Viruses, including the coronavirus that causes COVID-19, can get passed from person to person via contaminated surfaces. But can some surfaces reduce the risk of this type of transmission without the help of household disinfectants? As reported in ACS Applied Materials & Interfaces, wood has natural antiviral properties that can reduce the time viruses persist on its surface — and some species of wood are more effective than others at reducing infectivity.
Enveloped viruses, like the coronavirus, can live up to five days on surfaces; nonenveloped viruses, including enteroviruses linked to the common cold, can live for weeks, in some cases even if the surfaces are disinfected. Previous studies have shown that wood has antibacterial and antifungal properties, making it an ideal material for cutting boards. However, wood’s ability to inactivate viruses has yet to be explored, which is what Varpu Marjomäki and colleagues set out to study.
The researchers looked at how long enveloped and nonenveloped viruses remained infectious on the surface of six types of wood: Scots pine, silver birch, gray alder, eucalyptus, pedunculate oak and Norway spruce. To determine viral activity, they flushed a wood sample’s surface with a liquid solution at different time points and then placed that solution in a petri dish that contained cultured cells. After incubating the cells with the solution, they measured the number (if any) infected with the virus.
Results from their demonstrations with an enveloped coronavirus showed that pine, spruce, birch and alder need one hour to completely reduce the virus’ ability to infect cells, with eucalyptus and oak needing two hours. Pine had the fastest onset of antiviral activity, beginning after five minutes. Spruce came in second, showing a sharp drop in infectivity after 10 minutes.
For a nonenveloped enterovirus, the researchers found that incubation on oak and spruce surfaces resulted in a loss of infectivity within about an hour, with oak having an onset time of 7.5 minutes and spruce after 60 minutes. Pine, birch and eucalyptus reduced the virus’ infectivity after four hours, and alder showed no antiviral effect.
Based on their study data, the researchers concluded that the chemical composition of a wood’s surface is primarily responsible for its antiviral functionality. While determining the exact chemical mechanisms responsible for viral inactivation will require further study, they say these findings point to wood as a promising potential candidate for sustainable, natural antiviral materials.
The authors acknowledge funding from the Research Council of Finland and the Jane and Aatos Erkko Foundation.

Autoimmune diseases cannot currently be cured, only treated, and this is also true for neuromyelitis optica spectrum disorder, which affects the central nervous system. A Kobe University study of how the treatment acts on the immune system shows that it shifts the balance of types of immune cells. This finding may represent a step toward the development of personalized medicine for autoimmune diseases.
An autoimmune disease is the body’s immune system turning against parts of the body itself. Neuromyelitis optica disorder spectrum, or NMOSD, is one of them and it causes inflammation of the central nervous system, leading to vision and sensory loss, weakness and bladder dysfunction. The condition, which sometimes flares up in waves, has a treatment consisting of blinding the immune system to inflammation-promoting signals. But its biological action is broad and so it is also not understood why it doesn’t work in some patients and how to effectively ascertain which is the case.
The Kobe University neurologist CHIHARA Norio specializes on the disease and recently wondered: “B cells are a type of key immune cells that respond to inflammatory signals, and in autoimmune diseases like NMOSD, they produce antibodies against part of the body itself, exacerbating the condition. Therapies that inhibit inflammatory signals were therefore expected to change the activity of B cells in NMOSD. Since we observed that B cells were still present in the blood of patients after treatment, we decided to investigate the possibility that they were changing into a different type of B cell.” Chihara refers to so-called “regulatory B-cells,” a type of B cell that attenuates the immune system’s activity by secreting anti-inflammatory signal molecules and is thought to play an important role in keeping the body’s immune system from becoming too active, and in the case of autoimmune diseases may prevent disease flares.
The Kobe University team now reports that they created an experimental model of the immune cells during an NMOSD flare and could thus trace the effect of the drug on the different kinds of B cells. With the drug, there was a marked increase in the secretion of the anti-inflammatory signal, confirming their idea that not the number but the function of B cells responds to the treatment, according to the research published online on June 18, 2024, in Neurology® Neuroimmunology & Neuroinflammation, an official journal of the American Academy of Neurology.
In addition, Chihara’s team could also identify a molecular marker for B cells producing anti-inflammatory signals, a sort of ID that enables tracing the cells’ abundance. Having confirmed that healthy individuals and those under effective treatment show higher proportions of these cells than individuals in acute phases of the disease, Chihara thinks that this knowledge will enable clinicians to easily determine the effectiveness of the treatment in future diagnoses and thus is a step towards more personalized medicine.
Thinking about the bigger picture, the Kobe University neurologist thinks that this study will contribute to becoming able to not only treat but actually cure autoimmune diseases. He explains: “The essence of autoimmune diseases is a breakdown of autoimmune tolerance, the system that prevents us from attacking our own bodies. Our ultimate goal is to cure the disease by restoring this autoimmune tolerance, and the results of this study show one aspect of our work towards this goal.”
This research was funded by the Japan Society for the Promotion of Science (grants 21K20871, 23K14778, 20H03562 and 23H02797), the Japan Agency for Medical Research and Development (grant 22ek0109436h0003), the Japan Science and Technology Agency (grants JPMJMS2299 and JPMJMS229B), and the Ministry of Education, Culture, Sports, Science and Technology Japan (grants 22gm1710005h0001 and 23gm1710005h0002). It was conducted in collaboration with researchers from The University of Tokyo.

As space travel becomes more common, it is important to consider the impacts of space flight and altered gravity on the human body. Led by Dr. Ana Diaz Artiles, researchers at Texas A&M University are studying some of those impacts, specifically effects on the eye.
Gravitational changes experienced by astronauts during space travel can cause fluids within the body to shift. This can cause changes to the cardiovascular system, including vessels in and around the eyes.
As the commercialization of space flight becomes more common and individual space travel increases, astronauts will not be the only ones experiencing these changes. Individuals traveling to space with commercial companies may not be as fit or healthy as astronauts, making it even more important to understand the role that fluid shift plays in cardiovascular and eye health.
“When we experience microgravity conditions, we see changes in the cardiovascular system because gravity is not pulling down all these fluids as it typically does on Earth when we are in an upright position,” said Diaz Artiles, an assistant professor in the Department of Aerospace Engineering and a Williams Brothers Construction Company Faculty Fellow. “When we’re upright, a large part of our fluids are stored in our legs, but in microgravity we get a redistribution of fluids into the upper body.”
These fluid shifts may be related to a phenomenon known as Spaceflight Associated Neuro-ocular Syndrome (SANS), which can cause astronauts to experience changes in eye shape and other ocular symptoms, such as changes in ocular perfusion pressure (OPP). At this time, researchers are unsure of the exact cause of SANS, but Diaz Artiles hopes to shed light on the underlying mechanism behind it.
Diaz Artiles and her team are investigating potential countermeasures to help counteract the headward fluid shifts of SANS. In a recent study, they examined the potential aid of lower body negative pressure (LBNP) to combat SANS. This countermeasure has the potential to counteract the effects of microgravity by pooling fluid back into the lower body.
While the role of ocular perfusion pressure in the development of SANS remains undetermined, Diaz Artiles and her team hypothesized that microgravity exposure could lead to a slight but chronic elevation (compared to upright postures) in OPP, which may have a role in the development of SANS. The results of the recently published study showed that lower body negative pressure, while effective in inducing fluid shift toward the lower body, was not an effective method for reducing OPP. Should elevated ocular perfusion pressure be definitively linked to SANS, the use of LBNP could theoretically not be an effective countermeasure to this syndrome. But they emphasize that future work should seek to better understand the relationship between OPP and SANS, and the impact of LBNP on these ocular responses as part of the countermeasure development.
“This research is just one experiment of a three-part study to better understand the effects of fluid shift in the body and its relationship to SANS. Previous experiments in this study included the use of a tilt table for researchers to understand the cardiovascular effects of fluid shifts at different altered gravity levels, recreated by using different tilt angles,” said Diaz Artiles.
The published study, as well as upcoming research, focuses on countermeasures to the fluid shift; in this case, lower body negative pressure. In future studies, the researchers will examine the effects of using a centrifuge to combat the fluid shift and its effects. Diaz Artiles and her team aim to collect cardiovascular responses using each countermeasure and compare effects on ocular perfusion pressure and other cardiovascular functions that may be affected by microgravity environments. These studies are performed on Earth, so gravitational changes that occur in space may cause different outcomes. Thus, they hope to conduct future studies in true microgravity conditions, such as parabolic flights.

A sense of time is fundamental to how we understand, recall, and interact with the world. Tasks ranging from holding a conversation to driving a car require us to remember and perceive how long things take — a complex but largely unconscious calculation running constantly beneath the surface of our thoughts.
Now, researchers at University of Utah Health have found that, in mice, a specific population of “time cells” is essential for learning complex behaviors where timing is critical. Like the second hand of a clock, time cells fire in sequence to map out short periods of time.
But time cells aren’t just a simple clock, the researchers found — as animals learn to distinguish between differently timed events, the pattern of time cell activity changes to represent each pattern of events differently. The discovery could ultimately aid in early detection of neurodegenerative diseases, such as Alzheimer’s, that affect the sense of time.
The new study is published in Nature Neuroscience.
Mouse code
By combining a complex time-based learning task with advanced brain imaging, researchers were able to watch patterns of time cell activity become more complex as the mice learned. The researchers first set up a trial where learning the differences in the timing of events was critical. To get a reward, mice had to learn to distinguish between patterns of an odor stimulus that had variable timing, as if they were learning a very simple form of Morse code.
Before and after the mice learned, the researchers used cutting-edge microscopy to watch individual time cells fire in real time. At first, their time cells responded in the same way to every pattern of odor stimulus. But as they learned the differently timed patterns of stimulus, the mice developed different patterns of time cell activity for each pattern of events.

Notably, during trials that the mice got wrong, the researchers could see that their time cells had often fired in the wrong order, suggesting that the right sequence of time cell activity is critical for performing time-based tasks. “Time cells are supposed to be active at specific moments during the trial,” said Hyunwoo Lee, PhD, postdoctoral fellow in neurobiology in the Spencer Fox Eccles School of Medicine at the University of Utah and co-first author on the study. “But when the mice made mistakes, that selective activity became messy.”
Not just a stopwatch
Surprisingly, time cells play a more complicated role than merely tracking time, said Erin Bigus, graduate research assistant in neurobiology and co-first author on the study. When the researchers temporarily blocked the activity of the brain region that contains time cells, the medial entorhinal cortex (MEC), mice could still perceive and even anticipate the timing of events. But they couldn’t learn complex time-related tasks from scratch. “The MEC isn’t acting like a really simple stopwatch that’s necessary to track time in any simple circumstance,” Bigus said. “Its role seems to be in actually learning these more complex temporal relationships.”
Intriguingly, prior research on the MEC found that it’s also involved in learning spatial information and building “mental maps.” In the new study, researchers noticed that the patterns of brain activity that occur while learning time-based tasks show some similarities to previously observed patterns involved in spatial learning; aspects of both patterns persist even while an animal isn’t actively learning.
While more research is needed, these results suggest that the brain could process space and time in fundamentally similar ways, according to the researchers. “We believe that the entorhinal cortex might serve a dual purpose, acting both as an odometer to track distance and as a clock to track elapsed time,” said James Heys, PhD, assistant professor in neurobiology and the senior author on the study.
Learning how the brain processes time could ultimately aid in the detection of neurodegenerative diseases such as Alzheimer’s, the researchers say. The MEC is one of the first areas of the brain that Alzheimer’s affects, hinting that complex timing tasks could potentially be a way to catch the disease early.
Support was provided by the Whitehall Foundation, Brain and Behavior Research Foundation, the National Institutes of Health, and the National Science Foundation.

Women diagnosed with perinatal depression are more likely to develop cardiovascular disease in the following 20 years compared to women who have given birth without experiencing perinatal depression, according to research published in the European Heart Journal [1] today (Wednesday).
Perinatal depression, meaning depression during pregnancy or after birth is believed to affect one in five women giving birth worldwide.
The study is the first of its kind to look at cardiovascular health after perinatal depression and included data on around 600,000 women. It found the strongest links with risks of high blood pressure, ischemic heart disease and heart failure.
The research was by Dr Emma Bränn, Dr Donghao Lu and colleagues from the Karolinska Institutet, Stockholm, Sweden. Dr Lu said: “Our research group has already found that perinatal depression is linked to an increased risk of several other health issues, including premenstrual disorders, autoimmune disorders and suicidal behaviour, as well as premature death.
“Cardiovascular disease is one of the leading causes of death globally and there has been an ongoing discussion about including reproductive health when assessing the risk among women. We wanted to know if a history of perinatal depression could help predict cardiovascular disease risk.”
The study was based on the Swedish Medical Birth Register, which records all births in the country. The researchers compared 55,539 Swedish women who were diagnosed with perinatal depression between 2001 and 2014 with another group of 545,567 Swedish women who had also given birth during that time but were not diagnosed with perinatal depression. All the women were followed up through to 2020 to assess if they developed any cardiovascular disease.
Among the women with perinatal depression, 6.4% developed cardiovascular disease compared to 3.7% of women who had not suffered with perinatal depression. This equates to a 36% higher risk of developing cardiovascular disease. Their risk of high blood pressure was around 50% higher, the risk of ischemic heart disease around 37% higher, and the risk of heart failure around 36% higher.

Dr Bränn, the senior author, said: “Our findings may help identify people who are at a higher risk of cardiovascular disease so that steps can be taken to reduce this risk. This study also adds to the established health risks of perinatal depression. We know that perinatal depression is both preventable and treatable, and for many people it’s the first episode of depression they’ve ever experienced. Our findings provide more reason for ensuring maternal care is holistic, with equal attention on both physical and mental health.
“It remains unclear how and through what pathways perinatal depression leads to cardiovascular disease. We need to do more research to understand this so that we can find the best ways to prevent depression and lower the risk of cardiovascular disease.
Researchers also compared the women who suffered perinatal depression with their sisters and found they had a 20% higher risk of cardiovascular disease.
“The slightly lower difference in risk between sisters suggest that there could be genetic or familial factors partly involved,” Dr Bränn said. “There could also be other factors involved, as is the case for the link between other forms of depression and cardiovascular disease. These include alterations in the immune system, oxidative stress and lifestyle changes implicated in major depression.”
In an accompanying editorial [2] Dr. Amani Meaidi from the Danish Cancer Society: Kraeftens Bekaempelse, Copenhagen, Denmark said: “Although signs of mood disturbances following childbirth have been noticed since the time of Hippocrates, it was not until last year, in 2023, that the US Food and Drug Administration approved the first oral treatment for postpartum depression, making treatment much more accessible for the millions of women suffering from this condition. The late and lack of development of effective, safe, and accessible treatment options for perinatal depression is unmistakably a manifestation of the historical neglect of women’s health in medical research. The future will reveal if proper perinatal depression therapy reduces the observed increased risk of developing cardiovascular morbidity.
“Considering the rise in perinatal depression and the lack of knowledge on cardiovascular disease in women, the study by Bränn and colleagues is much needed and welcomed.”

Tuberculosis is still one of the deadliest infectious diseases, causing over one million deaths each year worldwide. Additionally, about one-fourth of the world’s population carries Mycobacterium tuberculosis (M. tuberculosis) without showing any symptoms, and most of these carriers do not develop the disease.
The current anti-tuberculosis vaccine, BCG, is administered worldwide. However, considering that more than 10 million new tuberculosis cases are reported each year, its effectiveness is deemed insufficient. As a result, the development of vaccines to replace BCG is underway. However, no new vaccine has yet surpassed BCG, which is a highly effective live vaccine. Actually BCG is very effective in preventing tuberculosis in children, creating a booster vaccine to strengthen immunity in adults is considered a promising and realistic option.
In developing tuberculosis vaccines, scientists have studied proteins from M. tuberculosis that trigger the protective immunity against tuberculosis. Especially IFN-gamma produced by T cells is known to be critical for protection against tuberculosis. Thus IFN-gamma responses are marker of vaccine candidate antigens and efficacy. However there’s a paradoxical situation where proteins that induce higher IFN-gamma production in tuberculosis patients, who already have developed the disease, rather than in asymptomatic carriers who prevent its onset, are being viewed as potential vaccine candidates. Furthermore, many of vaccine studies ignore the native three-dimensional structure of the proteins and the modification they undergo after being translated in M. tuberculosis.
On the productivity side, vaccine candidate molecules are being made in basic model organisms like Escherichia coli. However, certain molecules undergo specific changes after translation that are unique to the pathogen, such as M. tuberculosis. It’s been noted that these modifications might be crucial for mounting effective defenses against actual pathogen attacks.
Mycobacterial DNA-binding protein 1 (MDP1) is a major protein of both BCG and M. tuberculosis (Shaban et al., Sci Rep., 2024) with extensive post-translational modifications (Yoshida et al., BBRC., 2023). Recent studies show that IFN-gamma responses to MDP1 are higher in individuals who suppress tuberculosis progression compared to tuberculosis patients, making MDP1 a new vaccine candidate (Yasuda et al., Front Immunol., 2024). To evaluate MDP1 for a tuberculosis booster vaccine, Ozeki et al. produced recombinant MDP1 and tested its ability to induce IFN-gamma using blood from BCG-vaccinated adults.
Ozeki et al., expressed MDP1 in two different hosts: M. smegmatis, a non-pathogenic, fast-growing mycobacteria, and E. coli. Importantly, the MDP1 expressed in M. smegmatis (mMDP1) showed significant post-translational modifications, closely resembling the native MDP1 found in M. tuberculosis, while the one expressed in E. coli (eMDP1) did not.
When they cultured both variants of MDP1 with peripheral blood from adults vaccinated with BCG, they observed that mMDP1 triggered notably higher levels of IFN-gamma production compared to eMDP1. This implies that the immune system of BCG-vaccinated adults can recognize MDP1 with post-translational modifications.
Importantly, mMDP1 demonstrated a superior capacity for IFN-gamma production compared to other vaccine candidate antigens, such as Antigen 85 complex, which is currently in development. When utilizing protein antigens as vaccines, adjuvants are typically employed to prevent degradation or enhance immunogenicity. We previously reported that MDP1, due to its binding affinity to bacterial DNA, has protected mice from M. tuberculosis infection when co-administered. In this study we also demonstrated that the combination of mMDP1 and G9.1, a novel type of CpG-DNA, elicits a significant level of IFN-gamma from peripheral blood of BCG-vaccinated adults.
The results of this study suggest that combining mMDP1, which displays post-translational modifications, with G9.1 can reinvigorate the waning effect of BCG, indicating its potential as a booster vaccine.

Measuring the heart rate of great apes in captivity is essential for both health management and animal studies. However, existing most methods are either invasive or inaccurate. Now, researchers from Japan have investigated the potential of using millimeter-wave radar technology to estimate heart rate from subtle body movements in chimpanzees. Their efforts will hopefully pave the way to better practices and techniques for monitoring heart rates in wild and captive primates.
Just like in humans, heart rate is a critically important and informative vital sign in nonhuman primates. Heart diseases are among the main causes of death of nonhuman primates in captivity, and monitoring their heart rate regularly can help veterinarians catch symptoms early. Beyond the obvious health reasons, monitoring heart rate is also really useful in animal cognitive studies. For example, it has been well documented that a chimpanzee’s heart rate changes under psychological stress, when emotionally aroused by images, or when encountering familiar humans.
Thus, it’s no wonder a few techniques have been devised to measure heart rate in great apes. Besides standard contact measurements, the most prevailing one consists of attaching a wireless device to the animal to monitor and transmit its heart rate remotely. However, installing the device often requires anesthesia, which carries risks. Moreover, the device itself might cause stress to the animal or others in its group. A less invasive approach is the estimation of heart rate from video feed, which has been tested in some species of primates. Still, the accuracy of these methods is quite sensitive to lighting conditions and the movement of the animals.
Against all these backdrops, a research team including Asisstant Professor Takuya Matsumoto from Shinshu University, Japan, set out to find a better alternative. In their latest study, which was published in the American Journal of Primatology on May 22, 2024, the researchers investigated whether millimeter-wave radar-based techniques originally developed for humans could be used to measure heart rate in chimpanzees. The co-authors include Dr. Itsuki Iwata, Dr. Takuya Sakamoto, and Dr. Satoshi Hirata, all affiliated with Kyoto University.
In essence, the proposed approach involves emitting high-frequency electromagnetic pulses aimed at the chest of the animal and capturing the resulting echoes. From these echoes, one can detect subtle body movements, which are ultimately used to estimate heart rate using specialized algorithms. Dr. Matsumoto highlights the study’s motivation, stating, “Millimeter-wave radar technology has been extensively developed for applications in automated driving and medicine, but after speaking with a radar researcher at a reception at an academic conference, we felt that it could open up a new field of study if applied to primates other than humans; thus, we began our joint research.”
To test their approach, the researchers performed experiments during the annual health checks of two adult chimpanzees at Kumamoto Sanctuary, Wildlife Research Center, Kyoto University. During these checkups, the animals were anesthetized, and the radar system was hung about half a meter above their chest. Traditional electrocardiography (ECG) signals were also recorded and used to assess the accuracy of the radar-based technique.
Fortunately, the heart rates recorded via ECG closely matched those obtained using the millimeter-wave radar for both chimpanzees, validating the proposed strategy. “Despite chimpanzees having muscular bodies, which raised uncertainties about measuring their heart rate in a similar manner to measurements in humans, the results of this study demonstrated the feasibility of noncontact heart rate measurements through the analysis of subtle body surface movements,” highlights Dr. Matsumoto. He further adds “These findings could expand the potential applications of such techniques in studies of animal psychology and wild primatology.”
Using millimeter-wave radar-based methods for heart rate monitoring offers significant advantages over standard practices. These techniques are entirely noninvasive, allowing for frequent use without causing stress to the animals. Heart rate can also be remotely measured using video analysis with a digital visible light camera, which doesn’t need specialized equipment and can reuse existing videos. Two main techniques are used: imaging photoplethysmography, detecting blood volume changes, and periodic movement extraction, measuring heart and respiratory rates from body movements; both have been validated in nonhuman primates but have certain limitations.
The researchers hope that the findings of this work pave the way to more innovation in the methods used to monitor vital signs in captive animals, including heart rate and respiration rate. “If it becomes possible to remotely measure the heart rate of end angered apes, their health management and welfare in captivity, such as in zoos, could improve,” Dr. Matsumoto concludes. Further feasibility studies will be necessary to validate the use of the proposed method in regular practice, where animals are free to move in their enclosure.
With any luck, these techniques could help us not only keep our closest relatives healthy, but also lead to a better understanding of them. This advancement opens avenues for deeper research into primate behavior and physiology, benefiting captive and wild primates and enhancing our understanding of these creatures and their environment.

An innovative synthesis strategy opened up the way to 2D/3D fused frameworks using inexpensive quinolines as feedstock, report scientists from Tokyo Tech. By leveraging a light-sensitive borate intermediate, the scientists could transform quinoline derivatives into a great variety of 2D/3D fused frameworks in a straightforward and cost-effective manner. Their findings are expected to enable the synthesis of highly customizable drug candidates.
Quinolines have garnered much attention from chemists wanting to synthesize compounds known as 2D/3D fused frameworks. These complex organic molecules have a lot of medical potential due to their highly customizable structure and functional groups. Quinolines make synthesis of such frameworks possible thanks to their unique electronic configuration. They consist of an electron-abundant benzene ring fused to an electron-deficient pyridine ring; these electronically distinct rings can be modified independently by adjusting reaction conditions.
One of the most attractive ways to use quinolines as feedstock for 2D/3D frameworks is through dearomative photocycloadditions. This process involves destabilizing one of the aromatic rings in quinoline, using light and sometimes a catalyst, so that a reactant can ‘latch’ onto the ring, forming the target compound. Despite many efforts, most studies have reported photocycloadditions happening on quinoline’s benzene ring side, while few have targeted the pyridine side. Thus, the full potential of quinolines remains untapped.
Against this backdrop, a research team from Tokyo Institute of Technology, Japan, led by Assistant Professor Yuki Nagashima, in collaboration with scientists from The University of Tokyo, decided to step up to the challenge. In their latest study, which was published in Angewandte Chemie International Edition on 27 May 2024, they present a convenient methodology to access the pyridine side of quinolines and synthesize diverse 2D/3D frameworks.
The key to their approach lies in the use of a molecule known as pinacolborane, also known as H-B(pin). The researchers discovered that this boron-containing compound was extremely effective at inducing dearomative photocycloaddition almost exclusively on the pyridine side of quinoline. Not only were the yields obtained high but also could a wide variety of quinoline derivatives and reactants be used to obtain all sorts of 2D/3D frameworks.
Seeking to shed light on the mechanisms underlying their newfound strategy, the team conducted a series of experiments and theoretical analyses. They determined that quinoline reacts with an organolithium compound first and then with H-B(pin) to form an intermediate borate complex. This intermediate step is crucial, as Nagashima remarks: “Our detailed mechanistic studies revealed that the photoexcited borate complex both accelerates the cycloaddition and suppresses the rearomatization that usually occurs in conventional photocycloaddition reactions.” These effects combined lead to fewer unreacted compounds and undesired aromatics.
It is worth noting that the proposed methodology offers several advantages over competing techniques. For one, it requires less reaction time and steps than classic synthesis routes. Catalysts are not needed either, which reduces costs further. Moreover, multi-substituted starting molecules can be used, which provides access to countless target compounds. “To our knowledge, these transformations are the first boron-based photocycloadditions and unlock previously elusive organoboron compounds. The present strategy based around an intermediate borate complex should be useful for further functionalization of various types of multi-ringed aromatic hydrocarbons,” highlights Nagashima.

When low doses of cancer drugs are administered continuously near malignant brain tumours using so-called iontronic technology, cancer cell growth drastically decreases. Researchers at Linköping University, Sweden, and the Medical University of Graz, Austria, demonstrated this in experiments with bird embryos. The results, published in the Journal of Controlled Release, is one step closer to new types of effective treatments for severe cancer forms.
Malignant brain tumours often recur despite surgery and post-treatment with chemotherapy and radiation. This is because cancer cells can “hide” deep within tissue and then regrow. The most effective drugs cannot pass through the so-called blood-brain barrier — a tight network surrounding blood vessels in the brain that prevents many substances in the blood from entering it. Consequently, there are very few available options for treating aggressive brain tumours.
In 2021, a research group from Linköping University and the Medical University of Graz demonstrated how an iontronic pump could be used to locally administer drugs and inhibit cell growth for a particularly malignant and aggressive form of brain cancer — glioblastoma. At that time, experiments were conducted on tumour cells in a petri dish.
Now, the same research group has taken the next step towards using this technology in clinical cancer treatment. By allowing glioblastoma cells to grow using undeveloped bird embryos, new treatment methods can be tested on living tumours. The researchers showed that the growth of cancer cells decreased when low doses of strong drugs (gemcitabine) were continuously administered using an iontronic pump directly adjacent to the brain tumour.
“We have previously shown that the concept works. Now we use a model with a living tumour, and we can see that the pump administers the drug very effectively. So even though it is a simplified model of a human, we can say with greater certainty that it works,” says Daniel Simon, professor of organic electronics at Linköping University.
The concept behind a future treatment for glioblastoma involves surgically implanting an iontronic device directly into the brain, close to the tumour. This approach allows for the use of low doses of potent drugs while bypassing the blood-brain barrier. Precise dosing, both in terms of location and timing, is crucial for effective treatment. Additionally, this method can minimize side effects since the chemotherapy doesn’t need to circulate throughout the entire body.
Beyond brain tumours, researchers hope that iontronics can be applied to many types of difficult-to-treat cancer forms.

“It becomes a very persistent treatment that the tumour cannot hide from. Even though the tumour and surrounding tissue try remove the drug, the materials and control systems we use in iontronics can continuously deliver a locally high concentration of medication to the tissue adjacent to the tumour,” explains Theresia Arbring Sjöström, a researcher at the Laboratory for Organic Electronics at Linköping University.
The researchers compared the continuous drug delivery of the pump with once-daily dosing, which more closely resembles how chemotherapy is administered to patients today. They observed that tumour growth decreased with the ionic treatment but not with the daily-dose approach, even though the latter was twice as strong.
These experiments were conducted using bird embryos at an early developmental stage. According to Linda Waldherr, a researcher at the Medical University of Graz and a guest researcher at LiU, this model serves as a good bridge to larger animal experiments:
“In bird embryos, certain biological systems function similarly to those in living animals, such as the formation of blood vessels. However, we don’t need to surgically implant any devices in them yet. This demonstrates that the concept works, although there are still many challenges to address,” she says.
The researchers believe that human trials could be feasible within the next five to ten years. The next steps involve further developing materials to allow for the surgical implantation of iontronic pumps. Subsequent experiments will also be conducted on rats and larger animals to further evaluate this treatment method.

Scientists at EPFL have achieved a significant research milestone in the field of spinal cord injuries — mapping out the cellular and molecular dynamics of paralysis in unprecedented detail with their open-source project ‘Tabulae Paralytica’. Grégoire Courtine and his team have integrated cutting-edge cell and molecular mapping technologies with artificial intelligence to chart the complex molecular processes that unfold in each cell after spinal cord injuries (SCI). Published in Nature, this seminal work not only identifies a specific set of neurons and genes that plays a key role for recovery but also proposes a successful gene therapy derived from its discoveries.
Understanding why spinal cord injuries are nearly impossible to heal sheds light on the significance of this breakthrough. The human spinal cord is one of the most complex biological systems known to science — it is a mechanical, chemical, and electrical arrangement of different types of cells working in harmony to produce and regulate a multitude of neurological functions, including a natural, elegant gait. This cellular complexity amplifies the challenges to effectively treating paralysis caused by injury to the spinal cord.
Until now, traditional imaging and mapping methods have offered a generalized view of the cellular mechanisms of SCI. But this lack of specificity blurs the distinct roles and reactions of individual cell types and has hindered the development of targeted treatments, as therapies could not be finely tuned to address specific cellular dynamics.
“In this study, we aimed for nothing less than a revolution in the biological understanding of spinal cord injury,” says Courtine. “By offering an exceptionally detailed view of the cellular and molecular dynamics of spinal cord injury in mice across space and time, the four cell atlases comprising the Tabulae Paralytica close a historic knowledge gap, paving the way for targeted treatments and enhanced recovery.”
The first treatment to come from this new understanding of the intricate cellular dynamics of paralysis is a targeted gene therapy. Developed in collaboration with fellow EPFL Neuro X professor Bernard Schneider, the therapy leverages a crucial finding: the researchers found that a specific type of support cell called an astrocyte loses its ability to respond to injury in aged animals.
“For much of the last hundred years, it was believed that astrocytes were detrimental to neural repair. Our data further supports overturning this notion and suggests an essential protective role for these cells that can be exploited to repair spinal cord injuries,” says EPFL’s Mark Anderson, senior author of the study.
Another key result of the study is the identification of a specific subset of neurons, known as Vsx2 neurons, that are inherently equipped to promote recovery.

“Our previous studies have pointed in their direction, but with this new, fine-tuned understanding, we can now say for certain that Vsx2 neurons are largely responsible for neural circuit reorganization, meaning that they are by far the most interesting population of neurons for repairing spinal cord injury,” asserts Jordan Squair, another senior author of the study from EPFL.
To create the first-ever comprehensive cellular map of spinal cord injuries in rodent models, the researchers employed two innovative technologies. The first, single cell sequencing, examines the genetic makeup of each cell. While it has been employed for over a decade, recent advances allowed the scientists to scale up the process like never before, generating detailed accounts of millions of spinal cord cells.
Secondly, spatial transcriptomics — a cutting-edge technology that shows us where these cellular activities occur — expanded the map across the entire spinal cord, preserving the spatial context and relationships between different cell types.
The new data is so vast that new machine learning techniques needed to be developed specifically to harness its intricacy. This computational approach leverages artificial intelligence to not only chart the immediate genetic responses of individual cells but also situate these responses within the physical and temporal landscape of the spinal cord.
“We now have a detailed map that not only shows us which cells are involved but also how they interact and change over the course of the injury and recovery process,” explains Squair. “This comprehensive understanding is crucial for developing treatments that are precisely tailored to specific cells and unique requirements for repair of varying injuries, paving the way for more effective and personalized therapies.”
The ‘Tabulae Paralytica’ is a significant milestone in SCI research. It combines scientific insight with technological innovation to open new horizons in the understanding and treatment of SCI. Although this study has been conducted using rodent models, the insights gained are expected to translate into clinical applications, where Courtine and his team have been making significant advances for over a decade.