Publisher Health

Portable ultrasound devices could provide an alternative to x-ray machines for diagnosing forearm fractures in children in a move that could alleviate waiting times for families in hospital emergency departments (ED).
Griffith University researchers Professor Robert Ware from the Menzies Health Institute Queensland and Senior Lecturer Peter Snelling from the School of Medicine and Dentistry compared functional outcomes in children given an ultrasound and those who received an x-ray on a suspected distal forearm fracture.
Dr Snelling said the ultrasounds were performed by nurses, physiotherapists and emergency physicians at four south-east Queensland hospitals.
“They treated 270 children, aged between five and 15 years, during the randomised trial, which included a check-up 28 days later and another check-in at eight weeks,” Dr Snelling said.
“The findings show the majority of children had similar recoveries and returned to full physical function.”
Less than one-third of children who were given an ultrasound needed a follow-up x-ray and care at an orthopaedic clinic.

Those who didn’t have a buckle fracture or fractured arm were discharged from hospital without the need for further imaging.
Professor Ware said children who had an ultrasound initially had fewer x-rays, and shorter stays in the ED.
“Families were also more satisfied with the treatment they received,” he said.
“The results are promising and have wider implications beyond in hospital diagnosis and follow up care.
“By using a bedside ultrasound, this frees up the x-ray machine for patients who really need it and can potentially be a cost-cutting measure for hospitals as they reduce the number of x-rays without comprising the safety of patients.

“It also would be extremely beneficial in rural or remote areas eliminating the need for children and their families to travel to a larger hospital for an x-ray.”
Dr David Bade, Queensland Children’s Hospital Director of Orthopaedic Surgery said: “This research will allow us to achieve a more efficient diagnostic and treatment service for these common injuries, not only in big tertiary hospitals but possibly also in smaller regional and even rural centres, where there can be a delay for X-ray diagnosis.
“Collaborative research such as this, allows us to tackle such health inequality in a small but meaningful way.”
Professor Hugh Grantham ASM, Emergency Medicine Foundation Chair said: “This is a great example of emergency medicine research at its best: identifying practical, translatable interventions that provide immediate positive outcomes for patients, and help relieve the burden on our hospitals and health system.” ?
The research was funded through grants from the Emergency Medicine Foundation, Wishlist Sunshine Coast Hospital Foundation, Queensland Advancing Clinical Research Fellowships and the Gold Coast Health Study Education and Research Trust Fund.
Dr Snelling is a practicing Paediatric Emergency Physician Gold Coast Hospital and Health Service, which offered two of the sites where the study was undertaken.
The paper ‘Ultrasonography or x-ray for suspected paediatric distal forearm fractures’ has been published in the New England Journal of Medicine.

Health professionals are in urgent need of new antibiotics to tackle resistant bacteria. Researchers at the University of Zurich and the company Spexis have now modified the chemical structure of naturally occurring peptides to develop antimicrobial molecules that bind to novel targets in the bacteria’s metabolism.
Each year, more than five million people worldwide die as a result of bacteria that are resistant to most common antibiotics. New antibiotics are urgently needed to ensure that bacterial infections in patients can still be treated successfully. “Unfortunately, the development pipeline for new antibiotics is fairly empty,” says chemist Oliver Zerbe, head of the NMR facilities at the University of Zurich. “It’s been more than 50 years since the last antibiotics against previously unused target molecules were approved.”
In a study recently published in Science Advances, Zerbe now discusses the development of a highly effective class of antibiotics that fight Gram-negative bacteria in a novel way. The WHO classifies this group of bacteria as extremely dangerous. The group, whose resistance is particularly high due to their double cell membrane, includes carbapenem-resistant enterobacteria, for example. Besides the UZH team, researchers from the pharmaceutical company Spexis AG were also involved in the study as part of a collaboration co-funded by Innosuisse.
Natural peptide chemically optimized
The starting point for the researchers’ study was a naturally occurring peptide called thanatin, which insects use to fend off infections. Thanatin disrupts an important lipopolysaccharide transport bridge between the outer and inner membrane of Gram-negative bacteria, as revealed a few years ago in a study by now retired UZH professor John Robinson. As a result, these metabolites build up inside the cells, and the bacteria perish. However, thanatin isn’t suitable for use as an antibiotic drug, among other things due to its low effectiveness and because bacteria quickly become resistant to it.
The researchers therefore modified the chemical structure of thanatin to enhance the peptide’s characteristics. “To do this, structural analyses were essential,” says Zerbe. His team synthetically assembled the various components of the bacterial transport bridge and then used nuclear magnetic resonance (NMR) to visualize where and how thanatin binds to and disrupts the transport bridge. Using this information, researchers from Spexis AG planned the chemical modifications that were necessary to boost the peptide’s antibacterial effects. Further mutations were made to increase the molecule’s stability, among other things.
Effective, safe and immune to resistance
The synthetic peptides were then tested in mice with bacterial infections — and yielded outstanding results. “The novel antibiotics proved very effective, especially for treating lung infections,” says Zerbe. “They are also highly effective against carbapenem-resistant enterobacteria, where most other antibiotics fail.” In addition, the newly developed peptides aren’t toxic or harmful to the kidneys, and they also proved stable in the blood over a longer period — all of which are properties that are required for gaining approval as a drug. However, further preclinical studies are needed before the first tests in humans can begin.
When choosing the most promising peptides for their study, the researchers made sure that they would also be effective against bacteria that have already developed resistance to thanatin. “We’re confident this will significantly slow down the development of antibacterial resistance,” says Zerbe. “We now have the prospect of a new class of antibiotics becoming available that is also effective against resistant bacteria.”

In crisis, the nucleus calls antioxidant enzymes to the rescue. The nucleus being metabolically active is a profound paradigm shift with implications for cancer research.
Summary points The human nucleus is metabolically active, according to the findings of a new study in Molecular Systems Biology by researchers at the CRG in Barcelona and CeMM/Medical University of Vienna, In a state of crisis, such as widespread DNA damage, the nucleus protects itself by appropriates mitochondrial machinery to carry out urgent repairs that threaten the genome’s integrity The findings represent a paradigm shift because the nucleus has been historically considered to be metabolically inert, importing all its needs through supply chains in the cytoplasm Cancer hijacks cellular metabolism for unfettered growth. The findings can help guide future lines of cancer research by offering new clues to overcome drug resistance and eventually the design of new treatments Main text

A typical human cell is metabolically active, roaring with chemical reactions that convert nutrients into energy and useful products that sustain life. These reactions also create reactive oxygen species, dangerous by-products like hydrogen peroxide which damage the building blocks of DNA in the same way oxygen and water corrode metal and form rust. Just how buildings collapse from the cumulative effect of rust, reactive oxygen species threatens a genome’s integrity.
Cells are thought to delicately balance their energy needs and avoid damaging DNA by containing metabolic activity outside the nucleus and within the cytoplasm and mitochondria. Antioxidant enzymes are deployed to mop up reactive oxygen species at their source before they reach DNA, a defensive strategy that protects the roughly 3 billion nucleotides from suffering potentially catastrophic mutations. If DNA damage occurs anyway, cells pause momentarily and carry out repairs, synthesising new building blocks and filling in the gaps.
Despite the central role of cellular metabolism in maintaining genome integrity, there has been no systematic, unbiased study on how metabolic perturbations affect the DNA damage and repair process. This is particularly important for diseases like cancer, characterised by their ability to hijack metabolic processes for unfettered growth.
A research team led by Sara Sdelci at the Centre for Genomic Regulation (CRG) in Barcelona and Joanna Loizou at the CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences in Vienna and the Medical University of Vienna addressed this challenge by carrying out various experiments to identify which metabolic enzymes and processes are essential for a cell’s DNA damage response. The findings are published today in the journal Molecular Systems Biology.
The researchers experimentally induced DNA damage in human cell lines using a common chemotherapy medication known as etoposide. Etoposide works by breaking DNA strands and blocking an enzyme which helps repair the damage. Surprisingly, inducing DNA damage resulted in reactive oxygen species being generated and accumulating inside the nucleus. The researchers observed that cellular respiratory enzymes, a major source of reactive oxygen species, relocated from the mitochondria to the nucleus in response to DNA damage.

The findings represent a paradigm shift in cellular biology because it suggests the nucleus is metabolically active. “Where there’s smoke there’s fire, and where there’s reactive oxygen species there are metabolic enzymes at work. Historically, we’ve thought of the nucleus as a metabolically inert organelle that imports all its needs from the cytoplasm, but our study demonstrates that another type of metabolism exists in cells and is found in the nucleus,” says Dr. Sara Sdelci, corresponding author of the study and Group Leader at the Centre for Genomic Regulation.
The researchers also used CRISPR-Cas9 to identify all the metabolic genes that were important for cell survival in this scenario. These experiments revealed that cells order the enzyme PRDX1, an antioxidant enzyme also normally found in mitochondria, to travel to the nucleus and scavenge reactive oxygen species present to prevent further damage. PRDX1 was also found to repair the damage by regulating the cellular availability of aspartate, a raw material that is critical for synthesising nucleotides, the building blocks of DNA.
“PRDX1 is like a robotic pool cleaner. Cells are known to use it to keep their insides ‘clean’ and prevent the accumulation of reactive oxygen species, but never before at the nuclear level. This is evidence that, in a state of crisis, the nucleus responds by appropriating mitochondrial machinery and establishes an emergency rapid-industrialisation policy,” says Dr. Sdelci.
The findings can guide future lines of cancer research. Some anti-cancer drugs, such as etoposide used in this study, kill tumour cells by damaging their DNA and inhibiting the repair process. If enough damage accumulates, the cancer cell initiates a process where it autodestructs.
During their experiments, the researchers found that knocking out metabolic genes critical for cellular respiration — the process that generates energy from oxygen and nutrients — made normal healthy cells become resistant to etoposide. The finding is important because many cancer cells are glycolytic, meaning that even in the presence of oxygen they generate energy without doing cellular respiration. This means etoposide, and other chemotherapies with a similar mechanism, is likely to have a limited effect in treating glycolytic tumours.
The authors of the study call for the exploration of new strategies such as dual treatment combining etoposide with drugs that also boost the generation of reactive oxygen species to overcome drug resistance and kill cancer cells faster. They also hypothesise that combining etoposide with inhibitors of nucleotide synthesis processes could potentiate the effect of the drug by preventing the repair of DNA damage and ensuring cancer cells self-destruct correctly.
Dr. Joanna Loizou, corresponding author and Group Leader at the Centre for Molecular Medicine and the Medical University of Vienna, highlights the value of taking data-driven approaches to uncover new biological processes. ‘By using unbiased technologies such as CRISPR-Cas9 screening and metabolomics, we have learnt about how the two fundamental cellular processes of DNA repair and metabolism are intertwined. Our findings shed light on how targeting these two pathways in cancer might improve therapeutic outcomes for patients’.

While indigestible video capsule endoscopes have been around for many years, the capsules have been limited by the fact that they could not be controlled by physicians. They moved passively, driven only by gravity and the natural movement of the body. Now, according to a first-of-its-kind research study at George Washington University, physicians can remotely drive a miniature video capsule to all regions of the stomach to visualize and photograph potential problem areas. The new technology uses an external magnet and hand-held video game style joysticks to move the capsule in three-dimensions in the stomach. This new technology comes closer to the capabilities of a traditional tube-based endoscopy.
“A traditional endoscopy is an invasive procedure for patients, not to mention it is costly due to the need for anesthesia and time off work,” Andrew Meltzer, a professor of Emergency Medicine at the GW School of Medicine & Health Sciences, said. “If larger studies can prove this method is sufficiently sensitive to detect high-risk lesions, magnetically controlled capsules could be used as a quick and easy way to screen for health problems in the upper GI tract such as ulcers or stomach cancer.”
More than 7 million traditional endoscopies of the stomach and upper part of the intestine are performed every year in the United States to help doctors investigate and treat stomach pain, nausea, bleeding and other symptoms of disease, including cancer. Despite the benefits of traditional endoscopies, studies suggest some patients have trouble accessing the procedure.
In fact, Meltzer got interested in the magnetically controlled capsule endoscopy after seeing patients in the emergency room with stomach pain or suspected upper GI bleeding who faced barriers to getting a traditional endoscopy as an outpatient.
“I would have patients who came to the ER with concerns for a bleeding ulcer and, even if they were clinically stable, I would have no way to evaluate them without admitting them to the hospital for an endoscopy. We could not do an endoscopy in the ER and many patients faced unacceptable barriers to getting an outpatient endoscopy, a crucial diagnostic tool to preventing life-threatening hemorrhage,” Meltzer said. “To help address this problem, I started looking for less invasive ways to visualize the upper gastrointestinal tract for patients with suspected internal bleeding.”
The study is the first to test magnetically controlled capsule endoscopy in the United States. For patients who come to the ER or a doctor’s office with severe stomach pain, the ability to swallow a capsule and get a diagnosis on the spot — without a second appointment for a traditional endoscopy — is a real plus, not to mention potentially life-saving, says Meltzer. An external magnet allows the capsule to be painlessly driven to visualize all anatomic areas of the stomach and record video and photograph any possible bleeding, inflammatory or malignant lesions.
While using the joystick requires additional time and training, software is being developed that will use artificial intelligence to self-drive the capsule to all parts of the stomach with a push of the button and record any potential risky abnormalities. That would make it easier to use the system as a diagnostic tool or screening test. In addition, the videos can be easily transmitted for off-site review if a gastroenterologist is not on-site to over-read the images.
Meltzer and colleagues conducted a study of 40 patients at a physician office building using the magnetically controlled capsule endoscopy. They found that the doctor could direct the capsule to all major parts of the stomach with a 95 percent rate of visualization. Capsules were driven by the ER physician and then the study reports were reviewed by an attending gastroenterologist who was physically off-site.
To see how the new method compared with a traditional endoscopy, participants in the study also received a follow up endoscopy. No high-risk lesions were missed with the new method and 80 percent of the patients preferred the capsule method to the traditional endoscopy. The team found no safety problems associated with the new method.
Yet, Meltzer cautions that the study is a pilot and a much bigger trial with more patients must be conducted to make sure the method does not miss important lesions and can be used in place of an endoscopy. A major limitation of the capsule includes the inability to perform biopsies of lesions that are detected.
The study, “Magnetically Controlled Capsule for Assessment of the Gastric Mucosa in Symptomatic Patients (MAGNET): A Prospective, Single-Arm, Single-Center, Comparative Study,” was published in iGIE, the open-access, online journal of the American Society for Gastrointestinal Endoscopy.
The medical technology company AnX Robotica funded the research and is the creator of the capsule endoscopy system used in the study, called NaviCam®.

The body is pretty good at healing itself, though more severe wounds can require bandages or stitches. But researchers publishing in ACS Applied Materials & Interfaces have developed a wound-healing ink that can actively encourage the body to heal by exposing the cut to immune-system vesicles. The ink can be spread into a cut of any shape using a 3D-printing pen, and in mice, the technology nearly completely repaired wounds in just 12 days.
When the skin is cut or torn, the body’s natural “construction crew” kicks in to fix it back up — clearing out any bacterial invaders, regrowing broken blood vessels and eventually forming a scar. Many techniques used to heal wounds can’t do much beyond helping the body do its job better. Bandages or stitches are used to prevent further bleeding, while antibiotics work to prevent complications from infections. But by adding members of the construction crew to a wound-healing treatment or bandage, it could actually accelerate the natural healing process. Specifically, white blood cells or the extracellular vesicles (EVs) secreted from them play important roles in promoting blood vessel formation and reducing inflammation during healing. So, Dan Li, Xianguang Ding and Lianhui Wang wanted to incorporate these EVs into a hydrogel-based wound healing ink that could be painted into cuts of any shape.
The team developed a system called PAINT, or “portable bioactive ink for tissue healing,” using EVs secreted from macrophages combined with sodium alginate. These components were combined in a 3D-printing pen, where they mixed at the pen’s tip and formed a sturdy gel at the site of injury within three minutes. The EVs promoted blood vessel formation and reduced inflammatory markers in human epithelial cells, shifting them into the “proliferative,” or growth, phase of healing. PAINT was also tested on injured mice, where it promoted collagen fiber formation. Mice treated with PAINT had almost healed completely from a large wound after 12 days, compared to mice that didn’t receive the treatment, who were not nearly as far along in the healing process at this time point. The researchers say that this work could help heal a wide variety of cuts quickly and easily, without the need for complex procedures.

A tiny Central American country is charting a path to slowing climate change, while boosting the economy and making communities safer. A new Stanford-led study quantifies the value of Belize’s coastal mangrove forests in terms of how much carbon they can hold, the value they can add to tourism and fisheries, and the protection they can provide against coastal storms and other risks. Importantly, the findings, published June 1 in Nature Ecology and Evolution, have already provided a basis for Belize’s commitment to protect or restore additional mangrove forests totaling an area about the size of Washington, D.C., by 2030. The approach holds lessons for many other coastal countries.
“The U.S. has one of the largest coastlines in the world, and extensive wetlands,” said study lead author Katie Arkema, a scientist at the Stanford Natural Capital Project at the time of the research, now at the Pacific Northwest National Laboratory and the University of Washington. “This paper offers an approach we could use for setting evidence-based climate resilience and economic development goals.”
Many countries have been struggling to meet their international climate commitments. Nature-based solutions, such as locking up or sequestering carbon in mangroves, seagrasses, and salt marshes, provide a promising solution — they help nations reduce their greenhouse gas emissions and also adapt to climate change. Yet, major coastal countries, including the U.S., have largely overlooked these so-called blue carbon strategies. The oversight is due in part to the complexity of calculating how much carbon wetlands and other coastal ecosystems can sequester, and where to implement these strategies to maximize co-benefits for the economy, flood risk reduction, and other sectors.
Maximizing benefits
Working together with other scientists, as well as Belizean policymakers and stakeholders, the researchers quantified carbon storage and sequestration using land cover data from Belize and field estimates from Mexico. They quantified coastal flood risk reduction, tourism, and fisheries co-benefits by modeling related services — such as lobster breeding grounds — provided by mangroves currently and under future protection and restoration scenarios at various locations.
Among their findings: In some areas, relatively small amounts of mangrove restoration can have big tourism and fisheries benefits. In contrast, total organic carbon sequestration is initially lower when restoring mangrove areas than when protecting existing forests because it takes time for carbon stocks to accumulate in the soil and biomass.

Another key takeaway: The rate of increase for benefits other than carbon storage begins to decrease at a certain point as mangrove area continues to increase. Predicting these inflection points can help stakeholders and policymakers decide how to most effectively balance ecosystem protection with coastal development. Similarly, identifying locations where blue carbon strategies would provide the greatest delivery of co-benefits can help bolster local support.
Based on the findings, Belizean policymakers pledged to protect an additional 46 square miles of existing mangroves — bringing the national total under protection to 96 square miles — and to restore 15 square miles of mangroves by 2030. If realized, the effort will not only store and sequester millions of tons of carbon but also boost lobster fisheries by as much as 66%, generate mangrove tourism worth several million dollars annually, and reduce the risk of coastal hazards for at least 30% more people, according to the researchers’ models.
The numbers are significant for a country with a population smaller than Tulsa, Oklahoma, and a GDP equivalent to about 2% of New York City’s annual budget.
Because the approach addresses both climate and sustainable development goals, it opens new opportunities for financing nature-based solutions in countries like Belize. In the months to come, the Natural Capital Project, the InterAmerican Development Bank, and the Asian Development Bank will work with 10 countries, including Belize, to support the mainstreaming of and accounting for such nature-based approaches into policy and investment decision-making processes (read more).
“Belize’s example, illustrating the practical ways nature’s many benefits can be spatially quantified and inform a country’s climate policy and investments, are now primed to be scaled around the world with development banks and country leaders” said study co-author Mary Ruckelshaus, executive director of the Stanford Natural Capital Project.
The study was funded by the Gordon and Betty Moore Foundation, the Pew Charitable Trusts, and the World Wildlife Fund.
Study co-authors also include Jade Delevaux of the Natural Capital Project; Jessica Silver and Samantha Winder of the Natural Capital Project and the University of Washington; and researchers with Silvestrum Climate Associates, the World Wildlife Fund, the Pew Charitable Trusts, the University of Minnesota, Belize’s National Climate Change Office, and Belize’s Coastal Zone Management Authority and Institute.

Penn State researchers have developed a low-cost, RNA-based technology to detect and measure biomarkers, which can help decode the body’s physiology. The presence of protein biomarkers can indicate chronic or acute conditions, from arthritis to cancer to bacterial infections, for which conventional tests can cost anywhere from $100 to upwards of $1,000. The new technology can perform the same measurement for about a dollar.
The team published their results in Nature Communications, combining the efforts of Howard Salis, associate professor of biological engineering, chemical engineering and biomedical engineering; Grace Vezeau, who earned a doctorate in biological engineering from Penn State in 2021; and Lipika Gadila, who earned a bachelor of science in chemical engineering from Penn State in 2018.
The results demonstrate that RNA-based sensors can be engineered to detect human biomarker proteins, including monomeric C-reactive protein, which is involved in chronic inflammatory conditions such as heart disease and arthritis, and interleukin-32 gamma, a signaling protein for acute infections like viruses or bacterial infections. According to Salis, such sensors could be used to develop devices for diagnostic testing.
“These tests can help a clinician diagnose a patient, but it’s more informative to carry out multiple biomarker measurements periodically over the span of several weeks,” Salis said. “Right now, one test can be expensive, and they add up. With our new RNA-based technology, it’s now possible to carry out the same measurements for much less.”
The technology is a combination of a cell-free expression system and engineered RNA-based sensors called riboswitches. Cell-free expression systems contain cellular machinery to read DNA and produce proteins, but they are not restricted by cell membranes and allow bulky proteins to freely enter. The riboswitches are engineered to bind to a biomarker protein and regulate the activation or repression of an observable signal. The riboswitch itself is produced inside the cell-free expression system from DNA instructions. Altogether, the cost of these materials is about a dollar per reaction.
According to Salis, this is the first time that researchers have engineered a riboswitch sensor to detect biomarker proteins. The challenge, he said, is figuring out the best DNA instructions to generate the most sensitive protein sensors.
“Past efforts to engineer such riboswitch sensors have largely relied on trial-and-error experimentation, for example, constructing and characterizing large random libraries to identify riboswitch variants — the genetic blueprints and aptamers — that work best,” Salis said. “Using a combination of thermodynamic modeling and computational optimization, we rationally designed new riboswitches that are predicted to be excellent protein sensors and then we tested them. Our design algorithm is called the Riboswitch Calculator.”
Salis and the researchers tested their new technology to detect three proteins: MS2, a small protein found in a bacterial phage, as a proof-of-principle test; and the medically relevant biomarkers human monomeric C-reactive protein and human interleukin-32 gamma. The researchers engineered 32 riboswitches, most of which successfully sensed their target proteins.
“Current assays require expensive detection reagents, expensive and bulky instruments, sample cold chain storage and distribution, and trained personnel,” Salis said. “By applying modeling and computational design, we engineered low-cost protein sensors that can be freeze-dried and rehydrated. The next step is to develop an easy-to-use device that allows researchers and clinicians to use this new technology.”
Salis is also affiliated with the Penn State Institutes of Energy and Environment.
The Defense Advanced Research Projects Agency and the Air Force Office of Scientific Research supported this research.

When we’re driving to a new destination, we often turn down the stereo as we follow the directions. What had been music suddenly sounds like noise, and it interferes with our focus.
Our understanding of how infectious diseases like COVID affect human lungs has been similarly confounded by noise. Data from patient lung tissues greatly varies from person to person, obscuring the basic mechanisms of how, exactly, SARS-Co-V2 first infects lung cells. It’s also an after-the-fact analysis — as if we’re trying to map the route the virus took three states back.
Turning down the noise of variability by studying genetically identical tissues from the first moment of infection could light up the route the pathogen takes. Which cells are infected, and when? What is the level of infection, and how does it differ depending on cell type? How does it change in different conditions?
And what if it were possible to track thousands of these infections at once? It might revolutionize our understanding of both infections and the drug treatments used to combat them.
That’s the hope for new advanced tech capable of growing mini organs on microchips. The labs of Rockefeller’s Ali Brivanlou and Charles M. Rice collaborated to refine a cell culture technology platform that grows genetically identical lung buds — the embryonic structures that give rise to our breathing organs — from human embryonic stem cells (hESCs). Their findings were recently published in Stem Cell Reports.
When placed on an array of microchips and carefully dosed with a custom cocktail of signaling molecules, the hESCs rapidly organize themselves into “micro lungs” that have full tissue complexity. These buds can be cultured by the thousands, allowing for an unprecedented high-throughput analysis of lung tissue infection without all the noisy variables.

The result is unlimited, fast, and scalable access to lung tissue that has the key hallmarks of human lung development and can be used to track lung infections and identify candidate therapeutics.
“These lungs are basically clones,” says Ali Brivanlou. “They have the exact same DNA signature. That way we don’t have to worry about one patient responding differently from another. Quantification allows us to keep the genetic information constant and measure the key variable — the virus.”
Building a better mini lung
Embryonic stem cells are the Ur-cells of the human body. They can infinitely divide to create more stem cells or to differentiate into any other tissue. Brivanlou’s Laboratory of Synthetic Biology has long explored their potential.
Brivanlou joined forces with Rockefeller colleague Charles M. Rice during the COVID pandemic: his lab had the microchip technology to grow lung buds, and Rice’s lab had the necessary biosafety clearance required to infect them with SARS-Co-V2 and study the outcome.

In 2021, first authors Edwin Rosado-Olivieri, a stem cell biologist in Brivanlou’s lab, and Brandon Razooky, then a postdoc in Rice’s Laboratory of Virology and Infectious Disease, began coaxing the cells to organize into more specialized forms. Stem cells don’t just organize on their own. They need a confined space — such as a microchip well — and stimuli to spark change. The stimuli come from four main signaling pathways that induce stem cells to differentiate into specific cell types.
After about two weeks, the group’s lung cells had formed identical buds whose molecular profiles closely matched those seen in the earliest stages of fetal lung development — including the formation of airways and alveoli, structures known to be damaged in many people with severe COVID.
Identifying a key culprit
Since then, they’ve used the platform to understand how SARS-Co-V2 infects different lung cells.
Alveoli are tiny sacs at the end of the lung branches that manage the gas exchange performed with every breath: oxygen in, carbon dioxide out. By studying cloned alveoli cells en masse, the researchers discovered that alveoli were more susceptible to SARS-Co-V-2 infection than airway cells, which are the guardians of the organ — the first defense against all inhaled threats. If the virus got past them, the alveoli were sitting ducks.
Another view of virus particles (blue) infecting alveolar and airway tissues (red).
They also hit upon a winning combination of signaling proteins for creating the most robust batches of lung buds — a mix of keratinocyte growth factor (KGF) and bone morphogenetic protein 4 (BMP4). Both contribute to cell differentiation and growth.
Interestingly, the BMP pathway has a downside. When they compared infected lung buds to postmortem tissue of COVID patients, they found that the BMP signaling pathway was induced in both and rendered the tissues more vulnerable to infection. Blocking the BMP pathway made the cells less vulnerable.
Beyond COVID
The researchers note that the platform can also be used to investigate the mechanisms of influenza, RSV, pulmonary diseases, and lung cancer, among other diseases. Moreover, it can be used to screen for new drugs to treat them.
And lungs are far from the only organ of interest. “The broader focus of our work is understanding cellular development to make synthetic organs and tissues that we can use to model diseases and find therapeutic mechanisms,” says Rosado-Olivieri. The liver, kidney, and pancreas are all likely next targets.
“The platform will also allow us to respond to the next pandemic with much more speed and precision,” Brivanlou adds. “We can quickly capitalize on this platform to make a virus visible and develop therapies much faster than we did for COVID. It can be used to screen for drugs, compounds, vaccines, monoclonal antibodies, and more directly in human tissue. This technology is ready to confront all kinds of threats that may hit us in the future.”

Cutting boards are handy tools found in most homes and restaurant kitchens. But a small-scale study in ACS’ Environmental Science & Technology suggests that they are an overlooked source of micrometer-sized particles. The researchers report that chopping up carrots on wood and plastic boards could produce tens of millions of microparticles a year. However, a toxicity test showed no substantial effect on mouse cell survival from polyethylene or wood microparticles released during chopping.
Most cutting boards are made of rubber, bamboo, wood or plastic. Over time, these kitchen implements develop grooves and slash marks from mincing, slicing and chopping food. Recently, researchers have shown that some plastic board materials, including polypropylene and polyethylene, can shed nano- and micro-sized flecks when cut with knives. Yet those studies didn’t assess how many of these microplastics could be produced during realistic food preparation scenarios. This would be an important piece of information because the particles might have negative health impacts if ingested. So, Syeed Md Iskander and colleagues wanted to investigate the microparticles that would be released when chopping vegetables on plastic and wood boards, as well as any potential toxicity from these tiny materials.
The researchers collected and measured the micro-sized particles released from cutting boards, which were repeatedly struck by a knife. In their tests, they compared five people’s chopping patterns and one person’s chopping on different materials with and without carrots.
From the results, the team calculated that food preparation could produce 14 to 71 million polyethylene microplastics and 79 million polypropylene microplastics from their respective boards each year. The estimates could vary, depending on: An individual’s chopping style. The board material. The force needed to cut through foods. Whether ingredients are roughly or finely chopped. And how often a cutting board is used.Yearly estimates were not determined for wooden boards, though the researchers reported that these items sloughed off 4 to 22 times more microparticles than plastic ones in different tests.
But even though many microparticles formed, the researchers found that polyethylene microplastics and wood microparticles released when chopping carrots didn’t appear to significantly change mouse cells’ viability in lab tests. While plastic cutting boards are easy to clean, the researchers conclude that other options could be used to reduce potential microplastic contamination in foods.

For the first time ever, scientists have uncovered evidence that a species’ long-term adaptation to living in an extremely cold climate has led to the evolution of social behaviours including extended care by mothers, increased infant survival and the ability to live in large complex multilevel societies.
The new study, published today in the journal Science, was led by researchers from Northwest University in China and a team including the University of Bristol (UK) and the University of Western Australia, and examined how langurs and odd-nosed monkeys, part of the Asian colobine family, that can be found from tropical rainforests to snow-covered mountains, adapted over time.
These species were chosen by the researchers as they exhibit four distinct types of social organisation and provide a good model for examining the multiple mechanisms that have driven their social evolution from a common ancestral state to the diverse systems present today.
By integrating ecological, geological, fossil, behavioural and genomic analyses, the team found that colobine primates inhabiting colder environments tend to live in larger, more complex groups. More specifically, glacial periods during the past six million years promoted the selection of genes involved in cold-related energy metabolism and neuro-hormonal regulation.
They found that odd-nosed monkeys living in extremely cold locations had developed more efficient hormonal (dopamine and oxytocin) pathways that may lengthen maternal care, leading to longer periods of breast-feeding and an overall increase in infant survival.
These adaptive changes also appear to have strengthened relationships between individuals, increased tolerance between males and enabled the evolution from independent one-male, multi-female groups to large complex multilevel societies.
Dr Kit Opie, is one of the study’s authors from the Department of Anthropology and Archaeology at the University of Bristol. He said: “Our study identified, for the first time, a genetically regulated adaptation linked to the evolution of social systems in primates.
“This finding offers new insights into the mechanisms that underpin behavioural evolution in primates and could be used to address social evolutionary changes across a wide range of species including humans.
“In addition we would like to examine how changes in social and mating behaviour in many primate species may be the result of genetic changes due to past environments as well as other social and environmental factors.”
Dr Cyril Grueter is also an author of the study from the Department of Anatomy, Physiology and Human Biology at the University of Western Australia. He said: “With climate change becoming an hugely important environmental pressure on animals, it is hoped that this study will raise awareness for the need to investigate what course social evolution will take as the prevailing climate changes.”
“Our finding that complex multilevel societies have roots stretching back to climatic events in the distant evolutionary past also has implications for a reconstruction of the human social system which is decidedly multilevel.”