Publisher Health

Robotic prosthetic ankles that are controlled by nerve impulses allow amputees to move more “naturally,” improving their stability, according to a new study from North Carolina State University and the University of North Carolina at Chapel Hill.
“This work focused on ‘postural control,’ which is surprisingly complicated,” says Helen Huang, corresponding author of the study and the Jackson Family Distinguished Professor in the Joint Department of Biomedical Engineering at NC State and UNC.
“Basically, when we are standing still, our bodies are constantly making adjustments in order to keep us stable. For example, if someone bumps into us when we are standing in line, our legs make a wide range of movements that we are not even necessarily aware of in order to keep us upright. We work with people who have lower limb amputations, and they tell us that achieving this sort of stability with prosthetic devices is a significant challenge. And this study demonstrates that robotic prosthetic ankles which are controlled using electromyographic (EMG) signals are exceptionally good at allowing users to achieve this natural stability.” EMG signals are the electrical signals recorded from an individual’s muscles.
The new study builds on previous work, which demonstrated that neural control of a powered prosthetic ankle can restore a range of abilities, including standing on challenging surfaces and squatting.
For this study, the researchers worked with five people who had amputations below the knee on one leg. Study participants were fitted with a prototype robotic prosthetic ankle that responds to EMG signals that are picked up by sensors on the leg.
“Basically, the sensors are placed over the muscles at the site of the amputation,” says Aaron Fleming, co-author of the study and recent Ph.D. graduate from NC State. “When a study participant thinks about moving the amputated limb, this sends electrical signals through the residual muscle in the lower limb. The sensors pick these signals up through the skin and translate those signals into commands for the prosthetic device.”
The researchers conducted general training for study participants using the prototype device, so that they were somewhat familiar with the technology.

A new study carried out in mice, led by Queen Mary University of London, has identified cells that drive the spread of pancreatic cancer and discovered a weakness in these cells that could be targeted using existing drugs. This offers a promising new approach for treating pancreatic cancer.
The research, published in Science Advances and funded by Barts Charity and Cancer Research UK, found that many patients’ pancreatic cancer contains cells called amoeboid cells. These are aggressive, invasive and fast-moving cells that weaken the immune system. These cells have previously been identified in other cancers, such as melanoma, breast, liver and prostate cancer, and have been linked with poor survival rates. This is the first time that they have been found in pancreatic cancer.
Crucially, the new study discovered amoeboid cells in pancreatic cancer produce high levels of a molecule called CD73, which drives their ability to spread and weaken the immune system. When blocking this molecule, the researchers reduced the spread of cancer to the liver and decreased the number of immune cells that supported the tumour.
The research looked at mice given anti-CD73 treatment over the short term (3 weeks) and long term where clinical endpoints were met (when an outcome that represents direct clinical benefit was achieved, such as survival, decreased pain, or the absence of disease). In the long-term group, anti-CD73 treatment reduced the incidence of cancerous tumours that spread to the liver from 66.6 per cent to 36.4 per cent.
While further tests would be needed involving humans to confirm the conclusions, the study suggests that blocking CD73 could be a promising approach for treating pancreatic cancer and the spread of it, especially considering that drugs blocking CD73 have already been developed and are being tested in clinical trials for various types of cancer.
The amoeboid cells were present in both late and early-stage pancreatic cancer. This opens up a new possible avenue of treatment in blocking CD73 early in the disease and reducing the aggressive nature of these cells and the damage they cause in the body.
Professor Victoria Sanz-Moreno, Professor of Cancer Cell Biology at Queen Mary University of London, said:
“While the results would need to be replicated in humans, they are very promising in highlighting a potential way of treating the spread of one of the most aggressive and poorly survived cancers.

About 40,000 years ago, Neanderthals, who had lived for hundreds of thousands of years in the western part of the Eurasian continent, gave way to Homo sapiens, who had arrived from Africa. This replacement was not sudden, and the two species coexisted for a few millennia, resulting in the integration of Neanderthal DNA into the genome of Sapiens. Researchers at the University of Geneva (UNIGE) have analyzed the distribution of the portion of DNA inherited from Neanderthals in the genomes of humans (Homo sapiens) over the last 40,000 years. These statistical analyses revealed subtle variations in time and geographical space. This work, published in the journal Science Advances, helps us to understand the common history of these two species.
Thanks to genome sequencing and comparative analysis, it is established that Neanderthals and Sapiens interbred and that these encounters were sometimes fruitful, leading to the presence of about 2% of DNA of Neanderthal origin in present-day Eurasians. However, this percentage varies slightly between regions of Eurasia, since DNA from Neanderthals is somewhat more abundant in the genomes of Asian populations than in those of European populations.
One hypothesis to explain this difference is that natural selection would not have had the same effect on genes of Neanderthal origin in Asian and European populations. Mathias Currat’s team, senior lecturer in the Department of Genetics and Evolution at the UNIGE Faculty of Science, is working on another hypothesis. His previous work, based on computer simulations, suggests that such differences could be explained by migratory flows: when a migrant population hybridizes with a local population, in their area of cohabitation, the proportion of DNA of the local population tends to increase with distance from the point of departure of the migrant population.
Europe: a territory shared by both species
In the case of Sapiens and Neanderthals, the hypothesis is that the further one moves away from Africa, Homo sapiens’ point of origin, the greater the proportion of DNA from Neanderthal, a population mainly located in Europe. To test this hypothesis, the authors used a database made available by Harvard Medical School that includes more than 4,000 genomes from individuals who have lived in Eurasia over the past 40 millennia.
”Our study is mainly focused on European populations since we are obviously dependent on the discovery of bones and the state of conservation of DNA. It turns out that archaeological excavations have been much more numerous in Europe, which greatly facilitates the study of the genomes of European populations,” explains Claudio Quilodrán, senior research and teaching assistant in the Department of Genetics and Evolution at the UNIGE Faculty of Science, and co-first author of the study.
Statistical analyses revealed that, in the period following the dispersal of Homo sapiensfrom Africa, the genomes of Paleolithic hunter-gatherers who lived in Europe contained a slightly higher proportion of DNA of Neanderthal origin than the genomes of those who lived in Asia. This result is contrary to the current situation but in agreement with paleontological data, since the presence of Neanderthals was mainly reported in western Eurasia (no Neanderthal bones have been discovered further east than the Altai region of Siberia).
The arrival of Anatolian farmers modifies genomes
Subsequently, during the transition to the Neolithic, i.e. the transition from the hunter-gatherer lifestyle to the farmer lifestyle, 10,000 to 5,000 years ago, the study shows a decline in the proportion of DNA of Neanderthal origin in the genomes of European populations, resulting in a slightly lower percentage than that of Asian populations (as currently observed). This decrease coincided with the arrival in Europe of the first farmers from Anatolia (Turkey’s western peninsula) and the Aegean area, who themselves carried a lower proportion of DNA of Neanderthal origin than the inhabitants of Europe at the same time. By mixing with the populations of Europe, the genomes of farmers from Anatolia ”diluted” Neanderthal DNA a little more.
This study shows that the analysis of ancient genomes, coupled with archaeological data, makes it possible to trace different stages in the history of hybridized species. ”In addition, we are beginning to have enough data to describe more and more precisely the percentage of DNA of Neanderthal origin in the genome of Sapiens at certain periods of prehistory. Our work can therefore serve as a reference for future studies to more easily detect genetic profiles that deviate from the average and might therefore disclose an advantageous or disadvantageous effect,” concludes Mathias Currat, last author of the study.

A vaccine designed to protect against three different deadly coronaviruses shows success in mouse studies, demonstrating the viability of a pan-coronavirus vaccine developed by researchers at the Duke Human Vaccine Institute.
Publishing in the journal Cell Reports, the single nanoparticle vaccine included components of a previous vaccine that was shown to protect mice and primates against multiple variants of SARS-CoV-2, which is the virus that causes COVID-19. In this study, the vaccine protected mice from SARS-CoV-1, another form of SARS coronavirus that can infect humans, and a MERS coronavirus that has led to periodic, deadly outbreaks around the world.
“We are making important progress toward a broadly protective coronavirus vaccine,” said senior author Kevin O. Saunders, Ph.D., associate director of the Duke Human Vaccine Institute. “These are pathogens that cause or have the potential to cause significant human infections and loss of life, and a single vaccine that provides protection could slow down or even prevent another pandemic.”
Saunders and colleagues built the tri-valent vaccine using a nanoparticle loaded with a key fragment called a receptor binding domain from each of the coronaviruses. The fragment — a docking site on the virus that enables it to infiltrate the body’s cells — provides enough information for immune cells to build an effective response against actual coronaviruses that enter the body.
In earlier studies in mice and primates, the researchers demonstrated that an earlier iteration of the nanoparticle vaccine was effective against multiple SARS-CoV-2 variants. Human tests are planned next year for a version that carries immunogens to different SARS-CoV-2 strains, including those that have dominated since the original outbreak in late 2019.
The current work expands the components of the vaccine to include an additional SARS-related virus and MERS virus. In lab studies, as well as in mice, the researchers found that the vaccine candidate generated inhibitory immune molecules called antibodies against all three pathogenic human coronavirus types.
Importantly, vaccinated mice did not grow sick when challenged with either SARS-like or MERS-like viruses.
“This study demonstrates proof-of-concept that a single vaccine that protects against both MERS and SARS viruses is an achievable goal,” Saunders said. “Given that one MERS and two SARS viruses have infected humans in the last two decades, the development of universal coronavirus vaccines is a global health priority.”
In addition to Saunders, study authors include lead author David R. Martinez, who is now at Yale School of Medicine, and Alexandra Schäfer, Tyler D. Gavitt, Michael L. Mallory, Esther Lee, Nicholas J. Catanzaro, Haiyan Chen, Kendra Gully, Trevor Scobey, Pooja Korategere, Alecia Brown, Lena Smith, Rob Parks, Maggie Barr, Amanda Newman, Cindy Bowman, John M. Powers, Erik J. Soderblom, Katayoun Mansouri, Robert J. Edwards, Ralph S. Baric, and Barton F. Haynes.
The study received funding support from the National Institute of Allergy and Infectious Diseases, which is part of the National Institutes of Health (U54 CA260543, P01 AI158571).

Children fall broadly into four eating categories, according to new research at Aston University, and parents feed their children differently depending on those categories.
The four categories identified by Dr Abigail Pickard and the team in the School of Psychology are ‘avid’, ‘happy’, ‘typical’, and ‘fussy’.
In the UK, around a fifth of children are overweight or living with obesity when they begin school, rising to around a third by the time they leave primary school at age 11. The team sought to identify eating behaviour patterns and how these are associated with temperament, feeding practices and food insecurity, as a way to predict which children are more at risk of becoming overweight.
Typical eaters made up 44% of the children in the study, while fussy eaters accounted for 16%. But of greatest interest to the team was that around one in five young children in the study were found to show “avid eating,” including greater enjoyment of food, faster eating speed, and weaker sensitivity to internal cues of ‘fullness’. The behaviours that distinguish children with avid eating from those who show ‘happy’ eating (17.7% of children in the study), who have similarly positive responses to food, are wanting to eat (or eating more) in response to the sight, smell or taste of palatable food, and a higher level of emotional overeating. In combination, these eating behaviours can lead to overeating and subsequent weight gain.
Dr Pickard and the team, which includes academics from Aston University, Loughborough University, Kings College London and University College London (UCL), have also shown that there are significant differences in children’s temperament and caregivers’ feeding practices between each of the four eating behaviour patterns. Children with avid eating are more likely to be active and impulsive, and their caregivers are more likely to give them food to regulate their emotions or to restrict food for health reasons. Children with avid eating were also less food secure than children who showed happy or typical eating behaviours.
Principal investigator of the project, Professor Jackie Blissett, said:
“Whilst feeding practices are key intervention targets to change children’s eating behaviour and child weight outcomes, there has been little evaluation of how feeding practices interact with children’s food approach behaviours to predict eating behaviour.”
She explained that despite the knowledge of the influence of feeding practices on children’s weight, current public health advice is generic and does not reflect variability in children’s appetites. Parents and caregivers can be left feeling frustrated when trying to manage their child’s food intake. By defining the four eating behaviour profiles, this research project, which is funded by the Economic and Social Research Council and co-developed by Professor Claire Farrow, Dr Clare Llewellyn, Dr Moritz Herle, Professor Emma Haycraft and Dr Helen Croker will make it easier to identify the best feeding practices for each eating pattern and provide tailored, effective advice for parents.

As the COVID-19 pandemic scattered and isolated people, researchers across Virginia Tech connected for a data-driven collaboration seeking improved drugs to fight the disease and potentially many other illnesses.
A multidisciplinary collaboration spanning several colleges at Virginia Tech resulted in a newly published study, “Data Driven Computational Design and Experimental Validation of Drugs for Accelerated Mitigation of Pandemic-like Scenarios,” in the Journal of Physical Chemistry Letters.
The study focuses on using computer algorithms to generate adaptations to molecules in compounds for existing and potential medications that can improve those molecules’ ability to bind to the main protease, a protein-based enzyme that breaks down complex proteins, in SARS-CoV-2, the virus that causes COVID-19.
This process allows exponentially more molecular adaptations to be considered than traditional trial-and-error methods of testing drugs one by one could allow. Candidate molecule adaptations can be identified among myriad possibilities, then narrowed to a few or one that can be created in a laboratory and tested for effectiveness.
“We present a novel transferable data-driven framework that can be used to accelerate the design of new small molecules and materials, with desired properties, by changing the combination of building blocks as well as decorating them with functional groups,” said Sanket A. Deshmukh, associate professor of chemical engineering in the College of Engineering. A “functional group” is a cluster of atoms that generally retains its characteristic properties, regardless of the other atoms in the molecule.
“Interestingly, the newly designed functionalized drug not only had a better half maximal effective concentration value than its parent drug, but also several of the proposed and used antivirals including Remdesivir,” Deshmukh said, referring to a measure of compound potency.
Moving through all the phases of the study would not have been possible without extensive cross-departmental collaboration.

Engineers at the University of California San Diego have developed an experimental vaccine that could prevent the spread of metastatic cancers to the lungs. The key ingredients of the vaccine are nanoparticles — fashioned from bacterial viruses — that have been engineered to target a protein known to play a central role in cancer growth and spread. In mice, the vaccine significantly reduced the spread of metastatic breast and skin cancers to the lungs. It also improved the survival rate in mice with metastatic breast cancer after surgical removal of the primary tumor.
The findings were published on Oct. 16 in Proceedings of the National Academy of Sciences.
Metastasis is a process involving the migration of cancer cells from their primary site to other parts of the body. Recent studies have identified S100A9, a protein typically released by immune cells, as a key player in this process. Its normal role is to regulate inflammation. However, an excess of S100A9 can attract cancer cells like a magnet, causing them to form aggressive tumors and facilitating their spread to other organs, such as the lungs.
A team led by Nicole Steinmetz, a professor of nanoengineering at the UC San Diego Jacobs School of Engineering, developed a vaccine candidate that can modulate the levels of S100A9 when it goes haywire. When injected subcutaneously, the vaccine stimulated the immune system in mice to produce antibodies against S100A9, effectively reducing the protein levels and minimizing cancer metastasis to the lungs. The vaccine also increased the expression of immune-stimulating proteins with anti-tumor properties, while decreasing the levels of immune-suppressing proteins.
“S100A9 is known to form what is called a premetastatic niche within the lungs, creating an immunosuppressive environment that allows for tumor seeding and growth,” said study first author Young Hun (Eric) Chung, a UC San Diego bioengineering Ph.D. alumnus from Steinmetz’s lab. “By reducing S100A9 levels, we can effectively counteract the formation of this premetastatic niche, leading to a reduced attraction and increased clearance of cancer cells to the lungs.”
“This is a clever, new approach to vaccination in that we are not targeting tumor cells, but rather the tumor microenvironment so that it prevents the primary tumor from making new tumors,” said Steinmetz, who is the founding director of the UC San Diego Center for Nano-ImmunoEngineering and co-lead of the university’s Materials Research Science and Engineering Center (MRSEC). “We are essentially changing the whole immune system to be more anti-tumor.”
How it works
The vaccine consists of nanoparticles made from a bacterial virus called Q beta. The nanoparticles were grown from E. coli bacteria and isolated. Afterwards, a piece of the S100A9 protein was attached to the surface.

Artificial intelligence has exploded in popularity and is being harnessed by some scientists to predict which molecules could treat illnesses, or to quickly screen existing medicines for new applications. Researchers reporting in ACS Central Science have used one such deep learning algorithm, and found that dihydroartemisinin (DHA), an antimalarial drug and derivative of a traditional Chinese medicine, could treat osteoporosis as well. The team showed that in mice, DHA effectively reversed osteoporosis-related bone loss.
In healthy people, there is a balance between the osteoblasts that build new bone and osteoclasts that break it down. But when the “demolition crew” becomes overactive, it can result in bone loss and a disease called osteoporosis, which typically affects older adults. Current treatments for osteoporosis primarily focus on slowing the activity of osteoclasts. But osteoblasts — or more specifically, their precursors known as bone marrow mesenchymal stem cells (BMMSCs) — could be the basis for a different approach. During osteoporosis, these multipotent cells tend to turn into fat-creating cells instead, but they could be reprogrammed to help treat the disease. Previously, Zhengwei Xie and colleagues developed a deep learning algorithm that could predict how effectively certain small-molecule drugs reversed changes to gene expression associated with the disease. This time, joined by Yan Liu and Weiran Li, they wanted to use the algorithm to find a new treatment strategy for osteoporosis that focused on BMMSCs.
The team ran the program on a profile of differently expressed genes in newborn and adult mice. One of the top-ranked compounds identified was DHA, a derivative of artemisinin and a key component of malaria treatments. Administering DHA extract for six weeks to mice with induced osteoporosis significantly reduced bone loss in their femurs and nearly completely preserved bone structure. To improve delivery, the team designed a more robust system using injected, DHA-loaded nanoparticles. Bones of mice with osteoporosis that received the treatment were similar to those of the control group, and the treatment showed no evidence of toxicity. In further tests, the team determined that DHA interacted with BMMSCs to maintain their stemness and ultimately produce more osteoblasts. The researchers say that this work demonstrates that DHA is a promising therapeutic agent for osteoporosis.
The authors acknowledge funding from the National Natural Science Foundations of China, the Beijing International Science and Technology Cooperation, the Beijing Natural Science Foundation, Peking University Clinical Medicine Plus X — Young Scholars Project, the Ten-Thousand Talents Program, the Key R & D Plan of Ningxia Hui Autonomous Region, the Innovative Research Team of High-Level Local Universities in Shanghai, the Beijing Nova Program, the China National Postdoctoral Program for Innovative Talents, the China Postdoctoral Science Foundation, and the Peking University Medicine Sailing Program for Young Scholars’ Scientific & Technological Innovation.

Progressive strength training using resistance can protect against the detrimental effects of a high-protein diet, according to new research in mice.
The study, published today as a Reviewed Preprint in eLife, presents what the editors describe as a valuable finding on the relationship between a high-protein diet and resistance exercise on fat accumulation and glucose homeostasis, supported by solid evidence. They say the findings will be relevant to dietitians and others trying to understand links between dietary protein, diabetes and exercise.
Dietary protein provides essential nutrients that control a wide variety of processes in the body and can influence health and lifespan. Protein consumption is generally thought of as good, promoting muscle growth and strength, especially when combined with exercise. Yet in people with a sedentary lifestyle, too much protein can increase the risk of heart disease, diabetes and death.
“We know that low-protein diets and diets with reduced levels of specific amino acids promote healthspan and lifespan in animals, and that the short-term restriction of protein improves the health of metabolically unhealthy, adult humans,” explains lead author Michaela Trautman, Research Assistant at the Department of Medicine, School of Medicine and Public Health, University of Wisconsin, US. “But this presents a paradox — if high dietary protein is so harmful, many people with high-protein diets or protein supplements would be overweight and at an increased risk of diabetes, whereas athletes with high-protein diets are among the most metabolically healthy.”
To examine the possibility that exercise can protect against the detrimental effects of a high-protein diet, the researchers used a progressive resistance-based strength training program in mice. The animals pulled a cart carrying an increasing load of weight down a track three times per week for a three-month period, or pulled an identical cart without any load for the same time period. One group of mice were fed a low-protein diet (7% of calories from protein) and a second group were fed a high-protein diet (36% of calories from protein). The team then compared the body composition, weight and metabolic measurements, such as blood glucose, of the different groups.
The results were as the team expected: the high-protein diet impaired metabolic health in sedentary mice pulling no weight; these mice gained excess fat mass compared to the low-protein diet mice. But in the mice pulling the increasing weight, a high-protein diet led to muscle growth especially in the forearm, and protected the animals from gaining fat. However, the exercise did not protect the mice from the effects of high protein on blood sugar control.
Additionally, although the high-protein-fed mice gained strength more quickly than the low-protein-fed mice, there was no difference in the maximum weight each set of mice could pull by the end of the study period, even though the mice fed high-protein diets were bigger and had larger muscles.
Although the evidence supporting the claims of the study was considered to be solid, the editors highlight a couple of limitations. For instance, the use of mice might limit the generalisability of the findings to humans, due to inherent physiological differences. The editors note that the findings would also be strengthened further by the inclusion of a direct investigation into the underlying molecular mechanisms responsible for the observed results.
“We know that many people deliberately consuming high-protein diets or consuming protein supplements to support their exercise regimen are not metabolically unhealthy, despite the body of evidence showing that high-protein levels can have detrimental metabolic effects,” says senior author Dudley Lamming, Associate Professor of Medicine (Endocrinology) at the Department of Medicine, School of Medicine and Public Health, University of Wisconsin. “Our research may explain this conundrum, by showing that resistance exercise protects from high-protein-induced fat gain in mice. This suggests that metabolically unhealthy, sedentary individuals with a high-protein diet or protein supplements might benefit from either reducing their protein intake or more resistance exercise.”

Many efforts to reduce transmission of diseases like Covid-19 and the flu have focused on measures such as masking and isolation, but another useful approach is reducing the load of airborne pathogens through filtration or germicidal ultraviolet light. Conventional UV sources can be harmful to eyes and skin, but newer sources that emit at a different wavelength, 222 nanometers, are considered safe.
However, new research from MIT shows that these UV lights can produce potentially harmful compounds in indoor spaces. While the researchers emphasize that this doesn’t mean the new UV lights should be avoided entirely, they do say the research suggests it is important that the lights have the right strength for a given indoor situation, and that they are used along with appropriate ventilation.
The findings are reported in the journal Environmental Science and Technology, in a paper by recent MIT postdoc Victoria Barber, doctoral student Matthew Goss, Professor Jesse Kroll, and six others at MIT, Aerodyne Research, and Harvard University.
While Kroll and his team usually work on issues of outdoor air pollution, during the pandemic they became increasingly interested in indoor air quality. Usually, little photochemical reactivity happens indoors, unlike outdoors, where the air is constantly exposed to sunlight. But with the use of devices to clean indoor air using chemical methods or UV light, “all of a sudden some of this oxidation is brought indoors,” triggering a potential cascade of reactions, Kroll says.
Initially, the UV light interacts with oxygen in the air to form ozone, which is itself a health risk. “But also, once you make ozone, there’s a possibility for all these other oxidation reactions,” Kroll says. For example, the UV can interact with the ozone to produce compounds called OH radicals, which are also powerful oxidizers.
Barber, who is now an assistant professor at the University of California at Los Angeles, adds, “If you have volatile organic compounds in the environment, which you do basically in all indoor environments, then these oxidants react with them and you make these oxidized volatile organic compounds, which in some cases turn out to be more harmful to human health than their unoxidized precursors.” The process also leads to the formation of secondary organic aerosols, she says. “Again, this stuff is harmful to breathe, so having it in your indoor environment is not ideal.”
The formation of such compounds is particularly problematic in the indoors, Kroll says, because people spend so much of their time there, and low ventilation rates can mean these compounds could accumulate to relatively high levels.