Publisher Health

Regular physical activity and exercise may reduce bleeding in individuals with intracerebral hemorrhage, a University of Gothenburg study shows. The researchers emphasize the importance of physical activity to protect the brain.
The study, published in the journal Stroke and Vascular Neurology, analyzed data on 686 people treated for intracerebral hemorrhage at Sahlgrenska University Hospital in Gothenburg during the years 2014 to 2019.
The results are based on a retrospective analysis. Causal connections cannot be identified, but the findings are nonetheless clear: Those who reported regular physical activity had smaller hemorrhages than those who reported being inactive.
Physically active was defined as engaging in at least light physical activity, such as walking, cycling, swimming, gardening, or dancing, for at least four hours weekly.
50 percent less bleeding volume
The main author of the study is Adam Viktorisson, a PhD student in clinical neuroscience at Sahlgrenska Academy, University of Gothenburg, and doctor in general practice at Sahlgrenska University Hospital.

“We found that individuals who engage in regular physical activity had, on average, bleeding volumes that were 50 percent smaller upon arriving to the hospital. A similar connection has previously been seen in animal studies, but no prior study has demonstrated this in humans.”
Everyone who comes to the hospital with a suspected intracerebral hemorrhage undergoes a computerized tomography (CT) scan of the brain. Depending on the severity of the hemorrhage, neurosurgery may be required. However, in most cases, non-surgical methods and medications are used to manage symptoms and promote patient recovery.
Intracerebral hemorrhage is the most dangerous type of stroke and can lead to life-threatening conditions. The risk of severe consequences from the hemorrhage increases with the extent of the bleeding.
“In cases of major intracerebral hemorrhages, there is a risk of increased pressure within the skull that can potentially lead to fatal outcomes” says Thomas Skoglund, associate professor of neurosurgery at the University of Gothenburg, neurosurgeon at the University Hospital, and one of the study’s co-authors.
Better understanding of intracerebral hemorrhages
The findings were significant regardless of the location within the cerebrum. Physically active individuals exhibited reduced bleeding in both the deep regions of the brain, which are often associated with high blood pressure, and the surface regions, which are linked to age-related conditions like dementia.
The study creates scope for further research on intracerebral hemorrhages and physical activity. Katharina Stibrant Sunnerhagen, professor of rehabilitation medicine at the University of Gothenburg and senior consultant physician at Sahlgrenska University Hospital, oversees the study.
“We hope that our findings contribute to a deeper understanding of intracerebral hemorrhages and aid in the development of more effective preventive measures” she concludes.

Have you ever wondered why some people might get sicker than others, even when they catch the same virus? It is not yet clear why this is. Viral factors (such as differences in the strain of a virus) play a role in this variability, but they cannot account for the wide range of responses in different individuals infected by the same virus. A number of host factors have also been considered, including pre-existing immunity, age, sex, weight, and the microbiome.
Another important factor is the molecular biology within your cells. DNA is shown as one long double-helical strand. So, you might expect that the cell would always read genetic information in order, starting at one end and going to the other. But this isn’t the case. DNA contains transposable elements , sometimes called “junk DNA,” which can change the regions of the genome are being read at a given time.
The work published in Cell Genomics by an international team led by Dr. Guillaume Bourque, who studied the role of these transposable elements on the severity of illness after influenza A virus infection.
By examining data from 39 individuals before and after infection with influenza A virus, the researchers were able to identify changes in the accessibility (that is, the “readability”) of transposable elements. To do this, the researchers used an approach combining various sets of multiomics data, which characterize and quantify collections of biomolecules in cells or organisms. One was the transcriptome, which consists of all copies of RNA transcribed from DNA in the cell. The other was the epigenome, which is the collection of chemical changes to DNA that modify gene expression. An advantage of this multiomics approach is that they were able to identify families of transposable elements with changes in accessibility, which would have likely been missed by previous approaches.
By considering these changes in transposable elements after viral infection, they could identify several transcription factors (proteins that turn specific genes “on” or “off”) that likely contribute to someone’s response to infection. Using these findings, the researchers were able to create a model that could predict an individual’s viral load after influenza A infection.
“A number of questions remain, such as whether the link between transposable elements and viral load is actually causal and whether these changes would be consistent over time,” says lead author Xun Chen. “But these findings are an important step toward understanding the role that such factors play in the variability of illness severity among individuals.”
The authors include researchers from Kyoto University in Japan, McGill University and the Université de Montréal in Canada, and the University of Chicago in the US.

In the scientific literature, the total production of reactive oxygen species (ROS) such as H2O2 is commonly used as proxy for the toxicity of air pollutants and their ability to induce oxidative stress and inflammation. The research team led by Thomas Berkemeier from the MPIC in Mainz found that ROS concentrations in the epithelial lining fluid (ELF) of the human respiratory tract may be primarily determined by the release of endogenous H2O2 and the inhalation of ambient gas-phase H2O2, while the chemical production of H2O2 through inhaled PM2.5 is less important.
“Based on our simulations, we think that the overall concentrations of these reactive species in the lungs are large anyway, and not directly dependent on levels of air pollution,” says Dr. Thomas Berkemeier, head of the Chemical Kinetics & Reaction Mechanisms group at the MPIC. They use a computer model to understand the relevant physical, chemical, and biological processes, and quantify the health effects of different types of air pollutants.
“Our new model simulates the chemical reactions that happen in the respiratory tract. For the first time, we included production, diffusion, and removal of hydrogen peroxide from cells and the blood stream into our computer model. This was quite challenging, because it is not so easy to put these processes in biological tissues into equations,” explains Thomas Berkemeier.
New research directions
“The findings of this study suggest that the current paradigms for assessing the differential toxicity of individual PM2.5 components need to be critically reassessed,” says Prof. Dr. Ulrich Pöschl, Head of the Multiphase Chemistry Department at the MPIC. The study proposes that the chemical production of superoxide and H2O2 in a cell-free assay may not be a suitable metric for assessing the differential toxicity of individual PM2.5 components, and some acellular oxidative potential assays may not capture the actual deleterious effects of PM2.5.
Fine particulates might act through Fenton chemistry
However, the production of hydroxyl radicals (OH) was strongly correlated with Fenton chemistry of PM2.5 in the model calculations. “The model simulations suggest that PM2.5 mostly acts by conversion of peroxides into highly reactive OH radicals. Thus, PM2.5 is not so much the fuel, but rather the catalyst of the chemical reactions that cause damage to cells and tissues,” says Berkemeier explaining the role of inhaled particles in the model. Additionally, PM2.5 may stimulate the production of superoxide from endogenous sources, which further contributes to the adverse health effects of air pollution.
The study underscores the importance of continued research to better understand the chemical mechanisms underlying the health effects of air pollution and to develop effective strategies to mitigate these effects. The authors believe that this study will contribute significantly to this important research effort. Their findings are published in the scientific journal “Environmental Science: Atmospheres.”
Background information
Air pollution is a major health risk that affects millions of people worldwide, but the underlying chemical mechanisms are not yet fully understood. Fine particulate matter (PM2.5) typically contains chemical components that can trigger oxidation reactions. When inhaled and deposited in the human respiratory tract, they can induce and sustain radical reaction cycles that produce reactive oxygen species (ROS) in the epithelial lining fluid (ELF) that covers the airways and alveoli in human lungs. Numerous studies have shown that excess concentrations of ROS like hydrogen peroxide (H2O2) and hydroxyl radicals (OH) can cause oxidative stress injuring cells and tissues in the respiratory tract.

Ants’ brains are amazingly sophisticated organs that enable them to coordinate complex behaviour patterns such as the organisation of colonies. Now, a group of researchers led by Christian Gruber of MedUni Vienna’s Institute of Pharmacology have developed a method that allows them to study ants’ brain chemistry and gain insights into the insects’ neurobiological processes. The findings could help to explain the evolution of social behaviour in the animal kingdom, and shed light on the biochemistry of certain hormone systems that have developed similarly in both ants and humans. For the study, the researchers used a combination of high-resolution mass spectrometry imaging (MSI) and micro-computed tomography (µCT) to map the three-dimensional distribution of neuropeptides in the brains of two ant species: the leafcutter ant (Atta sexdens) and the black garden ant (Lasius niger).
Researchers from MedUni Vienna, the Max Planck Institute for Marine Microbiology in Bremen and the University of Bremen have developed a new method for studying social insects’ brains, which measure only a few millimetres in size. In future, their approach could play a decisive role in research into fundamental neurobiological processes. The method integrates three-dimensional chemical data into a high-definition anatomical model, allowing for unbiased visualisation of 3D neurochemistry in its particular anatomical environment. Published in the journal PNAS Nexus, the study showed that some ant peptides, such as the tachykinin-related peptides TK1 and TK4, are widely distributed in many areas of both species’ brains, while other peptides, including myosuppressin, are only found in particular regions. The researchers also noticed differences between the two species – a large number of peptides were found in the optic lobe of L. niger, but only one (an ITG-like peptide) was identified in the same region in A. sexdens.
The key feature of the new method is that a correlative approach is used to analyse data. This means that 3D maps of the distribution of neuropeptides and 3D anatomical models are precisely collated, generating two maps that help to navigate the ants’ brains. Each map contains different information, which is critical for studying organs with high plasticity, such as the brains of social insects, which are particularly hard to analyse due to the complex division of labour and caste system in ant colonies. Building on previous studies of MS imaging of neuropeptides in invertebrate model systems, this approach represents a promising method for studying fundamental neurobiological processes by visualising distortion-free 3D neurochemistry in its own complex anatomical environment.
“These findings have the potential to fundamentally alter the way we study complex neurobiological processes. Our method opens up new perspectives when it comes to observing the brains of social insects more closely and better understanding the functioning of nervous systems where chemistry and anatomy are fully attuned,” commented lead author Benedikt Geier, who worked alongside co-lead author Esther Gil Mansilla. “In terms of neurobiology, ants are a model species. Due to the extremely complex structures in ant colonies, this method could be applied in future to gain an understanding of various factors, including the evolution of social behaviour in the animal kingdom, or the biochemistry of certain hormone systems that have developed in a similar fashion in both ants and humans,” reported Christian Gruber.

Biosensors are artificial molecular complexes designed to detect the presence of target chemicals or even biomolecules. Consequently, biosensors have become important in diagnostics and synthetic cell biology. However, typical methods for engineering biosensors focus on optimizing the interactions between static binding surfaces, and current biosensor designs can only recognize structurally well-defined molecules, which can be too rigid for “real-life” biology.
“We developed a novel computational approach for designing protein-peptide ligand binding and applied it to engineer cell-surface chemotactic receptors that reprogrammed cell migration,” says EPFL professor Patrick Barth. “We think that our work could broadly impact the design of protein binding and cell engineering applications.”
The new biosensors developed by Barth’s group can sense flexible compounds and trigger complex cellular responses, which open up new possibilities for biosensor applications. The researchers created a ‘computational framework’, which is a computer-based system, for designing protein complexes that can change their shape and function dynamically — as opposed to the conventional static approaches. The framework can look at previously unexplored protein sequences to come up with new ways for the protein’s groups to be activated, even in ways that are different to their natural function.
The researchers used their new method to create synthetic receptors that can sense and respond to multiple natural or engineered molecular signals, providing optimal sensing of flexible ligands and strong allosteric signaling responses, a term that refers to changes in protein activity when a molecule binds to a different site on a protein, causing a change in the protein’s shape and activity at a different site.
The designed receptors act by interacting with the flexible ligands via allosteric triggers, like natural receptors, but they improve and rearrange how the signals are transferred, a bit like dialing the same number from a different cell phone with better service. Specifically, the triggers seem to funnel signals through the same set of “transmission hubs” as the natural ones, but considerably enhance signal transmission through optimally rewired dynamic couplings.
The research shows that combining a flexible sensing layer with a robust signal transmission layer may be a common hallmark of G protein-coupled receptors, a family of enormously important receptors in the cell, connected to virtually every major aspect of its life and function.
“We were able to leverage our biosensor design to drive cell migration in lymphocytes, which migrate more efficiently towards chemokines when equipped with designed biosensors,” says Rob Jefferson, the study’s first author. “Chemokines serve as chemical beacons for immune cell recruitment in the body, a suboptimal process in certain diseases that could be improved with our biosensors.”
The new method of designing synthetic receptors could be useful in a wide variety of therapeutic contexts. For example, engineered cytotoxic lymphocytes with enhanced chemotaxis toward tumor sites could prove useful in cancer treatment. Designing receptors that can sense and respond to specific signals, provides a promising new synthetic cell biology tool, leading to more precise control over cellular processes for a wide range of therapeutic applications.

Every day, millions of cells die in our body. Other than generally assumed, cells do not simply burst at the end of their lives but rather, a specific protein serves as a breaking point for cell membrane rupture. Researchers at the University of Basel have now been able to elucidate the exact mechanism at the atomic level. They have published their results in Nature.
Cell death is crucial for all organisms. Damaged cells or cells infected with viruses or bacteria eliminate themselves by starting a built-in “suicide” program, which prevents the development of tumors and the spread of pathogens in the body.
Until recently, it was assumed that cells simply burst and die at the end of their life. Now, researchers at the Biozentrum of the University of Basel, the University of Lausanne and the Department of Biosystems Science and Engineering (D-BSSE) at ETH Zurich have provided new insights into the final step of cell death. In the scientific journal “Nature,” they describe how a protein called ninjurin-1 assembles into filaments that work like a zipper and open the cell membrane, thus leading to the disintegration of the cell. The new insights are an important milestone in the understanding of cell death.
Protein acts as a breaking point in the cell membrane
Various signals, such as bacterial components, trigger the cell death machinery. At the final stage of this process, the cell’s protective membrane is compromised by tiny pores which allow ions to stream into the cell. “The common understanding was that the cell then swells until it finally bursts due to increasing osmotic pressure,” explains Professor Sebastian Hiller who heads a research group at the Biozentrum, University of Basel. “We are now resolving how the cells really rupture. Instead of bursting like a balloon, the protein ninjurin-1 provides a breaking point in the cell membrane, causing rupture at specific sites.”
Using advanced techniques such as highly sensitive microscopes and NMR spectroscopy, the scientists have been able to elucidate the mechanism by which ninjurin-1 induces membrane rupture at the level of individual atoms. Ninjurin-1 is a small protein embedded in the cell membrane.
“Upon receiving the suicide command, two ninjurin-1 proteins initially cluster together and drive a wedge into the membrane,” explains Morris Degen, first author of the study and PhD student at the PhD School of the Swiss Nanoscience Institute. “Large lesions and holes are formed by many further proteins attaching to the initial wedge. In this way, the cell membrane is cleaved open piece by piece until the cell disintegrates completely.” The cell debris is then removed by the body’s own cleaning service.
“It is now evident that the cells do not burst without ninjurin-1. They do swell to a certain extend due to the influx of ions, but membrane rupture is contingent on the function of this protein,” adds Hiller. “The textbooks chapter on cell death will be expanded with these beautiful structural insights.”
Therapy to prevent or promote cell death
The deeper understanding of cell death will facilitate the search for novel drug targets. Therapeutic interventions to treat cancer are conceivable, since some tumor cells evade programmed cell death. Also, in the case of premature cell death observed in neurodegenerative diseases such as Parkinson’s disease or in life-threatening conditions such as septic shock, drugs that interfere in this process are a potential treatment option.

Chronic wounds are open sores or injured tissue that fail to heal properly. These types of wounds are notoriously challenging to treat because of bacterial infections like Staphylococcus aureus, or S. aureus. Additionally, bacterial infections that are highly resistant to antibiotics, such as methicillin-resistant S. aureus (MRSA), are one of the main causes of life-threatening infections in hospital patients.
To defend itself from our immune system and other threats, S. aureus can band together, creating a slick, slimy forcefield — or biofilm — around itself. The biofilm barrier is so thick that neither immune cells nor antibiotics can penetrate through and neutralize the harmful bacteria.
Researchers at the UNC School of Medicine and the UNC-NC State Joint Department of Biomedical Engineering have developed a new method that combines palmitoleic acid, gentamicin, and non-invasive ultrasound to help improve drug delivery in chronic wounds that have been infected with S. aureus.
Using their new strategy, researchers were able to reduce the challenging MRSA infection in the wounds of diabetic mice by 94%. They were able to completely sterilize the wounds in several of the mice, and the rest had significantly reduced bacterial burden. Their results were published in Cell Chemical Biology.
“When bacteria are not completely cleared from chronic wounds, it puts the patient at high risk for the infection recurring or of developing a secondary infection,” said senior author Sarah Rowe-Conlon, PhD, a research associate professor in the Department of Microbiology and Immunology. “This therapeutic strategy has the potential to improve outcomes and reduce relapse of chronic wound infections in patients. We are excited about the potential of translating this to the clinic, and that’s what we’re exploring right now.”
Biofilms act as a physical barrier to many classes of antibiotics. Virginie Papadopoulou, PhD, a research assistant professor in the UNC-NCSU Joint Department of Biomedical Engineering, was curious to know if non-invasive cavitation-enhanced ultrasound could create enough agitation to form open spaces in the biofilm to facilitate drug-delivery.

Liquid droplets which can be activated by ultrasound, called phase change contrast agent (PCCA), are applied topically to the wound. An ultrasound transducer is focused on the wound and turned on, causing the liquid inside the droplets to expand and turn into microscopic gas-filled microbubbles, when then move rapidly.
The oscillation of these microbubbles agitates the biofilm, both mechanically disrupting it as well as increasing fluid flow. Ultimately, the combination of the biofilm disruption and the increased permeation of the drugs through the biofilm allowed the drugs to come in and kill the bacterial biofilm with very high efficiency.
“Microbubbles and phase change contrast agents act as local amplifiers of ultrasound energy, allowing us to precisely target wounds and areas of the body to achieve therapeutic outcomes not possible with standard ultrasound,” said Dayton, the William R. Kenan Jr. Distinguished Professor and Department Chair of the UNC-NCSU Joint Department of Biomedical Engineering. “We hope to be able to use similar technologies to locally delivery chemotherapeutics to stubborn tumors or drive new genetic material into damaged cells as well.”
When the bacterial cells are trapped inside the biofilm, they are left with little access to nutrients and oxygen. To conserve their resources and energy, they transition into a dormant or sleepy state. The bacteria, which are known as persister cells in this state, are extremely resistant to antibiotics.
Researchers chose gentamicin, a topical antibiotic typically ineffective against S. aureus due to widespread antibiotic resistance and poor activity against persister cells. The researchers also introduced a novel antibiotic adjuvant, palmitoleic acid, to their models.
Palmitoleic acid, an unsaturated fatty acid, is a natural product of the human body that has strong antibacterial properties. The fatty acid embeds itself into the membrane of bacterial cells, and the authors discovered that it facilitates the antibiotic’s successful entry into S. aureus cells and is able to kill persister cells and reverse antibiotic resistance.
Overall, the team is enthusiastic about the new topical, non-invasive approach because it may give scientists and doctors more tools to combat antibiotic resistance and to lessen the serious adverse effects of taking oral antibiotics.
“Systemic antibiotics, such as oral or IV, work very well, but there’s often a large risk associated with them such as toxicity, wiping out gut microflora and C. difficile infection,” said Rowe-Conlon. “Using this system, we are able to make topical drugs work and they can be applied to the site of infection at very high concentrations, without the risks associated with systemic delivery.”

For the first time, researchers have recorded pain-related data from inside the brain of individuals with chronic pain disorders caused by stroke or amputation (phantom limb pain). A long sought-after goal has been to understand how pain is represented by brain activity and how to modulate that activity to relieve suffering from chronic pain. Data were collected over months while patients were at home, and they were analyzed using machine learning tools. Doing so, the researchers identified an area of the brain associated with chronic pain and objective biomarkers of chronic pain in individual patients. These findings, published in Nature Neuroscience, were funded by both the National Institutes of Health’s Brain Research Through Advancing Innovative Neurotechnologies (BRAIN) Initiative and the Helping to End Addiction Long-term Initiative, or NIH HEAL Initiative, represent a first step towards developing novel methods for tracking and treating chronic pain.
“This is a great example of how tools for measuring brain activity originating from the BRAIN Initiative have been applied to the significant public health problem of relieving persistent, severe chronic pain,” said Walter Koroshetz, M.D., director of the National Institute of Neurological Disorders and Stroke. “We are hopeful that building from these preliminary findings could lead to effective, non-addictive pain treatments.”
Chronic pain is one of the largest contributors to disability worldwide. Neuropathic pain is caused by damage to the nervous system itself. It most commonly occurs due to injury to the nerves in our bodies, but for the individuals in this study, their pain is thought to originate from the brain itself. This kind of pain does not respond well to current treatments and can be debilitating for people living with it.
“When you think about it, pain is one of the most fundamental experiences an organism can have,” said Prasad Shirvalkar, M.D., Ph.D., associate professor of anesthesia and neurological surgery at the University of California, San Francisco, and lead author of this study. “Despite this, there is still so much we don’t understand about how pain works. By developing better tools to study and potentially affect pain responses in the brain, we hope to provide options to people living with chronic pain conditions.”
Traditionally, researchers gather data about chronic pain through self-reports from those living with the condition. Examples of this type of data include questionnaires about pain intensity and emotional impact of pain. This study however, also looked directly at changes in brain activity in two regions where pain responses are thought to occur — the anterior cingulate cortex (ACC) and the orbitofrontal cortex (OFC) — as participants reported their current levels of chronic pain.
“Functional MRI studies show that the ACC and OFC regions of the brain light up during acute pain experiments. We were interested to see whether these regions also played a role in how the brain processes chronic pain,” said Dr. Shirvalkar. “We were most interested in questions like how pain changes over time, and what brain signals might correspond to or predict high levels of chronic pain?”
Four participants, three with post-stroke pain and one with phantom limb pain, were surgically implanted with electrodes targeting their ACC and OFC. Several times a day, each participant was asked to answer questions related to how they would rate the pain they were experiencing, including strength, type of pain, and how their level of pain was making them feel emotionally. They would then initiate a brain recording by clicking a remote-control device, which provided a snapshot of the activity in the ACC and OFC at that exact moment. Using machine learning analyses, the research team was able to use activity in the OFC to predict the participants’ chronic pain state.
In a separate study, the researchers looked at how the ACC and OFC responded to acute pain, which was caused by applying heat to areas of the participants’ bodies. In two of the four patients, brain activity could again predict pain responses, but in this case the ACC appeared to be the region most involved. This suggests that the brain processes acute vs. chronic pain differently, though more studies are needed given that data from only two participants were used in this comparison.
This study represents an initial step towards uncovering the patterns of brain activity that underly our perception of pain. Identifying such a pain signature will enable the development of new therapies that can alter brain activity to relieve suffering due to chronic pain. The most immediate benefit may be in informing ongoing studies in HEAL and BRAIN to employ deep brain stimulation (DBS) to treat chronic pain. Ongoing and future work involving more participants will be key in determining whether different pain conditions share the OFC activity seen in these patients or how the signatures differ among persons with different pain conditions.
More modern approaches to DBS that fine-tune the stimulation based on activity biomarkers from the brain have been used to successfully treat some brain disorders including Parkinson’s disease and major depressive disorder, but those successes have required well-established brain biomarkers. For conditions such as chronic pain, the identification of biomarkers is in the early stages.
Effective and non-addictive treatments for chronic pain conditions is a main goal of NIH HEAL Initiative efforts to find scientific solutions to stem the opioid public health crisis. The findings are a key step to identifying pain-specific biomarkers toward personalizing pain management for individuals, leading to the development of new technologies and advances to better understand brain circuit, a major component of the NIH BRAIN Initiative.
This study was funded by the BRAIN Initiative (UH3NS109556), NIH HEAL Initiative (UH3NS115631) and Defense Advanced Research Projects Agency (DARPA).

Current climate policies will leave more than a fifth of humanity exposed to dangerously hot temperatures by 2100, new research suggests.
Despite the Paris Agreement pledge to keep global warming well below 2°C (compared to pre-industrial levels), current policies are projected to result in 2.7°C warming by the end of the century.
The new study, led by researchers at the Global Systems Institute, University of Exeter, associated with the Earth Commission, and Nanjing University, assessed what this would mean for the number of people living outside the “climate niche” in which our species has thrived.
It says about 60 million people are already exposed to dangerous heat (average temperature of 29°C or higher).
And two billion — 22% of the projected end-of-century population — would be exposed to this at 2.7°C of global warming.
The paper highlights the “huge potential” for decisive climate policy to limit the human costs and inequities of climate change.

Limiting warming to 1.5°C would leave 5% exposed — saving a sixth of humanity from dangerous heat compared to 2.7°C of warming.
The study also finds that the lifetime emissions of 3.5 average global citizens today — or just 1.2 US citizens — expose one future person to dangerous heat. This highlights the inequity of climate crisis, as these future heat-exposed people will live in places where emissions today are around half of the global average.
In “worst-case scenarios” of 3.6°C or even 4.4°C global warming, half of the world’s population could be left outside the climate niche, posing what the researchers call an “existential risk.”
“The costs of global warming are often expressed in financial terms, but our study highlights the phenomenal human cost of failing to tackle the climate emergency,” said Professor Tim Lenton, director of the Global Systems Institute at the University of Exeter.
“For every 0.1°C of warming above present levels, about 140 million more people will be exposed to dangerous heat.

“This reveals both the scale of the problem and the importance of decisive action to reduce carbon emissions.
“Limiting global warming to 1.5°C rather than 2.7°C would mean five times fewer people in 2100 being exposed to dangerous heat.”
Defining the niche
Human population density has historically peaked in places with an average temperature of about 13°C, with a secondary peak at about 27°C (monsoon climates, especially in South Asia).
Density of crops and livestock follow similar patterns, and wealth (measured by GDP) peaks at about 13°C.
Mortality increases at both higher and lower temperatures, supporting the idea of a human “niche.”
Although less than 1% of humanity currently live in places of dangerous heat exposure, the study shows climate change has already put 9% of the global population (more than 600 million people) outside the niche.
“Most of these people lived near the cooler 13°C peak of the niche and are now in the ‘middle ground’ between the two peaks. While not dangerously hot, these conditions tend to be much drier and have not historically supported dense human populations,” said Professor Chi Xu, of Nanjing University.
“Meanwhile, the vast majority of people set to be left outside the niche due to future warming will be exposed to dangerous heat.
“Such high temperatures have been linked to issues including increased mortality, decreased labour productivity, decreased cognitive performance, impaired learning, adverse pregnancy outcomes, decreased crop yield, increased conflict and infectious disease spread.”
While some cooler places may become more habitable due to climate change, population growth is projected to be highest in places at risk of dangerous heat, especially India and Nigeria.
The study also found: Exposure to dangerous heat starts to increase dramatically at 1.2°C (just above current global warming) and increases by about 140 million for every 0.1°C of further warming. Assuming a future population of 9.5 billion people, India would have the greatest population exposed at 2.7°C global warming — more than 600 million. At 1.5°C, this figure would be far lower, at about 90 million. Nigeria would have the second-largest heat-exposed population at 2.7°C global warming, more than 300 million. At 1.5°C warming this would be less than 40 million. India and Nigeria already show “hotspots” of dangerous temperatures. At 2.7°C, almost 100% of some countries including Burkina Faso and Mali will be dangerously hot for humans. Brazil would have the largest land area exposed to dangerous heat, despite almost no area being exposed at 1.5 °C. Australia and India would also experience massive increases in area exposed.The research team — which included the Potsdam Institute for Climate Impact Research, the International Institute for Applied Systems Analysis, and the Universities of Washington, North Carolina State, Aarhus and Wageningen — stress that the worst of these impacts can be avoided by rapid action to cut greenhouse gas emissions.
Speaking about the conception of their idea, Professor Marten Scheffer, of Wageningen University, said: “We were triggered by the fact that the economic costs of carbon emissions hardly reflect the impact on human wellbeing.
“Our calculations now help bridging this gap and should stimulate asking new, unorthodox questions about justice.”
Ashish Ghadiali, of Exeter’s Global Systems Institute, said: “These new findings from the leading edge of Earth systems science underline the profoundly racialised nature of projected climate impacts and should inspire a policy sea-change in thinking around the urgency of decarbonisation efforts as well as in the value of massively up-shifting global investment into the frontlines of climate vulnerability.”
The research was funded by the Open Society Foundations and the paper is also an output of the Earth Commission — convened by Future Earth, the Earth Commission is the scientific cornerstone of the Global Commons Alliance.
Wendy Broadgate, Executive Director of the Earth Commission at Future Earth, said: “We are already seeing effects of dangerous heat levels on people in different parts of the world today. This will only accelerate unless we take immediate and decisive action to reduce greenhouse gas emissions.”
Work on climate solutions by the Global Systems Institute at the University of Exeter has identified “positive tipping points” to accelerate action, including a recent report that highlighted three “super-leverage points” that could trigger a cascade of decarbonisation.

A team of engineers at the University of California San Diego has developed the first fully integrated wearable ultrasound system for deep-tissue monitoring, including for subjects on the go. It facilitates potentially life-saving cardiovascular monitoring and marks a major breakthrough for one of the world’s leading wearable ultrasound labs. The paper, “A fully integrated wearable ultrasound system to monitor deep tissues in moving subjects,” is published in the May 22, 2023 issue of Nature Biotechnology.
“This project gives a complete solution to wearable ultrasound technology — not only the wearable sensor, but also the control electronics are made in wearable form factors,” said Muyang Lin, a Ph.D. candidate in the Department of Nanoengineering at UC San Diego and the first author on the study. “We made a truly wearable device that can sense deep tissue vital signs wirelessly.”
The research emerges from the lab of Sheng Xu, a professor of nanoengineering at UC San Diego Jacobs School of Engineering and corresponding author of the study.
This fully integrated autonomous wearable ultrasonic system-on-patch (USoP) builds on the lab’s previous work in soft ultrasonic sensor design. However, previous soft ultrasonic sensors all require tethering cables for data and power transmission, which largely constrains the user’s mobility. In this work, it includes a small, flexible control circuit that communicates with an ultrasound transducer array to collect and transmit data wirelessly. A machine learning component helps interpret the data and track subjects in motion.
According to the lab’s findings, the ultrasonic system-on-patch allows continuous tracking of physiological signals from tissues as deep as 164 mm, continuously measuring central blood pressure, heart rate, cardiac output, and other physiological signals for up to twelve hours at a time.
“This technology has lots of potential to save and improve lives,” Lin said. “The sensor can evaluate cardiovascular function in motion. Abnormal values of blood pressure and cardiac output, at rest or during exercise, are hallmarks of heart failure. For healthy populations, our device can measure cardiovascular responses to exercise in real time and thus provide insights into the actual workout intensity exerted by each person, which can guide the formulation of personalized training plans.”
The USoP also represents a breakthrough in the development of the Internet of Medical Things (IoMT), a term for a network of medical devices connected to the internet, wirelessly transmitting physiological signals into the cloud for computing, analysis and professional diagnosis.

Thanks to technological advances and the hard work of clinicians over the last few decades, ultrasound has received an ongoing wave of interest, and the Xu lab is often mentioned in the first breath as an early and enduring leader in the field, particularly in wearable ultrasound. The lab took devices that were stationary and portable and made them stretchable and wearable, driving a transformation across the landscape of healthcare monitoring. Its strength rests in part on its close collaboration with clinicians. “Although we are engineers, we do know the medical problems that clinicians face,” Lin said. “We have a close relationship with our clinical collaborators and always get valuable feedback from them. This new wearable ultrasound technology is a unique solution to address many vital sign monitoring challenges in clinical practice.”
While developing its latest innovation, the team was surprised to discover that it had more capabilities than initially anticipated.
“At the very beginning of this project, we aimed to build a wireless blood pressure sensor,” said Lin. “Later on, as we were making the circuit, designing the algorithm and collecting clinical insights, we figured that this system could measure many more critical physiological parameters than blood pressure, such as cardiac output, arterial stiffness, expiratory volume and more, all of which are essential parameters for daily health care or in-hospital monitoring.”
Moreover, when the subject is in motion, there will be relative movement between the wearable ultrasonic sensor and the tissue target, which will require frequent manual readjustment of the wearable ultrasonic sensor to keep track of the moving target. In this work, the team developed a machine learning algorithm to automatically analyze the received signals and choose the most appropriate channel to keep track of the moving target.
However, when the algorithm is trained using one subject’s data, that learning may not be transferable to other subjects, making the results inconsistent and unreliable.
“We eventually made the machine learning model generalization work by applying an advanced adaptation algorithm,” said Ziyang Zhang, a master’s student in the Department of Computer Science and Engineering at UC San Diego and co-first author on the paper. “This algorithm can automatically minimize the domain distribution discrepancies between different subjects, which means the machine intelligence can be transferred from subject to subject. We can train the algorithm on one subject and apply it to many other new subjects with minimal retraining.”
Moving forward, the sensor will be tested among larger populations. “So far, we have only validated the device performance on a small but diverse population,” said Xiaoxiang Gao, a postdoctoral scholar in the Department of NanoEngineering at UC San Diego and co-first author on the study. “As we envision this device as the next generation of deep-tissue monitoring devices, clinical trials are our next step.”
Xu is the co-founder of Softsonics, LLC, which plans to commercialize the technology.