Culture

LAWRENCE -- Climate change is a problem facing countries around the world, but media coverage of the topic differs from one nation to the next. A new study from the University of Kansas shows the way media frame climate change coverage can be predicted by several national factors, yet none tend to frame it as an immediate problem requiring national policies to address the issue.

While richer countries tend to frame climate change coverage as a political issue, poorer countries more often frame it as an international issue that the world at large needs to address.

"Media can tell people what to think about. At the same time, framing can have an effect on how people think about certain issues," said Hong Vu, assistant professor of journalism at KU and the study's lead author. "Not only can framing have an impact on how an issue is perceived but on whether and how policy is made on the issue. With big data, machine-learning techniques, we were able to analyze a large amount of media climate change coverage from 45 countries and territories from 2011 to 2015."

Vu and co-authors Yuchen Liu, graduate student at KU; and Duc Vinh Tran of Hanoi University of Science and Technology published their findings in the journal Global Environmental Change. They analyzed over 37,000 articles and considered national factors such as economic development, weather and energy consumption. They reviewed headlines from nationally circulated publications of varying political ideologies that contained the keywords "greenhouse gas," "climate change" and/or "global warming," or the local language equivalent.

The most consistent predictor of how the issue was framed was a nation's gross domestic product per capita.

"We showed that the issue is more politicized in richer countries. In poorer countries, it was framed more as an international issue," Vu said. "Which makes sense, as poorer countries don't have the resources that richer countries do to fight it."

Even when richer countries framed the issue as one they could address with their more plentiful resources, it was often also framed as a political issue and would focus on debate or argument about political approaches as opposed to proposing policy solutions. Media from richer countries also focused more on the science of climate change.

When climate change was framed as an economic issue, it was in countries that had the most severe climates and those that have experienced the most adverse consequences of climate change and natural disasters, loss of life and property, and economic effects.

In terms of social progress framing, richer countries framed the issue in terms of energy policy and use. Those that emit the most carbon dioxide framed content in terms of energy issues, while poorer countries and those that had experienced the most severe climates focused more on natural impact.

The study also used independent nation-level variables from several databases, including the World Bank, the Center for Research on the Epidemiology of Disasters, the Global Carbon Atlas Project and Freedom House, all nongovernment organizations working in development or on climate change.

The authors argue that the international relations frame being the most widely used reflects the fact that climate change is a problem every nation needs to address. Economic effects being second most popular reflects that fighting climate change will have impacts on every economy and that when natural disasters and climate change were discussed, they were nearly always brought forth in an economic sense. They also contend that richer countries framing the issue as political reflects that climate change skeptics in those nations gaining more media prominence and the efforts of multiple groups trying to politicize the issue, influence media agendas and policymaking.

The study helps add to the understanding of media influence on climate change coverage, Vu said. Future work will address questions of framing the topic, if it's done on local, national or global levels, if communicators suggest solutions, if such solutions are attributed to individuals, businesses or governments and efficacy of proposed solutions. Three decades of communications on the topic show there is not a sense of immediacy in covering the problem and influencing policy.

"As communications researchers we want to know why, if climate change entered public discussion more than 30 years ago and we've been covering it as a global problem since, why can't we slow the warming climate down," Vu said. "If we want the public to have better awareness of climate change, we need to have media imparting it in an immediate sense. By looking at how they have portrayed it, we can better understand how to improve it, and hopefully make it a priority that is reflected in policy."

A new multicenter study at Columbia University links long-term exposure to air pollution, especially ozone, to development of emphysema, a chronic lung disease.

In Brief

Long-term exposure to outdoor air pollutants, especially the pollutant ozone, accelerates the development of emphysema and age-related decline in lung function, even among people who have never smoked, according to a study published in the Journal of the American Medical Association.

The findings may help explain why emphysema is relatively common in nonsmokers.

Background

Chronic lower respiratory disease--a catchall term for emphysema, chronic obstructive pulmonary disease (COPD), chronic bronchitis, and asthma--is the fourth-leading cause of death in the U.S. and third-leading cause of death worldwide. Short-term exposure to air pollutants is a major risk factor for poor lung health. But the long-term effects of air pollutants on the lungs are not well understood.

Study Details

The study, the largest and longest of its kind, looked at whether exposures to four major pollutants--ground-level ozone, fine particulate matter (PM), nitrogen oxide, and black carbon--were associated with the development of emphysema, measured by CT scan, and decline in lung function, measured by spirometry. (Ground-level ozone harms human health, but ozone high in the atmosphere ozone protects against the sun's harmful ultraviolet rays.)

The study included more than 7,000 adults (ages 45 to 84) living in Chicago, Los Angeles, Baltimore, St. Paul, New York City, and Winston-Salem, who were taking part in the Multi-Ethnic Study of Atherosclerosis Air Pollution (MESA Air) and MESA Lung studies. Participants were followed for a median of 10 years. Air pollutant levels were estimated at each participant's home address.

What the Study Found

The researchers found that exposure to each of the pollutants at the beginning of the study was independently linked to the development of emphysema during the study period. The strongest association was seen with ozone. Only ozone, at baseline and during follow-up, was associated with a decline in lung function.

Ambient concentrations of fine particulates and nitrous oxide, but not ozone, decreased significantly over the study period.

"The increase in emphysema we observed was relatively large, similar to the lung damage caused by 29 pack-years of smoking and 3 years of aging,"said R. Graham Barr, MD, DrPH, the Hamilton Southworth Professor of Medicine and Epidemiology at Columbia University Irving Medical Center and a senior author of the paper. (One pack-year is equal to smoking a pack a day for a year.)

What the Study Means

"These findings matter since ground-level ozone levels are rising, and the amount of emphysema on CT scans predicts hospitalization from and deaths due to chronic lower respiratory disease," says Barr.

"Ground-level ozone is produced when UV light reacts with pollutants from fossil fuels," adds Barr. "This process is accelerated by heatwaves, so ground-level ozone will likely continue to increase unless additional steps are taken to reduce fossil fuel emissions and curb climate change. But it's not clear what level of ozone, if any, is safe for human health."

Walter and Eliza Hall Institute researchers have identified a molecular switch that impacts immune responses to viral infections, and whether or not protective antibodies are produced.

The team also made the surprising discovery that the immune system protects against different viruses via distinct pathways. Their findings could lead to better strategies to develop vaccines for previously hard-to-prevent viruses.

The research, led by Dr Joanna Groom and PhD student Ms Amania Sheikh, was published today in the journal Cell Reports.

At a glance

Our researchers have identified that the protein T-bet determines how the immune system responds to viral infections.

The research showed that T-bet enables immune T cells to distinguish between different viral infections, controlling whether or not protective antibodies are produced.

Antibodies are an essential component of long-lived immunity to viruses, and this discovery could underpin the development of better vaccines to prevent viral diseases.

Molecular switch

Our immune system comprises a complex network of cells and signalling molecules that can produce a range of responses to infections, Ms Sheikh said. "Immune T cells are critical for coordinating specific immune responses, recruiting other cells and directing how we respond to different microbes such as bacteria, fungi or viruses," she said.

"We knew that the protein T-bet was important for the function of many immune cells, and wanted to understand its role in a subset of immune T cells that help in the formation of protective antibodies."

Antibodies are long-lived proteins that can be produced following an infection. They specifically bind to other proteins - such as those on a microbe's surface - and are important for protecting us against repeat infections by the same microbe. Vaccines work by stimulating the production of antibodies that are specific to an infectious disease, preventing the infection from establishing.

Ms Sheikh said the team discovered that T-bet was an essential switch that enabled T cells to stimulate antibody production in response to viral infections. "The level of T-bet in T cells is influenced by factors such as how a virus enters the body, and how much inflammation it triggers in its early stages. This in turn influences the immune response to the virus," she said.

Distinguishing viruses

These findings reconcile a controversy in the field about how the immune system can distinguish between different viral infections, and respond in distinct ways. "We compared the role of the T-bet switch in immune responses to two viruses, influenza and LCMV, a virus that can cause meningitis," Dr Groom said.

"These viruses are thought to activate similar immune cells, yet we demonstrated specific changes between the responses could lead to very different amounts of protective antibodies. We showed that T-bet was critical for scaling how much antibody production occurred in response to a viral infection."

The findings could underpin the development of more effective vaccines against viruses. "Most current vaccines to infectious diseases rely on robust and long-lived antibody production. If we can understand the precise triggers controlling how much antibody is produced in response to an infection, we should be able to develop vaccines that act similarly to stimulate protective antibody production," Dr Groom said.

Research published in the journal BMC Evolutionary Biology has shed new light on why some grey squirrels are black.

The study was led by Dr Helen McRobie of Anglia Ruskin University (ARU), who has previously mapped the spread of black squirrels across the UK. Black squirrels are the same species as grey squirrels, with the only difference being their fur colour.

The new work builds on Dr McRobie's research from 2014, which found that the black fur is caused by the grey squirrel having a pigment gene with a missing piece of DNA.

Working with colleagues from the University of Cambridge and the Virginia Museum of Natural History in the United States, Dr McRobie has found that the faulty pigment gene in grey squirrels is identical to a faulty gene found in the closely-related fox squirrel, a species which is native to North America and also has black variants.

Testing DNA from grey and fox squirrels found across the United States and British Columbia, Canada, the researchers discovered that other "signatures" on the mutated gene are more closely related to the fox squirrel. This suggests it is highly likely the mutation first arose in the fox squirrel and passed to the grey squirrel through interbreeding.

Dr McRobie, Senior Lecturer in Biomedical Science at Anglia Ruskin University (ARU), said: "Squirrels take part in 'mating chases' where a female squirrel is pursued by lots of male squirrels and eventually one male mates with the female.

"People have spotted 'mixed species' mating chases, with a mix of grey and fox squirrels pursing a female. The most likely explanation for the black version of the gene being found in the grey squirrel is that a male black fox squirrel mated with a female grey squirrel.

"The fact black grey squirrels have become so common right across North America is possibly because black fur offers a thermal advantage, helping them inhabit regions with extremely cold winters. This may have contributed to the expansion of the grey squirrel's range during the past 11,000 years, following the end of the most recent ice age, helping them spread further north into Canada."

The black squirrels living in the UK are believed to have escaped from a private zoo, having been imported from the United States. The first wild black squirrel was recorded in Woburn, Bedfordshire, in 1912, and they are now found across many parts of South East England.

The pain-relieving effect of salicylic acid, now sold as Aspirin, has been known for thousands of years. Besides being a useful drug with numerous health applications, it is a stress hormone made by plants which is essential in enabling them to fight off damaging pathogens. What was not known, however, is how plants generated this hormone. Now, an international research team led by the University of Göttingen with the University of British Columbia in Vancouver have at last unravelled the biosynthesis of this crucial hormone. Their results were published in Science.

As far back as Neanderthal times, bark containing salicylic acid was chewed to self-medicate; the first chemical extraction was in the 1820s, and an improved version has been marketed as Aspirin for over 120 years. But no-one understood how plants actually made it. Then, 20 years ago researchers using the plant Arabidopsis thaliana discovered the first gene involved in salicylic acid synthesis. Ever since, countless groups have tried to identify the missing steps on the way to salicylic acid.

Dmitrij Rekhter and colleagues from the Department of Plant Biochemistry at the University of Göttingen found a way to investigate. They used special Arabidopsis plants isolated by Professor Zhang's team at the University of British Columbia, which have extremely elevated levels of salicylic acid. Then the researchers found that the precursor to salicylic acid accumulates in these plants if a gene of previously unknown function (PBS3) is removed. The team in Göttingen was therefore able to deduce the action of the gene product.

As first author Rekhter explains, "PBS3 attaches isochorismic acid to glutamic acid resulting in the formation of the previously unknown compound isochorismate-9-glutamate. This highly unstable substance decomposes spontaneously into salicylic acid and by-product." Solving the riddle of how plants biosynthesise salicylic acid was a joint effort of the teams of Professor Ivo Feußner, Dr Marcel Wiermer and Professor Volker Lipka at the University of Göttingen together with the team of Professor Yuelin Zhang at the University of British Columbia in Vancouver, within the International Research Training Group "PRoTECT".

Furthermore, it looks like this pathway applies across the plant kingdom. Feußner from the Department of Plant Biochemistry at the University of Göttingen says, "This research not only increases our understanding of how plants synthesise this hormone, but also opens up new opportunities to breed crops that are more resistant to disease. The important role of salicylic acid for plants in their battle against disease make these findings of fundamental importance for research areas such as plant immunity and therefore also food production."

OAK BROOK, Ill. - A drug used to treat attention-deficit/hyperactivity disorder (ADHD) appears to affect the development of the brain's signal-carrying white matter in children with the disorder, according to a study published in the journal Radiology. The same effects were not found in adults with ADHD.

Methylphenidate (MPH), sold under trade names including Ritalin and Concerta, is a commonly prescribed treatment for ADHD that is effective in up to 80 percent of patients. However, not much is known about its effect on the development of the brain, including the brain's white matter, which is important for learning and brain functions and coordinating communication between different brain regions.

To find out more about MPH's effects on white matter development, Dutch researchers performed a study of 50 boys and 49 young adult men diagnosed with ADHD. All patients were medication-naïve; that is, they had never received MPH prior to the study.

"Previous studies all have tried to statistically control for the effects of ADHD medications," said study senior author Liesbeth Reneman, M.D., Ph.D., from the Department of Radiology and Nuclear Medicine at the Academic Medical Center, University of Amsterdam, the Netherlands. "But we are the first to study medication-naïve patients in this context, which, of course, is crucial if you want to know how ADHD medications affect the developing brain."

Patients received either MPH or a placebo for 16 weeks. Before and one week after treatment cessation, the participants underwent MRI including diffusion tensor imaging (DTI), a technique that helps assess white matter. DTI provides a measure called fractional anisotropy (FA), which is thought to reflect important aspects of white matter such as nerve fiber density, size and myelination--the process of coating nerve fibers to protect the nerve and help it carry signals more efficiently.

In boys with ADHD, four months of treatment with MPH was associated with increased white matter FA. The effects were age dependent, as they were not observed in adults treated with MPH.

"The results show that ADHD medications can have different effects on the development of brain structure in children versus adults," Dr. Reneman said. "In adult men with ADHD, and both boys and adult men receiving placebo, changes in FA measures were not present, suggesting that the effects of methylphenidate on brain white matter are modulated by age."

Dr. Reneman and colleagues are studying the long-term implications of these findings on ADHD behavior, which have yet to be established. Many ADHD patients are on medications for years, so the long-term effects of MPH treatment represent a vital area of research. In the meantime, the researchers want to see tighter regulations for prescribing ADHD medications, since MPH is being prescribed not only to increasing numbers of children, but also at younger ages.

"What our data already underscore is that the use of ADHD medications in children must be carefully considered until more is known about the long-term consequences of prescribing methylphenidate at a young age," Dr. Reneman said. "The drug should only be prescribed to children who actually have ADHD and are significantly affected by it."

According to the Center for Disease Control and Prevention, based on parent reporting, approximately 5.2 percent of American children between the ages of 2 and 17 take ADHD medication.

A team of scientists from the University of Southampton, Bangor University and the National Oceanography Centre have discovered several artificially introduced species in the coastal waters of southern England, using a technique that could help the early detection of non-native species if adopted more widely.

Among the species identified during the study was Cephalothrix simula, a worm, originating from the North West Pacific Ocean, which contains neurotoxins that are potentially fatal if they enter the human body.

The researchers, led by Luke Holman, a PhD student at the University of Southampton, collected water and sediment from four marinas around the UK and analysed the DNA of each sample to determine which species had been present in the ecosystems.

Organisms leave traces of their DNA in water systems through a variety of means, for example fish can lose scales and many species can release sperm or eggs during the spawning season. The team were able to extract this genetic material, known as environmental DNA (eDNA), and compare it to global DNA databases to identify the presence of species.

Luke Holman said "We are enormously excited about the potential for eDNA in the detection of invasive species. This initial work gives us confidence that the technique could be invaluable both for catching invasions early on and also for monitoring the success of eradication efforts."

There are many ways in which species that are not native to the UK arrive on our shores. They can be carried in ballast water tanks or on ship hulls from one international harbour to another, something especially common in places like Southampton. They can also hitch a lift on live fish stocks and oysters imported for British fish farms.

In total the team identified 18 non-indigenous species across the four sampled marinas - in Southampton Water, Anglesey, The Bristol Channel and the River Blackwater. The Cephalothrix simula worm had not been previously detected in the UK when this study was carried out in May 2017 although it was subsequently found in Cornwall the following year; a discovery which has been documented by the Centre for Environment, Fisheries and Aquaculture Science (Cefas). Other recently introduced species the researchers detected included Arcuatula senhousia (Asian date mussel) and another type of worm known as Paranais frici.

If not caught early, invasive species can have devastating effects on the country's native wildlife habitats. For example, Asian date mussels can alter sediment through the thread like cocoons they produce which weave together and change the seafloor from a muddy to a thick, sandy material. This in turn changes the creatures that inhabit the area.

Luke Holman added "We know that the muddy flats of Southampton water and the Solent area provide a great deal of food for foraging birds so we should be worried about any species with an ability to change the sediment."

eDNA metabarcoding surveys are increasingly common in biodiversity monitoring, but their use for the detection of invasive species remains limited and this study, published in the journal Scientific Reports, is the first of its kind in the UK.

The team hopes to build on their research by providing guidance for routine monitoring of non-indigenous species to natural resource agencies both in the UK and elsewhere.

In the human body the salt content of cells and their surrounding is regulated by sophisticated transport systems. Special channels in the cell membrane selectively permit salt ions to flow in and out of cells. A research team led by Professor Thomas Jentsch at the FMP and MDC has now identified the molecular components of a previously unknown ion channel.

The membranes that encase cells and cell organelles are normally impermeable for charged particles such as salt ions. But there are loopholes: Transmembrane proteins can form channels that pass ions. In most cases, such ion channels open or close on receiving a particular signal transmitted, for example, voltage or a signaling molecule. The channels are often specialized to allow only specific ions - such as chloride, potassium, or sodium - to pass.

A team led by Professor Thomas Jentsch from Leibniz-Forschungsinstitut für Molekulare Pharmakologie (FMP) and the Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC) has now identified a new transmembrane protein called TMEM206 as a new chloride ion channel. It is characterized by a so-far unique activation mechanism: When the pH level decreases in the cell environment, the channel opens and allows chloride, depending on the cell type, to flow out or into the cell. This type of ion channels may play a role in the development of heart attacks, strokes, and tumors, for these diseases are accompanied by an acidification in the affected tissue.

The starting point for the current research was an ion channel called ASOR (Acid-Sensitive Outwardly Rectifying anion channel). More than ten years ago, electrophysiological studies had detected and characterized pH-regulated chloride currents in cells of various vertebrates. "But the structure of the underlying channel had remained unknown. Back then, technology had not been advanced enough to perform a genome-wide screen to identify it. We have now discovered the gene encoding the protein that forms the ASOR channel," explains Professor Thomas Jentsch, head of the research group on Physiology and Pathology of Ion Transport at the MDC and FMP.

It took about four years to complete the study. Many methods had to be adapted or newly developed. For example, the team devised a special optical detection assay for the function of the ASOR channel that is compatible with high-throughput methods.

In order to search for DNA sequences relevant to the ASOR channel, the researchers performed a siRNA screen. This involves using small pieces of RNA (small interfering RNA, or siRNA) to systematically shut down genes one by one in cultured cells and then analyzing the functional consequences.

They also employed CRISPR-Cas9 technology and mutations changing channel properties to confirm that the thus identified gene was in fact coding for the channel. "For us, it was extremely helpful that the Screening Unit at the FMP, which has a facility specializing in these high-throughput methods, was our direct neighbor," says Jentsch. "There are numerous robots there that pipette the samples, and it is equipped with automated cell culture systems." The Screening Unit's siRNA library contains siRNAs for all 20,000 human genes, each of which must be evaluated separately. To be on the safe side, three runs were performed so that in the end a total of 60,000 individual results had to be analyzed bioinformatically.

"The identification of TMEM206 as central component of the ASOR channel is a major breakthrough. This opens the door to finally uncover the currently unknown physiological roles of the channel," summarizes Jentsch. Chloride ions are among the most important and prevalent electrolytes in the body. Their concentration can vary substantially between the extracellular space, the cytoplasm, and various intracellular organelles. The cell membrane forms a barrier for the negatively charged chloride, but special membrane proteins enable it to cross this barrier. Chloride ions either move along concentration gradients through channels or, by coupling to other ions, can be actively pumped across the membrane by transporter proteins. Chloride channels carry out very diverse biological functions. The underlying proteins are also molecularly very diverse. They are regulated in a host of ways to regulate the transport of chloride according to the need of the cell and the organism.

There is strong evidence that the ASOR channel plays a role in acid-induced cell death. The channel allows the passage of chloride ions only when the extracellular milieu is very acidic. Even though the channel is found in every mammalian cell, this occurs only in a few specialized cell types or under pathological conditions such as stroke or heart attack or within tumors. However, the fact that ASOR plays a harmful role in disease does not explain why it is found in all mammalian cells.

There are still many unanswered questions, says Jentsch. What is the significance of the strong pH-dependence of the channel? Why do all cells apparently have this ASOR channel? And where exactly is the channel located inside the cells? Is it also present in acidic organelles, such as lysosomes and endosomes? In order to further elucidate the structure and physiological functions of ASOR, the research group has developed antibodies against TMEM206 and are generating mice in which the gene for the channel is destroyed. They want to find out in which cell the channel protein is expressed and where exactly it is localized within the cells. In the future, they also hope to clarify the physiological function by using their mouse models.

A new study analyzing samples from patients with and without acute flaccid myelitis (AFM) provides additional evidence for an association between the rare but often serious condition that causes muscle weakness and paralysis, and infection with non-polio enteroviruses. The National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health, funded the research, which was conducted by investigators at Columbia University's Center for Infection and Immunity and investigators from the Centers for Disease Control and Prevention. The findings are reported in the online journal mBio.

There have been 570 confirmed cases since CDC began tracking AFM in August 2014. AFM outbreaks were reported to the CDC in 2014, 2016 and 2018. AFM affects the spinal cord and is characterized by the sudden onset of muscle weakness in one or more limbs. Spikes in AFM cases, primarily in children, have coincided in time and location with outbreaks of EV-D68 and a related enterovirus, EV-A71. Both of these viruses typically cause mild respiratory illness from which most people recover fully. Despite the epidemiological link between enterovirus circulation and AFM cases, evidence of direct causality has not been found.

The researchers first looked for direct evidence of enterovirus infection in the cerebrospinal fluid (CSF) of 13 children and one adult diagnosed with AFM in 2018. They also examined five CSF samples taken from people with other central nervous system diseases. The team used a new tool they developed called VirCapSeq-VERT, which can detect any viral genetic material that is at least 60% like that of any known vertebrate virus. They found enteroviral genetic material (EV-A71) in only the one adult AFM case and genetic material from another enterovirus (echovirus 25) in one of the non-AFM cases.

The investigators also sought indirect evidence of enterovirus infection by looking for antibodies to enteroviruses made by the immune system in response to an infection. The team developed a microchip assay, AFM-SeroChip-1, that detects the presence of antibodies generated in response to any human enterovirus (EV-A, EV-B, EV-C or EV-D) infection. Using this assay, the team tested the same 14 CSF samples from the AFM patients. They also tested CSF samples taken from 11 adults with central nervous system conditions, such as multiple sclerosis, and from 10 children with Kawasaki disease, none of whom had AFM.

EV-specific antibodies were detected in the CSF of 79% (11 of 14) of the AFM cases. Of those, six samples were positive for EV-D68, strongly indicating that enterovirus had been in the central nervous system, even though it had not been detected by VirCapSeq-VERT. None of the CSF samples from children with Kawasaki disease had antibodies that reacted with any enterovirus.

While other etiologies of AFM continue to be investigated, this study provides further evidence that enterovirus infection may be a factor in AFM. In the absence of direct detection of a pathogen, antibody evidence of pathogen exposure within the central nervous system can be an important indicator of the underlying cause of disease, the researchers note.

NEW YORK, August 13, 2019 -- Exposure to violence, social conflict, and other stressors increase risk for psychiatric conditions such as depression and post-traumatic stress disorder. Not everyone who experiences significant stress will develop such a response, however, and the cellular and molecular basis for an individual's underlying resilience or susceptibility to stressful events has remained poorly understood. Now, a newly published paper in the journal eLife from researchers at the Advanced Science Research Center (ASRC) at The Graduate Center, CUNY suggests that the behavior of oligodendrocytes -- the glial cells that produce the myelin sheath that protects nerve fibers -- plays a critical role in determining whether we succumb to or tolerate stress.

"Through our study, we were able to identify brain-region-specific differences in the number of mature oligodendrocytes and in the content of myelin between two groups of mice who were categorized based on their resilience or susceptibility to an identical social-defeat stressor," said the paper's corresponding author Jia Liu, a research associate professor with the ASRC's Neuroscience Initiative. "After repeated exposure to an aggressive mouse, some animals, called "susceptible," avoided any sort of social interaction with their peers, while others remained resilient and continued to be socially engaged."

In follow-up brain tissue analysis, the research team detected fewer mature oligodendrocytes and irregular myelin coverage in the medial prefrontal cortex -- a brain region that plays a critical role in emotional and cognitive processing -- in the susceptible mice. In contrast, healthy numbers of oligodendrocytes and myelin were detected in resilient mice.

Methodology

For the study, researchers exposed test mice to an aggressor for five minutes daily over 10 days. Following this period, the mice were placed in the presense of unfamiliar mouse and categorized either as susceptible if they showed signs of social withdrawal or resilient if they still showed interest in socializing with the new mouse -- a social behavior that is typically detected in normal mice.

Reseachers next sought to determine if there were myelination differences between susceptible and resilient mice. They looked at two areas of the brain that are known to play a critical role in determining the individual's response to stress. In one of those areas -- the medial prefrontal cortex -- they found that the myelinated segments of nerve fiber in susceptible mice were shorter in length and thinner than typical. They did not find this condition in the resilient or control mice groups. They also investigated the state of each mouse group's glial cells, and discovered that in susceptible mice fewer of these cells had differentiated into myelin-producing oligodendrocytes.

In a final experiment, researchers found that induced damage to the myelin in the medial prefrontal cortex caused altered social behavior in mice, but the behavior returned to normal when new myelin was formed.

"Dr. Liu's research has highlighted the importance of stressful social events in changing the epigenetic code of oligodendrocyte progenitors, which may account for the increased susceptibility to developing chronic psychiatric disorders in some individuals," said Patrizia Casaccia, founding director of the ASRC Neuroscience Initiative. "Her data suggest that oligodendrocyte progenitor differentiation can be affected by emotional and psychological events, and this provides a new concept for preventing and treating depression. Current treatments target neuronal function, but Dr. Liu's work identifies potential new therapy targets as it suggests glial cell dysfunction could be a cause of stress-related mental disorders."

Sufferers of recurring urinary tract infections (UTIs) could expect more effective treatments thanks to University of Queensland-led research.

UTIs are one of the most common bacterial infections according to Professor Mark Schembri from UQ's School of Chemistry and Molecular Biosciences.

"They're a major burden on global healthcare," he said.

"Approximately 25 per cent of women who suffer UTI will experience recurrent UTI within six months of initial infection.

"It's a problem magnified by increasing antibiotic resistance - antibiotic treatments can sometimes just stop working on these patients, with dire results."

The study, performed in collaboration with researchers from the University of Utah, followed a long-term recurrent UTI sufferer, using genetic analysis to find out whether the infection came from a single bacterial 'reservoir' in the body.

"The patient we examined has suffered from recurring UTIs for 45 years, since 1974," Professor Schembri said.

"The longest period she can recall being UTI-free is nine months.

"During that time she's taken almost every type of antibiotic and the same bacteria has been able to survive and escape treatment, even when the patient used some of the strongest antibiotics available in our armoury."

The research team isolated E. coli from the patient's urine during repeat infections and determined its entire DNA sequence.

UQ's Associate Professor Scott Beatson said the analysis showed the bacteria causing recurring UTIs were identical.

"This was proof - her infections did indeed originate from a common reservoir," he said.

"To find the reservoir, we also collected and sequenced the DNA of E. coli recovered from the patient's faecal samples.

"These E. coli were the same as those that caused the recurring UTI, proving that the woman had a persistent reservoir of E. coli residing in her intestine - the source of her infections.

"We now know that bacteria can reside in the intestine for very long periods and cause recurring UTIs, despite antibiotic treatment.

"Therefore, it's time we consider using antibiotics that will not just treat the UTI in the bladder, but also eliminate the infection reservoir in the intestine that seeds recurrent infection of the bladder."

The paper's first author, UQ's Dr Brian Forde, said when a patient suffered a UTI episode, a faecal sample could determine if the infecting strain also resided in the intestine, by combining bacterial culture with genome sequencing technology.

"If the same strain keeps being identified, we could design tailored treatment to eliminate the bacteria from not just the patient's urine, but also the intestinal reservoir," he said.

"We predict a treatment like this would lead to reduced incidences of recurring UTI in patients suffering from this debilitating, chronic disease for which there is currently no effective cure." Professor Schembri said.

Deforestation in Colombia has been linked to armed conflict and forests' proximity to coca crops, the plant from which cocaine is derived.

A University of Queensland-led study found that conflict between illegal groups and the governmental military forces, proximity to coca plantations, mining concessions, oil wells and roads were all associated with increased deforestation.

UQ PhD student Pablo Negret said the study identified how local drivers of deforestation in tropical countries affect deforestation risk.

"The relationship between conflict and deforestation is far from simple," he said.

"Many factors interact to increase or decrease deforestation risk, but stable governance can help forest retention."

Mr Negret said establishing governmental control where Colombia's largest dissident group, the Revolutionary Armed Forces of Colombia (FARC), was present was essential to avoiding further deforestation.

"We need clear policy and action to stop the uncontrolled deforestation that has occurred since the official peace treaty between the Colombian Government and FARC was signed in 2016.

"Our research shows that conservation projects need to work in parallel with social projects and substituting illegal coca crops.

"One way to do this is to work with the communities in Indigenous reserves and Afro-Colombian collective lands to reach conservation objectives, while fostering economic activity."

The researchers used forest cover information collected from satellites between 2000 and 2015, analysing the association of 17 variables with deforestation patterns in the country.

Fellow study author Professor Martine Maron said by determining the drivers of deforestation the study could help prompt action to save at-risk forests.

"We must stop the full-scale destruction of the world's forests if we are to control the biodiversity and climate crisis," she said.

"And by teasing out the complex factors that threaten forests in a country like Colombia, we may be able to find effective solutions for addressing social and environmental ills across the globe.

"Peace and sustainability make good bedfellows."

The existing astronomical observatories on Maunakea returned to operations this weekend, and it didn't take long for a significant result to be achieved, not only for science, but for assuring the safety of the Earth.

Observations of the near-Earth asteroid 2006 QV89 made on August 11 with the Canada-France-Hawaii Telescope (CFHT) have ruled out any potential future impact threat to the Earth by this asteroid for the next century.

2006 QV89 was discovered on August 29, 2006, with a telescope in Arizona, and observations were only possible through September 8, 2006, when the asteroid became unobservable from telescopes on Earth. The orbit determined from these limited observations had significant uncertainty, and it was not possible to rule out the low probability of the asteroid impacting Earth in the future, possibly as early as 2019. Last month, observations with the European Southern Observatory's Very Large Telescope (VLT) in Chile did not find the asteroid where it would have appeared if it was on a trajectory that would impact Earth this September. This ruled out an impact in 2019, but an impact for 2020 remained a possibility, along with nearly two dozen more over the next hundred years, with eight of those in the next decade.

"There is a big difference between knowing where a hazardous asteroid isn't, and knowing where it is," said David Tholen, astronomer at the University of Hawai'i's Institute for Astronomy, who led the effort to recover 2006 QV89.

This summer provided the first clear opportunity to recover the asteroid since its discovery, but the uncertainty in its position on the sky spanned roughly 30 degrees (60 times the diameter of the moon) in mid-July, growing even larger as the asteroid approached the Earth. "That made the use of a large telescope with a wide-field camera absolutely essential," noted Tholen. Only a fraction of that uncertainty region had been imaged with CFHT on July 14, but operations at the existing telescopes were suspended on July 16, due to the protest on Maunakea.

"We found at least a dozen asteroids in the July 14 data that fell close to the region where 2006 QV89 could have been, but the suspension of operations prevented us from confirming which, if any, of those objects was 2006 QV89," said Tholen.

With access to the Maunakea telescopes blocked, Tholen enlisted the aid of Marco Micheli of the European Space Agency's NEO Coordination Centre in Frascati, Italy. Micheli is a UH graduate who led the effort to rule out the 2019 impact scenario with ESO's VLT. He pointed a telescope in Spain at the position for the best of the candidate objects, but after two hours of data collection, the object at the predicted position could not be convincingly distinguished from electronic noise in the data. It came as a great relief to learn that CFHT would resume operations last weekend.

"Our highest priority target for Saturday night was the best 2006 QV89 candidate, and despite some thin cirrus clouds and a lot of moonlight, we needed only four minutes of data to obtain proof that we had found the right object," said Tholen.

The International Astronomical Union's Minor Planet Center announced the recovery to the world on Sunday, and the impact monitoring services at the Jet Propulsion Laboratory and the University of Pisa/SpaceDys in Italy immediately began crunching the numbers to update the impact predictions. A little over an hour later, Davide Farnocchia of Center of Near-Earth Object Studies at NASA's Jet Propulsion Laboratory in Pasadena reported that all the impact scenarios for the next century had been eliminated.

"This result is only one example of the telescopes on Maunakea protecting Earth by observing and studying the asteroids that enter Earth's neighborhood," said Kelly Fast, manager of the Near Earth Object Observations Program in NASA's Planetary Defense Coordination Office, which supported the observations.

Much in the same way that meteorologists use weather satellite imagery to track hurricanes to determine whether they represent a hazard to people and property, astronomers use telescopes to track asteroids near the Earth to determine whether they represent an impact hazard. "A different asteroid, 2019 NX5, got away from us while the Maunakea telescopes were shuttered, which is regrettable," Tholen said. "We are relieved that we were able to catch 2006 QV89 before our window closed. We are even more relieved that it won't impact the Earth."

Philadelphia, August 13, 2019 - The maturation of skin microbial communities during childhood is important for the skin health of children and development of the immune system into adulthood, but only a few studies have analyzed the microbiota in young children. In a new study, investigators in China found that bacterial genera in children were more similar to those of their own mothers than to those of unrelated women. Their data suggest that the mode of delivery at birth could be an important factor in shaping the child's microbiome. They report their findings in the Journal of Investigative Dermatology, published by Elsevier.

"To date, research into the maternal influence on her child's skin microbiome has been mostly limited to a narrow postpartum window in children younger than one year old and fewer studies have explored the maternal relationship with the child's microflora after infancy," explained lead investigator Zhe-Xue Quan, Ministry of Education Key Laboratory for Biodiversity Science and Ecological Engineering, Institute of Biodiversity Science, School of Life Sciences, Fudan University, Shanghai, China. "Therefore, we expanded the scope of our analysis to include sampling from different body sites and direct comparison to the mother of the child in order to provide novel insights."

Investigators examined the changes in the skin microbiota and analyzed relationships between the skin microbiome and microenvironment as well as between the microbiota composition of children and mothers in 158 children between one and ten years old. The mothers of 50 of these children were randomly selected and recruited to represent different child age groups. Microbiota structures between the children and their mothers were compared using 16S rRNA gene amplicon sequencing. Samples were taken from three skin sites: center of the cheek; one quarter of the length of the forearm from the hand; and the center of the calf. Data for 474 samples (three skin sites per child) were pooled into 36 groups according to age, gender, and skin site.

Sample location and age were the primary factors determining a child's skin bacterial composition, which differed significantly among the three sites. However, there was negative correlation between the abundances of Streptococcus and Granulicatella and age. The relative abundances of most bacterial genera in children were more similar to those of their own mothers than those of unrelated women. The facial bacterial composition of 10-year-old children was strongly associated with whether they were born by Caesarian section or vaginal delivery.

"By analyzing the microbial community structure at three very different skin sites of children, we demonstrated that the skin microbiome is strongly impacted by the surrounding microenvironment and that the alpha diversity of the skin microbiome increases during childhood," noted Professor Quan. "Our results suggest that the bacterial population on a child's skin is to a large extent similar to that of their mothers and is affected in the long term by the way they were delivered at birth. One possible explanation is that the developing skin microbiome interacts with the immune system, which may be educated by exposure to microbes during a critical window early in life. It means that microbial colonization runs in parallel with immune system development."

The skin serves as the body's first line of defense against environmental insult. It hosts approximately ten billion bacterial cells per 1.8 square meters. Skin-associated bacteria constitute a large proportion of the human microbiome and interact with the host immune system via numerous pathways. Depending on the skin microenvironment, certain bacteria can act as either beneficial microbes or opportunistic pathogens.

Researchers at EMBL's European Bioinformatics Institute (EMBL-EBI), the Babraham Institute and collaborators have used the epigenetic clock to explore the molecular mechanisms that may drive ageing in humans. They found one gene, called NSD1, that seems to be closely linked to the process. This type of research could advance our understanding of ageing.

There are different ways of measuring an organism's age. Chronological age is a measure of how long an organism has been alive, while biological age is a measure of how well the organism is functioning on a molecular level.

One useful tool for measuring biological age is the epigenetic clock, proposed first by Trey Ideker, and independently by Steve Horvath in 2013.

What is an epigenetic clock?

An epigenetic clock is a mathematical model that predicts age by measuring DNA methylation levels in different sites across the genome. DNA methylation is a process by which methyl groups are added to the DNA molecule, which can modify the function of a gene without changing its underlying DNA sequence. DNA methylation is essential for the healthy growth and development of cells and it is affected by lifestyle and environmental factors.

Epigenetic clocks can be used to estimate the biological age of a tissue, cell type or organ. By comparing 'DNA methylation age' or biological age with chronological age in different tissues, scientists can gain insights into how ageing works, the factors influencing it, and how ageing is linked to cancer, obesity, Alzheimer's disease and many other conditions.

A promising tool

The researchers examined different datasets - many of them publicly available - of people with developmental disorders, to see whether there were any associations between specific genes and an acceleration of biological age. They found that individuals with a mutation in gene NSD1 had an accelerated biological age according to the epigenetic clock, meaning they were ageing faster at a molecular level.

"The epigenetic clock is the most accurate tool available to measure the ageing process in humans," explains Daniel Elías Martín-Herranz, who recently completed his PhD at EMBL-EBI. "We wanted to 'peer inside' and better understand how it works. Specifically, we wanted to see if we could identify specific genes or proteins from the epigenetic machinery that accelerate or slow down the ageing process. The fact that we found one gene that, when mutated, results in a significant acceleration of biological age is very encouraging. It shows that the epigenetic clock is a promising tool for understanding ageing and that we may unravel the molecular mechanisms that control its ticking rate.

"There is a lot of potential for such studies, but it's also worth noting that they are not possible without access to relevant public datasets. We would like to thank our collaborators who made the data available to us."

Professor Wolf Reik from the Babraham Institute agrees. "Following on from the work with the mouse epigenetic ageing clock two years ago, this paper continues the productive collaboration between the Babraham Institute and EMBL-EBI on mammalian ageing," he says. "It's exciting to see that genes can be identified that may underlie an epigenetic ageing program and that they can make molecular sense. The gene identified here is implicated in ageing in other organisms, and in the regulation of the epigenome during the ageing process."