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A British biologist and blogger discovered faulty data in many studies conducted by top executives of the Dana-Farber Cancer Institute.A prominent cancer center affiliated with Harvard said it will ask medical journals to retract six research papers and correct dozens of others after a British scientist and blogger found that work by some of its top executives was rife with duplicated or manipulated data.The center, the Dana-Farber Cancer Institute in Boston, one of the nation’s foremost cancer treatment and research facilities, moved quickly in recent days to address allegations of faulty data in 58 studies, many of them influential, compiled by a British molecular biologist, Sholto David.In many cases, Dr. David found, images in the papers had been stretched, obscured or spliced together in a way that suggested deliberate attempts to mislead readers. The studies he flagged included some published by Dana-Farber’s chief executive, Dr. Laurie Glimcher, and its chief operating officer, Dr. William Hahn.The retractions come as researchers in the United States face growing pressure to account for instances of scientific misconduct, sloppy work or outright fraud. Image sleuths have recently found evidence of fabricated data in scores of influential papers on Alzheimer’s disease. Last year, Marc Tessier-Lavigne resigned as president of Stanford University after some of his published papers were found to contain manipulated results.Allegations of misconduct have ballooned in part because experts have access to new artificial intelligence tools that can flag suspicious images depicting experimental results.In the wake of recent high-profile misconduct claims, experts have drawn attention to a “publish or perish” culture in academia, which pressures researchers to generate striking results and place papers in major journals, whatever the merits of a study. Some researchers have also said that certain labs, explicitly or not, encourage junior researchers to take shortcuts.We are having trouble retrieving the article content.Please enable JavaScript in your browser settings.Thank you for your patience while we verify access. If you are in Reader mode please exit and log into your Times account, or subscribe for all of The Times.Thank you for your patience while we verify access.Already a subscriber? 

Researchers have identified a receptor protein known as CHRM1 as a key player in prostate cancer cells’ resistance to docetaxel, a commonly used chemotherapy drug to treat advanced cancer that has spread beyond the prostate. The discovery opens the door to new treatment strategies that could overcome this resistance. This could ultimately help extend the lives of those with prostate cancer, one of the leading causes of cancer deaths among men.
Led by a team of scientists at Washington State University, the study showed that blocking CHRM1 in resistant prostate cancer cell lines and an animal model based on patient-derived resistant tissue restored docetaxel’s ability to kill cells and stop tumor growth. The researchers did this by using dicyclomine, a drug that selectively inhibits CHRM1 activity. Dicyclomine is already on the market as a generic drug and is currently used to treat symptoms of irritable bowel syndrome.
“The effect was pretty dramatic in all the experimental models we tested,” said Boyang (Jason) Wu, an associate professor in the WSU College of Pharmacy and Pharmaceutical Sciences and co-senior author on the study. “And because dicyclomine already has a clinical use, this work has immediate translational potential.”
Published in the journal Cell Reports Medicine, the researchers’ findings support clinical testing to confirm whether combined use of docetaxel and dicyclomine could help overcome treatment resistance in prostate cancer patients. Docetaxel resistance can develop in prostate cancer after about six months of treatment. Chemotherapy drugs like docetaxel are among very few options available to patients with castration-resistant prostate cancer, a lethal form of the disease that no longer responds to hormone therapy.
Wu said this type of combination therapy could also potentially be used for other cancers that are currently being treated with docetaxel, such as breast and lung cancer. It may also be possible to use the same combination strategy with other similar chemotherapy drugs.
In addition to testing resistant cancer cell lines, the research team also tested cells that still responded to docetaxel treatment. They found that using dicyclomine to block CHRM1 in these cells made docetaxel more efficient at killing them. Wu said that this shows that prostate cancer patients could potentially benefit from a combination treatment strategy even before docetaxel resistance develops.
“What this suggests is that the lowest effective dose of docetaxel may be lower when the drug is combined with dicyclomine, compared to when docetaxel is used alone,” Wu said. “Being able to use a lower dose could help reduce unwanted side effects and make treatment more manageable for patients.”
Aside from Wu, co-authors on the study include co-senior author Tyler Bland — a former WSU postdoctoral fellow who is now a clinical assistant professor at the University of Idaho — as well as co-first authors Jing Wang, a recent WSU PhD graduate, and Jing Wei, a WSU postdoctoral fellow. The research team conducted the study in collaboration with scientists at the University of Washington, Medical University of Innsbruck in Austria and National Yang Ming Chiao Tung University in Taiwan.
Funding for this study came from a U.S. Department of Defense Prostate Cancer Research Program grant with additional support provided by the National Cancer Institute, a component of the National Institutes of Health, and WSU College of Pharmacy and Pharmaceutical Sciences startup funds.

Air conditioning in our workplaces and homes doesn’t just cool the air — it can also help trap particles from wildfire smoke and reduce our exposure to potentially harmful elements like soluble mercury, sulfate and nitrate, new research shows.
Wildfire smoke can cause or exacerbate health conditions such as asthma, chronic obstructive pulmonary disease (COPD) and heart disease, and lead to an increased risk of hospitalisation and death.
The study, recently published in the journal Environmental Pollution, was led by University of Technology Sydney (UTS) PhD candidate in environmental science Raissa Gill, a recipient of a UTS Research Excellence Scholarship, together with researchers from UTS and UNSW Sydney.
“The wildfires that raged across Australia during the 2019-2020 ‘Black Summer’ produced an enormous amount of air pollution, with plumes of smoke travelling long distances and cloaking Sydney and surrounding areas,” said Gill.
“We wanted to find out more about what was in the wildfire smoke we were breathing. By using commercial air conditioning filters, we were able to capture and analyse the chemical composition of particles that would otherwise have been inhaled,” she said.
The researchers collected particulate matter from heating, ventilation, and air-conditioning (HVAC) filters in UTS Buildings 4 and 7 during the peak of the Black Summer wildfires as well as one year later as a reference point.
They found daily particulate matter concentrations were generally 2-3 times higher than normal, with hourly concentrations reaching up to 10.5 times the usual maximum. This exceeded the national standards on 19% of days across the four-month sampling window. The particles were also finer and contained a different mixture of toxic chemicals.

“Wildfire aerosols contained much smaller, rounder particles than urban aerosols, making them more likely to be inhaled into our lungs and to transfer toxic elements into our blood stream,” said co-author UTS Professor Martina Doblin.
“These particles also contained more soluble forms of mercury, as well as higher concentrations of sulfate, nitrate and fluoride ions and metals including manganese, cobalt, and antimony. Mercury is quite toxic even in low concentrations and can cause neurological problems and lung damage.”
The study highlights the diverse chemical changes that severe wildfire events exert on the atmosphere. Understanding these changes is crucial for assessing the impact of wildfires and their potential consequences for human health and environmental quality.
“While air quality in Sydney is usually good by world standards, recent evidence has clearly shown that the handful of days that we get every year with high pollution loads from wildfires and dust storms lead to significant disease and death in the community,” said co-author UTS Associate Professor Fraser Torpy.
“Studies that build an understanding of these high pollution events are critical in helping us determine what is causing these health crises, and will lead towards a better understanding of how we can protect the vulnerable members of the community that suffer from them,” he said.
While HVAC systems are not designed specifically for wildfire smoke, research on indoor air quality in Canberra during the 2019-2020 fires showed that outdoor concentrations of fine particulate matter were up to 10 times higher than measured values indoors with air conditioning.
The current study shows the UTS HVAC filters were able to capture a significant portion of wildfire smoke, reducing exposure to toxic particles for staff and students working in these buildings. It also underscores the importance of considering higher-rated HVAC filters during fire seasons and maintaining and replacing the filters regularly.
“Australians face significant obstacles in achieving satisfactory air quality during major wildfire events. Many homes and older buildings rely on natural ventilation or have poor HVAC filtration efficiency and gaps that allow smoke to enter. These systems can also be costly and complicated to manage for effective protection during wildfires,” Gill said.
“Given that severe wildfires are projected to increase with climate change, the role of wildfire-ready infrastructure in maintaining public health, as well as the need to reduce greenhouse gas emissions, is now more pressing than ever.”

A groundbreaking study has unveiled a significant link between anxiety disorders and a brain receptor known as TACR3, as well as testosterone.
Prof. Shira Knafo, head of the Molecular Cognitive Lab at Ben-Gurion University, led the research published last month in the journal Molecular Psychiatry.
Anxiety is a common response to stress, but for those dealing with anxiety disorders, it can significantly impact daily life. Clinical evidence has hinted at a close connection between low testosterone levels and anxiety, particularly in men with hypogonadism, a condition characterized by reduced sexual function. However, the precise nature of this relationship has remained unclear until now.
Prof. Knafo discovered male rodents exhibiting exceedingly high anxiety levels had notably lower levels of a specific receptor called TACR3 in their hippocampus. The hippocampus is a brain region closely associated with learning and memory processes. TACR3 is part of the tachykinin receptor family and responds to a substance known as neurokinin. This observation piqued the researchers’ curiosity and was the foundation for an in-depth investigation into the link between TACR3 deficiency, sex hormones, anxiety, and synaptic plasticity.
The rodents were classified based on their behavior in a standard elevated plus maze test measuring anxiety levels. Subsequently, their hippocampi were isolated and underwent gene expression analysis to identify genes with varying expressions between rodents with extremely low anxiety and those with severe anxiety.
One gene that stood out was TACR3. Previous research had revealed that mutations in genes associated with TACR3 led to a condition known as “congenital hypogonadism,” resulting in reduced sex hormone production, including testosterone. Notably, young men with low testosterone often experienced delayed sexual development, accompanied by depression and heightened anxiety. This pairing led researchers to investigate the role of TACR3 further.
Prof. Knafo and her team were aided in their research by two innovative tools they crafted themselves. The first, known as FORTIS, detects changes in receptors critical for neuronal communication within living neurons. By utilizing FORTIS, they demonstrated that inhibiting TACR3 resulted in a sharp increase in these receptors on the cell surface, blocking the parallel process of long-term synaptic strengthening, known as LTP.

The second pioneering tool employed was a novel application of cross-correlation to measure neuronal connectivity within a multi-electrode array system. This tool played a pivotal role in uncovering the profound impact of TACR3 manipulations on synaptic plasticity.
Synaptic plasticity refers to the ability of synapses, the connections between brain cells, to change their strength and efficiency. This dynamic process is fundamental for the brain’s adaptation to the environment. Through synaptic plasticity, the brain can reorganize its neural circuitry in response to new experiences. This flexibility allows for the modification of synaptic connections, enabling neurons to strengthen or weaken their communication over time. Essentially, synaptic plasticity is a key mechanism by which the brain encodes and stores information, adapting continuously to the ever-changing external stimuli and internal states. Importantly, it revealed that deficiencies stemming from TACR3 inactivity could be efficiently rectified through testosterone administration, offering hope for novel approaches to address challenges related to anxiety associated with testosterone deficiency.
TACR3 is seemingly a central player in bridging anxiety and testosterone. The researchers have unraveled the complex mechanisms behind anxiety and opened avenues for novel therapies, including testosterone treatments, that could improve the quality of life for individuals grappling with sexual development disorders and associated anxiety and depression.
Prof. Knafo is a member of the Department of Physiology and Cell Biology in the Faculty of Health Sciences as well as The National Institute for Biotechnology in the Negev.
The research was supported by the Israel Science Foundation (Grant no. 536/19).

We typically don’t think about it whilst doing it, but walking is a complicated task. Controlled by our nervous system, our bones, joints, muscles, tendons, ligaments and other connective tissues (i.e., the musculoskeletal system) must move in coordination and respond to unexpected changes or disturbances at varying speeds in a highly efficient manner. Replicating this in robotic technologies is no small feat.
Now, a research group from Tohoku University Graduate School of Engineering has replicated human-like variable speed walking using a musculoskeletal model — one steered by a reflex control method reflective of the human nervous system. This breakthrough in biomechanics and robotics sets a new benchmark in understanding human movement and paves the way for innovative robotic technologies.
Details of their study were published in the journal PLoS Computational Biology on January 19, 2024.
“Our study has tackled the intricate challenge of replicating efficient walking at various speeds — a cornerstone of the human walking mechanism,” points out Associate Professor Dai Owaki, and co-author of the study along with Shunsuke Koseki and Professor Mitsuhiro Hayashibe. “These insights are pivotal in pushing the boundaries for understanding human locomotion, adaptation, and efficiency.”
The achievement was thanks to an innovative algorithm. The algorithm evolved beyond the conventional least squares method and helped devise a neural circuit model optimized for energy efficiency over diverse walking speeds. Intensive analysis of these neural circuits, particularly those controlling the muscles in the leg swing phase, unveiled critical elements of energy-saving walking strategies. These revelations enhance our grasp of the complex neural network mechanisms that underpin human gait and its effectiveness.
Owaki stresses that the knowledge uncovered in the study will help lay the groundwork for future technological advancements. “The successful emulation of variable-speed walking in a musculoskeletal model, combined with sophisticated neural circuitry, marks a pivotal advancement in merging neuroscience, biomechanics, and robotics. It will revolutionize the design and development of high-performance bipedal robots, advanced prosthetic limbs, and state-of-the-art- powered exoskeletons.”
Such developments could improve mobility solutions for individuals with disabilities and advance robotic technologies used in everyday life.
Looking ahead, Owaki and his team hope to further refine the reflex control framework to recreate a broader range of human walking speeds and movements. They also plan to apply the insights and algorithms from the study to create more adaptive and energy-efficient prosthetics, powered suits, and bipedal robots. This includes integrating the identified neural circuits into these applications to enhance their functionality and naturalness of movement.

A water-soluble, luminescent europium complex enables evaluation of malignancy grade in model glioma tumor cells.
An important part of choosing the most suitable cancer therapy is understanding the malignancy of the tumor; however, current methods for evaluating brain tumor malignancy are invasive and have a high risk of complications. Collaborative research led by Professor Yasuchika Hasegawa and Professor Shinya Tanaka of the Institute for Chemical Reaction Design and Discovery (WPI-ICReDD) at Hokkaido University have developed a non-destructive cancer grade probing system (GPS) for evaluating the malignancy grade of model glioma tumor cells using a water-soluble, luminescent europium complex. This method could lead to non-invasive tests for the determination of tumor malignancy in patients.
The team evaluated tumor malignancy by introducing the europium complex to model cells that mimic glioma, a common type of tumor that accounts for 26.3% of brain cancers (Source: CBTRUS). Three different model cells that mimic different grades of malignancy were tested, and researchers measured changes in the lifetime of the europium complex’s characteristic red-light emission. Researchers found that during the first three hours after adding the europium complex, larger changes in the lifetime of the light emission occurred in the more malignant cells.
“Visualization of cancer cells using luminescent complexes has previously been reported, but our hypothesis was that the photophysical signals sent by such complexes in cancer cells might reflect internal information from the cancer cells,” said Hasegawa.
To achieve this result, researchers first modified the europium complex so that it would be water soluble and stable among the amino acids in the cell culture medium. Upon addition to the cell culture medium, the europium complex initially forms an aggregate with itself. Interaction with model tumor cells results in the aggregates breaking into single molecules, which are then rapidly taken up by the cells. This process promotes structural changes in the europium complex, which cause changes in the lifetime of the complex’s red-light emission.
These differences in emission lifetimes were attributed to the varying tumor activity and growth processes of the different malignancy grades, which could cause different structural changes at different time scales in the europium complex. The team anticipates that using this method could enable continuous detection of tumor activity and provide doctors with key information when deciding appropriate treatment.
“Brain tumors occur in 4.6 out of every 100,000 people in Japan, and the 5-year survival rate is 16% for the most malignant grade 4 type of glioblastoma, which is an aggressive type of glioma brain tumor,” explained Tanaka. “The malignancy evaluation method we developed may be able to benefit these patients in the future.”

A new study conducted by researchers at the Center for Injury Research and Policy of the Abigail Wexner Research Institute at Nationwide Children’s Hospital and the Central Ohio Poison Center investigated trends in calls to poison centers across the country for exposures to liquid laundry detergent packets. The study investigators identified declines in the number, rate and severity of liquid laundry detergent packet exposures among children younger than 6 years. However, the exposure burden remained high. Additionally, exposures have increased among older children, teens and adults.
The study, published in Clinical Toxicology, found that in the most recent three years of the study, U.S. poison centers received 36,279 calls related to liquid laundry detergent packet exposures — an average of one call every 44 minutes. Most exposures involved children younger than 6 years (87%), a single substance (97%) or occurred at a residence (99%). Approximately 6% of single-substance exposures resulted in serious medical outcomes. During the study period, there were nine deaths associated with the ingestion of laundry detergent packets. All nine fatalities involved adults, seven of whom were older than 70 years.
According to previous research, in an effort to reduce unintentional exposures to the contents of liquid laundry detergent packets, ASTM published a voluntary Standard Safety Specification for Liquid Laundry Packets in 2015, but some experts feel it did not go far enough. Recent updates to the standard in March 2022 did not substantially change its scope. Multiple opportunities exist to strengthen the ASTM standard, including requiring Poison Prevention Packaging Act-compliant packaging or adopting additional “layers of protection,” such as individual packaging of each laundry packet.
“The voluntary standard, public awareness campaigns, and product and packaging changes to-date have improved the safety of these products, but a high number of children are still exposed each year,” said Christopher Gaw, MD, senior author of the study, emergency medicine physician and faculty of the Center for Injury Research and Policy at Nationwide Children’s. “There is still room for improvement.”
One reason for the less-than-expected decline in exposures among young children is likely because the voluntary safety standard permits manufacturers to meet the requirement for child resistant containers in six different ways rather than requiring them to conform to the Poison Prevention Packaging Act (PPPA) of 1970, which has been shown to be highly effective in preventing child access to poisons. “Requiring that all liquid laundry detergent packet packaging be PPPA-compliant would be an important next step in reducing child access to these products,” said Gary Smith, MD, DrPH, co-author of the study and director of the Center for Injury Research and Policy at Nationwide Children’s. “In addition, each laundry packet should be individually wrapped with child-resistant packaging, which would provide important layers of protection for this highly toxic product.”
Liquid laundry detergent packets are more toxic than traditional liquid and powder laundry detergents. The reasons for this increased toxicity are not completely understood, and further research is needed to determine how to make packet contents less toxic. Such reformulation would reduce the severity of exposures to liquid laundry detergent packets.
Pediatricians and other healthcare providers should continue to counsel patients and their families about the hazards of laundry detergent packet exposures and the importance of safe storage practices. Experts recommend that caregivers to children younger than 6 years old and adults with a history of dementia, Alzheimer’s disease or developmental disability use traditional laundry detergents instead of packets.
“Many families don’t realize how toxic these highly concentrated laundry detergent packets can be,” said Dr. Gaw. “If you have young children or vulnerable adults in your home, using traditional laundry detergents is a safer alternative.”

When people develop myelodysplastic neoplasms (MDS), the healthy maturation of blood cells is impaired. Severe forms, known as higher-risk MDS, are characterised by rapid progression, severe symptoms and often a transition to acute leukemia. Patients for whom potentially curative or intensive treatments, such as stem cell transplantation or high-dose chemotherapy, are not suitable, have very few alternative treatment options. An international clinical trial led by Professor Uwe Platzbecker from the University of Leipzig Medical Center, in collaboration with a large international team of researchers, tested a new treatment combination.
Every year, around 4,000 people in Germany are diagnosed with myelodysplastic neoplasms (MDS). The disease can lead to anemia, infections and an increased risk of bleeding. People with higher-risk MDS have a significantly lower life expectancy than the average person of the same age. In the higher-risk stage, the disease is treated with stem cell transplantation or chemotherapy. Patients for whom these intensive and physically demanding treatments are not an option, have very few therapeutic alternatives. Therefore, there is a great need for new approaches and combinations in higher-risk MDS.
In a current international trial at 54 sites in 17 countries, researchers tested a new treatment combination in 127 patients. Hypomethylating agents (HMA), the current standard of care in this patient population, were compared with a combination of HMA and the active ingredient sabatolimab. Sabatolimab is an intravenously administered new immunotherapeutic agent that targets domains located on myeloid immune and tumour cells. It belongs to a class of drugs known as immune checkpoint inhibitors. Checkpoint inhibitors target specific areas of the immune system to override tumour survival mechanisms. This could prevent the cancer from switching off the immune system that would otherwise attack it. “The study is the first randomised trial involving immunotherapy in combination with the standard of care in this patient population for myeloid neoplasms,” says Uwe Platzbecker, Professor of Haematology at Leipzig University and Director of the Department for Hematology, Cell Therapy, Hemostaseology and Infectious Diseases at the University of Leipzig Medical Center. Professor Platzbecker has been conducting clinical research into myelodysplastic neoplasms for more than 20 years.
The addition of the active ingredient sabatolimab to the standard of care did not significantly improve response rates or progression-free survival in this study. However, in most cases, sabatolimab showed a manageable safety profile in this difficult-to-treat patient population for whom only limited treatment options are available. The most common side effects were a reduction in white blood cells (neutropenia) and platelets (thrombocytopenia) — although these occurred in both the sabatolimab and placebo groups.
The researchers still see potential in combining the standard treatment with the new active ingredient sabatolimab. A randomised phase 3 trial is already underway. Phase 3 trials are the final stage of drug development and test new treatment options in large patient cohorts. This follow-up study is investigating the potential benefit — in terms of overall patient survival — of sabatolimab in combination with azacitidine, the most commonly used HMA. The clinical trial described above was sponsored by the pharmaceutical company Novartis.
Every year, around 4,000 people in Germany are diagnosed with myelodysplastic neoplasms (MDS). The disease can lead to anemia, infections and an increased risk of bleeding. People with higher-risk MDS have a significantly lower life expectancy than the average person of the same age. In the higher-risk stage, the disease is treated with stem cell transplantation or chemotherapy. Patients for whom these intensive and physically demanding treatments are not an option, have very few therapeutic alternatives. Therefore, there is a great need for new approaches and combinations in higher-risk MDS.
In a current international trial at 54 sites in 17 countries, researchers tested a new treatment combination in 127 patients. Hypomethylating agents (HMA), the current standard of care in this patient population, were compared with a combination of HMA and the active ingredient sabatolimab. Sabatolimab is an intravenously administered new immunotherapeutic agent that targets domains located on myeloid immune and tumour cells. It belongs to a class of drugs known as immune checkpoint inhibitors. Checkpoint inhibitors target specific areas of the immune system to override tumour survival mechanisms. This could prevent the cancer from switching off the immune system that would otherwise attack it. “The study is the first randomised trial involving immunotherapy in combination with the standard of care in this patient population for myeloid neoplasms,” says Uwe Platzbecker, Professor of Haematology at Leipzig University and Director of the Department for Hematology, Cell Therapy, Hemostaseology and Infectious Diseases at the University of Leipzig Medical Center. Professor Platzbecker has been conducting clinical research into myelodysplastic neoplasms for more than 20 years.
The addition of the active ingredient sabatolimab to the standard of care did not significantly improve response rates or progression-free survival in this study. However, in most cases, sabatolimab showed a manageable safety profile in this difficult-to-treat patient population for whom only limited treatment options are available. The most common side effects were a reduction in white blood cells (neutropenia) and platelets (thrombocytopenia) — although these occurred in both the sabatolimab and placebo groups.
The researchers still see potential in combining the standard treatment with the new active ingredient sabatolimab. A randomised phase 3 trial is already underway. Phase 3 trials are the final stage of drug development and test new treatment options in large patient cohorts. This follow-up study is investigating the potential benefit — in terms of overall patient survival — of sabatolimab in combination with azacitidine, the most commonly used HMA. The clinical trial described above was sponsored by the pharmaceutical company Novartis.

For the first time, scientists have successfully trapped atoms of krypton (Kr), a noble gas, inside a carbon nanotube to form a one-dimensional gas.
Scientists from the University of Nottingham’s School of Chemistry used advanced transmission electron microscopy (TEM) methods to capture the moment when Kr atoms joined together, one by one, inside a “nano test tube” container with diameter half a million times smaller than the width of a human hair. The research has been published in the journal of the American Chemical Society.
The behaviour of atoms has been studied by scientists ever since it was hypothesized that they are the basic units of the universe. The movement of atoms has significant impact on fundamental phenomena such as temperature, pressure, fluid flow and chemical reactions. Traditional spectroscopy methods can analyse the movement of large groups of atoms and then use averaged data to explain phenomena at the atomic scale. However, these methods don’t show what individual atoms are doing at a specific point in time.
The challenge researchers face when imaging atoms is that they are very small, ranging from 0.1 — 0.4 nanometres, and they can move at very high speeds of around 400 m/s in the gas phase, on the scale of the speed of sound. This makes the direct imaging of atoms in action very difficult, and the creation of continuous visual representations of atoms in real-time remains one of the most significant scientific challenges.
Professor Andrei Khlobystov, School of Chemistry, University of Nottingham, said: “Carbon nanotubes enable us to entrap atoms and accurately position and study them at the single-atom level in real-time. For instance, we successfully trapped noble gas krypton (Kr) atoms in this study. Because Kr has a high atomic number, it is easier to observe in a TEM than lighter elements. This allowed us to track the positions of Kr atoms as moving dots.”
Professor Ute Kaiser, former head of the Electron Microscopy of Materials Science group, senior professor at the University of Ulm, added: “We used our state-of-the-art SALVE TEM, which corrects chromatic and spherical aberrations, to observe the process of krypton atoms joining together to form Kr2 pairs. These pairs are held together by the van der Waals interaction, which is a mysterious force governing the world of molecules and atoms. This is an exciting innovation, as it allows us to see the van der Waals distance between two atoms in real space. It’s a significant development in the field of chemistry and physics that can help us better understand the workings of atoms and molecules.”
The researchers utilised Buckminster fullerenes, which are football-shaped molecules consisting of 60 carbon atoms, to transport individual Kr atoms into nano test tubes. The coalescence of buckminsterfullerene molecules to create nested carbon nanotubes helped to improve the precision of the experiments. Ian Cardillo-Zallo, a PhD student at the University of Nottingham, who was responsible for the preparation and analysis of these materials, says: “Krypton atoms can be released from the fullerene cavities by fusing the carbon cages. This can be achieved by heating at 1200oC or irradiating with an electron beam. Interatomic bonding between Kr atoms and their dynamic gas-like behaviour can both be studied in a single TEM experiment.”
The group have been able to directly observe Kr atoms exiting fullerene cages to form a one-dimensional gas. Once freed from their carrier molecules, Kr atoms can only move in one dimension along the nanotube channel due to the extremely narrow space. The atoms in the row of constrained Kr atoms cannot pass each other and are forced to slow down, like vehicles in traffic congestion. The team captured the crucial stage when isolated Kr atoms transition to a 1D gas, causing single-atom contrast to disappear in the TEM. Nonetheless, the complementary techniques of scanning TEM (STEM) imaging and electron energy loss spectroscopy (EELS) were able to trace the movement of atoms within each nanotube through the mapping of their chemical signatures.

Professor Quentin Ramasse, Director of SuperSTEM, an EPSRC National Research Facility, said: ‘By focusing the electron beam to a diameter much smaller than the atomic size, we are able to scan across the nano test tube and record spectra of individual atoms confined within, even if these atoms are moving. This gives us a spectral map of the one-dimensional gas, confirming that the atoms are delocalised and fill all available space, as a normal gas would do.’
Professor Paul Brown, director of the Nanoscale and Microscale Research Centre (nmRC), University of Nottingham, said: ‘As far as we know, this is the first time that chains of noble gas atoms have been imaged directly, leading to the creation of a one-dimensional gas in a solid material. Such strongly correlated atomic systems may exhibit highly unusual heat conductance and diffusion properties. Transmission electron microscopy has played a crucial role in understanding the dynamics of atoms in real-time and direct space.’
The team plans to use electron microscopy to image temperature-controlled phase transitions and chemical reactions in one-dimensional systems, to unlock the secrets of such unusual states of matter.

A team of scientists from Nanyang Technological University, Singapore (NTU Singapore) has demonstrated that communication among memory-coding neurons — nerve cells in the brain responsible for maintaining working memory — is disrupted with ageing and that this can begin in middle age.
Findings from the study, which was reported in Nature Communications, provide new insights into the ageing process of the human mind, and pave the way for therapies to maintain the mental well-being of an ageing individual.
Scientists have long studied the impact of ageing on the brain’s executive functions, such as poorer self-control and working memory. While it is well established that memory can worsen as people age, it has not been clear what changes occur at the individual brain neuron level to cause this — until now.
Previous studies used nerve cells from dead subjects, but the Lee Kong Chian School of Medicine (LKCMedicine) team measured the real-time activity of individual nerve cells in live mice. To make these measurements, the team adopted a recently unveiled optical imaging technique that allowed them to understand the function of each neuron by measuring its neural activity in the context of working memory.
In lab experiments, the NTU scientists investigated how neurons in mice of three different age groups — young, middle age, and old age — responded to tasks that required memory.
The researchers showed that compared to young mice, middle-aged and old mice required more training sessions to learn new tasks, indicating some decline in memory and learning abilities from middle age. But beyond that, they also found changes in the nerve cells of older mice.
Connections between neurons weaken with age
Using advanced optical techniques (calcium imaging and optogenetic manipulation) that allow researchers to observe multiple individual neurons and manipulate their activity, the NTU team discovered that neurons in one part of the brain, the prefrontal cortex, showed robust memory coding ability in young mice. However, this ability to hold memory diminishes in middle-aged and old mice due to weakening connections among the neurons, which causes the mice to take longer to recall and perform tasks.

While scientists know connections between neurons are crucial for storing memory, it has not previously been experimentally demonstrated in the live brain how ageing brain cell changes cause weakening connections.
The findings thus suggest that strengthening the weakened connections between the nerve cells, such as through memory training activities, could help delay the deterioration of people’s working memories as they age.
Lead investigator and Assistant Professor Tsukasa Kamigaki from NTU’s LKCMedicine said, “Our study highlights a significant reduction in communication among neurons responsible for encoding memories in the prefrontal cortex — a key factor in age-related working memory decline, which was a neurological process not widely understood until now. This discovery provides more evidence that proactive intervention can improve neuron communication. Examples of intervention include lifestyle changes such as cognitive training and regular exercise. These activities can potentially mitigate the impact of cognitive ageing and enhance people’s overall cognitive health as they age.”
Memory decline can begin in middle age
Further experiments also showed that the weakening connections between the nerve cells led to instability of neural circuits in the prefrontal cortex from as early as middle age, resulting in poorer ability to hold memory.
The NTU team used optogenetic technology — a method that uses genetically engineered light-sensitive ion channels in neurons which enables the control of neuronal activity through light stimulation — to briefly turn off neurons in the brain for one to two seconds and found that the working memory circuits in middle-aged mice are particularly sensitive to the short interruptions in neural activity.

Co-first author and LKCMedicine Research Assistant Huee Ru Chong said, “Our four-year study shows that the ongoing function of the prefrontal circuits is critical for memory tasks. The fact that the brain circuits showed signs of degradation from middle age highlights the need for clinical strategies to safeguard our mental well-being as early as possible.”
Co-first author and LKCMedicine Research Fellow Dr Yadollah Ranjbar-Slamloo said, “We found that the prefrontal cortex in mice stays active when they remember things, like humans. The finding suggests that mice could be a good model for studying how memory works and its ageing process. Our findings, therefore, indicate that just as in mice, our brain may start to degrade early on as we age.”
LKCMedicine Associate Professor Nagaendran Kandiah, Visiting Senior Consultant Neurologist at Singapore’s National University Hospital and Khoo Teck Puat Hospital, who is not involved in the study, said, “In humans, the prefrontal cortex plays a key role in organisation, retention, and retrieval of memory. The exciting findings from the NTU team provides insights into specific neural changes in the prefrontal cortex associated with ageing. This new knowledge will be of huge clinical relevance in designing cognitive interventions to delay age-related memory decline.”
Commenting as an independent expert, Dr Jun Nishiyama, Assistant Professor in the Neuroscience and Behavioural Disorders programme at Duke-NUS Medical School said, “It is well-known that brain performance declines with ageing, yet the underlying causes remained elusive. This groundbreaking study from NTU Singapore offers key neurological insights into age-related working memory decline, highlighting reduced neuronal communication in the mouse prefrontal cortex beginning from middle age. This research emphasises the importance of early, strategic interventions to combat cognitive decline, providing a vital framework for future ageing research and brain health maintenance.”
The next steps for this project are to investigate more brain-wide neural changes that occur during middle age to understand how proactive interventions may enhance communication among different brain areas.