Culture

Anyone who likes to sing in the shower probably knows that they sometimes sing out of tune. But what about professional singers? How well do they evaluate their own abilities? And what role does this self-assessment play in becoming a better musician? A research team from the Max Planck Institute for Empirical Aesthetics in Frankfurt, New York University, and the University of Hamburg has now investigated these questions scientifically in a study of professional singers.

The study participants, all female sopranos, were each recorded singing "Happy Birthday" in a studio. They were then asked to listen to all of the recordings and rate the pitch accuracy of both their own vocal performances and those of their colleagues. In Western culture, pitch accuracy--i.e., singing in tune--is associated with acoustic characteristics that can be quantified and thus serves as an objective measure of proficiency.

The research team derived a statistical model from the participants' evaluations of others. Using this, they were able to determine how well a singer rated others as well as her own performance.

"The results show that the singers were surprisingly inaccurate in their self-assessment. Most overestimated their own performance," says lead author Pauline Larrouy-Maestri of the Max Planck Institute for Empirical Aesthetics.

In addition, the researchers observed a correlation between singing competence and self-assessment ability: the better the singer (in terms of pitch-accuracy) the better they evaluated themselves. This outcome is surprising since experts in a certain domain usually tend to underestimate their abilities in this domain.

The study, the findings of which have just appeared in the Journal of Voice, thus not only underscores the fact that even professional singers do not necessarily evaluate their own vocal performance correctly. But it also suggests that self-evaluation itself may be a key factor in the development of exceptional musical skills.

Coral reefs are a favorite spot for scuba divers and are among the world's most diverse ecosystems. For example, the Hawaiian coral reefs, known as the "rainforests of the sea," host over 7,000 species of marine animals, fishes, birds and plants. But coral reefs are facing serious threats, including a number of diseases that have been linked to human activity.

To understand the connection between human activity and a type of tumorlike disease called growth anomalies (GAs), researchers at the National Institute of Standards and Technology (NIST) have collaborated with the U.S Geological Survey (USGS) and the National Oceanic and Atmospheric Administration (NOAA) to use an emerging molecular profiling method to identify 18 small molecules that promise to help them better understand the series of molecular reactions that lead to the disease.

GAs affect both the coral skeleton and its soft tissues. Scientists don't know the cause of the disease or how it spreads but have hypothesized that there is a strong correlation between GA prevalence in coral colonies and human population density nearby.

Almost all types of corals are made of hundreds to millions of individual soft-bodied animals called polyps. The polyps secrete calcium carbonate to form a hard skeleton that lays the foundation for the coral colony. GAs affect corals through irregular and accelerated growth of their skeleton, causing it to be less dense and filled with holes. This results in a tumorlike mass in the skeleton of a coral colony with fewer polyps and a diminished ability to reproduce.

Shallow water corals receive food like carbohydrates and oxygen as a byproduct of photosynthesis from the symbiotic relationship they have with zooxanthellae, photosynthetic algae that live inside coral tissues. GAs can lead to fewer symbiotic zooxanthellae and therefore less energy being absorbed from photosynthesis.

Even though GAs do not typically directly lead to coral death, they do affect the overall health of coral colonies and can pose an ecological threat to coral populations. To analyze the disease, NIST researchers chose the coral species Porites compressa as their target sample.

This coral species is known as the "finger" or "hump" coral and is part of the stony coral family, which is "one of the important reef-building species in Hawaii," said NIST chemist Tracey Schock. "They lay the foundation for the coral reef."

P. compressa is found in shallow lagoons off the Hawaiian Islands, and the researchers obtained their coral samples from Kaneohe Bay, Oahu. The bay has been studied widely as a site affected by human activity such as sewage discharge and metal pollution. GAs have previously been observed in the coral species there.

In order to analyze and study GAs in P. compressa, researchers turned to the field of metabolomics, which is the study of small molecules, such as those making up living organisms found in tissues, blood or urine. These small molecules, known as metabolites, are the intermediate and end products in a linked series of biochemical reactions known as molecular pathways in an organism.

Some examples of such small molecules include sugars like glucose, amino acids, lipids and fatty acids. Their production can be influenced by genetic and environmental factors and can help researchers better understand the biochemical activity of tissue or cells. In this case, chemical analysis of metabolites provides significant information that helps researchers understand the physiology of the disease.

For their study, researchers sampled a coral colony that had both healthy and diseased tissue. They split up their samples so they could assess the healthy coral and diseased coral separately. They also had a separate adjacent sample that was free of diseased tissue.

The samples were frozen in liquid nitrogen, and then freeze-dried for practical sample processing while maintaining metabolic integrity. The researchers then separated the diseased parts from the healthy colony using a hammer and stainless-steel chisel and collected the tissue from the skeleton with a brush. In one of the final stages of the sample preparation, they chemically extracted the metabolites from the coral tissue using a combination of methanol, water and chloroform.

"The method is novel for coral studies," said Schock. "With metabolomics, it is critical to preserve the state of all metabolites in a sample at the time of collection. This requires halting all biochemical activity using liquid nitrogen and maintaining this state until chemical extraction of the metabolome. The complexity of a coral structure necessitates stringent collection and processing protocols."

The researchers then produced a metabolomic analysis of the coral samples by using a reproducible profiling technique known as proton nuclear magnetic resonance (1H NMR).

The 1H NMR technique exposes the coral extract to electromagnetic fields and measures the radio frequency signals released by the hydrogens in the sample. The various kinds of metabolites are revealed by their unique signals which inform of their chemical environment. NMR detects all signals from the magnetic nuclei within a sample, making it an unbiased "all-in-one" technique. Two-dimensional NMR experiments that can identify both hydrogens (1H) and their directly bound carbon (13C) atoms provide more chemical information, giving confidence in the accuracy of the identities of the various metabolites within a sample.

The study identified 18 different metabolites and a new GA morphological form in P. compressa. The researchers found that GA tumors have distinct metabolite profiles compared with healthy areas of the same coral colony and detected specific metabolites and metabolic pathways that may be important for these profile differences. They also discovered that the loss of internal pH regulation is seemingly responsible for the hollow skeletons that are a characteristic of GAs.

"We have not only characterized new aspects of GA physiology, but have also discovered candidate pathways that provide a clear path forward for future research efforts aiming to further understand GA formation and coral metabolism, in general," said Schock.

As studies of this type accumulate, the researchers envision a database that could pull together coral metabolite information from multiple coral species into an accessible location for all scientists.

Collaborating with other researchers in different fields could increase understanding of the biological impacts of this disease on coral colonies. "We are going to learn which species are tolerant and which species are sensitive to stresses, and the physiological adaptations or mechanisms of both types will be important to conservation efforts," said Schock.

For now, the researchers hope these findings will be helpful for other scientists analyzing coral species and ultimately be beneficial for the coral reefs themselves, potentially aiding efforts to better preserve them.

Contrary to conventional thought, songbirds can taste sugar--even though songbirds are the descendants of meat-eating dinosaurs and are missing a key protein that allows humans and many other animals to taste sweetness. An international team investigated how many bird species can taste sweet and how far back that ability evolved. Their work was published today in the journal Science.

The researchers offered two species of songbirds a choice between sugar water and plain water--nectar-taking honeyeaters, as well as canaries, a grain-eating bird not known for consuming sweet foods. They also examined taste receptor responses sampled from a variety of other species. Regardless of whether their main diet consisted of seeds, grains, or insects, songbird taste receptors responded to sugars.

"This was a clear hint that we should concentrate on a range of songbirds, not only the nectar-specialized ones, when searching for the origins of avian sweet taste," explains senior author Maude Baldwin at the Max Planck Institute for Ornithology in Germany. Baldwin led this study with Yasuka Toda from Meiji University in Japan.

Sugar is a vital carbohydrate providing lots of energy and may have had far-reaching effects on songbird evolution. Though it is thought that most bird lineages can't taste sweetness at all, the scientists now believe that songbirds, which account for more than 40% of the world's bird species, can actually taste sweet, and that sugary food sources may have contributed to their success.

Baldwin and Toda dug down to the molecular level to understand the modifications to the "umami" taste receptor that enabled sweet perception among songbirds.

"Because sugar detection is complex, we needed to analyze more than one hundred receptor variants to reveal the molecular mechanisms underlying the sugar responses," says Toda. These exact changes coincide only slightly with those seen in the distantly-related hummingbirds, even though similar areas of the receptor are modified.

Though songbirds evolved similar workarounds to taste sweetness, they did so at different times, in different places, and in slightly different ways--an example of "convergent evolution." Some songbirds, such as honeyeaters, sunbirds, honeycreepers, and flowerpiercers are now just as dependent on nectar as the hummingbirds.

"This study fundamentally changes the way we think about the sensory perceptions of nearly half the world's birds," says study co-author Eliot Miller at the Cornell Lab of Ornithology. "It demonstrates that most songbirds definitely can taste sweet and got there by following nearly the same evolutionary path that hummingbirds did--it's a neat story about how convergence happens."

Exploring the songbird family tree, the researchers conclude that songbirds evolved to sense sweetness approximately 30 million years ago, before the early ancestors of songbirds left Australia, where all songbirds originated. Even after songbirds radiated across the world, they kept their ability to taste sugar.

Researchers in Japan, Germany, the United States, Hong Kong, and Australia participated in this study. Future studies will explore how sweet perception has coevolved with other physiological traits, such as changes in digestion and metabolism, across bird evolution.

A team of physicists from the Harvard-MIT Center for Ultracold Atoms and other universities has developed a special type of quantum computer known as a programmable quantum simulator capable of operating with 256 quantum bits, or "qubits."

The system marks a major step toward building large-scale quantum machines that could be used to shed light on a host of complex quantum processes and eventually help bring about real-world breakthroughs in material science, communication technologies, finance, and many other fields, overcoming research hurdles that are beyond the capabilities of even the fastest supercomputers today. Qubits are the fundamental building blocks on which quantum computers run and the source of their massive processing power.

"This moves the field into a new domain where no one has ever been to thus far," said Mikhail Lukin, the George Vasmer Leverett Professor of Physics, co-director of the Harvard Quantum Initiative, and one of the senior authors of the study published today in the journal Nature. "We are entering a completely new part of the quantum world."

According to Sepehr Ebadi, a physics student in the Graduate School of Arts and Sciences and the study's lead author, it is the combination of system's unprecedented size and programmability that puts it at the cutting edge of the race for a quantum computer, which harnesses the mysterious properties of matter at extremely small scales to greatly advance processing power. Under the right circumstances, the increase in qubits means the system can store and process exponentially more information than the classical bits on which standard computers run.

"The number of quantum states that are possible with only 256 qubits exceeds the number of atoms in the solar system," Ebadi said, explaining the system's vast size.

Already, the simulator has allowed researchers to observe several exotic quantum states of matter that had never before been realized experimentally, and to perform a quantum phase transition study so precise that it serves as the textbook example of how magnetism works at the quantum level.

These experiments provide powerful insights on the quantum physics underlying material properties and can help show scientists how to design new materials with exotic properties.

The project uses a significantly upgraded version of a platform the researchers developed in 2017, which was capable of reaching a size of 51 qubits. That older system allowed the researchers to capture ultra-cold rubidium atoms and arrange them in a specific order using a one-dimensional array of individually focused laser beams called optical tweezers.

This new system allows the atoms to be assembled in two-dimensional arrays of optical tweezers. This increases the achievable system size from 51 to 256 qubits. Using the tweezers, researchers can arrange the atoms in defect-free patterns and create programmable shapes like square, honeycomb, or triangular lattices to engineer different interactions between the qubits.

"The workhorse of this new platform is a device called the spatial light modulator, which is used to shape an optical wavefront to produce hundreds of individually focused optical tweezer beams," said Ebadi. "These devices are essentially the same as what is used inside a computer projector to display images on a screen, but we have adapted them to be a critical component of our quantum simulator."

The initial loading of the atoms into the optical tweezers is random, and the researchers must move the atoms around to arrange them into their target geometries. The researchers use a second set of moving optical tweezers to drag the atoms to their desired locations, eliminating the initial randomness. Lasers give the researchers complete control over the positioning of the atomic qubits and their coherent quantum manipulation.

Other senior authors of the study include Harvard Professors Subir Sachdev and Markus Greiner, who worked on the project along with Massachusetts Institute of Technology Professor Vladan Vuleti?, and scientists from Stanford, the University of California Berkeley, the University of Innsbruck in Austria, the Austrian Academy of Sciences, and QuEra Computing Inc. in Boston.

"Our work is part of a really intense, high-visibility global race to build bigger and better quantum computers," said Tout Wang, a research associate in physics at Harvard and one of the paper's authors. "The overall effort [beyond our own] has top academic research institutions involved and major private-sector investment from Google, IBM, Amazon, and many others."

The researchers are currently working to improve the system by improving laser control over qubits and making the system more programmable. They are also actively exploring how the system can be used for new applications, ranging from probing exotic forms of quantum matter to solving challenging real-world problems that can be naturally encoded on the qubits.

"This work enables a vast number of new scientific directions," Ebadi said. "We are nowhere near the limits of what can be done with these systems."

Although the giant panda is in practice a herbivore, its masticatory system functions differently from the other herbivores. Through the processes of natural selection, the giant panda's dietary preference has strongly impacted the evolution of its teeth and jaws. Researchers from the Institute of Dentistry at the University of Turku and the Biodiversity unit of the University of Turku together with researchers from the China Conservation and Research Center for Giant Panda (CCRCGP) have been the first in the world to solve the mystery of how the giant panda's special stomatognathic system functions.

The bamboo diet of the giant panda (Ailuropoda melanoleuca) has long been a mystery for researchers. The panda is in practice a herbivore, and its diet only consists of few dozen species of bamboo. Related to the consumption of bamboo, the giant panda has a special characteristic of peeling the green outer skin of all bamboo shoots, rich in abrasive and toxic compounds, by the highly adapted premolars.

Herbivores have usually evolved to have ridged molars that help them grind the plant material and jaws capable of moving sideways which is essential for grinding their food. Although the teeth of giant pandas have been studied extensively, until now, researchers have not paid attention to why the large canines of their upper jaw do not prevent the sideways movement of the lower jaw typical for herbivores - and also humans. The key to this has been the evolution of the temporomandibular joint and the premolar teeth.

Evolution of the Temporomandibular Joint Allows Sideways Movement

Using modern 3D scanning methods, the research group studied the movement of the giant panda's jaw and the structure of its teeth and found the answer to the question that had puzzled researchers for over a century: how are giant pandas able to use bamboo as their diet. The solution was that the panda's temporomandibular joint has evolved to differ from that of e.g. brown bear and polar bear. In addition to the open-closed movement reminding that of a hinge, the joint also allows the jaw to be moved sideways, which is required to peel the bamboo. Interestingly, this movement isn't prevented by the large canines the male pandas need to fight.

- The necessity to ensure adequate nutrition has helped evolve the temporomandibular joint and the shape of the teeth to allow efficient peeling of the bamboo without without exposing the premolars to the attritive or other damaging effect of bamboo diet, explains Professor Pekka Vallittu from the Institute of Dentistry.

The evolution of the giant panda's masticatory system, as demonstrated in the study, allowed them to be the only large mammals to access an endless source of nutrition in the form of bamboo in the early Pleistocene.

- The premolars giant pandas use for peeling bamboo are unique among the family of bears and allow the removal of the poisonous green skin of the bamboo which also includes mineral crystals which would wear their teeth, says Professor Juha Varrela from the Institute of Dentistry.

The study of how the giant panda's masticatory system functions also helps to understand human's occlusion and its characteristics better.

- Whether giant pandas grind their teeth still remains to be seen, ruminates Vallittu.

- This newly published study is of great scientific significance because it solves the long-prevailing mystery of the ecological interrelationship between the pandas and the bamboo plants, says Professor Jukka Salo from the Biodiversity Unit of the University of Turku.

12,000 people in Denmark and 7 to 10 million people worldwide suffer from Parkinson's Disease (PD). It is the second most common neurogenerative disorder of aging and the most common movement disorder, but the cause of the disease is largely unknown.

In a new study, researchers from the University of Copenhagen show that the most common form of the disease, encompassing 90 to 95 percent of all Parkinson's Disease cases known as sporadic PD, is caused by a blockage of a pathway that regulates the nerve cell's powerhouse, the mitochondria.

'Just like when people eat, cells take what they need and get rid of the rest waste products. But if our brain cells have this specific kind of signaling blockage, it means that the powerhouse of the cell - mitochondria - cannot get cleaned up after being damaged', explains corresponding author and group leader Professor Shohreh Issazadeh-Navikas at the Biotech Research & Innovation Centre.

The blockage leads to an accumulation of high amounts of damaged mitochondria, while not being able to produce enough energy for the cells. It causes neurons to gradually die, which is the reason for the development of Parkinson's Disease symptoms, and why it leads to dementia.

The blockage is caused by a dysregulation of the immune genes, more specifically a pathway called type 1 interferon, which is normally important for fight against viruses, but now we show that it is also responsible for regulating the energy supply of the nerve cells.

'Every part of our body needs to be regulated. We get a signal to stop eating, when we are full, and the same thing happens everywhere else in our body. If we get an infection, parts of our body need to fight it and stop it from replicating. But when the infection is cleaned up, the signal should subside. This is the job of a protein called PIAS2. That causes the blockage of the type 1 interferon-pathway, and when the infection is over, the blockage should stop and go back to normal. But that does not seem to be the case in patients with Parkinson's Disease. We further demonstrate that this dysregulation leads to a defect in the mitochondrial energy supply, as mentioned before', says Shohreh Issazadeh-Navikas.

These pathways are very important for brain functions, but they are also associated with microbial and virus recognition. For example, they are very important for fighting COVID-19, and a mutation in the related gene has been shown to be linked to a deadly outcome after contracting COVID-19.

The researchers combined and analyzed four data sets, which studied neurons from brains with Parkinson's Disease and looked at what type of genes they express.

They then looked at which gene patterns were disturbed in patients with Parkinson's Disease and especially those who had also developed PD with dementia.

In order to test the results, the major findings of the combined data was tried in three different mouse models using a negative regulator of the type I interferon pathway, PIAS2, which had been identified from the patients study as one of the key proteins linked to the progression of Parkinson's Disease and dementia.

'We show that a high accumulation of the PIAS2-protein is what is causing the blockage in the pathway, which should have activated the processes responsible for removing damaged protein and mitochondrial garbage', says Shohreh Issazadeh-Navikas.

'The accumulation of damaged mitochondrial mass further leads to increase of other toxic proteins. So when we compare patients to same-aged healthy patients without Parkinson's Disease, we see that this PIAS2-protein is highly expressed in the neurons, which is why this pathway should be evaluated for potential roles in the other forms of familial Parkinson's Disease that we have not studied here.'

The researchers hope the study will encourage research to counteract the pathway blockage, which could have a beneficial impact on the disease and towards preventing dementia.

In the next stages, the Shohreh Group will study how the pathway contributes to neuronal homeostasis and survival, as well as how its dysregulation causes neuronal cell death.

A presentation at this year's European Congress on Clinical Microbiology & Infectious Diseases (ECCMID), held online this year, will discuss the growing evidence that the beta SARS-CoV-2 variant first identified in South Africa is leading to more severe disease in people living with HIV, and that failure to clear SARS-CoV-2 infection in a patient with advanced HIV creates conditions that can lead to evolution of dangerous mutations in SARS-CoV-2.

Control of HIV with antiretroviral therapy could be the key to preventing such evolution of SARS-CoV-2 in patients with advanced HIV, since clearance of the virus is compromised if HIV is allowed to replicate for a long time and results in major damage to the immune system.

"Evolved mutations lead to escape from neutralisation, which means antibodies made as a result of previous natural infection or vaccination would work less well to protect you from a new infection," explains session presenter Dr Alex Sigal, Africa Health Research Institute, KwaZulu-Natal, South Africa, and Max Planck Institute for Infection Biology, Berlin, Germany. "SARS-CoV-2 may mutate extensively within one person if infection persists."

In his talk, Dr Sigal will present a case study of a patient with advanced HIV who, despite having only mild COVID-19 illness, tested SARS-CoV-2 positive for 216 days. Genomic sequencing revealed shifts in the patient's SARS-CoV-2 viral population over time, involving multiple mutations at key sites including the spike protein domain which SARS-CoV-2 uses to enter human cells. The evolved virus was tested and shown to have variant-like properties in terms of its ability to escape antibodies.

"Such findings underline the need to make sure everyone living with HIV has appropriate treatment. If not, it is possible that potentially more potent variants than the ones circulating now could emerge from people whose immune systems are severely damaged," he explains.

It is believed to be involved in the development of chronic inflammatory intestinal diseases, to trigger diabetes, to be responsible for obesity, even neurological diseases such as multiple sclerosis and Parkinson's could have their causes here - not to mention depressions and autistic disorders. We are talking about the microbiome - the vast collection of bacteria in the human gut. It is estimated that each person carries around 100 trillion bacterial cells in their digestive tract, belonging to several thousand species.

The microbiome has been the focus of research for 20 years - ever since a new technique made it possible to analyse these bacteria quickly and precisely: high-throughput sequencing. Since then, there has been an increasing body of findings that the microbiome, which is sometimes also referred to as the second human genome, is not only of central importance for digestion, but also influences, if not controls, at least a large number of body functions. The immune system is mentioned particularly frequently.

The microbiome influences the immune system

Scientists at the Universities of Würzburg and Marburg have now succeeded for the first time in experimentally demonstrating that bacterial metabolites are able to increase the cytotoxic activity of certain immune cells and thus positively influence the efficiency of tumour therapies. Ideally, the composition of the bacterial species in the microbiome could be used to control its influence on the success of the therapy.

The research team published the results of its study in the journal Nature Communications. Dr. Maik Luu, postdoc in the laboratory of Professor Michael Hudecek at the Medical Clinic and Polyclinic II of the University Hospital of Würzburg, was responsible for the finding. Another participant was Professor Alexander Visekruna from the Institute of Medical Microbiology and Hygiene at the Philipps University in Marburg, where Luu did research before moving to Würzburg.

Fatty acids increase the activity of killer cells

"We were able to show that the short-chain fatty acids butyrate and, in particular, pentanoate are able to increase the cytotoxic activity of CD8 T cells," Maik Luu describes the central result of the now published study. CD8 T cells are sometimes also called killer cells. As part of the immune system, it is their task to specifically kill cells that are harmful to the organism.

Short-chain fatty acids, in turn, belong to the most dominant class of metabolites of the gut microbiome. On the one hand, they can boost the metabolism of T cells by inducing central regulators of energy metabolism. On the other hand, they can inhibit specific enzymes that regulate the accessibility to the genetic material and thus the gene expression in the T cells. In doing so, they induce epigenetic changes.

Solid tumor models are combated more effectively

"When short-chain fatty acids reprogram CD8 T cells, one of the results is increased production of pro-inflammatory and cytotoxic molecules," Luu explains. In the experiment, treatment with the fatty acid pentanoate increased the ability of tumor-specific T cells to fight solid tumor models. "We were able to observe the same effect when fighting tumor cells with so-called CAR-T cells," says the scientist.

CAR-T cells are written out as "chimeric antigen receptor T cells". While normal T cells are largely "blind" to tumor cells, CAR T cells are able to recognize specific target antigens on the tumor surface and destroy the cancer cells thanks to a genetic modification. Michael Hudecek is one of the leading experts in the field of CAR-T cell research.

Targeted control via the composition of the microbiome

"The results are an example of how metabolites of intestinal bacteria can change the metabolism and gene regulation of our cells and thus positively influence the efficiency of tumor therapies," says Maik Luu. In particular, the use of CAR-T cells against solid tumors could benefit from this.

In these cases, therapy with genetically modified cells has so far been much less effective than the treatment of haematological tumours such as leukaemia. This could change if the CAR-T cells were treated with pentanoate or other short-chain fatty acids before being used in patients, the scientists hope.

This effect might specifically be exploited via the composition of the bacterial intestinal colonisation - especially since Luu and the others involved in the study were also able to identify the essential pentanoate producer of the intestinal flora: the bacterium Megasphaera massiliensis.

A long way to clinical applications

However, there is still a long way to go before the new findings will lead to new therapies for cancer patients. In a next step, the research team will initially expand the spectrum of tumour diseases investigated and, in addition to other solid tumours, also look at haematological tumour diseases such as multiple myeloma. In addition, it wants to investigate the functioning of short-chain fatty acids more intensively in order to identify starting points for targeted genetic modifications.

URBANA, Ill. - Food insecurity is a major problem in the U.S., and it worsened during the COVID-19 pandemic. The Supplemental Nutrition Assistance Program (SNAP) provides some relief, but millions of Americans still lack adequate access to healthy food. A new study from the University of Illinois proposes a potential solution.

"Restructuring SNAP as a Universal Basic Income (UBI) program or modified UBI is a straightforward way to eliminate food insecurity in United States. It's expensive but it is not difficult," says Craig Gundersen, distinguished professor in the Department of Agricultural and Consumer Economics at U of I. Gundersen authored the study, published in Food Policy.

While the existing SNAP program effectively reduces food insecurity, it has some limitations. For some SNAP recipients, the amount of aid they receive is insufficient. Some people who are food insecure and eligible for SNAP do not participate. And finally, more than half of those who are food insecure are not eligible for SNAP, Gundersen explains.

Using data from the 2019 Current Population Survey, Gundersen estimates the effects of expanding SNAP to become a UBI program under three different scenarios.

"The first scenario is a standard UBI program, where everybody in the United States gets SNAP at the maximum level," Gundersen explains. "Under the current program, your SNAP benefits go down if your income increases. Under this proposal, the amount would remain the same. If people wanted to work more and earn more money, they wouldn't lose their SNAP benefits."

Under this scenario, food insecurity could decline by 88.8 %, assuming the $730 billion cost would be funded through higher taxes for top-earning households.

"With the current distribution of taxes in the United States, the top 10% of incomes pay 70% of the taxes, and the top 50% pay 97%. Even if you were to raise taxes on the higher-income brackets to implement this program, it is unlikely to influence the probability of these households becoming food insecure," he states.

The second scenario in Gundersen's study would be a modified UBI program where households with incomes up to four times the poverty line; that is, approximately $100,000 for a family of four, would receive SNAP benefits.

Compared to the first scenario, the decline in food insecurity would be almost the same - 88.5% ¬ - but at a much lower cost of $408.5 billion.

Gundersen's third scenario addresses the issue that current SNAP benefits are not enough for some recipients to become food secure.

"Under this scenario, I consider what would happen if we increase the maximum SNAP benefit by 25% and give it to all households with incomes up to about $100,000 a year. In that case, there would be a 98.2% decline in food insecurity, and the cost would be $564.5 billion," he notes.

"I believe the third scenario is the best one," Gundersen says. "While the second one is also good, it would not be adequate for some of the most vulnerable groups; that is, SNAP recipients who need more assistance than they currently receive. The third scenario would ensure that they get what they need to become food secure."

Gundersen acknowledges that his proposals are costly, but so are other government programs.

"Essentially, I propose a way of eliminating food insecurity in United States, and the cost of this would be about a half trillion dollars per year. That seems like a lot, but to put it in context, the cost of the COVID-19 pandemic stimulus packages from the Trump administration and the Biden administration were roughly $6 trillion. It's a lot of money. But if we want to be serious about alleviating food insecurity, this is a simple, straightforward way to do it," he concludes.

Meningitis is associated with high mortality and frequently causes severe sequelae. Newborn infants are particularly susceptible to this type of infection; they develop meningitis 30 times more often than the general population. Group B streptococcus (GBS) bacteria are the most common cause of neonatal meningitis, but they are rarely responsible for disease in adults. Scientists from the Institut Pasteur, in collaboration with Inserm, Université de Paris and Necker-Enfants Malades Hospital (AP-HP), set out to explain neonatal susceptibility to GBS meningitis. In a mouse model, they demonstrated that the immaturity of both the gut microbiota and epithelial barriers such as the gut and choroid plexus play a role in the susceptibility of newborn infants to bacterial meningitis caused by GBS. The findings were published in the journal Cell Reports on June 29, 2021.

Newborn infants are more likely to develop bacterial meningitis than children and adults. Group B streptococcus (GBS) is the pathogen responsible for a significant proportion of cases of neonatal meningitis. In most instances, infection is preceded by bacterial colonization of the gut. The commensal bacterial gut flora (known as the microbiota) plays a key physiological role, as it is involved in digestion, offers protection from gut pathogens and contributes to tissue differentiation and immune development. Newborns have no gut microbiota; it gradually develops in the first few weeks after birth.

In a new study, scientists from the Institut Pasteur, in collaboration with Inserm, Université de Paris and Necker-Enfants malades Hospital (AP-HP), demonstrated in a mouse model that the immaturity of the gut microbiota in neonates is involved in neonatal susceptibility to meningitis caused by GBS. In the absence of a mature microbiota, the bacteria can extensively colonize the gut. In the absence of a mature microbiota, the barrier function of blood vessels in the gut that the bacteria must cross to reach the brain through the bloodstream is also less effective, and the immune system is unable to control infection.

Unexpectedly, the scientists also demonstrated that, independently of the microbiota, the epithelial barriers formed by the gut and the choroid plexus (the interface between the blood and the cerebrospinal fluid that irrigates the brain) are not entirely mature in newborns, which facilitates bacterial access to the brain. The signaling pathway known as the Wnt pathway, which is involved in tissue growth and differentiation, is more active in newborns, resulting in a less effective barrier function at the gut and choroid plexus levels in neonates.

"In this study, we show how two factors associated with infancy - the immaturity of the gut microbiota and the growth of gut and choroidal epithelial tissues - play a role in the susceptibility of newborn infants to meningitis caused by GBS, at all stages of infection from gut colonization to dissemination in the brain," explains Marc Lecuit (university professor/hospital practitioner, Université de Paris and Necker-Enfants Malades Hospital), head of the Biology of Infection Unit at the Institut Pasteur and Inserm and last author of the study.

The results of this research illustrate the importance of the microbiota and its critical role in protecting against infection.

DNA is composed of nucleobases represented by the letters A, T, G and C. They form the basis of the genetic code and are present in all living beings. But in a bacteriophage, another base, represented by the letter Z, exists. This exception, the only one observed to date, has long remained a mystery. Scientists from the Institut Pasteur and the CNRS, in collaboration with the CEA, have now elucidated the biosynthesis pathway of this base. This work has been published in the April 30th, 2021 issue of Science.

DNA, or deoxyribonucleic acid, is a molecule that serves as the medium for storing genetic information in all living organisms. It is a double helix characterized by alternating purine nucleobases (adenine and guanine) and pyrimidine nucleobases (cytidine and deoxycytidine). The bases of each DNA strand are located at the center of the helix and are bonded together, thereby linking the two DNA strands: adenine forms two hydrogen bonds with thymine (A-T), and guanine forms three hydrogen bonds with cytosine (G-C). This applies to all living beings, with one exception.

Cyanophage S-2L, an exception to conventional genetics

Cyanophage S-2L is a bacteriophage, in other words a virus that infects bacteria. In this phage, adenine is completely replaced by another base, 2-aminoadenine (represented by the letter Z). The latter forms three hydrogen bonds with thymine (Z-T), instead of the usual two bonds between adenine and thymine. This higher number of bonds increases the stability of the DNA at high temperatures and changes its conformation, meaning that the DNA is less well recognized by proteins and small molecules

2-aminoadenine biosynthesis pathway elucidated

Since it was discovered in 1977, cyanophage S-2L has been the only known exception, and the biosynthesis pathway of 2-aminoadenine has remained unknown. Scientists from the Institut Pasteur and the CNRS, in collaboration with the CEA, recently elucidated this biosynthesis pathway and demonstrated its enzymatic origins. They achieved this by identifying a homolog of the known enzyme succinoadenylate synthase (PurA) in the genome of cyanophage S-2L. A phylogenetic analysis of this enzyme family revealed a link between the homolog, known as PurZ, and the PurA enzyme in archaea. This indicates that the homolog is an ancient enzyme that probably conferred an evolutionary advantage. The research was carried out using the Institut Pasteur's Crystallography Platform.

The new Z-T base pair and the discovery of the biosynthesis pathway show that new bases can be enzymatically incorporated into genetic material. This increases the number of coding bases in DNA, paving the way for the development of synthetic genetic biopolymers.

Trust in science - but not trust in politicians or the media - significantly raises support across US racial groups for COVID-19 social distancing.

Changing climate patterns have left millions of people vulnerable to weather extremes. As temperature fluctuations become more commonplace around the world, conventional power-guzzling cooling and heating systems need a more innovative, energy-efficient alternative, and in turn, lessen the burden on already struggling power grids.

In a new study, researchers at Texas A&M University have created novel 3D printable phase-change material (PCM) composites that can regulate ambient temperatures inside buildings using a simpler and cost-effective manufacturing process. Furthermore, these composites can be added to building materials, like paint, or 3D printed as decorative home accents to seamlessly integrate into different indoor environments.

"The ability to integrate phase-change materials into building materials using a scalable method opens opportunities to produce more passive temperature regulation in both new builds and already existing structures," said Dr. Emily Pentzer, associate professor in the Department of Materials Science and Engineering and the Department of Chemistry.

This study was published in the June issue of the journal Matter.

Heating, ventilation and air conditioning (HVAC) systems are the most commonly used methods to regulate temperatures in residential and commercial establishments. However, these systems guzzle a lot of energy. Furthermore, they use greenhouse materials, called refrigerants, for generating cool, dry air. These ongoing issues with HVAC systems have triggered research into alternative materials and technologies that require less energy to function and can regulate temperature commensurate to HVAC systems.

One of the materials that have gained a lot of interest for temperature regulation is phase-change materials. As the name suggests, these compounds change their physical state depending on the temperature in the environment. So, when phase-change materials store heat, they convert from solid to liquid upon absorbing heat and vice versa when they release heat. Thus, unlike HVAC systems that rely solely on external power to heat and cool, these materials are passive components, requiring no external electricity to regulate temperature.

The traditional approach to manufacturing PCM building materials requires forming a separate shell around each PCM particle, like a cup to hold water, then adding these newly encased PCMs to building materials. However, finding building materials compatible with both the PCM and its shell has been a challenge. In addition, this conventional method also decreases the number of PCM particles that can be incorporated into building materials.

"Imagine filling a pot with eggs and water," said Ciera Cipriani, NASA Space Technology Graduate Research Fellow in the Department of Materials Science and Engineering. "If each egg has to be placed in an individual container to be hard-boiled, fewer eggs will fit in the pot. By removing the plastic containers, the veritable shell in our research, more eggs, or PCMs, can occupy a greater volume by packing closer together within the water/resin."

To overcome these challenges, past studies have shown that when using phase-changing paraffin wax mixed with liquid resin, the resin acts as both the shell and building material. This method locks the PCM particles inside their individual pockets, allowing them to safely undergo a phase change and manage thermal energy without leakage.

Similarly, Pentzer and her team first combined light-sensitive liquid resins with a phase-changing paraffin wax powder to create a new 3D printable ink composite, enhancing the production process for building materials containing PCMs and eliminating several steps, including encapsulation.

The resin/PCM mixture is soft, paste-like and malleable, making it ideal for 3D printing but not for building structures. Hence, by using a light-sensitive resin, they cured it with an ultraviolet light to solidify the 3D printable paste, making it suitable for real-world applications.

Additionally, they found that the phase-changing wax embedded within the resin was not affected by the ultraviolet light and made up 70% of the printed structure. This is a higher percentage when compared to most currently available materials being used in industry.

Next, they tested the thermoregulation of their phase-changing composites by 3D printing a small-scale house-shaped model and measuring the temperature inside the house when it was placed in an oven. Their analysis showed that the model's temperature differed by 40% compared to outside temperatures for both heating and cooling thermal cycles when compared to models made from traditional materials.

In the future, the researchers will experiment with different phase-change materials apart from paraffin wax so that these composites can operate at broader temperature ranges and manage more thermal energy during a given cycle.

"We're excited about the potential of our material to keep buildings comfortable while reducing energy consumption," said Dr. Peiran Wei, research scientist in the Department of Materials Science and Engineering and the Soft Matter Facility. "We can combine multiple PCMs with different melting temperatures and precisely distribute them into various areas of a single printed object to function throughout all four seasons and across the globe."

A specific police action, an arrest or a shooting, has an immediate and direct effect on the individuals involved, but how far and wide do the reverberations of that action spread through the community? What are the health consequences for a specific, though not necessarily geographically defined, population?

The authors of a new UW-led study looking into these questions write that because law enforcement directly interacts with a large number of people, "policing may be a conspicuous yet not-well understood driver of population health."

Understanding how law enforcement impacts the mental, physical, social and structural health and wellbeing of a community is a complex challenge, involving many academic and research disciplines such as criminology, sociology, psychology, public health and research into social justice, the environment, economics and history.

"We needed a map for how to think about the complex issues at the intersection of policing and health," said lead author Maayan Simckes, a recent doctoral graduate from UW's Department of Epidemiology who worked on this study as part of her dissertation.

So, Simckes said, she set out to create a conceptual model depicting the complex relationship between policing and population health and assembled an interdisciplinary team of researchers to collaborate.

"This model shows how different types of encounters with policing can affect population health at multiple levels, through different pathways, and that factors like community characteristics and state and local policy can play a role," said Simckes, who currently works for the Washington State Department of Health.

The study, published in early June in the journal Social Science & Medicine, walks through the various factors that may help explain the health impacts of policing by synthesizing the published research across several disciplines.

"This study provides a useful tool to researchers studying policing and population health across many different disciplines. It has the potential to help guide research on the critical topic of policing and health for many years to come," said senior author Anjum Hajat, an associate professor in the UW Department of Epidemiology

For example, the study points out when considering individual-level effects that "after physical injury and death, mental health may be the issue most frequently discussed in the context of police-community interaction ... One U.S. study found that among men, anxiety symptoms were significantly associated with frequency of police stops and perception of the intrusiveness of the encounter."

Among the many other research examples explored in the new model, the researchers also examine the cyclic nature of policing and population health. They point out that police stops tend to cluster in disadvantaged communities and "saturating these communities with invasive tactics may lead to more concentrated crime." Consequently, it may be "impossible" to determine whether police practices caused a neighborhood to experience more crime or if those practices were in response to crime. However, the model's aim is to capture these complex "bidirectional" relationships.

"Our model underscores the importance of reforming policing practices and policies to ensure they effectively promote population wellbeing at all levels," said Simckes. "I hope this study ignites more dialogue and action around the roles and responsibilities of those in higher education and in clinical and public-health professions for advancing and promoting social justice and equity in our communities."

Sea otters are the smallest marine mammal. As cold-water dwellers, staying warm is a top priority, but their dense fur only goes so far. We have long known that high metabolism generates the heat they need to survive, but we didn't know how they were producing the heat -- until now.

Researchers recently discovered that sea otters' muscles use enough energy through leak respiration, energy not used to perform tasks, that it accounts for their high metabolic rate. The finding explains how sea otters survive in cold water.

Physiologist Tray Wright, research assistant professor in Texas A&M University's College of Education & Human Development, conducted the study along with colleagues Melinda Sheffield-Moore, an expert on human skeletal muscle metabolism, Randall Davis and Heidi Pearson, marine mammal ecology experts, and Michael Murray, veterinarian at the Monterey Bay Aquarium. Their findings were published in the journal Science.

The team collected skeletal muscle samples from both northern and southern sea otters of varying ages and body masses. They measured respiratory capacity, the rate at which the muscle can use oxygen, finding that the energy produced by muscle is good for more than just movement.

"You mostly think of muscle as doing work to move the body," Wright said. "When muscles are active, the energy they use for movement also generates heat."

Wright said that because muscle makes up a large portion of body mass, often 40-50% in mammals, it can warm the body up quickly when it is active.

"Muscles can also generate heat without doing work to move by using a metabolic short circuit known as leak respiration," Wright said.

A form of muscle-generated heat we are more familiar with is shivering. Wright said this involuntary movement allows the body to activate muscle by contracting to generate heat, while leak respiration can do the same without the tremors.

Wright said one of the most surprising findings was that the muscle of even newborn sea otters had a metabolic rate that was just as high as the adults.

"This really highlights how heat production seems to be the driving factor in determining the metabolic ability of muscle in these animals," Wright said.

Sea otters require a lot of energy to live in cold water. They eat up to 25% of their body mass per day to keep up with their daily activities and fuel their high metabolism.

"They eat a lot of seafood, including crabs and clams that are popular with humans, which can cause conflict with fisheries in some areas," Wright said.

Wright said we know how critical muscle is to animals for activities like hunting, avoiding predators and finding mates, but this research highlights how other functions of muscle are also critical to animal survival and ecology.

"Regulating tissue metabolism is also an active area of research in the battle to prevent obesity," Wright said. "These animals may give us clues into how metabolism can be manipulated in healthy humans and those with diseases where muscle metabolism is affected."

As for future research, Wright said there is still a lot we don't know about otters, including how they regulate their muscle metabolism to turn up the heat on demand.

"This is really just the first look into the muscle of these animals, and we don't know if all the various muscle types are the same, or if other organs might also have an elevated ability to generate heat," Wright said.