Culture

People with gambling problems are less likely to consider important information that could prevent them from losing, according to new research published today from the UBC's Centre for Gambling Research.

Instead, people with gambling disorder pay more attention to irrelevant information from the previous gamble to inform their next choice.

"Our research may help explain why individuals with gambling disorder continue to gamble in the face of mounting losses, and on games that have a very small chance of winning," said Eve Limbrick-Oldfield, the study's lead author and a postdoctoral research fellow at the UBC department of psychology and Centre for Gambling Research.

To conduct the study, the researchers recruited two groups of participants, 48 of whom have gambling disorder and 35 control participants. The participants were asked to complete a computerized decision-making task where they repeatedly chose between two lotteries. The two lotteries varied in prize size and chance of winning - one lottery had a smaller prize, but higher chance of winning while the other had a larger prize, but a smaller chance of winning. The participants were given all the information that was needed to make an optimal decision.

"We found control participants paid attention to both the prize size and chance of winning when choosing between the lotteries but the individuals with gambling disorder were more likely to ignore that information. Instead, they relied on whether they won or lost in the last gamble to make a decision," said Limbrick-Oldfield. "The finding can be easily translated into real-world gambling situations. For example, someone using a slot machine that hasn't paid out in a while can believe that the machine is somehow 'due' a win."

This study is the first of its kind to see whether win size and probability information have an effect on how individuals with gambling disorder make decisions. The findings support the hypothesis that individuals with gambling disorder are susceptible to irrelevant sources of information to guide gambling decisions.

The researchers do not know whether this impaired decision-making predates the gambling disorder or is a consequence of prolonged gambling but they hope to find out in future research. They are currently working on another study that uses eye-tracking to see if problem gamblers pay more attention to certain information given to them.

"These findings could help inform psychological treatments for gambling disorder that work on dismantling erroneous beliefs and enhancing financial literacy," said Luke Clark, UBC Centre for Gambling Research director and a professor in the department of psychology.

The research team also hope the findings could be used when building algorithms for online gambling websites to identify those gamblers who might be at risk of having a gambling problem.

When Terrie Williams began hearing about the wide range of symptoms experienced by patients with COVID-19, she saw a connection between the various ways the disease is affecting people and the many physiological adaptations that have enabled marine mammals to tolerate low oxygen levels during dives.

Williams, a professor of ecology and evolutionary biology at UC Santa Cruz, has spent decades studying the physiology of marine mammals and their extraordinary ability to perform strenuous activities while holding their breath for long periods under water.

"Diving marine mammals experience a lifetime of rapid physiological transitions between normal oxygenation and hypoxia [low oxygen levels]," Williams said. "They've got ways to protect themselves and allow their organs to keep functioning while holding their breath for hours at a time, but there's a whole suite of biological adaptations that had to happen for them to be able to do that."

Lacking those adaptations, humans are vulnerable to rapid damage in a wide range of tissues when oxygen levels drop due to the effects on the lungs and cardiovascular system of infection with the coronavirus SARS-CoV-2. In a review article published December 3 in Comparative Biochemistry and Physiology, Williams explores how the diving physiology of marine mammals can help us understand the effects of COVID-19.

"It really highlights why it is so important for people to protect themselves from infection with this virus," she said. "Damage to oxygen-deprived tissues happens fast and can be irreversible, which may account for the long-term effects we are beginning to see in people after coronavirus infections."

The heart and brain are especially sensitive to oxygen deprivation, and marine mammals have multiple mechanisms to protect these and other critical organs. In the first place, marine mammals have much higher oxygen carrying capacity than humans due to their greater blood volume and hemoglobin concentrations. In addition, some marine mammals contract their spleen during dives to release a store of oxygen-rich blood cells into the circulation. To avoid blood clots resulting from such high concentrations of red blood cells, many species lack a key clotting factor found in other mammals.

Other adaptations include greatly increased concentrations of oxygen-carrying proteins such as myoglobin in heart and skeletal muscles and neuroglobin and cytoglobin in the brain. In addition, numerous safety factors and biochemical buffers enable even the most oxygen-dependent tissues in marine mammals to withstand not only low oxygen but also the subsequent reperfusion of tissues with oxygenated blood. In humans, reperfusion after a heart attack or stroke often leads to additional tissue damage.

According to Williams, the solutions that marine mammals have evolved for tolerating hypoxia provide a natural template for understanding the potential for damage to oxygen-deprived tissues in humans.

"Studying marine mammals allowed me to understand what it takes to protect the body when the availability of oxygen is low," she said. "There are so many ramifications of shutting down the oxygen pathway, and I think that's what we're seeing in these COVID patients."

Williams is particularly concerned about the so-called "long-haulers" who continue to have symptoms long after they were infected with the coronavirus.

"You hear people say it's just like the flu, but COVID scares the heck out of me because of the potential for long-term damage to the heart and brain," she said. "When you think about oxygen deprivation and the tissue repair process, it makes sense that many people are having a hard time getting back to normal life, even after a mild infection."

Williams urges people to do all they can to avoid becoming infected. "Our heart and brain cells are meant to last a lifetime, and we cannot replace them once they are damaged," she said. "Dolphins and whales have natural protections that humans lack, so we are highly vulnerable to hypoxia."

"Super-spreader" events and extensive person-to-person contact propelled an outbreak of hantavirus pulmonary syndrome in a small village in Argentina from 2018-2019, according to research published today in The New England Journal of Medicine.

In the paper, an international scientific team reports the genetic, clinical, and epidemiologic features of the outbreak caused by the Andes virus, a member of the hantavirus family. The group's analysis could aid clinicians and public health officials in managing outbreaks of other viral diseases with similar transmission patterns, including COVID-19.

Andes virus is carried by wild rodents native to South America, and people can be infected through exposure to infected animals or their droppings. Like other hantaviruses, Andes virus infection can lead to a severe and often fatal respiratory disease in humans, called Hantavirus Pulmonary Syndrome (HPS). Importantly, Andes virus is the only hantavirus known to spread person to person. Those who come into direct contact with an infected individual or their body fluids, or who spend time in close proximity to an ill person, may also become infected. Currently, no licensed vaccines or drugs are available to treat the disease.

According to the study, led by scientists at the U.S. Army Medical Research Institute of Infectious Diseases (USAMRIID) and Administracion Nacional de Laboratorios e Institutos de Salud Dr. Carlos G. Malbran (ANLIS), large social events and high viral load in infected individuals fueled person-to-person transmission of the Andes virus during the outbreak. Researchers teamed up with local health authorities to piece together a near-complete epidemiological "picture" reconstructing specific transmission events for the 34 confirmed cases. They traced the outbreak's origin to a single spillover event, and documented a 32 percent case fatality rate overall.

While person-to-person spread of Andes virus was first described in 1996, the recent outbreak had the most extensive recorded human-to-human transmission of the virus seen to date. The team's genomic analysis showed a striking similarity between the 2018-2019 and 1996 outbreak sequences. Understanding which genomic "signatures" correspond to the mechanisms necessary for person-to-person transmission may help scientists to develop new therapeutics to treat Andes virus infection.

Researchers found that droplets or aerosolized viral particles may have been routes of infection during the extensive person-to-person transmission of the 2018-2019 outbreak. They also noted that symptoms presented anywhere between 9 and 40 days after the infection took place. However, the authors pointed out that there might be a narrow window of infectiousness. Transmission often occurred on the first day of fever presentation in an infected patient. Interestingly, there was no clear association between the individuals transmitting the virus and their disease severity.

"This important observation indicates that, regardless of the severity of the disease, all HPS cases should be equally managed concerning their potential for virus transmission," said Gustavo Palacios, Ph.D., co-senior author of the paper and Division Chief of Molecular Biology at USAMRIID. "Furthermore, we need to re-evaluate the threat that this virus poses. The lack of existing medical countermeasures, super-spreading potential, and high case-fatality rate all should raise concern."

These findings could potentially help clinicians and public health officials deal with future outbreaks. As with the preventive measures currently being practiced for COVID-19, social distancing and the use of appropriate personal protective equipment were effective in controlling transmission. Moreover, widespread contact tracing and self-quarantining led to a detectable decrease in transmission.

"Although less than 10 percent of cases occurred in hospital settings, the threat to clinicians and hospital staff must not be underestimated," said Valeria Martinez, Ph.D., of ANLIS, co-first author of the study. "Doctors should remember that in the 1996 outbreak, many health care personnel got sick, and some died, when the appropriate personal protective equipment was not used."

According to the authors, the study also examined cytokines within patients to determine the types of immunological responses present in people with HPS caused by Andes virus. Cytokines are proteins that aid cell-to-cell communication in immune responses. They concluded that there was no clear mechanism, but more of a broad and dysfunctional immunologic response among patients.

"We hope that by further exploring this apparent immune dysregulation, we will expand our knowledge of how different hantavirus species cause hantavirus pulmonary syndrome," said co-author Mariano Sanchez-Lockhart, Ph.D., of USAMRIID. "Gaining a better understanding of how our immune system tackles Andes virus infection will certainly help clinicians to better manage severe cases and pave the way for new therapeutic interventions."

Based on their comprehensive data, the team confirmed the necessity to study the patterns of Andes virus emergence, super-spreading, person-to-person transmission, and pathology to improve public health response strategies. "The breadth of techniques and expertise used to piece together person-to-person transmission and super-spreading events could be applied beyond Andes virus outbreaks," said co-author Peter Larson, Ph.D., of USAMRIID. "We hope this approach serves as a model for future investigations of person-to-person transmission and for the identification of super-spreading events."

According to Palacios, the investigative foundation for this work was built and tested by USAMRIID's Center for Genome Sciences during outbreaks of Ebola virus disease in Western Africa and the Democratic Republic of the Congo, as well as the introduction of Zika virus into the United States. "While we are proud of this work and our track record, we believe this is only the beginning," said Palacios. "Having a comprehensive approach to track spillover events is a long-term goal we strive for every day."

Although separated by millions of years of evolution, plants and animals have independently alighted upon similar innate immune strategies to protect themselves against microbial infection. In both kingdoms of life, immune receptors called nucleotide-binding/leucine-rich-repeat (NLR) proteins form an important layer of defence inside cells against pathogen attack. NLRs are complex devices made up of several modules that recognize molecules from invading microbes termed effectors, and then locally activate resistance and cell death pathways to limit infection. Based on distinct structural and signalling features, plant NLRs are divided into two main classes: those that contain coiled-coiled (CC) modules (CNL proteins) and those that harbour Toll/interleukin-1 receptor/resistance (TIR) modules (TNL proteins). In a recent study, MPIPZ researchers and Humboldt Professor Jijie Chai and his team succeeded for the first time in piecing together the sequence of molecular events that convert an inactive TNL-type plant immune receptor into an active 'resistosome' complex that mediates host cell death.

Chai, who is also affiliated with the University of Cologne, joined forces with research group leader Jane Parker and MPIPZ director Paul Schulze-Lefert to determine the structural and biochemical features underlying activation of the Recognition of Peronospora parasitica 1 (RPP1) TNL-type NLR receptor, which protects the model plant Arabidopsis thaliana from infection by the oomycete pathogen Hyaloperonospora arabidopsidis (Hpa). To understand at a molecular level how RPP1 shields plants from Hpa infection, Chai, Schulze-Lefert, Parker and colleagues expressed RPP1 together with a recognized Hpa effector ATR1 protein in insect cells, a system that allows high levels of protein expression. The ATR1-activated RPP1 receptor is an enzyme that breaks down nicotinamide adenine dinucleotide (NAD+), which is important for defence signalling.

By isolating RPP1-ATR1 oligomeric complexes and subjecting them to cryo-electron microscopy, the authors have answered two outstanding questions in NLR biology: how direct effector binding induces the conformational activation of an NLR receptor, and how organization of the TNL receptor oligomer (in this case a tetramer composed of four tightly-packed receptor molecules) creates a unique surface within a portion of the receptor, which is necessary for cleaving NAD+ to initiate defence signalling. Specifically, the tetramerization of RPP1 induced by ATR1 at one end of the receptor complex forces - at the opposite end - the four TIR modules to form two asymmetric TIR pairs, which are the sites of NAD+ breakdown (Figure 1). Thus, the RPP1 resistosome functions as a 'holoenzyme', the active form of an enzyme for NAD cleavage.

Strikingly, findings from the groups of Eva Nogales and Brian Staskawicz at the University of California, Berkeley, on another TNL-type NLR, Roq1 from the tobacco relative Nicotiana benthamiana, also show that TNL activation involves direct effector recognition and adoption of a similar tetrameric structure. The effector recognized by Roq1 is produced by a bacterial pathogen and the activated Roq1 receptor complex provides resistance to bacterial infection. Thus, the discoveries of the MPIPZ researchers seem to have a broad relevance for understanding how these critical plant immune molecules protect their hosts from infection. More generally, the oligomeric configurations adopted by active RPP1 and Roq1 resemble induced oligomeric scaffolds of other plant and mammalian NLR receptor proteins, including human receptors of the innate immune system. This suggests that these receptors rely on a common structural principle to initiate intracellular immune signalling and cell death across different kingdoms of life.

A new paper in Science Advances describes for the first time how minerals come together at the molecular level to form bones and other hard tissues, like teeth and enamel.

The University of Illinois Chicago researchers who published the paper described their experiments -- which captured high-resolution, real-time images of the mineralization process in an artificial saliva model -- and their discovery of distinct pathways that support bone and teeth formation, or biomineralization.

"Until now these pathways, particularly at the early stages when molecules are first starting to organize into a structure, have not been understood clearly," Reza Shahbazian-Yasser, UIC professor of mechanical and industrial engineering at the College of Engineering and corresponding author of the paper.

Shahbazian-Yasser and his colleagues observed that both direct and indirect formations of hydroxyapatite crystals -- the foundation of hard tissues -- can be achieved by local variations in energetic pathways for nucleation and growth.

"The control over the dissolution of amorphous calcium phosphate affects the assembly of hydroxyapatite crystals into larger aggregates," Shahbazian-Yasser said. "Using technology developed at UIC, we found evidence that these pathways coexist simultaneously -- explaining why different groups had reported seemingly different or opposite results. In addition, we now understood how hydroxyapatite materials nucleate and grow on amorphous calcium phosphate templates. The control over the nucleation and growth of hydroxyapatite will aid in developing new drugs and medical treatments to heal lost or broken bone faster or cure tooth cavities."

To capture the images, the researchers used a unique micro-device that made it possible to use electron microscopy with a liquid model. Using this method, the researchers were able to monitor chemical reactions in the model on the smallest scale.

"Our study provides clear, new evidence of how minerals organize and grow into bone materials, and this finding has many important implications for further research on bone or teeth healing," Shahbazian-Yasser said.

"By better understanding these pathways, scientists are one step closer to engineering ways to better treat dental diseases and bone injuries -- like those from traumatic injuries -- or prevent medical conditions that can develop when normal mineralization processes in the body go awry," he said.

Medical conditions caused by dysfunctional mineralization in the body can include everything from a tendency to develop cavities to osteoporosis.

"In the next step, we would like to learn how molecular modifiers can affect the process of biomineralization, which is important to develop effective drugs," Shahbazian-Yasser said.

A new study has found that a novel T cell genetically engineered by University of Arizona Health Sciences researchers is able to target and attack pathogenic T cells that cause Type 1 diabetes, which could lead to new immunotherapy treatments.

The immune system fights bacteria, viruses and other pathogens by utilizing several types of T cells, all of which have receptors that are specific to particular antigens. On killer T cells, the receptor works in concert with three signaling modules and a coreceptor to destroy the infected cell. Michael Kuhns, PhD, an associate professor in the UArizona College of Medicine - Tucson Department of Immunobiology, copied the evolutionary design to engineer a five-module chimeric antigen receptor, or 5MCAR, T cell.

"The 5MCAR was an attempt to figure out if we could build something by biomimicry, using some of evolution's natural pieces, and redirect T cells to do what we want them to do. We engineered a 5MCAR that would direct killer T cells to target autoimmune T cells that mediate Type 1 diabetes," said Dr. Kuhns, who is member of the UArizona Cancer Center, BIO5 Institute and Arizona Center on Aging. "So now, a killer T cell will actually recognize another T cell. We flipped T cell-mediated immunity on its head."

Dr. Kuhns worked with Thomas Serwold, PhD, of the Harvard Medical School-affiliated Joslin Diabetes Center, to test the 5MCAR T cells in a non-obese diabetic mouse model with promising results. The findings recently were published in the Proceedings of the National Academy of Sciences.

"When we saw that the 5MCAR T cells completely eliminated the harmful T cells that invaded the pancreas, we were blown away," Dr. Serwold said. "It was like they hunted them down. That ability is why we think that 5MCAR T cells have tremendous potential for treating diseases like Type 1 diabetes."

In 2017, the U.S. Food and Drug Administration approved two chimeric antigen receptor (CAR) T cell therapies for specific types of cancer - one for the treatment of children with acute lymphoblastic leukemia and the other for adults with advanced lymphomas. Those CAR T cells focused solely on the receptor, not the surrounding signaling modules or coreceptor.

Dr. Kuhns believes that by mimicking the form and function of a natural T cell, including its complex five-module structure, researchers will be able to more specifically target antigens with greater sensitivity in the future. This type of personalized immunotherapy is a key initiative of the UArizona Health Sciences, as well as a focus of Dr. Kuhns' lab.

"I'm generally of the belief that evolution converges on related principles to execute related tasks," Dr. Kuhns said. "Basic research from labs around the world, including ours, has helped us to understand the complex structure and function of the five-module molecular machines that have evolved to drive T cell responses. We think these results show that a biomimetic approach holds promise for CAR engineering."

Drs. Kuhns and Serwold recently received a bridge grant from the National Institute of Allergy and Infectious Diseases to continue their research into using 5MCAR T cells to prevent autoimmune disease.

"There are many things we don't yet know about this technology," Dr. Kuhns said. "What we know is that it works, and it can be very effective in a mouse model of Type 1 diabetes, so that's great. Now, we have a lot more work to do."

Accelerating tree growth in recent years has been accompanied by a reduction in tree lifespan, which could eventually neutralize part of the increase in net uptake of carbon dioxide (CO2). This trade-off between tree growth and life expectancy applies to forests worldwide, including in the Amazon and other tropical regions, as well as temperate regions and the Arctic.

Models and projections of future forest carbon uptake based on the existing system may therefore overestimate the capacity of forests to absorb greenhouse gases over time. In other words, while tree planting is important to help reduce levels of these gases in the atmosphere, it is not sufficient. Efforts to reduce carbon emissions remain essential.

These are the key points discussed in an article published in Nature Communications. It reports the findings of a study conducted by a cross-border group of researchers, including Gregório Ceccantini and Giuliano Locosselli, researchers at the University of Paulo's Institute of Biosciences (IB-USP) in Brazil. Both are supported by FAPESP (São Paulo Research Foundation).

"There's an inverse relationship between tree growth and longevity," Locosselli told Agência FAPESP. "We consistently show that this relationship exists regardless of species and location. If trees are growing faster, they're also assimilating carbon faster. The problem is that they'll live shorter lives and the carbon will be stored for less time."

Trees need large amounts of CO2 to grow and develop, so this growth acceleration has led to substantial carbon uptake. Recent studies show that about a third of the greenhouse gas emissions resulting from human activities in the past 50 years has been absorbed by terrestrial ecosystems thanks to a combination of new trees and expanding secondary forest growth.

The paper published in Nature Communications questions how far forests will continue to absorb excess atmospheric carbon in the future, arguing that this "depends not only on the growth response of trees to a changing climate and atmospheric composition but also on changes in mortality rates that ultimately release carbon back to the atmosphere. [...] This negative feedback on carbon storage via increased mortality will offset - at least to some extent - the beneficial effects of increased growth on total carbon storage of forests. Our current, incomplete knowledge of the universality and causes of the feedback hinders its representation in Earth System Models and thus is an important uncertainty in predictions of future forest carbon uptake in response to global change".

According to Locosselli, most climate change projections and models of forest biomass dynamics take into consideration tree growth but not the negative relationship with longevity. The drivers of faster growth are not entirely clear, but they may include temperature and atmospheric CO2, as well as the production and use of fertilizer and fossil fuels, which have significantly altered the amount of nitrogen in the environment.

Climate change

A report issued in 2019 by the United Nations Environment Program (UNEP) warned that global greenhouse gas emissions must fall by at least 7.6% each year over the next decade to limit the average temperature rise to 1.5°C, as promised by the Paris Agreement.

If the average temperature rise exceeds this limit, the impacts across the planet will include more intense heat waves and more frequent storms, according to the Intergovernmental Panel on Climate Change (IPCC).
Greenhouse gas emissions have risen 1.5% per year in the last decade, largely owing to fossil fuels and land-use change such as deforestation.

The G20 countries account for about 75% of total greenhouse gas emissions, led by China and the United States. Brazil ranks 14th in the world, according to the Global Carbon Atlas. Deforestation and forest fires alone account for a significant proportion of Brazil's emissions. In its Paris Agreement climate commitments, Brazil undertook to achieve a 37% reduction in emissions from the 2005 level by 2025 and a 43% reduction by 2030.

The latest study by the World Meteorological Organization (WMO) shows global CO2 fossil fuel emissions reaching a record 36.7 gigatons in 2019, for an increase of 62% compared with 1990 when climate negotiations began.
Because the pandemic has forced countries to restrict mobility for several months, CO2 emissions are set to fall 4%-7% in 2020 compared with last year, according to the WMO. Although in April daily emissions reached the lowest level seen between January and August, they were the same as in 2006, when they were rising sharply.

The means to mitigate this rise in carbon emissions include more public policies to increase the use of renewable energy sources and low-carbon transportation and to eliminate coal, as well as reducing deforestation and forest fires throughout the world.

Last year a group of 66 countries, plus 10 regions, 102 cities, 93 businesses, and 12 investors, committed to achieving net-zero CO2 emissions by 2050. Carbon pricing mechanisms under discussion entail taxing emissions and incrementing the carbon credit market so that the polluter pays if mitigation is not performed domestically. The ultimate goal is to make low-carbon production steadily more advantageous.

Methodology

To return to the relationship between tree lifespan and net carbon uptake, Locosselli explained that the study was based on an analysis of annual growth rings. The researchers compiled and analyzed tree-ring datasets for more than 210,000 trees belonging to 110 species.

When a tree grows faster, it lays down more tissue in the year, resulting in a wider growth ring, and vice-versa. The age of a tree can be calculated by counting its annual rings.

"This is how we were able to measure the dynamics of trees that are 500 or 600 years old. We extrapolated time beyond what other studies did with permanent plots," said Locosselli, who is supported by FAPESP with a Young Investigator grant for the project "Functional forests: biodiversity to benefit cities".

Forest burning also accelerates tree mortality, but this factor was not included in the study, he said. Other research has shown that when the Amazon or any other tropical forest burns, it retains 25% less carbon even after three decades of regrowth.

Stars are rather patient. They can live for billions of years, and they typically make slow transitions -- sometimes over many millions of years -- between the different stages of their lives.

So when a previously typical star's behavior rapidly changes in a few decades, astronomers take note and get to work.

Such is the case with a star known as SAO 244567, which lies at the center of Hen 3-1357, commonly known as the Stingray Nebula. The Stingray Nebula is a planetary nebula -- an expanse of material sloughed off from a star as it enters a new phase of old age and then heated by that same star into colorful displays that can last for up to a million years.

The tiny Stingray Nebula unexpectedly appeared in the 1980s and was first imaged by scientists in the 1990s using NASA's Hubble Space Telescope. It is by far the youngest planetary nebula in our sky. A team of astronomers recently analyzed a more recent image of the nebula, taken in 2016 by Hubble, and found something unexpected: As they report in a paper accepted to the Astrophysical Journal, the Stingray Nebula has faded significantly and changed shape over the course of just 20 years.

If dimming continues at current rates, in 20 or 30 years the Stingray Nebula will be barely perceptible, and was likely already fading when Hubble obtained the first clear images of it in 1996, according to lead author Bruce Balick, an emeritus professor of astronomy at UW.

"This is an unprecedented departure from typical behavior for a planetary nebula," said Balick. "Over time, we would expect it to imperceptibly brighten and expand, which could easily go unnoticed in a century or more. But here we're seeing the Stingray nebula fade significantly in an incredibly compressed time frame of just 20 years. Moreover, its brightest inner structure has contracted -- not expanded -- as the nebula fades."

Planetary nebulae form after most stars, including stars like our own sun, swell into red giants as they exhaust hydrogen fuel. At the end of the red giant phase, the star then expels large amounts of its outer material as it gradually -- over the course of a million years -- transforms into a small, compact white dwarf. The sloughed-off material expands outward for several thousand years while the star heats the material, which eventually becomes ionized and glows.

Balick and his co-authors, Martín Guerrero at the Institute of Astrophysics of Andalusia in Spain and Gerardo Ramos-Larios at the University of Guadalajara in Mexico, compared Hubble images of the Stingray Nebula taken in 1996 and 2016. Hen 3-1357 changed shape markedly over 20 years, losing the sharp, sloping edges that gave the Stingray Nebula its name. Its colors have faded overall and once-prominent blue expanses of gas near its center are largely gone.

"In a planetary nebula, the star is really the center of all the activity," said Balick. "The material around it is directly responsive to the energy from its parent star."

The team analyzed light spectra from Hen 3-1357 emitted by chemical elements in the nebula. Emission levels of hydrogen, nitrogen, sulfur and oxygen all dropped between 1996 and 2016, particularly oxygen, which dropped by a factor of 900. The resulting fade in color and the nebula's change in shape are likely connected to the cooling of its parent star -- from a peak of about 107,500 degrees Fahrenheit in 2002 to just under 90,000 degrees Fahrenheit in 2015 -- which means it is giving off less ultraviolet ionizing radiation that heats the expelled gas and makes it glow.

"Like a doused forest fire, the smoke wanes more slowly than the flames that created it," said Balick. "Even so, we were amazed when the Hubble images revealed how quickly the nebula was fading. It took a month of work to believe it."

Astronomers have yet to understand why SAO 244567 made the Stingray Nebula light up and then fade almost as quickly. One theory, posited by a team led by Nicole Reindl at the University of Potsdam, is that the star underwent a brief burst of fresh helium fusion around its core, which stirred up its outer layers and caused its surface to both shrink and heat.

If so, then as its outer layers settle back down, the star may return to a more typical transition from red giant to white dwarf. Only future observations of the star and its nebula can confirm this.

"Unfortunately, the best tool to follow future changes in the Stingray Nebula, the Hubble Space Telescope, is near the end of its life as well," said Balick. "We can hope, but the odds aren't good for Hubble's survival as its three remaining gyroscopes start to fail. It's a good race to the finish."

A recent study examining perceptions of power suggests that individuals with lower socioeconomic statuses are more likely to have a negative view of policy or decision-makers.

Leanne ten Brinke, an assistant professor of psychology in the Irving K. Barber Faculty of Arts and Social Sciences and study co-author, says the study was inspired by her time living in the United States during the 2016 presidential election.

"I was a post-doc at University of California Berkley and remember being so struck by the different approaches to power being used by then-candidates Hillary Clinton and Donald Trump," she explains. "It occurred to me then that people have very different perspectives on what it takes to get to the top."

In a survey of over 1,000 participants, the study looked at their perceptions of two viable paths to power--one through the use of coercion, manipulation and fear-mongering, and the other rooted in collaboration and respect.

"We were interested in how socioeconomic status might affect one's view on how power is gained and maintained," says ten Brinke. "We also wondered how identifying with a theory of power might be associated with one's interpersonal and societal trust."

Results showed those with lower socioeconomic statuses were generally less-trusting and more inclined to hold a more coercive and less collaborative view of power, while people with higher socioeconomic statuses were more trusting and embraced the opposite view.

"We also found that people held one theory of power or the other--but not both simultaneously," explains ten Brinke. "As income inequality continues to rise, and we have a widening gap between the powerful and powerless, these results help us understand how these groups view the human hierarchy in which they live."

Though it's unclear exactly where the 'cut-off' is for one to have the income and status that leads to a more positive view on power, ten Brinke says this research provides much-needed insight into why people carry such differing views.

"I think a lot of it comes down to trust. If we can change peoples' theories of power, perhaps we can increase trust where it's due," she says, adding that further investigation may be helpful in understanding involvement in the democratic process or why some follow public health guidelines when others don't.

"There's considerable research that shows low socioeconomic individuals are less likely to vote than high," she says.

"Part of that is structural--it may be more difficult for them to get time off work--but I suspect theories of power play into it as well. If you think powerful people are coercive and corrupt and you can't trust any of them, perhaps you think it doesn't matter who is in office--but that's not a healthy democracy, so I see this research as a building block for future work in this area."

Forest leaves are teeming with bacterial life - but despite the vast extent of bacteria-covered foliage across the world, this habitat, known as the phyllosphere, remains full of mysteries. How do bacteria spread from tree to tree? Do certain types of bacteria only live on certain types of trees?

A new paper published in the Ecological Society of America's journal Ecological Monographs addresses some of these questions. The findings reveal that the leaf microbiomes of sugar maple trees vary across the species' range, changing in accordance with the types of trees in the surrounding "neighborhood."

Geneviève Lajoie, now a post-doctoral researcher at the University of British Columbia and the paper's lead author, performed the research as a Ph.D. student at the Université du Québec à Montréal. She and her field assistant spent a summer in hot pursuit of bacteria-covered foliage, camping at remote parks and rushing to get their leaf samples back to the lab for analysis before new conditions altered the leaves' resident microbes.

The team sampled foliage at sites across Québec, Ontario and the northeastern United States. Lajoie's analysis zeroed in on the iconic sugar maple - a species that is abundant at the southern end of the study range, but tapers off at more northern latitudes where conifers dominate the landscape. In fact, at the northern reaches of the study range, at sites like Monts-Valin National Park, sugar maples become anomalous enough that tracking them down among their evergreen neighbors was a challenge.

"To reach the site, we drove up north from Québec City and witnessed the gradual transition from the mixed deciduous forest of the Saint Lawrence Valley to a boreal landscape dominated by conifers," Lajoie said. "Going sampling over the next days, we were looking for sugar maple populations - our focal species. Even though we knew it could be found in the park despite it being the northern limit of its range, encountering these beautiful trees seemingly out of place but still thriving were particularly amazing moments for me."

However, despite being outliers on a conifer-dominated landscape, these northernmost sugar maple trees had adopted leaf microbiomes that blended in with their coniferous neighbors. LaJoie found a pattern along the latitudinal gradient of her study area: southern sugar maples, which are surrounded by lots of other sugar maples, tended to share a relatively similar microbiome - one that was distinct from other tree species in the area. But in more northern areas, where sugar maple trees are few and far between, the species hosted bacterial communities that resembled the microbiomes of other more dominant species.

The observations echo similar patterns that have been observed among animal microbiomes. Ground-dwelling animals, for instance, tend to have relatively similar microbiomes, possibly through increased contact with the feces of other animals, while canopy-dwelling animals have gut microbiomes that are less similar to each other.

While gut microbiomes are a hot research topic in the human health sciences, the forest phyllosphere remains a study system that is not well understood - and according to Lajoie, the fields of plant ecology and microbiology have been growing mostly in parallel for many years. This study's findings provide a more complete picture of the plant-microbe relationship: what kinds of bacteria go on which trees, and how this pattern varies depending on how well a tree fits in with the crowd.

It is already possible to produce food with a 3D printer, potentially delivering products that suit consumer preferences regarding taste, texture, cost, convenience, and nutrition. In the near future, it will be possible to produce food with personalized shapes, textures, flavors, and colors considered attractive and healthy for children and the elderly, for example.

A group of researchers at the University of São Paulo's Luiz de Queiroz College of Agriculture (ESALQ-USP) in Brazil, partnering with colleagues in France at Nantes Atlantic College of Veterinary Medicine, Food Science and Engineering (Oniris) and the National Institute for Research on Agriculture, Food and Environment (INRAE), have made strides toward achieving this goal. They are developing hydrogels based on modified starch for use as "ink" in 3D printing of foods.

Recent results of the project, supported by FAPESP (São Paulo Research Foundation), are published in the journal Food Research International. "In the past few years we've developed different technologies to modify starch and obtain gels with ideal characteristics for use as 'ink' to produce food by 3D printing," Pedro Esteves Duarte Augusto, a professor at ESALQ-USP and principal investigator for the project, told Agência FAPESP.

The first gels produced by the researchers were based on cassava starch. They themselves developed the method used to modify the structure and properties of the starch with ozone during a previous project also supported by FAPESP.

They produced ozone by applying an electrical discharge to oxygen, bubbled the gas in a container with a mixture of water and cassava starch in suspension, and dried the mixture by removing the water. The result was modified starch.

By varying aspects of the process such as ozone concentration, temperature, and time, they were able to obtain gels with different properties in terms of the right consistency for use in 3D printing.

"Control of the conditions enabled us to obtain weaker gels for other applications and firmer gels that are ideal for 3D printing because they retain the shape of the printed structure without flowing or losing moisture," Augusto said.

In the past two years, the researchers have developed another starch modification method. This involves dry heating of cassava and wheat starch in an oven while controlling both temperature and time.

Using the new method they were also able to obtain gels based on modified starch that displayed optimal printability, defined as the ability to make a 3D object by additive manufacturing (layer-by-layer deposition) and to maintain its structure once printed. Dry heat treatment also extended the textural possibilities of printed samples based on wheat starch hydrogels.

"We obtained good results with both methods. They're simple, cheap and easy to implement on an industrial scale," Augusto said.

Samples of gel based on cassava and wheat starch were printed at Oniris and INRAE in France via a project to develop functional starch-based gels for 3D printing funded by the Pays de la Loire regional innovation agency under a program called "Food 4 tomorrow".

Through the partnership with French scientists, ESALQ-USP researcher Bianca Chieregato Maniglia conducted postdoctoral research at Oniris and INRAE, applying the ozone and dry heating techniques to produce gels based on modified cassava and wheat starch for 3D printing of foods.

The techniques were developed with the collaboration of other researchers in ESALQ-USP's Process Engineering Research Group (Ge²P).

"The combined experience of all the researchers involved in the project enabled us to obtain gels with better printability, resulting in foods with better shape, definition and texture, which are essential parameters for product acceptability," Maniglia said.

Novel ingredientes

The ESALQ-USP group now plans to study other methods of modification and sources for the production of 3D food printing gels. ESALQ-USP has recently purchased a 3D printer, which they will use to produce the structures developed with the new gels.

The gels based on modified cassava and wheat starch can be used to print other things apart from food, such as biomedical products including drug capsules and nutraceuticals - foods designed not only to nourish but also to confer health benefits.

"We've demonstrated the feasibility of food production by 3D printing and fabrication of tailor-made ingredients. Now we plan to extend the applications and test other raw materials," Augusto said.

HOUSTON - (Dec. 3, 2020) - That carbon nanotubes fluoresce is no longer a surprise. Finding a second level of fluorescence is surprising and potentially useful.

How does it work? Wait for it.

The Rice University lab of Bruce Weisman, a professor of chemistry who led the pioneering discovery of nanotube fluorescence in 2002, found that single-walled nanotubes emit a delayed secondary fluorescence when triggered by a multistep process in a solution with dye molecules and dissolved oxygen.

The delay is only microseconds, but it's enough to be detected with some effort.

The complex process is detailed by Weisman, lead author and Rice alumnus Ching-Wei Lin, and research scientist Sergei Bachilo in the Journal of the American Chemical Society.

The reaction begins when light excites a solution containing a dye called rose bengal. Oxygen molecules dissolved in the solution capture energy from the dye, forming an energized form of O2. These then transfer their energy to nanotubes, where excitons -- quasiparticles made of electrons and electron holes -- are generated in their triplet state. With a bit of added thermal energy, those excitons get promoted to a higher energy singlet state that emits the observed fluorescence.

"For a number of years, we have been looking at interesting effects involving nanotubes and oxygen," Weisman said. "We've found quite a range of things that can happen, from physical effects like this energy transfer or the reversible quenching of fluorescence, to the triggering of chemical reactions between nanotubes and DNA. So this study was part of a larger program of exploration."

Their ability to excite dissolved oxygen molecules prompted the researchers to see how that would affect adjacent nanotubes, Weisman said.

"We make singlet oxygen by exciting a dye molecule with visible light, and then the oxygen deactivates the dye and gets excited itself," he said. "That idea goes back decades in photophysics and is very conventional. What's unusual here is that the singlet oxygen interacts with the nanotube to directly make triplet-state excitations in the tube. Those triplet states have been pretty elusive.

"Triplet states of organic molecules are the longest-lived excited states," Weisman said. "Their lifetimes are orders of magnitude greater than the singlet excited states, so they can hang around long enough to bump into something else and undergo chemical reactions.

"But because nanotube triplet states don't emit light or directly absorb light very well, they are tricky to study and not too much is known about them," he said. "What we've been doing is trying to understand them a little better."

Triggering fluorescence still required an extra step. "Just by random thermal agitation in their surroundings, these guys can sometimes get kicked up to the bright singlet state, and then they can tell you they're there by spitting out a photon," Weisman said.

Because the triplet state can last 10 microseconds or so, that upconverted emission is called delayed fluorescence.

The researchers had to find a way to detect the relatively weak effect amid the nanotubes' bright primary fluorescence. "It was like trying to see a dim object right after being blinded by a bright camera flash," Weisman said. "We had to devise some special instrumentation."

One device "is basically a fast mechanical shutter" that covers the short-wave infrared (SWIR) spectrometer during the bright flash and then quickly opens up, a kind of reverse camera that goes from covered to open in seven microseconds. The other device, he said, is a sensitive detector that's triggered with an electronic signal and measures how the weak emission fades away over time. "These systems were both built by Ching-Wei, who's a terrific experimentalist," he said.

Weisman and colleagues have employed nanotube fluorescence in medical imaging technologies and in nanotube-based smart skin to measure strain in surfaces, among other applications. He said the new discovery could eventually find its way into optoelectronics and solar energy.

"There's not a direct step where somebody's going to read this and make a new, more efficient device," Weisman said. "But this fundamental knowledge of processes and properties is the foundation on which new technologies are built."

More than 40 years since they launched, the Voyager spacecraft are still making discoveries.

In a new study, a team of physicists led by the University of Iowa report the first detection of bursts of cosmic ray electrons accelerated by shock waves originating from major eruptions on the sun. The detection, made by instruments onboard both the Voyager 1 and Voyager 2 spacecraft, occurred as the Voyagers continue their journey outward through interstellar space, thus making them the first craft to record this unique physics in the realm between stars.

These newly detected electron bursts are like an advanced guard accelerated along magnetic field lines in the interstellar medium; the electrons travel at nearly the speed of light, some 670 times faster than the shock waves that initially propelled them. The bursts were followed by plasma wave oscillations caused by lower-energy electrons arriving at the Voyagers' instruments days later--and finally, in some cases, the shock wave itself as long as a month after that.

The shock waves emanated from coronal mass ejections, expulsions of hot gas and energy that move outward from the sun at about one million miles per hour. Even at those speeds, it takes more than a year for the shock waves to reach the Voyager spacecraft, which have traveled further from the sun (more than 14 billion miles and counting) than any human-made object.

"What we see here specifically is a certain mechanism whereby when the shock wave first contacts the interstellar magnetic field lines passing through the spacecraft, it reflects and accelerates some of the cosmic ray electrons," says Don Gurnett, professor emeritus in physics and astronomy at Iowa and the study's corresponding author. "We have identified through the cosmic ray instruments these are electrons that were reflected and accelerated by interstellar shocks propagating outward from energetic solar events at the sun. That is a new mechanism."

The discovery could help physicists better understand the dynamics underpinning shock waves and cosmic radiation that come from flare stars (which can vary in brightness briefly due to violent activity on their surface) and exploding stars. The physics of such phenomena would be important to consider when sending astronauts on extended lunar or Martian excursions, for instance, during which they would be exposed to concentrations of cosmic rays far exceeding what we experience on Earth.

The physicists believe these electrons in the interstellar medium are reflected off of a strengthened magnetic field at the edge of the shock wave and subsequently accelerated by the motion of the shock wave. The reflected electrons then spiral along interstellar magnetic field lines, gaining speed as the distance between them and the shock increases.

In a 2014 paper in the journal Astrophysical Letters, physicists J.R. Jokipii and Jozsef Kota described theoretically how ions reflected from shock waves could be accelerated along interstellar magnetic field lines. The current study looks at bursts of electrons detected by the Voyager spacecraft that are thought to be accelerated by a similar process.

"The idea that shock waves accelerate particles is not new," Gurnett says. "It all has to do with how it works, the mechanism. And the fact we detected it in a new realm, the interstellar medium, which is much different than in the solar wind where similar processes have been observed. No one has seen it with an interstellar shock wave, in a whole new pristine medium."

Scientists have created an evolutionary model to predict how animals should react in stressful situations.

Almost all organisms have fast-acting stress responses, which help them respond to threats - but being stressed uses energy, and chronic stress can be damaging.

The new study - by an international team including the University of Exeter - suggests most animals remain stressed for longer than is optimal after a stress-inducing incident.

The reasons for this are not clear, but one possibility is that there is a limit to how quickly the body can remove stress hormones from circulation.

"We have created one of the first mathematical models to understand how organisms have evolved to deal with stressful events," said Dr Tim Fawcett, of the University of Exeter.

"It combines existing research on stress physiology in a variety of organisms with analysis of optimal responses that balance the costs and benefits of stress.

"We know stress responses vary hugely between different species and even among individuals of the same species - as we see in humans.

"Our study is a step towards understanding why stress responses are so variable."

The researchers define stress as the process of an organism responding to "stressors" (threats and challenges in their environment), including both detection and the stress response itself.

A key point highlighted in the study is the importance of how predictable threats are.

The model suggests that an animal living in a dangerous environment should have a high "baseline" stress level, while an animal in a safer environment would benefit from being able to raise and reduce stress levels rapidly.

"Our approach reveals environmental predictability and physiological limits as key factors shaping the evolution of stress responses," said lead author Professor Barbara Taborsky, of the University of Bern.

"More research is needed to advance scientific understanding of how this core physiological system has evolved."

A new study reveals how bacteria control the chemicals produced from consuming 'food.' The insight could lead to organisms that are more efficient at converting plants into biofuels.

The study, authored by scientists at UC Riverside and Pacific Northwest National Laboratory, has been published in the Journal of the Royal Society Interface.

In the article, the authors describe mathematical and computational modeling, artificial intelligence algorithms and experiments showing that cells have failsafe mechanisms preventing them from producing too many metabolic intermediates.

Metabolic intermediates are the chemicals that couple each reaction to one another in metabolism. Key to these control mechanisms are enzymes, which speed up chemical reactions involved in biological functions like growth and energy production.

"Cellular metabolism consists of a bunch of enzymes. When the cell encounters food, an enzyme breaks it down into a molecule that can be used by the next enzyme and the next, ultimately generating energy," explained study co-author, UCR adjunct math professor and Pacific Northwest National Laboratory computational scientist William Cannon.

The enzymes cannot produce an excessive amount of metabolic intermediates. They produce an amount that is controlled by how much of that product is already present in the cell.

"This way the metabolite concentrations don't get so high that the liquid inside the cell becomes thick and gooey like molasses, which could cause cell death," Cannon said.

One of the barriers to creating biofuels that are cost competitive with petroleum is the inefficiency of converting plant material into ethanol. Typically, E. coli bacteria are engineered to break down lignin, the tough part of plant cell walls, so it can be fermented into fuel.

Mark Alber, study co-author and UCR distinguished math professor, said that the study is a part of the project to understand the ways bacteria and fungi work together to affect the roots of plants grown for biofuels.

"One of the problems with engineering bacteria for biofuels is that most of the time the process just makes the bacteria sick," Cannon said. "We push them to overproduce proteins, and it becomes uncomfortable -- they could die. What we learned in this research could help us engineer them more intelligently."

Knowing which enzymes need to be prevented from overproducing can help scientists design cells that produce more of what they want and less of what they don't.

The research employed mathematical control theory, which learns how systems control themselves, as well as machine learning to predict which enzymes needed to be controlled to prevent excessive buildup of metabolites.

While this study examined central metabolism, which generates the cell's energy, going forward, Cannon said the research team would like to study other aspects of a cell's metabolism, including secondary metabolism -- how proteins and DNA are made -- and interactions between cells.

"I've worked in a lab that did this kind of thing manually, and it took months to understand how one particular enzyme is regulated," Cannon said. "Now, using these new methods, this can be done in a few days, which is extremely exciting."

The U.S. Department of Energy, seeking to diversify the nation's energy sources, funded this three-year research project with a $2.1 million grant.

The project is also a part of the broader initiatives under way in the newly established UCR Interdisciplinary Center for Quantitative Modeling in Biology.

Though this project focused on bacterial metabolism, the ability to learn how cells regulate and control themselves could also help develop new strategies for combatting diseases.

"We're focused on bacteria, but these same biological mechanisms and modeling methods apply to human cells that have become dysregulated, which is what happens when a person has cancer," Alber said. "If we really want to understand why a cell behaves the way it does, we have to understand this regulation."