD, professor of genetics. "But this finding allows us a deeper look into how those aggregates are made, and potentially how we can hinder that process."

The gene, RPS25, codes for a piece of cellular machinery necessary for creating the protein-based gunk that amasses in some forms of ALS and damages healthy neurons. When the gene's activity was experimentally depleted -- in yeast, in neurons derived from patients with ALS and in fruit flies -- Gitler and his team saw levels of the lethal protein drop by about 50 percent across the board.

The team also tested the function of RPS25 in human cells modeling Huntington's disease and spinocerebellar ataxia, two other neurodegenerative illnesses that have protein-aggregate "hallmarks" similar to ALS, said Shizuka Yamada, a graduate student in Gitler's lab. There, too, inhibiting the gene helped tamp down the levels of bad protein.

It's still early days, Yamada said, but hampering the RPS25 gene seems like a promising target for reducing the destructive proteins seen in ALS and even extending life span, as was seen in the fruit fly model of ALS with low activity levels of the gene.

A paper detailing the results of the research will be published July 29 in Nature Neuroscience. Gitler, who holds the Stanford Medicine Basic Science Professorship, is the senior author. Yamada is the lead author.

An alternate route

Also known as Lou Gehrig's disease, ALS is a condition that kills off motor neurons, which are crucial to all physical tasks, from brushing one's hair to breathing. The root cause behind every case is not always the same; there's a slew of genetic factors that play into the onset of ALS. Yet one gene is often the culprit. In ALS, it harbors a string of DNA that erroneously repeats itself.

It's these DNA repeats that are transformed into the harmful proteins that build up in the brain. As the proteins amass, they interfere with healthy neurons, blocking the cells' ability to function normally.

Outside of their toxic properties, what's notable about the protein aggregates is that they aren't made like other proteins found in the body, Yamada said. "These repeats actually shouldn't be made into proteins at all," she said. "They come from DNA that isn't supposed to code for anything, and yet somehow the proteins come to be anyway."

During run-of-the-mill protein formation, the ribosome, a sort of molecular machine that resides in the cell, processes messenger RNA, which contains genetic code based on DNA, and turns it into the raw materials of a protein. That process is called translation, and it's initiated by a code in the mRNA that shows the ribosome where to start translating. The ALS-associated DNA repeats don't have that start code, unlike normal mRNA.

"So regular translation doesn't work with the repeats," Yamada said. But it turns out there's a molecular workaround: an unconventional translation process called repeat-associated non-AUG translation, or RAN translation, that turns the ALS repeats into destructive protein bodies.

Putting the brakes on RPS25

The exact mechanism of RAN translation and its role in human biology is not clear, but scientists do know that it still depends on the ribosome. To better understand the process, Gitler and Yamada turned to yeast, a simple organism that still has the major proteins and pathways of human cells. One at a time, the researchers decreased the function of individual yeast genes and monitored the fungus' RAN function. When subdued, several genes swayed RAN function, but one in particular, RPS25, stood out. With the gene hindered, production of the toxic protein fell by 50 percent.

The researchers also saw a 50 percent dip in the toxic protein when they tested how neurons derived from patients with ALS fared without RPS25.

"We were really excited to see the decrease in repeat proteins carry over into human cells," Yamada said. "It's always pretty cool when yeast biology can directly inform human biology." Because these cells came from patients who suffer from ALS, the research offered a reliable glimpse into how the neurons of individuals with ALS would respond to lower levels of RPS25, she said.

"Through genomic analyses, we could see that the ALS-associated repeats were still there; the sequences hadn't changed," Yamada said. "What was changing was the output of the ribosome; the repeats weren't being made into toxic proteins nearly as often."

Slashing a part of the cell's protein-making machine might sound risky, but it turns out a defunct RPS25 gene doesn't spoil normal protein production. Yet the researchers also showed that an inactive RPS25 gene affects more than just the ALS repeats; the dysfunctional gene similarly stunted erroneous protein production in cellular models of Huntington's disease and spinocerebellar ataxia, two neurodegenerative illnesses that have hallmark protein aggregates similar to ALS.

Moving toward more complexity

Finally, the researchers turned to fruit fly models of ALS to investigate how depleting RPS25 affected the insect overall. Not only did they see a similar decrease in toxic protein levels, they also saw an increased life span in the flies that lacked fully functional RPS25. Flies that harbored both the ALS mutation and a working RPS25 gene died by day 29, on average, while those that had the ALS mutation and lower amounts of RPS25 lived on average for 38 days. A healthy fruit fly lives about 50 days on average.

The findings are intriguing, Yamada said, but before the scientists can begin to pursue RPS25 as a drug target, the team has a couple boxes to tick off. The team now is investigating how a more complex animal model -- like a mouse -- would fair without RPS25.

"With the fruit flies, we tampered with the gene; we didn't remove it completely," Yamada said. "Whether an animal can survive without the gene entirely is a big part of our next step."

Furthermore, Yamada said, she and Gitler are still after a clearer picture of RAN translation in humans, overall. "Does it only occur under neurogenerative conditions? Or is there a broader role for it in healthy individuals?" she said. "We don't know the answer to those questions yet, and it will be crucial to figure out before pursuing RPS25 as a therapeutic target."

Changing your identity to protect others might sound like something reserved for comic book vigilantes, but a study led by researchers at the Stanford University School of Medicine has found a select group of cells in artery walls do just that.

For these cells, the identity shift happens in a disease called atherosclerosis, which occurs when arteries get clogged by plaque, a buildup of fats, cholesterol and molecular particulate.

"We know that things like poor diet and lack of exercise contribute to atherosclerosis," said Thomas Quertermous, MD, professor of cardiovascular medicine at Stanford. "But molecularly speaking, researchers still don't know how the disease progresses or, conversely, is hindered." This new work, he said, takes a big step toward addressing that question.

Plaque grows within the layers of tissue that form the artery, as opposed to inside the tube itself, causing the blood conduit to narrow. Too much plaque tears open the tissue, allowing the built-up gunk to flood the interior of the tube. That leads to a clot, which can cause artery blockage and often a heart attack.

In people with atherosclerosis, cells that make up the artery wall transform and invade the area containing the plaque, or lesion, and form something called a fibrous cap, which acts kind of like a lid to prevent the plaque from bursting into the artery. Now, Quertermous and his colleagues have characterized the identity of these transformed cells, giving key insights into something called plaque stability, which determines the likelihood of a plaque bursting. The more robust the fibrous cap, the more stable the plaque and the less likely it is to rupture.

The team has also pinpointed a gene that seems to be behind the cells' transformation. What's more, when they looked at populationwide genomic data, they saw that individuals who had more activity in this particular gene were at a decreased risk for heart attack.

"Logically, it makes sense -- the more cells that help form the fibrous cap, the stronger the protection against plaque rupture and therefore the less risk of a heart attack," said Quertermous, who is the William G. Irwin Professor in Cardiovascular Medicine.

A paper describing the details of the study will be published July 29 in Nature Medicine. Quertermous and Juyong Kim, MD, instructor of medicine, are the senior authors. The lead author is Robert Wirka, MD, instructor of cardiovascular medicine.

Smooth muscle cells to the rescue

Under healthy conditions, the smooth muscle cells that make up the wall of arteries control the vessel's dilation, expanding and contracting to regulate blood flow and blood pressure. But when plaque in the artery starts to build, smooth muscle cells begin to shift.

The cells actually move toward the plaque lesion, Wirka said. The genes that make the smooth muscle cells begin to shut off and, in their place, new genes turn on. Then, like Clark Kent to Superman, the smooth muscle cells ditch their everyday identity for a heroic version of themselves -- the fibromyocyte, similar to a fibroblast, a cell type known for its role in connective tissue and collagen production. The fibromyocytes then form a protective cap over the cholesterol, fat and molecular debris that compose arterial plaque.

"It's kind of like a scab over a wound," Quertermous said. "Only in this case, the scab also keeps the plaque stable."

Researchers have known that smooth muscle cells reinvent themselves during atherosclerosis, but it wasn't clear exactly what their new identity was. Scientists thought these cells could have a beneficial role, but also suspected they could transform into dysfunctional immune cells that promote inflammation and worsen the condition.

To figure out the smooth muscle cells' intentions, Wirka, Quertermous and their colleagues used an experimental technique in mice called lineage tracing, which allowed the scientists to track the whereabouts of specific cells and cells derived from those cells. The group labeled arterial smooth muscle cells in the mice with a special chemical that turns the cells red under a microscope. Then, after inducing a mouse version of atherosclerosis, they checked the arteries for signs of smooth muscle cell movement. They observed that some of the red-labeled smooth muscle cells had moved into the plaque from their original homes in the artery.

New place, new name

Wirka and Quertermous then profiled all the cells in the artery, analyzed the collection of cells -- immune, smooth muscle, fibromyocyte and more -- and ran gene expression analyses to see which genes were "on" in each individual cell. According to the gene expression analysis, the red-labeled smooth muscle cells that migrated to the plaque were sporting a new look.

"These cells exhibited a sort of swap: Patterns of gene activity that track with smooth muscle cells decreased, and activity of genes that give rise to fibromyocytes increased," Quertermous said. "The data allowed us to, beyond a shadow of a doubt, characterize these particular cells in the plaque as smooth muscle cells that have turned into fibromyocytes." Remarkably, Wirka said, the researchers found no evidence that smooth muscle cells transformed into plaque-destabilizing immune cells, resolving a long-standing question in the field.

Next, Quertermous and Wirka used a form of computer modeling to bridge mouse biology to humans. They took tissue samples from human patients with atherosclerosis who'd received heart transplants. The scientists analyzed cells from the human arteries with the same single-cell gene expression method used in the mouse tissue.

With data from both human and mouse atherosclerotic tissue, the computer model accurately identified cell types, regardless of species. Importantly, the researchers found the same phenomenon occurring in the human arteries: Smooth muscle cells were also transforming into fibromyocytes during human disease.

The gene behind the transition

Quertermous and Wirka went even one step further, identifying the gene that seems to drive the transition from smooth muscle cell to fibromyocyte during atherosclerosis. In Quertermous' earlier work, he identified one particular gene, TCF21, that was associated with a person's risk for coronary artery disease.

"It's been my theory all along that TCF21 gets reactivated in the vessel wall and is a key contributor to this cell type transition," Quertermous said.

So he tested that theory in a mouse model of atherosclerosis, disabling the TCF21 gene to see if it exacerbated the disease. He and Wirka saw that mice without TCF21 formed fewer fibromyocytes overall, fewer fibromyocyte cells in the plaque and a less-sturdy fibrous cap.

Quertermous and Wirka said that TCF21 could likely help guide them toward a new therapy for coronary artery disease. But before taking steps in that direction, there's still more to understand about TCF21 and how it mediates this transformation at the molecular level, they said. "Now we have good evidence that the ability for smooth muscle cells to undergo this transformation to fibromyocytes is important to protect against clinically significant coronary disease, but the timing and extent of this transformation is likely also important," Wirka said.

DURHAM, NC -- Scientists at Duke University have identified one kind of lung cell that can hustle to repair its damaged DNA and survive an attack of the influenza A virus while other kinds of cells around it die in droves.

The finding reveals more about the battle between cells and viruses at the smallest level, and also may provide some important clues for respiratory conditions such as chronic obstructive pulmonary disease and asthma.

The resilient cell is called a club cell and it's found in the narrowest airways just above the alveoli of the lungs where gases are exchanged in the blood, said Nicholas Heaton, an assistant professor of molecular genetics and microbiology in the Duke School of Medicine. The cell's normal function is to produce surfactants and secrete various other proteins that coat the lining of the lungs. Their functions during a viral infection however, have remained incompletely understood.

Heaton and his team had found in 2014 that club cells could survive a flu infection that would kill most cells. In a 2016 study, they watched club cells crank up their protein-making machinery when under a viral assault and signal the immune system to produce high levels of pro-inflammatory molecules called cytokines.

The net result of club cell survival would be that the lungs remain somewhat hostile to new viruses even after an infection has cleared, Heaton said.

As evidence of that, he points to an intriguing clue from the 2009 influenza pandemic: The flu virus that year was actively replicating in the summer months, not its usual fall and winter months. That year another RNA-based seasonal virus, the respiratory syncytial virus (RSV), was unable to infect people at the same time that it normally would, as if the population were better able to resist it.

"It suggests that influenza makes some sort of changes that make you better able to resist another respiratory infection," Heaton said. And the club cells were probably players in this.

"We knew from previous work that club cells could survive, but we had no idea how," Heaton said.

In the latest work, appearing July 29 in Nature Microbiology, Heaton's lab, along with Sara Cherry, a colleague at the University of Pennsylvania, sorted through all of the club cell's viral response pathways during infection. They found that the club cells were ramping up DNA mismatch repair in response to infection.

An invading virus's weapon of choice is reactive oxygen, which it uses to damage any sections of DNA that are open and active within the host cell. Normally, that damage accumulates to the point that the cell can't express the genes it needs to fight off the virus, whereupon it dies.

But the club cell somehow redoubles its efforts to repair DNA damage and makes it through the infection.

To confirm that was the case, the researchers created an engineered virus that carried the necessary RNA to truly clobber all the DNA repair machinery in cultured human club cells, whereupon the club cells died from flu just like other respiratory cells.

Having patched their damaged DNA, and survived the influenza infection, club cells continue their work of producing surfactants and chemicals that encourage inflammation.

"If another virus comes in, the environment it normally comes into is pretty antiviral," Heaton said, which might explain the mystery of the missing respiratory syncytial virus in 2009.

But the survival of club cells is a two-edged sword, Heaton said. While a proinflammatory environment helps control virus levels, it's actually the over-activity of inflammation that can kill influenza patients, often after they've cleared the flu virus. The club cells that survive and stay active might actually contribute to this.

"Now we have a population of cells we know are going to be hyperinflammatory on the back side of an infection," Heaton said. "When we deplete club cells, there's less inflammation," which might be an important insight to addressing chronic obstructive pulmonary disease or asthma, Heaton said.

This research was supported by the National Institutes of Health, the Burroughs Wellcome Fund and Duke University. Duke has filed a provisional patent application for targeting DNA mismatch repair as a way to grow influenza vaccine strains in the lab.

A collection of new studies in The Journals of Gerontology, Series A: Biological Sciences and Medical Sciences further quantifies how blueberry consumption can contribute to healthy aging.

“Since the 1990s, research on the health benefits of blueberries has grown exponentially,” wrote guest editor Donald K. Ingram, PhD, FGSA, in an opening editorial. “Studies have documented that this fruit ranks highest in antioxidant activity compared to many other popular fruits. Moreover, other mechanisms for the health benefits of blueberries, such as their anti-inflammatory properties, have been identified.”

Ingram’s editorial is followed by four articles in a special section of the journal’s Biological Sciences section. One of the studies found that consuming 200 grams of blueberries (about one cup) daily can improve blood vessel function and decrease systolic blood pressure. As the cause, the authors cited anthocyanins, which are phytochemicals that give blueberries their dark color.

Other studies document the cognitive benefits of eating blueberries. One tied the fruit’s high polyphenol count to improved performance on memory tests by a group of older adults. Likewise, another journal article provides a review of several clinical studies focusing on benefits of blueberry supplementation — with a focus on specific memory effects in children as well as older adults with mild cognitive impairment.

The journal collection also includes a rodent study, which presents data on the improved memory performance of blueberry-supplemented aged rats compared to rats on a control diet.

The articles presented in this special collection emerged from a symposium titled “Blue versus Gray: Potential Health Benefits of Blueberries for Successful Aging,” held at the World Congress of Gerontology and Geriatrics in July 2017.

Researchers at North Carolina State University have developed portable technology that allows farmers to identify plant diseases in the field. The handheld device, which is plugged into a smartphone, works by sampling the airborne volatile organic compounds (VOCs) that plants release through their leaves.

"All plants release VOCs as they 'breathe,' but the type and concentration of those VOCs changes when a plant is diseased," says Qingshan Wei, an assistant professor of chemical and biomolecular engineering and corresponding author of a paper on the work. "Each disease has its own signature profile of VOCs. So, by measuring the type and concentration of VOCs being released by the plant, you can determine whether a plant is diseased and - if it is diseased - which disease it has.

"Our contribution here is the creation of a device that can be plugged into a smartphone and used to make those VOC measurements quickly in the field," says Wei, who is also a faculty member in NC State's Emerging Plant Disease and Global Food Security cluster.

Current disease identification techniques rely on molecular assays, which take hours to perform and - most importantly - have to be done in a lab. Getting a sample to the lab, where the sample may have to wait to be tested, can delay disease identification by days or weeks.

"Our technology will help farmers identify diseases more quickly, so they can limit the spread of the disease and related crop damage," says Jean Ristaino, William Neal Reynolds Distinguished Professor of Plant Pathology at NC State, co-author of the paper and director of the cluster. "We are now ready to scale up the technology."

Here's how the technology works. If a farmer suspects that a plant may be diseased, he or she can take a leaf from the relevant plant and place it in a test tube. The test tube is then capped for at least 15 minutes to allow the relevant VOCs to accumulate. After this incubation period, the cap is removed and the farmer uses a narrow, plastic tube to pump the VOC-laden air into a "reader" device connected to a smartphone.

The air is pumped into a chamber in the reader that contains a paper strip. The paper is embedded with an array of chemical reagents that change color when they come into contact with a specific chemical group. By evaluating the resulting color pattern on the strip, users can determine the nature of any plant disease that may be affecting the plant.

"For this technology to work, we had to develop reagents that could be embedded in the paper strips," says Zheng Li, a postdoctoral researcher at NC State and first author of the paper. "About half of the reagents were off-the-shelf organic dyes, but the other half were gold nanoparticles that we functionalized to respond to specific chemical groups. These functionalized nanoparticles allow us to be more precise in detecting various types of VOCs."

"We also had to design and build the reader device, since there is nothing like it on the market," says Wei.

In proof-of-concept testing, the researchers demonstrated the device's ability to detect and classify 10 plant VOCs down to the parts-per-million level. They were able to detect the late blight pathogen that caused the Irish famine two days after tomato plants were inoculated with the pathogen. Researchers could also distinguish tomato late blight from two other important fungal pathogens that produce similar symptoms on tomato leaves. In addition, the researchers showed they could detect the pathogen Phytophthora infestans in tomato leaves with greater than 95% accuracy.

"We've shown that the technology works," Wei says. "There are two areas where we could make it even better. First, we would like to automate the pattern analysis using software for the smartphone, which would make it easier for farmers to make disease determinations.

"Second, we envision the development of customized reader strips that are designed to measure the VOCs associated with other diseases specific to a given crop. Different crops in different regions face different threats, and we could develop paper strips that are tailored to address those specific concerns.

"This kind of innovation is an integral part of the goals of the NC State Plant Sciences Initiative, which aims to develop new technologies that will improve food production through interdisciplinary science," Wei says.

A study based on the Million Veteran Program of the U.S. Department of Veterans Affairs has identified multiple locations in the human genome related to the risk of re-experiencing traumatic memories, the most distinctive symptom of posttraumatic stress disorder.

Researchers from the VA Connecticut Healthcare System, Yale University School of Medicine, the VA San Diego Healthcare System, and the University of California San Diego collaborated with colleagues on this large genome-wide association study of more than 165,000 veterans.

In addition to providing valuable information on genetic factors that may put people at risk for PTSD, the study also demonstrates "the immediate utility of the MVP sample for disorders prevalent in U.S. veterans," say the researchers.

The results appear online July 29, 2019, in the journal Nature Neuroscience.

PTSD is usually considered to have three main clusters of symptoms: re-experiencing, avoidance, and hyperarousal. Avoidance and hyperarousal are common to other anxiety conditions as well, but re-experiencing is largely unique to PTSD. Re-experiencing refers to intrusive thoughts, nightmares, and flashbacks of the traumatic event.

Using the vast genetic and health record data available through MVP, the research team set out to identify gene variants that increase the likelihood of PTSD re-experiencing. This study was considerably more powerful than previous PTSD genome-wide association studies (studies that look at the genomes of a large group of people for connections between shared gene variations and medical conditions or other traits) because of a larger sample size.

The researchers compared the genomes of 146,660 white veterans and 19,983 black veterans who had volunteered for MVP.

The study revealed eight separate regions in the genome associated with re-experiencing symptoms among the white veterans. It did not show any significant regions for black veterans, considered separately as a group, because there were far fewer black study participants available, making it harder to draw conclusions. The association between PTSD re-experiencing and common variants in three of these genome regions were highly significant: gene CAMKV, a region near genes KANSL1 and CRHR1, and gene TCF4.

Key results were replicated using the UK Biobank sample, which has about 500,000 participants.

The results also showed genetic overlap between PTSD and many other psychiatric, behavioral, and medical conditions. Two genes previously associated with schizophrenia and bipolar disorder were found to be linked to re-experiencing in PTSD. This could mean that the hallucinations experienced in schizophrenia may share common biochemical pathways with the nightmares and flashbacks of people with PTSD, say the researchers.

The study also revealed that re-experiencing shares genetic risk factors with hypertension. Previous studies found that PTSD and hypertension often occur together. This result suggests that the link could be at the genetic level. The researchers explain that the finding could lead to new drug treatments based on patients' genes. It is possible that hypertension drugs that affect these same genes could be effective for treating PTSD.

The study also adds evidence to a theory of how PTSD develops. A variant located at the gene CRHR1 was linked to PTSD re-experiencing. This gene is involved with the body's stress response. In past studies, biological evidence has linked processes involving CRHR1 to PTSD. The new results provide additional strong evidence in support of the theory that CRHR1 and other genes related to the body's steroid-hormone stress response are linked to PTSD risk.

All together, the results "provide new insights into the biology of PTSD," say the researchers. They have implications for understanding PTSD risk factors, as well as identifying new drug targets.