Culture

Plants are constantly exposed to microbes: pathogens that cause disease, commensals that cause no harm or benefit, and mutualists that promote plant growth or help fend off pathogens. For example, most land plants can form positive relationships with arbuscular mycorrhizal fungi to improve nutrient uptake. How plants fight off pathogens without also killing beneficial microbes or wasting energy on commensal microbes is a largely unanswered question.

In fact, when scientists within the field of Molecular Plant-Microbe Interactions were asked to come up with their Top 10 Unanswered Questions, the #1 question was "How do plants engage with beneficial microorganisms while at the same time restricting pathogens?" Put more simply, how do plants tell good microbes from bad and what do they do about it? As part of a Top10MPMI review series in the open access MPMI Journal, this question of how plants and microbes engage in symbiosis was recently interrogated by Dr. Cara Haney and Dr. David Thoms, microbiologists at the University of British Columbia, in collaboration with Dr. Yan Liang at Zhejiang University in China.

"Maintaining a balance in plant disease resistance where plants can fight off pests and pathogens but still engage with microbes that can help with nutrient uptake is essential for the health of our crops," emphasizes Haney. To fully engage with such a large question, paradigms are needed to drive specific research questions towards the unanswered pieces. As Haney says, "this question is so broad, I think the review raises more questions than it answers. We attempted to highlight much of what was known, but also what wasn't known and to provide paradigms and models that could be frameworks going forward." In a proposed framework for considering mechanisms of symbiotic engagement, Haney, Thoms, and Liang distinguish three principles: chemical selection with metabolites, dual receptor recognition, and tuning of an immune thermostat.

Plants first use metabolite compounds like antimicrobials and chemical signals to recruit beneficial organisms and restrict pathogens, but not all pathogens are excluded. Once plant and microbe are in contact, Thoms proposes that "a dual input model" is used by the plant to distinguish both the type of microbe (bacterial, fungal, or nematode) and the lifestyle (mutualist, commensal, or pathogen). Microbes can be detected by receptor proteins on the surface of plant cells. When receptor proteins detect a piece of fungal cell wall known as chitin, the plant discovers a fungal microbe is present. But as chitin, and other microbe-associated molecular patterns (MAMPS), are often shared among microbes, they are insufficient signals to distinguish commensals from pathogens according to Thoms.

"Unlike most animals, plants do not have an adaptive immune system. However, plant genomes contain many more innate immune receptors than animals," Liang explains. "Plants also use similar receptors to sense signaling molecules from beneficial microbes, environments, as well as their own cells." So, additional receptors use a second layer of information to identify pathogens versus mutualists. Symbiosis receptors can identify signaling molecules specifically produced by beneficial microbes, while immune receptors can identify pathogen proteins intended to shut down plant defense. Addressing the need to know both the type and lifestyle of a microbe, Thoms remarks, "I think it's cool that plants can perceive so many types of MAMPs across different kingdoms of life and I think one use of that is recognizing where the microbe is coming from to give the appropriate physiological response." Essentially, a plant cell follows a flowchart to determine what reaction is needed in response to the type and lifestyle of microbe it perceives.

Yet, a plant can simultaneously engage with multiple microbes that require different responses, making it more complicated than following the flowchart directly. Energy use for immunity and symbiosis must be balanced based on present microbes and current plant needs. So, the remaining piece of the story is a "normal immune setpoint." "It is important to understand what this is and how it can be adjusted over a plant's life in order to maximize yields of our crops," explain Haney. Because of the impact of the environment and nutrient stress as well, how plants decide to use resources to engage in symbiosis or prevent infection is perhaps one of the biggest areas for exploration.

How to identify and respond to different microbes in variable environments is not a problem unique to plants. "Many living things, ranging from plants to humans, are faced with the challenge of engaging with beneficial microbes while restricting pathogens," highlights Haney. "As a result, paradigms in plant-microbe interactions may shed light on eukaryotic interactions with microbes in diverse organisms."

An exploratory investigation into the behavior of materials with desirable electric properties resulted in the discovery of a structural phase of two-dimensional (2D) materials. The new family of materials are electrides, wherein electrons occupy a space usually reserved for atoms or ions instead of orbiting the nucleus of an atom or ion. The stable, low-energy, tunable materials could have potential applications in nanotechnologies.

The international research team, led by Hannes Raebiger, associate professor in the Department of Physics at Yokohama National University in Japan, published their results on June 10th as frontispiece in Advanced Functional Materials.

Initially, the team set out to better understand the fundamental properties of a 2D system known as Sc2CO2. Containing two atoms of metallic scandium, one atom of carbon and two atoms of oxygens, the system belongs to a family of chemical compounds collectively referred to as MXenes. They are typically composed of a carbon or nitrogen layer one atom thick sandwiched between metal layers, dotted with oxygen or fluorine atoms.

The researchers were particularly interested in MXene Sc2CO2 due to the predictions that, when structured into a hexagonal phase, the system would have desired electrical properties.

"Despite these fascinating predictions of hexagonal phases of Sc2CO2, we are not aware of its successful fabrication as of yet," said Soungmin Bae, first author and researcher in the Department of Physics at Yokohama National University. "Analyzing its fundamental properties, we discovered a completely new structural phase."

The new structural phase results in new electride materials. The atomic-thin 2D structural phase is described as tiled shapes forming the central carbon plane. The previously predicted shape was a hexagon, with a carbon atom at every vertex and one in the middle. The new materials have a rhombus-like shape, with electrons at the vertices and a carbon trimer -- three carbon atoms in a row -- in the middle.

"Carbon is one of the most common materials on our planet, and quite important for living beings, but it is hardly ever found as trimers," Raebiger said. "The closest place where carbon trimers are typically found is interstellar space."

The overall shape is less symmetric than the previously described hexagonal structure, but it is more symmetric with regard to the central plane. This structure offers unique characteristics due to the appearance of the new family of electrides, according to Raebiger.

"Electrides contain electrons as a structural unit and often are extremely good electrical conductors," Raebiger said. "The present family of electrides are insulators, and while most insulators can be made conductive by adding or removing electrons, these materials simply become more insulating."

MXenes are particularly attractive as a material, because they can be reconfigured with other metallic elements to offer a cornucopia of properties, including tunable conductivity, various forms of magnetism, and/or accelerate chemical reactions as catalysts. On top of this, they are ultra-thin sheets only a few atoms thick, that is, 2D materials. The newly discovered electrides have electrons in lattice voids between atoms and ions, which can be readily emitted into surrounding space, such as the electron sources for large particle accelerators, as well as be borrowed to catalyze a specifically desired chemical reaction.

"We made this discovery because we wanted to understand how these materials work better," Bae said. "If you encounter something you don't understand, dig deeper."

Co-authors include William Espinosa-García and Gustavo M. Dalpian, Centro de Ciências Naturais e Humanas, Universidade Federal do ABC, Brazil; Yoon-Gu Kang and Myung Joon Han, Department of Physics, Korea Advanced Institute of Science and Technology; Juho Lee and Yong-Hoon Kim, Department of Electrical Engineering, Korea Advanced Institute of Science and Technology; Noriyuki Egawa, Kazuaki Kuwahata and Kaoru Ohno, Department of Physics at Yokohama National University; and Mohammad Khazaei and Hideo Hosono, Materials Research Center for Element Strategy, Tokyo Institute of Technology. Espinosa-García is also affiliated with Grupo de investigación en Modelamienot y Simulación Computacional, Facultad de Ingenierías, Universidad de San Buenaventura-Medellín.

The Iwaki Scholarship Foundation; São Paulo Research Foundation; Korea's National Research Foundation, Ministry of Science and ICT and Ministry of Education; KAIST (formerly the Korea Advanced Institute of Science and Technology); and Samsung Research Funding & Incubation Center of Samsung Electronics funded this work.

Music is a tool that has accompanied our evolutionary journey and provided a sense of comfort and social connection for millennia. New research published today in the American Psychologist provides a neuroscientific understanding of the social connection with a new map of the brain when playing music.

A team of social neuroscientists from Bar-Ilan University and the University of Chicago introduced a model of the brain that sheds light on the social functions and brain mechanisms that underlie the musical adaptations used for human connection. The model is unique because it focuses on what happens in the brain when people make music together, rather than when they listen to music individually.

The research was inspired by creative efforts of people around the world to reproduce music-making together while social distancing during the COVID-19 pandemic. This included people singing songs in unison from balcony to balcony, group singing on video conferencing platforms such as Zoom, and live living room concerts by the likes of Yo Yo Ma, Chris Martin from Coldplay, and Norah Jones.

The team fused the latest advances in social neuroscience and the field of music, including evolutionary theory. They synthesized these advances and highlighted five key functions and mechanisms of the brain that contribute to social connection through music.

These are (1) empathy circuits, (2) oxytocin secretion, (3) reward and motivation, including dopamine release, (4) language structures, and (5) cortisol. These five functions and mechanisms involve at least 12 important brain regions and two pathways which are mapped here.

Empathy helps us to tune into how other people are thinking and feeling, and can be improved through interpersonal musical coordination.

Oxytocin is sometimes called the "love hormone" because it contributes to our sense of feeling socially bonded with others. It is secreted when people sing together, even when the singing is improvised.

Dopamine is a neurotransmitter that produces a sense of pleasure and is released during musical anticipation and expectation, and pivotal for our sense of reward and motivation.

Language structures in the brain are involved in back-and-forth musical dialogue (sometimes referred to as "call" and "response").

Cortisol is a hormone that contributes to stress, but it is decreased in the brain when people sing together and when they listen to music together in groups.

The research provides the groundwork for an emerging field called the "social neuroscience of music", which builds on the previously established cognitive neuroscience of music, which largely focuses on music listening.

The authors say a better understanding of the social neuroscience of music can play an important role for helping to improve social bonding around the world, particularly in cultures that are in conflict. They conclude that music is a powerful tool that can bring individuals together, promote empathy and communication, and heal social divisions. They say that a better scientific understanding of how music provides brain-to-brain social connections helps highlight that music isn't mere entertainment, but instead is a core feature of human existence with important social implications.

Dr. David Greenberg, who led the research, is a social neuroscientist, professional musician, and Zuckerman Postdoctoral Scholar at Bar-Ilan University in Israel. He says, "Music connects us to our humanity. Through social neuroscience, we can discover that our sense of social connection isn't just subjective, but that it is rooted in important brain mechanisms. Especially in a time when there is so much social division around the world, we need to find new ways to to bridge cultures in conflict. Music is one of those ways. We hope our research will lead to more grass-roots programs like the West-Eastern Divan Orchestra and the Jerusalem Youth Chorus, which bring people from differing cultures together through music."

Dr. Ilanit Gordon, an Associate Professor at the Department of Psychology and Director of the Social Neuroscience Lab at the Gonda (Goldschmied) Multidisciplinary Brain Research Center at Bar-Ilan, says: "Human sociality is rooted in our biological makeup. Through music we can connect and interact with others, and via the scientific exploration of the neurobiological basis of music, we can further our understanding of major issues in social neuroscience."

Jean Decety, the Irving B. Harris Distinguished Service Professor in Psychology and Psychiatry, and director of Child Neurosuite at the University of Chicago, says, "Music is a fundamental part of our evolution, allowing for unique expressions of social ties. It can strengthen cohesion and mutual trust between people by signaling shared values. It is quite fascinating to understand the neurobiological mechanisms of music."

GRAND RAPIDS, Mich. (JUNE 10, 2021) -- Much like a supply truck crossing the countryside, the misfolded proteins that damage neurons in Alzheimer's disease travel the "roads" of the brain, sometimes stopping and sometimes re-routing to avoid roadblocks, reports a study published in Science Advances by researchers at Van Andel Institute and University of Pennsylvania.

The findings shed light on how tau proteins, which form tangled clumps that damage brain cells in Alzheimer's, move through the brain. The study also provides new insights into why some areas of the brain are more vulnerable to damage than other areas.

"While the interconnected structure of the brain is essential to its function, these misfolded proteins commandeer that structure to travel through the brain and cause progressive degeneration," said Michael X. Henderson, Ph.D., an assistant professor at Van Andel Institute and corresponding author of the study. "By understanding how these proteins travel through the brain and what causes certain neurons to be at risk for damage, we can develop new therapies that can be directed to the right place at the right time to have maximal impact on disease progression."

Using models of Alzheimer's disease, the team mapped misfolded tau proteins as they progressed through the brain. They found that tau pathology moved from region to region along the brain's neural networks, which are similar to biological highways, but that it did not travel to every connected region.

To find out why some areas of the brain seemed to resist the proteins' spread, the team turned to gene expression patterns.

They identified some genes that were expressed more in regions that had more tau pathology than expected from protein spread alone. By understanding the genetic factors that control protein accumulation in the brain, the team hopes to identify ways to interfere with misfolded protein movement and slow or stop the progression of Alzheimer's and similar neurodegenerative diseases.

"We used these network models to test our hypothesis that tau spreads both forward and backward along connections between brain regions," said Eli Cornblath, Ph.D., an M.D./Ph.D. student at University of Pennsylvania and the study's first author. "After using our models to account for this two-way spreading process, we found several genes that could help inform new molecular targets to clear or prevent these protein aggregates from forming."

Just as the governor announced the start of python hunting season in Florida this month, researchers at the University of Central Florida have published a first- of-its-kind study that shows that near-infrared (NIR) spectrum cameras can help hunters more effectively track down these invasive snakes, especially at night.

The snakes, which can reach 26 feet in length and 200 pounds, have invaded the Everglades in Florida -- threatening native species and disrupting the ecosystem. The number of common native species observed in the Everglades since the snakes were first discovered in the 1990s dropped in some species by 90% through 2010, according to an earlier study. Since then, the state has been implementing mitigation strategies and encouraging residents to hunt down the massive snakes. On average snakes removed from the Everglades are about eight feet long, according to the Florida Fish and Wildlife Conservation Commission.

The new study found that by using NIR cameras, pythons could be detected 20 percent farther away than with visible cameras. Researchers say that with more work they may be able to develop an automated snake detection system. That could be a game changer especially since the pythons are marching northward and could threaten native species as far north as Virginia and Texas to the west.

"Manual removal of Burmese pythons has been the most effective management strategy, but snakes are difficult to see due to their natural camouflage," says Kyle Renshaw, a co-author of the study and an assistant professor at CREOL - UCF's College of Optics and Photonics. "NIR cameras will help python hunters find and remove pythons. These small, inexpensive cameras could be mounted on trucks or drones to help catch the hard-to-find pythons. Using cameras also opens the possibility for automated detection using computer algorithms to search the imagery faster and more comprehensively than the hunters can do on their own."

Jennifer Hewitt, a graduate student in Renshaw's lab led the study, which was published this week in the journal Applied Optics.

This research is one example showing how cameras can be "tuned" to improve performance of a specific task, the researcher say. The detection band, time constants, lens parameters, image processing and algorithms provide a rich set of variables to optimize a camera system for a particular application. The work with the snakes was based on viewing from a stationary position, but the team hopes to expand its work to include moving sensors.

"That could have big applications in search & rescue, explosives detection, border security, etc.," Renshaw says. "Jen is developing and testing models for time-limited search using a moving camera as we speak as part of her thesis."

How did they do it?

The work builds on previous spectral reflectivity characterization of pythons conducted at CREOL by then UCF Professor Ron Driggers.

Hewitt collected images of pythons at different locations and with different background scenery. Images were collected using two similar cameras that differed only in their spectral sensitivity. Images were taken in the daytime and at night at 10 different locations with similar foliage.

Hewitt then wrote software to randomly present images to the volunteers, asking them to "click" on the snake in the scene. Some scenes had no snakes. User responses were collected and analyzed. Volunteers spent an hour looking at imagery on a computer to locate pythons and clicking on the python image.

"For both day and night conditions, volunteers were able to detect the pythons further away with NIR than with visible," Hewitt says. "From here, we are continuing to fine tune the camera system to further improve the detection rate."

The NIR cameras were tuned to the snakes and appear to be more effective at night because the snake's camouflage doesn't create the same glare it does in the sunlight.

Renshaw joined UCF in 2015. He has a doctorate in applied physics and a master's degree in electrical engineering from the University of Michigan. He also has a bachelor's degree in engineering physics from Cornell University. He leads the Thin-Film Optoelectronics (TFO) Lab, which conducts research and development on materials, components, and technologies for imaging systems.

Researchers remain perplexed as to what causes dementia and how to treat and reverse the cognitive decline seen in patients. In a first-of-its-kind study, researchers at the Medical University of South Carolina (MUSC) and Beth Israel Deaconess Medical Center (BIDMC), Harvard Medical School discovered that cis P-tau, a toxic, non-degradable version of a healthy brain protein, is an early marker of vascular dementia (VaD) and Alzheimer's disease (AD). Their results, published on June 2 in Science Translational Medicine, define the molecular mechanism that causes an accumulation of this toxic protein. Furthermore, they showed that a monoclonal antibody (mAb) that targets this toxic protein was able to prevent disease pathology and memory loss in AD- and VaD-like preclinical models. Additionally, this treatment was even capable of reversing cognitive impairment in an AD-like preclinical model.

"We believe our findings have not only discovered cis P-tau as a previously unrecognized major early driver of VaD and AD but also identified a highly effective and specific immunotherapy to target this common disease driver for treating and preventing AD and VaD at early stages," said Onder Albayram, Ph.D., co-lead author and assistant professor in the Division of Cardiology in the Department of Medicine at MUSC.

Aging is a normal part of life - we experience weakening of our bones and muscles, stiffening of our blood vessels and some memory lapses. But for around 50 million people worldwide, these memory lapses become progressively more severe, ultimately leading to a diagnosis of dementia.

Dementia is an umbrella term that covers AD, which accounts for 60% to 80% of cases; VaD, the second most common cause; and other less common pathologies. Currently, there are no effective treatments for AD. Interestingly, most AD cases have a vascular component, suggesting a broader relationship between cognitive function and healthy brain vasculature. A better understanding of that relationship could provide a platform to discover novel therapeutic targets.

"Our work provides evidence that cis P-tau may be a pathogenic factor that explains VaD, which is not generally linked to other dementias," added Chenxi Qiu, Ph.D., co-lead author and a postdoctoral research fellow at BIDMC, Harvard Medical School.

In a preclinical model of VaD, young mice showed signs of brain inflammation and memory loss within one month. However, treating these mice with the cis P-tau mAb prevented neural degradation and cognitive decline out to six months. In a separate preclinical model of AD, old mice showed severe cognitive impairment. Excitingly, this severe impairment was significantly reversed when mice were given the cis P-tau mAb.

"These data show that cis P-tau could be an early upstream pathogenic factor common to both diseases," said Albayram.

Translating information gained from preclinical models to humans is often difficult, but this study offers reasons to be optimistic. Accumulation of cis P-tau caused dramatic changes in the genetic architecture of affected cells in a VaD model; these changes were consistent with those seen in human AD patients. The researchers went on to show that treatment with the cis P-tau mAb reversed 85% to 90 % of those changes suggesting the power of this potential therapy.

"The genomic landscape really adapts after the silencing of this toxic protein," said Albayram. "That was a big discovery."

Not only are Albayram and Qiu excited about these findings, but colleagues at MUSC are already quite enthusiastic about this work.

"I can go on and on about this paper," said Adviye Ergul, M.D., Ph.D., professor in the College of Medicine, Department of Pathology and Laboratory Medicine at MUSC. "They provide robust evidence that there is accumulation of a specific form of the tau protein - cis P-tau - that highlights a different tau protein pathology in VaD research."

This groundbreaking research has opened the door for new potential immunotherapies and highlighted several new areas of research that need to be explored. While the researchers delineated a pathway that leads to the accumulation of cis P-tau, the underlying linkage between vascular abnormalities and activation of the pathway needs to be identified. A better understanding of how toxic cis P-tau interacts with the healthy trans P-tau could provide further insights into the progression of AD disease.

AD and VaD might not be the only diseases affected by high levels of cis P-tau. Other brain disorders with a vascular component might also arise from this toxic protein, but further study will be required to establish such a link.

"Cis P-tau may be a common, early and pathogenic factor underlying traumatic brain injury, VaD and AD," said Qiu.

As we get older and our memory begins to lapse - misplacing our car keys or forgetting the name of a new acquaintance - we fear the possibility that these are the first signs of dementia. And while there is currently no approved treatment to reverse the physiological effects of dementia, this new research may provide hope that new therapies are around the corner.

WACO, Texas (June 9, 2021) - Most people listen to music throughout their day and often near bedtime to wind down. But can that actually cause your sleep to suffer? When sleep researcher Michael Scullin, Ph.D., associate professor of psychology and neuroscience at Baylor University, realized he was waking in the middle of the night with a song stuck in his head, he saw an opportunity to study how music -- and particularly stuck songs -- might affect sleep patterns.

Scullin's recent study, published in Psychological Science, investigated the relationship between music listening and sleep, focusing on a rarely-explored mechanism: involuntary musical imagery, or "earworms," when a song or tune replays over and over in a person's mind. These commonly happen while awake, but Scullin found that they also can happen while trying to sleep.

"Our brains continue to process music even when none is playing, including apparently while we are asleep," Scullin said. "Everyone knows that music listening feels good. Adolescents and young adults routinely listen to music near bedtime. But sometimes you can have too much of a good thing. The more you listen to music, the more likely you are to catch an earworm that won't go away at bedtime. When that happens, chances are your sleep is going to suffer."

People who experience earworms regularly at night -- one or more times per week -- are six times as likely to have poor sleep quality compared to people who rarely experience earworms. Surprisingly, the study found that some instrumental music is more likely to lead to earworms and disrupt sleep quality than lyrical music.

The study involved a survey and a laboratory experiment. The survey involved 209 participants who completed a series of surveys on sleep quality, music listening habits and earworm frequency, including how often they experienced an earworm while trying to fall asleep, waking up in the middle of the night and immediately upon waking in the morning.

In the experimental study, 50 participants were brought into Scullin's Sleep Neuroscience and Cognition Laboratory at Baylor, where the research team attempted to induce earworms to determine how it affected sleep quality. Polysomnography -- a comprehensive test and the gold standard measurement for sleep -- was used to record the participants' brain waves, heart rate, breathing and more while they slept.

"Before bedtime, we played three popular and catchy songs -- Taylor Swift's 'Shake It Off,' Carly Rae Jepsen's 'Call Me Maybe' and Journey's 'Don't Stop Believin'," Scullin said. "We randomly assigned participants to listen to the original versions of those songs or the de-lyricized instrumental versions of the songs. Participants responded whether and when they experienced an earworm. Then we analyzed whether that impacted their nighttime sleep physiology. People who caught an earworm had greater difficulty falling asleep, more nighttime awakenings, and spent more time in light stages of sleep."

Additionally, EEG readings -- records of electrical activity in the brain -- from the experimental study were quantitatively analyzed to examine physiological markers of sleep-dependent memory consolidation. Memory consolidation is the process by which temporary memories are spontaneously reactived during sleep and transformed into a more long-term form.

"We thought that people would have earworms at bedtime when they were trying to fall asleep, but we certainly didn't know that people would report regularly waking up from sleep with an earworm. But we saw that in both the survey and experimental study," he said.

Participants who had a sleep earworm showed more slow oscillations during sleep, a marker of memory reactivation. The increase in slow oscillations was dominant over the region corresponding to the primary auditory cortex which is implicated in earworm processing when people are awake.

"Almost everyone thought music improves their sleep, but we found those who listened to more music slept worse," Scullin said. "What was really surprising was that instrumental music led to worse sleep quality -- instrumental music leads to about twice as many earworms."

The study found that individuals with greater music listening habits experienced persistent earworms and a decline in sleep quality. These results are contrary to the idea of music as a hypnotic that might help sleep. Health organizations commonly recommend listening to quiet music before bedtime -- recommendations that largely arise from self-reported studies. Instead, Scullin has objectively measured that the sleeping brain continues to process music for several hours, even after the music stops.

Knowing that earworms negatively affect sleep, Scullin recommends first trying to moderate music listening or taking occasional breaks if bothered by earworms. Timing of music also is important -- try to avoid it before bed.

"If you commonly pair listening to music while being in bed, then you'll have that association where being in that context might trigger an earworm even when you're not listening to music, such as when you're trying to fall asleep," he said.

Another way to get rid of an earworm is to engage in cognitive activity -- fully focusing on a task, problem or activity helps to distract your brain from earworms. Near bedtime, rather than engaging in a demanding activity or something that would disrupt your sleep, like watching TV or playing video games, Scullin suggests spending five to 10 minutes writing out a to-do list and putting thoughts to paper. A previous study by Scullin -- partially funded by a National Institutes of Health grant and the Sleep Research Society Foundation -- found that participants who took five minutes to write down upcoming tasks before bed helped "offload" those worrying thoughts about the future and led to faster sleep.

June 10, 2021, CLEVELAND: A new Cleveland Clinic-led study has identified mechanisms by which COVID-19 can lead to Alzheimer's disease-like dementia. The findings, published in Alzheimer's Research & Therapy, indicate an overlap between COVID-19 and brain changes common in Alzheimer's, and may help inform risk management and therapeutic strategies for COVID-19-associated cognitive impairment.

Reports of neurological complications in COVID-19 patients and "long-hauler" patients whose symptoms persist after the infection clears are becoming more common, suggesting that SARS-CoV-2 (the virus that causes COVID-19) may have lasting effects on brain function. However, it is not yet well understood how the virus leads to neurological issues.

"While some studies suggest that SARS-CoV-2 infects brain cells directly, others found no evidence of the virus in the brain," says Feixiong Cheng, Ph.D., assistant staff in Cleveland Clinic's Genomic Medicine Institute and lead author on the study. "Identifying how COVID-19 and neurological problems are linked will be critical for developing effective preventive and therapeutic strategies to address the surge in neurocognitive impairments that we expect to see in the near future."

In the study, the researchers harnessed artificial intelligence using existing datasets of patients with Alzheimer's and COVID-19. They measured the proximity between SARS-CoV-2 host genes/proteins and those associated with several neurological diseases where closer proximity suggests related or shared disease pathways. The researchers also analyzed the genetic factors that enabled SARS-COV-2 to infect brain tissues and cells.

While researchers found little evidence that the virus targets the brain directly, they discovered close network relationships between the virus and genes/proteins associated with several neurological diseases, most notably Alzheimer's, pointing to pathways by which COVID-19 could lead to Alzheimer’s disease-like dementia. To explore this further, they investigated potential associations between COVID-19 and neuroinflammation and brain microvascular injury, which are both hallmarks of Alzheimer's.

"We discovered that SARS-CoV-2 infection significantly altered Alzheimer's markers implicated in brain inflammation and that certain viral entry factors are highly expressed in cells in the blood-brain barrier," explained Dr. Cheng. "These findings indicate that the virus may impact several genes or pathways involved in neuroinflammation and brain microvascular injury, which could lead to Alzehimer's disease-like cognitive impairment."

The researchers also found that individuals with the allele APOE E4/E4, the greatest genetic risk factor for Alzheimer's, had decreased expression of antiviral defense genes, which could make these patients more susceptible to COVID-19.

"Ultimately, we hope to have paved the way for research that leads to testable and measurable biomarkers that can identify patients at the highest risk for neurological complications with COVID-19," said Dr. Cheng.

Dr. Cheng and his team are now working to identify actionable biomarkers and new therapeutic targets for COVID-19-associated neurological issues in COVID long-haulers using cutting-edge network medicine and artificial intelligence technologies.

Metformin is a widely prescribed blood sugar-lowering drug. It is often used as an early therapy (in combination with diet and lifestyle changes) for type 2 diabetes, which afflicts more than 34 million Americans.

Metformin works by lowering glucose production in the liver, reducing blood sugar levels that, in turn, improve the body's response to insulin. But scientists have also noted that metformin possesses anti-inflammatory properties, though the basis for this activity was not known.

In a study published online June 8, 2021 in the journal Immunity, a multi-institution team led by researchers at University of California San Diego School of Medicine identified the molecular mechanism for the anti-inflammatory activity of metformin and, in mouse studies, found that metformin prevents pulmonary or lung inflammation in animals infected with SARS-CoV-2, the virus that causes COVID-19.

Over the past year, several retrospective clinical studies had reported that metformin use by diabetic and obese patients prior to hospital admission for COVID-19 correlated to reduced severity and mortality. Both diabetes and obesity are recognized risk factors for COVID-19, and are linked to more severe outcomes. Notably, other drugs used to control blood sugar levels do not appear to produce a similar effect.

But while these clinical studies suggested metformin's anti-inflammatory activity, rather than lowering of blood glucose, could be responsible for reduced COVID-19 severity and mortality, none of the studies offered an explanation or prompted large, randomized clinical trials needed for obtaining conclusive answers.

"The clinical studies were plagued by confounders that made conclusions hard to reach. There was some skepticism in their findings," said corresponding study author Michael Karin, PhD, Distinguished Professor of Pharmacology and Pathology and Ben and Wanda Hildyard Chair for Mitochondrial and Metabolic Diseases at UC San Diego School of Medicine. "And because metformin is an out-of-patent, low-cost drug, there is little impetus to conduct large-scale trials, which are quite expensive."

Karin, with co-senior author Elsa Sanchez-Lopez, PhD, an assistant professor at the Department of Orthopedic Surgery, postdoctoral fellow Hongxu Xian, PhD, and others, turned their focus to a mouse model of acute respiratory distress syndrome (ARDS), a life-threatening condition in which fluids leak into the lungs, making breathing difficult and restricting oxygen supply to essential organs.

ARDS is triggered by trauma and by bacterial or viral infections. It is a frequent cause of death in patients hospitalized with COVID-19. The researchers found that metformin administered to mice prior to or after exposure to bacterial endotoxin, a surrogate for bacterial pneumonia, resulted in the inhibition of ARDS onset and lessening of its symptoms. Metformin also produced a marked reduction in mortality in endotoxin-challenged mice and inhibited IL-1β production and inflammasome assembly within alveolar macrophages -- immune cells found in the lungs.

IL-1β, along with IL-6, are small proteins called cytokines that cause inflammation as an early immune response. Their amounts are often highly elevated in persons infected by SARS-CoV-2, creating "cytokine storms" in which the body starts attacking its own cells and tissues. They are signs of an acute immune response gone awry.

Production of IL-1β depends on a large protein complex called the inflammasome, whose presence in lung tissue is found to be highly increased in deceased COVID-19 patients, a discovery made by co-authors Moshe Arditi, MD, and Timothy R. Crother, PhD, at Cedars-Sinai Medical Center in Los Angeles.

Working with colleagues at The Scripps Research Institute, the UC San Diego researchers confirmed that metformin inhibited inflammasome activation and prevented SARS-CoV-2-induced pulmonary inflammation in mice.

Cell culture studies using macrophages revealed the underlying mechanism by which metformin exerts its anti-inflammatory activity: reduced production of ATP by mitochondria. ATP is the molecule that mitochondria use to store chemical energy for cells. It is essential to all cellular processes, but blunted ATP production in liver cells is responsible for the glucose lowering effect of metformin.

Lower amounts of ATP in macrophages led to inhibition of mitochondrial DNA synthesis, which had been previously identified by Karin's lab as a critical step in NLRP3 inflammasome activation. Subsequent research found that clearing away damaged mitochondria reduced NLRP3 inflammasome activity and reduced inflammation.

UC San Diego researchers also confirmed that specific interference with mitochondrial DNA synthesis in macrophages caused by removal of the enzyme CMPK2 (cytidine monophosphate kinase 2) inhibited IL-1β (but not IL-6) production and prevented ARDS onset.

"These experiments strongly suggest that improved delivery of metformin or CMPK2 inhibitors into lung macrophages can provide new treatments for severe COVID-19 and other forms of ARDS," said Sanchez Lopez.

The authors said the findings suggest metformin may have therapeutic potential for treating a variety of neurodegenerative and cardiovascular diseases in which NLRP3 inflammasome activation is a factor. "Inhibition of inflammasome activation may also account for the poorly explained anti-aging effect of metformin," said Karin.

Married men who don't help out around the house tend to bring home bigger paychecks than husbands who play a bigger role on the domestic chores front.

New research from the University of Notre Dame shows that "disagreeable" men in opposite-sex marriages are less helpful with domestic work, allowing them to devote greater resources to their jobs, which results in higher pay.

In contemporary psychology, "agreeableness" is one of the "Big Five" dimensions used to describe human personality. It generally refers to someone who is warm, sympathetic, kind and cooperative. Disagreeable people do not tend to exhibit these characteristics, and they tend to be more self-interested and competitive.

"Why Disagreeableness (in Married Men) Leads to Earning More: A Theory and Test of Social Exchange at Home" is forthcoming in Personnel Psychology from lead author Brittany Solomon and Cindy Muir (Zapata), management professors at Notre Dame's Mendoza College of Business, along with Matthew Hall, the David A. Potenziani Memorial College Professor of Constitutional Studies and concurrent law professor at Notre Dame, and Elizabeth Campbell from the University of Minnesota.

"Across two studies, we find evidence that disagreeable men tend to earn more money relative to their more agreeable male counterparts because they are more self-interested and less helpful to their wives at home, which allows for greater job involvement and, ultimately, higher pay," Solomon said. "This effect is even stronger among disagreeable men with more traditional gender role attitudes and when their wives are highly conscientious, presumably because in these cases their wives take on more household management and more seamlessly carry out the responsibilities."

The concept may bring to mind the '50s and '60s sitcom "Leave it to Beaver," where Ward Cleaver always arrived home in time for dinner and June Cleaver wore dresses and pearls to clean floors. Did they have advanced understanding of their respective roles?

The study suggests that because these men are able to preserve more time and energy at home, they can invest these resources into their work and earn more. However, the team found that disagreeableness does not predict career success for more egalitarian men, those whose wives are less conscientious or any men outside opposite-sex marriages.

"While disagreeableness in the workplace may lead some employees to success, those hoping to attain higher pay should at least hesitate before leaning into a disagreeable workplace persona," Solomon cautioned. "Indeed, if self-interested and less communal work behavior was the only key to higher pay, then disagreeable men would tend to earn more, regardless of whether they were married, how they viewed gender roles or to whom they were married."

Prior research has shown that disagreeableness predicts financial success (especially for men), and this association is attributed to workplace behavior. However, this effect remains puzzling given that disagreeableness is negatively associated with valued workplace behaviors, such as cooperation and prosocial behavior. In contrast, the team theorizes the male disagreeableness premium can be further understood by considering imbalanced social exchanges at home, specifically with one's spouse. 

"Our findings build on the conventional wisdom that organizations seem to reward disagreeable workplace behaviors and highlight the importance of social exchange at home for success at work," Solomon said. "Our research suggests that organizations acknowledge the role that spousal exchange plays in individual success and points to the potential for organizations to refocus efforts to fuel job involvement on lightening the burden of at-home responsibilities. Doing so could allow employees to preserve resources that could then be invested in their jobs.

"Presumably, this type of initiative would be especially beneficial to those who do not have the persona and gender that, we found, naturally drives individually advantageous spousal exchange -- that is, everyone other than disagreeable, married men," she said. "To help those who do not have the built-in at-home arrangement that enhances job involvement and pay, organizations may consider investing in infrastructure that helps establish more level career-related playing fields."

These may include providing non-work resources, such as lists of reputable providers for home services and maintenance, establishing child care programs, pre-vetting caregivers or having couriers on retainer, which Solomon speculates may enhance job involvement even more than traditional work-focused incentives like bonuses.

"Practices that situate employees more equitably outside of work may offer more employees the opportunity to succeed," Solomon said. "Also, some research shows that men are stigmatized for taking advantage of flex work policies. Changing the organizational culture, in addition to implementing such policies, may influence calculations within a marriage or partnership about whose career should take priority and who should do more at home. Consequently, organizations may also help support initiatives aimed to promote gender diversity and inclusion, especially efforts to reduce male dominance in high-income positions."

The study also carries implications for career self-management. Most notably, the findings may influence how employees view other people's roles in their own success, beyond their boss and other organizational members, and help improve the understanding of how one's choice of romantic partner and social exchange at home can have substantial implications for one's career success.

"Professionals often publicly thank their spouses when receiving achievement awards or earning promotion," Solomon said. "And, at least for disagreeable men, our findings quantify the truth behind this sentiment."

Have you ever been cut off in traffic by another driver, leaving you still seething miles later? Or been interrupted by a colleague in a meeting, and found yourself replaying the event in your head even after you've left work for the day? Minor rude events like this happen frequently, and you may be surprised by the magnitude of the effects they have on our decision-making and functioning. In fact, recent research co-authored by management professor Trevor Foulk at the University of Maryland's Robert H. Smith School of Business suggests that in certain situations, incidental rudeness like this can be deadly.

In "Trapped by A First Hypothesis: How Rudeness Leads to Anchoring" forthcoming in the Journal of Applied Psychology, Foulk and co-authors Binyamin Cooper of Carnegie Mellon University, Christopher R. Giordano and Amir Erez of the University of Florida, Heather Reed of Envision Physician Services, and Kent B. Berg of Thomas Jefferson University Hospital looked at how experiencing rudeness amplifies the "anchoring bias." The anchoring bias is the tendency to get fixated on one piece of information when making a decision (even if that piece of information is irrelevant).

For example, if someone asks, "Do you think the Mississippi River is shorter or longer than 500 miles?," that suggestion of 500 miles can become an anchor that can influence how long you think the Mississippi River is. When it happens, it's difficult to stray very far from that initial suggestion, says Foulk.

The anchoring bias can happen in a lot of different situations, but it's very common in medical diagnoses and negotiations. "If you go into the doctor and say 'I think I'm having a heart attack,' that can become an anchor and the doctor may get fixated on that diagnosis, even if you're just having indigestion," Foulk explains. "If doctors don't move off anchors enough, they'll start treating the wrong thing."

Because anchoring can happen in many scenarios, Foulk and his co-authors wanted to study more about the phenomenon and what factors exacerbate or mitigate it. They have been studying rudeness in the workplace for years and knew from previous studies that when people experience rudeness, it takes up a lot of their psychological resources and narrows their mindset. They suspected this might play a role in the anchoring effect.

To test their theory, the researchers ran a medical simulation with anesthesiology residents. The residents had to diagnose and treat the patient, and right before the simulation started, the participants were given an (incorrect) suggestion about the patient's condition. This suggestion served as the anchor, but then throughout the exercise, the simulator provided feedback that the ailment was not the suggested diagnosis, but instead something else.

In some iterations, before the simulation started, the researchers had one doctor enter the room and act rudely toward another doctor in front of the residents.

"What we find is that when they experienced rudeness prior to the simulation starting, they kept on treating the wrong thing, even in the presence of consistent information that it was actually something else," says Foulk. "They kept treating the anchor, even though they had plenty of reason to understand that the anchor diagnosis was not what the patient was suffering from."

This effect was replicated across a variety of other tasks, including negotiations as well as general knowledge tasks. Across the different studies, the results were consistent - experiencing rudeness makes it more likely that a person will get anchored to the first suggestion they hear.

"Across the four studies, we find that both witnessed and directly-experienced rudeness seemed to have a similar effect," says Foulk. "Basically, what we're observing is a narrowing effect. Rudeness narrows your perspective, and that narrowed perspective makes anchoring more likely."

In general, the anchoring tendency is usually not a big deal, says Foulk. "But when you're in these important, critical decision-making domains - like medical diagnoses or big negotiations - interpersonal interactions really matter a lot. Minor things can stay on top of us in a way that we don't realize."

To provide additional insights into this phenomenon, the researchers also explored ways to counteract it. Rudeness makes you more likely to anchor because it narrows your perspective, so the researchers explored two tasks that have been shown to expand your perspective - perspective-taking and information elaboration.

Perspective-taking helps you expand your perspective by seeing the world from another person's point of view, and information elaboration helps you see the situation from a wider perspective by thinking about it more broadly. Across their studies, the researchers found that both behaviors could counteract the effect of rudeness on anchoring.

While these interventions can help make rudeness less likely to anchor people, Foulk says these should be a last resort. The best remedy for the rudeness problem?

"In important domains, where people are making critical decisions, we really need to rethink the way we treat people," he says. "We never really did allow aggressive behavior at work. But we're fine with rudeness, and now we're learning more and more that small insults are equally impactful on people's performance."

And it needs to stop, he says.

"We tend to underestimate the performance implications of interpersonal treatment. We hear 'If you can't stand the heat, get out of the kitchen.' It's almost like being able to tolerate people's treatment of you is like a badge of honor. But the reality is that this bad treatment is having really deleterious effects on performance in domains that we care about - like medicine. It matters."

This is the fourth paper in a string of Foulk's research showing that rudeness negatively impacts medical performance, where the impacts can be much bigger - and much more dire - than the insults, he says.

"In simulations, we're finding that mortality is increased by rudeness. People could be dying because somebody insulted the surgeon before they started operating."

HOUSTON - (June 10, 2021) - Leaders who encourage their employees to learn on the job and speak up with ideas and suggestions for change have teams that are more effective and resilient in the face of unexpected situations, according to new research from Rice University and the University of Windsor.

"A Resource Model of Team Resilience Capacity and Learning" will appear in a special issue of Group & Organization Management. Authors Kyle Brykman, an assistant professor at the Odette School of Business at the University of Windsor, and Danielle King, an assistant professor of psychological sciences at Rice, studied what makes employees more resilient and fosters learning in the workplace. The researchers specifically examined the interactions of 48 teams from five Canadian technology startups.

"Understanding what organizations can do to help employees become more resilient is the focus our work in my WorKing Resilience Research Laboratory," King said. "This research project offered an opportunity to uncover the important role of leadership and employee voice in the resilience process."

Brykman and King found that teams that were more effective and resilient if their bosses encourage employees to take risks, make suggestions and learn from the process. Creating a work environment centered around learning and open communication is helpful as teams grow and take on new tasks, King said. Leaders must reinforce this workplace culture with positive language that signals openness and a focus on their development, she said.

"Knowing that you have a leader who is focused on learning and not just on performance outcomes is critical," King said. "It's also important for them to be intentional about communicating this regularly to employees, as it can make all the difference in building more resilient teams. Leaders need to verbally reward a learning mindset. For example, when a boss responds to an employee who makes an on-the-job error by saying, 'Great, now you can learn from this experience,' rather than berating them for making a mistake, it makes a big difference."

To request a copy of the study, contact Amy McCaig, senior media relations specialist at Rice, at 713-348-6777 or amym@rice.edu.

DALLAS - June 9, 2021 - A phenomenon in which an RNA named NORAD drives a protein named Pumilio to form liquid droplets in cells, much like oil in water, appears to tightly regulate the activity of Pumilio. A new study led by UT Southwestern scientists suggests that such RNA-driven "phase separation," in turn, protects against genome instability, premature aging, and neurodegenerative diseases, and may represent a previously unrecognized way for RNAs to regulate cellular processes.

"It's becoming more and more clear that phase separation is an important organizing principle in cells," says Joshua Mendell, M.D., Ph.D., professor of molecular biology and a Howard Hughes Medical Institute investigator at UTSW who led the study published online today in Nature.

Other scientists at UTSW, including Michael Rosen, Ph.D., chair of biophysics, a member of the National Academy of Sciences (NAS), and a Howard Hughes Medical Institute investigator, and Steven McKnight, Ph.D., professor of biochemistry and a member of NAS and the National Academy of Medicine, have previously found that phase separation participates in many cellular pathways. "Our work," says Mendell, "builds upon their findings, uncovering how phase separation enables some RNAs to regulate the activity of proteins that they interact with."

Mendell and Mahmoud Elguindy, a student in UTSW's Medical Scientist Training Program, uncovered this role for phase separation by studying an RNA known as "non-coding RNA activated by DNA damage," or NORAD. Although NORAD isn't directly responsible for generating proteins, it binds and inhibits Pumilio, a protein that represses the expression of hundreds of other messenger RNAs that encode proteins involved in cell division.

Previous work from the Mendell lab showed that human cells and lab animals genetically engineered to lack NORAD have too much active Pumilio, which prevents them from maintaining consistent numbers of chromosomes during cell division and causes them to prematurely age. On the flip side, mutations that lead to too little Pumilio have been linked to neurodegenerative diseases in humans.

But a fundamental question remained as to how NORAD regulates Pumilio to prevent disease. Because NORAD is only one RNA of hundreds in the cell that is bound by Pumilio, it was unclear how NORAD is able to outcompete these other RNAs to control levels of active Pumilio.

To answer this question, Mendell and Elguindy used microscopy to locate NORAD-Pumilio complexes in cells. They found that these complexes dotted the cells' interiors, forming their own oil droplet-like structures separate from the cytoplasm, which they named "NORAD-Pumilio bodies."

Further investigation showed that about half the Pumilio in cells was sequestered in NORAD-Pumilio bodies, and that phase separation was critical for concentrating Pumilio in these structures. Not only did Pumilio bind to numerous sites on each NORAD molecule, but interactions between Pumilio molecules also played a central role in droplet formation. This combination of attraction between the RNA and protein molecules provides a strong driving force that separates Pumilio proteins from the surrounding cellular environment, Elguindy says, preventing them from interacting with other RNAs.

When the researchers used techniques to disrupt this phase separation, NORAD was no longer able to sequester enough Pumilio, leading to chromosomal abnormalities.

"While phase separation has been observed in many different settings in cells, the scientific community has debated which cellular activities require this process," says Elguindy. "Our study showed that in this instance, when you perturb phase separation, there are real consequences."

Mendell adds that better understanding the NORAD-Pumilio system could lead to new ways to counter symptoms associated with aging and to treat neurodegenerative diseases. In addition, looking for more examples of phase separation by other RNA molecules could shed light on how cells regulate other key processes.

Young clownfish living closest to shore are dying faster than those further offshore because they are being exposed to artificial lighting, says an international research team.

Working on the reefs around Moorea in French Polynesia, scientists from France, the United Kingdom, Chile and Australia found that nearshore juvenile clownfish living in anemones under lights had higher mortality than juveniles in anemones not exposed to artificial light.

The scientists also found that the surviving clownfish grew 44 per cent more slowly than clownfish under natural lighting conditions.

Professor Stephen Swearer, a marine ecologist, from the University of Melbourne, said the team exposed 42 clownfish in their host anemones to either artificial light at night (ALAN) or natural light in the lagoon.

The clownfish were monitored over nearly two years, individually identified as survivors, and captured to measure their growth.

"The impacts of light pollution found here are probably underestimated and mitigation measures and policy changes are urgently required," said Professor Swearer.

Lead author, Jules Schligler, from the École Pratique des Hautes Études PSL Université Paris (EPHE) and the Centre of Island Research and Environmental Observatory (CRIOBE), said clownfish can live in shallow coastal waters and are highly sedentary living in anemones, which means they can be easily impacted by light at night coming from streetlights, piers or ports.

"As with many other reef fish, clownfish feed, reproduce, defend their territories and interact with other fish during the day and reset whilst sleeping at night. However, 36 per cent of the clownfish exposed to light pollution were more likely to die than fish under natural light cycles," he said.

"Like humans, fish need a period of inactivity, which is crucial for their well-being."

In the research paper "Longterm exposure to artificial light at night in the wild decreases survival and growth of a coral reef fish" published in Royal Society B, the scientists say "even those fish that survived didn't entirely escape the effects of artificial light at night as they grew less than fish from the control group."

"This is the first time that the impacts of ALAN have been tested on a coral reef fish in the wild and over such a long time," said Daphne Cortese, a former EPHE and CRIOBE student, who is now post-doctoral fellow at the University of Glasgow.

"As 12 per cent of all coral reef fish live in close association with another sedentary species, such as a coral or anemone, light pollution could already be having severe negative impacts on a fifth of fringing reef fish populations," she said.

The international team hope the research will help raise awareness of the impacts of ALAN on coastal marine ecosystems.

"Many marine protected areas are impacted by light pollution at night, and authorities are not taking this pollution into account," said Ricardo Beldade, Associate Professor at the Pontificia Universidad Católica de Chile. "We hope that policy makers take this threat much more seriously for future management strategies."

New Curtin research has shown how a readily available, cheap and safe-to-use product found in the medicine cabinet of most homes could be the key to better ecological restoration practices with major benefits for the environment and agriculture.

The study revealed that aspirin, which naturally occurs in the bark of the willow tree and other plants, can improve the survival of grass species important for ecological restoration and sustainable pasture when applied in a seed coating.

Lead researcher Dr Simone Pedrini from the ARC Centre for Mine Site Restoration in Curtin's School of Molecular and Life Sciences, said salicylic acid has been used for its medicinal properties for more than 4000 years and its modern synthetic version, acetylsalicylic acid, or aspirin, is one of the most widely used medications in the world.

"Our research found that aspirin can do more than just ease a headache; it can also help restore degraded land and ecosystems and establish sustainable pastures through improving plant growth and survival," Dr Pedrini said.

"This study was performed on native perennial grasses and showed that applying very low concentrations of salicylic acid to the seed can improve plant survival and therefore its effectiveness in reaching restoration goals.

"Salicylic acid was already known for its ability to improve stress resistance for plants such as tomatoes, making it useful for the agricultural industry, but its effect on native species and potential to aid landscape restoration was still unknown."

Research team member and Director of the ARC Centre for Mine Site Restoration, John Curtin Distinguished Professor Kingsley Dixon said salicylic acid was applied to the seeds of the native grass species using a technology called seed coating, perfected by Curtin University researchers, that allows seed shape and size to be modified, improving seeding efficiency, and can be used to carry growth benefiting compounds.

"This is the first study to deliver aspirin via coating on native species which means the technology can be scaled up for improving restoration targets such as the UN Decade on Ecosystem Restoration to be launched on 5 June 2021," Professor Dixon said.

"Further research is now needed to test salicylic acid as a coating in other wild species to improve native plant resistance to drought, extreme temperatures, salinity, pathogens, and herbicides.

"Moreover, coating with salicylic acid in combination with other beneficial compounds should be tested on a broader array of plant species used in restoration, as their combined impact on seed germination, emergence, growth and plant establishment could improve the successful deployment of native seed onto degraded landscapes, ultimately allowing for a more efficient seed-based restoration."

The full paper, 'Seed encrusting with salicylic acid: a novel approach to improve establishment of grass species in ecological restoration' will be published in PLOS ONE.