Culture

The risk of being bullied at work is twice as high if you were born abroad. And if you come from a culture that is culturally dissimilar to Sweden's, the risk is even higher. These are the results of a Swedish study from Linköping University that was recently published in The International Journal of Human Resource Management.

Employers in Sweden have a duty to ensure that the workplace is safe, with a healthy atmosphere. Despite this, some employees are treated poorly, excluded and ignored. When such treatment has continued for a longer period, it is defined as bullying.

Researchers at Linköping University wanted to see if people born abroad run a greater risk of being bullied at work.

"Our results show an increased risk of bullying for people who work in Sweden but were born in another country. The results also show the importance of addressing these issues. Bullying can cause serious problems for a person, and for the workplace where it occurs", says Michael Rosander, associate professor in psychology at Linköping University's Department of Behavioural Sciences and Learning.

Michael Rosander's research investigates what happens at different types of workplaces and how different organisational factors affect individuals, working groups and the organisation as a whole. He conducted the study together with Stefan Blomberg, doctoral student at Linköping University.

Excluded from the work community

In this study, the researchers investigated two types of bullying: work-related and person-related bullying. In work-related bullying, one is subjected to negative actions related to one's work, for example having responsibilities taken away, being given trivial work duties, or having one's work monitored excessively.

Person-related bullying, on the other hand, is being subjected to negative actions related to one's person. It can include being humiliated, ridiculed, or ignored and excluded from social contexts.

The results show that people who are born abroad are subjected to more person-related bullying than people born in Sweden. For foreign-born, the risk of being bullied at work is twice as high as for natives. And for people from cultures dissimilar to the Swedish, the risk is quadrupled. Most exposed are people born in Asia.

However, for work-related bullying the researchers found no increased risk for foreign-born, compared to Swedish-born.

Thus, the person-related bullying that foreign-born are subjected to is based on who they are - not on work-related factors.

"They are subjected to what we call predatory bullying. It doesn't matter what they do. Their very presence, the way they look, can be a reason for the negative treatment. It became clear in the study, says Michael Rosander.

To measure the experience of being bullied, the researchers used the Swedish version of the Negative Acts Questionnaire-Revised (NAQ-R), where the respondents estimate their exposure to bullying at work in various situations on a five-point scale. Using register data from Statistics Sweden, the researchers sent the questionnaire to a representative selection of the Swedish workforce. The questionnaire was completed by 1856 people from workplaces of 10 people or more. The majority of respondents (1625) were born in Sweden, while 229 were born abroad.

Because it was already known that poor working conditions can be a breeding ground for bullying, the researchers also looked at certain work-related factors, in order to ensure that the responses concerned bullying specifically, and were not just general workplace dissatisfaction. But the analysis showed that these people don't have worse work environments - they are at a greater risk of being bullied.

The headquarter of a eukaryotic cell is the nucleus, and most of the cell's information and instructions are stored there in the form of DNA (Deoxyribonucleic acid). The DNA, which is twisted, rolled and bundled two-meter-long chain, together with protein molecules, makes up the chromatin fiber that lays inside the nucleus. For years, scientists were curious how these components are organized. How is it possible that proteins necessary in biochemical reactions move efficiently within the nucleus full of DNA? Recent studies have finally solved the mystery. Findings describing it in detail were published in the Journal of Physical Chemistry Letters on December 21st, 2020.

Molecules in a crowded nucleus

The nucleus of each cell hides a two-meter-long chain of a most amazing and unique molecule: DNA. Along with histones and various related proteins, DNA builds up a chromatin framework filled with a viscous fluid that exhibits excellent molecular composition diversity. For decades, the mobility of molecules in the nucleus was not sufficiently explored, but recent developments have altered this status quo. Thanks to in-depth research by a group of researchers from the Institute of Physical Chemistry of the Polish Academy of Sciences (IPC PAS) led by professor Robert Ho?yst, the mobility of molecules at length-scales from single to tens of nanometers in the nucleus is presented in detail.

A Molecular superstore

Due to its small size, one might assume that the nucleus has a simple structure and a random molecule distribution. That is by no means the case. The nucleus has an unbelievably complex and fine-tuned layout. The DNA does not resemble a messy tangle of spaghetti; it is efficiently packed into compact structures. Even the nanoscale viscosity of the nucleus determines the mobility of the individual objects inside. To better visualize how well-organized this all is, the nucleus can be described as a superstore. The chromatin fibers work like shelves, holding an assortment of necessary genetic information (i.e., DNA) just like the shop shelves are filled with products. These shelves don't take up the entire space, but rather they are separated within an aisle-like distance that works as a channel. The people crossing the aisles in specific patterns as they shop could be compared to the protein molecules that move somewhat randomly within the nucleus' channels according to the rules of Brownian motion. No matter how crowded the aisle gets, people always find a way to pass by each other, maintaining some distance as they go. The molecules crossing molecular channels do the same without any traffic problems on their way. This allows each molecule to travel efficiently, maintaining the orderliness of a superstore.

Viscosity impact

The molecules that are present in the eukaryotic cells have different sizes. For example, ions are subnanometer in size, protein radii are typically few nanometers; a nucleosome's radius is about 5.5 nm, while folded up chromatin fibers have a radius of about 15 nm. Furthermore, condensed loops of chromatin form higher-level compact structures are boasting a radius of about 150 nm. To understand their mobility within the nucleus, professor Ho?yst's team proposed to place nanometer-sized objects covering the whole spectrum of natural components length-scales found in the nucleus. Polymers, proteins, and nanoparticles having radius from 1.3 to 86 nm in were considered.

To see this intriguing organization at the nanoscale level, specific molecules' mobility was studied using non-invasive techniques such as fluorescence correlation spectroscopy (FCS) and raster image correlation spectroscopy (RICS). Thanks to substances like the GFP (green fluorescent protein) or the rhodamine-based nanoparticles in nanomolar concentration, it was possible to observe the mobility of particular molecules and determine the nucleoplasm viscosity without causing any disruption to cellular activity. These techniques allow scientists to investigate even the most minor changes at the molecular level. The mobility of large nanoparticles was reduced by as much as 6 times compared to the diffusion in an aqueous medium. However, the typical protein-sized molecules diffusion was reduced only 2-3 times. The mobility drastically decreases when the radius of injected objects is larger than 20, more significance on estimations of the diffusion coefficient, it is possible to look closer at the movement and interaction of molecules that happen between particular objects in the nucleus' channels and within the packed structure inside the nucleus. These measurements expand our current understanding of the structure of the nucleus. Having a good understanding of the complexity of the channels within nuclei is crucial as it directly contributes to our knowledge of how large biostructures, perhaps including the medicine of the near future, are transported within the cell.

The first author, dr. Grzegorz Bubak remarks, "Our experiments revealed that eukaryotic cell nucleus is percolated by ?150 nm-wide interchromosomal channels filled with the aqueous diluted protein solution of low viscosity."

The studies quantifying the crowding within cells' nuclei reveal that most molecules can freely pass through this complex structure. Based on experiments supported by theoretical models, it was possible to estimate channels' width (~150 nm) between the chromatin structure. The nuclei channels can constitute as much as 34% of the nuclei's volume which is around 240 fL. If they were narrower, the chromatin fibers would be more dispersed, making the molecules' efficient movement inside impossible. It is fascinating that the nucleus can contain such large amounts of DNA and other chemical elements without disturbing the molecules' migration. This is all thanks to the well-arranged chromatin fibers made by DNA with structural proteins that give the double helix its shape. The mobility of particular chemical elements through the biological fluid in molecular channels is essential in many processes, such as creating specific molecules and forming new protein complex structures.

"These results can be of great importance when designing biological drugs such as therapeutic proteins, enzymes, and monoclonal antibodies, which can have the hydrodynamic radii larger than conventional chemical drugs based on synthetic compounds." - concludes dr. Bubak

As a result of these studies, the mobility of the molecules in the nuclear channels is now described in detail and well-understood for the first time. Thanks to the research presented in this work, we now know how the chromatin fibers govern molecule organization, revealing the intriguing molecular machinery hidden deep inside the nucleus. We are now one step closer to developing therapeutic agents that can be effectively transported into the nucleus.

In 1991, scientists Brian O'Regan and Michael Grätzel at EPFL published a seminal paper describing a new type of solar cell: the dye-sensitized solar cell (DSSC), also known as "Grätzel cell". Simple and cheap to build while being flexible and versatile, DSSCs are already manufactured on a multi-megawatt scale, cutting a significant slice of the photovoltaic market, which currently supplies almost 3% of all the world's electricity, well in the race to reduce carbon emissions.

Now, Dan Zhang and Marko Stojanovic, two PhD students in Grätzel's lab at EPFL's School of Basic Sciences, have led the development of a simple dye for DSSCs, called MS5. In devices, this new sensitizer can either be used as single dye, and produce an open-circuit voltage - the maximum voltage a solar cell can reach in full sunlight - of 1.24 Volts or as co-sensitizer, along with the commercial dye XY1b, and enable a power conversion efficiency of 13.5 %. Both are among the highest in the field of DSSCs.

The work is published in Nature Communications.

The team used this new dye in combination with another organic sensitizer coded XY1b. Apart from absorbing photons from the blue and yellow domain of the solar emission, the role of the new dye in this tandem is to boost the voltage output of the device by retarding the recombination of charge carriers generated by light. Called MS5, the photosensitizer was used with a copper (II/I) electrolyte to enable the DSSC achieve its impressive efficiency.

"Our work constitutes an important breakthrough in the work of DSSCs and especially dye design," says Michael Grätzel. "It shows that high performances are achievable with a relatively simple dye through judicious molecular engineering of the sensitizer's molecular structure."

Tested under ambient light conditions, the dye showed impressive performance, which is crucial for photovoltaics to be effective under cloudy conditions, or in-door applications to power electronic devices applied e.g. for the internet of things. And last but not least, MS5 is easy to synthesize up to the gram scale using a one-step procedure that researchers describe in their paper.

"Our results not only push the field of dye-sensitized solar cells further, but demonstrate EPFL's leading expertise in the field," says Marko Stojanovic.

Flashlight fish have the ability to generate situation-specific blink patterns resembling a visual Morse code. Researchers at Ruhr-Universität Bochum have shown in laboratory and field experiments that the animals use these light signals to coordinate their behaviour in the school when visibility is limited. Both the light intensity and the blinking frequency affected the animals' behaviour. The team headed by Peter Jägers and Professor Stefan Herlitze from the Department of General Zoology and Neurobiology has shared their findings in the journal Scientific Reports, published online on 19 March 2021. "Our data show that flashlight fish are attracted by the light signals emitted by other school members," points out Jägers.

Milky Way in the water

Flashlight fish of the species Anomalops katoptron have a luminescent organ under their eyes that is filled with luminescent bacteria and which they can occlude so that it looks as if they are blinking. During the day, the animals hide in caves, rock crevices or in dark, deep water. "On moonless nights, up to a thousand individuals migrate in a school into the plankton-rich surface water," says Peter Jägers, who observed the fish in the wild during a diving expedition in the Indo-Pacific. "It is a surreal experience to see the schools - like a Milky Way in the water."

To understand the function of the flashing patterns, the researchers first studied Anomalops katoptron in the lab in a large water tank containing fish dummies that could be digitally controlled to mimic the animals' light signals. They also used infrared cameras to record the movements of individual animals in response to the artificial flashing lights. During the experiments, only one animal was in the tank at a time, with several individuals being tested one after the other.

Flashlight dummies attract fish

When the researchers placed a single dummy that was flashing light in the middle of the tank, the fish moved closer to it the faster the light flashed. In another experiment, 13 lights were positioned around the tank and lit up one after the other at varying time intervals. "We observed a high motivation among the flashlight fish to head towards the light," says Peter Jägers.

Based on the laboratory experiments, the researchers deduced that a faster flashing is a signal for Anomalops katoptron to stay closer to their fellow fish in the school, as the group offers, for example, protection from predators. This theory was confirmed in field experiments. On a diving expedition, the researchers showed that the animals reacted to stress by blinking more rapidly.

Waiting for the school at night in the sea

Diving at night in the dark, the researchers waited until a school of flashlight fish got close. The animals avoided light brighter than moonlight by fleeing immediately. The Bochum team triggered the escape response with dim red light and simultaneously recorded the animals and their blinking patterns with special cameras. This is how they showed that stress was associated with an increased blinking frequency. "We assume that the increased blinking frequency is the signal to follow the other group members more closely under stress," concludes Peter Jägers. "In our study, we demonstrated for the first time that there is a direct link between visually communicated signals under limited light conditions, such as those prevailing at night or in the deep sea, and the school formation of fish. We hope that this can be of help in future studies of, for example, the largely unexplored deep sea."

COLUMBUS, Ohio - Recent generations show a worrying decline in health compared to their parents and grandparents when they were the same age, a new national study reveals.

Researchers found that, compared to previous generations, members of Generation X and Generation Y showed poorer physical health, higher levels of unhealthy behaviors such as alcohol use and smoking, and more depression and anxiety.

The results suggest the likelihood of higher levels of diseases and more deaths in younger generations than we have seen in the past, said Hui Zheng, lead author of the study and professor of sociology at The Ohio State University.

"The worsening health profiles we found in Gen X and Gen Y is alarming," Zheng said.

"If we don't find a way to slow this trend, we are potentially going to see an expansion of morbidity and mortality rates in the United States as these generations get older."

Zheng conducted the study with Paola Echave, a graduate student in sociology at Ohio State. The results were published yesterday (March 18, 2021) in the American Journal of Epidemiology.

The researchers used data from the National Health and Nutrition Examination Survey 1988-2016 (62,833 respondents) and the National Health Interview Survey 1997-2018 (625,221 respondents), both conducted by the National Center for Health Statistics.

To measure physical health, the researchers used eight markers of a condition called metabolic syndrome, a constellation of risk factors for heart disease, stroke, kidney disease and diabetes. Some of the markers include waist circumference, blood pressure, cholesterol level and body mass index (BMI). They also used one marker of chronic inflammation, low urinary albumin, and one additional marker of renal function, creatinine clearance.

The researchers found that the measures of physical health have worsened from the Baby Boomer generation through Gen X (born 1965-80) and Gen Y (born 1981-99). For whites, increases in metabolic syndrome were the main culprit, while increases in chronic inflammation were seen most in Black Americans, particularly men.

"The declining health trends in recent generations is a shocking finding," Zheng said. "It suggests we may have a challenging health prospect in the United State in coming years."

Zheng said it is beyond the scope of the study to comprehensively explain the reasons behind the health decline. But the researchers did check two factors. They found smoking couldn't explain the decline. Obesity could help explain the increase in metabolic syndrome, but not the increases seen in chronic inflammation.

It wasn't just the overall health markers that were concerning for some members of the younger generations, Zheng said.

Results showed that levels of anxiety and depression have increased for each generation of whites from the War Babies generation (born 1943-45) through Gen Y.

While levels of these two mental health indicators did increase for Blacks up through the early Baby Boomers, the rate has been generally flat since then.

Health behaviors also show worrying trends.

The probability of heavy drinking has continuously increased across generations for whites and Black males, especially after late-Gen X (born 1973-80).

For whites and Blacks, the probability of using street drugs peaked at late-Boomers (born 1956-64), decreased afterward, then rose again for late-Gen X. For Hispanics, it has continuously increased since early-Baby Boomers.

Surprisingly, results suggest the probability of having ever smoked has continuously increased across generations for all groups.

How can this be true with other research showing a decline in overall cigarette consumption since the 1970s?

"One possibility is that people in older generations are quitting smoking in larger numbers while younger generations are more likely to start smoking," Zheng said. "But we need further research to see if that is correct."

Zheng said these results may be just an early warning of what is to come.

"People in Gen X and Gen Y are still relatively young, so we may be underestimating their health problems," he said. "When they get older and chronic diseases become more prevalent, we'll have a better view of their health status."

Zheng noted that the United States has already seen recent decreases in life expectancy and increases in disability and morbidity.

"Our results suggest that without effective policy interventions, these disturbing trends won't be temporary, but a battle we'll have to continue to fight."

Most drugs operate via the membranes that surround the body's cells. A study by researchers at Karolinska Institutet in Sweden has now mapped the structure and mechanism of MGST2, a membrane enzyme that, amongst other things, plays a part in chronic inflammation and cancer. The study, which is published in the journal Nature Communications, can make a significant contribution to the development of future drugs.

All our cells are enclosed in a fat-rich membrane. The cells' equivalent to organs, the organelles, are also enclosed by membranes. Embedded in the cell's internal and external membranes are proteins that regulate a large number of vital functions. Almost half of all drugs are effective via membrane proteins, such as enzymes, receptors and transporters.

Researchers at Karolinska Institutet have now, with the aid of X-ray crystallography, molecular dynamics simulations and biochemical techniques, been able to determine the 3D structure and mechanism of an important enzyme embedded in the cell's nuclear membrane.

The membrane enzyme MGST2 (Microsomal Glutathione S-Transferase 2) is the motor of a biochemical process that causes oxidative stress and the formation of oxygen radicals and, subsequently, DNA damage and cell death.

"Membrane proteins are hard to study and it's fantastic that we've managed to determine the crystal structure for MGST2 at high resolution," says the study's first author Madhuranayaki Thulasingam, researcher at the Department of Medical Biochemistry and Biophysics, Karolinska Institutet. "One of the study's findings is that MGST2 is made up of three functional units that are controlled in an unusually sophisticated manner. The three units are involved in mutually coordinated movements, taking turns to perform the enzyme's function one active unit at a time."

MGST2 belongs to a larger family of enzymes that control the formation of prostaglandins and leukotrienes, signal molecules that regulate fever, pain and inflammation of the airways, joints, heart and blood vessels.

The results provide valuable information on the molecular regulation of other members of the enzyme family, many of which are important targets for future drug development.

"We hope that our results will be able to contribute to the development of drugs for many diseases characterised by increased synthesis of oxygen radicals and cell death, such as chronic inflammation, cancer and side-effects of radio- and chemotherapy," says principal investigator Jesper Z. Haeggström, professor at the Department of Medical Biochemistry and Biophysics, Karolinska Institutet.

Parkinson's disease is the second most common, age-related, neurodegenerative disease: In Germany alone, about 300,000 people are affected and experience sometimes major limitations to their quality of life. Although Parkinson's is so widespread, there is still no treatment that targets the cause of the disease and can stop it in its tracks.
However, current research provides new hope: A research team at the University of Konstanz led by Professor Marcus Groettrup describes a new approach for developing future treatments for Parkinson's. The biologists demonstrated that the ubiquitin-like protein FAT10 inhibits the molecular defence mechanisms protecting the brain from Parkinson's disease. The biological mechanism is tricky: FAT10 causes processes in our own body that degrade the body's molecular "guardians" against Parkinson's disease (the enzyme Parkin). Instead of getting rid of damaged mitochondria in brain cells, Parkin is itself disposed of by the body. The research results were published in the scientific journal Cell Reports on 16 March 2021.

Damaged power plants of the cells

Parkinson's disease develops as a result of nerve cells dying off in the mesencephalon (midbrain). This is caused by faulty disposal of damaged mitochondria, the cells' "power plants". When damaged mitochondria are not disposed of by the body, oxygen radicals develop in the brain. These, in turn, damage the nerve cells, causing them to die.

So that the body can dispose of mitochondria, they have to be marked by a signalling substance. This can be compared with labelling them as "broken - please throw away". The enzyme Parkin is responsible for labelling damaged mitochondria. The molecular label it gives them contains the protein ubiquitin.

Wrongly labelled

This is where the protein FAT10 comes into play. FAT10 has a very similar structure and function to ubiquitin. It is also a signalling substance that labels other molecules for disposal. Unfortunately, FAT10 is the wrong label for mitochondria. FAT10 not only labels the damaged mitochondria, but also the enzyme Parkin for the body to dispose of.

To use a picture: It would be like labelling the cell's own guardians for disposal - the very ones that otherwise label damaged mitochondria for disposal. The body then does what the labels tell it to do. The more guardians are disposed of, the fewer damaged mitochondria can be correctly labelled for disposal. What happens as a result? The body's defence processes do not dispose of the damaged mitochondria - and the brain cells themselves are damaged over time.

"We hope this discovery provides a new approach to developing an effective treatment for Parkinson's. An inhibitor for FAT10 could possibly be used to limit the disposal of Parkin and ensure that damaged mitochondria are disposed of correctly", says Marcus Groettrup.

A study by Monash University has uncovered that liver metabolism is disrupted in people with obesity-related type 2 diabetes, which contributes to high blood sugar and muscle loss - also known as skeletal muscle atrophy.

Using human trials as well as mouse models, collaborative research led by Dr Adam Rose at Monash Biomedicine Discovery Institute has found the liver metabolism of the amino acid alanine is altered in people with obesity-related type 2 diabetes. By selectively silencing enzymes that break down alanine in liver cells, high blood sugar and muscle loss can be reversed by the restoration of skeletal muscle protein synthesis, a critical determinant of muscle size and strength.

The research, published today in Nature Metabolism, has shown the altered liver metabolism directly affects muscle size and strength and the mechanism behind this is driven by elevated levels of the hormones cortisol and glucagon which enhance the cycling of amino acids between liver and skeletal muscle, causing muscles to become smaller and weaker.

Along with metabolic dysfunction and related complications, an often overlooked co-morbidity of obesity is skeletal muscle atrophy, which causes frailty, and is related to reduced life-quality and death.

"The ageing-related diseases of skeletal muscle loss and type 2 diabetes are very prevalent and are a huge societal and economic burden. We have known for some time that the ageing-related diseases of skeletal muscle loss and type 2 diabetes were linked but we didn't know how," Dr Rose said.

He adds: "Our studies demonstrate that the liver is a critical control point for muscle protein metabolism; a discovery that is quite surprising. We believe that our new findings highlight the need to examine the role of skeletal muscle atrophy in type 2 diabetes more closely in human clinical populations."

The study solidifies the long-known metabolic biochemistry staple, the glucose-alanine cycle, as a fundamental part of metabolism in health and disease.

Mitochondria are important cellular power plants whose diminished activity has been previously demonstrated to be associated with obesity by a group of researchers at the University of Helsinki. Now, in a new international study coordinated by the University of Helsinki, the researchers have determined that the method of weight loss affects the metabolic pathways of mitochondria in fat tissue, also known as adipose tissue.

The study was recently published in the Journal of Clinical Endocrinology and Metabolism.

The researchers combined two datasets on calorie restriction diets and two datasets on weight loss surgery, or bariatric surgery, from Europe, monitoring dieters' weight loss as well as metabolism. A biopsy was taken from the study subjects' adipose tissue both at the beginning and the end of their weight reduction.

Ordinary dieting based on calorie restrictions put the mitochondria in the adipose tissue out of tune, further reducing the expression of related genes. In the case of similar weight loss resulting from bariatric surgery, the function of mitochondrial genes was improved and the activity level of mitochondrial metabolic pathways was higher.

The analyses conducted in the study were set in proportion to weight loss so that the results did not depend on greater weight loss in patients who had undergone surgery.

Why does lost weight come back? Impaired mitochondrial function is a potential cause

Weight loss brings improvements to many metabolic changes associated with obesity, including disorders of glucose and lipid metabolism. Such beneficial effects were also observed in the new study, both in those who followed a regular diet and in those who underwent bariatric surgery.

"This is why it was astonishing to see that the activity of mitochondrial metabolic pathways in adipose tissue was entirely opposite in the two different groups," says researcher Birgitta van der Kolk from the University of Helsinki's Obesity Research Unit.

"Our observations indicate that impaired mitochondrial activity after losing weight by dieting may be the cause of adipose tissue rapidly building up again after weight loss. At the same time, bariatric surgery patients are better protected against regaining weight, which makes us suspect that a recovery of activity by mitochondria in the adipose tissue may be a factor underlying this phenomenon," says Professor Kirsi Pietiläinen, who led the study.

The study utilised a technique known as transcriptomics analysis, which makes it possible to read the genome as a whole.

"By combining these broad-based techniques, biocomputing and extensive European datasets, we observed entirely unexpected links between dieting and the mitochondria of adipose tissue. In the future, it is important to investigate the relevance of these mechanisms to the functioning of such tissue and weight regain," Pietiläinen adds.

Atypical teratoid rhabdoid tumor (ATRT) is a rare brain tumor that predominantly occurs in young children. Scientists at St. Jude Children's Research Hospital used data from two clinical trials to study the molecular groups of ATRT and correlate them with clinical outcomes. A paper detailing the findings was published today in Clinical Cancer Research, a journal of the American Association for Cancer Research.

"If you look at the biology of ATRT, we have learned in the last few years that this is not a single disease but instead there are at least three biologically different groups of the same disease," said first and corresponding author Santhosh Upadhyaya, M.D., St. Jude Department of Oncology. "But what are the outcomes for these different groups? That is where the current St. Jude study offers insight into how these different groups of ATRT can present, and what their outcomes may be with different treatment regimens."

There are three previously established molecular groups of ATRT: ATRT-MYC, ATRT-SHH, and ATRT-TYR. Researchers used data from the SJYC07 and SJMB03 clinical trials to look at treatment outcomes from 74 children with ATRT. This is one of the largest cohorts of children with this disease, because ATRT is a rare pediatric cancer.

Findings showed that ATRT-TYR typically occurs in children younger than 3 years old and is less likely to metastasize. They also found that ATRT-SHH tends to occur in very young children and has a higher chance of metastasis at presentation. Additionally, although children with ATRT-TYR had the best overall response, those with ATRT-SHH and ATRT-MYC had comparable treatment responses in the absence of metastases.

The researchers also looked at the SMARCB1 gene in the blood--a hallmark genetic mutation found in ATRT. The scientists showed that approximately a third of tested children have an abnormality in the SMARCB1 gene. These children tend to develop ATRT at a younger age and are more likely to have the ATRT-SHH group. The researchers found that having this abnormality did not predict treatment outcome.

"While we have clearly made giant strides in understanding the molecular basis of ATRT, substantial progress is still required before treatment decisions can be made on the basis of different molecular groups," Upadhyaya said.

Age and metastasis still guide the way

The mortality rate for ATRT is around 70%, and children are typically diagnosed under the age of 3. Age of the child at diagnosis and the extent of metastatic spread remain the two most important factors to consider for prognosis and treatment of this disease.

Children who are older when they are diagnosed and who do not have metastatic spread typically experience the best outcomes. Children under the age of 3 cannot be treated with the radiation therapy offered to older children, which affects outcomes. The researchers stress that children in each group have a chance for a positive outcome, keeping in mind their age and metastatic status.

"Although a better understanding of the molecular groups of ATRT is important for developing the next generation of treatments for this disease, age at diagnosis and metastatic spread are still the most important clinical factors to consider," said senior author Amar Gajjar, M.D., St. Jude Department of Pediatric Medicine chair.

Ticket inspection on public transport can prompt law-abiding people to behave dishonestly once they have gotten off the bus, according to a study published in The Economic Journal. The study was written by three experimental economists: Fabio Galeotti and Marie Claire Villeval of The French National Centre for Scientific Research (CNRS) in the Groupe d'Analyse et de Théorie Economique Lyon St-Etienne (GATE), and Valeria Maggian from Ca' Foscari University of Venice.

In order to study the "side effects" of ticket inspection, researchers designed and carried out a complex large-scale study on public transport and in the streets of Lyon, France. During typical weekdays and avoiding rush hours, research assistants and professional actors/actresses, in pairs, got onto a bus or tram.

The research assistants took note of the passengers who, after getting on board, validated their ticket and of those who did not, in a context in which ticket validation was compulsory. The research assistant and the actor/actress both got off at the same stop of the targeted passenger and, once on the street, the actor/actress pretend to find a €5 banknote on the ground, and call the attention of the targeted passenger by asking whether he or she had lost the banknote. In total, the researchers tested 708 individuals.

"One third of the passengers who had validated their ticket subsequently claimed ownership of the banknote. Surprisingly, that percentage jumped to 50% if a team of ticket inspectors had previously controlled the people on the bus" says Valeria Maggian, professor of experimental economics at Ca' Foscari. "This indicates that inspections can influence our perception of how widespread dishonest behaviour in society is. In other words, the more ticket inspectors get on board, the more passengers perceive that there are dishonest people around. In fact, a plausible explanation is that honest people claimed ownership of the €5 banknote in an effort to conform to prevailing dishonesty, with a negative unexpected consequence or spillover effect."

This study is the first to show that ticket inspections can affect the honesty of passengers in their everyday life. In fact, among the passengers who had not validated their ticket, 53% claimed ownership of the banknote without ticket inspection, while 67% did so after ticket inspection. Among the passengers who had validated their ticket, 32% claimed ownership of the banknote without ticket inspection, while 51% did so after ticket inspection.

"This study does not recommend eliminating inspections," Maggian states "but it indicates that sanctioning dishonest behaviour in public might not be the best way to discourage such behaviour. Other actions might be more effective, such as more discrete inspections carried out in smaller groups and in civilian clothing. It is important that actions that are meant to encourage honest behaviour do not end up promoting dishonesty. In order to study the effects of a policy, in fact, we need to look beyond a specific situation."

The study was conducted in the most realistic way possible and the people who participated were not aware that their behaviour was being monitored. Research assistants and actors/actresses carried out their tasks without knowing what the aim of the project was, in order to avoid their being influenced. Moreover, the actors/actresses were selected by means of special auditions organised by an acting school in Lyon. The credibility of the actors' and actresses' performance in the banknote scene was evaluated via video by 20 people. The two female actresses and two male actors were selected in order to ensure a similar performance (across conditions), so that the individual actor's or actresses' style would not influence the target passenger's response.

Once they had gotten off the bus or tram, the actors/actresses pretended to be engaged in a phone conversation. On the one hand, this was meant to minimise interactions that might compromise the experiment; on the other hand, this allowed the actors/actresses to record her voice when asking the passenger about the €5 banknote. The recordings were then submitted to another group of people who were asked to predict whether the targeted passenger would accept or refuse the €5 banknote. This final step in the experiment revealed that the tone of voice used by the actors/actresses did not influence the target passenger's choice.

Though our galaxy is an immense city of at least 200 billion stars, the details of how they formed remain largely cloaked in mystery.

Scientists know that stars form from the collapse of huge hydrogen clouds that are squeezed under gravity to the point where nuclear fusion ignites. But only about 30 percent of the cloud's initial mass winds up as a newborn star. Where does the rest of the hydrogen go during such a terribly inefficient process?

It has been assumed that a newly forming star blows off a lot of hot gas through lightsaber-shaped outflowing jets and hurricane-like winds launched from the encircling disk by powerful magnetic fields. These fireworks should squelch further growth of the central star. But a new, comprehensive Hubble survey shows that this most common explanation doesn't seem to work, leaving astronomers puzzled.

Researchers used data previously collected from NASA's Hubble and Spitzer space telescopes and the European Space Agency's Herschel Space Telescope to analyze 304 developing stars, called protostars, in the Orion Complex, the nearest major star-forming region to Earth. (Spitzer and Herschel are no longer operational).

In this largest-ever survey of nascent stars to date, researchers are finding that gas-clearing by a star's outflow may not be as important in determining its final mass as conventional theories suggest. The researchers' goal was to determine whether stellar outflows halt the infall of gas onto a star and stop it from growing.

Instead, they found that the cavities in the surrounding gas cloud sculpted by a forming star's outflow did not grow regularly as they matured, as theories propose.

"In one stellar formation model, if you start out with a small cavity, as the protostar rapidly becomes more evolved, its outflow creates an ever-larger cavity until the surrounding gas is eventually blown away, leaving an isolated star," explained lead researcher Nolan Habel of the University of Toledo in Ohio.

"Our observations indicate there is no progressive growth that we can find, so the cavities are not growing until they push out all of the mass in the cloud. So, there must be some other process going on that gets rid of the gas that doesn't end up in the star."

The team's results will appear in an upcoming issue of The Astrophysical Journal.

A Star is Born

During a star's relatively brief birthing stage, lasting only about 500,000 years, the star quickly bulks up on mass. What gets messy is that, as the star grows, it launches a wind, as well as a pair of spinning, lawn-sprinkler-style jets shooting off in opposite directions. These outflows begin to eat away at the surrounding cloud, creating cavities in the gas.

Popular theories predict that as the young star evolves and the outflows continue, the cavities grow wider until the entire gas cloud around the star is completely pushed away. With its gas tank empty, the star stops accreting mass - in other words, it stops growing.

To look for cavity growth, the researchers first sorted the protostars by age by analyzing Herschel and Spitzer data of each star's light output. The protostars in the Hubble observations were also observed as part of the Herschel telescope's Herschel Orion Protostar Survey.

Then the astronomers observed the cavities in near-infrared light with Hubble's Near-infrared Camera and Multi-object Spectrometer and Wide Field Camera 3. The observations were taken between 2008 and 2017. Although the stars themselves are shrouded in dust, they emit powerful radiation which strikes the cavity walls and scatters off dust grains, illuminating the gaps in the gaseous envelopes in infrared light.

The Hubble images reveal the details of the cavities produced by protostars at various stages of evolution. Habel's team used the images to measure the structures' shapes and estimate the volumes of gas cleared out to form the cavities. From this analysis, they could estimate the amount of mass that had been cleared out by the stars' outbursts.

"We find that at the end of the protostellar phase, where most of the gas has fallen from the surrounding cloud onto the star, a number of young stars still have fairly narrow cavities," said team member Tom Megeath of the University of Toledo. "So, this picture that is still commonly held of what determines the mass of a star and what halts the infall of gas is that this growing outflow cavity scoops up all of the gas. This has been pretty fundamental to our idea of how star formation proceeds, but it just doesn't seem to fit the data here."

Future telescopes such as NASA's upcoming James Webb Space Telescope will probe deeper into a protostar's formation process. Webb spectroscopic observations will observe the inner regions of disks surrounding protostars in infrared light, looking for jets in the youngest sources. Webb also will help astronomers measure the accretion rate of material from the disk onto the star, and study how the inner disk is interacting with the outflow.

A Russian-German research team has created a quantum sensor that grants access to measurement and manipulation of individual two-level defects in qubits. The study by NUST MISIS, Russian Quantum Center and the Karlsruhe Institute of Technology, published in npj Quantum Information, may pave the way for quantum computing.

In quantum computing the information is encoded in qubits. Qubits (or quantum bits), the quantum mechanical analogue of a classical bit, are coherent two-level systems. A leading qubit modality today superconducting qubits based on the Josephson junction. That is the kind of qubit IBM and Google used in their quantum processors. However, scientists are still searching for the perfect qubit -- the one that can be precisely measured and controlled, while remaining unaffected by its environment.

The key element of a superconducting qubit is the nanoscale superconductor--insulator--superconductor Josephson junction. A Josephson junction is a tunnel junction made of two pieces of superconducting metal separated by a very thin insulating barrier. The most commonly used insulator is aluminum oxide.

Modern techniques do not allow to build a qubit with 100% precision, resulting in so-called tunneling two-level defects that limit the performance of superconducting quantum devices and cause computational errors. Those defects contribute to a qubit's extremely short life span, or decoherence.

Tunneling defects in aluminum oxide and at surfaces of superconductors are an important source of fluctuations and energy losses in superconducting qubits, ultimately limiting the computer run-time. The more material defects occur, the more they affect the cubit's performance, causing more computational errors, the researchers noted.

The new quantum sensor grants access to measurement and manipulation of individual two-level defects in quantum systems. According to Prof. Alexey Ustinov, Head of the Laboratory for Superconducting Metamaterials at NUST MISIS and Group Head at Russian Quantum Center, who co-authored the study, the sensor itself is a superconducting qubit, and it allows the detection and manipulation of individual defects. Traditional techniques for studying material structure, such as small-angle X-ray scattering (SAXS), are not sensitive enough to spot small individual defects, therefore using those techniques won't help to build the best qubit. The study may open avenues for quantum material spectroscopy to investigate the structure of tunneling defects and to develop low-loss dielectrics that are urgently required for the advancement of superconducting quantum computers, the researchers believe.

UNIVERSITY PARK, Pa. -- A team led by researchers in Penn State's College of Agricultural Sciences has developed a diagnostic test that can identify virulent forms of the swine bacterial pathogen Streptococcus equi subspecies zooepidemicus -- often referred to as "Strep zoo" -- which can cause severe illness and death in pigs, other animals and rarely people.

Outbreaks of S. zooepidemicus causing high mortality in swine first were reported in Asia in 1977, and until recently, the pathogen was not thought to be a major concern in North America. However, high-mortality Strep zoo outbreaks occurred in swine herds in Canada, Tennessee, Ohio and Pennsylvania in 2019. Different versions of the pathogen also can cause a range of disease symptoms in horses, ruminants, guinea pigs, monkeys, cats, dogs, poultry and humans.

Pigs infected with Strep zoo may suffer a sudden onset of lethargy, weakness, high fever and rapidly escalating mortality that can approach 30% to 50% of infected animals. However, the bacterium that causes these symptoms presents a diagnostic challenge because virulent strains are largely indistinguishable from benign strains, according to lead researcher Suresh Kuchipudi, clinical professor of veterinary and biomedical sciences.

"Rapid and accurate diagnosis is absolutely critical for controlling and limiting the spread of this emerging disease of swine," said Kuchipudi, who also is the associate director of Penn State's Animal Diagnostic Laboratory. "But the version of the bacterium that is deadly is very similar -- with only minor genetic differences -- to bacteria that are commonly found in healthy pigs and in other animals. As a result, conventional methods can't selectively identify this virulent version."

To address this issue, the team set out to identify genetic factors that are unique to virulent Strep zoo bacteria. Using cutting edge tools including next-generation sequencing, the researchers looked at bacterial isolates from a lethal Pennsylvania Strep zoo outbreak. Their analysis zeroed in on the SzM gene, which had been identified in previous research as a key virulence factor of S. zooepidemicus for swine but was not found in avirulent strains of the pathogen.

Targeting the SzM gene, researchers developed a probe-based, real-time polymerase chain reaction, or PCR, diagnostic assay for the detection of virulent Strep zoo isolates. They evaluated the assay's specificity and sensitivity by using it to test a panel of reference bacterial isolates and viral pathogens commonly associated with swine respiratory disease. In addition, they applied the newly developed assay to test avirulent strains of S. zooepidemicus.

The team's study, reported recently in Frontiers in Veterinary Science, found that the new PCR test reliably identified virulent Strep zoo strains, while producing negative results when testing other pathogens that can cause porcine respiratory diseases, as well as avirulent S. zooepidemicus.

Kuchipudi noted that emerging and reemerging animal infectious diseases have the potential to negatively impact animal health, food safety and trade.

"Several animal infectious diseases also have zoonotic potential, meaning they can have a significant impact on public health," he said. "For these reasons, accurate and rapid diagnosis is of utmost importance. This novel assay -- which can return results in less than four hours and is the first test that can detect virulent S. zooepidemicus selectively in pigs -- provides a practical solution to the previously unsolved problem of diagnosing Strep zoo in swine herds."

Kuchipudi added that a key question yet to be answered is whether susceptible animals of other species serve as reservoirs for S. zooepidemicus. "This PCR assay also can be used to answer this question and further investigate the host range of S. zooepidemicus," he said.

BOSTON - Patients who regurgitate regularly but without any known cause may have a condition called rumination. Unfortunately, rumination is often confused with other gastrointestinal conditions, which means many patients may not be getting prompt treatment. But a new study by investigators at Massachusetts General Hospital (MGH) in Neurogastroenterology and Motility clearly describes this syndrome, how to distinguish it from other conditions, and how to treat it.

Rumination syndrome is a behavioral problem, in which patients effortlessly and repeatedly regurgitate food into their mouths while eating and sitting upright. It is a learned behavior that is classified as a disorder of the gut-brain interaction (DGBI). Many experts think that regurgitations develop as a habit involving an uncomfortable, mounting sensation or inner tension (similar to patients with tics) that results in contraction of the abdominal walls after eating. This pattern gets reinforced with positive associations (such as relief of anxiety and stress after regurgitation) as well as negative associations (such as the discomfort of trying to suppress the inner tension without regurgitating).

"This condition causes a lot of embarrassment and may stop people from eating with others," explains Trisha Satya Pasricha, MD, co-lead author with Helen Burton Murray, PhD, both of MGH's Division of Gastroenterology. "It is not well understood, and is often mistaken for other disorders."

One reason rumination symptoms are missed is because they overlap with other DGBIs, such as functional dyspepsia (stomach pain or indigestion) or gastroparesis, which is when patients feel nauseous and full after eating just a small amount. Patients may incorrectly describe their symptoms as reflux or vomiting. As a result, the condition may go undiagnosed or misdiagnosed for a long period. That can lead to significant social constraint and possibly weight loss.

Pasricha and her colleagues screened 242 patients who were referred to specialists for gastric symptoms that could indicate they were experiencing rumination. The symptoms that brought these patients to a gastroenterologist included dyspepsia and gastroparesis.

Thirty-one of the 242 (12.8%) patients met criteria for rumination syndrome, which is determined using a gastric symptom scoring system. Almost half of those patients (48%) reported associated psychosocial impairment, meaning that they experienced difficulty in social situations because of their condition.

Comparing those patients with rumination and those without, there were no differences in race, gender, frequency of diabetes, or frequency of gastroparesis. "There is little demographically that distinguishes these patients other than their tendency to regurgitate when eating," says Pasricha. "They are not more likely to have a history of an eating disorder or weight problems."

However, the patients with rumination were more likely to also experience heartburn, particularly daytime symptoms. The researchers suggest that screening for heartburn and regurgitation could help identify more patients with this condition.

The treatment for rumination is behavioral and involves the practice of diaphragmatic, or deep, breathing. Two pilot trials have shown that this significantly improves gastroesophageal reflux. Comprehensive cognitive behavioral therapy for rumination syndrome (CBT-RS) is also recommended. CBT is an increasingly popular type of behavior therapy that helps people re-orient their thinking, teaching them new thought processes to replace old patterns that lead to self-harm and other poor outcomes.