Category: Medical Research & Technology

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Preventing Drug Damage to the Vestibular System

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Photo by Dylann Hendricks on Unsplash

The vestibular system is responsible for the sense of balance in the inner ear. Prolonged use of toxic substances, such as certain antibiotics or anticancer drugs, can damage the hair cells that form part of this system, leading to alterations in balance and other motor skills. Now, a team from the University of Barcelona and the Bellvitge Biomedical Research Institute (IDIBELL) has identified the genetic mechanisms involved in the degradation of the vestibular system regarding the damage caused by these ototoxic compounds that affect the vestibule. The results could help improve the diagnosis of chronic vestibular ototoxicity and other pathologies related to the hair cells of the vestibular system.

The study, published in the Journal of Biomedical Science, is led by Jordi Llorens, professor at the UB’s Faculty of Medicine and Health Sciences and researcher at the Institute of Neurosciences (UBneuro) and IDIBELL. Researchers from the National Centre for Genomic Analysis (CNAG) also took part in the study.

The main causes of chronic vestibular ototoxicity are antibiotics of the aminoglycoside family, such as streptomycin – an antibiotic of choice in case of tuberculosis relapses – or anticancer drugs, such as cisplatin. Continued use of these drugs initiates a process of degeneration that causes “the hair cells to detach from the neurons, begin to deform and end up being expelled from their place in the sensory tissue,” explains Llorens.

This is a serious problem because the hair cells of the vestibular system do not regenerate. “We only have the ones we are born with. If we lose them, we also lose our balance, with very diverse consequences: from not being able to ride a bicycle to suffering blurred vision while moving, falls, orientation difficulties, dizziness or vertigo,” explains the UB professor.

Using RNA-seq analysis, i.e. a study of the global expression of genes that reveals which genes are activated or deactivated in the tissues of the vestibular system, the researchers discovered that, in the initial stages of degeneration, the hair cells change the expression of their genes to adapt to the progressive damage caused by otototoxic drugs. “The expression of many genes that define the identity of the hair cell, i.e. those that determine its shape and its ability to respond to movement by generating the signals that are sent to the brain, is reduced,” explains Llorens.

These results, together with the fact, discovered by the researchers, that the damage is reversible during the early stages of the degeneration process, indicate that it is essential to detect the problem as early as possible to stop the toxicity and avoid irreversible damage. “Hair cells become disconnected from neurons and stop sending information to the brain, but if the toxicity is interrupted, the connections can be repaired and function is restored. This increases the chances of avoiding a permanent loss of function,” the researcher stresses.

A potential biomarker

This study may also contribute to advances in the diagnosis and treatment of the pathology, since, according to the researchers, the genetic mechanisms they have identified in response to the stress caused by ototoxic drugs will make it possible, in the future, to “measure this stress and evaluate the effect of possible therapies, such as the development of drugs capable of stopping the process of eliminating hair cells or promoting their repair.”

In addition, the study has identified a new gene, Vsig10l2, expressed by hair cells, which significantly reduces its expression in all the models analysed. “This gene is of great interest as a possible marker of chronic ototoxicity in preclinical studies,” says Llorens.

The same response to different toxics

One of the most remarkable elements of the study is that the analysis has been carried out with four different models of chronic ototoxicity, using two different animal species and two different toxins, and then cross-checking the results of all experiments.

This comprehensive analysis has allowed them to determine that the degradation process occurs in response to very different toxins. “It is not a response conditioned by a particular toxin, it is the basic response of hair cells, which is always there, in response to chronic ototoxicity of any kind,” stresses the UB professor.

These results, together with the fact, discovered by the researchers, that the damage is reversible during the early stages of the degeneration process, indicate that it is essential to detect the problem as early as possible to stop the toxicity and avoid irreversible damage.

Impact on other pathologies

The study could have implications for understanding other pathologies, as the researchers suggest that the response they have demonstrated in chronic ototoxicity might represent a general response to chronic stress of any origin. “The results could be relevant to any chronic pathology with progressive loss of vestibular hair cells, including age-related loss of vestibular function. We also hypothesise that auditory hair cells might respond in a similar way, so they could help understanding deafness,” explains Llorens.

In this sense, the research team is studying – within the framework of a project funded by La Marató de TV3 – the possible relevance of the loss of vestibular function in patients with vestibular schwannoma, a tumour of the audiovestibular nerve that appears spontaneously or as a consequence of a minority disease, neurofibromatosis type 2. “Thanks to this project, we have been able to develop a culture model that allows us to study these chronic effects or how the hair cells become progressively more damaged before dying,” he concludes. 

Source: University of Barcelona

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Solving Africa’s Hidden Snakebite Problem with a New Universal Antivenom

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Photo by Nivedh P on Unsplash

In Sub-Saharan Africa, more than 300 000 people are bitten by venomous snakes annually, 3000 of whom die – but with the underreporting that goes hand in hand with the lack of healthcare infrastructure, the real number could be as much as five times higher. Many more face amputations. Even if patients manage to make it to a clinic or hospital in time, there is no guarantee that there will be any anti-venom available to treat them. As a South African case study shows, just having antivenom in the right place is a problem even in Western Cape’s relatively well-developed healthcare system, with antivenom’s three-year shelf life and cold chain failures posing a major problem for rural healthcare centres.

But now, scientists have developed a new kind of antivenom that is effective for 17 different snake species, including mambas, cobras and a rinkhals. The study, published in Nature, makes use of a nanobody-based cocktail that targets common mechanisms across venoms – and which is also more effective at preventing the tissue damage that leads to amputations.

A huge obstacle to creating broad-spectrum antivenoms is the enormous diversity of venomous snakes and the complexity of their venoms – a single species’ venom may contain 100 toxins from multiple different protein families. Listen to our podcast to hear a deep dive into Africa’s snakebite burden and how the international team of researchers accomplished their feat:

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How an Old Drug Could Help Treat Mitochondrial Diseases

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Credit: Pixabay CC0

Oxybutynin is usually prescribed for an unglamorous problem: bladder incontinence. But researchers have discovered a surprising new role for this decades-old drug – one that could open the door to treatments for a devastating class of genetic illnesses known as mitochondrial diseases.

In a paper published Sept. 8 in the American Journal of Physiology-Cell Physiology, a team of Cornell researchers described their finding that the molecule oxybutynin can overcome mitochondrial dysfunction by enhancing cellular glycolysis to improve healthy muscle formation by interacting with a suite of proteins involved in mRNA function. 

“Mitochondria are essential for our body to produce energy,” said Joeva Barrow, assistant professor of nutritional sciences in the College of Human Ecology who led the study. “If mitochondria are damaged and can no longer produce energy, the cells die, the tissues die and, eventually, the person dies.”

Mitochondrial diseases affect about one in every 5000 people and a large proportion of them are children, Barrow said. Patients often experience profound muscle weakness, neurological decline, heart problems and, in the most severe cases, shortened lives. There are no cures and virtually no effective treatments.

“Our approach was to test a series of small molecules that have never been used to treat mitochondrial disease before,” Barrow said. “Previous attempts at small molecules therapy were unsuccessful because of the use of artificial cell systems, but our plan was to use these molecules directly at the source – the muscle stem cells themselves.”

After running a screen of thousands of small molecules, they saw oxybutynin emerge as a clear frontrunner. They found that oxybutynin treatment can help muscle stem cells overcome one of the most severe forms of the condition, Complex III mitochondrial dysfunction. Normally, cells rely on mitochondria to generate ATP, the molecule that powers nearly every biological process. In Complex III disorders, that system grinds down, leaving cells starved.

The researchers tested oxybutynin on mouse and human muscle stem cells, the cells responsible for repairing and growing new muscle. These cells, normally stunted by the disease, began multiplying and forming muscle fibers again when treated with the drug.

The effect didn’t come from fixing the broken mitochondria. Instead, oxybutynin rewires the cellular energetic pathways to perform glycolysis: the quick-burning process of breaking down glucose. That backup system provided just enough energy to revive growth.

Using a high-tech small molecule binding protein analysis method, the team discovered that oxybutynin binds to proteins involved in RNA processing – the machinery that fine-tunes how cells interpret their genetic code. That interaction set off a cascade of changes, including a boost in amino acid and glucose transport into the cells.

In other words, the drug seems to rewire how diseased muscle cells fuel themselves, finding clever ways to survive without fully functioning mitochondria.

The results held true not only for mouse stem cells but also for human ones. Treated muscle stem cells grew stronger, produced more muscle fibres and maintained higher energy levels than untreated controls.

“Translating these findings to children with mitochondrial disease is happening in real time at the Children’s Hospital of Philadelphia with collaboration with Dr Marni Falk,” Barrow said. Dr Marni Falk, is the executive director of the Mitochondrial Medicine Frontier Program at the Children’s Hospital of Philadelphia. “Their team performs biopsies with kids with mitochondrial diseases, and they are currently testing oxybutynin with those cells.”

While this is still far from a clinical therapy – no human patients have yet received oxybutynin for mitochondrial disease – the findings raise hopes that an old, inexpensive drug might be repurposed for a devastating illness. “Oxybutynin already has FDA approval for treatment of bladder disorders” she said. 

For families facing mitochondrial disease, even small advances can be a lifeline. Most patients today rely only on supportive care, managing symptoms without any way to slow or reverse the disease.

If further studies confirm its benefits, oxybutynin could speed its way into trials, bypassing years of costly development, Barrow said.

Source: Cornell University

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South African Hunters Chewed the Kanna Plant for Endurance: New Study Tests its Effects on Mouse Brain Chemistry

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Sceletium tortuosum – Kougoed. Source: Wikimedia Commons.

Catherine H Kaschula, Stellenbosch University

Sceletium tortuosum is a little succulent plant that grows in the semi-arid Karoo and Namaqualand regions of South Africa. It has a long history of traditional use among the hunter-gatherers of the region.

The plant, known as kanna or kougoed by the San and Khoikhoi people, was mainly chewed or smoked to stay alert and suppress appetite during long hunts. The San were traditionally hunter-gatherers, while the Khoikhoi were pastoralists who herded livestock.

The name kanna (meaning “eland” in the click language of the San), has a symbolic reference to this large antelope, as the “trance animal”, which was called upon during religious and spiritual gatherings. Kougoed is Afrikaans for “something to chew”. The plant can be chewed after being dried and fermented, which is believed to intensify its effects.

The first colonial governor of the Cape colony, Simon van der Stel, in 1685 wrote about kanna in his journal:

They chew mostly a certain plant which they call Canna and which they bruise, roots as well as the stem, between the stones and store and preserve in sewn-up sheepskins.

I’m part of a group of scientists from different disciplines with an interest in this plant and we pooled our expertise to understand its effects on neurochemical concentrations in different parts of the brain.

Our studies were done in mice, so there is caution about establishing effectiveness on humans. Still, the results are striking.

As a chemist with an interest in natural products, I wanted to know which alkaloids in the plant were important in bringing about these effects.

Our latest study explored the effects of Sceletium tortuosum extracts on mouse brain chemistry.

We found that Sceletium increased the levels of certain brain chemicals which may balance mood and reduce stress. These findings lend support to the calming and mood-enhancing use of this plant in traditional medicine.

Plant chemistry

Our study examined how extracts from different chemotypes of Sceletium tortuosum can have different effects on brain chemistry. Chemotypes are groups of the same plant species that differ in the alkaloids they produce. This is because plants often produce alkaloids in response to external cues such as the weather or the presence of a plant-eating animal or pathogen.

Alkaloids are carbon-based compounds produced by plants. They are often toxic or taste bitter, making the plants less appealing or even harmful to the predators or invaders that want to eat or inhabit them. Alkaloids generally have physiological effects of use to humans. Some commonly used ones include caffeine, morphine and quinine.

We harvested two chemotypes of kanna from the Touwsrivier and De Rust regions of South Africa. These areas were chosen because of their interesting and unusual alkaloid profiles. The chemotypes were given to healthy mice as a supplement once a day for one month. The mice were monitored every day for behavioural or unexpected adverse reactions but none were noted.

At the end of the month, the levels of chemicals in the mouse brain were measured. Both the chemotypes were found to cause a marked increase in noradrenaline and a decrease in GABA in all brain regions studied. Both molecules are neurotransmitters that transmit nerve signals in the brain affecting memory, mood, attention and sleep.

This effect on noradrenaline supports kanna’s traditional use as an appetite suppressing drug. Increased noradrenergic stimulation is also the basis of many anti-depressants as well as drugs that improve attention and alertness.

We also found an impact on the brain chemicals serotonin and dopamine which may act together to balance mood and reduce stress. Serotonin affects emotional well-being and mood; dopamine motivates feelings of pleasure and satisfaction. These findings lend support to the calming and mood-enhancing use of this plant in traditional medicine.

Importantly, the control kanna extracts that did not have the interesting alkaloid profiles did not cause any of these chemical changes in the mouse brain.

Most studies on kanna have focused on the alkaloid mesembrine. The two specific chemotypes of kanna harvested from the Touwsrivier and De Rust regions of South Africa do have the mesembrine, but they are also packed with some other lesser-known or “minor” alkaloids. These differences in alkaloids may arise from a combination of geographic, environmental and inherent genetic factors found in a particular subset of plants.

Both the Touwsrivier and De Rust plants contained higher levels of alkaloids called mesembrine alcohols, which are different from mesembrine, and were barely present in the control extract. Another minor alkaloid, known as sceletium A4, was also identified as possibly being important. Mesembrine alcohols and sceletium A4 may be the ones responsible for the activity.

This suggests that the source of the plant, and the area in which it is grown, can influence its potential as a natural treatment for mood disorders and sleep.

What the results tell us

Stress, anxiety and depression pose a risk to the ability to lead a meaningful life. The World Health Organization has reported a 25% increase in anxiety and depression worldwide since the emergence of COVID-19.

Our study showed that the plant extracts had a broad noradrenergic effect in mice. But we have to be careful about making connections between results in mice and in humans. We need to explore the behavioural impact of these extracts in both mice and humans, especially in relation to sleep, alertness and mood.

The results also highlighted that without understanding the complex chemical composition of these plants, we risk overgeneralising their benefits, or worse, using them inappropriately.

Our findings have two implications.

First, they point towards a future of precision phytotherapy (use of plants for medicinal purposes), where natural remedies are tailored not just to individuals but to selecting certain plant chemotypes that produce certain combinations of alkaloids. Manipulating the growing conditions and genetic make-up of plants to optimise for alkaloid content is an age-old art.

Second, they remind us of the enormous, still largely untapped potential of African medicinal plants in global health innovation if we invest in research that honours both indigenous knowledge and scientific rigour.

As the world searches for safer, more sustainable ways to treat mental health conditions, South Africa’s kanna plant may hold secrets worth rediscovering.

Catherine H Kaschula, Senior Lecturer, Stellenbosch University

This article is republished from The Conversation under a Creative Commons license. Read the original article.

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Research Findings Offer New Insight into Heparin and Bone Builders

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Photo by Mufid Majnun on Unsplash

The blood thinner heparin is used during and after surgery and is essential to kidney dialysis. Most of today’s heparin comes from pigs, but the Federal Drug Administration is encouraging the use of alternative sources, including cows and synthetic forms of heparin, to diversify the supply chain.

Unfortunately, heparin from animals other than pigs just doesn’t work as well.

The reasons are connected to ongoing questions in modern cell biology. Now, an interdisciplinary Virginia Tech team has uncovered new molecular clues that may explain why some sources of heparin are more effective than others. The findings, published recently in the Proceedings of the National Academy of Sciences, may open doors for designing safer, more reliable heparin therapies.

“The structure of heparin and how that structure impacts function is an ongoing puzzle,” said Brenna Knight, first author of the study and recent graduate student studying in the Department of Chemistry. “Seemingly small differences in the content and arrangement of [chemical entities called] sulfates on the molecule cause substantial differences in the energetics that drive chemical activity.”

From mineralization to medicine

Heparin hails from a family called heparan sulfates, or heparans, present in all living creatures. These chains of sugars are diverse, serve many functions in organisms, and many, including heparin, are incredibly complex.

As a student of Patricia Dove in the Departments of Geosciences and Chemistry, Knight was originally looking at heparans for a completely different reason: to understand how the sulfates could impact biological mineralisation, which is the process by which organisms build crystal-strengthened tissues such as bones, teeth, shells, and corals.

Dove is one of today’s pre-eminent geochemists and was elected to the National Academy of Sciences in 2012. Unravelling the process of biomineralisation has been one of her major passions over the past three decades.  

“Animals grow crystals in specific places, usually to make structures that serve to support, defend, or feed themselves.” said Dove. “It’s a coordinated result of many chemical reactions within the organism and a crowning achievement of biology. We’ve been trying to better understand the reactions that produce these working biomaterials for a long time.”

That mineralization process unexpectedly linked back to medicine.

Heparan sulfates are just one of many different agents that interact with calcium to trigger a diverse portfolio of biochemical operations. One of those operations is integral to blood clotting.

Team science

To better understand how heparan sulfates help facilitate biomineralisation, Dove and Knight teamed with Kevin Edgar, professor in the Department of Sustainable Biomaterials, who was interested in heparans from the healthcare angle. To study interactions of calcium with heparin, they worked with Michael Schulz and graduate student Connor Gallagher in the chemistry department.  

When they applied their combined expertise to calcium-heparin interactions, they found that slight variations in heparin’s molecular composition changed how effective it was at binding calcium. These differences could affect its ability to form biominerals and blood thinners.  

“This paper provides insights for how to bioengineer synthetic pathways to effective heparin products for applications in therapeutics and drug delivery,” Edgar said.

Source: Virginia Tech

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Synthetic Torpor has the Potential to Redefine Medicine

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A team of researchers at Washington University in St. Louis is in pursuit of translating induced, or synthetic, torpor into potential solutions for humans, such as when there is reduced blood flow to tissues or organs, to preserve organs for transplantation or to protect from radiation during space travel. (Credit: Chen lab)

Nature is often the best model for science. For nearly a century, scientists have been trying to recreate the ability of some mammals and birds to survive extreme environmental conditions for brief or extended periods by going into torpor, when their body temperature and metabolic rate drop, allowing them to preserve energy and heat.

Taking inspiration from nature, Hong Chen, professor of biomedical engineering in the McKelvey School of Engineering and of neurosurgery at WashU Medicine, and an interdisciplinary team induced a reversible torpor-like state in mice by using focused ultrasound to stimulate the hypothalamus preoptic area in the brain, which helps to regulate body temperature and metabolism. In addition to the mouse, which naturally goes into torpor, Chen and her team induced torpor in a rat, which does not. Their findings, published in 2023 in Nature Metabolism, showed the first noninvasive and safe method to induce a torpor-like state by targeting the central nervous system.

Now, the team is in pursuit of translating induced, or synthetic, torpor into potential solutions for humans, such as when there is reduced blood flow to tissues or organs, to preserve organs for transplantation or to protect from radiation during space travel.

Conventional medical interventions focus on increasing energy supply, such as restoring blood flow to the brain after a stroke. Synthetic torpor seeks to do the opposite by reducing energy demand.

“The capability of synthetic torpor to regulate whole-body metabolism promises to transform medicine by offering novel strategies for medical interventions,” said Chen in a Perspectives paper published in Nature Metabolism July 31, 2025. 

Synthetic torpor has been used successfully in preclinical models with medications and specialised targeting of the neural circuit, but there are challenges to adapting these methods for humans. Previous human trials with hydrogen sulfide were terminated early due to safety concerns.

“Our challenges include overcoming metabolic differences among animals and humans, choosing the correct dose of medication and creating ways to allow a reversible torpor-like state,” said Wenbo Wu, a biomedical engineering doctoral student in Chen’s lab and first author of the Perspectives paper, a collaboration between Chen’s team and Genshiro Sunagawa from the RIKEN Center for Biosystems Dynamics Research in Japan. “Collaboration among scientists, clinicians and ethicists will be critical to develop safe, effective and scalable solutions for synthetic torpor to become a practical solution in medicine.”

Chen’s team, including Yaoheng (Mack) Yang, who was a postdoctoral research associate in her lab and is now assistant professor of biomedical engineering at the University of Southern California, targeted the neural circuit with their induced torpor solution in mice. They created a wearable ultrasound transducer to stimulate the neurons in the hypothalamus preoptic area. When stimulated, the mice showed a drop in body temperature of about 3 degrees C for about one hour. In addition, the mice’s metabolism showed a change from using both carbohydrates and fat for energy to only fat, a key feature of torpor, and their heart rates fell by about 47%, all while at room temperature.

“Ultrasound is the only noninvasive energy modality capable of safely penetrating the skull and precisely targeting deep brain structures,” Chen said. “While ultrasound neuromodulation lacks cell-type specificity compared with genetic-based neuromodulation, it provides a noninvasive alternative for inducing synthetic torpor without the need for genetic modifications.”

Chen and her team indicate that synthetic torpor offers a promising therapeutic strategy with additional applications, including inhibiting tumour growth and potential development of new therapies for tau protein related diseases, such as Alzheimer’s disease. However, much remains unknown about how brain regions, peripheral organs and cellular pathways coordinate metabolic suppression and arousal. Researchers also need to study the long-term risks and potential side effects and call for more preclinical studies and technological innovations that will facilitate a dual approach, which would include modulating neural circuits associated with hypometabolism and influencing peripheral metabolic pathways through systemic interventions, such as with drugs or peripheral neuromodulation.

“Synthetic torpor is no longer just a theoretical concept – it is an emerging field with the potential to redefine medicine,” Chen said. “Bridging fundamental neuroscience, bioengineering and translational medicine will be key to overcoming current challenges and advancing synthetic torpor toward real-world applications. Synthetic torpor could transition from a scientific curiosity to a human reality through interdisciplinary collaborations.”

Source: Washington University McKelvey School of Engineering

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Vibration Technique Controls Strength of Lab-grown Tissues

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Photo by Pawel Czerwinski on Unsplash

Researchers in McGill’s Department of Mechanical Engineering have discovered a safe and low-cost method of engineering living materials such as tissues, organs and blood clots. By simply vibrating these materials as they form, scientists can dramatically influence how strong or, weak they become.

The findings, published in the journal Advanced Functional Materials, could have a range of innovative applications, including in organ transplants, wound healing and regenerative medicine.

Good vibrations

The researchers used a speaker to apply controlled vibration, gently agitating the living materials during formation. By doing so, they found they could influence how cells organized and how strong or weak the final material became.

The technique works across a range of soft cellular materials, including blood clots made from real blood and other human tissues.

Aram Bahmani, study co-author and Yale postdoctoral fellow, conducted the research at McGill as a PhD student with Associate Professor Jianyu Li’s Biomaterials Engineering lab. Bahmani explained that strong, fast-forming blood clots are vital for use in emergencies like traumatic injuries. They’re also useful for people with clotting disorders.

“On the other hand, the same approach could help design clots that break down more easily as necessary, helping to prevent dangerous conditions like stroke or deep vein thrombosis,” he added. “Mechanical nudging allows us to make the material up to four times stronger or weaker, depending on what we need it to do.”

Why previous methods fell short

Earlier approaches to shaping living tissues relied on physical forces like magnets or ultrasound waves. While promising, these methods often fail to replicate the complexity of real tissues, which contain billions of cells and have thick, three-dimensional structures. In addition, they are often limited to specific materials, can damage healthy tissues and sometimes trigger immune responses.

The researchers’ study is the first to show that mechanical agitation, a very simple and widely accessible tool, can control the inner structure and performance of living materials in a “safe, scalable and highly tunable way.”

From the lab bench to living systems

To validate their findings, the team ran a series of tests to measure how vibration affected various cell-laden materials such as blood-based gels, plasma and seaweed-derived alginate. Using imaging and mechanical analysis, they assessed how broadly the method could be applied. Next, they tested the technique in animals.

The results showed that the technique works when applied inside the body, without harming surrounding healthy tissues.

Toward advanced medical technology

Bahmani said he believes the simple method could one day be integrated into advanced medical devices or wound-healing techniques.

“What makes this especially exciting is that our method is non-invasive, low-cost and easy to implement,” he said. “It does not rely on expensive machines or complex chemicals, meaning it could one day be built into portable medical devices, like a hand-held tool to stop bleeding, or a smart bandage that speeds up healing.” 

He noted that the method requires further testing, such as in irregular wounds or in combination with certain medications, before it can be used in real-life medical settings.

“Moving toward clinical use will require miniaturising the devices, optimising settings for different medical scenarios and completing regulatory testing to ensure safety and effectiveness in humans,” he said.

Source: McGill University

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Cold Plasma Penetrates Deep into Tissue to Attack Tumours

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Researchers at the Leibniz Institute for Plasma Science and Technology (INP) have collaborated with partners at Greifswald University Hospital and University Medical Centre Rostock to demonstrate that cold plasma can effectively combat tumour cells even in deeper tissue layers. What is particularly noteworthy is that, by developing new tissue models, they were able to precisely investigate the effect of individual plasma components on tumour cells for the first time.

The results of the study were published in the journal Trends in Biotechnology.

What is cold plasma?

Plasma is an ionised gas that produces a large number of chemically reactive molecules known as reactive oxygen and nitrogen species. These short-lived molecules can have a strong influence on biological processes such as the growth or death of tumour cells.

New tissue models provide important insights

“The effect of plasma in tissue is very complex and little understood. We have therefore developed a 3D model made of hydrogels that mimics real tumour tissue. In this model, we were able to observe exactly how deep the molecules from the plasma penetrate – and which of these molecules are important for the effect on tumour cells,” explains Lea Miebach, first author of the study. Particularly short-lived molecules such as peroxynitrite penetrated several millimetres deep into the tissue. Hydrogen peroxide, which had previously been considered the main active ingredient in laboratory research, showed little effect: even when it was specifically removed, the effect of the plasma remained strong.

Use during surgery also conceivable

Another model investigated how well plasma could work in the follow-up treatment of tumour surgery. Residual tumour cells at the edge of an artificial surgical wound were specifically treated with plasma. The result: here too, a strong effect was observed, especially in cells that had already spread into the surrounding tissue. These findings could help to better prevent relapses after surgery.

Important step for plasma medicine

“Our results could significantly improve the medical application of plasma,” says Prof Dr Sander Bekeschus, head of the Plasma Medicine research programme at INP. “The better we understand which molecules are active in the tissue, the more precisely plasma devices can be used for specific types of cancer.”

The work was carried out using the medically approved plasma jet “kINPen”. In the long term, the method could help make therapies more effective and gentler.

Source: Leibniz-Institut für Plasmaforschung und Technologie e.V.

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Podcast: Could Infrared Light Have Deeper Biological Effects than Believed?

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Light transmission through the hand from an 850nm LED source. Because the tissues are relatively
thin compared with the thorax it was possible to map the spectrum here against known biological absorbers.
The images clearly show that deoxygenated blood is a key absorber. Also, bone can not be seen and hence is
relatively transparent at these longer wavelengths. Source: Jeffery et al., Scientific Reports, 2025.

In this podcast, we explore how some infrared wavelengths of sunlight can penetrate the human body – even through clothing – and have a systemic positive impact on physiological functions. Sounds like something out of science fiction, but a recent article published in Scientific Reports has demonstrated this effect in humans.

In this study, exposing the torsos of human participants to 830–860nm infrared light was found to boost mitochondrial function and ATP production. There were notable improvements in vision, despite the eyes being shielded from the infrared light. If infrared light is indeed beneficial, what does this mean for our current way of life, indoors and illuminated by LED lights – which notably lack infrared light?

Categories : Medical Research & Technology Respiratory DiseasesTags :

No Benefits Seen from Conservative Oxygen in the ICU

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A UK trial involving 16 500 mechanically ventilated intensive care unit (ICU) patients found no 90-day survival benefit for conservative supplemental oxygen over usual oxygen therapy. Nevertheless, the study, published in JAMA, did demonstrate the accuracy and cost-effectiveness of conducting a large trial with a simple intervention.

Oxygen is one of the most commonly administered treatments to patients in ICUs, but liberal oxygen therapy to avoid the risks of hypoxaemia may lead to harm, so finding the right level could optimise outcomes. Trials to date have shown mixed results.

For COVID patients admitted to the ICU with severe hypoxaemia, survival without life support was extended with conservative oxygen therapy. In a paediatric ICU study, conservative oxygen therapy resulted in a reduction in a composite of organ support at 30 days or death. A meta-analysis of 13 trials showed no differences between liberal and conservative oxygen therapy.

Even with just a small difference in survival benefit, with tens of millions of patients mechanically ventilated in the ICU would still mean significant numbers of lives saved. Other tests of new drugs and procedures in the ICU are hampered by high cost, as Seitz et al. noted in an accompanying editorial, so this sort of trial comparing two approaches to a common therapy is much more affordable.

The UK Intensive Care Unit Randomised Trial Comparing Two Approaches to Oxygen Therapy (UK-ROX) trial was initiated to determine if there was a difference between conservative and usual oxygen therapy.

The trial randomised 16 500 patients across 97 ICUs in the UK to either conservative oxygen therapy or usual oxygen therapy, in adults receiving mechanical ventilation and supplemental oxygen in the ICU. The primary outcome was mortality at 90 days. Conservative oxygen therapy targeted a peripheral oxygen saturation (Spo2) of 90% (range, 88%-92%), while usual oxygen therapy was at the discretion of the treating clinician.

Patients were early in mechanical ventilation (median, 5 hours), were severely ill (median predicted mortality risk, 35%), had a range of critical illnesses (eg, > 5000 patients with sepsis and > 1500 patients with hypoxic-ischaemic encephalopathy) and with significant hypoxaemia (eg, > 11 000 patients with a Pao2:Fio2 ratio, consistent with acute respiratory distress syndrome). Obtaining informed consent from the patients was, of course, largely not feasible, so this requirement was waived for the study.

Exposure to supplemental oxygen was 29% lower for those in the conservative oxygen therapy group compared with the usual oxygen therapy group. Of the patients randomised to conservative oxygen therapy, 35.4% died by 90 days compared with 34.9% of patients receiving usual oxygen therapy.

No differences were seen for secondary outcomes, including ICU stay, days free of life support and mortality at various time points. No interactions for confirmed or suspected COVID, ethnicity or other illnesses were observed.

Post hoc analysis showed weak evidence of increased harm from conservative oxygen therapy among the first 10 patients in each site but no difference for the random enhanced data collection sample compared with standard data collection.

Seitz et al. pointed out that the high level of adherence to the conservative target resulted in a mean oxygen saturation of 93.3%, versus 95.1% for usual care. The differences in oxygen saturation (1.9%) and Fio2 (0.04) between the trial groups in UK-ROX were about half the magnitude of some prior trials, due to not aiming for widely separated targets, and usual care varies considerably depending on location and clinical considerations.

Therefore, the researchers concluded that the findings do not support an approach of reducing oxygen exposure by targeting an Spo2 of 90% in mechanically ventilated adults receiving oxygen in the ICU. They suggest that future research may involve using AI to determine specific situations where conservative or liberal oxygen therapy may have beneficial outcomes.

References:

Martin DS, Gould DW, Shahid T, et al. Conservative Oxygen Therapy in Mechanically Ventilated Critically Ill Adult Patients: The UK-ROX Randomized Clinical Trial. JAMA. 2025;334(5):398–408. doi:10.1001/jama.2025.9663

Seitz KP, Casey JD, Semler MW. Patient, Treatment, Outcome—Large Simple Trials of Common Therapies. JAMA. 2025;334(5):395–397. doi:10.1001/jama.2025.9657