Its additional role, say the researchers, may shift from trash sorter to signal messenger in dorsal root ganglion neurons — cells that convey sensory signals from nerve cells close to the skin to the central nervous system.

Results of their experiments, published April 12 in Cell Reports, show that proteasomes may help those specialized neurons sense the surrounding environment, send signals to each other and potentially differentiate between sensing pain and itch, a finding that could help scientists better understand these sensory processes and new targets for treating pain and other sensory problems.

“Neurons live next to each other for a long time, and they need ways to communicate with each other about what they’re doing and who they are,” says Seth S. Margolis, Ph.D., associate professor of biological chemistry at the Johns Hopkins University School of Medicine. “Proteasomes in the membrane of neurons may help the cells fine tune this messaging process.”

“Proteasomes are more complicated than they appear,” says Margolis. He and his colleagues first found proteasomes in the plasma membranes of central nervous system neurons in mice in 2017, which they dubbed neuronal membrane proteasomes, and have continued studying how these special proteasomes promote messaging, or crosstalk, among neurons.

At the time, Margolis’ focus was on the central nervous system, encompassing the brain and spinal cord. But later, he collaborated with neurobiologist Eric Villalón Landeros, Ph.D., postdoctoral fellow in Margolis’ laboratory at Johns Hopkins, whose work focuses on the peripheral nervous system, the network of neurons running through the rest of the body, closer to the skin, capturing sensory information from the environment.

Margolis and Villalón Landeros wondered whether proteasomes could be found in peripheral neurons, and if so, what they might do.

Using mouse antibodies that glom on to proteasomes, and other methods, the investigators found the proteasomes on the surface of neurons in the spinal cord, dorsal root ganglia, sciatic nerve and peripheral nerves innervating skin.

The researchers were also able to find proteasomes in the same type of peripheral neurons grown in laboratory culture dishes.

To understand the proteasome’s function in peripheral sensory neurons, the researchers gave mice biotin-epoxomicin, a cell membrane-impermeable proteasome inhibitor that blocks the function of neuronal membrane proteasomes. Then, they performed classic sensory tests.

The researchers found that the mice that got injections of the proteasome-blocking drug biotin-epoxomicin on one side of the body were between 25% to 50% slower than the other side to respond to sensory tests.

“This suggests that membrane proteasomes are important for sensation, and they must be facilitating this at the signaling level,” says Margolis.

The researchers used single cell sequencing technology to determine that membrane proteasomes were expressed in a subpopulation of neurons involved in itch sensation and known to be sensitive to histamine, an immune system compound that launches an animal’s (including human’s) response to allergens.

In laboratory culture dishes, the researchers stimulated both itch-related and non-itch related neurons and blocked their membrane proteasomes with biotin-epoxomicin. This resulted in changes to activity in all of the cells. “Blocking proteasomes seems to have an activity-modulatory effect across all the cells, despite being expressed in a subpopulation, suggesting that proteasomes facilitate a kind of cross talk between these cells,” says Margolis.

Proteasome blockers, including one called Velcade, are currently used to treat certain types of cancer.

Villalón Landeros and Margolis plan to continue working together to determine how neuronal membrane proteasomes function in sensory neurons and in sensing pain versus itch. “We want to see if we can manipulate neuronal membrane proteasomes to have a different outcome on pain and itch sensation,” says Villalón Landeros.

Additional scientists who contributed to the research are Samuel Kho, Taylor Church, Anna Brennan, Fulya Türker, Michael Delannoy and Michael Caterina from Johns Hopkins.

Funding for the research was provided by the National Institutes of Health (F32NS119202, R01 NS110754) and a Merkin Peripheral Neuropathy and Nerve Regeneration Center grant.

Researchers are urgently trying to find ways to prevent or slow idiopathic pulmonary fibrosis (IPF) and related lung conditions, which can cause worsening shortness of breath, dry cough, and extreme fatigue. Average survival following diagnosis of IPF is just three to five years, and the disease has no cure.

A recent U-M study from a team led by Sean Fortier, M.D. and Marc Peters-Golden, M.D. of the Division of Pulmonary and Critical Care Medicine at U-M Medical School uncovers a pathway used during normal wound healing that has the potential to reverse IPF.

Using a mouse model, they simulated IPF by administering bleomycin, a chemotherapy agent that causes cell injury and confirmed that the resulting lung scarring resolved itself over the span of about six weeks.

Because of this, “studying fibrosis is kind of tough,” said Fortier. “If we’re going to give experimental drugs to try and resolve fibrosis, we have to do it before it resolves on its own.

Otherwise, we will not be able to tell if the resolution was the action of the drug or natural repair mechanisms of the body.”

However, he said, “there’s actually a lot to learn about how the mouse gets better on its own. If we can learn the molecular mechanisms by which this occurs, we may uncover new targets for IPF.”

The process by which lung injury either leads to healing or fibrosis relies in part on what happens to a cell called a fibroblast, which forms connective tissue.

During injury or illness, fibroblasts are activated, becoming myofibroblasts that form scar tissue by secreting collagen. When the job is done, these fibroblasts must be deactivated, or de-differentiated, to go back to their quiet state or undergo programmed cell death and be cleared.

“This is the major distinction between normal wound healing and fibrosis — the persistence of activated myofibroblasts,” explained Fortier. That deactivation is controlled by molecular brakes. The study examined one of these brakes, called MKP1 — which the team found was expressed at lower levels in fibroblasts from patients with IPF.

By genetically eliminating MKP1 in fibroblasts of mice after establishing lung injury, the team saw that fibrosis continued uncontrolled.

“Instead of at day 63, seeing that nice resolution, you still see fibrosis,” said Fortier.

“We argued by contradiction: when you knock out this brake, fibrosis that would otherwise naturally disappear, persists and therefore MKP1 is necessary for spontaneous resolution of fibrosis.”

They performed several additional studies using CRISPR techniques to demonstrate how MKP1 applies the brakes, mainly by deactivating the enzyme p38α, which is implicated in a cell’s reaction to stress.

Furthermore, they demonstrated that neither of the two current FDA approved drugs for lung fibrosis, pirfenidone and nintedanib, are able to turn off myofibroblasts.

“That’s totally in keeping with the fact that they do slow the progression, but they don’t halt or reverse disease,” said Fortier.

Fortier hopes the discovery that this pathway reverses fibrosis leads to exploration of additional brakes on fibrosis.

“So much work on fibrosis has focused on how we can prevent it, but when a patient presents to my clinic with a dry cough, shortness of breath, and low oxygen as a result of underlying IPF, the scarring is already present. Of course, we’d love a way to prevent the scarring from getting worse, but the Holy Grail is to reverse it.”

Duke University’s Marine Geospatial Ecology Lab led a collaboration of 11 institutions in the United States that pooled 17 years of available visual survey data covering 9.7 million square kilometers of the U.S. Atlantic — roughly the same area as the entire contiguous United States.

This information was coupled with auditory data from almost 500 hydrophone recorders in US Atlantic waters that captured whales’ calls. Lining up visual and acoustic datasets for the first time, researchers built a statistical model to estimate the number of whales per square kilometer at different points in time. Researchers published their findings on March 20, 2024 in Marine Ecology Progress Series.

“The more accurate and detailed the mapping, the better chance we have to save dwindling numbers of right whales from preventable injury and fatality,” said Patrick Halpin, director of Duke’s Marine Geospatial Ecology Lab. The lab studies marine ecology, resource management, and ocean conservation, using data to inform ocean management and governance.

Other current real-time efforts to track and protect the whales from deadly encounters with human activities have been incomplete or ineffective. Electronic tagging can harm whale health, and it is infeasible to continuously monitor more than a small fraction of the population that way.

The statistical model is a revision of a 2016 model that predicts whale density from environmental data, like sea surface temperature. This latest version incorporates new data to reflect whales’ changing migration and feeding patterns, including their presence in new areas that lack protection measures for marine life.

“With nearly three times more aerial survey data than we had before, and confirming evidence from the hydrophones, we were able to show how strongly the population has shifted its distribution,” said Jason Roberts, a Duke research associate and lead author of the study.

Right whales maintain the health and balance of marine environments and the entire food web through their feeding habits. As climate change has reduced the population of their prey, whale migration patterns have become more unpredictable, increasing the chances that human activities, like commercial fishing, may harm whale health and chances of reproduction.

Using maps obtained by satellite ocean monitoring, or from physical ocean models like the recently published one, researchers can more accurately predict whale density across the U.S. east coast.

Muscle strength, especially hand grip strength, can indicate an individual’s physiological resources to protect against age-related diseases and disabilities, as well as their ability to cope with them. Age-related loss of muscle strength is individual and influenced not only by lifestyle but also by genetics.

The study revealed that individuals with a genetic predisposition for higher muscle strength have a slightly lower risk for common noncommunicable diseases and premature mortality. However, it did not predict better survival after acute adverse health events compared to the time before illness onset.

“It seems that a genetic predisposition for higher muscle strength reflects more on an individual’s intrinsic ability to resist and protect oneself against pathological changes that occur during aging than the ability to recover or completely bounce back after severe adversity,” says doctoral researcher Päivi Herranen from the Faculty of Sport and Health Sciences.

The research utilized a unique study population

Muscle strength is a multifactorial trait influenced by lifestyle and environmental factors but also by numerous genetic variants, each with a very small effect on muscle strength. In this study, the genetic predisposition for muscle strength was defined by constructing a polygenic score for muscle strength, which summarizes the effects of hundreds of thousands of genetic variants into a single score. The polygenic score makes it possible to compare participants with an exceptionally high or low genetic predisposition for muscle strength, and to investigate associations with inherited muscle strength and other phenotypes, in this case, common diseases.

“In this study, we were able to utilize both genetic information and health outcomes from over 340,000 Finnish men and women,” Herranen explains.

“To our knowledge, this is the first study to investigate the association between a genetic predisposition for muscle strength and various diseases on this scale.”

Further research on the effects of lifestyles is still needed

Information about the genetic predisposition for muscle strength could be used alongside traditional risk assessment in identifying individuals who are at particularly high risk of common diseases and health adversities. However, further research on the topic is still needed.

“Based on these results, we cannot say how lifestyle factors, such as physical activity, modify an individual’s intrinsic ability to resist diseases and whether their impact on health differs among individuals due to genetics,” Herranen notes.

The study utilized the internationally unique FinnGen dataset, compiled through the collaboration of Finnish biobanks. The dataset consisted of 342,443 Finns who had given their consent and provided a biobank sample. The participants were aged 40 to 108 years, and 53% of them were women. The diagnoses selected for the study were based on the leading causes of death and the most significant noncommunicable diseases in Finland. Selected diagnoses included the most common cardiometabolic and pulmonary diseases, musculoskeletal and connective tissue diseases, falls and fractures, mental health and cognitive disorders, cancers, as well as overall mortality and mortality from cardiovascular diseases.

The study is the second publication of Päivi Herranen’s doctoral thesis, which investigates how genetics and environmental factors affect biological aging, particularly the weakening of muscle strength and functional capacity with age. The research is part of the GenActive project, funded by the Research Council of Finland and the Juho Vainio and Päivikki and Sakari Sohlberg foundations. The project is led by Assistant Professor and Academy Research Fellow Elina Sillanpää. The research was conducted in collaboration with the Gerontology Research Center (GEREC), the Institute for Molecular Medicine Finland (FIMM), and the FinnGen research project.

The design and development of novel materials with superior properties demands a comprehensive analysis of their atomic and electronic structures. Electron energy parameters such as ionization potential (IP), the energy needed to remove an electron from the valence band maximum, and electron affinity (EA), the amount of energy released upon the attachment of an electron to the conduction band minimum, reveal important information about the electronic band structure of surfaces of semiconductors, insulators, and dielectrics. The accurate estimation of IPs and EAs in such nonmetallic materials can indicate their applicability for use as functional surfaces and interfaces in photosensitive equipment and optoelectronic devices.

Additionally, IPs and EAs depend significantly on the surface structures, which adds another dimension to the complex procedure of their quantification. Traditional computation of IPs and EAs involves the use of accurate first-principles calculations, where the bulk and surface systems are separately quantified. This time-consuming process prevents quantifying IPs and EAs for many surfaces, which necessitates the use of computationally efficient approaches.

To address the wide-ranging issues affecting the quantification of IPs and EAs of nonmetallic solids, a team of scientists from Tokyo Institute of Technology (Tokyo Tech), led by Professor Fumiyasu Oba, have turned their focus towards machine learning (ML). Their research findings have been published in theJournal of the American Chemical Society.

Prof. Oba shares the motivation behind the present research, “In recent years, ML has gained a lot of attention in materials science research. The ability to virtually screen materials based on ML technology is a very efficient way to explore novel materials with superior properties. Also, the ability to train large datasets using accurate theoretical calculations allows for the successful prediction of important surface characteristics and their functional implications.”

The researchers employed an artificial neural network to develop a regression model, incorporating the smooth overlap of atom positions (SOAPs) as numerical input data. Their model accurately and efficiently predicted the IPs and EAs of binary oxide surfaces by using the information on bulk crystal structures and surface termination planes.

Moreover, the ML-based prediction model could ‘transfer learning,’ a scenario where a model developed for a particular purpose can be made to incorporate newer datasets and reapplied for additional tasks. The scientists included the effects of multiple cations in their model by developing ‘learnable’ SOAPs and predicted the IPs and EAs of ternary oxides using transfer learning.

Prof. Oba concludes by saying, “Our model is not restricted to the prediction of surface properties of oxides but can be extended to study other compounds and their properties.”

“Chimpanzees and bonobos use aggression in different ways for specific reasons,” says anthropologist and lead author Maud Mouginot of Boston University. “The idea is not to invalidate the image of bonobos being peaceful — the idea is that there is a lot more complexity in both species.”

Though previous studies have investigated aggression in bonobos and chimpanzees, this is the first study to directly compare the species’ behavior using the same field methods. The researchers focused on male aggression, which is often tied to reproduction, but they note that female bonobos and chimpanzees are not passive, and their aggression warrants its own future research.

To compare bonobo and chimpanzee aggression, the team scrutinized rates of male aggression in three bonobo communities at the Kokolopori Bonobo Reserve (Democratic Republic of Congo) and two chimpanzee communities at Gombe National Park (Tanzania). Overall, they examined the behavior of 12 bonobos and 14 chimpanzees by conducting “focal follows,” which involved tracking one individual’s behavior for an entire day and taking note of how often they engaged in aggressive interactions, who these interactions were with, and whether they were physical or not (e.g., whether the aggressor engaged in pushing and biting or simply chased their adversary).

“You go to their nests and wait for them to wake up and then you just follow them the entire day — from the moment they wake up to the moment they go to sleep at night — and record everything they do,” says Mouginot.

To their surprise, the researchers found that male bonobos were more frequently aggressive than chimpanzees. Overall, bonobos engaged in 2.8 times more aggressive interactions and 3 times as many physical aggressions.

While male bonobos were almost exclusively aggressive toward other males, chimpanzees were more likely to act aggressively toward females. Chimpanzee aggression was also more likely to involve “coalitions” of males (13.2% vs. 1% of bonobo aggressions). The researchers think that these coalitions might be one reason why aggression is less frequent among chimpanzees. Altercations involving groups of males have the potential to cause more injuries, and within-community fighting could also weaken the group’s ability to fight off other groups of chimpanzees. Bonobos don’t have this issue because most of their disputes are one on one, they have never been observed to kill one another, and they are not thought to be territorial, which leaves their communities free to bicker among themselves.

For both chimpanzees and bonobos, more aggressive males had greater mating success. The researchers were surprised to find this in bonobos, which have a co-dominant social dynamic in which females often outrank males, compared to chimpanzees, which have male-dominated hierarchies in which male coalitions coerce females into mating.

“Male bonobos that are more aggressive obtain more copulations with females, which is something that we would not expect,” said Mouginot. “It means that females do not necessarily go for nicer males.”

These findings partially contradict a prevailing hypothesis in primate and anthropological behavior — the self-domesticating hypothesis — which posits that aggression has been selected against in bonobos and humans but not chimpanzees.

The researchers were not able to assess the severity of aggressive interactions in terms of whether they resulted in wounds or injuries, but this is data that they hope to collect in future. They also want to compare aggressive behavior in other groups of chimpanzees and bonobos as it’s possible that behavior varies between communities and subspecies.

“I’d love to have the study complemented with comparable data from other field sites so we can get a broader understanding of variation within and between species,” says Mouginot.

“This is a big genomic resource that will open the door for many more studies,” says co-first author and algal biologist Alexandra Mystikou of New York University Abu Dhabi and the Technology Innovation Institute, United Arab Emirates. “Macroalgae play an important role in global climate regulation and ecosystems, and they have numerous commercial and ecoengineering applications, but until now, there wasn’t a lot of information about their genomes.”

Macroalgae live in both fresh and seawater and are complex multicellular organisms with distinct organs and tissues, in contrast to microalgae, which are microscopic and unicellular. There are three main groups of macroalgae — red (Rhodophyta), green (Chlorophyta), and brown (Ochrophyta) — that independently evolved multicellularity at very different times and in very different environmental conditions. Rhodophytes and Chlorophytes both evolved multicellularity over a billion years ago, while Ochrophytes only became multicellular in the past 200,000 years.

To investigate the evolution of macroalgal multicellularity, the researchers sequenced 110 new macroalgal genomes from 105 different species originating from fresh and saltwater habitats in diverse geographies and climates.

The researchers identified several metabolic pathways that distinguish macroalgae from microalgae, some of which may be responsible for the success of invasive macroalgal species. Many of these metabolic genes appear to have been donated by algae-infecting viruses, and genes with a viral origin were especially prevalent in the more recently evolved brown algae.

They found that macroalgae acquired many new genes that are not present in microalgae on their road to multicellularity. For all three lineages, key acquisitions included genes involved in cell adhesion (which enables cells to stick together), cell differentiation (which allows different cells to develop specialized functions), cell communication, and inter-cellular transport.

“Many brown algal genes associated with multicellular functions had signature motifs that were only otherwise present in the viruses that infect them,” says co-first author and bioinformatician David Nelson of New York University Abu Dhabi. “It’s kind of a wild theory that’s only been hinted at in the past, but from our data it looks like these horizontally transferred genes were critical factors for evolving multicellularity in the brown algae.”

The team also identified other features that were distinct between the macroalgal lineages. They observed much more diversity between different species of Rhodophyte, which evolved multicellularity first and have thus had longer to diverge. They also found that Chlorophytes share many genomic features with land plants, suggesting that these genes may have already been present in the last common ancestor of Chlorophytes and plants.

“By no means have we exhaustively explored all that there is in these genomes,” says senior author and systems biologist Kourosh Salehi-Ashtiani of New York University Abu Dhabi. “There is a ton of information that we have not touched in the present paper that can be mined by whoever who is interested.”

The researchers are already digging into the dataset to investigate environmental and habitat adaptations amongst macroalgae. In future, they hope to sequence and analyze even more macroalgal genomes.

“We want to explore some of these features in more detail, meaning more genomes if we can get our hands on them,” says Salehi-Ashtiani.

This research was supported by the NYUAD Faculty Research Funds and Tamkeen.

Led by Professor Ashok Venkitaraman, this ground-breaking study was conducted by scientists from the Cancer Science Institute of Singapore (CSI Singapore) at NUS and NUS Centre for Cancer Research (N2CR) under the Yong Loo Lin School of Medicine, with colleagues from the Agency for Science, Technology and Research (A*STAR).

Prof Venkitaraman, Director of CSI Singapore, explained, “Cancer is caused by the interaction between our genes and factors in our environment, such as diet, exercise, and pollution. How such environmental factors increase cancer risk is not yet very clear, but it is vital to understand the connection if we are to take preventive measures that help us stay healthy longer.”

A chemical linked to diabetes, obesity, and poor diet can heighten cancer risk

The research team first studied patients who are at a high risk of developing breast or ovarian cancers because they inherit a faulty copy of the cancer gene — BRCA2 — from their parents. They demonstrated that cells from such patients were particularly sensitive to the effects of methylglyoxal, which is a chemical produced when our cells break down glucose to create energy. The study showed that this chemical can cause faults in our DNA that are early warning signs of cancer development.

The team’s research also suggested that people who do not inherit a faulty copy of BRCA2 but could experience higher-than-normal levels of methylglyoxal — such as patients with diabetes or pre-diabetes, which are connected with obesity or poor diet — can accumulate similar warning signs indicating a higher risk of developing cancer.

Prof Venkitaraman elaborated, “Our research suggests that patients with high methylglyoxal levels may have higher cancer risk. Methylglyoxal can be easily detected by a blood test for HbA1C, which could potentially be used as a marker. Furthermore, high methylglyoxal levels can usually be controlled with medicines and a good diet, creating avenues for proactive measures against the initiation of cancer.”

The study’s first author, Dr Li Ren Kong, Lee Kuan Yew Fellow from N2CR, added, “We started the study aiming to understand what factors elevate risk in families susceptible to cancer, but ended up discovering a deeper mechanism linking an essential energy consumption pathway to cancer development. These findings raise awareness of the impact of diet and weight control in the management of cancer risks.”

Novel mechanism for tumour formation

Interestingly, the research team’s work also revised a longstanding theory about certain cancer-preventing genes. This theory — called the Knudson’s ‘two-hit’ paradigm — was first formulated in 1971, and it was proposed that these genes must be inactivated permanently in our cells before cancer can arise. The NUS team has now found that methylglyoxal can temporarily inactivate such cancer-preventing genes, suggesting that repeated episodes of poor diet or uncontrolled diabetes can ‘add up’ over time to increase cancer risk. This new knowledge is likely to be influential in changing the direction of future research in this area.

Next phase of research

Building on their novel discoveries, the researchers aim to conduct further studies to understand if metabolic disorders, such as diabetes or poor diets, affect cancer risk in Singapore and other Asian countries.

The research team also hopes to identify new mechanisms underlying the connection between metabolism, diet and cancer that they have discovered, to develop more effective approaches to prevent or delay the onset of cancer.

The study analysed samples collected alongside some of the busiest routes in South West England and the Midlands, many used by more than 100,000 vehicles each day.

Tyre particles were discovered in each of the 70 samples taken, confirming the findings of previous research which has shown them to pose a considerable environmental threat.

However, the presence of wetlands and retention ponds led to an average reduction of almost 75% in the mass of tyre wear particles being discharged to aquatic waters, thus providing protection for rivers and the ocean beyond.

The study also found that tyre wear particles significantly outweighed other forms of microplastics, such as plastic fibres and fragments, in the samples collected but that they were also removed in far greater quantities.

The researchers say that while the number of retention ponds and wetlands is quite small, in terms of the UK’s entire road network, the study has international significance as to the most effective ways to mitigate against the potential impacts of tyre pollution on a global scale.

They have also recommended that the maintenance of retention ponds and wetlands should be considered a major priority so that their apparent benefits, when it comes to reducing the flow of tyre particles from roads to rivers, continue to be realised.

The research is published in the Environmental Science and Pollution Research journal, and was carried out by scientists from the University of Plymouth and Newcastle University. It was funded by UK National Highways.

Florence Parker-Jurd, Associate Research Fellow in the University of Plymouth’s International Marine Litter Research Unit, is the study’s lead author.

She said: “Retention ponds and wetlands are constructed as part of highways projects primarily to attenuate flow and prevent downstream flooding, but also to remove pollutants. This study set out to establish if these existing drainage measures in place along parts of the UK’s strategic road network have the potential to halt the spread of tyre pollution. Our results are positive in that regard, and provide a much improved understanding on the extent and nature of tyre pollution. Similar drainage assets are used on a global scale; hence these results are of broad relevance to the management of tyre wear particle pollution.”

Dr Geoff Abbott, Reader in Organic Geochemistry in the School of Natural and Environmental Sciences (SNES) at Newcastle University, has previously developed a breakthrough method using pyrolysis-gas chromatography-mass spectrometry (Py-GC-MS) to detect tyre-derived particles in the environment.

He explained: “Py-GC-MS is a really productive approach that can unravel and quantify the monomeric components of microplastics in the environment. We used it to identify specific components of micro- and nanoplastics that can be unequivocally linked to vehicle tyre tread. That has enabled us to get hard numbers on the total amount of tyre wear particles that are collecting in the influent, effluent, and sediments of the retention ponds and wetlands in this study.”

The new research builds on previous studies involving researchers from Plymouth and Newcastle showing that tyre particles can be transported directly to the ocean through the atmosphere or carried by rainwater into rivers and sewers.

Professor Richard Thompson OBE FRS, Head of the International Marine Litter Research Unit, is senior author on the current study.

He added: “Tyre particles are thought to be among the greatest sources of microplastic pollution worldwide. This finding suggests that existing features of the road network can halt their flow into rivers and seas. But the number of these features is small compared to the total road network and our earlier work has shown substantial quantities of tyre wear particles are dispersed by wind rater then water. Ultimately, we need to seek more systemic solutions perhaps via improved vehicle tyre design.”

Professor Thompson is also currently leading the ongoing TYRE-LOSS project, which aims to highlight the effects of tyre pollution in the marine environment.

A study published by scientists involved in that project earlier this year also found that particles released into the environment from common road tyres should be treated as a “high concern” pollutant.