Culture

The team reported on their findings and conclusions in the British Journal of Sports Medicine on 26 August 2020.

In the first step, Christian Klein, Dr. Patrick Luig, Dr. Thomas Henke, Hendrik Bloch and Professor Petra Platen searched for the match scenes of all moderate and severe football injuries in the period from 2014 to 2017 that had resulted in more than one week of absence for the injured player. For this purpose, they viewed the relevant video sequences via the media portal of the German Football League. In order to systematically analyse all match scenes, they developed an observation sheet in which they recorded, for example, on which surface, after how many minutes and where on the pitch the injury occurred, whether there had been a foul, what position the player was in and where on the body the injury was located.

Predominantly knees, thighs and ankle joints

The team conclusively identified and analysed 345 situations that had led to injuries. "The majority of all injuries affected the knee joint with 24.3 percent, the thigh with 23.5 percent and the ankle joint with 19.1 percent," lists Christian Klein, PhD student in the Department of Sports Medicine and Sport Nutrition at RUB and sports consultant at VBG. Less frequent injuries concerned the shoulder (8.4 percent) and the head (7.8 percent).

Head injuries were often caused by contact between players who, for example, tried to head a ball at the same time. Shoulder injuries often resulted from indirect contact mechanisms, for example when a player falls on his shoulder after tripping on contact with an opponent. Thigh injuries often occurred without contact between players. Fouls were rarely the cause of injuries: more than 70 percent of all contact injuries were not accompanied by foul play by the opponent. In just under 20 percent of all contact injuries, the researchers found a violation of the rules by the injured player himself.

Tackling is dangerous

"Looking at the overall injury pattern, we can describe nine typical injury patterns for moderate and severe injuries," explains co-author Thomas Henke. One of the main findings of the study is that tackling is linked to a high risk of injury for the attacking player himself. Many knee injuries occur due to the respective player tackling, not through the attack of an opponent. "Tackling could therefore be a focus for preventive measures," says Petra Platen, Head of the Department of Sports Medicine and Sport Nutrition at RUB. "Didactic teaching methods for tackling as a component of technical training should be developed and implemented already in youth football."

Preventive training for fast running

Injuries without physical contact occurred mainly when a player was running fast. Injuries to the thigh muscles in particular are caused by sprints or lunges. In these cases, overload is the main injury mechanism. These findings demonstrate a great potential for preventive measures, as the causes result from physiological conditions of the injured person himself. As a preventive measure, the experts consider running training consisting of aerobic elements, anaerobic elements at high continuous speed and sprinting elements.

The large and constantly growing video database developed for the present study should be used in education programmes for coaches, referees and other professions to deliver specific training on injuries and their possible prevention for all parties involved in professional football. The research team also proposes a consensus that takes into account the definitions of playing situations, player and opponent behaviour and biomechanical injury mechanisms, using the study's observation sheet as a basis.

Apps such as Uber are an important mobility feature in many big cities. Driving others from A to B in their own car has become a job for many people. However, many drivers complain that their income is too low. In May 2019, the US television station ABC reported how Uber drivers at Washington airport artificially inflated the price of the service by all going offline at the same time. Within a few minutes, the price of the service had risen by 13 dollars, which almost doubled the amount.

How exactly does this strategy work and when is it used? This is what Dr. Malte Schröder and Professor Marc Timme from the Chair for Network Dynamics at the Center for Advancing Electronics Dresden (cfaed) and the Institute for Theoretical Physics at TU Dresden have been investigating alongside PhD students David-Maximilian Storch and Philip Marszal. The two researchers published a study in the journal Nature Communications: The applied dynamic price mechanisms generally provide incentives to artificially reduce offers and consequently increase the price.

With the dynamic price adjustment, the providers want to bring the market into balance: If demand exceeds the availability, travel costs increase. The idea is to attract more drivers to meet the high demand. At the same time, customers will have an incentive to wait.

Nevertheless, the drivers can activate the price increase themselves: "If many drivers go offline at the same time, the algorithm 'thinks' there is a shortage of drivers," explains Schröder. "It tries to attract more drivers by increasing the price: A flexible surcharge is added to the basic price for the service, which can double or even triple its cost".

By using analytical methods from game theory, Schröder and his colleagues demonstrate when the strategy is profitable. First, the demand must be sufficiently high. Otherwise, the drivers risk not finding customers after their offline phase. Moreover, people should be willing to pay the high price instead of waiting for a taxi or taking the bus. "For the drivers, these are empirical values," Storch assumes. "They have learned over time when the planes arrive with stressed business people whose journey is paid for by their employers anyway."

Moreover, the tactics are only optimal for all drivers if each of them participates in the game. Otherwise, any one of them could run the risk of being the only one to go offline and miss potential customers. Therefore, drivers have to trust each other or make arrangements - like in Washington. "The drivers at the airport know each other and all wait in the same car park," says Marszal. "Of course, communication is much easier this way than if they are spread all over the city."

The researchers have developed a model that enables the identification of offline tactics based on price trends without knowing the exact ratio of availability to demand. They analysed price data of the service in 59 cities around the world. At over 15 locations in America, Asia and Europe, the price developments for services from airports, train stations or exhibition centres were similar to those in Washington. In these cases, Uber limited the surcharge to ten dollars. "This is the most inefficient way to prevent increases in prices," says Schröder. "The trip will cost a maximum of ten dollars more, but this does not change the general incentives or the behaviour of the drivers. In principle, research has only just begun: "The collective dynamics of these kinds of apps are difficult to understand, and many questions are still open, especially in the rapidly changing mobility sector". In any case, an approach would be to offer customers alternatives, such as good local transport, and to pay drivers sufficiently. Until then, travellers should think about having a quick coffee when the journey is too expensive. Outside rush hours, prices usually fall quickly back to their normal level.

New dedicated hubs for Deaf children are needed around the country to provide new social spaces, education and support, an expert has said.

Special schools for Deaf children have had an important role in the Deaf community, acting as places people can meet and learn BSL together. But the move to inclusive education and new technology such as cochlear implants means most children with hearing loss are now educated in mainstream schools.

Deaf education should be remodelled to replace the role previously provided by specialist schools which have closed, Dr Hannah Anglin-Jaffe argues in a study in the British Education Research Journal.

Dr Anglin-Jaffe proposes Deaf education and support could be run in the same way as existing community provision in schools and other social spaces such as libraries or community centres. These hubs could act as a new iteration of the special school for the Deaf and host Deaf clubs, specialist provision, pastoral support and social activity.

The hubs could provide expertise on visual learning methods, sign language tuition for children and their families and could also facilitate a meeting place for Deaf people of all ages. The hubs would work in partnership with mainstream schools and peripatetic Teachers of the Deaf to enable access to a broad mainstream curriculum.

Dr Anglin-Jaffe said: "There is a need for Deaf children to access Deaf culture and sign language, whilst maintaining the positive achievements of inclusive practice such as raised expectations, family and community belonging and high academic achievement.

"Statistics suggest there are now less specialist provision for Deaf children in mainstream schools. We need to find new social spaces which meets the needs of Deaf children and adults."

Many special schools have closed and those that survive are faced with the threat of closure. They also support children with complex and additional needs. Whenever a school is threatened with closure grass roots activism from the Deaf community is mobilised, showing they inspire strong feelings of loyalty from parents, pupils, staff and the Deaf community.

The key features of the new Deaf education hubs proposed by Dr Anglin-Jaffe would be the ability for Deaf children to meet with their peers and use sign language. This would safeguard the existence of culturally significant places and social spaces for the Deaf community.

Hubs could be set up in areas where there are Deaf children who could benefit from access to BSL. They could be coordinated by local authorities and social enterprises.

Dr Anglin-Jaffe said: "New hubs within communities could provide linguistic support, social space and access to a peer group. Young Deaf children would spend part of their time learning and socialising there, and the majority in mainstream schools local to their families.

"From this hub 'ripples' could expand allowing Deaf children to engage as bilingual and bicultural learners moving between different languages and developing positive identities. This will challenge the perception of a hostile, inaccessible 'hearing world'. Empowering young Deaf children to see the whole world as theirs to inhabit would be a profound but welcome change at the heart of Deaf education."

New research published in EPJ B reveals that the higher-than-expected efficiency of PLEDs can be reached through interactions between triplet excitons, and impurities embedded in their polymer layers.

Molecular dynamics simulations have shown that the mysteriously high efficiency of polymer LEDs arises from interactions between triplet excitons in their polymer chains, and unpaired electrons in their molecular impurities.

Polymer LEDs (PLEDs) are devices containing single layers of luminescent polymers, sandwiched between two metal electrodes. They produce light as the metal layers inject electrons and holes into the polymer, creating distortions which can combine to form two different types of electron-hole pair: either light-emitting 'singlets,' or a non-emitting 'triplets.' Previous theories have suggested that the ratio between these two types should be around 1:3, which would produce a light emission efficiency of 25%.

However, subsequent experiments showed that the real value can be as high as 83%. In new research published in EPJ B, physicists in China, led by Yadong Wang at Hebei North University, found that this higher-than-expected efficiency can be reached through interactions between triplet excitons, and impurities embedded in the polymer.

Owing to their scientific and commercial value, PLEDs are becoming an increasingly popular field of research. The discoveries of Wang's team could now lead to more widespread applications of the devices in the future.

Within PLED polymer layers, excitons are known to be produced through the recombination of 'polarons' - distortions in electrical charges which form and disappear as electrons move through solid materials. However, other mechanisms must also be involved to explain why their luminescence efficiencies are so much higher than previous theories predicted. One proposal suggests that their electrical and optical properties of PLEDs are strongly influenced by unpaired electrons trapped within molecular impurities.

Wang and colleagues explored this idea through molecular dynamics simulations, which allowed them to recreate collisions between a non-emitting triplet exciton in a polymer chain, and an unpaired impurity electron. Their calculations revealed that light-emitting singlet excitons are among the main products of this reaction; with their overall proportion varying with the size of the impurity, and its degree of coupling with the polymer chain. For the first time, the result offers conclusive evidence that impurities can significantly boost the efficiency of PLEDs, and offers new clues about the molecular mechanisms involved.

Lesbian, gay and bisexual (LGB) individuals report higher rates of medical, non-medical, and illegal stimulant use compared to heterosexuals, mirroring patterns seen in other substance use. The study by Columbia University Mailman School of Public Health researchers provides the most detailed picture to date on stimulant use by LGB subgroups and gender. Findings are published in the American Journal of Preventive Medicine.

The researchers analyzed data from the 2015-2017 National Survey on Drug Use and Health to examine associations between sexual identity and past-year use of medical and non-medical stimulants (i.e., Adderall, Ritalin) and illegal stimulants (i.e., cocaine, crack, methamphetamine). They found that bisexual women's illegal stimulant use in the past year was fivefold that of heterosexual women (7.8% vs. 1.5%), while gay men's use was threefold that of heterosexual men (9.2% vs. 3.2%). Non-medical use of prescription stimulants was higher among gay and bisexual men than heterosexual men (5.4% and 6.6% vs. 2.4%) and among gay/lesbian and bisexual women versus heterosexual women (3.3% and 6.8% vs. 1.6%). Past-year medical use of prescription stimulants was higher among gay men than heterosexual men (6.6% vs. 4.1%) and bisexual women than heterosexual women (7.9% vs. 4.9%). There were no differences between bisexual men and women compared to their gay/lesbian counterparts.

Potential consequences of stimulant include substance use disorder and overdose, particularly given increases in fentanyl contamination in illegally produced pills and cocaine and methamphetamine. As many as half of LGB individuals who reported nonmedical and illegal stimulant use also reported nonmedical prescription opioid use.

"This study highlights the need for future interventions to target stimulant use among LGB populations, with a particular focus on harm reduction approaches," says first author Morgan Philbin, PhD, assistant professor of sociomedical sciences. "The findings have important implications across sexual identities, and demonstrate the need to disaggregate stimulant use by subgroup and gender, particularly related to polysubstance use."

Higher drug use among LGB individuals is likely a result of minority stress--that is, the fact that exposure to stigma and discrimination based on sexual orientation results in health disparities. Structural stigma (e.g., employment or housing discrimination) drives psychological and physical health morbidities among LGB populations, and perceived stigma is associated with cocaine use. Bisexuals can also experience "double discrimination" from heterosexuals and lesbian and gay communities, which the researchers say may account for the particularly high substance use among bisexual individuals.

The paper outlines several avenues to address stimulant use, including by educating healthcare providers who focus on LGB communities to screen for and discuss substance use, including stimulants. Communities and providers can also scale-up access to medication disposal and harm reduction services.

The researchers note that their dataset started assessing sexual identity among adults in 2015, so these relationships could not be examined in earlier years or among adolescents. The options for gender included only "male" or "female" and thus did not allow researchers to differentiate between transgender and cis-gender individuals. The dataset does not assess sexual behavior, so this study only captured associations based on individuals' sexual identity.

Survey of geosynchronous orbital debris led by University of Warwick found over 75% of debris detected could not be matched to known objects in public satellite catalogues

Astronomers are calling for more regular surveys with large telescopes to help quantify the risks posed to active satellites

Many of the objects detected show optical signatures of tumbling, providing insight into the dynamical evolution of debris within the geosynchronous environment

First instalment of DebrisWatch, an ongoing collaboration between the University of Warwick and the Defence Science and Technology Laboratory (UK)

University of Warwick astronomers are warning that orbital debris posing a threat to operational satellites is not being monitored closely enough, as they publish a new survey finding that over 75% of the orbital debris they detected could not be matched to known objects in public satellite catalogues.

The astronomers are calling for more regular deep surveys of orbital debris at high altitudes to help characterise the resident objects and better determine the risks posed to the active satellites that we rely on for essential services, including communications, weather monitoring and navigation.

The research forms part of DebrisWatch, an ongoing collaboration between the University of Warwick and the Defence Science and Technology Laboratory (UK) aiming to provide a fresh take on surveys of the geosynchronous region that have been conducted in the past. The results are reported in the journal Advances in Space Research. The research was part-funded by the Science and Technology Facilities Council (STFC), part of UK Research and Innovation, and was supported by the Royal Society.

This survey was optimised to search for faint debris, objects that are too small or poorly reflective to be regularly monitored and recorded in publicly available catalogues. The US Strategic Command (USSTRATCOM) maintains the most complete public catalogue of space objects, using its global Space Surveillance Network (SSN) comprising over 30 ground-based radars and optical telescopes, alongside 6 satellites in orbit. The SSN is able to monitor high-altitude objects down to roughly 1 metre in diameter. Although certain residents of the geosynchronous region are often referred to as 'stationary', collisions can still occur with relative velocities of kilometres per second. With this in mind, even small objects could cause a lot of damage to an active satellite.

Images from the survey were analysed using a custom software pipeline designed to pick out candidate debris objects and investigate their brightness over time. The resulting 'light curves' contain a wealth of information about the objects themselves, including their shape, surface properties and attitude, but are also affected by other factors like viewing geometry and atmospheric interference. Disentangling these components remains a very difficult task, and large quantities of high-quality data will be key to developing and refining the necessary techniques.

The astronomers focused their survey on the geosynchronous region, located roughly 36,000 kilometres above the Equator, where satellites orbit with a period that matches the Earth's rotation. Far above the outermost layer of the Earth's atmosphere, there are no natural mechanisms (like atmospheric drag) to induce orbital decay, so debris generated in the vicinity of the geosynchronous region will remain there for a very long time indeed.

To help them uncover faint debris, the astronomers made use of the Isaac Newton Telescope on the Canary Island of La Palma, which has a large 2.54 m aperture, allowing it to collect photons of light over a large area. They used an optimised strategy to ensure that the sunlight reflecting off of candidate objects would fall within the same pixels of the camera, to increase their chances of being detected. Strips of sky were scanned above, along and below the geostationary belt, where most of the operational geosynchronous satellites reside.

The majority of the orbital tracks detected by the astronomers had brightnesses corresponding to roughly 1 metre or less. Sure enough, over 95% of these faint detections failed to match with a known object in the publicly available USSTRATCOM catalogue, as they are too faint to be regularly and reliably monitored by the SSN. When the researchers included all their detections - including those above and below 1m - over 75% failed to match.

Lead author James Blake, a PhD student in the University of Warwick Department of Physics, said: "The light curves extracted from our survey images show just how varied these objects can be, both in terms of their physical nature and of their attitude or behaviour within orbit. Many of the faint, uncatalogued debris appear to be tumbling, showing significant brightness variation across the observation window. These sorts of features can tell us a lot about the perturbative forces acting on residents of the geosynchronous region, but also highlight that we need to be more careful when making assumptions about the properties of these objects. We need to probe the faint debris population further and obtain more data to gain a better understanding of what's out there.

"It's important that we continue to observe the geosynchronous region with large telescopes wherever possible, to start to build up a more complete feel for the faint debris environment. With this survey, we've probed deeper than ever before, and still the population appears to be climbing as our sensitivity limit is reached. While we're dealing with small number statistics here, it's unsurprising that we see many more small, faint objects than large, bright ones."

Artificial debris orbiting the Earth can originate for a number of reasons: the satellites themselves become debris when they reach the end of their mission lifetime; rocket bodies abandoned after successfully launching their payloads can explode or 'break-up' after many years in orbit; collisions can occur between orbiting bodies, sometimes resulting in thousands of new fragments; the harsh environment of space can deteriorate satellites over time, shedding bits of insulating blanket and paint flakes.

The astronomers are now investigating ways to extract even more information from the survey data, using simultaneous observations that were taken with a second, smaller instrument. They aim to foster new collaborations to ensure this survey can act as a gateway to an enduring activity.

Co-author Professor Don Pollacco, from the University of Warwick Department of Physics, said: "This kind of data will be key in the development of algorithms to characterise objects in the geosynchronous region. Remember that we're not dealing with close-up photographs here, even the big satellites appear as non-resolved blobs of light in our images. Light curves offer a great opportunity to learn more about the way these objects behave and what they might be. The more high-quality data we take, the better chance we have of developing these tools."

WASHINGTON--Scientists have spotted a once-in-a-century climate anomaly during World War I that likely increased mortality during the war and the influenza pandemic in the years that followed.

Well-documented torrential rains and unusually cold temperatures affected the outcomes of many major battles on the Western Front during the war years of 1914 to 1918. Most notably, the poor conditions played a role in the battles of Verdun and the Somme, during which more than one million soldiers were killed or wounded.

The bad weather may also have exacerbated the Spanish flu pandemic that claimed 50 to 100 million lives between 1917 and 1919, according to the new study. Scientists have long studied the spread of the H1N1 influenza strain that caused the pandemic, but little research has focused on whether environmental conditions played a role.

In a new study in AGU's journal GeoHealth, scientists analyzed an ice core taken from a glacier in the European Alps to reconstruct climate conditions during the war years. They found an extremely unusual influx of air from the North Atlantic Ocean affected weather on the European continent from 1914 to 1919. The incessant rain and cold caused by this influx of ocean air hung over major battlefields on the Western Front but also affected the migratory patterns of mallard ducks, the main animal host for H1N1 flu virus strains.

Mallard ducks likely stayed put in western Europe in the autumns of 1917 and 1918 because of the bad weather, rather than migrating northeast to Russia as they normally do, according to the new study. This kept them close to military and civilian populations and may have allowed the birds to transfer a particularly virulent strain of H1N1 influenza to humans through bodies of water. Listen to the latest episode of AGU's podcast Third Pod from the Sun to learn more about climate and pandemics.

The findings help scientists better understand the factors that contributed to making the war and pandemic so deadly, according to Alexander More, a climate scientist and historian at the Harvard University/Climate Change Institute, associate professor of environmental health at Long Island University and lead author of the new study.

"I'm not saying that this was 'the' cause of the pandemic, but it was certainly a potentiator, an added exacerbating factor to an already explosive situation," More said.

"It's interesting to think that very heavy rainfall may have accelerated the spread of the virus," said Philip Landrigan, director of the Global Public Health Program at Boston College who was not connected to the new study. "One of the things we've learned in the COVID pandemic is that some viruses seem to stay viable for longer time periods in humid air than in dry air. So it makes sense that if the air in Europe were unusually wet and humid during the years of World War I, transmission of the virus might have been accelerated."

War and weather

The rainy, cold, muddy landscapes of the Western Front are well documented by historians. Poet Mary Borden described it as "the liquid grave of our armies" in her poem "The Song of the Mud" about 1916's Battle of the Somme.

Historical accounts of early battles in France describe how the intense rain affected British, French and German troops. Newly dug trenches and tunnels filled with rainwater; muddy fields slowed the movement of troops during the day; and cold nighttime temperatures caused thousands to endure frostbite. However, little research has been done on the environmental conditions that may have caused the torrential rains and unusual cold.

In the new study, More and his colleagues reconstructed the environmental conditions over Europe during the war using data from an ice core taken from the Alps. They then compared the environmental conditions to historical records of deaths during the war years.

They found mortality in Europe peaked three times during the war, and these peaks occurred during or soon after periods of cold temperatures and heavy rain caused by extremely unusual influxes of ocean air in the winters of 1915, 1916 and 1918.

"Atmospheric circulation changed and there was much more rain, much colder weather all over Europe for six years," More said. "In this particular case, it was a once in a 100-year anomaly."

The new ice core record corroborates historical accounts of torrential rain on battlefields of the Western Front, which caused many soldiers to die from drowning, exposure, pneumonia and other infections.

Interestingly, the results suggest the bad weather may have kept mallard ducks and other migratory birds in Europe during the war years, where they could easily transmit influenza to humans by water contaminated with their fecal droppings. Mallard ducks are the main animal reservoir of H1N1 flu viruses and as many as 60 percent of mallard ducks can be infected with H1N1 every year. Previous research has shown that migratory patterns of mallards and other birds are disrupted during bouts of unusual weather.

"Mallards have been shown to be very sensitive to climate anomalies in their migration patterns," More said. "So it is likely is that they stayed put for much of that period."

The first wave of H1N1 influenza infection in Europe occurred in the spring of 1918, most likely originating among allied troops arriving in France from Asia in the fall and winter of 1917, according to previous research. The new study found the deadliest wave of the pandemic in Europe began in the autumn of 1918, closely following a period of heavy precipitation and cold temperatures.

"These atmospheric reorganizations happen and they affect people," More said. "They affect how we move, how much water is available, what animals are around. Animals bring their own diseases with them in their movements, and their migrations are due to the environment and how it changes, or how we change it."

"I think it's a very credible, provocative study that makes us think in new ways about the interplay between infectious diseases and the environment," Landrigan said.

ABERDEEN PROVING GROUND, Md. -- Future technology may be able to monitor and modify the brain to produce enhanced team performance, while increasing the efficiency and accuracy of decisions.

The U.S. Army may be able to use this information to enhance future operations.

"We are working toward fused human-technology systems that work synergistically to not only impact perceptions, decisions and actions of the Soldier, but also to enhance the hybrid human system's capabilities for rapid and adaptive decision making," said Dr. Javier Garcia, an Army neuroscientist.

The U.S. Army Combat Capabilities Development Command's Army Research Laboratory, the Italian Institute of Technology, Italy, Harvard Medical School and the University of California, Irvine teamed up to study and advance research on the complexities of the human brain. Scientific Reports recently published the discoveries from their study.

Building on previous studies, the researchers used transcranial magnetic stimulation, or TMS, and within minutes of continuous stimulation, subjects were placed in a functional magnetic resonance imaging, or fMRI, scanner and asked to perform a very challenging attention tracking task.

"TMS is the type of neurostimulation that is simply an electromagnet that you put on your head and as you quickly send pulses through the electromagnetic, it induces current into whatever conductive body is next to it will, modifying neural activity -- and sometimes behavior," Garcia said. "We are stimulating the brain, except in this stimulation protocol, we use very rapid and consecutive pulses to the brain to inhibit a part of the brain."

Researchers used a stroke model to see neural changes after a specific part of the brain was inhibited and then tracked the brain's recovery. They wanted to know how long the changes would last, the brain network changes due to the stimulation, and the behavioral consequences.

"Noninvasive brain stimulation is a tool that allows neuroscientists to gain insight into disease spreading and compensatory reorganization following stroke," said Prof. Emily Grossman, UCI professor of cognitive science. "We know from patient and brain imaging work that brain injury to a focal, or localized, brain site has a spreading effect that destabilizes connected circuits far from the actual site of impact."

She said in many cases the downstream effects are significant, but also difficult to predict due to the complicated nature of brain organization -- best described as a set of large-scale networks that have various points of connection.

"In this study, we target the attention network of the brain, which consists of a specialized set of brain regions involved in controlling where and when we best encode information about the world around us," Grossman said. "Visual attention is essential for everything we do in daily life, including tasks like monitoring streams of visual information when driving, engaging in conversation and tracking our children on a busy soccer field."

When individuals experience an injury to the attention network, tracking skills become impaired and it is more difficult to maintain focus on individual items embedded in a cluttered environment, she said.

"This study suggests that recovery may depend, in part, on the compensatory reorganization of brain networks downstream and connected to the site of impact," Grossman said. "These downstream networks experienced a brief interval of dynamic reorganization after stimulation, and are known to be important for manipulating information that we are attending to and are using to make decisions about events in the visual environment."

Researchers at the lab are investing in a variety of techniques and methods to extend the state of the art in real-world neuroimaging.

"This unique collaboration brings cognitive, clinical, and army researchers together from across the globe to probe the dynamic network changes as a consequence of neurostimulation," Garcia said. "While we provided the innovative methods and analysis to this research -- others brought the clinical and cognitive aspects."

Together they plan to explore more neurostimulation protocols and bring this technology to a closed-loop, human-autonomy teaming perspective, building upon the work that proves the brain may be nudged to specific behaviorally-relevant configurations.

Kidney injury is a dreaded complication in patients hospitalized for COVID-19, with more than a third of patients ending up in need of dialysis. Patients with COVID-19-related kidney injury are also at much higher risk of death.

"We don't known exactly why patients with severe COVID-19 have a high rate of kidney injury," says Salim Hayek, M.D., a cardiologist at the Michigan Medicine (University of Michigan) Frankel Cardiovascular Center and senior author of a new observational study." It is, however, becoming clearer that a hyperactive immune system plays a major role in the morbidity of COVID-19, including kidney-related complications."

In the multi-center study published in the Journal of the American Society of Nephrology, Hayek and an international team of experts report that levels of a protein in blood produced by immune cells and known to be involved in causing kidney disease are very high in patients hospitalized for COVID-19 and strongly predictive of kidney injury.

The research team tested soluble urokinase plasminogen activator receptor (suPAR) levels of 352 study participants when they were admitted to the hospital for COVID-19 infection.

A quarter of the participants developed acute kidney injury while hospitalized, and their median suPAR levels were more than 60% higher than those of the rest of the participants. The risk of needing dialysis was increased 20-fold in patients with the highest suPAR levels. Overall, median suPAR levels for these study participants hospitalized with severe COVID-19 were almost three times higher than levels of healthy people.

"SuPAR is an immune-derived circulating factor we've seen contribute to kidney injury in thousands of patients," says Jochen Reiser, M.D., Ph.D., a professor of medicine at Rush University and expert in the biology of suPAR. "RNA viruses such as HIV and SARS-CoV-2 elicit a suPAR response of the innate immune system leading to a rise in blood suPAR levels. If there is a hyperinflammatory suPAR response, kidney cells may be damaged."

Study author Subramaniam Pennathur, M.D., a professor of nephrology at Michigan Medicine, says identifying suPAR levels at hospital admission as a strong predictor for AKI during the hospitalization has important implications for future care.

"For example, obtaining suPAR levels may allow us to risk-stratify, i.e., identify high risk patients early, and institute appropriate preventive treatment, thereby reducing AKI risk and improving COVID-19 outcomes," he says. "Second, therapies aimed at interrupting suPAR pathway may also be explored for preventative as well as a therapeutic option for COVID-19 AKI."

Hayek, an expert on this protein is currently researching how best to reduce suPAR levels in those people at highest risk.

"We're preparing to launch the first clinical trial targeting suPAR to prevent COVID-19 related kidney injury, and by doing so hope to alleviate the burden of kidney disease in both COVID-19 and non-COVID-19 patients with high suPAR levels," he says.

Two scientists from IP2I (CNRS/Université Claude Bernard Lyon 1), in collaboration with a researcher from the University of Southern Denmark and the University of Naples Federico II, have developed a new mathematical model inspired by high energy physics to predict the next waves of the Covid-19 pandemic. The extension of this technique to epidemiology, referred to as the epidemic Renormalisation group,[1] and widely used in particle physics and condensed matter physics, yields a mathematical model that can characterise the evolution of the pandemic across European territories. Their simulations, which were conducted on the basis of infection rates and travel within and between European countries from March to July 2020, suggest that a second wave will impact Europe between July 2020 and January 2021.[2] While it is not possible to provide specific details of this second wave, or to identify when exactly the next peak of infections will take place in France, the simulations underscore the importance of human behaviour in slowing the pandemic. According to this research, the precise moment of peak infection rates for each country can be controlled through social distancing, the control of local "clusters," and border control measures. The study was published in Scientific Reports on 23 September 2020.

Further information: the authors modelled the temporal dynamic of a second wave in numerous European countries, and created a simulation video of when a second wave is likely to peak in each country. This animation is the result of many simulations of the second wave. The researchers assumed that the countries included would adopt measures for the second wave similar to those for the first, and that group immunity is not yet reached. The simulations begin on calendar week 25. The fact that some countries have already experienced a second wave beginning on August 5 is taken into consideration.

People infected by the novel coronavirus can have symptoms that range from mild to deadly. Now, two new analyses suggest that some life-threatening cases can be traced to weak spots in patients' immune systems.

At least 3.5 percent of study patients with severe COVID-19, the disease caused by the novel coronavirus, have mutations in genes involved in antiviral defense. And at least 10 percent of patients with severe disease create "auto-antibodies" that attack the immune system, instead of fighting the virus. The results, reported in two papers in the journal Science on September 24, 2020, identify some root causes of life-threatening COVID-19, says study leader Jean-Laurent Casanova, a Howard Hughes Medical Institute Investigator at The Rockefeller University.

Seeing these harmful antibodies in so many patients - 101 out of 987 - was "a stunning observation," he says. "These two papers provide the first explanation for why COVID-19 can be so severe in some people, while most others infected by the same virus are okay."

The work has immediate implications for diagnostics and treatment, Casanova says. If someone tests positive for the virus, they should "absolutely" be tested for the auto-antibodies, too, he adds, "with medical follow-up if those tests are positive." It's possible that removing such antibodies from the blood could ease symptoms of the disease.

A global effort

Casanova's team, in collaboration with clinicians around the world, first began enrolling COVID-19 patients in their study in February. At the time, they were seeking young people with severe forms of the disease to investigate whether these patients might have underlying weaknesses in their immune systems that made them especially vulnerable to the virus.

The plan was to scan patients' genomes - in particular, a set of 13 genes involved in interferon immunity against influenza. In healthy people, interferon molecules act as the body's security system. They detect invading viruses and bacteria and sound the alarm, which brings other immune defenders to the scene.

Casanova's team has previously discovered genetic mutations that hinder interferon production and function. People with these mutations are more vulnerable to certain pathogens, including those that cause influenza. Finding similar mutations in people with COVID-19, the team thought, could help doctors identify patients at risk of developing severe forms of the disease. It could also point to new directions for treatment, he says.

In March, Casanova's team was aiming to enroll 500 patients with severe COVID-19 worldwide in their study. By August, they had more than 1,500, and they now have over 3,000. As the researchers began analyzing patient samples, they started to uncover harmful mutations, in people young and old. The team found that 23 out of 659 patients studied carried errors in genes involved in producing antiviral interferons.

Without a full complement of these antiviral defenders, COVID-19 patients wouldn't be able to fend off the virus, the researchers suspected. That thought sparked a new idea. Maybe other patients with severe COVID-19 also lacked interferons - but for a different reason. Maybe some patients' bodies were harming these molecules themselves. As in autoimmune disorders such as type 1 diabetes and rheumatoid arthritis, some patients might be making antibodies that target the body. "That was the eureka moment for us," Casanova says.

The team's analysis of 987 patients with life-threatening COVID-19 revealed just that. At least 101 of the patients had auto-antibodies against an assortment of interferon proteins. "We said, 'bingo'!" Casanova remembers. These antibodies blocked interferon action and were not present in patients with mild COVID-19 cases, the researchers discovered.

"It's an unprecedented finding," says study co-author Isabelle Meyts, a pediatrician at the University Hospitals KU Leuven, in Belgium, who earlier this year helped enroll patients in the study, gather samples, and perform experiments. By testing for the presence of these antibodies, she says, "you can almost predict who will become severely ill."

The vast majority - 94 percent - of patients with the harmful antibodies were men, the team found. Men are more likely to develop severe forms of COVID-19, and this work offers one explanation for that gender variability, Meyts says.

Casanova's lab is now looking for the genetic driver behind those auto-antibodies. They could be linked to mutations on the X chromosome, he says. Such mutations might not affect women, because they have a second X chromosome to compensate for any defects in the first. But for men, who carry only a single X, even small genetic errors can be consequential.

Looking ahead
Clinically, the team's new work could change how doctors and health officials think about vaccination distribution strategies, and even potential treatments. A clinical trial could examine, for instance, whether infected people who have the auto-antibodies benefit from treatment with one of the 17 interferons not neutralized by the auto-antibodies, or with plasmapheresis, a medical procedure that strips the antibodies from patients' blood. Either method could potentially counteract the effect of these harmful antibodies, Meyts says.

In addition to the current work, Meyts, Casanova, and hundreds of other scientists involved with an international consortium called the COVID Human Genetic Effort are working to understand a second piece of the coronavirus puzzle. Instead of hunting for factors that make patients especially vulnerable to COVID-19, they're looking for the opposite - genetic factors that might be protective. They're now recruiting people from the households of patients with severe COVID-19 - people who were exposed to the virus but did not develop the disease. "Our lab is currently running at full speed," Casanova says.

More than 10 percent of young and healthy people who develop severe COVID-19 have misguided antibodies that attack not the virus, but the immune system itself, new research shows. Another 3.5 percent, at least, carry a specific kind of genetic mutation.

In both groups, the upshot is basically the same: The patients lack type I interferon, a set of 17 proteins crucial for protecting cells and the body from viruses. Whether the proteins have been neutralized by so-called auto-antibodies, or were not produced in sufficient amounts in the first place due to a faulty gene, their missing-in-action appears to be a common theme among a subgroup of COVID-19 sufferers whose disease has thus far been a mystery.

Published in two papers in Science, the findings help explain why some people develop a disease much more severe than others in their age group--including, for example, individuals who required admission to the ICU despite being in their 20s and free of underlying conditions. They may also provide the first molecular explanation for why more men than women die from the disease.

"These findings provide compelling evidence that the disruption of type I interferon is often the cause of life-threatening COVID-19," says Jean-Laurent Casanova, head of the St. Giles Laboratory of Human Genetics of Infectious Diseases at The Rockefeller University and a Howard Hughes Medical Institute investigator. "And at least in theory, such interferon problems could be treated with existing medications and interventions."

The findings are the first results being published out of the COVID Human Genetic Effort, an ongoing international project spanning over 50 sequencing hubs and hundreds of hospitals around the world, co-led by Casanova and Helen Su at the National Institute of Allergy and Infectious Diseases. The study participants included various nationalities from Asia, Europe, Latin America, and the Middle East. "COVID-19 may now be the best understood acute infectious disease in terms of having a molecular and genetic explanation for nearly 15% of critical cases across diverse ancestries," Casanova says.

Genetics of COVID-19 outliers

The way SARS-CoV-2 affects people differently has been puzzling. The virus can cause a symptom-free infection and go away quietly, or it can kill in a few days. Casanova's research over the past two decades has shown that unusual susceptibility to certain infectious diseases can be traced to single-gene mutations that affect an individual's immune response.

Since February, his team and their collaborators have been enrolling thousands of COVID-19 patients to find out whether something in their genetic make-up drives the disparate clinical outcomes the disease produces.

In one study, the researchers genetically analyzed blood samples from more than 650 patients who had been hospitalized for life-threatening pneumonia due to SARS-CoV-2, 14 percent of whom had died. They also included samples from another group of over 530 people with asymptomatic or benign infection. They initially searched for differences between the two groups across 13 genes known to be critical for the body's defense against the influenza virus. These genes govern type I interferons.

It soon became obvious that a significant number of people with severe disease carried rare variants in these 13 genes, and more than 3 percent of them were in fact missing a functioning gene. Further experiments showed that immune cells from these patients did not produce any detectable type I interferons in response to SARS-CoV-2.

Interferons are part of the intrinsic and innate immunity, kicking in before the adaptive immune system mounts an antibody response. They are known to play an important role in immediately heightening the cells' defenses in response to several viruses. Follow up experiments led by Rockefeller's Charles M. Rice showed that this is also the case for SARS-CoV-2: Human fibroblast cells with mutations affecting the interferon type I pathway were more vulnerable to the virus, and died in higher numbers--and faster--than cells without those mutations.

A mysterious autoimmune condition

Three other infectious diseases caused by mutations affecting an immune signaling protein can also be caused by auto-antibodies against that protein. So next, the team checked for the possibility of a similar scenario.

Examining 987 patients with life-threatening COVID-19 pneumonia, they found that more than 10 percent had auto-antibodies against interferons at the onset of their infection. The majority of them, 95%, were men.

Biochemical experiments confirmed these auto-antibodies can effectively curb the activity of interferon type I. In some cases, they could be detected in blood samples taken before patients became infected; in others, they were found in the early stages of the infection, before the immune system had the time to mount a response.

These auto-antibodies seem to be rare in the general population. Out of 1,227 randomly selected healthy people, only four were found to have them.

"All of these findings strongly indicate that these auto-antibodies are actually the underlying reason some people get very sick, and not the consequence of the infection," Casanova says.

The findings point to certain medical interventions to consider for further investigation, Casanova says. For example, there are already two types of interferons available as drugs and approved for use to treat certain conditions such as chronic viral hepatitis.

The team continues to look for genetic variations that may affect other types of interferons or additional aspects of the immune response in COVID-19 outliers.

Two new studies report specific mechanisms of impaired type I interferon (IFN) signaling in some hospitalized patients suffering from severe cases of COVID-19, suggesting that screens for these defects could help identify patients at the highest risk of life-threatening complications from SARS-CoV-2 infection. The results of the paired studies - which report that mutations in type I IFN-associated genes and high titers of neutralizing autoantibodies against type I IFNs may both be associated with severe COVID-19 respiratory symptoms - also suggest that administering specific type I IFNs to select high-risk patients could offer therapeutic benefits, especially early in the course of the disease. To test whether severe COVID-19 respiratory symptoms may be associated with the genetics of type I IFN signaling, Qian Zhang and colleagues performed whole-genome or whole-exome sequencing of 659 patients hospitalized with life-threatening COVID-19 pneumonia and 534 patients with asymptomatic or mild infection. Focusing on 13 gene loci known to govern TLR3- and IRF7-dependent type I IFN immunity to influenza virus, the researchers found rare loss-of-function gene variants in 3.5% of the patients with severe COVID-19 symptoms, but not in the asymptomatic/mild cohort. This subgroup of patients (23 in total) ranged in age from 17 to 77, with representation of both sexes and various ancestries. Based on their findings, the researchers suggest that mutations in other type I IFN-related genes may exist in other patients with life-threatening COVID-19 symptoms. In a related study, Paul Bastard and colleagues investigated whether neutralizing autoantibodies (which aberrantly recognize, bind to, and neutralize a patient's own proteins) against type I IFNs might also underlie severe COVID-19 pneumonia. In a screen of 987 patients with dire cases of COVID-19, the researchers found that 101 patients had autoantibodies against IFN-ω, IFN-a, or both. In contrast, 663 patients with asymptomatic or mild cases of COVID-19 had none of the autoantibodies, and only 4 of 1,227 healthy individuals, sampled before the pandemic, had one or more of the autoantibody types. Based on their findings, Bastard et al. conclude that "the neutralizing [autoantibodies] against type I IFNs, like inborn errors of type I IFN production, tip the balance in favor of the virus, resulting in devastating disease, with insufficient, and even perhaps deleterious, innate and adaptive immune responses."

Researchers from North Carolina State University have demonstrated the utility of artificial intelligence (AI) in identifying and categorizing neural degeneration in the model organism C. elegans. The tool uses deep learning, a form of AI, and should facilitate and expedite research into neural degeneration.

"Researchers want to study the mechanisms that drive neural degeneration, with the long-term goal of finding ways to slow or prevent the degeneration associated with age or disease," says Adriana San Miguel, corresponding author of a paper on the work and an assistant professor of chemical and biomolecular engineering at NC State. "Our work here shows that deep learning can accurately identify physical symptoms of neural degeneration; can do it more quickly than humans; and can distinguish between neural degeneration caused by different factors.

"Having tools that allow us to identify these patterns of neural degeneration will help us determine the role that different genes play in these processes," San Miguel says. "It will also help us evaluate the effect of various pharmaceutical interventions on neural degeneration in the model organism. This is one way we can identify promising candidates for therapeutic drugs to address neurological disorders."

For this study, researchers focused on C. elegans, or roundworm, which is a model organism widely used to study aging and the development of the nervous system. Specifically, the researchers focused on PVD neurons, which are nerve cells that can detect both touch and temperature. The researchers chose the PVD neuron because it is found throughout the nervous system of C. elegans and it is known to degenerate due to aging.

Roundworms are tiny and transparent - meaning that it is possible to see their nervous systems while they are still alive. Traditionally, identifying degeneration in C. elegans neurons requires researchers to look for microscopic changes in the cell, such as the appearance of bubbles that form on parts of individual neurons. Researchers can analyze the extent of neural degeneration by tracking the size, number and location of these bubbles.

"Counting these bubbles is a time-consuming and labor-intensive process," says Kevin Flores, co-author of the study and an assistant professor of mathematics at NC State. "We've demonstrated that we can collect all of the relevant data from an image in a matter of seconds, by combining the power of deep-learning with the advanced speed of so-called GPU computing. This enables a much faster quantitative assessment of neuronal degeneration than traditional techniques."

In addition to monitoring the effects of age on neural degeneration, the researchers also examined the effects of "cold shock," or prolonged exposure to low temperatures. The researchers were surprised to learn that cold shock could also induce neural degeneration.

"We also found that neural degeneration caused by cold shock had a different pattern of bubbles than the degeneration caused by aging," San Miguel says. "It is difficult or impossible to distinguish the difference with the naked eye, but the deep learning program found it consistently.

"This work tells us that deep learning tools are able to spot patterns we may be missing - and we may be just scratching the surface of their utility in advancing our understanding of neural degeneration."

Tiny crystals, ten thousand times thinner than a human hair, can cause explosive volcanic eruptions. This surprising connection has recently been discovered by a German-British research team led by Dr. Danilo Di Genova from the Bavarian Research Institute of Experimental Geochemistry & Geophysics (BGI) at the University of Bayreuth. The crystals increase the viscosity of the underground magma. As a result, a build-up of rising gases occurs. The continuously rising pressure finally discharges in massive eruptions. The scientists present the results of their nanogeoscientific research in the journal "Science Advances".

"Exactly what causes the sudden and violent eruption of apparently peaceful volcanoes has always been a mystery in geology research. Nanogeoscience research has now allowed us to find an explanation. Tiny crystal grains containing mostly iron, silicon, and aluminium are the first link in a chain of cause and effect that can end in catastrophe for people living in the vicinity of a volcano. The most powerful volcanic eruption in human history was Mount Tambora in Indonesia in 1815", says Dr. Danilo Di Genova. For the recently published study, he worked closely with scientists from the University of Bristol, the Clausthal University of Technology, and two European synchrotron radiation facilities.

Because of their diameter of a few nanometres, the crystals are also known as nanolites. Using spectroscopic and electron microscopy methods, the researchers have detected traces of these particles, invisible to the eye, in the ashes of active volcanoes. In the BGI's laboratory, they were then able to describe these crystals and finally to demonstrate how they influence the properties of volcanic magma. The investigations focused on magma of low silicon oxide content cooling to form basalt on the earth's surface after a volcanic eruption. Low silica magma is known for its low viscosity: It forms a thin lava that flows quickly and easily. The situation is different, however, if it contains a large number of nanolites. This makes the magma viscous - and far less permeable to gases rising from the earth's interior. Instead of continuously escaping from the volcanic cone, the gases in the depths of the volcano become trapped in the hot magma. As a result, the magma is subjected to increasing pressure until it is finally ejected explosively from the volcano.

"Constant light plumes of smoke above a volcanic cone need not necessarily be interpreted as a sign of an imminent dangerous eruption. Conversely, however, the inactivity of apparently peaceful volcanoes can be deceptive. Rock analyses, written and archaeological sources suggest, for example, that people in the vicinity of Vesuvius were surprised by an extremely violent eruption of the volcano in 79 AD. Numerous fatalities and severe damage to buildings were the result", says Di Genova. In his further research, the Bayreuth scientist hopes to use high-pressure facilites and computer simulation to model the geochemical processes that lead to such unexpected violent eruptions. The aim is to better understand these processes and thus also to reduce the risks for the population in the vicinity of volcanoes.