Culture

Stroke is the third leading cause of death and disability in the United States. More than 87 percent are ischemic strokes, caused by obstruction of one or more cerebral arteries. With limited progress in developing treatments, there is a critical need for neuroprotective agents to effectively treat stroke.

A study from Florida Atlantic University's Schmidt College of Medicine holds promise for a new way to treat stroke using an already FDA-approved drug - granulocyte colony-stimulating factor (GCSF). GCSF enhances blood cellular development and is currently used to treat neutropenia (low white blood cells) caused by chemotherapy and has successfully been used with very few side effects for patients who require bone marrow transplants to stimulate blood cell formation.

The study, published in the Journal of Biomedical Science, is the first to report on the neuroprotective effect of GCSF against autophagy and mitochondrial stress in vivo. The data support the hypothesis that GCSF is one of the few growth factors that can reduce infarction by decreasing endoplasmic reticulum (ER) and mitochondrial stress while improving behavioral performance.

Results showed that GCSF improved neurological deficits that occur in the first few days following cerebral ischemia and improved long-term behavioral outcomes while also stimulating a neural progenitor recovery response. Researchers tested behavioral performance on corner and locomotor tests, used as an indicator of brain injury.

Using a mouse model, researchers investigated the efficacy of GCSF beyond the typical four-hour thrombolytic therapy (tPA) clot-busting drug - the gold standard to treat stroke for global ischemia. They examined the pro-survival mechanisms of GCSF against apoptosis resulting from autophagy, mitochondrial stress and ER stress.

"In recent years, many studies including ours have shown that as an endogenous growth factor and immune system modulator factor, GCSF is beneficial in models of neurological disorders such as stroke and traumatic brain injury," said Jang-Yen (John) Wu, Ph.D., corresponding author, distinguished professor of biomedical science in FAU's Schmidt College of Medicine, and a member of the FAU Brain Institute (I-BRAIN). "Although the anti-apoptotic activity of GCSF is reported in global cerebral ischemia, this mechanism has not been fully explored."

Researchers used a mechanism-based therapeutic approach for stroke first to examine the connection of mitochondrial, autophagy and ER stress inhibition in the protective action of GCSF and then to analyze relevant ER stress pathways in the bilateral common carotid artery occlusion (BCAO) model of stroke. They confirmed the neuroprotection of GCSF gene therapy in the BCAO mouse stroke model by a decrease of dynamin-related protein (DRP1), a marker of mitochondrial stress, in the frontal and middle brain of the GCSF treated group.

The initial dose of GCSF was administered 24 hours post-BCAO and then followed by a single application of the same dose for another three days for a total of four days of administration. Researchers examined behavior and used immunoblotting to analyze key proteins in ER stress, autophagy and mitochondrial stress-induced apoptosis. BCAO mice receiving GCSF protein showed significantly less asymmetric turning in the corner test than BCAO mice without GCSF. In the behavioral assays, GCSF elicited increased locomotor sensitization verified by greater activity in the locomotor activity test, demonstrating the neuroprotective properties of the drug.

"More than 15 million people worldwide suffer from stroke and our study provides new and important insights into GCSF induced protection as it relates to ER stress and mitochondrial stress activated apoptosis, " said Howard Prentice, Ph.D., corresponding author, a professor of biomedical sciences in FAU's Schmidt College of Medicine, and a member of FAU's I-BRAIN. "Future research will need to focus on uncovering the complete mechanisms by which GCSF retains the ER and mitochondrial homeostasis."

Wu and Prentice have been developing GCSF as a therapeutic method to replenish new brain cells because of its ability to preserve the central nervous system, suppress cell death and at the same time elicit neurogenesis as well as angiogenesis. GCSF works the same way for other neurological diseases such as Parkinson's disease due to its neuroprotective properties.

Wu and Prentice have received a patent with the U.S. Patent Office (USPTO) for the neuroprotective properties of GCSF in stroke. Wu and Dipnarine Maharaj, M.D., Maharaj Institute of Immune Regenerative Medicine, also received a patent from the USPTO for use of GCSF for treatment of Parkinson's disease. A patent application with the USPTO also has been filed by WU for the neuroprotective and neurogenesis properties of GCSF gene therapy for treatment of stroke and Alzheimer's disease.

A team of researchers led by Yale-NUS College Professor of Science (Environmental Studies) Stephen Pointing has discovered a link between two different ecosystems, continental Australia and the Great Barrier Reef, due to airborne microbes that travel from the former to the latter. The finding showed that the health of these two ecosystems are more interconnected than previously believed, hence holistic conservation efforts need to span different ecosystems.

Microbes are fundamental to the health of ecosystems, playing roles such as providing energy, oxygen and carbon to other organisms and recycling nutrients from other organisms' waste products. Prof Pointing's team recently published two papers in established scientific journals Nature Microbiology and The ISME Journal (a Nature partner journal) on the role of microbes in connecting ecosystems, specifically how microbes from one ecosystem can have significant effects on the well-being of a completely different ecosystem.

The team's success has grown from development of a new apparatus and methodology to accurately study microbes in air - something that has never been previously done due to the low abundance of airborne microbes and how quickly they degrade once captured for sampling. The team's first paper, published in the June 2019 issue of the peer-reviewed journal Nature Microbiology, revealed this method and highlighted how some microbes survive better than others during transport in the air over the Southern Ocean.

Their second paper, published in The ISME Journal in November 2019, focused on the interconnectedness between earth, sea, and sky. Prof Pointing and his team observed that vital microbes essential for the flourishing of the Great Barrier Reef are present in the air, and are in fact transported through the air from other ecosystems like the Australian continental landmass.

While there has long been speculation that airborne microbes are absorbed into the Reef, this was the first study that confirmed the existence of such a link. Genetic testing highlighted that the most abundant shared species in the air and coral played important functional roles in both coral and soil ecosystems, suggesting that the atmosphere acts to connect these ecosystems by transporting microbes essential to the health of each between them.

Prof Pointing, who is also Director of the Division of Science at Yale-NUS, said, "In order to make effective policy decisions to protect our natural environment, it is vital to have reliable data on the level of connectivity between different ecosystems. The role that the air plays in ecosystem connectivity has not been appreciated until now. Our research provides empirical evidence that distant ecosystems on land and at sea are connected by the multitude of microorganisms such as bacteria and fungi that are transported in air currents between these ecosystems. Because microorganisms are so important to ecosystem health, any change to their transport patterns can have potentially catastrophic environmental impacts."

The team's third paper, specially commissioned by Nature Microbiology and published on 28 January 2020, is a position paper setting the direction of research in the field for the next five to 10 years. It explores ways in which human activity affects how microbes are transported in air, such as how pollution particles in the atmosphere can kill microbes, or disrupt or alter their transport patterns. It also explores the potential of some microbes to detoxify toxic polycyclic aromatic hydrocarbons (PAH) compounds in the air, which are known to cause cancer in humans, although further research is required to determine the feasibility of such an endeavour.

Regular consumers of popular caffeinated energy drinks may need help kicking the habit.

New research at Flinders University in Australia, published in the international journal PLOS One, put a form of cognitive incentive retraining - a form of computer-based training aimed at reducing decision-making biases in purchasing energy drinks - to the test on more than 200 regular consumers of energy drinks aged between 18 and 25.

With the powerful marketing by brands such as Red Bull, V, Mother and Monster, the Australian Research Council-funded research is focusing on finding ways to reduce or combat the rising levels of energy and soft drink consumption.

The training aimed to reduce energy drink consumption by either reducing the extent to which energy drink cans capture the attention of regular energy drink consumers (attentional bias) or reducing the tendency for these consumers to approach energy drinks (approach bias).

"We are keen to expand these trial methods on consumers to combat through their attentional and approach bias towards energy drinks," says Mind, Body and Cognition research leader Professor of Psychology Eva Kemps.

"By giving participants some simple techniques, we examined whether they were prepared to moderate their bias toward choosing energy drinks over soft drinks and more healthy options, and perhaps reduce consumption before they become addicted."

While an occasional energy drink is not problematic, it has been reported that some individuals consume four or more energy drinks a day. Excessive intake can lead to the development of intolerance and serious withdrawal symptoms upon cessation.

Energy drink consumption is rising, with one estimate of it doubling in the past 10-15 years to more than 11.5 billion litres a year globally, with a majority of consumers young adults.

Side-effects of excessive intake of the high caffeine drinks, with other stimulants taurine, guarana and ginseng, can lead to a range of negative physical and mental health consequences, including anxiety, depression, or even stress PTSD and substance abuse.

Reported adverse effects range in severity from headaches to heart palpitations, renal failure, seizures, and in rare cases death.

The 226 volunteers in the study - many of them university students - said they consumed 1 or more cans a fortnight, for an energy boost, to relieve fatigue, improve sporting or academic performance, or as a party mixer with alcohol.

The training aimed to reduce energy drink consumption by tackling either the extent to which the products capture the attention of regular energy drink consumers (attentional bias) or the tendency for these consumers to approach energy drinks (approach bias).

Attentional and approach biases have been demonstrated for a range of appetitive substances, including alcohol, tobacco, drugs and chocolate.

The research is part of an ARC Discovery Project (2018-21) looking at the role of automatic processing in the (over)consumption of soft drinks, and follows previous attentional retraining research to reduce food cravings and promote healthier eating and weight loss.

Urinary tract infections (UTI's) are painful and usually short lived - but for millions of people this is simply not the case.

Low levels of infection can be found long after it's thought to have cleared, and research suggests this could be an unknown, but leading cause of chronic bladder dysfunction.

But the fight against pain, discomfort and a constant urge to urinate has taken a step forward with scientists identifying how the immune systems defence against bladder infection causes nerves to magnify the sensations felt by patients.

Flinders University researchers at SAHMRI in collaboration with Griffith University on the Gold Coast, have analysed how the immune system responds to urinary tract infections and the direct link this response has to magnifying bladder pain.

Clinical Pharmacology Research Fellow & Head of Bladder Research, Dr Luke Grundy, says understanding how nerves in the bladder transmit different sensations to the brain could potentially help limit bladder dysfunction in overactive bladder patients.

"We believe that chronic pain and bladder dysfunction are a failure of these nerves to reset after inflammation, so by understanding how these nerves function with a UTI and what causes them to become more sensitive over time, we can develop effective treatments."

"This is important, as many people diagnosed with an overactive bladder, a disorder that is currently considered to have no specific cause, have a history of urinary tract infections, and have been shown to have persistent low levels of UTI. This may lead to enhanced patient diagnosis and alternative treatment options for those suffering with an overactive bladder."

With the number of antibiotic resistant UTI's growing globally each year, many can no longer be treated with common antibiotics despite the fact one in every two women will develop a UTI in their lifetime.

Dr Grundy says this study provides new information into how UTI causes hypersensitivity of the nerves that carry sensation from the bladder to the brain, resulting in the symptoms of urinary frequency, urgency, and pelvic or suprapubic pain.

"Our study provides a new understanding of why some overactive bladder patients do not respond to traditional medications and continue to suffer in silence, and opens the door for the development of more specific and effective treatments in the future".

Chaired by two of Flinders University's renowned gut researchers, Professor Nick Spencer and Professor Stuart Brierley, a week long conference will delve into the latest gut / brain breakthroughs at the annual meeting of the Federation of Neurogastroenterology and Motility, from 24 to 28 March 2020.

The 4th Meeting of the Federation of NeuroGastroenterology and Motility is hosted by the Australasian NeuroGastro­enterology and Motility Association Inc, the American NeuroGastro­enterology and Motility Society, the Asian NeuroGastro­enterology and Motility Association, the European Society of Neurogastro­enterology and Motility, and the Latin-American Society of Neurogastroenterology.

Hokkaido University scientists are getting closer to understanding how a rare hereditary disease impairs the skin's barrier function, which determines how well the skin is protected.

The gene mutation that causes ichthyosis prematurity syndrome--characterized by premature birth; difficulty breathing shortly after birth; and very dry, thick and scaly skin--dramatically reduces the synthesis of acylceramide, a key skin lipid in forming the skin barrier. The discovery provides us with a better understanding of the condition, which is currently untreatable.

Ichthyosis prematurity syndrome is caused by a gene mutation in fatty acid transporter member 4 (FATP4), but the details of how the mutation impairs the skin's barrier function, leading to dry, scaly skin, has been unclear.

Molecular biologist Akio Kihara of Hokkaido University led a team of researchers in Japan and Germany to investigate the molecular mechanisms behind the disease. When they disrupted the FATP4 gene in mice, the offspring had rigid skin, low body weight, and died within an hour of birth. Water loss from their skin was more than four times higher than normal mice, and their skin was delicate, susceptible to staining.

Investigations revealed microscopic changes in the skin similar to those that occur in people born with ichthyosis prematurity syndrome. These included abnormalities in the outermost layer of the epidermis.

Upon further analysis, the researchers found a group of skin lipids called acylceramides were significantly reduced in the mice, having only 10% of the normal amount. Acylceramide plays a pivotal role in making the skin barrier largely impermeable to pathogens, allergens and chemicals. It also prevents water loss from the body.

Similarly, when the FATP4 gene expression was decreased in human keratin-producing skin cells, they showed a 40% reduction in acylceramide levels compared to normal human keratinocytes.

The evidence suggests FATP4 plays a critical role in synthesizing acylceramides in both humans and mice, providing the missing link in the synthetic pathway. "Our findings help explain acylceramide synthesis and, with further research, could help in the development of treatments for ichthyosis prematurity syndrome and other skin barrier-related symptoms such as atopic dermatitis," says Akio Kihara.

Why do BMW and Audi owners often seem to drive like idiots? Is it the car that makes them behave aggressively behind the wheel, or are specific types of people drawn to such cars as well being more likely to break traffic regulations? New research at the University of Helsinki provides some answers.

Jan-Erik Lönnqvist (link), professor of social psychology, had made the same observation in traffic as many others: Audi and BMW drivers seemed much more likely to ignore traffic regulations and drive recklessly.

"I had noticed that the ones most likely to run a red light, not give way to pedestrians and generally drive recklessly and too fast were often the ones driving fast German cars," says Lönnqvist of the University of Helsinki's Swedish School of Social Science.

Previous research has also confirmed that the drivers of expensive cars are more likely to break traffic regulations. This phenomenon has been explained with the common assumption that wealth has a corrupting effect on people, resulting, for example, in high-status consumption and unethical behaviour in various situations.

Lönnqvist approached the question from a different angle by asking whether specific types of people are drawn to high-status cars regardless of their financial assets and also have a tendency to break traffic laws.

To gain answers, researchers carried out a study of Finnish consumers. A total of 1,892 car owners answered not only questions about their car, consumption habits and wealth, but also questions exploring personality traits. The answers were analysed using the Five?Factor Model, the most widely used framework for assessing personality traits in five key domains (openness, conscientiousness, neuroticism, extraversion, agreeableness).

The answers were unambiguous: self-centred men who are argumentative, stubborn, disagreeable and unempathetic are much more likely to own a high-status car such as an Audi, BMW or Mercedes.

"These personality traits explain the desire to own high-status products, and the same traits also explain why such people break traffic regulations more frequently than others," says Lönnqvist.

He points out that money is, of course, necessary to buy high-status products, which is why rich people are more likely to drive high-status cars.

"But we also found that those whose personality was deemed more disagreeable were more drawn to high-status cars. These are people who often see themselves as superior and are keen to display this to others."

Conscientious people also drawn to high-status cars

One of the more unexpected results was that another personality type is also drawn to high-status cars: the conscientious. People with this type of personality are, as a rule, respectable, ambitious, reliable and well-organised. They take care of themselves and their health and often perform well at work.

"The link is presumably explained by the importance they attach to high quality. All makes of car have a specific image, and by driving a reliable car they are sending out the message that they themselves are reliable," Lönnqvist explains.

The link between conscientious personality traits and interest in high-status cars was found among both men and women. In contrast, the connection between self-centred personality traits and high-status cars was only found among men, not women. Lönnqvist has no clear answer as to why this is the case. One possibility is that cars simply do not have the same significance as status symbols for women.

Few researchers have explored the consumption of luxury products using the Five-Factor Model, but Lönnqvist believes that more research could lead to an increased understanding of the reasons behind this kind of consumption.

"It would be great if consumers had other, sustainable ways of showing their status rather than the superficial consumption of luxury goods that often has negative consequences. We are already seeing that driving an electric car is becoming something of a status symbol, whereas SUVs with their high emissions are no longer considered as cool."

The new mitochondrial DNA (mtDNA) variant drastically speeds up the disease progression in a mouse model of GRACILE syndrome. This discovery provides a new tool for studies of mitochondrial diseases.

GRACILE syndrome, a member of the Finnish disease heritage, is a severe neonatal metabolic disease caused by a point mutation in the nuclear BCS1L gene.

About 10 years ago, Professor Vineta Fellman's group at Lund University generated GRACILE patient mutation-carrying mice to investigate disease mechanisms and develop therapies. Later on, the researchers exported the mice to Helsinki and maintained the mutants in a slightly different genetic background.

Astonishingly, the mutant mice lived five times longer in Helsinki than in the original strain in Lund. By whole genome sequencing, a novel point mutation was discovered in the mitochondrial DNA (mtDNA) of the short-lived Lund strain.

The work, carried out at the Folkhälsan Research Center and the University of Helsinki, revealed that, due to an extremely unlikely coincidence, a random mutation in the mt-Cyb gene had appeared, affecting exactly the same part of mitochondria as the GRACILE mutation and worsening the disease of the mice.

According to computer simulations and spectroscopic measurements performed by collaborators in Finland and Poland, the amino acid change identified in the mice slows down the movement of a part of Rieske protein needed in electron transfer during cellular respiration. The researchers say that this is the first time such an interaction between the nuclear and mitochondrial genomes has been delineated down to almost atomic level.

Docent Jukka Kallijärvi tells that the discovery is an extreme example of an unexpectedly large effect of the genetic background on the course of an inherited disease.

"Modifying the nuclear genome has been commonplace in experimental animal models for a long time, but we are yet to develop a technique with which to transfer mutations in a targeted manner to as many as thousands of copies of the mitochondrial genome in every cell. Our unique mouse model, which carries the spontaneous mtDNA variant, could prove a valuable tool in studies of both mitochondrial diseases and the function of mitochondria in general," Kallijärvi notes.

The otherwise wild-type mice carrying the newly discovered variant appear healthy, but their metabolism is not entirely normal. An equivalent mutation is found naturally in the three-toed sloth species of South America, an animal with an extremely slow metabolism and an energy-poor diet.

"It is interesting to speculate that the mtDNA variant may be beneficial in certain conditions, which is why it occurs in nature. In further studies, we are interested in the effect of this variant, which subtly affects mitochondrial functions, on metabolism and ageing in mice", Kallijärvi says.

Researchers at the RIKEN Center for Integrative Medical Sciences (IMS) in Japan and colleagues at Osaka University have found genetic variations in humans related to specific dietary habits. Published in Nature Human Behaviour, the genome-wide association study found 9 gene locations associated with eating and drinking foods like meat, tofu, cheese, tea, and coffee. Among them, three were also related to having particular diseases such as cancer or diabetes.

Genome-wide association studies are usually carried out when scientists want to know if a disease is related to a specific genetic variation. To do this, they group hundreds of thousands of people depending on whether or not they have the disease and compare the genomes across groups. They scan the whole genome looking at variations in DNA called single nucleotide polymorphisms (SNPs). If they find an SNP that is consistently associated with the disease group, they can say that people with that genetic variation might be at risk for the disease.

Rather than first looking at diseases, the RIKEN team looked at dietary habits. They wanted to find out if there are any specific genetic variations that make people "at risk" for habitually eating certain foods. "We know that what we eat defines what we are, but we found that what we are also defines what we eat," says Yukinori Okada, Senior Visiting Scientist at RIKEN IMS and professor at Osaka University.

Using genetic data from over 160,000 Japanese people who had filled out a food-frequency questionnaire, they found 9 genetic loci--positions on chromosomes--that were associated with consuming coffee, tea, alcohol, yogurt, cheese, natto (fermented soy beans), tofu, fish, vegetables, or meat. Initial diet-genome associations showed that the ingredients mattered. For example, they found positive genetic correlations between eating cheese and eating yogurt.

Overall, the study found 10 diet-genome associations that have never been reported before; four related to coffee and three related to alcohol. One SNP already known to be associated with coffee and alcohol was found to be related to almost all of the dietary items that were examined. "We found that this particular variation in a single DNA nucleotide at the ALDH2 gene was related to consuming less alcohol, natto, tofu, and fish, and at the same time, related to consuming more coffee, green tea, milk, and yogurt," says Okada.

Just as the genome comprises all the genetic material of an organism, the phenome comprises all the possible observable traits, known as phenotypes. In order to determine whether any of the SNPs associated with diet were also related to diseases, the researchers performed a phenome-wide association study. The results indicated that six of the SNPs were related to at least one disease phenotype, including several types of cancer as well as type-2 diabetes.

As with genome-wide association studies for diseases, the current results can benefit society in the long run. As Okada explains, "by estimating individual differences in dietary habits from genetics, especially the 'risk' of being an alcohol drinker, we can help create a healthier society."

The reprocessing of spent nuclear fuel could become safer and more efficient in future after researchers found a way to modify the structure of molecules to remove radioactive materials.

The research is published in a recent edition of the influential Chemistry - A European Journal (7th January 2020) and is described by the editors of the journal as being of great significance.

The reprocessing operation

Nuclear energy offers a clean, low carbon source of electricity and is becoming a growing part of the energy provision in many countries worldwide. About 10% of the world's electricity is produced by nuclear power. However, nuclear power stations need fuel to produce electricity and this fuel becomes less efficient over time, and needs to be replaced after approximately five years.

Spent fuel is still highly radioactive and generates intense amounts of heat. Before being reprocessed or disposed of, it needs to be submerged in specialist cooling ponds under more than 40 feet of water. The water provides shielding from radioactivity and is continuously cooled to remove the intense heat from the fuel rods.

It takes more than a year for the fuel rods to cool to a point where they can be reprocessed to remove the uranium and plutonium elements, which can then be reused as fuel.

However, the elements americium, curium and neptunium, which are called the minor actinides, are still present and produce most of the heat and radioactivity of the remaining spent fuel. In addition, these elements remain highly radioactive for approximately 9,000 years, which makes the long-term storage and disposal of spent fuel extremely difficult to manage safely.

If these harmful radioactive elements could be removed it would significantly improve the safety and sustainability of nuclear energy because the remaining spent fuel would remain radioactive for approximately 300 years, which is a much more manageable timeframe.

Modifying the molecules

Molecules called triazines are capable of removing (or extracting) these harmful elements from spent nuclear fuel in a highly selective way, and have been known for some time. The researchers aimed to find out how modifying a certain part of these molecules could influence their ability to bind and extract these minor actinides at the molecular level. The knowledge and insights gained could be exploited to design better, more efficient molecules for spent nuclear fuel reprocessing in future.

The researchers changed the size of the aliphatic rings in the established benchmark molecules from 6-membered rings to 5-membered rings. They found that this small but subtle change had unexpected effects on how efficiently these molecules bind and extract the minor actinides compared to the benchmark molecules. The exact reasons for these effects were then determined at the molecular level using a range of experimental techniques.

Dr Frank Lewis, senior lecturer in organic chemistry in Northumbria University's Department of Applied Sciences said: "The findings are significant as they could allow better molecules to be designed in a more rational way, rather than simply by trial and error.

"The knowledge and insights we have gained by tuning the cyclic aliphatic part of these molecules could pave the way for the rational design of improved actinide selective ligands for reprocessing spent nuclear fuels. Modifying these molecules in different ways to improve their extraction properties could make future reprocessing more efficient and could be essential if they are to be used industrially in future.

"We believe that these results are of great importance to the field of nuclear energy, and this has been confirmed by the panel who reviewed the paper before publication."

Significant results

The editorial team at Chemistry A European Journal wrote to Dr Lewis and his colleagues saying: "According to the evaluation of referees, the results reported in this article are of great significance. Less than 20% of manuscripts receive such a positive review." The paper was also selected by the editors as a 'Hot Paper', and was highlighted in a Frontispiece graphic artwork.

Workers in many industries inadvertently bring home toxic contaminants, endangering the health of their families. Those at greatest risk are the least likely to benefit from current regulations.

A new review by researchers from the Boston University School of Public Health (BUSPH) and the Harvard T.H. Chan School of Public Health calls for recognition of "take-home" exposures--exposures to toxic contaminants inadvertently brought home from a family member's work--as a public health hazard. The review was published in Annals of Work Exposures and Health.

Take-home exposures often fall into a regulatory blind spot, says corresponding author Dr. Diana Ceballos, assistant professor of environmental health at BUSPH.

"Although OSHA [Occupational Safety and Health Administration] does regulate some key workplace exposures that can become take-home exposures, such as asbestos, lead, and pesticides, often regulations are not up to date or enforced enough to be protective of health at the family level," she says.

Ceballos says cases tied to take-home exposures are all too common. When she was an industrial hygienist at the Center for Disease Control and Prevention (CDC), she worked on several such cases, including one where two young children had been poisoned by lead from their father's work at an electronics recycling facility. Grinding up the lead glass from cathode ray tubes, the father was not exposed to enough lead to immediately affect the health of a grown man, but the lead dust that came home with him on his body and clothing quickly affected the health of his young daughter and son. "The father had only worked at this facility for about a year when his kids' physician found they were poisoned," Ceballos says. "Within just a few years, the kids exhibited textbook health effects of lead, including behavioral, developmental, and learning difficulties."

In their review of research related to take-home exposure, Ceballos and her colleagues make the case that the issue is not simply a matter of worker carelessness, a view that has been expressed with the simplistic--and dehumanizing--expression "soiling one's own nest." Instead, they argue, take-home exposures are part of much larger and more complex systemic issues, where workers and their families face myriad challenges to their health and safety at work and at home.

The authors write that workers who are most likely to take home exposures are often--and increasingly--not only low-income, but also in precarious employment situations, such as contractors working in construction, and undocumented immigrants. These workers rarely benefit from safety regulations or employment protections, and could easily lose their jobs (and even face deportation) if they raise concerns about their working conditions.

Because of economic inequality, racist housing practices, and other systemic factors, the authors write, the health risks that these vulnerable workers and families face from workplace exposures are also compounded by being more likely to live in unsafe and contaminated housing, and in communities that face broader environmental injustices. A child may not be exposed to dangerous levels of a toxic contaminant from a parent's workplace, from their home, or from their neighborhood, but the low levels of exposure from two or three of these sources together can be enough to harm their development, the authors note.

"To prevent the chronic, low-level, take-home exposures that are particularly harmful for developing children, a multi-tier intervention approach including interventions at the workplace, home, and community levels are needed," Ceballos says.

Such interventions would include not just better workplace regulations, but also efforts to improve the housing conditions of workers' families and take on environmental injustices in their neighborhoods. The authors also propose a role for schools to screen children for the effects of exposures--whether from their parents' workplaces, housing, neighborhood, or all of the above.

Despite the immense progress in the field of AI in recent years, we are still very far from human intelligence. Indeed, if current AI techniques allow to train computer agents to perform certain tasks better than humans when they are trained specifically for them, the performance of these same agents is often very disappointing when they are put in conditions (even slightly) different from those experienced during training.

The human being is capable of adapting to new situations very effectively by using the skills he has acquired throughout his life. For example, a child who has learned to walk in a living room will quickly learn to walk in a garden as well. In such a context, learning to walk is associated with synaptic plasticity, which modifies the connections between neurons, while the rapid adaptation of walking skills learned in the living room to those needed to walk in the garden is associated with neuromodulation. Neuromodulation modifies the input-output properties of the neurons themselves via chemical neuromodulators.

Synaptic plasticity is the basis of all the latest advances in AI. However, no scientific work has so far proposed a way to introduce a neuromodulation mechanism into artificial neural networks. This result, described this week in the journal PLOS ONE, is the result of an extremely fruitful collaboration between neuroscientists and artificial intelligence researchers at the University of Liège developing intelligent algorithms: two PhD researchers, Nicolas Vecoven and Antoine Wehenkel, as well as two professors, Damien Ernst (specialist in artificial intelligence) and Guillaume Drion (neuroscientist).

These ULiège researchers have developed a completely original artificial neural network architecture, introducing an interaction between two sub-networks. The first one takes into account all the contextual information concerning the task to be solved and, on the basis of this information, neuromodule the second subnetwork in the manner of the brain's chemical neuromodulators. Thanks to neuromodulation, this second sub-network, which determines the actions to be performed by the intelligent agent, can therefore be adapted extremely quickly to the current task. This allows the agent to efficiently solve new tasks.

This innovative architecture has been successfully tested on classes of navigation problems for which adaptation is necessary. In particular, agents trained to move towards a target, while avoiding obstacles, were able to adapt to situations in which their movement was disrupted by extremely variable wind directions.

Prof. Damien Ernst: "The novelty of this research is that, for the first time, cognitive mechanisms identified in neuroscience are finding algorithmic applications in a multi-tasking context. This research opens perspectives in the exploitation in AI of neuromodulation, a key mechanism in the functioning of the human brain."

New antiviral materials made from sugar have been developed to destroy viruses on contact and may help in the fight against viral outbreaks.

This new development from a collaborative team of international scientists shows promise for the treatment of herpes simplex (cold sore virus), respiratory syncytial virus, hepatitis C, HIV, and Zika virus to name a few. The team have demonstrated success treating a range of viruses in the lab - including respiratory infections to genital herpes.

The research is a result of a collaboration between scientists from The University of Manchester, the University of Geneva (UNIGE) and the EPFL in Lausanne, Switzerland. Although at a very early stage of development, the broad spectrum activity of this new approach could also be effective against newly prevalent viral diseases such as the recent coronavirus outbreak.

So called 'virucidal' substances, such as bleach, are typically capable of destroying viruses on contact but are extremely toxic to humans and so cannot be taken or applied to the human body without causing severe harm. Developing virucides from sugar has allowed for the advent of a new type of antiviral drug, which destroys viruses yet is non-toxic to humans.

Current antiviral drugs work by inhibiting virus growth, but they are not always reliable as viruses can mutate and become resistant to these treatments.

Using modified sugar molecules the team showed that the outer shell of a virus can be disrupted, thereby destroying the infectious particles on contact, as oppose to simply restricting its growth. This new approach has also been shown to defend against drug resistance.

Publishing their work in the journal Science Advances the team showed that they successfully engineered new modified molecules using natural glucose derivatives, known as cyclodextrins. The molecules attract viruses before breaking them down on contact, destroying the virus and fighting the infection.

Dr Samuel Jones, from The University of Manchester and a member of the Henry Royce Institute for Advanced Materials, jointly led the pioneering research with Dr Valeria Cagno from the University of Geneva. "We have successfully engineered a new molecule, which is a modified sugar that shows broad-spectrum antiviral properties. The antiviral mechanism is virucidal meaning that viruses struggle to develop resistance. As this is a new type of antiviral and one of the first to ever show broad-spectrum efficacy, it has potential to be a game changer in treating viral infections." said Sam.

Professor Caroline Tapparel from the University of Geneva and Prof Francesco Stellacci from EPFL were both also senior authors of the study. Prof Tapparel declared: "We developed a powerful molecule able to work against very different viruses, therefore, we think this could be game changing also for emerging infections."

The molecule is patented and a spin-out company is being set up to continue pushing this new antiviral towards real-world use. With further testing the treatment could find a use in creams, ointments and nasal sprays or other similar treatments for viral infections. This exciting new material can work to break down multiple viruses making for cost-effective new treatments even for resistant viruses.

The number of plant species that extract organic nutrients from fungi could be much higher than previously assumed. This was discovered by researchers from the University of Bayreuth and the University of Copenhagen through isotope investigations on Paris quadrifolia, otherwise known as Herb Paris or True Lover's Knot. This forest-floor plant, which is widespread in Europe, is regarded in botany as a prototype for plants that have a specific exchange relationship with fungi, which in fact accounts for around 40 percent of all plant species. In "The New Phytologist" journal, the scientists report on their surprising results.

The research results show that the ecological importance of fungi is still considerably underestimated. "If it is confirmed that far more plant species than previously known obtain part of their organic nutrients from fungi, fungi will be shown to have a major impact on the biodiversity and function of ecosystems. Programmes and measures in nature conservation and environmental protection should therefore also increasingly consider fungi", says Philipp Giesemann M.Sc., the lead author of the study, who is currently doing his doctorate in biology at the University of Bayreuth and has been awarded a scholarship from the Elite Network of Bavaria (ENB).

Underground networks

Well over 90 percent of all plant species are linked to fungi via their underground root systems. Such a symbiosis of plants and fungi is called "mycorrhiza". Very often it is advantageous for both partners: While fungi supply the plant with minerals and water, the plant supplies local fungi with carbonaceous nutrients it has previously produced by photosynthesis. However, it also happens that plants "unfairly" exploit the fungi cross-linked with them. They then extract organic nutrients from their fungal partners instead of producing them themselves through photosynthesis. These nutrients have been transferred from trees to fungi, for example, and are now being tapped by a third plant using an underground root network. Such plants are therefore called "mycoheterotrophs". The best known example are the orchids: Because they can be partially or completely fed by fungi via underground root networks, they are not exclusively dependent on photosynthesis. Hence, they can thrive even in the darkest forests.

However, of the 80 per cent of all green plant species that utilize a form of mycorrhiza, researchers have up to now assumed it to always involve "fair" exchange relationships between plants and fungi. In this "arbuscular mycorrhiza" - so it was believed - the green plants are always completely autotrophic partners, producing vital organic nutrients themselves and partially releasing them to their fungal partners. But the studies on Paris quadrifolia now published refute this general assumption. The Bayreuth researchers were able to prove beyond doubt that this plant obtains part of its carbon-rich nutrients from fungal partners.

Herb Paris as prototype

"This finding could have far-reaching consequences for botany", explains the Bayreuth biologist Prof. Dr. Gerhard Gebauer, who coordinated the research work. "This is because experts distinguish between two forms of arbuscular mycorrhiza, each of which is used by about 40 percent of all plant species. In a sense, Herb Paris is considered a model for one of these two forms of plant symbiosis with fungi. In this respect, it is a prototype for far more than a third of all plant species. This raises the question of whether the number of plant species living at the expense of fungi is possibly much higher than previously thought. We have already discovered that another plant utilizing arbuscular mycorrhiza, the wood anemone, also enjoys a mycoheterotrophic way of life," said the biologist from Bayreuth.

In parallel, the researchers have also carried out analogous investigations on Arum maculatum, also known as Cuckoo Pint or Wild Arum. This plant is regarded as a prototype for the second form of arbuscular mycorrhiza, which is preferred by numerous agricultural crops. It behaves in a clearly autotrophic way and supplies itself by photosynthesis with all the carbonaceous nutrients it needs.

Background

The research results on the mycoheterotrophic lifestyle of Herb Paris are based on isotope studies. It has long been known that plants supplied with carbon and nitrogen by fungi have a comparatively high proportion of heavy carbon, hydrogen, and nitrogen isotopes. In autotrophic plants the proportion of these isotopes is lower. The Laboratory for Isotope Biogeochemistry at the Bayreuth Center for Ecology and Environmental Research (BayCEER) is specialized in determining nutrient fluxes within ecosystems using isotopes.

These days, many people are concerned about plastic waste; however, the convenience, mechanical properties and cost of plastic food packaging are hard to beat. But now, a growing number of innovators and entrepreneurs are trying to make edible packaging and tableware from foods like seaweed, milk proteins and potato starch, according to an article in Chemical & Engineering News (C&EN), the weekly newsmagazine of the American Chemical Society, produced in collaboration with ACS Central Science. 

Edible films, wrappers and straws have already found a specialty market and are starting to attract attention from larger food and beverage companies, according to freelance contributor Prachi Patel. At the 2019 London Marathon, the start-up company Notpla handed out sports drink pods, packaged in seaweed-based capsules, to thirsty runners. Although the packaging is safe to swallow, runners can choose to spit out the film. In that case, it biodegrades in only 4-6 weeks. The New York-based company Loliware is making seaweed- and algae-based straws that feel like plastic for 24 hours after getting wet. Once used, they can be eaten, or they will degrade in the environment within 2 months. Marriott Hotels and alcoholic-beverage firm Pernod Ricard have already started using the straws.

Although edible packaging is gaining ground, challenges remain. Some worry about the hygiene of eating packaging that has been touched or exposed to germs during transport or while sitting on the shelf. Experts agree that edible packaging will require an outer layer, but these materials could also be made from compostable or sustainable materials, such as paper. Another obstacle is public acceptance: will people eat something that is usually thrown away? Consumers could perhaps be convinced if the packaging includes nutrients, such as vitamins or proteins, or just tastes good. And finally, improvements in heat and moisture stability need to be made before edible packaging can enjoy widespread use.

Tougher early lives could help captive-bred game birds develop survival skills for adulthood in the wild, new research suggests.

Captive-bred pheasants and partridges start life in unnatural conditions, in sheds and pens with no adult birds, more densely packed and eating different food than they would in the wild.

They may grow well and avoid disease and predators for the first six to eight weeks, but then they are released into the wild - and they may be unprepared for this dramatic change in their living conditions.

University of Exeter scientists, working with Dr Francesco Santilli from the Italian Hunting Federation, say the current approach may be cruel while trying to be kind.

They say a "careful balance" is needed between conditions essential to maintain bird welfare in captivity and the welfare of birds once they are released.

More than 110 million game birds - mostly pheasants and partridges - are reared and released each year worldwide for recreational hunting.

"We know a vast amount of about the welfare of other captive-bred animals, such as chickens," said Dr Mark Whiteside, of the University of Exeter.

"However, our review of the existing research reveals that we know almost nothing about how captive rearing affects the welfare of game birds after they're released into the wild.

"We do know that captive-reared pheasants are much more likely to be killed by predators or suffer starvation after release than wild birds.

"We can't be sure why this is the case. It might be because their early life conditions don't allow them to develop the right behaviours to survive.

"We've been studying what changes would help reduce this problem and it appears that 'mimicking' natural conditions in captivity could promote more natural behaviour and make birds better able to cope with natural hazards."

Dr Whiteside added: "Some of these changes may be good for birds both before and after release. Adding perches allows chicks to escape harassment by other chicks and also teaches them to roost off the ground at night - a good way to avoid predators in the wild.

"However, other changes - such as exposing chicks to imitation predators or making the food supply 'unpredictable' by changing the timing and location of feeding within the chicks' enclosure - might be more realistic of conditions in the wild, but might also increase stress and reduce the short-term welfare of young birds in captivity.

"For the best possible welfare, we need to find the right balance."

The researchers say the impact of any changes on later-life welfare would have to be tested, and the possible financial costs have not yet been assessed.