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The children of families who fall upon hard times are at significantly greater risk of being involved in violent crime and harming themselves as young adults, according to a major new study.

The research by University of Manchester epidemiologists is a major addition to our understanding of the risk factors for self-harm and violent criminality.

The knowledge was generated from a study funded by the European Research Council of the young adult population of Denmark published today in The Lancet Public Health.

The results are highly relevant to the UK context argue Professor Roger Webb and Dr Pearl Mok, two of the study's authors.

Children who remained in the top 20% of wealthiest families over their first 15 years of life were the least likely to harm themselves or commit violent crime between the ages of 15 and 33.

Compared to the wealthiest fifth, children from families who remained in the least affluent fifth of society were 7 times more likely to harm themselves and 13 times more likely to commit violent crime as young adults.

Children from families whose income dropped from the top fifth to the bottom fifth were 2.9 times more likely to commit violent crime and 2.3 times more likely to self-harm as young adults.

And children from families whose income rose from the bottom fifth to the top fifth were 1.6 times more likely to self-harm and to commit violent crime as young adults.

Using Danish national registers of over one million young adults, the study analysed 21,267 patients who presented to hospital with self-harm episodes and 23,724 people who were convicted for violent crime aged 15 to 33.

Parental income was measured at birth-year, and at ages 5, 10 and 15.

Professor Webb said: "This study casts new light on our understanding of the deep-rooted causes of self-harm and violent behaviour. Though to some extent, we all make choices, what children go through does have a powerful effect on these harmful behaviours.

"Though the report drew on data relating to the entire population of Denmark, its results are relevant to the UK, whose population demographics are similar, as is their health system.

"In fact, income inequality in Denmark is one of the lowest in the world, so we'd expect these findings to be even more pronounced in countries with greater levels of income inequality, such as the UK."

He added: "These two harmful behaviours pose serious societal challenges. After accidents, intentional self-harm and assault are the next two most common causes of death among young people globally.

"Exposure to poverty can have an adverse impact on early child development as well as parental conflict and separation, harming children's psychosocial development and well-being.

"We would also imagine that ten years of austerity in the UK would escalate and entrench these problems: Poverty still affects more than one in four children in the UK today according to Child Poverty Action group.

"So this study underlines just how important it is to tackle socioeconomic inequalities during childhood.

"That encompasses access to public services, good housing and education but also things like local and social environments."

High levels of air pollutants, especially fine particulate matter (PM2.5) and to a lesser extent, ozone, may be linked to a heightened risk of developing mouth cancer, suggests the first study of its kind, published online in the Journal of Investigative Medicine.

The number of new cases, and deaths from, mouth cancer is increasing in many parts of the world. Known risk factors include smoking, drinking, human papilloma virus, and in parts of South East Asia, the chewing of betel quid ('paan'), a mix of ingredients wrapped in betel leaf.

Exposure to heavy metals and emissions from petrochemical plants are also thought to be implicated in the development of the disease, while air pollution, especially PM2.5, is known to be harmful to respiratory and cardiovascular health.

To find out if air pollutants might have a role in the development of mouth cancer, the researchers mined national cancer, health, insurance, and air quality databases.

They drew on average levels of air pollutants (sulphur dioxide, carbon monoxide, ozone, nitrogen monoxide, nitrogen dioxide, and varying sizes of fine particulate matter), measured in 2009 at 66 air quality monitoring stations across Taiwan.

In 2012-13, they checked the health records of 482,659 men aged 40 and older who had attended preventive health services, and had provided information on smoking/betel quid chewing.

Diagnoses of mouth cancer were then linked to local area readings for air pollutants taken in 2009.

In 2012-13, 1617 cases of mouth cancer were diagnosed among the men. Unsurprisingly, smoking and frequent betel quid chewing were significantly associated with heightened risk of a diagnosis.

But so too were high levels of PM2.5. After taking account of potentially influential factors, increasing levels of PM2.5 were associated with an increasing risk of mouth cancer.

When compared with levels below 26.74 ug/m3, those above 40.37 ug/ m3 were associated with a 43 per cent heightened risk of a mouth cancer diagnosis.

A significant association was also observed for ozone levels below 28.69-30.97 parts per billion.

This is an observational study, and as such, can't establish cause. And there are certain caveats to consider, say the researchers. These include the lack of data on how much PM2.5 enters the mouth, or on long term exposure to this pollutant.

Nor is it clear how air pollutants might contribute to mouth cancer, they acknowledge, and further research would be needed to delve further into this.

But some of the components of PM2.5 include heavy metals, as well as compounds such as polycyclic aromatic hydrocarbons-known cancer causing agents-they say.

And the smaller diameter, but larger surface area, of PM2.5 means that it can be relatively easily absorbed while at the same time potentially wreaking greater havoc on the body, they suggest.

"This study, with a large sample size, is the first to associate oral cancer with PM2.5...These findings add to the growing evidence on the adverse effects of PM2.5 on human health," they conclude.

Philadelphia, PA, October 9, 2018 - Each year 15 million infants are born preterm and face high risks of short- and long-term complications, including sepsis, severe inflammation of the gut, and neurodevelopmental disorders. A new report in the American Journal of Pathology demonstrates a link between prenatal inflammation and postnatal immune status and organ function in preterm pigs, suggesting that early intervention (eg, antibiotics or anti-inflammatory drugs) may be warranted for infants born preterm with signs of inflammation of fetal membranes.

"Our study may urge clinicians to be more aware of the population of preterm infants with chorioamnionitis (inflammation of the fetal membrane) as they have higher risks of systemic inflammation and neonatal sepsis," explained lead investigator Per T. Sangild, DVSc, DMSc, PhD, of the Section of Comparative Pediatrics and Nutrition, Department of Veterinary and Animal Sciences, University of Copenhagen, Frederiksberg, Denmark, and the Department of Pediatrics and Adolescent Medicine, Rigshospitalet, Copenhagen, Denmark.

"The data imply the importance of the integrity of barriers between epithelial tissues (eg, gut, lungs, and skin) and the circulation. Those barriers are more fragile in preterm neonates, and they can facilitate translocation of bacteria and inflammatory molecules, leading to systemic inflammation and internal organ disorders."

To induce prenatal inflammation, the bacterial endotoxin lipopolysaccharide (LPS) was injected into the amniotic sacs of prenatal pigs. LPS and control groups were analyzed at birth, three days after birth, and five days after birth (formula feeding).

At birth, prenatal LPS induced mild histologic chorioamnionitis and strong fetal lung and gut innate immune responses with elevated inflammatory cytokines and neutrophil/macrophage infiltration. "We believe the epithelial responses were likely derived from direct exposure to intra-amniotic LPS or LPS-induced cytokines," noted Dr. Sangild.

Five days later, the gut and lung inflammation subsided; however, the pigs exposed to LPS prenatally gradually developed systemic inflammation, with high levels of blood leukocyte subsets (eg, neutrophils, lymphocytes) and plasma cytokines (eg, IL-1β), similar to symptoms found in septic infants. Among those who survived, the pigs in the control group were on their feet and walked for the first time before the LPS-exposed animals. High levels of bacteria were also found in the spleen in the LPS-exposed pigs, indicating increased systemic infection or decreased capacity to clear translocated bacteria. The in utero death rate was higher in the LPS-exposed fetuses compared to the control group, as was the incidence of severe diarrhea. Interestingly, intra-amniotic LPS did not increase the incidence of formula-induced necrotizing enterocolitis (NEC) on Day 5. This is important as it has been suspected that systemic inflammation at birth might also predispose to later NEC in the gut of preterm infants; however, this hypothesis was not supported by this study.

"These data suggest that the postnatal systemic effects of short-term prenatal LPS were indirectly initiated from the preceding local inflammation of epithelial tissues in the fetal period, and the effects were gradually amplified systemically during the first few days after preterm birth," commented Dr. Sangild.

The results of this study highlight the importance of early diagnosis of prenatal inflammation to facilitate nutritional, medical, or pharmaceutical interventions that attenuate the detrimental postnatal responses to prenatal inflammation. The problem still remains that a pregnant woman with intra-amniotic inflammation may be asymptomatic and, therefore, unaware she has an infection that could harm her baby.

A bacterium named Moorella thermoacetica won't work for free. But UC Berkeley researchers have figured out it has an appetite for gold. And in exchange for this special treat, the bacterium has revealed a more efficient path to producing solar fuels through artificial photosynthesis.

M. thermoacetica first made its debut as the first non-photosensitive bacterium to carry out artificial photosynthesis in a study led by Peidong Yang, a professor in UC Berkeley's College of Chemistry. By attaching light-absorbing nanoparticles made of cadmium sulfide (CdS) to the bacterial membrane exterior, the researchers turned M. thermoacetica into a tiny photosynthesis machine, converting sunlight and carbon dioxide into useful chemicals.

Now Yang and his team of researchers have found a better way to entice this CO2-hungry bacterium into being even more productive. By placing light-absorbing gold nanoclusters inside the bacterium, they have created a biohybrid system that produces a higher yield of chemical products than previously demonstrated. The research, funded by the National Institutes of Health, was published on Oct. 1 in Nature Nanotechnology.

For the first hybrid model, M. thermoacetica-CdS, the researchers chose cadmium sulfide as the semiconductor for its ability to absorb visible light. But because cadmium sulfide is toxic to bacteria, the nanoparticles had to be attached to the cell membrane "extracellularly," or outside the M. thermoacetica-CdS system. Sunlight excites each cadmium-sulfide nanoparticle into generating a charged particle known as an electron. As these light-generated electrons travel through the bacterium, they interact with multiple enzymes in a process known as "CO2 reduction," triggering a cascade of reactions that eventually turns CO2 into acetate, a valuable chemical for making solar fuels.

But within the extracellular model, the electrons end up interacting with other chemicals that have no part in turning CO2 into acetate. And as a result, some electrons are lost and never reach the enzymes. So to improve what's known as "quantum efficiency," or the bacterium's ability to produce acetate each time it gains an electron, the researchers found another semiconductor: nanoclusters made of 22 gold atoms (Au22), a material that M. thermoacetica took a surprising shine to.

"We selected Au22 because it's ideal for absorbing visible light and has the potential for driving the CO2 reduction process, but we weren't sure whether it would be compatible with the bacteria," Yang said. "When we inspected them under the microscope, we discovered that the bacteria were loaded with these Au22 clusters - and were still happily alive."

Imaging of the M. thermoacetica-Au22 system was done at UC Berkeley's Molecular Imaging Center.

The researchers also selected Au22 ¬- dubbed by the researchers as "magic" gold nanoclusters - for its ultrasmall size: A single Au22 nanocluster is only 1 nanometer in diameter, allowing each nanocluster to easily slip through the bacterial cell wall.

"By feeding bacteria with Au22 nanoclusters, we've effectively streamlined the electron transfer process for the CO2 reduction pathway inside the bacteria, as evidenced by a 2.86 percent quantum efficiency - or 33 percent more acetate produced within the M. thermoacetica-Au22 system than the CdS model," Yang said.

The magic gold nanocluster is the latest discovery coming out of Yang's lab, which for the past six years has focused on using biohybrid nanostructures to convert CO2 into useful chemicals as part of an ongoing effort to find affordable, abundant resources for renewable fuels, and potential solutions to thwart the effects of climate change.

"Next, we'd like to find a way to reduce costs, improve the lifetimes for these biohybrid systems, and improve quantum efficiency," Yang said. "By continuing to look at the fundamental aspect of how gold nanoclusters are being photoactivated, and by following the electron transfer process within the CO2 reduction pathway, we hope to find even better solutions."

A study led by researchers at Université de Montréal quantifies for the first time the maximum amount of nutrients - specifically, phosphorus - that can accumulate in a watershed before additional pollution is discharged into downriver ecosystems.

That average threshold amount is 2.1 tonnes per square kilometre of land, the researchers estimate in their study published today in Nature Geoscience. "Beyond this, further phosphorus inputs to watersheds cause a significant acceleration of (phosphorus) loss in runoff."

This amount is shockingly low, the researchers say; given current nutrient application rates in most agricultural watersheds around the world, tipping points in some cases could be reached in less than a decade.

The study was led by Jean-Olivier Goyette, a doctoral student in biology at UdeM, and supervised by UdeM aquatic ecosystem ecologist Roxane Maranger in collaboration with sustainability scientist Elena Bennett at McGill University.

Phosphorus, an element in fertilizer, is essential to the growth of plant food. But the mineral is also harmful when overused. When it gets into surface water, it can lead to excessive plant growth in lakes and rivers and proliferation of toxic algae, harmful to human and animal health.

23 watersheds studied

Focusing on 23 watersheds feeding the St. Lawrence River in Quebec, the researchers reconstructed historic land-use practices in order to calculate how much phosphorus has accumulated on the land over the past century.

The two main sources of phosphorus to watersheds, the land adjacent to tributaries, come from agriculture (fertilizers and animal manure) and from the human population (through food needs and sewage).

Using Quebec government data, the researchers matched the estimated accumulation with phosphorus concentrations measured in the water for the last 26 years. Since the watersheds they studied had different histories - some had been used intensively for agriculture for decades whereas others were forested and pristine - this method allowed the researchers to establish a gradient of different phosphorus accumulations among sites. In so doing, they were able to see at what point the watershed "tipped" or reached a threshold and began to leak considerably more phosphorus into the water.

"Think of the land as a sponge," Maranger said. "After a while, sponges that absorb too much water will leak. In the case of phosphorus, the landscape absorbs it year after year after year, and after a while, its retention capacity is reduced. At that point historical phosphorus inputs contribute more to what reaches our water."

Until now, no-one had been able to put a number to the amount of accumulated phosphorus at the watershed scale that's needed to reach a tipping point in terms of accelerating the amount of the mineral flowing into the aquatic ecosystem.

'Really important contribution'

"This is a very important finding," Bennett said. "It takes our farm-scale knowledge of fertilizers and pollution and scales it up to understand how whole watersheds respond within a historical context."

Agriculture on a mass scale began in Quebec only in the 1950s, but some of the province's more historical agricultural watersheds had already passed the tipping point by the 1920s, the study found.

Even if phosphorus inputs ceased immediately, eliminating the accumulated phosphorus in saturated Quebec watersheds would take between 100 and 2,000 years, the researchers estimate.

In some countries, including China, Canada, and the US, phosphorus is so heavily used now that the saturation point is reached in as little as five years.

"Nutrient management strategies developed using novel creative approaches ... are urgently required for the long-term sustainability of water resources," the researchers urge in their study.

Recycle and reuse

"One possible mitigating measure would be to do what is already being done in some European countries: instead of adding more and more to help plants grow, phosphorus already stored in soils can be accessed using new practices and approaches," Goyette said.

"Furthermore, phosphorus can be recycled and reused as fertilizer rather than accessing more of the raw mined material."

The dilemma is this: humans need to eat but need to have clean water, yet growing food requires phosphorus that pollutes the water when too much leaves the watershed and pollutes adjacent aquatic ecosystems.

"Are some of our more extreme (agricultural) watersheds impossible to repair?" Maranger asked. "I can't answer that. It's a societal issue and there are solutions. We should never despair, but it's a wicked problem."

TORONTO, ON - Scientists at the University of Toronto have found a way to select the outcome of chemical reaction by employing an elusive and long-sought factor known as the 'impact parameter'.

The team of U of T chemists, led by Nobel Prize-winning researcher John Polanyi, have found a means to select the impact parameter or miss-distance by which a reagent molecule misses a target molecule, thereby altering the products of chemical reaction. The findings are published today in Science Advances.

"Chemists toss molecules at other molecules all the time in hopes of making something new," says Polanyi, University Professor in the Department of Chemistry at U of T. "In this study we have found a way to control the outcome by aiming a projectile molecule at a target molecule, with an accuracy of a small fraction of the diameter of the target molecule."

Molecular dynamics in chemistry is a lot like a game of billiards. Just as a billiard player sends the incoming ball towards the target ball, chemists launch one molecule towards another to produce a chemical reaction. However, this can be done, it is now clear, either by chance as has been the norm, or by design as the new work shows to be possible.

Previously the inherent randomness in molecular motions has prevented chemists from aiming their projectile molecules at the chemical targets, as billiards players do. Instead, they have been obliged to play their game of billiards blindfold.

"Over the years chemists have become very good at playing billiards blindfold, using sticky balls and throwing them strongly or weakly," Polanyi says. "But we have found a way to take off the blindfold, and aim each shot."

The researchers achieved this by depositing molecules on a metal crystal, then applying a small current from an atomically sharp metal tip to one of the molecules. This addition of energy caused a 'projectile' molecule to shoot across the surface in a straight line, along one of the rail-like ridges on the metal crystal toward a nearby 'target' molecule present on the crystal, missing it by a controlled amount.

Different miss-distances, called 'impact parameters', were shown reproducibly to give different outcomes, that is to say different patterns of reaction.

"The underlying crystalline surface is our billiard table," said Kelvin Anggara, a postdoctoral fellow in Polanyi's research group and a lead author of the study. "By taking advantage of the grooves that nature has conveniently scored across the surface of crystals, we found we could guide the travelling molecular projectile so that it hit the target either head-on or in a glancing collision that missed the target by a desired amount. That way, just as in billiards, we can control the outcome of the molecular collision."

Selecting the miss-distance or impact parameter in collisions between reagent molecules has till now been termed the "forbidden fruit of reaction dynamics" by Harvard University professor Dudley R. Herschbach, with whom Polanyi shared the 1986 Nobel Prize in Chemistry along with Yuan T. Lee. While the discoveries made by the trio enabled chemists to infer many of the forces at play in a chemical reaction, the impact parameter has defied direct control.

This is true even in the famously well-controlled conditions of "crossed molecular beams". It is frequently overlooked that though the beams in this elegant method are aimed at one another, the molecules are not. Now the individual molecules can be aimed at one another, quite precisely.

"We believe that this is a major step forward in the control of chemical reactions," said Anggara, who performed the study along with Polanyi, senior research associate Lydie Leung and graduate student Matthew Timm.

Global sustainability is important now more than ever due to increasing urban populations and the resulting stress it can have on natural resources. But increased populations in cities may lead to greater efficiency, as a team of Penn State researchers discovered when they analyzed the water footprint of 65 mid- to large-sized U.S. cities.

"Human life on the planet has never been more complex," said Caitlin Grady, assistant professor of civil engineering. "We're so intertwined with so many aspects of the global trade and global economy. People in rural areas are still buying food like bananas from across the world and because of this we need more complex and rigorous tools to analyze how to manage our limited resources."

In order to develop these tools, researchers first need to better understand the urban water footprint. Grady and her colleagues set out to do just that.

"We looked at the overall picture of water consumption," Grady said. "Not just the water that comes out of your tap but also the water that goes into the food that each city produces and consumes, so it's both the direct water use and indirect water use, which we call your water footprint."

They analyzed agricultural, livestock and industrial commodity flows, and the corresponding virtual water contents using data from the U.S. Department of Agriculture, the U.S. Geological Survey and the U.S. Department of Transportation. The team then used these values to calculate an overall water footprint for each city. Their results were published in August in PLOS ONE.

What they found was that on average, larger cities, for their populations, consume less water.

"As the population increases, cities are consuming less per capita of the water resources, so the larger cities are getting more out of the water that they have based on population," Grady said.

Tasnuva Mahjabin, a doctoral student in civil engineering and contributing researcher on the project, said that multiple factors are likely contributing to these results.

"Water footprint consumption and production are tied to the changing composition of urban economic activities with city size, suggesting that large cities are more service-oriented with less prevalence to secondary sector industries," Mahjabin said. "This allows large cities to have reduced water footprints by shifting water-intensive economic activities to less populated regions."

And although the overall water usage decreased in correlation with a city's size, the researchers noted that not all types of water usage yielded a more efficient footprint.

Water that has been sourced from surface or groundwater resources mainly mirrored water-related weather patterns and showed little correlation with population. However, the amount of water used from precipitation contributed to consumption both positively - by transferring the dependence of food consumption on population into the water footprint - and negatively - by increasing diversity.

Several exceptions did arise. New Orleans, for example, has a much larger water footprint for their size and their population compared to the trend, whereas Las Vegas falls well below the average for water footprint production. The team is tracking the complexity of these findings in an effort to more accurately dissect the results.

The researchers hope to use their findings to benchmark cities and potentially set realistic targets to support the development of strategies for reducing the water footprint. This information could also be valuable to policy makers and city planners concerned with designing economic incentives that support water sustainability.

"A city in California may have a very strong campaign to have people take shorter showers and reduce water consumption, but they may also be a huge food producer," said Grady. "That's not necessarily a bad thing, but if you look at these things together you have a more complete picture of how you can manage the limited resources you have, and how you can prioritize the use of those resources."

In the future, the researchers plan to make their analyses more robust by incorporating more locations and including the water consumption needed to provide electricity to different regions. They would also like to analyze network resilience and network risk. Ultimately, they hope to create a platform where not only the public could investigate linkages but the government, as well.

BLOOMINGTON, Ind. -- More and more breweries are investing in practices to save energy and reduce greenhouse gases. Will it pay off? A study by Indiana University researchers suggests it may.

Drawing on survey research, they find that a majority of U.S. beer drinkers would be willing to pay more for beer produced with sustainable practices. On average, they would pay about $1.30 more per six-pack.

"The takeaway for the brewing industry is that it is financially feasible to introduce energy-saving practices into the brewing process," said Sanya Carley, associate professor in the IU Bloomington School of Public and Environmental Affairs and the first author of the paper. "Even if it ends up adding costs, more than half of all beer consumers are willing to absorb those extra costs."

The study, "Willingness-to-pay for Sustainable Beer," was published by the journal PLOS ONE. Lilian Yahng, director of research and development for IU's Center for Survey Research, is a co-author.

The research highlights potential for energy savings and sustainability in an energy-intensive industry that is growing rapidly, especially in the craft-beer segment. The number of craft breweries grew by over 200 percent between 2005 and 2015, and their production increased by over 12 percent each year.

The industry has considerable potential for reducing energy use and mitigating its impact on climate change. Some breweries have already added solar panels, installed onsite wastewater treatment plants, insulated brewing vessels and recaptured steam from the brewing process.

But those kinds of measures require upfront investments that are likely to increase prices. To determine whether consumers would be willing to pay more for sustainably brewed beer, the researchers drew on a survey of over 1,000 self-reported beer drinkers, all over age 21. They found that 59 percent said they would pay more.

Consumers who already pay more for their beer were most likely to be willing to pay a premium for sustainability. Also, those who said they would pay more for sustainable beer were likely to report lifestyle activities associated with the common good. For example, they spent time in volunteer work or engaged in recycling, composting, and buying locally produced food and products.

Surprisingly, however, there was no significant correlation between the type of beer that consumers preferred and their willingness to pay more for sustainability, after controlling for differences in price. Consumers of traditional American lagers -- think Budweiser and Coors -- were as likely to be willing to pay more as those who prefer craft beers, a category that includes such exotic brews as avocado honey ale and a wild ale brewed with yeast cultured from the brewmaster's beard hairs.

That said, the proliferation of beer varieties suggests that brewers will have to find new ways to distinguish themselves in an increasingly crowded market. Carley said the research suggests that going green could be a way for beer companies to do just that.

NASA's Aqua satellite passed over the Central Atlantic Ocean and obtained infrared data on Leslie, now weakened to a large tropical storm.

The National Hurricane Center or NHC said that Leslie remains a large tropical storm, with tropical-storm-force winds extending outward up to 290 miles (465 km) from the center. Because of the size and strength of Tropical Storm Leslie, waves from Leslie are expected to increase along the coasts of Atlantic Canada and New England today, Oct. 5.

At 1:40 a.m. EDT (0540 UTC) on Oct. 5, the Moderate Resolution Imaging Spectroradiometer or MODIS instrument aboard NASA's Aqua satellite revealed strongest storms with the coldest cloud top temperatures northwest of Leslie's center. MODIS found coldest cloud tops had temperatures near minus 63 degrees Fahrenheit (minus 53 degrees Celsius). NASA research has found that cloud top temperatures that cold have the capability to generate heavy rainfall.

At 5 a.m. EDT (0900 UTC), the center of Tropical Storm Leslie was located near 35.9 degrees north latitude and 58.3 degrees west longitude. Leslie is moving toward the north-northwest near 14 mph (22 kph). A slower northward motion is expected to occur today, but Leslie will make a sharp turn toward the east and east-southeast over the weekend.

Maximum sustained winds are near 65 mph (100 kph) with higher gusts. Little change in strength is forecast during the next several days.

NHC cautioned, "Large swells generated by Leslie will continue to affect portions of the southeastern coast of the United States, Bermuda, the Bahamas, and the Greater and Lesser Antilles during the next few days. Swells are expected to increase near the coasts of New England and Atlantic Canada today."

Philadelphia, October 5, 2018 - Energy drinks represent a new category of nonalcoholic beverage with global sales of over USD 50 billion. Containing caffeine as a main ingredient, energy drinks are a central part of partying and sporting culture. A new study published in the Journal of Nutrition Education and Behavior found that digital marketing of energy drinks was more persuasive with young adults than other marketing methods.

"Consumption of energy drinks is a public health concern in children and young adults because they may cause dental problems, cardiovascular and neurological issues, and in rare cases, death," said lead author Limin Buchanan, PhD candidate, School of Health and Society, Early Start, Faculty of Social Sciences, University of Wollongong, Wollongong, Australia. "Because Internet usage among this age group is so prevalent, digital marketing of unhealthy food and beverages may have a greater effect."

To study this possibility, researchers recruited 359 young adults from the New South Wales region through flyers, online ads, and mentions in lectures. The group was primarily middle-class students who worked part-time. Over half of the student subjects had consumed energy drinks. They were asked to take a 44-question survey asking about exposure to and engagement with energy drink marketing, attitudes toward energy drink use, and frequency of consuming energy drinks. The results identified differences between users and non-users, although few respondents reported high levels of energy drink consumption.

Energy drink users reported both greater exposure to and engagement with digital marketing than non-users. While exposure alone was not a significant predictor of energy drink usage, engagement with digital marketing did increase usage. Examples of engagement include clicking on a social media ad or playing an online game. This engagement also increased their attitude towards the normalcy of energy drinks and their perceived likelihood to use energy drinks when pressured by peers. However, the study also showed that impact of digital marketing engagement was mediated by young adults' attitudes against energy drink usage and its normalcy, indicating that enhancing nutrition education knowledge among these individuals may reduce the effects of such marketing.

"Public health professionals have advocated for stronger regulations on marketing unhealthy foods to children through traditional media," said Ms. Buchanan. "This advocacy could be expanded to include restrictions on digital marketing to young adults based on current research. Future nutrition education interventions may focus on strategies to lessen the appeal of energy drinks, denormalize energy drink use, and strengthen young adults' ability to reject this drink option when with peers."

The research, led by Georgetown University Medical Center (GUMC) investigators and published in Neurotoxicity Research, complements findings from another GUMC-led study, published Oct. 3, that found a subset of breast cancer patients who experience long lasting cognitive deficits also have the APOE4 gene. Cancer survivors often report memory difficulties and this study, published in the Journal of Clinical Oncology (JCO), was the first large U.S. study of cognition in older breast cancer patients and the first to zero in on the cause of difficulties in memory, among other issues.

While the JCO study did not examine the specific type of chemotherapy used in the breast cancer patients, the mouse study investigated a single drug, doxorubicin, which is commonly used to treat the disease.

"These two studies took completely different approaches, yet they are telling the same story, and that is a real strength," says G. William Rebeck, PhD, a professor in the GUMC Department of Neuroscience and senior author of the Neurotoxicity Research study.

"The data in the mice is very clear -- APOE4 works in concert with doxorubicin to produce significant changes in the cortex and hippocampus and to markedly impair learning," he says.

"Given how well this mouse model works, we believe we can now methodically test chemotherapy drugs, one by one, and see what effects the drugs may be producing in the brain. We could also test agents to prevent cognitive decline in cancer patients with APOE4," Rebeck says.

"These kind of direct studies can't be done in humans; our mouse models may be able to provide some valuable insight into which drugs may work best for individual patients," he says.

Rebeck, a neuroscientist, started working on this project several years ago when geriatrician Jeanne Mandelblatt, MD, MPH, came to see Rebeck. Mandelblatt, who led the JCO study, wondered, early in the study, whether APOE4 could be a culprit in the cognitive issues that some of the patients in her study were having. Rebeck is well known for his work of the link between APOE4 and Alzheimer's disease.

They talked about how chemotherapy could affect brain function in APOE4-positive patients, which led Rebeck to test a mouse model of human APOE3 (the most common variant) and APOE4. These mice lack the mouse APOE gene (which is different from the human) and instead express one of two human APOE alleles.

While both APOE3 and APOE4 chemotherapy-treated mice had brain changes, compared to a control group of knock-in mice that were not treated with doxorubicin, the difference was more severe in APOE4 treated mice. These mice also had significantly impaired functioning on learning tasks.

Rebeck cannot say why chemotherapy and APOE4 may work together to affect brain function, but "good hypotheses" are that the combination increases inflammation in the periphery of the brain that accelerates aging -- and aging is linked to development of Alzheimer's disease -- or that APOE4 inhibits normal growth of new brain neurons that helps replace damaged neurons.

"Our group is delighted that we can provide some insights to our colleagues who study cancer," he says. "We hope to collaborate a great deal in the future on these issues."

Scientists using a powerful new technology that sequences RNA in 20,000 individual cell nuclei have uncovered new insights into biological events in heart disease. In animal studies, the researchers identified a broad variety of cell types in both healthy and diseased hearts, and investigated in rich detail the "transcriptional landscape," in which DNA transfers genetic information into RNA and proteins.

"This is the first time to our knowledge that massively parallel single-nucleus RNA sequencing has been applied to postnatal mouse hearts, and it provides a wealth of detail about biological events in both normal heart development and heart disease," said study leader Liming Pei, PhD, a molecular biologist in the Center for Mitochondrial and Epigenomic Medicine (CMEM) at Children's Hospital of Philadelphia (CHOP) and an assistant professor in the Department of Pathology and Laboratory Medicine in the Perelman School of Medicine at the University of Pennsylvania. "Ultimately, our goal is to use this knowledge to discover new targeted treatments for heart disease. In addition, this type of large-scale sequencing may be broadly applied in many other fields of medicine."

Pei and co-study leader Hao Wu, PhD, also of the CMEM and an assistant professor of Genetics at Penn Medicine, published their findings online Sept. 25, 2018 in Genes & Development.

While massively parallel single-cell RNA sequencing (scRNA-seq) has been available to researchers in the past three years, it is technically challenging to study single cells in postnatal hearts due to the large size of cardiac muscle cells.

To enable single-cell analysis of large cells such as muscle cells, or cells with complex morphology such as neurons, robust massively parallel single-nucleus sequencing (snRNA-seq) methods have been developed recently in Wu's laboratory, as well as by others in the field. To date, massively parallel snRNA-seq has been applied only to the central nervous system. Pei and colleagues are the first to adapt the technology for use in postnatal heart tissue.

The research team used the snRNA-Seq method termed sNucDrop-seq to analyze nearly 20,000 nuclei in heart tissue from normal and diseased mice. "We are excited to further develop sNucDrop-seq and apply it to mammalian postnatal hearts, which are of critical medical relevance but difficult to study with standard scRNA-seq," said Wu.

The current study focused on cardiomyopathy, a group of diseases characterized by progressive weakening of the heart muscle, and representing a leading worldwide cause of heart failure. Pei and colleagues used mice developed to model a type of pediatric mitochondrial cardiomyopathy.

"The heart is a complex organ, with a multitude of cell types, and much still remains poorly understood about mammalian heart development and heart disease, especially during the postnatal period," said Pei. "Our study provides key insights in three areas: normal heart development, heart disease, and gene regulatory mechanisms of a heart hormone called GDF15."

The sequencing tool identified major types of heart cells, such as cardiomyocytes, fibroblasts and endothelial cells, as well as rarer cardiac cell types. The study team found great variety among each cell type, as well as indications of functional changes in the heart cells during both normal and diseased conditions. For example, the researchers detected metabolic changes in fibroblasts, the fibrous cells that make the heart abnormally stiff in heart disease.

Another finding concerned gene networks that regulate production of cardiac hormones in heart disease--specifically GDF15, which slows overall body growth, presumably to reduce the energetic demands on a damaged heart. Such signaling, said Pei, could reveal more about the biological mechanisms that underlie the growth restriction commonly seen in children with congenital heart disease.

Greater understanding of cardiac biology, as provided in this research, said Pei, may lead to targeted therapies aimed at key gene networks that could offer better treatments for heart patients.

"This research was a first step in defining the transcriptional landscape of normal and diseased heart at high resolution," said Pei, who added that future work in his and his collaborator's laboratory will investigate how heart disease progresses over a longer timespan than the early postnatal period. The research tool may also offer opportunities to investigate diseases in organs and systems beyond the heart.

Previous research has shown that the bacillus Calmette-Guerin (BCG) vaccine, used to prevent tuberculosis, can reduce blood sugar levels in people with advanced type 1 diabetes in the long term. New research being presented at this year's European Association for the Study of Diabetes (EASD) Annual Meeting in Berlin, Germany (1-5 October) reveals the mechanism through which the vaccine can make durable, beneficial changes to the immune system and lower blood sugars.

The new findings suggest that the immune-metabolic imbalance in type 1 diabetes could stem from too few microbial (ie, germ) exposures that have been eliminated in today's more sterile environments, and that reintroduction of a bacterium (BCG) might reset abnormal metabolic functions boosting the immune system to consume sugar and reduce blood glucose levels over time.

"It has long been believed that the move to cleaner and more urban environments is involved in not only how type 1 diabetes develops, but increased incidence of the disease", explains Dr Faustman, Director of the Massachusetts General Hospital Immunobiology Laboratory, who led the study. "In particular, reduced exposures to certain microbes, the consequence of better sanitation, greater use of antibiotics, smaller family sizes, cleaner houses, less daily exposures to the soil, and less exposure to domesticated animals, appears to have changed the modern metabolic function."

The BCG vaccine, based on a harmless strain of bacteria related to the one that causes tuberculosis, appears to have the effect of safely mimicking the microbial exposures modern societies have lost.

In an earlier phase 1 randomised trial, two injections of the BCG vaccine 2 weeks apart reduced average blood sugar to near normal levels by the 3-year mark in people with advanced type 1 diabetes, an improvement that was sustained for 5 more years. [1] Faustman and colleagues from Massachusetts General Hospital in the USA also identified that the BCG vaccine uses a novel mechanism to change the way the body consumes glucose--from oxidative phosphorylation (the most common pathway by which cells convert glucose to energy) to aerobic glycolysis, a state that speeds up the rate cells turn glucose into energy, leading to reduced blood sugar levels over time.

These new findings show that type 1 diabetics have metabolism consistent with less microbial exposure. As a result, type 1 diabetic patients have white blood cells that use minimal blood sugar compared to non-diabetics control subjects. Exposing the patients to microbes in the BCG vaccine seems to result in the white blood cells using more blood sugar by increasing aerobic glycolysis.

"BCG is an organism that needs a lot of energy sources. It lives inside white blood cells and elevates the sugar utilisation", explains Dr Faustman.

The findings support the hygiene hypothesis which suggests that early life exposure to microbes that promote aerobic glycolysis is actually beneficial to the development of the immune system and is an important determinant of sensitivity to autoimmune diseases such as type 1 diabetes.

"The BGC vaccinations like tuberculosis itself, convert a depressed lymphatic system deficient in sugar utilisation into a highly efficient process, a restoration similar to normal subjects without diabetes", says Dr Faustman.

"Our discovery that type 1 diabetic patients have too little lymphoid sugar utilisation opens the door for more clinical trials using the BCG vaccine, even in advanced type 1 diabetes, to permanently lower blood sugar with the potential to reduce the substantial illness and mortality associated with this disease."

The authors note some limitations including that this is an early, small study, and a large 5-year phase 2 trial of 150 type 1 diabetic subjects approved by the US Food and Drug Administration is currently underway to test whether repeat BCG vaccine can clinically improve type 1 diabetes in adults with existing disease.

It is not so long ago that immunotherapy against cancer was positioned as emerging or even promising but not as proven. Novel immunotherapeutics across different tumor types, either as mono therapy or in combination, are increasingly becoming one of the most innovative and powerful anti-cancer strategies.

One of the major challenges in ensuring that these novel treatments realize their true potential has been successfully equipping the immune system to launch its attack exclusively on tumour cells excluding all healthy tissues. Up until now.

Research led by Joaquín Arribas, Director of Preclinical Research at the Vall d'Hebron Institute of Oncology (VHIO), ICREA Professor, and Scientific Director of the Center for the Biomedical Research Network in Oncology (CIBERONC), has turned this obstacle into therapeutic opportunity.

Published in Science Translational Medicine, the study, first co-authored by Irene Rius-Ruiz, Graduate Student of VHIO's Growth Factors Group, reveals that p95HER2-T cell bispecific antibody (TCB) can successfully guide immune cells, known as lymphocytes, directly to cancerous ones for their targeted killing.

This direct delivery is achieved thanks to the p95HER2 protein, which is only located in tumor cells. Representing a new therapeutic avenue and fresh hope for patients who have ceased to respond to current therapies, this novel immune-based approach can be used to tackle certain HER2+ breast cancers through its exclusive targeting of cancerous cells.

p95HER2-TCB: guiding the immune system for the targeted killing of HER2-positive breast cancer cells

T cell bispecific antibodies constitute a promising approach in harnessing the immune system to mount its anti-cancer response, and represent an increasingly valuable addition to the current arsenal of armory against cancer. Not only are they highly specific but they can also hone in on one protein among tens of thousands, in this particular case, p95HER2.

Furthermore, each antibody molecule has a bipartite structure containing two protein-binding sites. This means that they can simultaneously attach to immune cells and cancerous ones as well as take the lymphocytes hand-in-hand directly to the malignant cells for their subsequent destruction.

Acting as a magnet that lures the patient's immune system solely to tumor cells, p95HER2-TCB enables a targeted response by attacking these cells directly without affecting normal cells. "The immune system has the natural capacity to fight against disseminated disease. To do so more effectively, it must be better equipped to recognize and act against malignant cells. While bispecific antibodies are designed to do just that, they often signpost T cells to healthy ones," explains Joaquín Arribas, corresponding author of the study.

He continues, "Thanks to the distinct specificity of p95HER2-TCB and p95HER2's exclusive location in tumor cells, we have achieved a 'home delivery' of immune-based therapy. Our findings represent an important step towards ensuring that the immune system can successfully deliver its powerful anti-cancer blows."

Immunotherapies for cancer are proving increasingly more effective in the treatment of metastatic disease. Generally, advanced and metastatic cancers eventually develop resistance to different lines of therapies. When patients eventually cease to respond to current therapies, leading to cancer cell spread, they have few therapeutic options available.

While the immune system represents powerful weaponry in thwarting the spread of disease, it can only effectively do so by recognizing and launching its attack on malignant cells. "The real added value of our findings is that the bispecific antibody, p95HER2-TCB, directs lymphocytes exclusively to tumour cells harboring p95HER2," observes Irene Rius Ruiz, first author of the study.

Approximately 10% of patients with HER2-positive breast cancers expressing p95HER2 could stand to benefit from this novel strategy.

"While our approach can only be extended to a relatively small subset of patients with HER2-positive disease, for those who stand to gain, the benefits could be significant. By more precisely matching novel therapy to a particular patient population, we are getting closer to delivering on the true promise of precision medicine in oncology," says Irene Rius Ruiz.

These findings are the fruit of a decade of research at VHIO, beginning with Joaquín Arribas' group's identification of the p95HER2 protein, which was initially used as a biomarker to identify a subgroup of patients with HER2-positive breast cancer who no longer responded to standard therapies.

Their later discovery that this protein only resides on the surface of tumour cells as opposed to healthy cells led to the development of a specific targeted therapy.

As a leading reference in advancing modelling systems, VHIO is dedicated to delivering the predictive data required to reliably inform the clinical development of innovative agents and evidence reproducibility before moving to the clinic.

VHIO's Growth Factors Group focuses on more accurately modeling anti-tumor immunotherapy strategies and has generated humanized patient-derived xenograft models (Hu PDXs), in which the human immune system is established in immunodeficient mice. These experimental models have been invaluable in validating the efficacy of the p95HER2-T cell bispecific antibody.

Having now completed the pre-clinical phase of development, Arribas' team will seek to advance the therapy so that it can be administered in humans for investigation in clinical trials. Next steps will also include developing additional therapies against p95HER2 such as antibody-drug conjugates or chimeric antigen receptors (CARs).

"These future treatments will likely be as effective and safe as p95HER2-TCB. We are confident that our findings will enable the exclusive targeting of malignant cells by different means through p95HER2," concludes Joaquín Arribas.

Reflective of VHIO's purely multidisciplinary and translational research model, several of its preclinical, translational and clinical groups, along with colleagues belonging to CIBERONC, have collaborated in this research.

The project has also counted on the participation of other physician-scientists and oncology professionals of the Vall d´Hebron University Hospital across the Vall d´Hebron Barcelona Hospital Campus.

A study published in Family Practice indicates that healthcare providers outside of the Veterans Affairs (VA) Department are uncertain how to address veterans' needs. The study says that this is due to limited knowledge of resources and coordination problems.

Between 2011 and 2015 there were 20 million veterans living in the United States, comprising approximately 6% of the total population. Non-VA healthcare providers in the US have been called to screen patients for veteran status in order to better identify health conditions related to military service. Despite this, many service members are still not asked about veteran status. Even once a patient is identified as a current or former service member, providers admit they are uncertain about how to manage specific treatments.

Researchers completed interviews with non-VA primary care providers as part of a larger quantitative survey study of their attitudes around veteran care. Providers were asked about their approach to addressing veteran status in their practice and their thoughts on how to address the needs of this population. Researchers analysed and categorized data retrieved from the transcripts to identify major themes.

All participants expressed a sense that knowing about military participation was important for assessing someone's health; asking a few additional questions about military service may improve treatment recommendations and allow for referrals for specific mental health services. However, responses generally indicated limited insight into the possible health impacts of military experience beyond psychological concerns.

Overall, the interviews revealed that providers had inconsistent knowledge about the military population, admitting that they never learned about veterans or the military during their medical training, and so had limited exposure. Providers discussed that a lack of information, lack of available services (particularly in rural areas), and uncertainty about veterans' insurance coverage reduce their ability to care for veteran patients.

"Given the significant numbers of veterans who use non-VA sources of care and the potentially broad-ranging impacts of military service on health, supporting providers in their ability to recognize and address the needs of these patients--and to do so in a culturally competent manner--is critically important to improving these patients' overall health and well-being," said Bonnie Vest, research assistant professor in the department of family medicine at the University at Buffalo and the principal investigator for the project.