Culture

WASHINGTON - Headline issues, from immigration to sexual assault, are causing significant stress among members of Generation Z - those between ages 15 and 21 - with mass shootings topping the list of stressful current events, according to the American Psychological Association's report Stress in America™: Generation Z released today.

Despite these concerns, Gen Z adults who are 18 to 21 years old are the generation least likely to vote in the 2018 midterm elections, the report found.

Specifically, 75 percent of Gen Z members said that mass shootings are a significant source of stress, according to the survey, which was conducted online by The Harris Poll on behalf of APA in July and August 2018 among 3,458 adults and 300 15- to17-year-olds.

Gen Z members are also more stressed than adults overall about other issues in the news, such as the separation and deportation of immigrant and migrant families (57 percent of Gen Z vs. 45 percent of all adults reported the issue is a significant source of stress) and sexual harassment and assault reports (53 percent vs. 39 percent). Despite this, just more than half of Gen Z adults, between ages 18 and 21, (54 percent) said they intend to vote in the U.S. midterm elections, compared with 70 percent of adults overall.

America's youngest generation is also significantly more likely (27 percent) than other generations, including Millennials (15 percent) and Gen Xers (13 percent), to report their mental health as fair or poor, the survey found. They are also more likely (37 percent), along with Millennials (35 percent), to report they have received treatment or therapy from a mental health professional, compared with 26 percent of Gen Xers, 22 percent of baby boomers and 15 percent of older adults.

"Current events are clearly stressful for everyone in the country, but young people are really feeling the impact of issues in the news, particularly those issues that may feel beyond their control," said Arthur C. Evans Jr., PhD, APA's chief executive officer. "At the same time, the high percentage of Gen Z reporting fair or poor mental health could be an indicator that they are more aware of and accepting of mental health issues. Their openness to mental health topics represents an opportunity to start discussions about managing their stress, no matter the cause."

More than nine in 10 Gen Z adults (91 percent) said they have experienced at least one physical or emotional symptom because of stress, such as feeling depressed or sad (58 percent) or lacking interest, motivation or energy (55 percent). Only half of all Gen Zs feel like they do enough to manage their stress.

Money and work continued to top the list of significant stressors tracked annually by the Stress in America survey for adults overall. Nearly two-thirds of adults (64 percent) reported money and work each to be a stressor. A new question added this year asking about additional sources of stress revealed that for more than three in 10 Gen Zs, personal debt (33 percent) and housing instability (31 percent) were a significant source of stress, while nearly three in 10 (28 percent) cited hunger or getting enough to eat.

One notable finding was a potential increased tolerance for stress across all generations. The average perceived healthy level of stress increased significantly over the past year, from 3.7 in 2017 to 3.9 in 2018 (on a scale from 1 to 10, where "1" is "little or no stress" and "10" is "a great deal of stress").

Americans Increasingly Stressed about the Future of the Nation

More than six in 10 Americans (62 percent) reported that the current political climate is a significant stressor, and more than two-thirds (69 percent) reported that the nation's future causes them stress. This was a significant increase from those who said the same in 2017 (63 percent). Most Americans (61 percent) also disagreed that the country is on a path to being stronger than ever. Because of their concern for the state of the nation, nearly half of Americans (45 percent) said they feel more compelled to volunteer or support causes they value.

Another key finding was that nearly one-quarter (24 percent) of adults identified discrimination as a significant source of stress, the highest percentage since this was first included in the survey in 2015. In 2018, black adults (46 percent) and Hispanic adults (36 percent) reported discrimination as a significant source of stress, compared with 14 percent of white adults.

Research by the University of Liverpool could help scientists unlock the full potential of new clean energy technologies.

Finding sustainable ways to replace fossil fuels is a key priority for researchers across the globe. Carbon dioxide (CO2) is a hugely abundant waste product that can be converted into energy-rich by-products, such as carbon monoxide. However, this process needs to be made far more efficient for it to work on a global, industrial scale.

Electrocatalysts have shown promise as a potential way to achieve this required efficiency 'step-change' in CO2 reduction, but the mechanisms by which they operate are often unknown making it hard for researchers to design new ones in a rational manner.

New research published in Nature Catalysis by researchers at the University's Department of Chemistry, in collaboration with Beijing Computational Science Research Center and STFC Rutherford Appleton Laboratory, demonstrates a laser-based spectroscopy technique that can be used to study the electrochemical reduction of CO2 in-situ and provide much-needed insights into these complex chemical pathways.

The researchers used a technique called Vibrational Sum-Frequency Generation (VSFG) spectroscopy coupled with electrochemical experiments to explore the chemistry of a particular catalyst called Mn(bpy)(CO)3Br, which is one of the most promising and intensely studied CO2 reduction electrocatalysts.

Using VSFG the researchers were able to observe key intermediates that are only present at an electrode surface for a very short time - something that has not been achieved in previous experimental studies.

At Liverpool, the work was carried out by the Cowan Group, a team of researchers who study and develop new catalytic systems for the sustainable production of fuels.

Dr Gaia Neri, who was part of the Liverpool team, said: "A huge challenge in studying electrocatalysts in situ is having to discriminate between the single layer of short-lived intermediate molecules at the electrode surface and the surrounding 'noise' from inactive molecules in the solution.

"We've shown that VSFG makes it possible to follow the behaviour of even very short-lived species in the catalytic cycle. This is exciting as it provides researchers with new opportunities to better understand how electrocatalysts operate, which is an important next step towards commercialising the process of electrochemical CO2 conversation into clean fuel technologies."

Following on from this research, the team is now working to further improve the sensitivity of the technique and is developing a new detection system that will allow for a better signal-to-noise ratio.

The future looks challenging for plants. Climate change is forecast to bring widespread drought to parts of the planet already struggling with dry conditions. To mitigate the potentially devastating effects to agriculture, researchers are seeking strategies to help plants withstand extreme environmental hazards including drought and salt stress, a problem exacerbated when irrigated water passes through the soil, depositing salts which can then absorbed by plant roots, lowering their overall productivity.

One tack is to look at ways that plants have naturally evolved to cope with stresses such as too much salt. In a new study out in Cell Reports, researchers led by University of Pennsylvania biologist Brian D. Gregory and graduate student Stephen J. Anderson have identified a mechanism that could potentially be manipulated to develop more salt-tolerant crops.

Their work shows that a tiny tag on RNA molecules--the transcripts that are translated to produce proteins--serves to stabilize and protect these strands of genetic material. When plants are exposed to high-salt conditions, the RNA mark, known as N6-methyladenosine, or m6A, prevents the breakdown of transcripts encoding proteins that help plants more effectively deal with the challenging conditions.

"This is how we're going to help farmers," says Gregory, an associate professor in Penn's Department of Biology in the School of Arts and Sciences and the senior author on the paper. "We need to identify ways that we can make more salt-resistant and drought-resistant plants, and manipulating this pathway might be one way to do it."

For an organism to produce any protein, it must first possess the corresponding strand of messenger RNA (mRNA). But not all mRNAs are turned into proteins; some are degraded before they reach that stage. In recent years, both mammalian and plant biologists have been paying attention to the m6A mark as a player in the process by which mRNAs are targeted to either keep around or destroy.

"There's been an explosion of interest in this mark," Gregory says. "It's been found to be the most abundant internal modification in mRNA."

In mammals, the bulk of research points to the mark labeling mRNA for destruction. And, while some studies have suggested it may function the same way in plants, Gregory, Anderson, and colleagues wanted to get a more global view.

Analyzing leaves from mature Arabidopsis, the researchers globally identified m6A in normal plants as well as in those in which the enzyme that adds m6A had been eliminated, thus experimentally depleting them of the mark.

They found that transcripts that were abundant when marked by m6A in the normal plants were much lower in the m6A-depleted mutant plants, a sign that the mark was acting in a protective capacity to stabilize the transcripts.

Closely comparing the normal and the mutant plants, the team found that m6A, when present, protected the transcripts by preventing an enzyme from degrading them. When this mark was missing, the transcripts were cleaved and subsequently degraded.

"It was kind of serendipitous," says Anderson, "but it turned out that this destabilization was occurring right next to where these marks should have been but weren't in the experimental group of plants."

The next step was to ask why the plants might have evolved this mechanism in the first place. The researchers had hints that m6A labeling might be involved in stress response, judging from the affected genes between the normal and mutant plants. But, to put it to the test, they grew plants in a high-salt soil and repeated their experiments.

The salt treatment, they discovered, caused plants to affix more m6A marks on mRNA transcripts associated with responding to salt stress, as well as drought stress. In other words, the plants were girding themselves to deal with an environmental challenge.

"This gives plants a dynamic and really powerful mechanism to regulate stress response," Gregory says. "You can move this mark onto transcripts you want to keep around."

"There's also evidence," Anderson says, "that plants may be able to actively remove the mark from transcripts they don't need. We're still investigating that mechanism."

"This work," says Karen Cone at the National Science Foundation, which funded the research, "provides exciting new understanding of how genomic information interacts with signals from the environment to produce beneficial outcomes for the organism. The results promise to open the door to future discoveries of how organisms use RNA-based mechanisms to maintain the robustness and adaptability they need to survive in the face of changing environments, a finding that is directly relevant to one of NSF's 10 Big Ideas, Understanding the Rules of Life: Predicting Phenotype."

In additional follow-up experiments, Gregory's lab will examine this mark's involvement in other stressful situations for plants, like when they are subject to damage from organisms like bacteria or fungi. Gregory and colleagues also plan to pursue experiments in plant species important to agriculture, such as soy beans.

Further study may also help them zero in on the mechanism by which plants attach this mark to transcripts, helping in the development of strategies for engineering plants that may better resist the challenging conditions posed by drought.

A genetic defect tied to a variety of neurodegenerative diseases and mental illnesses changes how cells starved of sugar metabolize fatty compounds known as lipids, a new study led by researchers from the Johns Hopkins Bloomberg School of Public Health shows. The finding could lead to new targets to treat these diseases, which currently have no cure or fully effective treatments.

Taken together, these results suggest that the genetic defect, mutations in a gene called C9orf72, lead to greater amounts of a protein that causes cells to overproduce lipids and an enzyme called NOX2. The enzyme NOX2, which is known to cause oxidative stress that can damage cells, has also been shown to be elevated in patients with amyotrophic lateral sclerosis (ALS) and frontotemporal dementia.

The findings were published online Oct. 26 in the journal Genes & Development.

"Cells with this mutation act as if they're chronically under stress, which could underlie the pathology of diseases associated with this defect," says Jiou Wang, MD, PhD, an associate professor in the Bloomberg School's Department of Biochemistry and Molecular Biology. "Our study raises the question of whether we should be looking at problems with lipid metabolism as a potential cause for these diseases."

Researchers identified the mutation in the C9orf72 gene several years ago, and it has since been associated with ALS, frontotemporal dementia, Alzheimer's disease and bipolar disorder, and other neurologic diseases. Although researchers have known that this mutation decreases the amount of the protein coded by the C9orf72 gene in cells, it was unknown exactly what this C9orf72-coded protein does.

To learn its function, the researchers created mouse cells in which C9orf72 was effectively removed, preventing the production of its protein in order to study what happens in cells naturally carrying the gene's mutated form. They then compared these cells to those with the gene, looking broadly at the levels of all proteins produced in both types of cells. They studied these protein levels both under normal conditions as well as when the cells lived in environments devoid of the sugar known as glucose, an important cellular energy source. Previous studies have hinted, Wang explains, that C9orf72 might play a role in how cells protect themselves from nutrient starvation stress.

When healthy cells are deprived of glucose, Wang says, they tend to make and store more lipid droplets. However, the researchers' protein level analysis showed that when deprived of glucose, the cells lacking the C9orf72 protein produced significantly more lipid metabolism-related proteins compared to cells with this gene. When the researchers compared the number of lipid droplets between the two types of cells in glucose-devoid conditions, the cells lacking C9orf72 protein held significantly more. They also had more free fatty acids, the individual components that come together to form these lipid droplets.

To better understand why lipids increased in cells without the C9orf72 gene, the researchers looked at the two different pathways that cells use to create lipid droplets: either creating them from scratch, a process called de novo lipid biogenesis, or by digesting other components of the cell to make lipids, a process called autophagy. They found higher amounts of the proteins associated with both routes in cells without the C9orf72 gene, suggesting that each lipid-producing pathway was abnormally regulated.

Digging even deeper to find out how cells without C9orf72 boosted both pathways, they did another protein analysis to find which proteins are associated with C9orf72. Their search led them to CARM1, a protein known to broadly affect which genes produce proteins, and how much. It turns out that C9orf72 is important for a previously unknown pathway to degrade the CARM1 protein by the lysosome, the cell's digestive organelle. Further investigation showed that in C9orf72 knockout cells, CARM1 levels increase, leading to greater expression of genes related to lipid production.

To see if these results translate to what happens in patients with C9orf72 mutations, the researchers studied cells and tissues from patients with ALS and frontotemporal dementia. Starving these samples of glucose led to the same results they saw in the mouse-derived cells: increased lipid levels caused by dysregulation of both lipid-producing pathways, along with increased levels of CARM1 and NOX2.

Taken together, Wang says, these results suggest that mutations in C9orf72 lead to greater amounts of CARM1, which causes cells to overproduce lipids and NOX2 in response to glucose starvation.

"As we learn more about this newly discovered biological pathway," says Wang, "it could lead to new therapeutic interventions that protect cells that carry this mutation from harm."

In the United States, suicide is twice as common as homicide -- and more often involves firearms -- but public perception is just the opposite.

News reports, movies and TV shows may contribute to the perception of a high risk of firearm homicide, authors of a new study say, leaving a substantial gap between ideas and reality and potentially leading to further danger.

Now, first-of-its kind research, led by the University of Washington, Northeastern University and Harvard University, delves into public perceptions of gun violence and the leading causes of death in the U.S. The study, published Tuesday in the Annals of Internal Medicine, seeks to facilitate national public discussions about firearm ownership and storage.

"This research indicates that in the scope of violent death, the majority of U.S. adults don't know how people are dying," said Erin Morgan, lead author and doctoral student in the Department of Epidemiology at the UW School of Public Health. "Knowing that the presence of a firearm increases the risk for suicide, and that firearm suicide is substantially more common than firearm homicide, may lead people to think twice about whether or not firearm ownership and their storage practices are really the safest options for them and their household."

To analyze national public perceptions, researchers used data from the 2015 National Firearms Survey, a web-based survey of nearly 4,000 U.S. adults. In that survey, individuals were asked to rank the relative causes of violent death in their state over the past year. The data were then compared to each state's official death count. The results indicated that although suicide was more common than homicide in all 50 states, the majority of respondents did not identify it as such.

"The relative frequencies that respondents reported didn't match up with the state's data when we compared them to vital statistics," Morgan said. "The inconsistency between the true causes and what the public perceives to be frequent causes of death indicates a gap in knowledge and a place where additional education can be helpful."

Researchers say education about the actual risks is critical. If people believe homicide is the top risk, for example, they might purchase a gun to protect themselves. And without an understanding of the high risk of suicide, people may be less inclined to store firearms safely.

To Morgan and her colleagues, this education on firearm risks needs to extend to the media and entertainment industries.

"By having mass media and other communication mechanisms enable further discussions of suicide, we, as a society, can have a more informed conversation about suicide prevention," Morgan said.

Moving forward, the researchers are interested in learning more about how people form their perceptions of gun violence, in order to begin shifting those beliefs.

"We know that this is a mixture of mass and individual communication, but what really leads people to draw the conclusions that they do?" Morgan said. "If people think that the rate of homicide is really high because that's what is shown on the news and on fictional TV shows, then these are opportunities to start to portray a more realistic picture of what's happening."

Researchers studying the sharp decline between 1980 and 2010 in documented landings of the four most commercially-important bivalve mollusks - eastern oysters, northern quahogs, softshell clams and northern bay scallops - have identified the causes.

Warming ocean temperatures associated with a positive shift in the North Atlantic Oscillation (NAO), which led to habitat degradation including increased predation, are the key reasons for the decline of these four species in estuaries and bays from Maine to North Carolina.

The NAO is an irregular fluctuation of atmospheric pressure over the North Atlantic Ocean that impacts both weather and climate, especially in the winter and early spring in eastern North America and Europe. Shifts in the NAO affect the timing of species' reproduction, growth and availability of phytoplankton for food, and predator-prey relationships, all of which contribute to species abundance. The findings appear in Marine Fisheries Review.

"In the past, declines in bivalve mollusks have often been attributed to overfishing," said Clyde Mackenzie, a shellfish researcher at NOAA Fisheries' James J. Howard Marine Sciences Laboratory in Sandy Hook, NJ and lead author of the study. "We tried to understand the true causes of the decline, and after a lot of research and interviews with shellfishermen, shellfish constables, and others, we suggest that habitat degradation from a variety of environmental factors, not overfishing, is the primary reason."

Northern Quahogs, American Lobsters Exceptions

Mackenzie and co-author Mitchell Tarnowski, a shellfish biologist with the Maryland Department of Natural Resources, provide details on the declines of these four species. They also note the related decline by an average of 89 percent in the numbers of shellfishermen who harvested the mollusks. The landings declines between 1980 and 2010 are in contrast to much higher and consistent shellfish landings between 1950 and 1980.

Exceptions to these declines have been a sharp increase in the landings of northern quahogs in Connecticut and American lobsters in Maine. Landings of American lobsters from southern Massachusetts to New Jersey, however, have fallen sharply as water temperatures in those areas have risen.

"A major change to the bivalve habitats occurred when the North Atlantic Oscillation (NAO) index switched from negative during about 1950 to 1980, when winter temperatures were relatively cool, to positive, resulting in warmer winter temperatures from about 1982 until about 2003," Mackenzie said. "We suggest that this climate shift affected the bivalves and their associated biota enough to cause the declines."

Factors Affecting Decline

Research from extensive habitat studies in Narragansett Bay, RI and in the Netherlands, where environments including salinities are very similar to the northeastern U.S, show that body weights of the bivalves, their nutrition, timing of spawning, and mortalities from predation were sufficient to force the decline. Other factors likely affecting the decline were poor water quality, loss of eelgrass in some locations for larvae to attach to and grow, and not enough food available for adult shellfish and their larvae.

"In the northeast U.S., annual recruitments of juvenile bivalves can vary by two or three orders of magnitude," said Mackenzie, who has been studying bay scallop beds on Martha's Vineyard with local shellfish constables and fishermen monthly during warm seasons for several years. In late spring-early summer of 2018, a cool spell combined with extremely cloudy weather may have interrupted scallop spawning, leading to what looks like poor recruitment this year. Last year, Nantucket and Martha's Vineyard had very good harvests due to large recruitments in 2016.

"The rates of survival and growth to eventual market size for shellfish vary as much as the weather and climate," Mackenzie said.

Oyster Demand Increases

Weak consumer demand for shellfish, particularly oysters, in the 1980s and early 1990s has shifted to fairly strong demand as strict guidelines were put in place by the Interstate Shellfish Sanitation Conference in the late 1990s regarding safe shellfish handling, processing and testing for bacteria and other pathogens. Enforcement by state health officials has been strict. The development of oyster aquaculture and increased marketing of branded oysters in raw bars and restaurants has led to a large rise in oyster consumption in recent years.

Since the late 2000s, the NAO index has generally been fairly neutral, neither very positive nor negative. As a consequence, landings of all four shellfish species have been increasing in some locations. Poor weather for bay scallop recruitment in both 2017 and 2018, however, will likely mean a downturn in landings during the next two seasons.

It may simply be that having a big brain is itself the cause.

That's what doctor and PhD candidate Even Hovig Fyllingen at the Norwegian University of Science and Technology (NTNU) has determined with his research colleagues.

"Aggressive brain cancer is a rare type of cancer, but once you have it, the chance of survival is relatively low," he says.

Lifestyle matters less

For some types of cancer, lifestyle makes a big difference. People who smoke have a greater risk of lung cancer than non-smokers, for example. A person's lifestyle matters less for brain tumor development.

A large brain means more brain cells. And the more cells you have, the more cell divisions that can go wrong and create mutations that lead to cancer.

Big organs, bigger risk

"Several studies have shown that the size of different organs is an important factor in cancer development. For example, women with larger breasts have a greater risk of breast cancer. We wanted to check if this was also the case for brain tumors," says Fyllingen.

To tackle the question, he relied on material from the Nord-Trøndelag Health Study (HUNT). It comprises health data and blood samples that have been collected in multiple waves of data gathering from thousands of Norwegians in the Nord-Trøndelag county region. The purpose of the study is to find out why some individuals become ill while others stay healthy, what affects our health and how our health affects our lives.

Fyllingen used the third version of the survey, called HUNT3, and compared it to St. Olavs Hospital's neurosurgery database. He extracted data on everyone who had been operated on for high-grade gliomas (brain tumors) between 2007 and 2015 and compared their data with healthy controls from the HUNT study.

The researchers used MRI scans to measure the size of the brain. Then 3D models were made from them so that the intracranial brain volume could be measured in millilitres.

Mostly men who get brain tumors

The study also shows that more men than women develop brain tumours.

"Men have a larger brain than women because men's bodies are generally larger. It doesn't mean that men are smarter, but you need to have more brain cells to control a large body. This is also the case with animals. In bigger bodies, organs like the heart, lungs and brain are also bigger," says Fyllingen.

Yet it turns out that women with big brains have a greater risk of developing brain tumors compared to men with big brains.

"Seventy per cent more men than women develop brain tumors, but when we correct for head size, it's no longer beneficial to be female. Women with large brains are particularly susceptible. Why that is I have no idea," says Fyllingen.

New Vanderbilt research finds how long humans and other warm-blooded animals live--and when they reach sexual maturity-- may have more to do with their brain than their body. More specifically, it is not animals with larger bodies or slower metabolic rates that live longer; it is animals with more neurons in the cerebral cortex, whatever the size of the body.

"Whether you're looking at birds or primates or humans, the number of neurons that you find in the cortex of a species predicts around 75 percent of all of the variation in longevity across species," said study author associate professor of psychology and biological sciences Suzana Herculano-Houzel.

Body size and metabolism, in comparison, to usual standards for comparing animals, only predicted between 20-30 percent of longevity depending on species, and left many inconsistencies, like birds that live ten times longer than mammals of same size.

Most importantly, humans were considered to be a "special" evolutionary oddity, with long childhood and postmenopausal periods. But this research, published in the Journal of Comparative Neurology, finds that's not accurate. Humans take just as long to mature as expected of their number of cortical neurons - and live just as long as expected thereafter.

THE STUDY

In the study, Herculano-Houzel examined more than 700 warm-blooded animal species from the AnAge database which collects comprehensive longevity records. She then compared these records with her extensive data on the number of neurons in the brains of different species of animals.

Herculano-Houzel color-coded the data for hundreds of species and found that parrots and songbirds, including corvids, live systematically longer than primates of similar body mass, which in turn live longer than non-primate mammals of similar body mass.

"Likewise, for similar specific basal metabolic rates, parrots and songbirds live longer and take longer to reach sexual maturity than many mammalian species, especially non-primates," said Herculano-Houzel.

She had seen that pattern before: her previous studies determining what brains are made of showed that parrots and songbirds have more cortical neurons than similar-sized primates, which have more cortical neurons than any other mammal of comparable body size.

Her new analysis confirmed her suspicion: that longevity increases uniformly across warm-blooded species together with the absolute number of neurons in the cerebral cortex.

"The more cortical neurons a species has, the longer it lives - doesn't matter if it is a bird, a primate or some other mammal, how large it is, and how fast it burns energy", says Herculano-Houzel.

ARE HUMANS UNIQUE? ASK GRANDMA

Anthropologists and researchers interested in evolution and human behavior have been working under the assumption that one of the ways the human species is unique is that humans have an uncommonly long childhood and adolescent period to allow for learning and social interactions. If larger animals live longer, then gorillas should live longer than humans - but they don't: humans outlive them. One favored hypothesis is that being cared for by grandmothers could have led humans to delayed sexual maturity and increased postmenopausal longevity beyond the expected.

But Herculano-Houzel's new data show that humans are not an exception from other mammalian species. Given the number of neurons in our cortex, humans take as long as they should to reach sexual maturity - and live just as long as expected for their number of neurons. Body size, it turns out, is irrelevant in matters of longevity.

"Now we can say that humans spend just as long in childhood and live exactly as long after reaching maturity as you would expect for the number of neurons in our cerebral cortex," said Herculano-Houzel.

Which is longer, compared to other species - gorillas included -simply because humans have the most neurons in the cerebral cortex.

"It makes sense that the more neurons you have in the cortex, the longer it should take a species to reach that point where it's not only physiologically mature, but also mentally capable of being independent," says Herculano-Houzel. "The delay also gives those species with more cortical neurons more time to learn from experience, as they interact with the environment."

And if longer lives also accompany more cortical neurons, those species will also enjoy a greater overlap between generations, and so more opportunities to pass along what they learned.

"Which means that grandma is still fundamental in the lives of those with plenty of cortical neurons; she's just probably not the reason why our species is long-lived," argues Herculano-Houzel.

FUNCTION OF THE CORTEX

What is the link between having more neurons in the cortex and living longer lives? Herculano-Houzel says that's the new big question researchers need to tackle.

"The data suggest that warm-blooded species accumulate damages at the same rate as they age. But what curtails life are damages to the cerebral cortex, not the rest of the body; the more cortical neurons you have, the longer you will still have enough to keep your body functional", she says.

Contrary to the rest of the body, which gets new cells that replenish old ones, cortical neurons are thought to have to last a lifetime.

While the cortex is usually associated with cognition, Herculano-Houzel believes a much more basic function of the cortex is key to longevity.

"The cortex is the part of your brain that is capable of making our behavior complex and flexible, yes, but that extends well beyond cognition and doing mental math and logic reasoning," said Herculano-Houzel. "The cerebral cortex also gives your body adaptability, as it adjusts and learns how to react to stresses and predict them. That includes keeping your physiological functions running smoothly and making sure your heart rate, your respiratory rate, and your metabolism are on track with what you're doing, with how you feel, and with what you expect to happen next. And that, apparently, is a key factor that impacts longevity," she adds.

BRAIN SOUP

Herculano-Houzel pioneered the method for rapidly and accurately measuring the number of neurons in brains. She creates "brain soup" by taking brain tissue and breaking down the cells, then applying fluorescent tags to the nuclei floating in the "brain soup" and counting them.

In collaboration with Vanderbilt Distinguished Professor of Psychology Jon Kaas, she studied how many neurons compose different primate brains, including great apes. With colleagues in Brazil, she produced the first accurate count of the number of neurons in the human brain--an average 86 billion, which makes it simply an enlarged primate brain.

TAKE CARE OF YOUR BRAIN!

Aging starts once humans and other species reach adolescence, and there's no way to gain back neurons. In fact, research shows humans can lose neurons in the prefrontal cortex. So Herculano-Houzel says taking good care of your mind, and keeping those cortical neurons healthy and busy, is the best bet to live long and well.

ANN ARBOR, Mich. - From games inspired by popular TV shows to digital play labeled as educational, children's apps continue to explode on smartphones and tablets.

But parents may not realize that while their little ones are learning letters and numbers or enjoying virtual adventures, they're also likely being targeted by advertisers.

Ninety-five percent of commonly downloaded apps marketed to or played by children ages 5 and under contain at least one type of advertising, according to a new study led by University of Michigan C.S. Mott Children's Hospital.

Published in the Journal of Developmental & Behavioral Pediatrics, the study reviewed 135 different apps -- and it marks the first effort to examine the prevalence of advertising in children's apps.

Researchers found play was frequently interrupted by pop-up video ads, persuasion by commercial characters to make in-app purchases to enhance the game experience and overt banner ads that could be distracting, misleading and not always age-appropriate.

"With young children now using mobile devices on an average of one hour a day, it's important to understand how this type of commercial exposure may impact children's health and well-being," says senior author Jenny Radesky, M.D., a developmental behavioral expert and pediatrician at Mott.

Radesky notes that her team found high rates of mobile advertising through manipulative and disruptive methods -- with exposure to ads even surpassing time spent playing the game in some cases.

"Our findings show that the early childhood app market is a wild west, with a lot of apps appearing more focused on making money than the child's play experience," she says. "This has important implications for advertising regulation, the ethics of child app design, as well as how parents discern which children's apps are worth downloading."

Ads target youngest players

Researchers detailed experiences with advertisements during gameplay of the most popular children's apps.

Although 100 percent of surveyed free apps contained advertising content (compared to 88 percent of purchased apps), the ads occurred at similar rates in both types of apps categorized as educational.

Ad videos interrupting play were prevalent in more than a third of all analyzed apps and in more than half of free apps. In-app purchases were also present in a third of all apps, and in 41 percent of all free apps.

This discrepancy worries Radesky: "I'm concerned about digital disparities, as children from lower-income families are more likely to play free apps, which are packed with more distracting and persuasive ads."

Some ads were particularly deceptive: Familiar commercial characters would appear on-screen to remind players that paying for certain in-app upgrades and purchases would give them access to more appealing options and make the game more fun.

Overt banner ads covering the sides or top and/or bottom of the screen during gameplay were also present in 17 percent of all apps and 27 percent of free apps. Some banners promoted adult-appropriate apps that required a user to watch the full promo before a box could be closed.

Authors note that prior research has found children ages 8 and younger can't distinguish between media content and advertising -- and that fewer regulations apply to advertising in apps than on television -- which raises further ethical questions around the practice.

"Commercial influences may negatively impact children's play and creativity," Radesky says. "Digital-based advertising is more personalized, on-demand and embedded within interactive mobile devices, and children may think it's just part of the game."

Youths' privacy at risk

Researchers also documented prompts within the apps to share information, most commonly asking players to share their progress or score on social media sites.

However, 17 of the apps reviewed requested phone permission, 11 asked for microphone permission, nine asked for camera permission and six requested location permission.

While some of the permissions were likely requested to allow certain functions during play, authors point out that collecting data on a child's location is a potential violation of the Children's Online Privacy Protection Act. The law, managed by the Federal Trade Commission, was created to protect the privacy of children under 13.

TV advertising regulations also limit commercial breaks during viewing segments, but there are no regulations focused on digital advertising approaches for children.

There is also growing concern among pediatricians and other experts that low-quality content and distracting visual and sound effects in popular apps may not be designed appropriately for children to learn, says Marisa Meyer, the study's lead author.

That prevalence also diminishes the educational quality of apps, she says.

"We know that time on mobile devices is displacing time children used to spend watching TV," says Meyer, research assistant at the U-M Medical School. "Parents may view apps that are marketed as educational as harmless and even beneficial to their child's learning and development."

The findings, Meyer says, suggest the need for heightened scrutiny of apps in the educational category.

"We hope further research will help us better understand the consequences of digital media advertisement, which hasn't caught up with the rapid growth of digital media products catered to children," she says.

Child consumer advocacy groups, led by Campaign for a Commercial Free Childhood, plan to file a complaint with the Federal Trade Commission about the study's findings.

BLOOMINGTON, Ind. -- Scientists at Indiana University found high levels of a previously unsuspected pollutant in homes, in an electronic waste recycling facility and in the natural environment. People are likely to be exposed to this pollutant by breathing contaminated dust or through skin contact.

The chemical, tri(2,4-di-t-butylphenyl) phosphate or TDTBPP, is part of a family of organophosphates that are known to be toxic. However, little information is known about the toxicity of TDTBPP or how it gets into our environment. The chemical may be used as a flame retardant or as a plasticizer in consumer products. It may also be formed as other chemicals degrade. It may even be an impurity in a structurally related compound.

"We found surprisingly high levels of TDTBPP everywhere we looked," said Marta Venier, a scientist at the IU School of Public and Environmental Affairs and the first author of the study. "The fact that this potentially toxic chemical is so abundant, but was previously unknown, is another example of the ineffective management of chemicals in the United States."

Many common commercial chemicals, including TDTBPP, are not subject to regulatory scrutiny under the U.S. Toxic Substances Control Act unless they are used for new purposes, and much of the information about their commercial use is private. Therefore, it is difficult for environmental chemists to track how these pollutants enter the environment and what kind of effects they might cause once they do. Many chemicals go undetected until scientists perform a general environmental scan, like this study conducted by scientists at IU.

The researchers studied dust samples from an e-waste dismantling facility in Ontario, Canada. Chemicals similar to TDTBPP are often used in the production of plastics, wires, printed circuit boards and electronic equipment, making e-waste recycling facilities an important place to search for previously undetected pollutants.

The researchers also studied dust from 20 residential homes in Ontario and analyzed outdoor samples from southwestern Lake Michigan to measure the amounts of TDTBPP in ambient air, water and sediment. They found that levels of TDTBPP were particularly high in house dust.

"Our research is the first step," Venier said. "Now that we know that TDTBPP is prevalent, especially in homes, scientists can flag it for further study and focus on understanding the effects of TDTBPP on people."

The study, "Tri(2,4-di-t-butylphenyl) Phosphate: A Previously Unrecognized, Abundant, Ubiquitous Pollutant in the Built and Natural Environment," will be published Oct. 30 in Environmental Science & Technology. The authors were Venier, William Stubbings, Jiehong Guo, Kevin Romanak and Ronald A. Hites of Indiana University; Liisa Jantunen of Environment and Climate Change Canada; Lisa Melymuk of Masaryk University in the Czech Republic; and Linh V. Nguyen, Victoria Arrandale and Miriam L. Diamond of the University of Toronto.

WASHINGTON (Oct. 29, 2018) -- Accepting an organ that has an increased risk of potentially transmitting disease offers a higher one-year survival rate for candidates on the heart transplant list over waiting for an organ with less risk, according to a study published today in the Journal of the American College of Cardiology. Increased risk donors make up a growing number in the donor pool for organs, offering a potential strategy to reduce waitlist mortality for patients awaiting transplant. For many of these patients, the benefit of proceeding with transplantation sooner outweighs the low risk of disease transmission associated with these donors.

Increased risk donors are defined as organ donors who carry an increased risk for inadvertent disease transmission to the transplant recipient, including HIV, Hepatitis B Virus and Hepatitis C Virus. In 2015, increased risk donors represented 19.5 percent of the donor pool.

"For patients with end-stage heart failure, heart transplantation is not only the gold-standard of care but an increasingly-utilized therapy by clinicians treating these patients," said Michael S. Mulvihill, MD, a surgical research fellow in the division of cardiovascular and thoracic surgery at Duke University. "Through this study we discovered that acceptance of an increased risk donor heart offer has a significant survival benefit that should be part of the shared decision-making process for clinicians and patients."

Researchers performed a retrospective registry analysis to examine the impact of declining an increased risk donor heart for heart transplant candidates compared to candidates who accepted the offer. Using United Network of Organ Sharing data, a total of 2,602 increased risk donor hearts were offered to 10,851 heart transplant candidates from 2007 to 2017. To measure competing outcomes, researchers followed candidates who declined an increased donor risk heart until eventual heart transplant (increased donor risk or non-increased donor risk), death or decompensation precluding heart transplant, or ongoing time on the transplant waitlist. These candidates were compared with candidates who accepted an increased risk donor heart to determine the survival benefit associated with acceptance of the increased risk donor organ.

"It's important to understand that patients who turn down an increased risk donor heart don't immediately get offered another, non-increased risk donor heart," Mulvihill said. "These patients are returned to the waitlist for an uncertain amount of time. We wanted to measure the risks of competing outcomes for these patients compared to patients who accepted the increased risk donor heart."

Of the patients who declined the initial increased risk donor offer, 58 percent underwent a non-increased risk donor heart transplant, 12.4 percent underwent a later increased risk donor heart transplant, 7.9 percent were removed from the waitlist due to death or decompensation, and 21.1 percent were still waiting for a heart transplant one year after the initial offer. Patients who accepted the initial increased risk donor offer had 92.1 percent survival rates after one year compared to 83.1 percent for those who declined. Researchers found this benefit persisted five years post-offer.

"Increased risk donor organs offer an opportunity to decrease waitlist mortality for patients awaiting heart transplant," Mulvihill said. "It's worth making sure candidates, clinicians and listing centers discuss the risks and benefits of increased risk donor offers for these patients."

Limitations include the potential for unmeasured confounders, especially with respect to uncertainty in the reasons for the organ offer decline. Researchers were also unable to assess the rate of disease transmission after transplantation based on available data.

Delivering an effective therapeutic payload to specific target cells with few adverse effects is considered by many to be the holy grail of medical research. A new Tel Aviv University study explores a biological approach to directing nanocarriers loaded with protein "game changers" to specific cells. The groundbreaking method may prove useful in treating myriad malignancies, inflammatory diseases and rare genetic disorders.

Prof. Dan Peer, director of the Laboratory of Precision Nanomedicine at the School of Molecular Cell Biology at TAU's Faculty of Life Sciences, led the research for the new study, which was conducted by TAU graduate student Nuphar Veiga and lab colleagues Meir Goldsmith, Yasmin Granot, Daniel Rosenblum, Niels Dammes, Ranit Kedmi and Srinivas Ramishetti. The research was published in Nature Communications.

Over the past few years, lipid carriers encapsulating messenger RNAs (mRNAs) have been shown to be extremely useful in altering the protein expressions for a host of diseases. But directing this information to specific cells has remained a major challenge.

"In our new research, we utilized mRNA-loaded carriers -- nanovehicles carrying a set of genetic instructions via a biological platform called ASSET -- to target the genetic instructions of an anti-inflammatory protein in immune cells," says Prof. Peer. "We were able to demonstrate that selective anti-inflammatory protein in the target cells resulted in reduced symptoms and disease severity in colitis.

"This research is revolutionary. It paves the way for the introduction of an mRNA that could encode any protein lacking in cells, with direct applications for genetic, inflammatory and autoimmune diseases -- not to mention cancer, in which certain genes overexpress themselves."

ASSET (Anchored Secondary scFv Enabling Targeting) uses a biological approach to direct nanocarriers into specific cells to promote gene manipulation.

"This study opens new avenues in cell-specific delivery of mRNA molecules and ultimately might introduce the specific anti-inflammatory (interleukin 10) mRNA as a novel therapeutic modality for inflammatory bowel diseases," says Ms. Veiga.

"Targeted mRNA-based protein production has both therapeutic and research applications," she concludes. "Going forward, we intend to utilize targeted mRNA delivery for the investigation of novel therapeutics treating inflammation disorders, cancer and rare genetic diseases."

CHICAGO - Oct. 29, 2018 - A study examining the diagnoses generated by WebMD Symptom Checker showed the online tool was correct only 26 percent of the time. And the recommendation for the top diagnosis was often inappropriate, at times recommending self-care at home instead of going to the emergency room. The research will be presented today at AAO 2018, the 122nd Annual Meeting of the American Academy of Ophthalmology. The researcher suggests ophthalmology-related symptom checkers have an inherent limitation because most eye diseases and conditions require an in-person examination.

Lead researcher Carl Shen, M.D., an ophthalmology resident at McMaster University in Canada, was inspired to conduct the study by his patients, who often come to appointments with an incorrect self-diagnosis or preconceived notions about their condition. He wants to help patients better understand and interpret the eye health information they find online.

To conduct the study, both medical and non-medical personnel input 42 clinical scenarios into the popular WebMD Symptom Checker. Results were then compared with the known diagnosis. The top diagnosis returned was correct in just 26 percent of cases. While the correct diagnosis did appear within the top three results 40 percent of the time, it wasn't even an option in 43 percent of the cases.

The assessment of symptom severity was also often incorrect. In 14 of 17 cases, the online symptom checker made incorrect recommendations about what the patient should do next, such as self-care at home or getting immediate treatment.

While WebMD can arrive at the correct clinical diagnosis, a significant proportion of common ophthalmic diagnoses are not captured, Dr. Shen concluded.

"Sometimes doing research online can be helpful in identifying possible conditions, and it's good to be an informed patient," Dr. Shen said. "But it's also true that often these online symptom checkers do not arrive at the correct diagnosis. And the wrong recommendation on what to do with that diagnosis could be dangerous. The technology used in these online symptom checkers still have a long way to go in terms of accuracy."

CHICAGO--October 29, 2018--Lifestyle interventions, medication and surgery for patients diagnosed with pre-diabetes is proven to delay or prevent Type 2 diabetes in the majority of patients, but limited access to the often expensive treatments is fueling rising rates of the disease, according to research in The Journal of the American Osteopathic Association.

Currently, one in three American adults has prediabetes and more than 70% of adults are overweight or obese. Evidence shows lifestyle interventions, medication or surgery that results in weight loss effective prevents or delays the onset of Type 2 diabetes for as many as 70% of patients with prediabetes, said researcher Jay Shubrook, DO, who specializes in the treatment of diabetes.

"We know that it's much more cost effective to prevent disease than to treat it, particularly when it comes to diabetes. The short-term focus on immediate costs means patients are missing out on the opportunity to keep their disease from progressing. It's a false economy and if nothing changes, a third of Americans are expected to have diabetes by 2050," Dr. Shubrook explained.

Evidence-based interventions

Common lifestyle interventions focus on nutrition and increasing physical activity to promote weight loss. Most prioritize offering a supportive group environment to help participants achieve their goals, typically a mean weight loss of 7%. In a 3,200 participant study, lifestyle intervention reduced the incidence of type 2 diabetes by 58% in patients with prediabetes. A 10-year follow up reported a 34% decrease in the incidence of diabetes for the original study participants. The results and projected cost savings were so impressive that the Diabetes Prevention Program is now a mandated benefit for people with prediabetes who have Medicare.

The prescription medication metformin and other drug interventions were somewhat less effective than lifestyle changes, but also resulted in preventing or delaying the onset of diabetes. Metabolic, or weight-loss, surgery was more effective than lifestyle interventions at preventing diabetes onset and had longer lasting benefits, with a relative risk reduction of 78%.

"Weight loss is a central treatment target for most chronic diseases because the benefit is spread across numerous conditions," Dr. Shubrook noted. "We have the tools to change the trajectory for millions of patients at risk for diabetes. Using them wisely will save not only money, but lives, in the long run."

Evidence has been building in recent years that our diet, our habits or traumatic experiences can have consequences for the health of our children - and even our grandchildren. The explanation that has gained most currency for how this occurs is so-called 'epigenetic inheritance' - patterns of chemical 'marks' on or around our DNA that are hypothesised to be passed down the generations. But new research from the University of Cambridge suggests that this mechanism of non-genetic inheritance is likely to be very rare.

A second study, also from Cambridge, suggests, however, that one way that environmental effects are passed on may in fact be through molecules produced from the DNA known as RNA that are found in a father's sperm.

The mechanism by which we inherit innate characteristics from our parents is well understood: we inherit half of our genes from our mother and half from our father. However, the mechanism whereby a 'memory' of the parent's environment and behaviour might be passed down through the generations is not understood.

Epigenetic inheritance has proved a compelling and popular explanation. The human genome is made up of DNA - our genetic blueprint. But our genome is complemented by a number of 'epigenomes' that vary by cell type and developmental time point. Epigenetic marks are attached to our DNA and dictate in part whether a gene is on or off, influencing the function of the gene. The best understood epigenetic modification is DNA methylation, which places a methyl group on one of the bases of DNA (the A, C, G or T that make up our genetic code).

One model in which DNA methylation is associated with epigenetic inheritance is a mouse mutant called Agouti Viable Yellow. The coat of this mouse can be completely yellow, completely brown, or a pattern of these two colours - yet, remarkably, despite their different coat colours, the mice are genetically identical.

The explanation of how this occurs lies with epigenetics. Next to one of the key genes for coat colour lies a section of genetic code known as a 'transposable element' - a small mobile DNA 'cassette' that is actually repeated many times in the mouse genome but here acts to regulate the coat colour gene.

As many of these transposable elements come from external sources - for example, from a virus's genome - they could be dangerous to the host's DNA. But organisms have evolved a way of controlling their movement through methylation, which is most often a silencing epigenetic mark.

In the case of the gene for coat colour, if methylation switches off the transposable element completely, the mouse will be brown; if acquisition of methylation fails completely, the mouse will be yellow. But this does not affect the genetic code itself, just the epigenetic landscape of that DNA segment.

And yet, a yellow-coated female is more likely to have yellow-coated offspring and a brown-coated female is more likely to have brown-coated offspring. In other words, the epigenetically regulated behaviour of the transposable element is somehow being inherited from parent to offspring.

A team led by Professor Anne Ferguson-Smith at Cambridge's Department of Genetics set out to examine this phenomenon in more detail, asking whether similar variably-methylated transposable elements existed elsewhere that could influence a mouse's traits, and whether the 'memory' of these methylation patterns could be passed from one generation to the next. Their results are published in the journal Cell.

The researchers found that while these transposable elements were common throughout the genome - transposable elements comprise around 40% of a mouse's total genome - the vast majority were completely silenced by methylation and hence had no influence on genes.

Only around one in a hundred of these sequences were variably-methylated. Some of these are able to regulate nearby genes, whereas others may have the ability to regulate genes located further away in the genome in a long-range capacity.

When the team looked at the extent to which the methylation patterns on these regions could be passed down to subsequent generations, only one of the six regions they studied in detail showed evidence of epigenetic inheritance - and even then, the effect size was small. Furthermore, only methylation patterns from the mother, not the father, were passed on.

"One might have assumed that all the variably-methylated elements we identified would show memory of parental epigenetic state, as is observed for coat colour in Agouti Viable Yellow mice," says Tessa Bertozzi, a PhD candidate and one of the study's first authors. "There's been a lot of excitement and hype surrounding the extent to which our epigenetic information is passed on to subsequent generations, but our work suggests that it's not as pervasive as was previously thought."

"In fact, what we showed was that methylation marks at these transposable elements are reprogrammed from one generation to the next," adds Professor Ferguson-Smith. "There's a mechanism that removes methylation from the vast majority of the genome and puts it back on again, once in the process of generating eggs and sperms and again before the fertilised egg implants into the uterus. How the methylation patterns at the regions we have identified get reconstructed after this genome-wide erasure is still somewhat of a mystery.

"We know there are some genes - imprinted genes for example- that do not get reprogrammed in this way in the early embryo. But these are exceptions, not the rule."

Professor Ferguson-Smith says that there is evidence that some environmentally-induced information can somehow be passed down generations. For example, her studies in mice show that the offspring of a mother who is undernourished during pregnancy are at increased risk of type 2 diabetes and obesity - and their offspring will in turn go on to be obese and diabetic. Again, she showed that DNA methylation was not the culprit - so how does this occur?

The answer may come from research at the Wellcome/Cancer Research UK Gurdon Institute, also at the University of Cambridge, in collaboration with the lab of Professor Isabelle Mansuy from the University of Zürich and Swiss Federal Institute of Technology. In a study carried out in mice and published in the journal Molecular Psychiatry, they report how the 'memory' of early life trauma can be passed down to the next generation via RNA molecules carried by sperm.

Dr Katharina Gapp from the Gurdon Institute and the Mansuy lab have previously shown that trauma in postnatal life increases the risk of behavioural and metabolic disorders not only in the directly exposed individuals but also in their subsequent offspring.

Now, the team has shown that the trauma can cause alterations in 'long RNA' (RNA molecules containing more than 200 nucleotides) in the father's sperm and that these contribute to the inter-generational effect. This complements earlier research that found alterations in 'short RNA' molecules (with fewer than 200 nucleotides) in the sperm. RNA is a molecule that serves a number of functions, including, for some of the long versions called messenger RNA, 'translating' DNA code into functional proteins and regulating functions within cells.

Using a set of behavioural tests, the team showed that specific effects on the resulting offspring mediated by long RNA included risk-taking, increased insulin sensitivity and overeating, whereas small RNA conveyed the depressive-like behaviour of despair.

Dr Gapp said: "While other research groups have recently shown that small RNAs contribute to inheritance of the effects of chronic stress or changes in nutrition, our study indicates that long RNA can also contribute to transmitting some of the effects of early life trauma. We have added another piece to the puzzle for potential interventions in transfer of information down the generations."