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Amsterdam, NL, January 30, 2020 - A new study shows for the first time that low and high exercise intensities differentially influence brain function. Using resting state functional magnetic resonance imaging (Rs-fMRI), a noninvasive technique that allows for studies on brain connectivity, researchers discovered that low-intensity exercise triggers brain networks involved in cognition control and attention processing, while high-intensity exercise primarily activates networks involved in affective/emotion processing. The results appear in a special issue of Brain Plasticity devoted to Exercise and Cognition.

"We believe that functional neuroimaging will have a major impact for unraveling body-brain interactions," said lead investigators Angelika Schmitt, MSc, and Henning Boecker, MD, Functional Neuroimaging Group, Department of Radiology, University Hospital Bonn, Bonn, Germany. "These novel methods allow us to 'look' directly into the brains of a group of athletes, and, maybe even more importantly, understand the dynamic changes in brain structure and function associated with the transition from a sedentary to a healthy lifestyle.

Twenty-five male athletes underwent individual assessments using an incremental treadmill test. On separate days they performed low- and high-intensity exercise bouts for 30 minutes. Before and after exercising, Rs-fMRI was used to examine functional connectivity of different brain regions that are linked to specific behavioral processes. Participants also completed a questionnaire to measure positive and negative mood before and after the exercise.

The behavioral data showed a significant increase in positive mood after both exercise intensities and no significant change in negative mood. The results of the Rs-fMRI tests showed that low-intensity exercise led to increased functional connectivity in networks associated with cognitive processing and attention. High-intensity exercise, on the other hand, led to increased functional connectivity in networks related to affective, emotional processes. High-intensity exercise also led to a decreased functional connectivity in networks associated with motor function.

The investigators note that this is the first study to report distinct effects of exercise intensity on specific functional networks within the brain at rest. Future research in this area will help provide neurobiological evidence about what type of exercise intensity is best suited for certain neurological or behavioral modulations and may pave the way for supportive clinical applications in patients or for enhancing brain functional plasticity.

The mechanism behind how HIV can develop resistance to a widely-prescribed group of drugs has been uncovered by new research from the Crick and Dana-Farber Cancer Institute, with the findings opening the door to the development of more effective treatments.

Today, a number of drugs are available which help to control HIV infection, including a group called integrase strand transfer inhibitors. There are four drugs within this family of medication: raltegravir, elvitegravir, dolutegravir and bictegravir. They all work by binding with one of HIV's key enzymes, called integrase, to stop it from inserting the virus' genetic information into DNA of human cells. While initially highly effective, over time HIV can develop resistance to these drugs.

The study, published on-line in Science 30 January 2020, discovered the mechanism HIV uses to develop resistance to this group of drugs. Although the drugs are normally very effective at binding and blocking integrase, over time, the virus can weaken this bond and thus enable its key enzyme to work again.

The researchers at the Francis Crick Institute in London uncovered this by exploring the structure of integrase from a virus that is highly similar to the ancestor of HIV, using cryo-electron microscopy. This technique uses a powerful microscope which fires electrons at a frozen sample of the drug-enzyme complex. By recording how the electrons interact with the samples, the researchers created detailed images, at a nearly atom-by-atom level.

"The unusual property of these drugs is that they interact with metal ions, which normally allows them to make very strong bonds to the viral enzyme's active site. We found that HIV can subtly alter the chemical environment of the metals, and as if using a remote control, reduce the strength of drug binding. This is an unexpected chink in the armour of strand transfer inhibitors," says Peter Cherepanov, co-lead author and group leader in the Chromatin and Mobile DNA Laboratory at the Crick and Professor of Molecular Virology at Imperial College London.

"The good news is that we have finally visualised the precise structure of the viral enzyme's active site, right where the drugs bind. These blueprints will inform the design of more effective integrase inhibitors that could improve the lives of the many millions of people living with HIV," says Alan Engelman, co-lead author from the Department of Cancer Immunology and Virology at the Dana-Farber Cancer Institute and Professor of Medicine at Harvard Medical School in Boston, USA.

"The weakening of drug binding occurs due to a combined effect of mutations and a loss of key water molecules in the active site. Understanding this mechanism will help improve this class of drugs in the future," comments Edina Rosta, co-author from the Crick and Reader of Computational Chemistry at Kings College London, whose team conducted complex computations on the integrase structures.

Daniel Kuritzkes, Chief of Infectious Diseases at Brigham and Women's Hospital and Professor of Medicine at Harvard Medical School, who was not directly involved in the study, adds: "The work by the Cherepanov and Engelman laboratories importantly informs the mechanism of resistance to a class of drugs that are now recommended first-line treatment for HIV worldwide."

"This research is an outstanding example of how we can use cryo-electron microscopy to reveal the intricate relationships between drugs and their targets, providing results that could lead to clinical benefit," explains Peter Rosenthal, the head of the Structural Biology of Cells and Viruses laboratory at the Francis Crick Institute.

Biodiversity loss is the biggest environmental problem we face today, according to a UN report that came out last year. One of the main reasons is that large forest areas are disappearing due to human impact.

A lack of connected forests can prevent trees from multiplying efficiently. The more fragmented the forest becomes, the greater the problem for the trees.

"Forest fragmentation has a negative effect on seed dispersal by means of animals," says Emma-Liina Marjakangas at the Centre for Biodiversity Dynamics (CBD) at the Norwegian University of Science and Technology (NTNU).

While working on her doctorate, Marjakangas studied 1424 tree species and 407 animal species from 912 sites in forested areas along the Atlantic coast of South America.
The data includes both known networks and probable networks, based in part on what species can be found in the same place.

Marjakangas' goal was to look at which species are found along the coast of South America, and to find relationships between these species.

Climate is the main reason for the variation between the different areas, with 26 per cent of variations attributable to climate causes. The use of areas around the forest areas accounts for almost as much variation.

Forest fragmentation can explain about 11 per cent of the total variation. But this percentage increases as the forest becomes more fragmented.

"When connected forest areas shrink, this has a greater effect on seed dispersal than the edge effects of various other activities around the forest," says Marjakangas.

Many tree species live in interaction with animals that spread their seeds. Birds and large mammals in particular often contribute significantly to seed dispersal. In return, the trees contribute food, housing and hiding places for the animals.

Large forests often have room for more species than small forests do. Some species that would normally scatter seeds are not able to survive in small patches of forest, or fragmentation hinders their ability to move from one area to another.

If the activity of the animals becomes restricted, so does the dispersal of seeds. And should the animals disappear completely, this quickly becomes a major problem for the plants.

"This imbalance can lead to a cascade effect," Marjakangas says.

When one species disappears, other species may also develop problems, precisely because species are interdependent.

Species disappear or decrease in number for many reasons. They may disappear from a single area or the species may die out. But the underlying cause is usually human activity.
Although it may occur in exceptional circumstances, rarely do we eradicate species on purpose. As a rule, species disappear because we destroy their habitats.

Most often this happens because the areas are needed for other activities like agriculture, or because we need resources such as wood or minerals. Sometimes species disappear because people eat the animals and plants.

But mechanisms exist to make the situation better again. Other animal species may mitigate some of the negative effects by taking over the seed dispersal.

For example, when one animal species disappears, it may allow one or more other species to help themselves to a tree's fruits and seeds.

"Reintroducing some bird species that are generalists to an area, along with some rarer specialists, is the most effective method of restoring seed dispersal," says Marjakangas.

Naturally, this applies exclusively to species that previously inhabited the area, since no alien species should be introduced. Species in the wrong place are themselves an environmental problem, but reintroducing species that are at home in an area can be very beneficial.

Some species seem to contribute much more to seed distribution than others. Of the more than 400 animal species studied, Marjakangas found that only 21 of them accounted for more than 40 per cent of the seed dispersal.

These are keystone species that warrant extra care if the goal is to preserve as many species as possible. Often these animals are generalists that eat a lot of fruit. In many instances, they are species that are not very discriminating and that can cope under varying conditions.

he trees that struggle the most are often rare specialists that are pollinated by animals and that produce few and large seeds. Several tree species may depend on specialized animal species to spread their seeds.

"Finding out how species interact with each other can give us valuable insights as we try to understand how humans affect biological diversity and ecosystems," says Marjakangas.

New research from a team of Florida State University scientists shows that rapid weather variability as a result of climate change could increase the risk of a flu epidemic in some highly populated regions in the late 21st century.
The research was published today in the journal Environmental Research Letters.

Zhaohua Wu, an associate professor in the Department of Earth, Ocean and Atmospheric Science and scientist with the Center for Ocean-Atmospheric Prediction Studies, and an international team looked at historical data to see how significant weather swings in the autumn months affect flu season in highly populated regions of northern-mid latitudes of the world. They specifically looked at the United States, mainland China, Italy and France.

Using surface air temperatures from Jan. 1, 1997 to Feb. 28, 2018, researchers analyzed weather patterns and average temperatures over 7,729 days. Simultaneously, they conducted statistical analysis on influenza data sets from the four countries over the same time period.

Previous research suggested low temperatures and humidity in the winter create a favorable environment for transmitting the flu virus. However, the 2017-2018 flu season was one of warmest on record and yet also one of the deadliest. The Centers for Disease Control reported 186 children's deaths during the 2017-2018 season. The previous high was 171 during the 2012-2013 season.

During the 2017-2018 flu season, scientists found that the extreme fluctuations in weather during the autumn months essentially kick-started the flu, building a patient population early in the season that snowballed in densely populated areas given the contagious nature of the virus.

"The historical flu data from different parts of the world showed that the spread of flu epidemic has been more closely tied to rapid weather variability, implying that the lapsed human immune system in winter caused by rapidly changing weather makes a person more susceptible to flu virus," Wu said.

The issue going forward, scientists noted, is that rapid weather variability is common in warming climates. Having a better understanding of those weather patterns may be key to determining the severity of any future flu season threat. If these climate models are correct, there is an anticipation of increased flu risk in highly populated areas. Under this scenario, Europe could see a 50 percent increase in deaths tied to flu.

"The autumn rapid weather variability and its characteristic change in a warming climate may serve not only as a skillful predictor for spread of flu in the following season but also a good estimator of future flu risk," Wu said. "Including this factor in flu spread models may lead to significantly improved predictions of flu epidemic."

Wu said he and his team are continuing to pursue this line of research with the ultimate goal of creating a model that incorporates both traditional flu indicators on the health and medicine side with environmental factors such as weather patterns.

A study inspired by street performers making gigantic soap bubbles led to a discovery in fluid mechanics: Mixing different molecular sizes of polymers within a solution increases the ability of a thin film to stretch without breaking.

The journal Physical Review Fluids published the results of the study by physicists at Emory University. The findings could potentially lead to improving processes such as the flow of oils through industrial pipes and the clearance of polluting foams in streams and rivers.

The results also hold implications for backyard bubble-blowing enthusiasts.

"This study definitely puts the fun into fundamental science," says Justin Burton, associate professor of physics at Emory University and senior author of the paper.

Fluid dynamics is one of the focuses of Burton's lab. "The processes of fluid dynamics are visually beautiful and they are everywhere on our planet, from the formation and breakup of droplets and bubbles to the aerodynamics of airplanes and the deep-sea overturning of the world's oceans," he says.

While Burton was in Barcelona for a conference a few years ago, he happened to see street performers making huge bubbles using a soap solution and thick cotton string. "These bubbles were about the diameter of a hula hoop and as much as a car-length long," he recalls. "They were also beautiful, with color changes from red to green to bluish tones on their surface."

This rainbow effect shows that a film's thickness is comparable to the wavelength of light, or just a few microns, he explains.

Viewing the performance sparked a physics question in Burton's mind: How could such a microscopically thin film maintain its integrity over such a large distance without breaking up? He began investigating, both in his backyard and in his lab.

As Burton researched bubble recipes he came across the Soap Bubble Wiki, an online, open-source project. The wiki states that it aims to help "bubblers" create "the perfect bubble" by separating fact from folklore regarding soap bubble-making recipes and ingredients.

In addition to water and dishwashing liquid, the Soap Bubble Wiki recipes usually included a polymer -- a substance made up of long chains of repeating molecules. The most common polymers in the recipes were natural guar, a powder used as an additive in some foods, or industrial polyethylene glycol (PEO), a lubricant used in some medicines. Guided by the wiki recommendations, Burton conducted laboratory experiments along with two student co-authors who have since graduated: Stephen Frazier, who received a master's in physics in May and is first author, and undergraduate Xinyi Jiang.

"We basically started making bubbles and popping them, and recorded the speed and dynamics of that process," Burton says. "Focusing on a fluid at its most violent moments can tell you a lot about its underlying physics."

Soap films absorb infrared light, so the researchers shone it through the bubbles to measure the thickness of the films. They also measured the molecular weights of the different polymers they used in the bubble recipes. And they let gravity pull droplets of the various soap films off a nozzle, in order to measure how long the resulting thread of liquid could stretch between the nozzle and the droplet before breaking.

The results revealed that polymers were the key ingredient to making colossal bubbles. The long, fibrous strands of polymers enable the bubbles to flow smoothly and stretch further without popping.

"The polymer strands become entangled, something like a hairball, forming longer strands that don't want to break apart," Burton explains. "In the right combination, a polymer allows a soap film to reach a 'sweet spot' that's viscous but also stretchy -- just not so stretchy that it rips apart."

The work confirms what many expert "bubblers" already had figured out -- a good giant soap bubble recipe should include a polymer.

"We did the physics to explain why and how polymers can make a fluid film stretch as far as 100 square meters without breaking," Burton says.

The physicists also found that varying the molecular sizes of the polymers helps strengthen soap film. That discovery happened by accident.

The researchers worked on the project for more than a year and stored some containers of PEO they had purchased. They realized that PEO from containers that had aged about six months produced stronger soap bubble films compared to PEO from containers used when it was first purchased. Upon investigation, they realized that the polymers in the aged PEO had degraded over time, varying the length of the molecular strands.

"Polymers of different sizes become even more entangled than single-sized polymers, strengthening the elasticity of the film," Burton says. "That's a fundamental physics discovery."

Understanding how fluids and thin films response to stress, Burton says, could lead to an array of applications, such as improving the flow of industrial materials through pipes, or the clean-up of toxic foams.

"As with all fundamental research, you have to follow your instincts and heart," Burton says of his soap bubble odyssey. "Sometimes your bubble gets burst, but in this case, we discovered something interesting."

Vascular dementia is caused by a defect on blood flow arrival to the brain, which consequently generates neuronal damage. Since now, its diagnosis has been quite complicated because only neuroimaging methods, such as a scanner, and the appearance of symptoms were available. The lack of more precise and specific methods creates confusion with other neurodegenerative diseases, like Alzheimer's. A study, developed between Medical Center of Göttingen University (UMG) and Bellvitge Biomedical Research Institute (IDIBELL), has described a new biomarker for this disease, lipocalin 2 protein. This protein is present in the cerebrospinal fluid that bathes the brain.

Patient samples from four independent groups have unequivocally demonstrated that the cerebrospinal fluid of people affected by vascular dementia has higher levels of lipocalin 2. Patients from four European centers have participated in this multicenter study: Sahlgrenska University Hospital (Sweden ), the University of Coimbra (Portugal), the University Paris Diderot (France) and the University Medical Center of Göttingen (Germany); and has been led by Dr. Franc Llorens, researcher from IDIBELL and the Center for Biomedical Research in Neurodegenerative Diseases Network (CIBERNED), and Dr. Inga Zerr (UMG). The result reproducibility in four sample groups converts lipocalin 2 to a firm candidate for vascular dementias diagnosis.

In contrast to diagnosis methods available until now, lipocalin 2 could discriminate vascular dementia from Alzheimer's, since the second does not show lipocalin 2 increase. The study shows that only patients with vascular dementia, but not those with cerebral vascular damage without dementia, exhibit this increase. The high diagnostic specificity of this protein further highlights its potential as a biomarker.

To determine the role of lipocalin 2 in the brain of patients with vascular dementia, brain tissue samples from the biobank HUB-ICO-IDIBELL (Bellvitge University Hospital, Catalan Institute of Oncology and IDIBELL) were studied. These studies were performed with the collaboration of Dr. Isidre Ferrer, head of the Neuropathology group of IDIBELL and CIBERNED, and showed that glial cells are expressing lipocalin 2, and its expression pattern is different in vascular dementia or Alzheimer's.

Going on a journey alone. Sitting in a plane for hours at a height of twelve kilometres above the Atlantic Ocean. With turbulence and all the inconveniences that are part of a long-haul flight. This is the situation Michaela B. is afraid of. If only a friend would be with her on the trip! Then she would certainly feel better.

But Michaela B. shouldn't be afraid of the situation in the plane. She could easily do without her friend as an escort. Because it would help her to have someone sitting next to her. And this person wouldn't even have to talk to her or turn to her in any other way. The mere presence would be enough to reduce her fear.

This is the result of a study conducted by a group led by Professor Grit Hein from Julius-Maximilians-Universität (JMU) Würzburg in Bavaria, Germany. The results are published in the Journal Proceedings of the Royal Society B: Biological Science.

Physiological tension measured via skin resistance

"Our results show that fear and the resulting physiological tension can be reduced by the mere presence of another person, even if this person is unknown and does not provide active support," explains Grit Hein. She holds a professorship for Translational Social Neuroscience at JMU and investigates how social interactions effect decisions, fear and pain.

The reduced anxiety reaction occurred regardless of whether the unknown person belonged to the same or a different ethnic group. "Interestingly, the anxiety-reducing effect was stronger when the subjects perceived the other person as less similar - probably because they then assumed that the other person, unlike themselves, was not afraid," says the JMU professor.

In the study, the test subjects were listening to either neutral or fear-inducing sounds via headphones - the splashing of water or human cries. Their physical reactions to these sounds were measured via skin resistance - when anxious, the electrical conductivity of the skin changes. The unknown person that was present in the room during the tests was not allowed to say anything and remained physically aloof from the test person. This setting prevented social interaction between the two.

Follow-up studies with men and women

So far, only women have been tested in the presence of women. In follow-up studies, the Würzburg research team now also wants to measure the effects when men with men or men with women are exposed to the uncanny situation in the laboratory.

Differences may become apparent in the process. "There are hints from stress research that the gender of the present person could play a role," says the JMU professor. The findings from this research could possibly be used for the treatment of anxiety disorders.

BOZEMAN - A Montana State University biotechnology researcher was part of an international team that recently discovered an internal mechanism which may protect human cells from oxidative damage. The discovery could lead to strides in understanding many problems associated with aging and some chronic illnesses.

Ed Schmidt, a professor in the Department of Microbiology and Immunology in MSU's colleges of Agriculture and Letters and Science, worked with research teams from Hungary, Sweden and Japan on the project, published earlier this month in the journal Science Advances. The mechanism, Schmidt said, is a previously unknown tool that cells can use to protect their proteins from being irreversibly damaged by cellular processes called redox reactions, which are common and necessary but which, in excess, can cause extensive damage.

"Redox reactions are any reaction where you're moving electrons from one molecule to another," said Schmidt. "Almost everything that goes on in our cells, chemically and energetically, involves the transfer of electrons. But it's critical that these be kept in balance. Our cells invest an enormous amount of effort and machinery into maintaining the right redox balance."

The discovery made by Schmidt's team focuses on sulfur atoms as part of protein molecules inside cells. When cells are exposed to external stressors -- from things humans eat, chemicals the cells are exposed to or any number of other sources -- that oxidative stress can damage parts of the proteins. It was previously thought that cells had no way to reverse that oxidation, instead relying upon making new proteins to replace the damaged ones. However, said Schmidt, it appears that our cells are sometimes able to protect themselves by adding an extra sulfur atom onto existing sulfurs in certain protein molecules. Then when the cell is exposed to stress, only that extra sulfur is damaged and can then be cleaved off by the cell, leaving behind a whole and undamaged protein.

"We suspect that once exposure begins, it's too late for the cell to do this," said Schmidt. "We think that cells have a subset of proteins already in this state with extra sulfur atoms, which makes them probably inactive, but kind of on reserve. These proteins on reserve get damaged but can be repaired and allow the cell to begin recovery to make new proteins."

Extreme oxidative damage can cause DNA mutations, said Schmidt. When those mutations accumulate, there is some evidence that points to an increased risk for cancers, inflammatory diseases and illnesses such as Parkinson's disease, Alzheimer's disease and diabetes. This new discovery may help lead to future strides in medicine by helping to predict or even mitigate those health problems, if human cells can utilize this mechanism more efficiently, Schmidt said, adding that there are even potential applications for medical procedures such as organ transplants.

"During transplants, the organ goes through a period where it doesn't have any oxygen or blood flow, but once it is transplanted, it gets a rush of oxygenated blood that causes a burst of oxidative stress," said Schmidt. "Now that we're starting to understand these mechanisms, maybe we can do something more sophisticated to allow the cells in a transplanted organ to prepare and protect themselves."

Schmidt's research team, which is also a part of the Montana Agricultural Experiment Station, worked with four other teams that brought expertise in biological sulfur chemistry, redox biology, cell biology and cell signaling from around the world. Next steps in this research, Schmidt said, include investigating exactly how cells manage to add those extra sulfur molecules and how that process is regulated.

"It's possible that by understanding this system more, we could make progress," said Schmidt. "Understanding some of these mechanisms allows us to come up with new ideas."

DURHAM, N.C. -- A modified form of poliovirus, pioneered at Duke Cancer Institute as a therapy for glioblastoma brain tumors, appears in laboratory studies to also have applicability for pediatric brain tumors when used as part of a cancer vaccine.

In preclinical studies using mice and human cancer cells, an injection of the modified poliovirus vector instigated an immune response that homed in on mutated cancer cells that predominate in diffuse midline glioma (DMG) tumors. The cancer strikes children and is universally deadly.

Reporting this week in the journal Nature Communications, the researchers described how a polio-rhinovirus chimera (PVSRIPO), modified to express a mutate tumor antigen found in DMG, is able to infect and induce the activity of dendritic cells.

Dendritic cells prime tumor antigen-specific T-cells to migrate to the tumor site, attack tumor cells, delay tumor growth and enhance survival in animal tumor models. But their activity can be difficult to control.

"Polioviruses have several advantages for generating antigen-specific CD8 T-cells as a potential cancer vaccine vector," said senior author Matthias Gromeier, M.D., who developed the poliovirus-based therapy as a member of Duke's Preston Robert Tisch Brain Tumor Center.

"They have naturally evolved to have a relationship with the human immune system, activating dendritic cells, inducing CD8 T-cell immunity and eliciting inflammation. As a result, they lack interference with innate or adaptive immunity."

Gromeier said the vaccine approach continues to be tested with the goal of initiating a phase 1 clinical trial.

"We are hopeful that this approach could be tested as a potential therapy for DMG tumors, which exact a terrible burden on children and their families," Gromeier said.

In addition to Gromeier, study authors Mubeen M. Mosaheb, Elena Y. Dobrikova, Michael C. Brown, Yuanfan Yang, Jana Cable, Hideho Okada, Smita K. Nair, Darell D. Bigner and David M. Ashley.

The work received support from the Public Health Service (R01 NS108773, F32 CA224593), a Defeat DIPG Research Grant and the V Foundation.

Authors Gromeier, Dobrikova, Brown, Nair, Bigner and Ashley are co-inventors of intellectual property for the PVSRIPO therapy that was licensed to Istari Oncology.

In response to the youth vaping crisis, experts at The University of Texas Health Science Center at Houston (UTHealth) developed CATCH My Breath, a program to prevent electronic cigarette use among fifth - 12th grade students. Research published in Public Health Reports reveals the program significantly reduces the likelihood of e-cigarette use among students who complete the curriculum.

Since a 2018 declaration citing the vaping crisis a public health epidemic, the number of middle school students who use e-cigarettes has more than doubled. According to 2019 data from the Centers for Disease Control and Prevention, about 1 in 10 middle school students reported using e-cigarettes in the last 30 days. This marks a troubling trend with dangerous consequences, as 60 deaths in the U.S. have been linked to lung injury associated with vaping product use.

The research collected from the program's pilot study found that students in schools that received the CATCH My Breath program were half as likely to experiment with e-cigarettes compared with those in schools that did not receive the program.

According to the research team, CATCH My Breath is the only evidence-based e-cigarette prevention program that has demonstrated effectiveness for middle school-aged youth. While the program focuses primarily on vaping, it also educates students to resist other forms of tobacco. Research has shown that around 40% of youth tobacco users reported using more than one tobacco product.

"This program was created to address the youth vaping crisis and to reverse the growing trend of e-cigarette use among adolescents," said Steven H. Kelder, PhD, MPH, Beth Toby Grossman Distinguished Professor in Spirituality and Healing at UTHealth School of Public Health in Austin and the study's lead author. "Most children are using JUUL devices, which has the nicotine equivalent of 20 cigarettes for one pod. Many do not know there is nicotine in these devices, much less such a high level. This is why it is urgent to educate schools, families, and kids."

Experts at UTHealth School of Public Health who developed the program received input from school administrators, health education coordinators, and tobacco prevention educators, as well as teachers, students, and parents.

The curriculum emphasizes active, student-centered learning through group discussions, goal setting, refusal skills training, capacity building with analyzing tobacco company advertising, and creating counter-advertising and non-smoking policies. The program is disseminated by the nonprofit CATCH Global Foundation and has been implemented in over 2,000 schools across all 50 states.

"We designed CATCH My Breath to be easy for teachers to implement in their classrooms. All program materials are available online and are age-appropriate for middle and high school students," said Kelder, who developed the program as part of his ongoing research at the Michael & Susan Dell Center for Healthy Living at UTHealth School of Public Health in Austin.

The research team was recently awarded a $3.1 million grant from the National Institutes of Health to conduct a long-term assessment of the program, a first-of-its-kind study on a nationwide nicotine vaping prevention program. Through this large-scale study, the research team will add a parent component to the CATCH My Breath program to further enhance support for e-cigarette prevention.

"CATCH My Breath offers theory- and practice-informed strategies for parents to understand the vaping epidemic and how to talk to their children as well," said Andrew Springer, DrPH, an associate professor at UTHealth School of Public Health in Austin and co-investigator of the CATCH My Breath study.

The Atlantic Ocean acts as a key pacemaker for Middle East surface air temperature (ME-SAT) multidecadal variability in summer. This is the important result of a study published on NPJ Climate and Atmospheric Science unveiling and demonstrating the existence of a North Atlantic-Middle East teleconnection, that is a remote influence of the Atlantic multidecadal variability on the decadal variability of Middle East summer temperatures. This Atlantic-ME summer connection involves ocean-atmosphere interactions through multiple ocean basins, with an influence from the Indian Ocean and the Arabian Sea.

The study, led by Muhammad Azhar Ehsan currently at ICTP and co-authored by Dario Nicolì, Alessio Bellucci and Paolo Ruggieri, CMCC scientists at the Climate Simulation and Prediction Division, examined the impact of North Atlantic sea surface temperature (SST) variations, one of the main drivers for Northern Hemisphere climate, on summer ME-SAT.

The SST variability was analyzed through an important indicator, termed AMV - Atlantic Multidecadal Variability or AMO - Atlantic Multidecadal Oscillation to remind of its apparent oscillatory behavior; the instrumental records show that AMO/AMV is associated with a low frequency fluctuation of basin-wide anomalously warm and cold phases, with a typical 40-80-year time scale.

The phenomenon is not only interesting from an academic point of view, but also for its impacts on the climate across a large area: on the regional and local scale, it drives the climate of North America and western Europe, Mediterranean surface temperatures, influences the global monsoon, the current high levels of Atlantic hurricane activity, controls Sahel rainfall, and impacts Eurasian climate and the South Asian summer monsoon.

"This study", explains Alessio Bellucci, "identified this teleconnection between North Atlantic and Middle East and shed light on its causal nexus. Correlation analysis indicates a significant in-phase relationship between the summer ME-SAT and AMV observations, and the ME-SAT decadal variability can be largely explained by the AMV signal."

Understanding the nature and drivers of this multiscale climate variability is a fundamental step in developing robust climate predictions and risk assessments over the ME. Surface air temperature over the ME shows a statistically significant positive trend (0.28 °C/decade) with accelerated warming from the 1980s, which is projected to continue into the future. The study shows that the strong recent warming trend over the Middle East could persist as long as the North Atlantic remains anomalously warm.

In order to investigate the relationship between Atlantic multidecadal variability and ME temperatures, researchers used observational evidence and numerical simulations. The CMCC provided in particular a suite of idealized numerical simulations that contributed to understand the causal network linking the basin-wide north Atlantic SST fluctuations and the summer ME-SAT multidecadal variability.

"Due to the identified teleconnection", adds Bellucci, "summer air temperatures over the Arabian Peninsula are potentially highly predictable on multiyear time scale and this has a high societal relevance, because during the next decade, 'Hajj', the largest annual pilgrimage in the Holy city of Makkah gathering several million of Muslims in the Arabian Peninsula, will occur during boreal summer (in 2020, it will occur from 28 July to 2 Aug). Therefore, knowing the physical mechanism of the SAT variability during summer could inform government agencies in adopting timely appropriate mitigation and adaption strategies that may provide ease and comfort to Pilgrims."

How these results can be correlated to global warming? The AMV oscillatory-like alternation of warm and cold phases modulates the current temperature trend, amplifying or mitigating the global warming signal. "Well, if we were able to predict the trend of this signal in the North Atlantic, we could be able to predict if this signal will exacerbate or not the trend of increasing temperatures due to climate change. It will be crucial to understand whether and when a turning point of this signal will occur. The recent pattern of summer Middle East climate may be expected to continue as long as the present warm phase of AMV persists; in the future, temperatures in this region could increase or decrease, according to the evolution in the next decades of this signal in the North Atlantic. Understanding the nature and drivers of the AMV phase transitions and its impact on the regional scale climatic changes is a very active research area, and will be further explored in future research."

To improve behavior in class, teachers should focus on praising children for good behavior, rather than telling them off for being disruptive, according to a new study published in Educational Psychology.

Researchers spent three years observing 2,536 students, across three US states, from kindergarten age through to sixth grade (5 to 12 years of age).

The children observed were shown to focus on tasks up to 20% to 30% more when teachers were required to consider the number of praise statements given, compared to the number of reprimands.

The study lead by Dr Paul Caldarella, at Brigham Young University, involved a research team that sat in 151 classes, in 19 elementary schools across Missouri, Tennessee and Utah.

In half of the classrooms, teachers followed a behavioral intervention programme called CW-FIT, where students are told about the social skills they are expected to show in lessons and rewarded for doing so. In the other half of the classes, teachers used their typical classroom management practices.

The study showed a relationship between the ratio of praise to reprimands (PRR) used by the teachers and the extent students focused on class activities. In other words, the more teachers praised and the less that they scolded, the more students attended to the teacher, or worked on assigned tasks.

The difference was such that children in classes where the PRR was highest, the pupils spent 20-30% longer focusing on the teacher or task compared to those in classes where the praise to reprimand ratio was lowest. This relationship was present across both CW-FIT and ordinary classes.

"Unfortunately, previous research has shown that teachers often tend to reprimand students for problem behavior as much or more than they praise pupils for appropriate behavior, which can often have a negative effect on classrooms and student behavior," says Dr Caldarella, from the David O. McKay School of Education at Brigham Young.

"Praise is a form of teacher feedback, and students need that feedback to understand what behavior is expected of them, and what behavior is valued by teachers.

"Even if teachers praised as much as they reprimanded, students' on-task behavior reached 60%. However, if teachers could increase their praise to reprimand ratio to 2:1 or higher, they would see even more improvements in the classroom."

The results suggest that praise is a powerful tool in a teacher's arsenal, inspiring students to work harder - particularly those difficult to reach children who may struggle academically or be disruptive in class. Previous studies have shown a clear link between the time spent by students attending to lessons and their academic achievement, suggesting that praise could boost learning and improve children's grades too.

"Everyone values being praised and recognised for their endeavours - it is a huge part of nurturing children's self-esteem and confidence," Dr Caldarella adds.

"Also from a behavioral perspective, behavior that is reinforced tends to increase - so if teachers are praising students for good behavior - such as attending to the teacher, asking for help appropriately, etc - it stands to reason that this behavior will increase, and learning will improve."

Although the study shows that praise plays an important role in boosting student's focus in class, the researchers are keen to stress that sound instructional techniques and other evidence-based classroom management strategies must also be used to maintain children's attention.

Researchers are at work to find effective treatments to help young patients with brain tumors. Hundreds of brain organoids have been developed in the laboratories of the University of Trento to understand the genetic mechanisms responsible for these hard to treat diseases.

In this way, the research team coordinated by Luca Tiberi of the Armenise-Harvard Laboratory of Brain Disorders and Cancer of Cibio Department of the University of Trento developed a new strategy to study brain tumors of childhood.

The University of Trento led the research study, coordinating a research team involving Sapienza University of Rome, Ospedale pediatrico Bambino Gesù in Rome, and Irccs Neuromed-Istituto neurologico mediterraneo in Pozzilli (Isernia), with support from the Armenise-Harvard Foundation, the Italian Association for Cancer Research-Airc, and Fondazione Caritro in Trento.

The organoids were used to create in vitro tumor models. The results achieved will make it possible to advance brain cancer research, as in the near future the large-scale production of in vitro tumors could provide a low-cost method for the screening of new drugs compared with previous technologies.

"Creating brain tumor organoids is very difficult - underlined Tiberi, the research team coordinator - and requires specific scientific capabilities that Cibio department managed to attract and develop in its research laboratories".

"Organoids, generated from skin or blood cells, shaped like irregular spheres the size of a small peanut, were grown by the University of Trento and examined and characterized with Sapienza University of Rome and Ospedale pediatrico Bambino Gesù in Rome. They can show signs of disease and provide a model of the tumors affecting young patients - he added. This work demonstrates how important it is to collaborate for universities and research institutes to initiate innovative projects".

"We also have grown organoids from the cells of healthy donors - explained Tiberi - and these gave us the opportunity to understand some of the genetic mechanisms responsible for the onset and development of brain tumors. In particular, the study confirmed the key role of two proteins (Otx2 and c-Myc) and investigated the efficacy of a number of therapeutic options (based on the drug Tazemetostat)".

Tiberi continued: "These in vitro tumors will help us fine-tune research on the genes that cause cancer and on possible prevention and treatment strategies. Organoids give us the opportunity to study brain tumors without using experimental animals in a context that is similar to a real-patient scenario. They can be a reliable tool for developing personalized therapies".

Brain tumors in childhood

Brain tumors are the first cause of death due to cancer in children. They are very aggressive and require a multidisciplinary and integrated approach. While significant progress has been made in treating these tumors, surviving patients may suffer long-term side effects that significantly compromise their quality of life. When the tumor reappears after some time, therapies are usually ineffective. Medulloblastoma, the focus of this study, is the most common malignant brain tumor in children affecting the central nervous system. The survival rate at five years from the diagnosis of medulloblastoma is around 70% (source: AIRC Italian Association for Cancer Research).

When we think of climate change, we tend to think about greenhouse gases, fossil fuels and pollution. Most of us don't think about fungi.

But Kathleen Treseder does. Treseder, an ecologist at the University of California, Irvine, studies how fungi can affect climate and vice-versa.

"Fungi are important to consider," she says. "They can influence nearly every aspect of ecosystems, especially processes that occur in soils."

New research from her lab shows that fungi can have different lifestyles in response to climate change. These findings can be incorporated into computational models that simulate ecosystems.

"We may be able to better predict shifts in atmospheric carbon dioxide levels and climate change," says Treseder. "That can help us estimate how much, when and where climate change will affect human societies."

It's important to be able to forecast which places will be hit by climate change and how quickly. These early warnings can help preparations, such as building sea walls or flood channels, or direct the development of new crop varieties.

Fungi are terrific decomposers. They break down organic material to get nutrients and energy. In doing so, they turn complex chemicals into simpler elements, such as carbon. In fact, "fungi are an integral part of the global carbon cycle," says Treseder. "They can move carbon from decomposing material into the atmosphere as carbon dioxide."

But fungi don't just release carbon. They can also store it. For example, environmental stress can cause fungi to strengthen their cell walls. They do so by using organic compounds that contain carbon. These carbon compounds can stay in soils for years to decades or even longer.

Treseder's research explores how fungi decide whether to use limited energy and resources to decompose material or for other processes. "No one can do everything well, and the same goes for fungi," says Treseder. "If fungi invest resources into one activity like decomposition, then those resources won't be available to support another activity like tolerating environmental stress."

These resource allocation decisions become even more important in a world with changing climate. "For example, will more extreme climates select for fungi that tolerate stress well, but cannot decompose dead material as efficiently?" says Treseder. "If so, then their production of carbon dioxide might decrease, slowing climate change."

To answer these questions, Treseder traveled to Alaska and Costa Rica. Experiments were set up in Alaskan Boreal forests and the cloud forests of Costa Rica. "

"We chose these locations because they are both endangered by climate change," says Treseder. "Northern ecosystems are warming particularly fast. Clouds are disappearing from the mountaintops of Costa Rica."

Treseder and colleagues exposed areas of the forests to drought-like conditions or more mellow environments. They collected soil samples from the different experimental areas.

Then they analyzed products made by fungal genes. These gene products served as indicators for whether the fungi were investing more resources toward decomposition or strengthening cell walls.

"We found that where drought stress increased, the amount of fungi that invested more in strengthening cell walls and less in decomposition tended to increase," says Treseder. In contrast, in more moderate conditions, the reverse occurred. Fungi that decomposed more efficiently became more common.

These findings suggest that fungi might store more carbon as global climate becomes more extreme. On the other hand, they might release more carbon dioxide in moderate climates. "These opposing feedbacks would not have been apparent without examining trade-offs among fungal traits," says Treseder.

Treseder is working to incorporate these findings into new and existing models of climate change. One particular area of focus are Earth system models that the Intergovernmental Panel on Climate Change uses for its official predictions. "We hope our research improves predictions of future trajectories of climate change," says Treseder.

Tampa, FL (Jan. 29, 2020) -- Many diseases arise from abnormalities in our capillaries, tiny exquisitely branching blood vessel networks that play a critical role in tissue health. Researchers have learned a lot about the molecular communication underlying capillary formation and growth, but much less is understood about what causes these critical regulators of normal tissue function to collapse and disappear.

"Capillary regression (loss) is an underappreciated, yet profound, feature of many diseases, especially those affecting organs requiring a lot of oxygen to work properly," said George Davis, MD PhD, professor of molecular pharmacology and physiology at the University of South Florida Health (USF Health) Morsani College of Medicine, Tampa, Fla.

"If we know how blood vessels are altered or begin to break down we should be able to fix it pharmacologically," said Dr. Davis, a member of the USF Health Heart Institute.

A team led by Dr. Davis advanced the understanding of how capillaries regress in a study published Dec. 19 in the American Heart Association journal Arteriosclerosis, Thrombosis, and Vascular Biology. The USF Health researchers worked with the laboratory of Courtney Griffin, PhD, at Oklahoma Medical Research Foundation.

The researchers discovered that three major proinflammatory mediators - interlukin-1 beta (IL-1β), tumor necrosis factor alpha (TNFα) and thrombin - individually and especially when combined, directly drive capillary regression (loss) known to occur in diseases such as hypertension, diabetes, cardiovascular diseases, neurodegenerative diseases and malignant cancer. They also identified combinations of drugs - neutralizing antibodies to specifically block IL-1β and TNFα, or combinations of pharmacologic inhibitors - that significantly interfered with capillary regression.

Capillaries, our body's tiniest and most abundant blood vessels, connect arteries with veins and exchange oxygen, nutrients and waste between the bloodstream and tissues throughout the body. The Davis laboratory grows three-dimensional human "blood vessel networks in a dish" under defined, serum-free conditions to delve into the complexity of how capillaries take shape to sustain healthy tissues. Lately, his team has begun applying what they've learned using this innovative in vitro model to attack, and possibly protect against, diseases.

For this study the researchers cultured two types of human cells: endothelial cells, which line the inner surface of capillaries, and pericytes, which are recruited to fortify the outer surface of the endothelial-lined tubes. Cross-communication between these cells controls how the blood vessel networks emerge, branch and stabilize. Macrophages, a type of immune cell, were activated in the cell culture media to simulate a tissue-injury environment highly conducive to capillary regression.

Among the key study findings:

- Macrophage-derived molecules IL-1β and TNFα, combined with thrombin, selectively cause endothelial-lined capillary tube networks to regress; however, pericytes continue to proliferate around the degenerating capillaries. Why the pericytes are spared remains an intriguing question to be answered, but Dr. Davis suggests these more resilient cells may be left behind to help repair tissue damaged by inflammation.

- IL-1β and TNFα, combined with thrombin, induce a unique set of molecular signals contributing to the loss of blood vessels. This "capillary regression signaling signature" is opposite of the physiological pathways previously identified by Dr. Davis and others as characterizing capillary formation and growth.

- Certain drug combinations (two were identified by the researchers) can block the capillary loss promoted by IL-1β, TNFα and thrombin.

The USF Health researchers found several other proinflammatory molecules that promoted capillary loss, but none proved as powerful as IL-1β, TNFα and thrombin, especially when all three were combined.

Antibodies to counteract the effects of IL-1β and TNFα are already used to treat patients with some inflammatory diseases, including atherosclerosis, rheumatoid arthritis, and Crohn's disease. And physicians prescribe direct thrombin inhibitors for certain patients with atrial fibrillation, deep vein thrombosis and pulmonary embolism.

"These drugs are out there and they work. Our data suggests that, if combined, they may actually prevent vessel breakdown (earlier in the disease process) and improve outcomes," Dr. Davis said.

The USF Health team plans to investigate how abnormal capillary response may influence the loss of cells and tissues specific to disease states like sepsis, ischemic heart disease and stroke. Their model of 3D blood vessel networks can also be easily used to screen more potential drug candidates, Dr. Davis said. "We've identified some promising (existing) drugs to rescue capillary regression -- but there may be more therapeutic opportunities."