Culture

Elastic can stretch too far and that could be problematic in wearable sensors. A team of researchers at Yokohama National University has proposed a fix to prevent too much stretching while improving the sensing ability of electronics. This could lead to advanced prosthetics or disaster recovery robotics.

They published their results on July 29 in the Scientific Reports.

"Stretchable physical sensors are crucial for the development of advanced electrical systems, particularly wearable devices and soft robotics," said Hiroki Ota, paper author and associate professor in the Faculty of Engineering at Yokohama National University. "However, current stretchable pressure sensors composed of elastic materials can be highly deformed during the strain of the devices."

The bend of an elbow or a knee can push the sensor past its structural integrity, producing a large error on the pressure movement measurement. This stops the sensor from being able to measure pressure and strain at the same time, but as independent variables.

To help combat this, the researchers proposed a monolithic array of pressure and strain sensors that can simultaneously and independently detect the force and bend deformation of motion. They used two different materials--one soft and one hard--to protect the sensor's ability to stretch and still accurately measure movement. They placed a hard silicone, called PDMS, along electrodes over the array. At the center of each PDMS placement, they positioned soft porous silicone, which senses pressure.

"The PDMS around the pressure-sensing elements prevents the development of large deformations of the elements during the developed device tension," Ota said.

The soft porous silicone pressure sensor is contained within the hard shell of the PDMS, so it can measure the force of pressure without being overextended past reliable margins of error. The containment also allows the sensors to identify and measure both pressure and strain as independent contributors to movement.

"In addition, resistances of column and row electrodes in the matrix of the mapped array are much lower than the ones of the pressure sensors," Ota said. "This substrate and control of electrode resistances can prevent stretch deformation of the device from affecting the sensing of pressure."

The electrodes in the stretchable array can measure strain at a much lower rate than is required to detect pressure.

"We could recognize pressure and strain sensing of our device independently," Ota said.

Ota said the team plans to apply the new stretchable sensor approach to a physical keyboard that can be mounted on the surface of a body, which could bend with the strain of the body and still detect fingertip pressure, as well as a physical sensor on a soft robot. They also hope to use the sensor to better understand the motion and touch of the human hand.

"In the future, by molding this sensor into a glove shape, it can be applied to the device which electronically analyzes the finger movement and tactile sense of the hand," Ota said.

Through a one-of-a-kind experiment at the Department of Energy's Oak Ridge National Laboratory, nuclear physicists have precisely measured the weak interaction between protons and neutrons. The result quantifies the weak force theory as predicted by the Standard Model of Particle Physics.

The team's weak force observation, detailed in Physical Review Letters, was measured through a precision experiment called n3He, or n-helium-3, that ran at ORNL's Spallation Neutron Source, or SNS. Their finding yielded the smallest uncertainty of any comparable weak force measurement in the nucleus of an atom to date, which establishes an important benchmark.

The Standard Model describes the basic building blocks of matter in the universe and fundamental forces acting between them. Calculating and measuring the weak force between protons and neutrons is an extremely difficult task.

"Because the interactions we're looking for are very weak, the effects that we want to detect in precision nuclear physics experiments are very small and, therefore, extremely difficult to observe," said David Bowman, co-author and team leader for fundamental neutron physics at ORNL.

The weak force is one of four fundamental forces in nature, along with the strong nuclear force, electromagnetism and gravity, and describes interactions between subatomic particles called quarks that make up protons and neutrons. The weak force is also responsible for an atom's radioactive decay. Certain mechanisms of the weak force are among the least understood aspects of the Standard Model.

Detecting the elusive weak interactions requires high-precision experiments, led by large international teams with a state-of-the-art apparatus and a world-class cold neutron source with very high neutron flux, such as the Fundamental Neutron Physics Beamline at SNS. Neutrons produced at SNS are ideal for precision experiments that address the role the weak force plays in the reaction between neutrons and other nuclei.

Bowman, a leading scientist in this field, has been studying nuclear physics and subatomic interactions since the early 1960s.

"In the beginning, there were phenomenological nuclear models gleaned from an empirical research point of view. But, in recent years, there have been major advances in calculations of weak force interactions in the nuclear environment," he said. "New nuclear techniques have become available with different degrees of freedom, and the calculations now are at a very advanced level."

The scientists' latest experiment focused on helium-3, which is a light and stable isotope consisting of two protons and one neutron, the only element in nature that has more protons than neutrons in the nucleus. "When a neutron and a helium-3 nucleus combine, the reaction produces an excited, unstable helium-4 isotope, decaying to one proton and one triton (consisting of two neutrons and one proton), both of which produce a tiny but detectable electrical signal as they move through the helium gas in the target cell," said Michael Gericke, corresponding author and professor for subatomic physics at the University of Manitoba.

The n-helium-3 experiment used the same neutron beamline, polarizer and diagnostics as its predecessor, NPDGamma, which used a liquid hydrogen target that produced gamma rays from neutron-proton interactions. The team found that more gamma rays go down than up with respect to neutron spin direction, which led to the successful measurement of a mirror-asymmetric component of the weak force.

Similar to NPDGamma, the n-helium-3 experiment is the culmination of a decade of research, preparation and analysis. The experiment's configuration created an extremely low background environment where neutrons can be controlled before entering a container of helium-3 gas. Gericke led the group that built the combined helium-3 target and detector system designed to pick up the very small signals and led the subsequent analysis.

In the experiment, a beam of slow-moving, or cold, neutrons at SNS entered the helium-3 target. One instrument was designed to control the nuclear spin direction of the helium-3 atoms. When the neutrons interact with the magnetic field, another apparatus flipped their spin direction either up or down, defining the spin state. When the neutrons reached the target, they interacted with the protons within the helium-3 atoms, sending out the current signals that were measured by sensitive electronics.

"We had to develop a unique target gas cell that simultaneously served as a position-sensitive detector to measure the subatomic products of the reaction," Gericke said.

"In order to accommodate different running conditions of this experiment, we invented a novel apparatus needed to reverse the spin direction of neutrons right before they reacted with the helium-3 target," said co-author and nuclear physics professor Christopher Crawford of the University of Kentucky. "This universal spin flipper was able to operate in the large neutron velocity range with high efficiency."

Weak force experiments have to contend with the dominating nature of the strong force and background noise that could distort the data. "The n-helium-3 experiment had to be sensitive to very small effects -- 100 million times smaller than the background," Crawford said. "That is akin to searching for a 1-inch needle in a 40-foot-high barn full of hay."

For about a year, the team collected and analyzed the data to determine the strength of the parity-violation, which is a specific property of the weak force between a neutron and a proton. This phenomenon is unique to the weak force and is not observed in the strong force, electromagnetism or gravity.

N-helium-3 exploited the symmetry of the experimental configuration obtained by the well-controlled neutron polarization, by measuring a combination of the neutron spin and outgoing momentum of reaction products for both neutron polarizations. "This has a certain handedness," Crawford said. "Since right and left hands look opposite in the mirror, this observation was completely insensitive to the effects of the other three forces."

The results of n-helium-3, along with NPDGamma, have changed the way nuclear physicists understand the role of the weak force in atomic nuclei. Both help answer outstanding questions in the Standard Model through the ability to make accurate calculations.

"Now what's going to happen after this, we need more measurements - like these very precise measurements we get at SNS," Bowman said. "Advancements in this field require a dialogue between the experimentalists and theorists. As results from experiments like ours become available, they benchmark theories, and that allows theorists to improve the models that predict new observables that then could be experimentally reachable."

Black, South Asian and Aboriginal populations from disadvantaged socioeconomic backgrounds in Canada are nearly four times more likely to have three or more medical conditions that have been identified as risk factors for severe illness from COVID-19.

Shen (Lamson) Lin, a doctoral candidate in gerontology and course instructor at the University of Toronto's Factor-Inwentash Faculty of Social Work and Institute for Life Course and Aging, compared 1,102 racialized immigrants and 338 Aboriginal Canadians with 23,802 Canadian-born Whites, aged 45 and older, using population-based data from the baseline Canadian Longitudinal Study on Aging (CLSA, 2012-2015). His findings were recently published in The Gerontologist (Special collection: Gerontology in a Time of Pandemic).

"We know that COVID-19 outbreak is not affecting everyone at the same levels, and the prevalence of multiple chronic conditions within an individual -- known as multimorbidity -- has also been linked to social inequalities for decades," says Lin, the sole author of the study. "I was curious to explore how one's family income, education levels and experience of racism and nativism -- and the intersection of these three social standings -- shape the health of aging populations."

Lin's study examined nine chronic conditions associated with an increased likelihood that one will experience severe illness due to COVID-19 infection, requiring hospitalization, intensive care and the use of a ventilator. These medical conditions include diabetes, asthma, cancer, previous heart attack or myocardial infarction, kidney disease, cardiovascular disease, hypertension, chronic obstructive pulmonary disease and obesity.

The odds of having three or more of these medical conditions was greater for Black and South Asian immigrants and close to double for Aboriginal populations in Canada, relative to Canadian-born Whites. Black, South Asian and Aboriginal populations from disadvantaged socioeconomic backgrounds (those without any post-secondary education and/or those who earned less than the median household income) had the highest odds of having three or more medial conditions.

The multimorbidity differences associated with these populations were enhanced for older adults (aged 66 to 85) compared to their middle-aged counterparts (aged 45-65). Among older respondents, Black immigrants were five times more likely and Aboriginal Canadians three times more likely to have three or more medical conditions.

"These observed health gaps illustrate various minority struggles that are often obscured within a discourse of multiculturalism and diversity" says Lin, "Given the lack of socio-demographic and race-based data in Canadian health systems, my study provides a timely frame of reference for public-health decision makers to reconsider measuring upstream health inequalities to mitigate the pandemic's long-term societal harms."

Additional risk factors for multimorbidity were identified. These included being male, experiencing chronic pain, having a physical impairment, living without partners, and a lifetime of smoking.

"Widespread chronic disease and racism in addition to the contemporary pandemic make living conditions more difficult for vulnerable older adults, especially those from racialized, immigrant, and impoverished communities," says Lin. "With COVID-19 spreading globally, health equity should be placed at the center of all policy responses designed to mitigate the disproportionate impact of the pandemic on underserved aging communities."

BOSTON - Emergency departments of hospitals generate significant amounts of environmentally harmful waste which could be reduced through basic changes to disposal policies and practices, while producing lower operating costs, researchers from Massachusetts General Hospital (MGH) have found. Efforts to optimize the daily waste stream through improvements such as switching from disposable to reusable items in the ED, better sorting of infectious waste, and more effective recycling of items like glass and aluminum could have meaningful impact both environmentally and financially, according to the study published in the Western Journal of Emergency Medicine.

"People working in emergency departments have no idea how much waste they routinely generate, nor that the environmental impact is totally at odds with their professional mission to improve health and save lives," says Jonathan E. Slutzman, MD, investigator in the Department of Emergency Medicine at MGH and senior author of the study. "A greater awareness of the harm that's being done, along with the opportunities that are available to turn that situation around, should be on the agenda of every hospital in America."

Healthcare facilities in the U.S. generate 6,600 metric tons of waste each day, making them the second largest contributor to landfill waste (next to the food industry). They also produce 10 percent of all greenhouse gas emission as well as other pollutants known to adversely affect human health. The MGH investigation is the first to quantify and characterize the volume of waste emanating from emergency departments. To that end, researchers conducted a 24-hour waste audit in July 2019 at MGH's Level 1 trauma center in Boston. The team collected, manually sorted into separate categories, and weighed each waste stream component. It also calculated direct pollutant emissions from ED waste disposal activities.

Among the findings was that 85 percent of all items disposed of as regulated medical waste (RMW) -- the most hazardous ED materials that must be deposited in red bags and autoclaved to render them safe prior to being sent to landfills -- did not meet the criteria for regulated medical waste. "We always want healthcare workers to err on the side of caution when it comes to waste disposal, but the fact is regulated medical waste costs up to ten times as much to dispose of as solid waste," notes Sarah Hsu, with the Warren Alpert Medical School at Brown University, and lead author of the study. "But if we could divert through better sorting some fraction of medical waste that now goes into red biohazard bags to regular solid waste, it would open up significant cost-saving opportunities for hospitals."

Another area rife with opportunity, according to the researchers, is transitioning from the use of disposable devices to more durable, reusable alternatives that would lead to waste reduction and supply savings. One example is the laryngoscope, commonly used in the ED to insert a breathing tube into the trachea, which could be reprocessed onsite and safely used multiple times rather than discarding it after a single use. Rethinking the use of plastic packaging, which was estimated by the MGH study to be responsible for over 40 percent of all emergency department solid waste, also holds the potential for significant waste reduction. MGH, for its part, asks suppliers to ship products in non-disposable bulk packaging, whenever possible, enabling reuse. Suppliers are also "debulking" items at distribution centers, enabling packaging to be reused from that point rather than being shipped all the way to the hospital.

To determine the best opportunities for waste reduction, Slutzman suggests that hospitals conduct their own audits of emergency department waste. "Gaining a full awareness of the problem and its downstream consequences on the health of the community is an important first step toward a solution," he says. "In addition to audits, hospitals should assemble all stakeholders around the table to explore alternatives to their current waste disposal practices. Our study shows that significant improvements can be made to optimize ED waste management, and as healthcare professionals we owe it to our patients and the community to take responsible action."

For the first time, researchers have discovered how antibiotic resistance genes are spreading, at a continental scale, via bacterial plasmids in the hospital superbug, Klebsiella pneumoniae.

Researchers from the Centre for Genomic Pathogen Surveillance, based jointly at the Wellcome Sanger Institute and the Big Data Institute, University of Oxford, together with their collaborators used genome sequencing technology to analyse plasmids - genetic structures in bacteria that can carry antibiotic resistance genes - as well as bacterial chromosomes from K. pneumoniae samples taken from European hospital patients.

The findings, published today (24th September) in Proceedings of the National Academy of Sciences, reveal three different pathways by which antibiotic resistance genes spread via plasmids through bacterial populations. Researchers say it is critical that plasmids are included when tracking antibiotic resistance in order to have the best chance of stopping superbugs.

Members of the Enterobacteriaceae family of bacteria can become resistant to last-line antibiotics called carbapenems, and are listed as a critical threat in the World Health Organisation's list of priority pathogens*. Within this family, Klebsiella pneumoniae is an opportunistic pathogen that causes serious diseases, including pneumonia and meningitis.

K. pneumoniae becomes resistant to carbapenems by acquiring antibiotic resistance genes, known as carbapenemase genes, which code for an enzyme that 'chews up' the antibiotic.

In K. pneumoniae, these carbapenemase genes are usually found on plasmids - smaller circular pieces of DNA that are additional to the bacterial chromosome. Plasmids can 'jump' between different strains and species of bacteria, meaning antibiotic resistance genes can quickly spread and drive the rapid rise in antibiotic resistant bacterial infections worldwide.

Therefore, researchers must include plasmids when tracking the evolution and spread of bacteria to get a true picture of how antibiotic resistance genes are spreading. However it has previously been difficult to use genome sequencing to reliably track plasmid evolution, due to the variability in size and structure of their genetic sequences.

Now with long-read sequencing technology** researchers are able to read and reconstruct complete sequences for plasmids.

In a new study, researchers from the Centre for Genomic Pathogen Surveillance and their collaborators conducted long-read genome sequencing on 79 K. pneumoniae samples from patients, taken from a Europe-wide survey.

The team generated complete plasmid sequences from these samples, and studied them along with more than 1700 previously short-read sequenced K. pneumoniae samples from the same survey to understand how antibiotic resistance genes are spreading through the bacterial population in European hospitals.

Dr Sophia David, first author from the Centre for Genomic Pathogen Surveillance said: "To fully understand how antibiotic resistance is spreading, we need to consider the role of plasmids. In this study, which is the first to analyse the genetic sequences of plasmids at a continental scale, we discovered three primary routes by which antibiotic resistance genes are spreading via plasmids through the K. pneumoniae population."

The three pathways of transmission involve one plasmid jumping between multiple strains, multiple plasmids spreading among multiple strains, and multiple plasmids spreading within one strain of K. pneumoniae.

Professor Hajo Grundmann, co-lead author from the University of Freiburg in Germany, said: "These new insights into the three routes of spread of antibiotic resistance genes in K. pneumoniae are critical for controlling outbreaks of antibiotic resistant infections. Knowing these transmission strategies enables tailoring of interventions, either to control the dominant plasmid, control the dominant strain, or in complicated situations, control both. For example, if there was a hospital outbreak and the strain carried a high-risk plasmid, there's a chance this plasmid might jump into other bacterial strains or species, which would need to be monitored."

The team also found that plasmids encoding carbapenemase genes were most successful in spreading when acquired by a high-risk strain. This reinforces the importance of preventing transmission of high-risk strains through early detection and rigorous infection control in healthcare environments.

Professor David Aanensen, co-lead author and Director of the Centre for Genomic Pathogen Surveillance said: "When tracking certain antibiotic resistant bacteria, plasmids are one of the missing parts of the puzzle. Analysing the genetic sequences of both bacterial chromosomes and plasmids can give us a more detailed picture of how antibiotic resistance genes and mechanisms spread in a population. Genomic surveillance of bacteria should include plasmids and other mobile elements in order to tackle the rise in antibiotic resistant infections."

Leesburg, VA, September 24, 2020--According to an open-access article in ARRS' American Journal of Roentgenology (AJR), because coronavirus disease (COVID-19) may present with medium to large arterial and venous abdominal and extremity macrothrombi, radiologists should raise concern for COVID-19 when identifying thromboembolic abdominopelvic findings.

Bari Dane of NYU Langone Medical Center in New York City and colleagues at NYU Winthrop in Mineola, New York retrospectively compared 82 patients (58 men, 24 women; mean age 58.8) with COVID-19 who underwent abdominal ultrasound or CT with 82 patients (43 men, 39 women; mean age 53.5) without COVID-19 for thromboembolism and solid-organ infarction.

Nine (11%) patients with COVID-19 had thromboembolic findings (seven men, two women; mean age 67.0). Thromboembolism was described in four of the 38 CT reports (10.5%). Two others described splenic infarctions with patent vasculature (overall positivity rate, 15.8% [6/38]). Three patients had arterial thromboembolism in the aorta or major branches.

Noting one patient without COVID-19 had known portal vein thrombus on CT, "thromboembolic findings occurred more frequently in patients with than without COVID-19 (p = 0.02)," Dane et al. concluded.

Acknowledging this study's small sample size and single-institution nature, Dane pointed out that the cohort describing patients with "COVID" in the radiology report may not include all patients with COVID-19.

"Additionally," the authors of this AJR article continued, "not all patients with thromboembolism undergo confirmative imaging, and some may not experience symptoms. Consequently, the prevalence is likely larger than reported."

Scientists have for the first time documented all of the different cell types and genes expressed in the healthy human heart, in new research published in the journal Nature.

Cardiologists from the Mazankowski Alberta Heart Institute at the University of Alberta joined teams from Cambridge, Boston and Berlin to use state-of-the-art analytical techniques to sequence the ribonucleic acids (RNA) in nine types of single cells from six regions of the heart.

"Now we have a single-cell atlas of the normal human heart, including cellular composition and gene expression," said Gavin Oudit, professor in the Faculty of Medicine & Dentistry, Canada Research Chair in Heart Failure, and director of the Mazankowski's Heart Function Clinic and its Human Explanted Heart Program.

Oudit said this is the first step toward understanding heart disease and developing new targeted treatments to stop it.

"What we are working on now is to see how the cell types and gene expression are changed in patients with genetic cardiomyopathies--a significant cause of end-stage heart failure and sudden cardiac death," he said.

Next, researchers will be able to select specific mutations as treatment targets. "We want to correct those mutations, either with drugs or gene therapy, and start to reverse cardiomyopathies, ideally at an early stage," Oudit said.

The Edmonton team helped the international consortium to isolate single cells and code the gene expressions from seven male and seven female healthy donor hearts.

"This technique is truly remarkable," Oudit said. "Rather than grinding up a piece of heart tissue and losing the cellular composition, this allows us to track the gene expression of every single cell."

The U of A research was funded by the Canadian Institutes of Health Research, Alberta Innovates and the University Hospital Foundation.

Oudit said the research could not have happened without the integrated team of transplant co-ordinators, cardiologists and cardiac surgeons working together in Canada's largest research-integrated human heart transplant program at the Mazankowski Alberta Heart Institute.

"The dedication and efforts of our trainees over the past decade have been invaluable, including our current PhD trainees, Hao Zhang and Anissa Viveiros," Oudit said.

"We have a wonderful clinical program which is also a fabulous research tool, and it will ultimately influence patient care and our approaches to treating heart disease."

LA JOLLA--Your lungs and airways need to be stretchy, sort of like balloons. Take a big breath, and they'll open right up.

Damaged lungs can't open properly. Patients with asthma, idiopathic pulmonary fibrosis and systemic sclerosis suffer from fibrosis and tissue remodeling, where a build-up of tissue and immune cells, and proteins that form a glue-like substance, keep the airways from expanding. As fibrosis gets worse, taking a breath feels like blowing up a balloon filled with concrete.

In a new study, researchers at La Jolla Institute for Immunology (LJI) report that a protein called TL1A drives fibrosis in several mouse models, triggering tissue remodeling, and making it harder for lungs and airways to function normally.

"Our new study suggests that TL1A and its receptor on cells could be targets for therapeutics aimed at reducing fibrosis and tissue remodeling in patients with severe lung disease," says LJI Professor Michael Croft, Ph.D., director of scientific affairs at LJI and senior author of the new study in The Journal of Immunology.

Croft's laboratory is focused on understanding the importance of a family of proteins, called tumor necrosis factors (TNF) and tumor necrosis factor receptors (TNFR), in inflammatory and autoimmune diseases. By investigating these molecules, researchers hope to track down the root causes of inflammation and stop tissue damage before it's too late.

Previous research had shown that a TNF protein called TL1A can act on immune cells involved in allergic reactions and drive those immune cells to make inflammatory molecules. The Croft Lab wondered--if TL1A leads to inflammation, could it contribute to fibrosis in the lungs?

For the new study, Croft and his colleagues used genetic and therapeutic interventions, tissue staining, and fluorescence imaging techniques to study protein interactions in mouse models of severe asthma, idiopathic pulmonary fibrosis and systemic sclerosis. They first discovered that TL1A acts directly on a receptor on cells in the lungs and bronchial tubes, which leads to fibrosis and tissue remodeling.

We're all familiar with the idea of tissue remodeling. When a wound on the skin heals, the new area of skin is sometimes shiner, darker or tougher than the skin around it. The tissue has been remodeled. When lungs and airways try to heal--in response to an asthma attack, for example-- the cells in the area also change. The damaged area accumulates cells called fibroblasts, which make several glue-like proteins, including collagen. Too much collagen makes the lungs and airways less elastic--and less functional.

As Croft describes it, tissue remodeling is like wound healing, "but wound healing that goes wrong and becomes so exaggerated that it blocks tissue from behaving in its normal way." With the new study, scientists now know that TL1A is driving this harmful remodeling in the lungs.

In addition to causing fibroblasts to make collagen, the researchers found that TL1A also helps fibroblasts to behave like smooth muscle cells. A thin layer of smooth muscle cells naturally lines the bronchial tubes allowing them to dilate and constrict, but a thick layer of these smooth muscle cells--that includes fibroblasts--will keep the airways from expanding and contracting normally, making it even hard for a patient to breathe.

The scientists then studied lung tissue remodeling in mice that lacked the receptor for TL1A, called DR3, or were given a reagent that blocked TL1A activity. These mice showed less lung remodeling, less collagen deposition and reduced smooth muscle mass in the lungs.

These animal model data may support recent research in humans. Researchers have found that patients with severe asthma have excessive production of TL1A. This could explain why these patients are more vulnerable to lung fibrosis and remodeling.

"This type of research needs to be expanded to really understand if there are subsets of patients with asthma or other inflammatory lung diseases who might express TL1A at higher levels than other patients--which could potentially guide future therapies for targeting TL1A to reduce remodeling and fibrosis," says Croft.

Going forward, Croft and his team plan to investigate how the DR3 receptor is expressed on tissue cells and whether it is affected by other inflammatory factors. They also want to know how active TL1A is in human patients and how many inflammatory activities the protein might be responsible for.

In the United States, individual state laws barring 18- to 20-year-olds from buying or possessing a handgun make little difference in the rate of homicides involving a gun by people in that age group, a new University of Washington study has found.

"The central issue is that there's a very high degree of informal access to firearms, such as through family members or illicit channels," said Caitlin Moe, the study's lead author and a PhD student in epidemiology in the UW School of Public Health. "And we can't address that kind of availability with age limits."

The UW study compared homicide rates involving firearms in this age group between five states that increased the minimum age to buy or possess a firearm higher than the nationwide limits set by the 1994 federal law and the 32 states that did not.

The five states were Massachusetts, Maryland, New Jersey, New York and Wyoming. With the exception of Wyoming, these states also increased the minimum age for possession of a handgun. (States that raised age limits before 1994 were not included. Washington was not included for this reason, and the initiative passed in 2018 increasing age limits became law after the study period, which was 1995 to 2017.)

In the study, published in JAMA Pediatrics, UW researchers found that rates of firearm homicides perpetrated by young adults aged 18 to 20 years old were not significantly different in the two groups of states.

Determining what laws do have an effect on homicide rates is paramount, she added, because of the roughly 275,000 homicides involving a firearm during the years studied nearly 36,000 were perpetrated by people in the study's age range. Because most handguns used in crimes by young adults are acquired from sources unlikely to be affected by age restrictions, "it is not surprising that we found no association" between state laws and homicides, the study said.

Also, Moe emphasized, firearms are the second leading cause of death of American youth, after motor vehicle crashes.

"It's incredibly important that we address this major cause of death in young people," said Moe, who is also affiliated with the Harborview Injury Prevention & Research Center. And that solution will need to be a country-wide, unified effort to address the "de facto availability" of firearms, especially among youth.

As Natsumi Hookabe snorkeled around Panama's Bocas del Toro archipelago, during the Smithsonian Tropical Research Institute's Training in Tropical Taxonomy program, she encountered an unusual ribbon worm or nemertean: large and dark colored, with numerous pale spots. It was her first field trip outside of Japan, so she wondered if it was a rare species or just one that she had never seen before.

Natsumi had been interested in worms since childhood, but when nemerteans were introduced during a university course, she was hooked.

"I was mesmerized by their body movement while crawling, which involves beautiful muscular waves," she recalled. "This led me to pursue nemertean biology for my bachelor's and master's degrees."

She then found out about the Training in Tropical Taxonomy workshop offered by the Smithsonian Tropical Research Institute (STRI) in Panama, and did not have to think for long before flying from Tokyo and plunging into the warm waters of the Caribbean in the Bocas del Toro archipelago.

The two-week course, supported by the U.S. National Science Foundation, teaches skills for the identification of understudied marine organisms, including nemerteans. It also offers an opportunity for students to make connections with other researchers from around the world.

"Hosting the courses has been a really fantastic way, not just to train the next generation of biodiversity researchers, but to also have the Bocas fauna carefully surveyed and identified by experts," said Rachel Collin, STRI staff scientist and director of the Bocas del Toro Research Station. "Over the years this has led to the discovery and description of many new species in Bocas del Toro. For some groups, Bocas has the most documented species for anywhere in the Caribbean."

During her stay in Bocas del Toro, Natsumi met Maycol Madrid, a biologist and assistant in Dr. Collin's lab. She quickly noted Maycol's deep knowledge about Japanese culture. In their spare time, they talked about Japanese manga, anime, and games and taught each other Japanese and Spanish words, respectively.

When Natsumi collected the unusual-looking nemertean, she knew she wanted to study it further in her lab in Japan, but this required sorting out a few bureaucratic processes. Maycol jumped in and lent his hand in getting the permissions to collect specimens, transportation to Japan, among other tasks.

All these efforts paid off: what seemed at first sight like a rare worm to Natsumi, turned out to be a new species of nemertean.

"Without Maycol's help, my trip would not have been as successful as it actually was," said Natsumi. "I really appreciate his sincere assistance throughout the period of my stay in Bocas."

She recently described the new species in the journal Marine Biodiversity, and named it Euborlasia maycoli sp. nov. after Maycol Madrid, as a token of appreciation for all his help. This new Panamanian species became the first Caribbean representative of the genus.

"For me it was a great surprise that Natsumi decided to name the new species of Euborlasia in my honor," said Maycol. "It fills me with great pleasure, knowing that I was somehow able to help Natsumi in the discovery of this new species."

Researchers have sequenced the genome of Alexander Fleming's penicillin mould for the first time and compared it to later versions.

Alexander Fleming famously discovered the first antibiotic, penicillin, in 1928 while working at St Mary's Hospital Medical School, which is now part of Imperial College London. The antibiotic was produced by a mould in the genus Penicillium that accidentally started growing in a Petri dish.

Now, researchers from Imperial College London, CABI and the University of Oxford have sequenced the genome of Fleming's original Penicillium strain using samples that were frozen alive more than fifty years ago.

The team also used the new genome to compare Fleming's mould with two strains of Penicillium from the US that are used to produce the antibiotic on an industrial scale. The results, published today in Scientific Reports, reveal that the UK and US strains use slightly different methods to produce penicillin, potentially suggesting new routes for industrial production.

Lead researcher Professor Timothy Barraclough, from the Department of Life Sciences at Imperial and the Department of Zoology at Oxford, said: "We originally set out to use Alexander Fleming's fungus for some different experiments, but we realised, to our surprise, that no-one had sequenced the genome of this original Penicillium, despite its historical significance to the field."

Although Fleming's mould is famous as the original source of penicillin, industrial production quickly moved to using fungus from mouldy cantaloupes in the US. From these natural beginnings, the Penicillium samples were artificially selected for strains that produce higher volumes of penicillin.

The team re-grew Fleming's original Penicillium from a frozen sample kept at the culture collection at CABI and extracted the DNA for sequencing. The resulting genome was compared to the previously published genomes of two industrial strains of Penicillium used later in the US.

The researchers looked in particular at two kinds of genes: those encoding the enzymes that the fungus uses to produce penicillin; and those that regulate the enzymes, for example by controlling how many enzymes are made.

In both the UK and US strains, the regulatory genes had the same genetic code, but the US strains had more copies of the regulatory genes, helping those strains produce more penicillin.

However, the genes coding for penicillin-producing enzymes differed between the strains isolated in the UK and US. The researchers say this shows that wild Penicillium in the UK and US evolved naturally to produce slightly different versions of these enzymes.

Moulds like Penicillium produce antibiotics to fight off microbes, and are in a constant arms race as microbes evolve ways to evade these defences. The UK and US strains likely evolved differently to adapt to their local microbes.

Microbial evolution is a big problem today, as many are becoming resistant to our antibiotics. Although the researchers say they don't yet know the consequences of the different enzyme sequences in the UK and US strains for the eventual antibiotic, they say it does raise the intriguing prospect of new ways to modify penicillin production.

First author Ayush Pathak, from the Department of Life Sciences at Imperial, said: "Our research could help inspire novel solutions to combatting antibiotic resistance. Industrial production of penicillin concentrated on the amount produced, and the steps used to artificially improve production led to changes in numbers of genes.

"But it is possible that industrial methods might have missed some solutions for optimising penicillin design, and we can learn from natural responses to the evolution of antibiotic resistance."

The COVID-19 pandemic has fired up interest in outdoor activities in our parks and forests. Now a new UBC study highlights the need to be mindful of how these activities may affect wildlife living in protected areas.

Researchers placed motion-activated cameras on the trails in and around the South Chilcotin Mountains Provincial Park in southwestern B.C., a region popular for its wildlife and recreational activities such as hiking, horseback riding, ATV riding and mountain biking. Overall, they found that environmental factors—like the elevation or the condition of the forest around a camera location—were generally more important than human activity in determining how often wildlife used the trails.

However, there were still significant impacts. Deeper analysis of trail use captured by the cameras showed that all wildlife tended to avoid places that were recently visited by recreational users. And they avoided mountain bikers and motorized vehicles significantly more than they did hikers and horseback riders.

The researchers focused on 13 species including grizzly bear, black bear, moose, mule deer and wolf.

“We wanted to better understand the relative impacts of human recreation in this region, given its increasing popularity. We already know that motorized vehicle access can disrupt wildlife; our initial findings suggest that other types of recreation may also be having impacts,” said study author Robin Naidoo, a UBC adjunct professor at the Institute for Resources, Environment and Sustainability.

Like many parks, the South Chilcotin Mountains provincial park and nearby regions are experiencing growing pressure from human activities—both recreational and industrial. According to Naidoo, the study confirms that camera traps can effectively monitor both wildlife and human trail use in these and other remote regions. “We’ll be able to collect more information over time and build a solid basis for research findings that can ultimately inform public policy,” he added

"Study co-author Cole Burton, a professor of forestry at UBC and the Canada Research Chair in terrestrial mammal conservation, says further research will be needed before any firm conclusions can be drawn.

“This is the first year of our multiyear study of the region. We’ll continue to observe and to analyze, so that we can better understand and mitigate the effects of these different human activities on wildlife,” said Burton. “Outdoor recreation and sustainable use of forest landscapes are important, but we need to balance them with potential disruption of the ecosystem and the loss of important species.”

Why are some tarantulas so vividly coloured? Scientists have puzzled over why these large, hairy spiders, active primarily during the evening and at night-time, would sport such vibrant blue and green colouration - especially as they were long thought to be unable to differentiate between colours, let alone possess true colour vision.

In a recent study, researchers from Yale-NUS College and Carnegie Mellon University (CMU) find support for new hypotheses: that these vibrant blue colours may be used to communicate between potential mates, while green colouration confers the ability to conceal among foliage. Their research also suggests that tarantulas are not as colour-blind as previously believed, and that these arachnids may be able to perceive the bright blue tones on their bodies. The study was published in Proceedings of the Royal Society B on 23 September, and is featured on the front cover of the current (30 September 2020) issue.

The research was jointly led by Dr Saoirse Foley from CMU, and Dr Vinod Kumar Saranathan, in collaboration with Dr William Piel, both from the Division of Science at Yale-NUS College. To understand the evolutionary basis of tarantula colouration, they surveyed the bodily expression of various opsins (light-sensitive proteins usually found in animal eyes) in tarantulas. They found, contrary to current assumptions, that most tarantulas have nearly an entire complement of opsins that are normally expressed in day-active spiders with good colour vision, such as the Peacock Spider.

These findings suggest that tarantulas, long thought to be colour-blind, can perceive the bright blue colours of other tarantulas. Using comparative phylogenetic analyses, the team reconstructed the colours of 110 million-year-old tarantula ancestors and found that they were most likely blue. They further found that blue colouration does not correlate with the ability to urticate or stridulate - both common defence mechanisms -- suggesting that it did not evolve as a means of deterring predators, but might instead be a means of attracting potential mates.

The team also found that the evolution of green colouration appears to depend on whether the species in question is arboreal (tree-dwelling), suggesting that this colour likely functions in camouflage.

"While the precise function of blueness remains unclear, our results suggest that tarantulas may be able to see these blue displays, so mate choice is a likely potential explanation. We have set an impetus for future projects to include a behavioural element to fully explore these hypotheses, and it is very exciting to consider how further studies will build upon our results," said Dr Foley.

The team's survey of the presence of blue and green colouration across tarantulas turned up more interesting results. They found that the blue colouration has been lost more frequently than it is gained across tarantulas. The losses are mainly in species living in the Americas and Oceania, while many of the gains are in the Old World (European, Asian, and African) species. They also found that green colouration has evolved only a few times, but never lost.

"Our finding that blueness was lost multiple times in the New World, while regained in the Old, is very intriguing. This leaves several fascinating avenues for future research, when considering how the ecological pressures in the New and the Old Worlds vary," said Dr Saranathan. "For instance, one hypothesis would be differences in the light environments of the habitats between the New and the Old World, which can affect how these colours might be perceived, if indeed they can be, as our results suggest."

A comprehensive search of genetic variation databases has revealed no significant differences across populations and ethnic groups in seven genes associated with viral entry of SARS-CoV-2.

African Americans and Latinos in the United States and ethnic minorities in the United Kingdom are disproportionately affected by COVID-19. They are more likely to develop severe symptoms and also show significantly higher mortality compared with other regional and ethnic groups.

To investigate if this disparity could be caused by genetic variation, a team of three researchers - including Assistant Professor Ji-Won Lee of Hokkaido University's Graduate School of Dental Medicine - surveyed publicly available databases of genomic variants, including gnomAD, the Korean Reference Genome Database, TogoVar (a Japanese genetic variation database) and the 1000 Genomes Project. They studied variants across multiple regional and ethnic groups in seven genes known to play roles in viral entry into host cells and recognition of viral RNA in host cells.

SARS-CoV-2 has spiked protein (S protein) on its envelope, which encloses the virus. Before the virus can enter host cells, the S protein has to bind with the ACE2 receptor on the cell surface. It is then broken into two pieces by the enzymes TMPRSS2 and cathepsin B and L. After the virus enters the cells, the viral RNA binds with proteins such as TLR3, TLR7 and TLR8, triggering an innate immune response.

According to the results, there were genetic variants in these seven proteins, with the largest number of variants in ACE2. However, very few of these variations alter the functions of these proteins. Since the overall variation frequency was extremely low (less than 0.01 percent), the scientists determined there is no significant difference across populations or ethnic groups in the functions of the seven proteins involved in infection.

The team's findings suggest that differences in morbidity and mortality are not the result of genetic variations in genes for viral entry across populations. Rather, it is more likely that preexisting medical conditions, individual medical histories, environmental factors and healthcare disparities play a significant role in affecting the morbidity and mortality of COVID-19. However, due to the limited size of the population databases used in this study, additional research using more diverse human genome databases is required. Additionally, other studies have shown that genetic factors may contribute to serious cases.

Philadelphia, September 24, 2020 - According to a new study in the Journal of the Academy of Nutrition and Dietetics, published by Elsevier, the percentage of heavy sugar-sweetened beverage (SSB) consumers - those who drink more than 500 calories of SSBs daily - trended downwards in the United States between 2003 and 2016. Among children, the percentage of heavy SSB consumers declined from 11 percent to 3 percent consistently across age group, sex, family income level, and most race/ethnicities. For adults, the percentage of heavy SSB consumers declined from about 13 percent to 9 percent overall, but there was variation among different age, sex, and racial/ethnic groups.

"Our study contributes important new evidence and insights to research on SSB consumption, and it tells a public health success story. The percentage of children and adults who are heavy sugary beverage drinkers has declined significantly, which is similar to trends in overall SSB consumption. Public health strategies to reduce excessive intake of sugary beverages appear to be working," said senior investigator Sara N. Bleich, PhD, Professor, Department of Health Policy and Management, Harvard T.H. Chan School of Public Health, Boston, MA, USA.

SSBs are widely consumed in the US, by about 60 percent of children and 50 percent of adults on a typical day, and they represent one of the largest sources of added sugar in the diet. Heavy sugary beverage drinkers are an important group to monitor since excessive intake is linked to chronic conditions like obesity and diabetes as well as cavities. In recent years, concern about excessive SSB consumption has been addressed through various strategies. For example, a number of cities and counties have imposed beverage taxes and passed several healthy beverage ordinances requiring restaurants to offer only healthy beverages with children's meals.

Studies looking at the changing consumption of sugary beverages have generally shown declines over the past decade. Unlike this study, however, little of the prior research has concentrated on heavy SSB drinkers, people who consume more than the equivalent of about 3.5 cans of soda daily.

The investigators used data from 2003 to 2016 for a sample of more than 20,000 children and 30,000 adults from the National Health Examination and Nutrition survey (NHANES), which provided a nationally representative look at beverage consumption for adults and children. In addition to looking at changes in consumption over time by heavy SSB consumers overall, the investigators looked at trends by age, sex, race/ethnicity, and family income level, as well as purchase and consumption locations.

The results showed that the percentage of heavy SSB drinkers has increased among people 60 years old and older, although the absolute percentage of heavy SSB consumers in this group was low. There was no significant change in the percentage of heavy SSB drinkers (no improvement) over the period among the 40-59-year old group and among non-Mexican Hispanic adults, while most other race/ethnicities experienced a decline (improvement). Finally, the investigators looked at the most recent years of data (2015-2016) and found that the majority of SSB calories consumed by heavy SSB drinkers were from stores and about half of the SSB calories were consumed at home.

First author Kelsey A. Vercammen, MSc, Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA, commented, "The insights gleaned from our study can help reduce consumption even further. Because the results zeroed in on several groups who showed no improvement or actually increased their intake, these can be used to better target interventions. Ongoing surveillance is also important to keeping these trends moving in the right direction."