Culture

When the famous Spanish physician Santiago Ramón y Cajal looked through his microscope in 1910, he discovered irregular and "transparent lumps" that appeared throughout the nucleus of a neuron. What these nuclear speckles are all about is still largely unclear, even though the biological and medical sciences have experienced several revolutions since then. "Even though we know quite a bit about their function, we didn't know how nuclear speckles originate, i.e. what their core consists of," says Tuçe Akta from the Max Planck Institute for Molecular Genetics.

A Berlin team of scientists led by the Max Planck Research Group leader now identified the molecules that form the scaffold of nuclear speckles.The two proteins in question are SON and SRRM2, which are present in different variations throughout the entire animal kingdom. Both molecules are involved in the processing of RNA, which is produced when genes are transcribed. Without these proteins, the speckles dissolve.

Unlike other cell structures, speckles do not have a membrane envelope. They consist of an aggregation of molecules that can dynamically dissolve and reassemble, exhibiting the properties of solids as well as those of liquids. These "condensates" can be found throughout the cell. "Each cellular condensate has a protein that represents its nucleus - in the case of nuclear speckles, there are two," says Akta.

Of red herrings and finding the right path

It is no coincidence that past attempts to identify the lowest common denominator of the mysterious structures have not been successful. "For 30 years scientists have been staining nuclear speckles with a reagent that they did not know very well", says Akta. "We did not realize that we have been in the dark for decades."

Since the early nineties, nuclear speckles have been visualised with a substance called SC35, which is an antibody that specifically attaches to certain sites in the speckles and can stain them with the help of pigments. Until recently, however, it was assumed that the antibody only recognizes the small protein SRSF2 - an assumption that now turned out to be wrong. "We wanted to use the antibody as a bait to fish for speckles in the cell," says brahim Avar Ilk, the lead author of the study. "It was a great surprise to find the protein SRRM2, which was not the intended prey for our experiment." It turned out that the antibody not only adheres to the already known SRSF2, but especially and particularly well to SRRM2.

Quest in the evolutionary family tree

While the sequence of SRRM2 varies widely in different animal species, the protein has a small section that has been preserved over hundreds of millions of years of evolution. Looking for similar proteins in the evolutionary family tree, the researchers also noticed the protein SON, which was considered by other research groups as a possible critical component of the speckles, too. "We had the idea that the combination of the two proteins could be the fundamental building block of the speckles", says Ilk.

To test their hypothesis, the team grew human cells with the genes for either SRRM2 or SON switched off. This resulted in only spherical remnants of the speckles in the cell's nuclei. Once the researchers knocked down both proteins simultaneously, all the speckles dissolved completely and associated proteins were found to be distributed throughout the cell nucleus. "We concluded that SRRM2 and SON must be the scaffold for nuclear speckles," says Ilk. "Next, we will investigate how the two proteins bind to other molecules and how this process is controlled".

Historical misinterpretation has consequences

But the results have even more, and perhaps far-reaching consequences. "Now that it is clear that SC35 binds to a different protein than assumed, previous research results on nuclear speckles must be carefully reevaluated," says Akta.

The antibody SC35 has also been widely used in disease research, since the speckles have been implicated in several neurodegenerative conditions such as Huntington's disease, spinocerebellar ataxia and dentatorubro-pallidoluysis atrophy. "There may be entirely new perspectives for research into these diseases," says Akta.

DURHAM, N.C. - The proliferation of pits and ponds created in recent years by miners digging for small deposits of alluvial gold in Peru's Amazon has dramatically altered the landscape and increased the risk of mercury exposure for indigenous communities and wildlife, a new study shows.

"In heavily mined watersheds, there's been a 670% increase in the extent of ponds across the landscape since 1985. These ponds are almost entirely artificial lakes created as thousands of former mining pits fill in with rainwater and groundwater over time," said Simon Topp, a doctoral student in geological sciences at the University of North Carolina at Chapel Hill, who co-led the study.

Landscapes formerly dominated by forests are now increasingly dotted by these small lakes, which, the study finds, provide low-oxygen conditions in which submerged mercury - a toxic leftover from the gold mining process - can be converted by microbial activity into an even more toxic form of the element, called methylmercury, at net rates 5-to-7 times greater than in rivers.

"Methylmercury poses especially high risks for humans and large predators because it bioaccumulates in body tissue as it moves up the food chain. That's particularly concerning given the high biodiversity and the large number of indigenous populations that live in the Peruvian Amazon," said Jacqueline Gerson, a doctoral student in ecology at Duke University, who also co-led the study.

These heightened risks likely also occur in other locations where unregulated artisanal small-scale gold mining takes place, including Asia, sub-Saharan Africa and other parts of South America, she said.

Topp, Gerson and their colleagues published their peer-reviewed study Nov. 27 in Science Advances.

Artisanal gold miners use mercury, a potent neurotoxin, to separate their gold ore from soil and sediments, often without adequate safety precautions to protect themselves or the environment.

Mercury poisoning can cause a wide range of health impacts, including tremors, muscle weakness, vision and hearing impairments, and loss of coordination and balance. In severe cases, it can lead to birth defects or death.

Some of the mercury used by the miners is burned off into the air or spilled into nearby rivers, creating far-reaching environmental and human health risks that have been well documented in past studies. The new study is the first to document how the mining has altered the landscape and simultaneously amplified the risks of mercury poisoning through the creation of ponds and the microbial processing of mercury into methylmercury that occurs there.

To conduct the study, the scientists collected water and sediment samples at sites upstream and downstream of artisanal gold mining sites along Peru's Madre de Dios River, its tributaries, surrounding lakes, and mining ponds during the dry season in July and August of 2019. They measured each sample for total mercury content and for the proportion of that mercury that was in the more toxic form of methylmercury.

By combining these measurements with more than three decades of high-resolution satellite data from the region, they were able to determine the extent of artificial ponding and mercury contamination at each site and identify causal links.

"You can clearly see that the increase in artificial lakes and ponds in heavily mined areas accelerated after 2008, when gold prices dramatically increased along with mining activity," Topp said. By contrast, the total surface area of ponds in areas without heavy mining increased by an average of only 20% over the entire study period.

"We expect that this trend, and the environmental and human health risks it causes, will continue as long as gold prices remain high and artisanal small-scale gold mining is a profitable activity," he said.

We’ve all been there. Whether we’re waiting for a bus that is stuck in traffic, or eagerly anticipating the release of a new book, film or album, there are times when we need to be patient. Learning to suppress the impulse for instant gratification is often vital for future success, but how patience is regulated in the brain remains poorly understood.

Now, in a study on mice conducted by the Neural Computation Unit at the Okinawa Institute of Science and Technology Graduate University (OIST), the co-authors, Dr. Katsuhiko Miyazaki and Dr. Kayoko Miyazaki, pinpoint specific areas of the brain that individually promote patience through the action of serotonin. Their findings were published 27th November in Science Advances.

“Serotonin is one of the most famous neuromodulators of behavior, helping to regulate mood, sleep-wake cycles and appetite,” said Dr. Katsuhiko Miyazaki. “Our research shows that release of this chemical messenger also plays a crucial role in promoting patience, increasing the time that mice are willing to wait for a food reward.”

Their most recent work draws heavily on previous research, where the unit used a powerful technique called optogenetics – using light to stimulate specific neurons in the brain – to establish a causal link between serotonin and patience.

The scientists bred genetically engineered mice which had serotonin-releasing neurons that expressed a light-sensitive protein. This meant that the researchers could stimulate these neurons to release serotonin at precise times by shining light, using an optical fiber implanted in the brain.

The researchers found that stimulating these neurons while the mice were waiting for food increased their waiting time, with the maximum effect seen when the probability of receiving a reward was high but when the timing of the reward was uncertain.

“In other words, for the serotonin to promote patience, the mice had to be confident that a reward would come but uncertain about when it would arrive,” said Dr. Miyazaki.

In the previous study, the scientists focused on an area of the brain called the dorsal raphe nucleus – the central hub of serotonin-releasing neurons. Neurons from the dorsal raphe nucleus reach out into other areas of the forebrain and in their most recent study, the scientists explored specifically which of these other brain areas contributed to regulating patience.

The team focused on three brain areas that had been shown to increase impulsive behaviors when they were damaged – a deep brain structure called the nucleus accumbens, and two parts of the frontal lobe called the orbitofrontal cortex and the medial prefrontal cortex.

“Impulse behaviors are intrinsically linked to patience – the more impulsive an individual is, the less patient – so these brain areas were prime candidates,” explained Dr. Miyazaki.

Good things come to those who wait (or not...)

In the study, the scientists implanted optical fibers into the dorsal raphe nucleus and also one of either the nucleus accumbens, the orbitofrontal cortex, or the medial prefrontal cortex.

The researchers trained mice to perform a waiting task where the mice held with their nose inside a hole, called a “nose poke”, until a food pellet was delivered. The scientists rewarded the mice in 75% of trials. In some test conditions, the timing of the reward was fixed at six or ten seconds after the mice started the nose poke and in other test conditions, the timing of the reward varied.

In the remaining 25% of trials, called the omission trials, the scientists did not provide a food reward to the mice. They measured how long the mice continued performing the nose poke during omission trials – in other words, how patient they were – when serotonin-releasing neurons were and were not stimulated.

When the researchers stimulated serotonin-releasing neural fibers that reached into the nucleus accumbens, they found no increase in waiting time, suggesting that serotonin in this area of the brain has no role in regulating patience.

But when the scientists stimulated serotonin release in the orbitofrontal cortex and the medial prefrontal cortex while the mice were holding the nose poke, they found the mice waited longer, with a few crucial differences.

In the orbitofrontal cortex, release of serotonin promoted patience as effectively as serotonin activation in the dorsal raphe nucleus; both when reward timing was fixed and when reward timing was uncertain, with stronger effects in the latter.

But in the medial prefrontal cortex, the scientists only saw an increase in patience when the timing of the reward was varied, with no effect observed when the timing was fixed.

“The differences seen in how each area of the brain responded to serotonin suggests that each brain area contributes to the overall waiting behavior of the mice in separate ways,” said Dr. Miyazaki.

Modelling patience

To investigate this further, the scientists constructed a computational model to explain the waiting behavior of the mice.

The model assumes that the mice have a predictive model of the timing of reward delivery and estimate the probability that a reward will be delivered. While they keep waiting without receiving a food pellet, the estimated probability for the trial to be a reward trial gradually goes down, and the mice accordingly decide whether or not to keep waiting. The model also assumes that the orbitofrontal cortex and the medial prefrontal cortex use different predictive models of reward timing to calculate reward probabilities individually, with the latter being more sensitive to variations in timing.

The researchers found that the model best fitted the experimental data of waiting time by increasing the initially expected reward probability from 75% to 94% under serotonin stimulation. Put more simply, serotonin increased the mice’s belief that they were in a reward trial, and so they waited longer.

Importantly, the model assumed that stimulation of the orbital frontal cortex and the medial prefrontal cortex separately increased the initial reward probability from 75% to 94% only in that particular area, whereas stimulation of the dorsal raphe nucleus increased the probability in both areas. Only under these assumptions was the model able to successfully reproduce all the behavioral data.

“This confirmed the idea that these two brain areas are calculating the probability of a reward independently from each other, and that these independent calculations are then combined to ultimately determine how long the mice will wait,” explained Dr. Miyazaki. “This sort of complementary system allows animals to behave more flexibly to changing environments.”

Ultimately, increasing our knowledge of how different areas of the brain are more or less affected by serotonin could have vital implications in future development of drugs. For example, selective serotonin reuptake inhibitors (SSRIs) are drugs that boost levels of serotonin in the brain and are used to treat depression.

“This is an area we are keen to explore in the future, by using depression models of mice,” said Dr. Miyazaki. “We may find under certain genetic or environmental conditions that some of these identified brain areas have altered functions. By pinning down these regions, this could open avenues to provide more targeted treatments that act on specific areas of the brain, rather than the whole brain.”

Does poverty cause lying? An international research team led by behavioral economist Agne Kajackaite from the WZB Berlin Social Science Center, Suparee Boonmanunt (Mahidol University, Bangkok) and Stephan Meier (Columbia Business School) examined whether poverty-stricken individuals were especially prone to acts of dishonesty. The researchers ran a field experiment with rice farmers in Thailand which incentivized cheating during a card game. They found that poverty itself did not cause individuals to act dishonestly.

Whether income influences ethical behavior is a topic of much debate. One approach holds that ethical acts are limited to those who can 'afford' them. Poverty, in this view, causes individuals to behave immorally. Empirically, the question whether poverty fosters or dampens prosocial behavior, has thus far remained unanswered.

The research team is now shedding new light on this relation. To provide a causal link between poverty and cheating behavior, the researchers conducted a field experiment with several hundred rice farmers in Thailand. The experiment consisted of a simple card game that rewarded individuals financially for lying about a card they had drawn blindly from a stack. The researchers found that participants cheated to a similar extent both during periods of relative poverty and relative wealth, that is, before and after harvesting season. "Contrary to the standard economic model - where no cash leads to cheating for cash - we show that poverty itself does not lead persons to behave more immorally", says Agne Kajackaite, head of the research group Ethics and Behavioral Economics at the WZB Berlin Social Science Center.

The study also provides evidence for the effectiveness of social interventions. Briefing subjects on the ethical implications of cheating changed the participants' behavior when the population was somewhat richer (after harvest), but had no effect when the population was poorer (before harvest). "This suggests that the timing of interventions to improve people's behavior matters", Kajackaite explains the study's policy implication.

LAWRENCE -- Researchers from the University of Kansas have described a galaxy more than 5.25 billion light years away undergoing a rarely seen stage in its galactic life cycle. Their findings recently were published in the Astrophysical Journal.

The galaxy, dubbed CQ 4479, shows characteristics that normally don't coexist: an X-ray luminous active galactic nuclei (AGN) and a cold gas supply fueling high star formation rates.

"Massive galaxies, such as our own Milky Way, host a supermassive black hole at their hearts -- these are black holes that grow by accreting interstellar gas onto themselves to become more massive," said Kevin Cooke, lead author and postdoctoral researcher in KU's Department of Physics & Astronomy. "The end of galactic growth is thought to happen when this gas accretion onto the black hole occurs in sufficient quantities that it produces a tremendous amount of energy. Then, all of that energy surrounding the black hole will actually heat up the rest of the gas throughout the galaxy in such a way that it can't condense any more to form stars and the galaxy's growth stops."

The KU researchers instead found CQ 4479, a galaxy which never had been closely studied before, to be still generating new stars in spite of the luminous AGN at the galaxy's center.

"Normally, we expect that to shut everything else off," Cooke said. "But instead, we see massive amounts of new stars being formed in this galaxy. So, it's a very limited time window where you can see both the black hole growing and the stars surrounding it growing at the same time."

The researchers observed the cold quasar primarily using NASA's SOFIA infrared telescope, which is flown aboard a Boeing 747 aircraft. Other measurements were made using FUV-FIR photometry and optical spectroscopy. The work was supported by a NASA grant to primary investigator Allison Kirkpatrick, assistant professor of physics & astronomy at KU, who co-wrote the new paper.

Kirkpatrick said the team's various methods of observing the galaxy showed contradictory data, making the nature of CQ 4479 even more of a puzzle.

"What's really unique about this source is we have different measurements of the energy output near the black hole," Kirkpatrick said. "That tells you how fast the black hole is growing and also its feedback into the host galaxy that can shut down star formation. We have everything from X-ray, to optical and the infrared, so we're able to measure several different signatures of the black hole's energy output. And the signatures don't agree -- that's really rare. One interpretation is the growth of the black hole is slowing, because the X-rays come from right next to the black hole, while the optical signatures come from a little bit further out, and the infrared signatures come from further out as well. Essentially, less energy seems to be being produced right around the black hole now than it was in the past."

The researchers seem to be looking at a snapshot of the galaxy during a pivotal stage of its lifespan.

"I think this is a galaxy undergoing a midlife crisis," Kirkpatrick said. "It's going through one last burst of star formation. Most of its solar mass is already in place. It's forming a few more stars now, and the thing that's ultimately going to kill it is starting to kick in."

In part, the research at KU was performed by Kirkpatrick's undergraduate student and co-author Michael Estrada, now a graduate student at University of Florida.

"He did the data analysis of the optical spectroscopy and measured the black hole mass for us," Kirkpatrick said.

Other questions about the physical structure of the galaxy remain because current instrumentation available to astronomers don't provide clear enough images of CQ 4479.

"The image we have shows a central blob and then a little smaller blob below it," Kirkpatrick said. "So we don't have a good sense for how this galaxy looks because the central AGN is so bright that it out shines the rest of the host galaxy. This is a real problem that plagues all AGN studies -- when you're dealing with the most luminous things they tend to outshine your host at nearly every wavelength."

The researchers said CQ 4479 would require more study, particularly using the ALMA Observatory and the NASA's James Webb Space Telescope -- the most powerful space telescope ever designed and currently slated for launch Oct. 31, 2021. Both Cooke and Kirkpatrick hope to perform more investigations of the strange cold quasar once the telescope is launched.

"We're currently banking on James Webb, because it will have excellent resolution and we should be able to look at wavelengths where we can see the shape of the galaxy," Kirkpatrick said. "Another good option would be ALMA. But ALMA has unfortunately shut down temporarily because of COVID. We've kind of been stymied at seeing the host galaxy."

The importance of understanding the strange processes underway in a galaxy 5.25 billion light years from Earth might seem vague at first, but Cooke said a better understanding of the cold quasar could improve understanding of the cosmos and the fate of our own galaxy.

"This very much ties into asking 'where do we come from?' and 'what processes were involved in the creation of galaxies?,' and that's important because we live in a galaxy," Cooke said. "We live in one of these vast collections of billions of stars and knowing the processes of what created our home is valuable information. Trying to understand big ticket questions like these also spur important engineering developments here on Earth, such as the detector technology and all the fancy engineering that goes into the SOFIA telescope -- there are plenty of ways how this type of work it benefits us here on Earth."

In new research presented at Euroanaesthesia (the annual meeting of the European Society of Anaesthesiology and Intensive Care [ESAIC]), doctors report a highly unusual case of a right-handed patient performing unconscious 'mirror-writing' with her left hand while in the midst of having epileptic seizures in the emergency room. The study is by Dr Laura Freitas and Dr Sofia R. de Valdoleiros, Centro Hospitalar Universitário do Porto, Portugal, and colleagues.

Mirror writing is writing which runs in the opposite direction to normal, with individual letters also reversed, nearly always undertaken with the left hand. It can be seen in healthy individuals or associated with various focal lesions that most commonly involve the left hemisphere. However, it has not yet been described in people with epilepsy.

This new case involved a 42-year-old right-handed female patient, with a form of epilepsy called non-lesional left frontal epilepsy diagnosed at age 18 years. She was being treated with various medications and had needed previous hospitalisations due to seizures requiring coma induction.

On this occasion, she presented to the emergency room of Centro Hospitalar Universitário do Porto with another episode of focal seizures involving her right arm. Infectious and metabolic causes were excluded, and despite the administration of diazepam 40mg IV and levetiracetam 1500mg IV to help sedate her, the seizures continued.

Between seizures, the patient presented with an episode of mirror writing (see link to image below) with her left hand. The writing said (in Portuguese) '"My head can't take it anymore I need You to stop my head it doesn't stop". General anaesthesia and deep sedation were required to bring the seizures under control.

The patient's relatives, who accompanied her to the hospital, said that she had performed mirror writing after previous seizures. When she regained consciousness, the woman had no memory of the mirror writing, and is unable to repeat it when not having seizures.

The authors say: "Unaware mirror writing with the left hand was present in this right-handed patient with epilepsy affecting the right upper limb. Stroke patients with right-sided partial paralysis can rarely present with spontaneous mirror writing, using the left hand. We hypothesise that our patient, while feeling impaired to write normally with her right hand during seizures, attempts to do so with her left hand, and mirror writing occurs."

They add: "To the best of our knowledge, this is the first case of mirror writing reported in a patient with epilepsy. Physicians should be aware of this condition, which may be underreported."

People borrowing money for the first time should only be given small amounts until they have proved their competence, a new study says.

The paper argues that new borrowers - especially young people and those of an "impulsive" disposition - need protection to prevent them falling into long-term debt.

It says lenders should have a duty of care, requiring them to consider age, experience and personality traits, which can be detected by psychometric tests.

The study, by Professor Stephen Lea of the University of Exeter, reviews evidence on the psychology of debt, and makes recommendations to help reduce debt problems.

"I argue that - similar to obtaining a driving licence - people should have to demonstrate their competence before taking out debts that could have long-term negative consequences," Professor Lea said.

"Some people are particularly susceptible to debt problems.

"This includes those of an impulsive disposition, but it particularly applies to young people - and debts contracted early in life can have long-term ill effects.

"Accordingly, steps need to be taken to protect people at this vulnerable life stage.

"Although this would involve a restriction of the financial freedom of people who are legally adults, the evidence suggests that access to credit should be controlled more carefully."

Speaking about rules relating to people of an "impulsive" disposition, Professor Lea said: "Lenders might well resist such regulations, but in fact financial advisors are already required to assess risk preference when advising people on investments.

"This shows that such a measure can be brought in without too much difficulty or expense to those who have to implement it."

Professor Lea acknowledges that debt is heavily influenced by economic inequality, and that no psychological factor can prevent debt if excessive socio-economic disadvantage is not addressed.

He also says the current Covid-19 pandemic is likely to increase debt problems.

His recommendations include tackling poverty (reducing the "decades-long drift towards greater inequality in almost all countries") and intensifying regulation of high-cost lenders.

Recommending better financial education of children, Professor Lea said: "Many people are shockingly bad at assessing credit deals.

"What seems to be needed is fluency in seeing, without effortful calculation, what is or is not a good deal when borrowing money."

The paper calls for policies to improve people's awareness of their credit position, and says debtors should be advised to seek independent advice before dealing with lenders to whom they owe money.

He concludes: "If all these recommendations were adopted overnight, the problems of debt in society would not go away.

"Credit enhances consumer choice and is a necessary function in a modern economy, and so long is credit is available, some people will get into difficulties with debt.

"But, as is the case with poverty itself, neither the extent nor the level of debt is fixed.

"Appropriate policies, such as those proposed here, could reduce both."

Decreases in hospital attendances and admissions amid fears of COVID-19 may result in avoidable harm for under 16s say researchers, who warn against the "unintended consequences of pandemic control measures".

Research led by Dr Rachel Isba from Lancaster University, Dr Rachel Jenner from Royal Manchester Children's Hospital, and Dr Marc Auerbach from Yale University analysed attendances and admissions to Paediatric Emergency Departments (PED) at the Royal Manchester Children's Hospital in the UK and Yale New Haven Children's Hospital in the US.

The Royal Manchester Children's Hospital, part of Manchester University NHS Foundation Trust is the largest and busiest children's hospital in the UK and the PED sees approximately 50,000 patients per year. The PED at Yale New Haven Children's Hospital sees over 38,000 patients per year. Both hospitals are in geographical areas that went into "lockdown" on March 23, 2020.

The international team compared the differences between weekly attendances and admissions (via the PED) from January 1, 2020, to May 20, 2020 compared with the same period in 2019.

Following lockdown, they found "a striking decrease" in the number of children and young people attending the PED at both hospitals.

Despite this, after lockdown they were up to 60% more likely to be admitted to hospital in 2020 compared to the same period in 2019, suggesting they may have been more unwell by the time they attended hospital.

The researchers said: "These observations likely reflect both a genuine decrease in need (eg, fewer viral infections) but also an increase in delayed and unmet need. Children and adolescents presenting later on in their illness are more likely to have a negative outcome."

"Although the direct effects of COVID-19 currently appear to be less severe in children and adolescents, only time will reveal the indirect negative impacts on this age group, including deaths, because of delayed Paediatric Emergency Department presentation."

They said that fear of COVID-19 was likely to have been a factor in the reduced numbers of under 16s attending hospital PEDs.

"Although not explored here, contributing factors are likely to include the parent or caregiver's fear of the virus, resulting in higher personal thresholds for needing to attend, and will need to be addressed proactively in case of future lockdowns.

"Those with responsibility for making and communicating decisions around lockdown need to be aware of the unintended consequences of pandemic control measures. As a minimum, there needs to be clear and consistent messaging around when it is appropriate to take an ill or injured child to hospital--emphasising that a PED visit can be made safely-- delivered at the start of any future periods of lockdown."

Jena, Germany (27.11.2020) Antibiotics work in different ways. Some, including penicillin, attack the cell wall of the bacteria by inhibiting their synthesis. But the bacteria are not helpless against this attack. "We have been able to identify a small ribonucleic acid that has a decisive influence on the antibiotic-resistance of the cholera-triggering bacterium Vibrio cholerae," says Kai Papenfort, Professor of General Microbiology at the University of Jena, Germany.

The protein CrvA is found in the periplasmic space of the bacterium. This lies between the outer cell wall and the basic substance of the cell, the cytoplasm, which is also surrounded by a membrane. There CrvA determines the curvature of the rod-shaped bacterium V. cholerae. "Until now, however, it was not known what controls the activity of this protein. With the small ribonucleic acid VadR we were able to identify a post-transcriptional inhibitor of the synthesis of this protein," says Prof. Papenfort. In contrast to messenger RNA, small ribonucleic acids do not contain any genetic information, but do influence its expression - usually after the DNA has been transcribed into messenger RNA.

Maintenance of the cell form is crucial for antibiotic resistance

"Cholera bacteria in which the protein CrvA is not suppressed by VadR show a reduced survival rate on contact with penicillin," says Papenfort. This indicates that the maintenance of the cell form by the small RNA is crucial for antibiotic resistance, the microbiologist adds. The researchers revealed other functions of the small RNA VadR, including the formation of biofilms, which play an important role in the pathogenicity of V. cholerae.

"VadR is one of many molecules that can intervene in gene expression in V. cholerae. If we understand all these molecules, their functions and their interaction, we can derive new therapeutic approaches. The increasing resistance to antibiotics makes this urgently necessary", says Papenfort, whose research contributes to the Cluster of Excellence „Balance of the Microverse" at the University of Jena.

A new sensing method has made tracking movement easier and more efficient. A research group from Tohoku University has captured dexterous 3D motion data from a flexible magnetic flux sensor array, using deep learning and a structure-aware temporal bilateral filter.

"We can now track complex motions with higher accuracy," said Yoshifumi Kitamura, co-author of the study.

Dexterous 3D motion data can be used for multiple purposes: biologists can use the data to record detailed movements of small animals in their living environments, scientists can track the flow of fluids, and researchers can track finger movements and objects being manipulated by users in virtual reality.

Currently, optical cameras are the most prominent method of tracking movements. Yet optical cameras struggle with accuracy and reliability. If a small animal burrows away or if fingers or objects obscure the view, the camera will fail to detect the motion.

Magnetic tracking technology is also used for dexterous motion. However, even state-of-the-art magnetic systems face limitations. The classic tracking method creates bias and magnetic sources have a dead-angle problem or bulky markers.

The research team invented their new method by applying a deep neural network and a novel structure-aware temporal bilateral filter on a new magnetic tracking principle. First, the neural networks learn the regression from the simulation flux values to the LC coils 3D configuration at any location and orientation.

The new filter further compensates the data to reconstruct smooth and accurate motion. Markers do not require batteries, so observation time can be maximized.

As a result, the new integrated system can track multiple LC coils at 100Hz speed at millimetre level accuracy. Tracking loss due to dead-angle can be reconstructed because of the system's self-learning.

"The application of our research is widespread. Hand motions can be tracked to make creating smooth animations easier, markers can be put into fluids to track its flow, and tracking can be placed on small animals," added Kitamura.

The pilot project aims to examine the costs and benefits of avoided crises - so-called "non-events" - in the domain of consumer health protection from an economic and psychological point of view, and will begin in January 2021. The project will also analyse whether and how cost-benefit considerations can be used in communication with different participants in risk communication and reputation management. For this reason, BfR President Professor Dr. Dr. Andreas Hensel and HSU President Professor Dr. Klaus Beckmann signed a cooperation agreement yesterday.

"Risk communication is defined as a continuous and interactive process and characterised by a participatory dialogue with different target groups," says BfR President Professor Dr. Dr. Andreas Hensel. "It can help every person and every interest group to make informed and independent decisions. Our interdisciplinary research group aims to make contributions to the scientific basis of this decision-making problem and, therefore, also increase economic efficiency and transparency," states Hensel, explaining the idea behind the joint project. The research project will primarily deal with the interaction between risk assessment and risk communication in consumer health protection. So-called "non-events" present a particular challenge: these are crisis events that have been avoided and that, due to successful prevention and treatment measures, do not present themselves as such to the individual. Sometimes, preventing a crisis then leads to society questioning the risk and the measures taken - this is also known as a "prevention paradox". The new research group will now analyse the social significance of these non-events in consumer health protection from an economic and psychological point of view and explore the use of cost-benefit considerations to improve risk communication.

HSU President Professor Dr. Klaus Beckmann welcomes the cooperation between the two institutions: "Our first collaboration in socio-scientific research gives our two departments a massive boost in the domain of risk research and once again illustrates the direct application benefit that interdisciplinary explanatory models can have for our society; in this case, the consumer interested in health."

To answer the multifaceted question of how to assess avoided crises, the BfR and HSU rely on a broad range of expertise: the HSU notably contributes with its economic and psychological competence and the use of its experimental psychological laboratory. The interdisciplinary team at BfR with expertise in psychology and communication science has many years of research experience in the fields of risk communication and crisis prevention.

In a ground-breaking new study, scientists used innovative molecular techniques to explain how corals on the east coast of Australia survived previous tough conditions--enabling the Great Barrier Reef to become the vast reef it is today.

"We sequenced the genomes of 150 individual colonies of the same species of corals and used this to find out which genes are important for survival in inshore reefs," said the study's lead author Dr Ira Cooke from James Cook University.

"Genomes are like a time capsule containing an enormous wealth of historical information," said co-author Professor David Miller from the ARC Centre of Excellence for Coral Reef Studies (Coral CoE).

"Generally, single genomes are really useful in coral studies, but hundreds of genomes for the same species are a goldmine of information," Prof Miller said.

The team delved into the ancient history of reefs, back some one million years, to when inshore corals from Magnetic Island first diverged from their northern reef kin.

The scientists mapped the rise and fall of these two coral populations on the Great Barrier Reef, tracking which genes rapidly evolved to endure changing conditions, while measuring the flow of genes between locations.

They say the results are important for the current and future conservation of coral reefs.

Dr Cooke and his team already knew corals on the inshore Great Barrier Reef were able to flourish despite a disruptive environment of high turbidity and highly variable salinity and temperature parameters. By looking at the variation between genomes the team discovered exactly how the corals achieved this feat.

The survival strategies used by the reef's inshore corals include a set of genes that evolved rapidly during the past 10,000 years. This time period includes flooding after the last ice-age. Another strategy includes the assimilation of specialist strains of coral symbiotic algae. These were found in reefs with some of the toughest conditions--often close to rivers.

"These two strategies deserve special attention in future studies, as possible keys to the survival of corals under similar conditions," Dr Cooke said.

"Losing these reefs is a future possibility as coral reefs currently experience unprecedented, drastic and rapid changes due to human influence," Prof Miller said.

"Coral reefs are threatened by climate change, over-fishing and pollution."

In addressing the latter, Dr Cooke says it's highly important to care for water catchments and water quality.

"As high-quality genome assemblies are derived from a broader range of corals and their symbionts, this and related approaches will become key tools," the authors said.

"These bring us closer to understanding the interaction between past climate conditions and the evolution of corals and coral reefs."

In the field of economics, the concept of a market economy is largely considered a modern phenomenon. Influential economists such as Karl Marx and Max Weber, for example, argued that although markets existed in antiquity, economies in which structures of production and distribution responded to the laws of supply and demand developed only as recently as the 19th century. A recent study by an international team of researchers, including Adam Izdebski of the Max Planck Institute for the Science of Human History, uses palynology - the study of pollen remains extracted from cored sediments - to challenge this belief and provide evidence for an integrated market economy existing in ancient Greece.

Market integration began earlier than assumed

Using publicly available data from the European Pollen Database, as well as data from other investigators, researchers analyzed pollen assemblages from 115 samples taken from six sites in southern Greece to measure landscape change. Using radiocarbon dating to tie their measurements to historical time, researchers followed the change in percentage values for individual plant taxa between 1000 BCE and 600 CE and observed a decrease in pollen from cereals, a staple of the ancient Greek diet, during a period of apparent population growth. This decrease occurred at the same time as an increase in the proportion of olive and vine pollen. These trends raise an important question: why would local producers chose to plant olives and vines instead of cereal grains, when the demand for this staple food must have been high and mounting?

In the current study, researchers argue that pollen data from southern Greece reveals an export economy based on cash cropping as early as the Archaic period, primarily through olive cultivation. Although archeological evidence from these periods documents the movement of goods, quantifiable data on market integration and structural changes in agricultural production have been very limited. "In this paper," says lead author Adam Izdebski, "we introduce pollen records as a new source of quantitative data in ancient economic history."

From mud to markets: Integrated scientific approaches reveal an integrated ancient economy

Before arriving at their conclusions, researchers compared the trends they observed in the pollen data with three other sources of data in an instance of pioneering scientific research. First, researchers observed a decrease in pollen from uncultivated landscapes corresponding with each increase in settlement numbers. This correlation between the number of settlements and the exploitation of the land supports the methodology of the study and indicates the potential of palynology for future studies in a variety of scientific disciplines.

Researchers then looked for evidence of increased trade activity in Mediterranean shipwrecks, which are routinely used to estimate maritime trade and overall economic activity. After restricting their search to wrecks from the appropriate period and region, scientists observed trends in shipwrecks consistent with trends found in cereal, olive, and vine pollen. Both sources of data suggest an economic boom in the 1st and 2nd century CE, a decline in the 4th and 5th century, and a smaller boom in the 6th century.

Finally, researchers examined trends in the presence of large-scale oil and wine presses in the Mediterranean. The presence of these machines, although not located in Greece, indicates a pattern of broad economic trends in the region and changing incentives for the production of large quantities of olive oil and wine. Again, the researchers found that trends in archaeological findings of oil and wine presses were consistent with trends in cereal, olive, and vine pollen.

As the emergence of integrated markets and capitalist economies of the early modern era is believed to have been at the roots of the Anthropocene, the current epoch in which humanity has become a major geological force, the current study shows that the structural developments that occurred on a large scale through European colonization from the 15th century onward were possible several thousand years before.

An international collaboration between researchers at the Niels Bohr Institute, University of Copenhagen, Oxford University, and University of Sheffield has revealed that colonies of slow moving bacteria can expand significantly quicker than their fast moving counterparts. The result is now published in Nature Physics.

The researchers combined genetics, experiments, custom image analysis algorithms and theoretical physics to investigate the efficiency of the bacterial invasion. It turned out that bacteria move slowly and prudently in order to avoid crashes and jams, making them capable of moving efficiently in dense and massive, multimillion population crowds. The result may have implications for how we treat infections in a future in which super bacteria, immune to antibiotics, pose a threat to human health.

Pathogenic bacteria, Pseudomonas ariginosa, move around by grabbing the surfaces with tiny feet called pili. The researchers at Oxford Zoology and Sheffield University set up an experiment in which they modified the individual bacteria by simply adding the number of feet. No other features or properties were changed. The individual bacteria were now able to move approximately two times faster than before, and the researchers asked the question if this enhancement of the individual's abilities would also enhance the population's ability to invade new territories. "We wanted to understand the behavior of the bacteria, both on an individual level and on the level of the collective", Amin Doostmohammadi from the Niels Bohr Institute says.

The tortoise beats the hare - again

The researchers literally made a race between the fast moving and the slow moving colonies, and very counterintuitively, the genetically enhanced, fast population was overtaken by the slower moving wildtype bacteria population. In the beginning, the fast population was ahead, but was, over the course of few hours, overtaken by the slower moving, but apparently more efficient wildtype population. The researchers also put the two different types of bacteria together, to have them compete directly, and again the slower moving, wildtype bacteria population ended up being better at expanding their population. "We find that a mutant that produces a larger number of pili could move more rapidly than the wildtype on an individual level, but in large groups they tended to crash into one another at high speeds. These collisions rotate the mutant cells vertically and trap them in place. As a result, the slower moving wildtype cells can move past them and ultimately win the race into new territory."

Basic physics is at play in a colony of bacteria

By characterizing the orientation of bacteria the researchers found that collisions take place at specific locations: singular points in cell alignment in the form of aster-like structures that are known as +1 topological defects in physics. "Considering how much biology goes into the machinery of bacteria and their behavior, it is striking that we were able to recreate almost exactly the same patterns by using basic physics principles and modelling them in a computer. In other words, the bacteria are obeying a simple, physical principle that limits their pace as individuals, but still allows for a very efficient invasion of a colony. Evolution seems to have put a fundamental speed limit on bacteria: if they move faster than certain amount, they collide together and get trapped in structures of their own creation".

Infections may in the future be dealt with in other ways than with antibiotics

Control of an infection typically means adding a drug to the bacteria colony to influence the individual bacteria - slow it down or kill the individuals in a population with antibiotics, but the surprising new discovery seems to show that speeding up the pace of the crowd of bacteria may actually cause the infection to self-destruct. If the bacteria population, through evolution, have solved the problem of crowding by gaining new territory at a very specific speed, if you then turn up the speed dial, the infection "crashes" and dies out. "From the physics perspective, we may be able to say what property exactly we need to control in a bacteria population, and from the genetics perspective they (biologists) may say 'we know how to control that', and then we can move on to do so. It is a quite new way of thinking, linking different fields of expertise together. Understanding how to control the crowd, rather than the individual in an infection, we hope, will lead to new strategies to control infections in the future" Amin Doostmohammadi says.

Interdisciplinarity was key to the success of the experiment

It was impossible to do this work without a continuous cross talk between researchers within different fields: the expertise in genetic modifications, image analysis, and bacterial ecology from Dr. Oliver Meacock and Dr. William Durham at Sheffield, and Professor Kevin Foster at Oxford Zoology, was combined with theoretical expertise on topological defects from Professor Julia Yeomans in Oxford Physics, and Dr. Amin Doostmohamamdi at the Niels Bohr Institute to discover and explain a counterintuitive phenomenon of how nature has favored slow individuals to make fast collectives.

Nearly one million people in the UK have dementia. People living with the most common form, Alzheimer's disease, can experience difficulties working out where they are, meaning they often get lost even in familiar environments. Today (Friday 27 November) research funded by Alzheimer's Research UK at the University of Exeter Medical School sheds new light about why this might happen.

The brain contains specialised nerve cells called 'speed-sensitive cells', which change their firing rate depending how fast someone is moving. Much like a speedometer in a car, these nerve cells encode how fast, and therefore how far, an individual has travelled. This process helps us to know where we are in relation to where we were, and to navigate our environment.

In this study, Dr Jon Brown led a team of scientists to examine how these speed-sensing nerve cells in a specific part of the brain known as the entorhinal cortex might be affected in Alzheimer's disease.

They investigated this in mice with features of Alzheimer's disease. The mice produced the tau protein - a hallmark protein of Alzheimer's and other forms of dementia.

The team found that while roughly 60% of the nerve cells in normal mice were speed-sensitive, a much lower proportion (13%) were speed-sensitive in the mice with features of disease.

When this speedometer malfunctions, the brain's map does not receive correct distance-travelled information.

The team believe that this malfunction will disrupt other elements of our internal map, and the team found that other cells in the mice producing the toxic tau protein did not function.

Dr Jon Brown, from the University of Exeter's Medical School, who led the research, said

"People with Alzheimer's disease and other dementias can experience profound deficits in spatial memory, meaning they often get lost even in familiar environments. We need to understand this if we are ever to provide treatments for this distressing symptom.

"Our discovery has revealed that cells acting like a "speedometer" and feeding information into the brain's neural map appear to malfunction in dementia brains, and this could help solve part of the puzzle. If this translates to humans, it could identify new pathways for potential treatment."

Dr Rosa Sancho, Head of Research at Alzheimer's Research UK who funded the work said:

"We often hear heart-breaking stories about people with dementia who get lost and can't find their way home and we know spatial navigation difficulties like these are some of the earliest warning signs for the condition.

"Research shows us that the brain changes associated with diseases like Alzheimer's begin decades before symptoms like memory loss start and for future Alzheimer's treatments to be effective, it's likely they must be given at the earliest stages of disease, before there's too much damage to the brain.

"Supporting fundamental research like this is incredibly important to build our knowledge of how the disease works. With the ongoing pandemic making its impact felt on people with dementia and our fundraising efforts, we are incredibly grateful for our dedicated supporters."