Culture

EUGENE, Ore. -- Researchers at the University of Oregon have uncovered a molecular mechanism by which the human stomach pathogen Helicobacter pylori is attracted to bleach, also known as hypochlorous acid or HOCI. The study revealed that H. pylori uses a protein called TlpD to sense bleach and swim toward it, and that the bacteria Salmonella enterica and Escherichia coli can use TlpD-like proteins to detect bleach in the environment.

The researchers propose H. pylori uses the protein TlpD to sense sites of tissue inflammation, which could help the bacteria colonize the stomach and perhaps locate damaged tissue and nutrients. The paper, "Helicobacter pylori senses bleach (HOCI) as a chemoattractant using a cytosolic chemoreceptor," appeared Aug. 29 in the journal PLOS Biology.

The health burden caused by H. pylori is particularly large, researchers say, because it infects about half the world's population with nearly 100 percent infection rates in some developing regions. The bacterium takes up residence inside small pockets in the stomach, called stomach glands, that are thought to shelter it from the hostile gastric environment.

H. pylori causes chronic inflammation and stomach ulcers. It is a major risk factor for stomach cancer, one of the most common forms of cancer worldwide.

"Part of the rationale for studying this particular protein is that we know the navigation system that Helicobacter pylori has is really important for the bacteria to be able to infect and cause disease," said lead author Arden Perkins, a postdoctoral fellow at the University of Oregon. "If we come to learn what the function of this protein is, there is potential that we might be able to disrupt its function with a new drug."

H. pylori, like most bacteria, use special proteins to sense chemicals in their environment. The process, known as chemotaxis, allows them to regulate their flagella to swim toward or away from compounds they encounter.

The research team set out to determine how bacteria respond to the presence of bleach, which is produced by white blood cells in the body and is a key part of how the immune system fights bacteria.

"It's important that we understand the protein machinery of bleach sensing," said study co-author Karen Guillemin, a professor of biology and member of the UO's Institute of Molecular Biology. "It turns out that this is not a machinery that is exclusive to Helicobacter pylori and it allows us insights into other bacteria that have similar proteins."

Work began 2.5 years ago to determine the molecular function of the TlpD protein, which the researchers knew was involved in regulating the bacteria's flagella. They knew TlpD was a sensor molecule but didn't know what it might be sensing. In order to get to the bottom of the uncharacterized protein's function, Perkins isolated the TlpD protein and two other proteins involved in transmitting the molecular signal to the flagella.

"Isolating the components of the molecular signaling system gave us a much clearer understanding of what was going on," Guillemin said.

Previous research had revealed that reactive oxygen species might be the compounds that were sensed by the TlpD protein, so Perkins tested different compounds, including hydrogen peroxide, superoxide and bleach. The surprising results showed that TlpD produced an attractant signal when exposed to bleach.

Although it seemed counterintuitive for the bacteria to be attracted to a noxious chemical, further studies using live bacteria confirmed that the bacteria are unharmed by and attracted to sources of bleach at concentrations produced by the human body.

Perkins and co-workers couldn't deny what they were seeing after repeatedly performing the experiment and controlling for different explanations.

"This project started from this really rigorous molecular insight, and then we progressed to thinking about what this means for the behavior of the bacteria," Guillemin said. "We were able to proceed with really strong confidence that the phenomenon we were studying made sense at a molecular level."

Normally, bleach produced during inflammation is effective at killing bacteria. But H. pylori is unusual in making its home in inflamed tissue for decades apparently without being eradicated by the bleach. The research team believes H. pylori may be attracted to bleach as a means of locating and persisting inside the stomach glands, which are full of white blood cells but serve as crucial reservoirs for the bacteria.

Surprisingly, the researchers found, the toxic compound produced by the white blood cells could be interpreted as an attraction signal by the invading bacteria.

"We know that in the course of its infection, the bacteria is able to live in inflamed tissue for years and years, so this result suggests that maybe part of the way it does that is by being attracted to inflamed tissue," Perkins said. "It's clearly evolved sufficient protections to be able to endure that environment even though there are potentially high concentrations of bleach there."

Researchers found TlpD-like proteins from Salmonella enterica and Escherichia coli are also able to detect bleach, indicating that bleach-sensing may be a previously unrecognized phenomena performed by many types of bacteria.

The research eventually could lead to new therapies to disrupt the ability of harmful bacteria to sense their environment and could have implications for reducing antibiotic resistance.

Typical antibiotics used clinically today kill or prevent bacteria from dividing by targeting things like the bacterial cell wall. As a result, bacteria face selective pressures to develop resistance to those kinds of drugs in order to survive.

In the case of Helicobacter pylori, approximately 30 percent of infections are resistant to antibiotic treatment. With a more thorough understanding of the mechanisms at work, Guillemin said, researchers may then be able to develop more effective means of combatting bacteria.

"It might be that there are less strong selective pressures for bacteria to overcome a drug that just makes them disoriented," Guillemin said. "By 2050 there's going to be pandemics of antibiotic-resistant bacteria, so there's a real need to think about new strategies."

ANN ARBOR--Researchers have identified a receptor protein that can detect when winter is coming.

The findings, scheduled for publication Aug. 29 in the journal Cell, reveal the first known cold-sensing protein to respond to extreme cold.

"Clearly, nerves in the skin can sense cold. But no one has been able to pinpoint exactly how they sense it," said Shawn Xu, a faculty member at the University of Michigan Life Sciences Institute and senior author of the study. "Now, I think we have an answer."

When environmental temperatures drop to uncomfortable, and even dangerous levels, receptor proteins within the sensory nerves in the skin perceive the change, and they relay that information to the brain. This is true for organisms from humans all the way down to the tiny, millimeter-long worms that researchers study in Xu's lab at the Life Sciences Institute: the model system Caenorhabditis elegans.

"When you step outside and you sense it's too cold, you're going to take action to get back to a warmer environment as soon as you can," said Xu, who is also a professor in the U-M Medical School's Department of Molecular and Integrative Physiology. "When the worms sense cold, they also engage in avoidance behavior--moving away from cold temperatures, just like humans."

But unlike humans or other complex organisms, C. elegans have a simple, well-mapped genome and a short lifespan, making them a valuable model system for studying sensory responses.

Previous searches for a cold receptor have been unsuccessful because researchers were focusing on specific groups of genes that are related to sensation, which is a biased approach, Xu said. Capitalizing on the simplicity of C. elegans, he and his colleagues instead took an unbiased approach. They looked across thousands of random genetic variations to determine which affected the worms' responses to cold.

The researchers found that worms missing the glutamate receptor gene glr-3 no longer responded when temperatures dipped below 18 degrees Celsius (64 F). This gene is responsible for making the GLR-3 receptor protein. Without this protein, the worms became insensitive to cold temperatures, indicating that the protein is required for the worms to sense cold.

What's more, the glr-3 gene is evolutionarily conserved across species, including humans. And it turns out the vertebrate versions of the gene can also function as a cold-sensing receptor.

When the researchers added the mammalian version of the gene to mutant worms lacking glr-3--and were thus insensitive to cold--they found that it rescued the worms' cold sensitivity. They also added the worm, zebrafish, mouse and human versions of the genes to cold-insensitive mammalian cells. With all versions of the gene, the cells became sensitive to cold temperatures.

The mouse version of the gene, GluK2 (for glutamate ionotropic receptor kainate type subunit 2), is well known for its role in transmitting chemical signals within the brain. The researchers discovered, however, that this gene is also active in a group of mouse sensory neurons that detect environmental stimuli, such as temperature, through sensory endings in the animals' skin.

Reducing the expression of GluK2 in mouse sensory neurons suppressed their ability to sense cold, but not cool, temperatures. The findings provide additional evidence that the GluK2 protein serves as a cold receptor in mammals.

"For all these years, attention has been focused on this gene's function in the brain. Now, we've found that it has a role in the peripheral sensory system, as well," Xu said. "It's really exciting. This was one of the few remaining sensory receptors that had not yet been identified in nature."

In addition to Xu, study authors are: Elizabeth Ronan, Wei Cai, Mahar Fatima, Hankyu Lee, Zhaoyu Li, Kevin Pipe and Bo Duan of U-M; Jianke Gong, Jinzhi Liu, Feiteng He and Wenyuan Zhang of Huazhong University of Science and Technology in China and U-M; Jianfeng Liu of Huazhong University of Science and Technology; and Gun-Ho Kim of the Ulsan National Institute of Science and Technology in South Korea.

WASHINGTON -- Even the most powerful computers are still no match for the human brain when it comes to pattern recognition, risk management, and other similarly complex tasks. Recent advances in optical neural networks, however, are closing that gap by simulating the way neurons respond in the human brain.

In a key step toward making large-scale optical neural networks practical, researchers have demonstrated a first-of-its-kind multilayer all-optical artificial neural network. Generally, this type of artificial intelligence can tackle complex problems that are impossible with traditional computational approaches, but current designs require extensive computational resources that are both time-consuming and energy intensive. For this reason, there is great interest developing practical optical artificial neural networks, which are faster and consume less power than those based on traditional computers.

In Optica, The Optical Society's journal for high-impact research, researchers from The Hong Kong University of Science and Technology, Hong Kong detail their two-layer all-optical neural network and successfully apply it to a complex classification task.

"Our all-optical scheme could enable a neural network that performs optical parallel computation at the speed of light while consuming little energy," said Junwei Liu, a member of the research team. "Large-scale, all-optical neural networks could be used for applications ranging from image recognition to scientific research."

Building an all-optical network

In conventional hybrid optical neural networks, optical components are typically used for linear operations while nonlinear activation functions--the functions that simulate the way neurons in the human brain respond--are usually implemented electronically because nonlinear optics typically require high-power lasers that are difficult to implement in an optical neural network.

To overcome this challenge, the researchers used cold atoms with electromagnetically induced transparency to perform nonlinear functions. "This light-induced effect can be achieved with very weak laser power," said Shengwang Du, a member of the research team. "Because this effect is based on nonlinear quantum interference, it might be possible to extend our system into a quantum neural network that could solve problems intractable by classical methods."

To confirm the capability and feasibility of the new approach, the researchers constructed a two-layer fully-connected all optical neural network with 16 inputs and two outputs. The researchers used their all-optical network to classify the order and disorder phases of the Ising model, a statistical model of magnetism. The results showed that the all-optical neural network was as accurate as a well-trained computer-based neural network.

Optical neural networks at larger scales

The researchers plan to expand the all-optical approach to large-scale all-optical deep neural networks with complex architectures designed for specific practical applications such as image recognition. This will help demonstrate that the scheme works at larger scales.

"Although our work is a proof-of-principle demonstration, it shows that it may become possible in the future to develop optical versions of artificial intelligence," said Du. "The next generation of artificial intelligence hardware will be intrinsically much faster and exhibit lower power consumption compared to today's computer-based artificial intelligence," added Liu.

The Feinstein Institutes for Medical Research Professor and Senior Vice President Karina W. Davidson, PhD, MASc, reviews clinical practices for social determinants of health screening and referrals in the September 17 issue of The Journal of the American Medical Association (JAMA).

Conditions in the places where people live, learn, work and play affect a wide range of health risks and outcomes - these conditions are called social determinants of health. Screening for social determinants helps health care professionals better understand patient health risks and improves patient health. The health care community generally agrees that clinicians should screen social determinants for their patients.

"For optimal health of our patients, we must address and eventually eliminate patients' social determinants of health disparities," said Dr. Davidson, who heads the Center for Personalized Health at the Feinstein Institutes and is a professor of Behavioral Medicine at the Donald and Barbara Zucker School of Medicine at Hofstra/Northwell. "Continued advances and debate about how to best implement social determinants screening and referrals will ensure continued progress towards this goal and will give clinicians and patients hope for a healthier future."

Dr. Davidson, along with co-author Thomas McGinn, MD, MPH, Director of the Institute for Health Innovations and Outcomes Research at the Feinstein Institutes and senior vice president of physician network operations at Northwell Health, note in their JAMA review that it is well known in the clinic that disparities in the social determinants are harmful to health. But less is known about who should screen, identify and deliver programs to reduce these harms and successfully address patients' social determinants, either individually or at the societal level. The authors note that there have been successes in identifying social screening needs and implementing co-location care models, for example. They also note that, "identifying and addressing/improving patients' social determinants will only be successful if these clinical practices occur with broad structural, community, and societal changes to the determinants that currently perpetuate poor health."

Drs. Davidson and McGinn also note that there is a debate to implementing comprehensive and universal screening for social determinants. One of the debates is that doctors don't have time. In a 2019 survey, 70 percent of physicians reported "lack of time" as an issue that prevents social determinants screening. There is already concern that many physicians are spending too little time in meaningful patient care, and too much time on electronic health record entry and other administrative responsibilities, and that adding screening for social determinants of health many only exacerbate this issue.

"Dr. Davidson is a research leader in chronic disease management who exemplifies our mission to produce knowledge to cure disease," said Kevin J. Tracey, MD, president and CEO of the Feinstein Institutes. "This paper is another example of how she brilliantly applies research to find future cures."

Dr. Davidson joined the Feinstein Institutes last year. Her current research focuses on Personalized (N-of-1) trials to identify precise therapies that improve a single patients' symptoms, conditions, or behaviors. Dr. Davidson has been the principal investigator of more than 22 federally funded grants and authored over 200 peer reviewed articles. She was recently awarded a Transformative R01 grant to accomplish this vision of re-imagining the process by which therapies are tested in the clinical encounter, which helped identify maximal benefit and minimal harm for each individual patient. For more than 25 years, she has served in leadership roles with diverse teams focused on improving scientific and educational missions.

Encouraging citizens to take part in almost every step of scientific air quality research improves their understanding of how air pollution affects their health, finds a new study from the University of Surrey.

In a paper published in Sustainable Cities and Society journal, researchers from Surrey's Global Centre for Clean Air Research (GCARE) together with the IAAC Fab Lab Barcelona, Connected Places Catapult and T6 Ecosystems under the iSCAPE project, provide details about how introducing a multi-component, 'citizen science' approach that allows people to take part in the scientific process of research - e.g., finding research problems, methodologies and conclusions, in collaboration with the researchers - helps them to better understand their pollution exposure levels.

GCARE's strategy is based on three basic ideas:

Inclusion: introducing seminars and workshops to involve people from different genders, ages and ethnic groups

Collaboration: constant interaction between researchers, communities and policy makers

Reciprocation: citizen scientists are encouraged to debate their research with each other in a workshop setting.

Scientists from GCARE also used questionnaires and interactive quizzes to monitor people's perception of exposure levels and introduced low-cost sensors to allow individuals to conduct their own research studies.

The project allowed citizens to create detailed and well thought out investigations that looked into issues such as the air quality inside of their homes at different times of the day to explored when and how traffic jams worsen air quality in nearby residential areas.

Professor Prashant Kumar, Director of GCARE at the University of Surrey, said: "Until recently, citizens' involvement in air quality research has been limited to monitoring their environment and raising awareness of pollution in their local area, while tasks such as the design, planning and analysis of research were carried out by scientists. What we have found is that when local residents play an integral part in scientific research, they acquire knowledge that can more directly impact their day-to-day lives and actions.

"Citizens should no longer be treated as participants of a study; we should rather embrace them as partners. This work is an example of bringing together citizens and their representatives, public authorities and researchers for all-round actions against pollution."

Councillor Caroline Reeves, Leader of Guildford Borough Council, said: "The involvement of members of our community with the work done at the University of Surrey has highlighted the interest in the issues around air quality in a very strong and meaningful way. Residents and businesses have far greater awareness, and are keen to find resolutions to the problems rather than dismissing it at someone else's problem. It has meant that air quality is very high on the list of targets to be addressed locally as well as nationally."

Scientists at the Institute for Research in Biomedicine (IRB Barcelona) and the Molecular Biology Institute of Barcelona (IBMB-CSIC) have published a study in the journal Nature Communications revealing the structure of a key protein, known as a portal, in Epstein-Barr virus infection.

The Epstein-Barr virus, which belongs to the herpesvirus family, is one of the most widespread human viruses and the main cause of infectious mononucleosis (also known as glandular fever). In addition, it causes several kinds of cancer, including Burkitt and Hodgkins lymphoma, stomach cancer and nasopharyngeal cancer, as well as several autoimmune diseases. There is currently no treatment for infections caused by this virus.

"Understanding the structure of the portal protein could prove useful for the design of inhibitors for the treatment of herpesvirus infections such as Epstein-Barr. Also, given that this protein is found only in herpesviruses, these inhibitors would be virus-specific and may be less toxic for humans," says Miquel Coll, head of the Structural Biology of Protein & Nucleic Acid Complexes and Molecular Machines Lab at IRB Barcelona and professor at CSIC.

All herpesviruses have a similar infection mechanism. Having entered the cell and reached the nucleus, the viruses release their DNA, which can remain latent for years until certain conditions trigger its replication. After this process, DNA is then introduced into new viral capsids, thereby forming new viruses that can attack other cells. The portal protein is the route through which DNA enters the viral capsid and through which it leaves to infect cells.

In a second study recently published in the same journal, the researchers have also characterised the structure of the portal protein in bacteriophage T7. This phage is a virus that infects only bacteria and, interestingly, its DNA packaging system resembles that used by herpesviruses.

"By solving the structure of the portal protein of bacteriophage T7, we have been able to infer how the portal from Epstein-Barr virus works," explain Cristina Machón and Montserrat Fàbrega, postdoctoral fellows at IRB Barcelona and IBMB-CSIC, and first authors --together with Ana Cuervo, from the National Centre for Biotechnology (CNB-CSIC)--of the studies published.

"In both viruses, the portal protein comprises 12 subunits, forming a large mushroom-shaped structure, with a central channel through which DNA passes. This channel has a valve that regulates the entry and exit of the virus' genetic material," explains Coll.

To study the structure of this protein, the researchers used both synchrotron X-ray diffraction and high-resolution electron cryomicroscopy. Both studies were performed in collaboration with the CNB-CSIC and the University of Oxford (UK).

The expression of many genes that have previously been associated with autism is abnormal also in violent psychopathy, a new study shows. The researchers used stem cell technology to analyse the expression of genes and proteins in the brain cells of psychopathic violent offenders. Published in Molecular Psychiatry, the findings may open up new avenues for the treatment of psychopathy. The study was carried out in collaboration between the University of Eastern Finland, the University of Helsinki and Karolinska Institutet in Sweden.

Psychopathy is an extreme form of antisocial behaviour, with about 1% prevalence in the general population, and 10-30% prevalence among incarcerated criminal offenders. Psychopathy is known to be strongly hereditary, but whether or not it is associated with abnormal expression of genes or proteins in neurons has remained unclear- up until now.

In the newly published study, the researchers used stem cell technology to analyse the expression of genes and proteins that have been associated with psychopathy. The study participants' skin cells were used to create pluripotent stem cells, which were then differentiated into cortical neurons and astrocytes. The study population comprised psychopathic violent offenders and healthy controls. Since psychopathy was accompanied by substance abuse, the study population also included non-psychopathic substance abusers. This made it possible for the researchers to determine which abnormalities were associated exclusively with psychopathy.

The study shows that psychopathy is associated with robust alterations in the expression of genes and immune-response-related molecular pathways. Several of these genes have also been linked to autism. In neurons, psychopathy was associated with marked upregulation of RPL10P9 and ZNF132, and downregulation of CDH5 and OPRD1. In astrocytes, RPL10P9 and MT-RNR2 were upregulated. The expression of these genes explained 30-92% of the variance of psychopathic symptoms. Psychopathy was also associated with altered expression of proteins related to glucose metabolism and the opioid system.

Several earlier studies have suggested that violent and psychotic behaviour are associated with alterations in glucose metabolism and opioidergic neurotransmission. The new findings support the idea of abnormal opioid system function being a factor underlying psychopathy. This suggests that using long-lasting injections of naltrexone or buprenorphine to balance the opioid system could be a feasible treatment for psychopathy.

Opioid dependence has become a national crisis with serious impact on economic and social welfare, and numerous casualties. A big goal of ongoing research in combating opioid use disorder is understanding drug withdrawal. The physical and emotional symptoms of withdrawal can be life threatening and make up a powerfully negative experience; the fear of these symptoms strongly motivates addiction.

Researchers in the lab of James Schwaber at the Daniel Baugh Institute for Functional Genomics and Computational Biology at Thomas Jefferson University are studying how inflammation contributes to drug withdrawal and dependence. Their study was published in Frontiers of Neuroscience on July 3.

Opioids can cause inflammation in the brain by inducing immune cells to release inflammatory molecules called cytokines. The main immune cells in the brain are microglia and astrocytes. Inflammatory responses induced by opioids have been observed in the central amygdala, a brain region that has been strongly implicated in opioid dependence because of its role in emotion and motivation. The central amygdala can also be affected by inflammation in other parts of the body, like the gut. In fact, the communication between the gut and the brain can shape a variety of motivated behaviors and emotional states, including those associated with drug dependence and withdrawal.

The researchers including first author Sean O'Sullivan in Dr. Schwaber's lab isolated single neurons, microglia, and astrocytes from the central amygdala and studied their genetic profiles in normal, opioid-dependent, and withdrawn rats. They were surprised to find that the profile of astrocytes changed the most, shifting genetic expression to a more activated state. This shift correlated strongly with opioid withdrawal. Furthermore, all three cell types showed a considerable increase in an inflammatory cytokine called TNF alpha in withdrawn animals.

In addition, the researchers also assayed different types of bacteria in the gut of rats and found that certain anti-inflammatory bacteria were suppressed in withdrawn animals, shifting the ratio of gut microbiota and causing a phenomenon called dysbiosis, which can cause inflammation in the digestive system. It is unclear how these changes influence opioid withdrawal, but the authors propose that the simultaneous inflammation in the gut and central amygdala may be linked to the negative emotional experience of withdrawal.

The findings underscore the highly complex relationship between the gut and the brain, and suggest that inflammation in the gut and brain may exacerbate symptoms associated with withdrawal. Targeting inflammation in these regions may alleviate the negative experience of drug withdrawal, and therefore prevent dependence.

How active matter, such as assemblages of bacterial or epithelial cells, manages to expand into narrow spaces largely depends on their growth dynamics, as Ludwig-Maximilians-Universitaet (LMU) in Munich physicists demonstrate in a newly published study.

Biological forms of active matter, such as bacterial biofilms or sheets of epithelial cells, are often found in confined microspaces. Working out how such systems colonize their environment and extend their range by invading new territories will enhance our understanding of many of the normal functions and disease states observed in higher organisms. In cooperation with Dr. Amin Doostmohammadi (University of Oxford), LMU physicists Felix Kempf and Professor Erwin Frey have now demonstrated with the aid of computer simulations that cell collectives exhibit a variety of motility patterns as they approach and pass through local constrictions. The authors of the new study go on to show that the pattern adopted depends on the level of active motility that develops at the leading edge of the assemblage. The findings appear in the journal Soft Matter.

Several previous publications had suggested that the collective motions of biological matter are influenced by the nature of the terrain in which such systems find themselves. In particular, in-vitro experiments carried out with epithelial and bacterial cells, and with mixtures consisting of isolated intracellular biofilaments and molecular motors, have revealed that spatial boundaries have a significant impact on motility. "So far, this type of research has concentrated primarily on the interactions between the shape of the obstacle employed and the motile activity of the particles concerned," says Kempf, the lead author of the new paper. However, in most of these systems, the number of particles does not remain constant. Under natural conditions, epithelial or bacterial cells divide at regular intervals and, when confined in capillary tubes, they form an advancing invasion front. Therefore, in order to understand how these patterns form and evolve, it is necessary to take the growth dynamics of these systems into account. Kempf and colleagues used computer simulations to explore the effects of this factor.

They observed three fundamentally distinct modes of invasion, which can be distinguished on the basis of the overall activity of the growing system and the behavior of the invasion front as it approaches the constriction. If the level of motile activity is low, the invasion front retains its smooth and sharply defined outline as it advances at a constant speed. At higher levels of activity, the leading edge takes on an irregular outline. Finally, once the activity level exceeds a certain threshold, small clusters of cells detach from the advancing front, which can then worm their way through the narrow gap. The simulations also enabled the researchers to characterize the processes that drive the transitions observed as the invasion front evolves, and to quantify their impact on the speed with which the cells advanced into the ever more confined space. "These findings make a significant contribution to our understanding of active matter, and have several implications that can be tested in future experiments," says Kempf.

Plant genetic varieties in Central Europe could collapse due to temperature extremes and drought brought on by climate change. According to a new paper published in Nature today, only a few individuals of a species have already adapted to extreme climate conditions. These findings suggest that the overall species genetic diversity could be greatly diminished. The publication was led by Moises Exposito-Alonso, who joins Carnegie next month from the Max Planck Institute for Developmental Biology and the University of California Berkeley.

An international team of researchers from the Max Planck Institute for Developmental Biology, University of Tübingen, Technical University of Madrid, and UC Berkeley studied populations of the thale cress plant, Arabidopsis thaliana, collected from over 500 geographic locations in Europe, commonly used for biological research. Growing these plants in Spain and Germany under dry conditions revealed how individual plants responded to heat and drought.

The investigators were particularly interested in how the unique blend of genetic mutations enables the different individuals of the same species to resist experimentally simulated climates. As some of these mutations may confer physiological advantages, the main goal of this study was to rank their fitness for the future survival of the species.

Mathematical models forecast shrink potential of European biodiversity

This data was then combined with models predicting how temperatures and precipitation are expected to shift geographically in the next few decades in order to understand how plant biodiversity will be affected by climate change caused by human activity.

"On the basis of our calculations up to the year 2050, we can determine a significant change in the mutations that will be needed for the thale cress to survive in Southern to Central Europe," first author Moi Exposito-Alonso said. "It is remarkable how much individuals from different parts of Europe differ in their ability to withstand future climate conditions," added Detlef Weigel, Director at the Max Planck Institute, where the work was coordinated.

Many of the continent's predominant plant populations won't be able to survive

As precipitation decreases and temperatures rise, especially in so-called transition zones between the Mediterranean and northern Europe, the team's predictions indicate that many of the continent's predominant plant populations will not possess the necessary genetic mutations to survive. These patterns might be shared across many plant species of Europe. While genetic information for most species is still lacking, the rapid advance in modern genetic methods allows researchers to obtain such information for more and more species. With such information in hand, it will be possible to improve predictions of where a species is most at risk of suffering from the consequences of climate change.

Researchers at the German Center for Neurodegenerative Diseases (DZNE) and the Institute for Stroke and Dementia Research (ISD) at the University Hospital of the Ludwig-Maximilians-Universität (LMU) in Munich have found that a protein called TREM2 could positively influence the course of Alzheimer's disease. When TREM2 is present in the cerebrospinal fluid at higher concentrations, patients at any stage of the disease have a better prognosis. This observation provides a starting point for the development of new therapeutic strategies. The study was led by Prof. Christian Haass (DZNE) and Prof. Michael Ewers (ISD, LMU) and is published in the journal "Science Translational Medicine".

In the brain, TREM2 is exclusively produced by microglia, the immune cells of the brain. These cells patrol the brain and clear it from cellular waste products and debris to keep it healthy. In previous studies on mice, Haass and his colleagues demonstrated that TREM2 activates microglia to enclose and selectively destroy toxic protein aggregates typical for Alzheimer's disease. "These observations indicate that TREM2 can protect the brain from the degenerative effects of the disease - at least in animal models," said Haass.

But what about patients with Alzheimer's disease? Does TREM2 protect the human brain as well? To answer these questions, Haass, Ewers, and their colleagues correlated the concentration of TREM2 in the cerebrospinal fluid of Alzheimer patients with their respective disease progression over several years. To this end, they used data of 385 subjects from the Alzheimer's Disease Neuroimaging Initiative (ADNI), a large clinical dataset containing records and samples from patients and healthy seniors taken at regular checkups over many years. The study thus allows to establish associations between certain biochemical changes and disease progression.

Indeed, Haass and Ewers found that high levels of TREM2 improved the prognosis of subjects at all stages of the disease. Their memory remained more stable and the degradation of the hippocampus, a brain region responsible for learning and recollection, was less pronounced. "Our findings are clinically relevant because we found that higher levels of TREM2 were associated also with a reduced rate of the development of full blown dementia over a time period up to 11 years", explained Ewers. "Microglia activation is a double-edged sword, entailing both protective effects and neurotoxic inflammation. TREM2 signaling may play a key role in the regulation of the brain's protective immune response".

The concentration of TREM2 in the cerebrospinal fluid usually increases at early stages of the disease, when the first symptoms appear. "TREM2 production is a response to brain damage that has already occurred," said Haass. "It stimulates the microglia to protect the brain. However, this protection does not seem to be sufficient in patients with Alzheimer's disease". This is where Haass and his colleagues see an option for new therapeutic strategies. "We are currently developing a therapeutic antibody that stimulates the TREM2 function and thus improves its protective function," said Haass.

Jugglers are skilled at keeping several objects in motion at the same time using a combination of tossing motions and eye movement. As objects are added to a juggler's routine, their gaze moves as the juggler tries to focus on all of the objects and avoid dropping one or two.

People who often multitask at work might feel like a juggler at times. In a work setting -- such as an oil refinery -- where a person needs to keep tabs on multiple gauges and systems to keep systems working properly, a change in a person's eye movement could cause a mistake, and possibly cost a life. With the ever-increasing connectivity of today's society, the demand for a real-time way to evaluate how well an employee understands their current situation -- often called situational awareness -- has become a paramount safety issue for employers, especially those in industrial and manufacturing industries. Researchers at the University of Missouri believe studying a person's eyes could help with this.

"An employee with poor situational awareness will miss some critical things that happen in their work area," said Jung Hyup Kim, an assistant professor of industrial and manufacturing systems engineering in the MU College of Engineering. "If I am tired, burdened by other things, or my workload is beyond what I can handle, my awareness will go down, and there is no way to measure that in real-time."

Researchers said the current method to evaluate a person's situational awareness involves only asking questions; this is not enough. In the study, they created a simulated multitasking environment of an oil refinery control room. Participants had to monitor multiple gauges and other controls on a computer screen while simultaneously responding to unexpected events, such as alarms.

"We found a relationship between situational awareness and self-terminating visual search -- or once you find a solution, you end the search," Kim said. "So, if a person has a good understanding about the situation, then they can directly target the cause of the problem in a short amount of time. But if they do not have good awareness, then they may spend a long time searching randomly for the cause."

Kim and Xiaonan Yang, a graduate student at MU, hope to test their model in a real-life environment to see if any changes are observed between that situation and their simulation.

A medication that boosts the body's own cannabis-like substances, endocannabinoids, shows promise to help the brain un-learn fear memories when these are no longer meaningful. These results, obtained in an early-stage, experimental study on healthy volunteers at Linköping University in Sweden, give hope that a new treatment can be developed for post-traumatic stress disorder, PTSD. The study has been published in the scientific journal Biological Psychiatry.

"We have used a medication that blocks the way the body breaks down its own cannabis-like substances, or 'endocannabinoids'. Our study shows that this class of medications, called FAAH inhibitors, may offer a new way to treat PTSD and perhaps also other stress-related psychiatric conditions. The next important step will be to see if this type of medication works in patients, particularly those with PTSD", says Leah Mayo, senior post-doctoral fellow and lead investigator on the study, which was carried out in the laboratory of Professor Markus Heilig at the Center for Social and Affective Neuroscience, CSAN, Linköping University.

Post-traumatic stress disorder, PTSD, arises in some - but not all - people who have experienced life-threatening events. A person affected by PTSD avoids reminders of the trauma, even when the danger is long gone. Over time, these patients become tense, withdrawn, and experience sleep difficulties. This condition is particularly common among women, where it is often the result of physical or sexual abuse. It is highly debilitating, and current treatment options are limited.

PTSD is currently best treated using prolonged exposure therapy, PE. In this treatment, patients are repeatedly exposed to their traumatic memory with the help of a therapist. This ultimately allows patients to acquire new learning: that these memories no longer signal imminent danger. Although clinically useful, effects of PE are limited. Many patients do not benefit, and among those who do, fears frequently return over time. The scientists who carried out the current study examined whether fear extinction learning, the principle behind PE therapy, can be boosted by a medication.

The researchers tested a pharmaceutical that affects the endocannabinoid system, which uses the body's own cannabis-like substances to regulate fear and stress-related behaviors. The experimental medication results in increased levels of anandamide, a key endocannabinoid, in regions of the brain that control fear and anxiety. The medication accomplishes this by blocking an enzyme, FAAH (fatty acid amide hydrolase), that normally breaks down anandamide. The FAAH inhibitor tested by the researchers was originally developed for use as a pain killer, but was not effective enough when tested clinically.

This early-stage experimental study was randomised, placebo-controlled and double-blind, which means that neither the participants nor the scientists knew who was receiving the active drug (16 people) and who was receiving placebo (29 people). Participants were healthy volunteers. After taking the drug for 10 days, they underwent several psychological and physiological tests. In one of these, participants learned to associate a highly unpleasant sound, that of fingernails scraping across a blackboard, with a specific visual cue - an image of a red or blue lamp. Once they had learned to respond with fear to the previously innocuous image of the lamp, they were repeatedly re-exposed to it, but now in the absence of the unpleasant sound. This allowed them to unlearn the fear memory. The following day, the scientists measured how well participants remembered this new learning: that the lamp was no longer a threat signal. This process of un-learning fear is the same principle on which PE therapy for PTSD is based.

"We saw that participants who had received the FAAH inhibitor remembered the fear extinction memory much better. This is very exciting", say Leah Mayo.

"Numerous promising treatments coming out of basic research on psychiatric disorders have failed when tested in humans. This has created quite a disappointment in the field. This is the first mechanism in a long time where promising results from animal experiments seem to hold up when put to test in people. The next step, of course, is to see whether the treatment works in people with PTSD", adds professor Markus Heilig.

East Hanover, NJ. August 29, 2019. A recent study by Kessler Foundation researchers linked the deficits in social cognition in multiple sclerosis with symptoms in other domains. The article, "Relationship between social cognition and fatigue, depressive symptoms, and anxiety in multiple sclerosis," was epublished on June 1, 2019 by the Journal of Neuropsychology.

The authors are Helen Genova, PhD, Katie Lancaster, PhD, Jean Lengenfelder, PhD, Christopher Bober, John DeLuca, PhD, and Nancy Chiaravalloti, PhD, of Kessler Foundation. Link to abstract: https://doi.org/10.1111/jnp.12185

Researchers tested 28 individuals with multiple sclerosis for impairments of social cognition using tests of facial affect recognition and Theory of Mind, and looked for associations between deficits of social cognition with common conditions in this population by screening for fatigue, depression and anxiety. They also measured non-social cognitive ability, i.e., attention and processing speed, using the Symbol Digit Modality Test.

Preliminary findings showed consistent associations between poorer performance on measures of social cognition and increased symptoms of depression, anxiety, and fatigue, most notably psychosocial fatigue. Cognitive ability was not a factor in these associations.

The study raises issues of causality and reciprocal effects, according to Dr. Genova, the Foundation's assistant director of the Center for Neuropsychology and Neuroscience Research. "The nature of the relationships among these variables remains unclear," said Dr. Genova. "We cannot say whether deficits of social cognition worsen mood condition and fatigue, or vice versa," she explained. "The relationships may be reciprocal in nature," she observed. "Poor social cognition may worsen fatigue, depression and anxiety, leading to greater social isolation. That, in turn, may worsen social cognitive function."

The researchers emphasized the preliminary nature of their findings and recommended further research into the relationships among these factors in individuals with MS, as well in other populations with non-neurologic conditions, and healthy controls. "All of these conditions adversely affect quality of life," concluded Dr. Genova. "To alleviate their impact, we need to understand the interplay of social cognition, mood, and fatigue. Our study is an initial step toward understanding these dynamics in the population with MS.'

Engineers at the University of Birmingham have successfully designed a robotic system that can perform a key task in disassembling component parts.

The research is an important advance for manufacturers looking for more efficient ways to build products from a combination of reused, repaired and new parts.

Known as remanufacturing, this process is becoming increasingly commonplace in manufacturing and is attractive because it can use as little as 10 per cent of the energy and raw materials required to build the product from scratch. It can also reduce CO2 emissions by more than 80 per cent.

A key part of the process is the ability to disassemble the 'core', the returned product. It's a challenge because of the huge variety within these products, with lots of unknowns in the size, shape and condition of components.

The new study, published in Royal Society Open Science, demonstrates a process for removing pins from holes - components like these are extremely common in a wide variety of machines, such as internal combustion engines. The research is the first to investigate this operation in depth and identify the key parameters required to automate the process.

Yongquan Zhang, of the Autonomous Remanufacturing Laboratory at the University of Birmingham is lead author on the paper. "Processes currently used for automating disassembly are fairly ad hoc," he explained. "We need to be able to design robust systems that can handle the uncertainties that are inherent in disassembly processes - and to do that, we need a better fundamental understanding of disassembly."

"The results of this study demonstrate how that fundamental understanding can be used to design robotic systems for reliably performing one common disassembly operation."