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The effect of iron supplementation on skeletal muscle atrophy in cancer patients and sufferers from other wasting diseases has been investigated by a team of Italian and Belgian scientists which studied causes of these conditions in humans and mouse models. The findings, published today in EMBO Reports, shed light on wasting mechanisms in advanced stage cancer patients, for whom prevalence of devastating skeletal muscle atrophy known generally as cachexia reaches 80%.
Furthermore, since at least 20% of all cancer-related deaths are estimated to be caused directly by cachexia, reversing the loss of muscle mass and function could at least prolong quality of life in such patients. Cancer patients with cachexia usually suffer from uncontrollable decrease in quality of life, insulin resistance, liver dysfunction, chronic inflammation, altered gut microbiota, and nutrient absorption.
The researchers firstly set about investigating whether iron deficiency, already known to be highly prevalent among cancer patients and associated with poor prognosis, is causally linked to cachexia. To do this, severe iron deficient anaemia typical of cancer patients was induced in mice by a combination of iron-free diet and phlebotomy, which reduces the volume of circulating blood. This resulted in muscle atrophy among those mice, supporting the hypothesis that disturbance of iron metabolism is associated with onset of cancer-associated muscle wasting.
Then it was found that muscle function, mass, and even longer survival in mouse models of colon cancer could be sustained by iron supplementation, preventing, or reversing cachexia. A finding was that intravenous injections of iron resulted in healthier and more physically active mice that survived far beyond the usual two weeks, as well as notably improved grip strength within 24 hours, all sustained until the end of the experiment.
A moderate strength improvement was observed in a small group of human cancer patients a few days after injection of ferric carboxymaltose, a preparation of iron commonly used as a supplement. Nevertheless, there is also a need for further human studies to validate the results as there was no placebo group to act as a control in the study discussed here.
Further study is necessary to identify fully the underlying mechanisms involved, but the mice experiments indicate that iron is not deficient overall but confined to the cytosol, the primary fluid of cells, and lacking in mitochondria for production of adenosine triphosphate (ATP), the energy source of cells and processes such as muscle contraction. It appears that iron supplementation remedies this deficit by making iron available to mitochondria in muscle cells.
Apart from cancer, skeletal muscle atrophy is a hallmark of various chronic diseases such as cardiac failure and COPD (Chronic Obstructive Pulmonary Disease). Therefore, there is hope that iron supplementation might at least alleviate symptoms of these conditions when muscle atrophy is involved.
At the same time though, the beneficial effects of iron supplementation remain to be validated in other cancer models. It cannot be assumed that the results are transferable to other cancers because some types rely more on iron than others, and therefore iron supplementation might have varying levels of success.
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Both SARS-CoV-1, the virus that caused the 2003 outbreak of Severe Acute Respiratory Syndrome (SARS), and SARS-CoV-2, which causes COVID-19, originate from a group of betacoronaviruses known as “subgroup 2b.” Coronaviruses from this subgroup have been highlighted as having significant potential to cross from animal hosts to humans with deleterious consequences, COVID-19 being the most recent one.
A coronavirus enzyme called papain-like protease, or PLpro, is one of two proteases that are required for the initial replication steps of the virus as well as silencing host immune responses, making this enzyme a sought-after drug target.
Scott Pegan, a professor of biomedical sciences in the School of Medicine at the University of California, Riverside, has led a team that investigated the PLpro from a subgroup 2b bat coronavirus, BtSCoV-Rfl.2004, to determine if identifiable trends in enzymatic activity exist within all subgroup 2b PLpros.
In a paper published in ACS Infectious Diseases, the team lays out the similarities in biochemical function among PLpros from SARS-CoV-2, SARS-CoV-1, and those of other SARS-like viruses already circulating among bats and other species. The work has revealed that unlike other types of coronaviruses, these subgroup 2b SARS and SARS-like coronaviruses seek to selectively target a specific form of ubiquitin — a small protein that exists in all eukaryotic cells — linked to key host immune pathways. Additionally, these PLpros have evolved to selectively target a ubiquitin-like protein known as ISG15 only from a subset of species.
With this information in hand, researchers can further zero in on how SARS and SARS-like viruses go undetected by the host immune system during the early stages of infection and which hosts specific coronaviruses have frequented.
“The pandemic has highlighted the urgent need to develop effective coronavirus therapeutics that can prevent current and future coronavirus subgroup 2b health threats,” Pegan said. “Our paper highlights that PLpro is not just a valid drug target for the current threat of COVID-19, but for other coronaviruses from that group that could cross from animals to humans in the future. Our work has potential to develop a therapy effective against SARS-CoV-2 and other coronaviruses lurking around the corner.”
Pegan explained that the conserved nature of PLpros among subgroup 2b coronaviruses presents an opportunity to develop inhibitors that can be used to thwart viral threats.

Deaths during pregnancy and the first six weeks after childbirth increased, especially for Black and Hispanic women, according to a new report.The number of women in the United States who died during pregnancy or shortly after giving birth increased sharply during the first year of the coronavirus pandemic, according to a new study, an increase that health officials attribute partly to Covid and pandemic-related disruptions.The new report, from the National Center for Health Statistics, found that the number of maternal deaths rose 14 percent, to 861 in 2020 from 754 in 2019.The United States already has a much higher maternal mortality rate than other developed countries, and the increase in deaths pushes the nation’s maternal mortality rate to 23.8 deaths per 100,000 live births in 2020 from 20.1 deaths in 2019. Maternal mortality rates in developed countries have in recent years ranged from fewer than two deaths per 100,000 live births in Norway and New Zealand to just below nine deaths per 100,000 live births in France and Canada.Black women in America experienced the most deaths: One-third of the pregnant women and new mothers who died in 2020 were Black, though Black Americans make up just over 13 percent of the population. Their mortality rate was nearly three times that of white women.The mortality rate for Hispanic women, which has historically been lower than for white women, also increased significantly in 2020 and is now almost on par with the rate for white women. Death rates increased among all pregnant women older than 24, but particularly in those 40 and over, whose mortality rate was nearly eight times that of women younger than 25.“Our maternal morbidity and mortality is the highest in the developed world, and the trend is continuing despite our awareness of it, despite our maternal-mortality review committees, despite attention in the press,” said Kara Zivin, a professor of psychiatry, obstetrics and gynecology at the University of Michigan who studies access to care during and after pregnancy. “Whatever we’re doing is clearly not enough to address either the overall rate or the disparities.”Although the new report is sparse on details — no maternal mortality figures were provided for American Indian/Alaska Native women, who have higher pregnancy-related deaths than white, Hispanic and Asian/Pacific Islander women — experts said some of the deaths were most likely related to the coronavirus pandemic. Pregnancy puts women at risk for more severe disease if they are infected with the SARS-CoV-2 virus, which causes Covid, and vaccines were not available for them in 2020.Dr. Chaniece Wallace died in 2020 from pregnancy complications after delivering her first child.Chaniece Wallace Memorial Facebook Page“We actually said when the lockdown started that we anticipated an increase in maternal deaths, both due to Covid and the responses to Covid,” said Dr. Denise Jamieson, an obstetrician at Emory University in Atlanta and a member of the Covid expert group at the American College of Obstetricians and Gynecologists, adding that she was not surprised by the increases.In addition to the greater risks faced by pregnant women who have Covid, she said, “we hadn’t figured out how to deliver obstetric care safely in 2020.”“Our health systems weren’t set up yet to manage telehealth,” she said, “and there were other barriers: Kids were home from school, and parents couldn’t get away for medical appointments.”Many doctors had stopped seeing patients in person, hospitals were often crowded and patients avoided emergency rooms filled with Covid patients.Pregnant women who develop Covid face a higher risk of requiring intensive care or mechanical ventilation. And despite the relative youth of pregnant women, they face a higher risk of dying, studies found. Health experts have been urging them to be vaccinated, but their vaccination rates have remained low.Black Americans overall suffered disproportionately from the pandemic, with higher hospitalization and death rates than their white counterparts, but the racial disparities in maternal mortality predate and extend beyond Covid, and stem from structural health inequities that have complex root causes.Stress, mental health problems and substance abuse increased during the pandemic and might also have contributed to worse outcomes, said Dr. Mary D’Alton, chair of the department of obstetrics and gynecology at Columbia University Irving Medical Center.New programs that provide enhanced services for patients, such as doulas, who can support and advocate for patients, are positive advances, she said.“We also have to educate our providers on listening to patients,” Dr. D’Alton said. “My dad was a primary care doctor and he used to say, ‘Mary, if you want to know what’s wrong with the patient, ask them and they’ll tell you. But first of all, you’ve got to listen to them.’”“Pregnant women’s complaints are often dismissed, and that is probably much more significant for Black and brown women,” she added.Generally speaking, the leading causes of pregnancy-related deaths are cardiovascular conditions, other medical conditions and infections. Research has found that cardiomyopathy, a disease of the heart muscle; blood clots to the lung; and hypertensive disorders of pregnancy contribute to a higher proportion of pregnancy-related deaths among Black women than among white women.One of the new mothers who died in 2020, whose story was widely reported, was Dr. Chaniece Wallace, a Black physician who was the chief pediatric resident at the Indiana University School of Medicine in Indianapolis.Dr. Wallace developed a pregnancy complication called pre-eclampsia and her baby girl was delivered early by cesarean section in October 2020. But Dr. Wallace went on to develop additional complications, and she died just days after giving birth.

A common building material, asbestos is the term used to describe a range of naturally growing minerals. Serious diseases, including mesothelioma and lung cancer, can arise decades after coming into contact with asbestos.
Biomedical researchers have spent many years trying to understand how asbestos causes disease, though multiple pieces of the puzzle remain unknown. Taking a completely different approach, an international team led by researchers at the University of Pennsylvania, looked instead at how the interactions change the mineral itself.
“Many studies have looked at the toxicity of asbestos, and we wanted to approach this issue from the opposite side, not investigating the effects on the cells, but rather exploring what happens to the mineral once inside the cell,” says Reto Gieré, a professor in Penn’s Department of Earth and Environmental Science in the School of Arts & Sciences, and senior author on the work, published in Scientific Reports.
“We used cutting-edge experimental techniques, going down to the nanoscale and even the atomic scale to see the transformation of the minerals,” says first author Ruggero Vigliaturo, now a tenure-track assistant professor at Italy’s University of Turin who completed the research during a postdoctoral fellowship at Penn. “What we saw is that the minerals are undergoing changes that almost look like they’re defending themselves from the cells.”
The research grew out of a larger set of experiments on asbestos undertaken through Penn’s Center of Excellence in Environmental Toxicology. Though a common term, the word “asbestos” is not a scientific one, but rather is used in industry to refer to a wide range of minerals with varying structures and chemical compositions. In the current work, Vigliaturo, Gieré, and colleagues focused on amphibole asbestos, which is hypothesized to be more hazardous than other varieties.
While much research into asbestos toxicity has focused on how the body’s tissues respond to the mineral, here the researchers wanted to observe how the mineral responded to being taken up by human lung cells. Collaborating with researchers at the National Institute of Chemistry in Slovenia, Vigliaturo and Gieré made use of imaging technology with an extremely high-spatial resolution to characterize the minerals after two days spent inside human lung cells. In contrast, most asbestos research has so far focused on impacts on the body when long asbestos fibers remain in areas of tissue outside of cells.

Ultrasound scans — best known for monitoring pregnancies or imaging organs — can also be used to stimulate cells and direct cell function. A team of Penn State researchers has developed an easier, more effective way to harness the technology for biomedical applications.
The team created a transparent, biocompatible ultrasound transducer chip that resembles a microscope glass slide and can be inserted into any optical microscope for easy viewing. Cells can be cultured and stimulated directly on top of the transducer chip and the cells’ resulting changes can be imaged with optical microscopy techniques.
Published in the Royal Society of Chemistry’s journal Lab on a Chip, the paper was selected as the cover article for the December 2021 issue. Future applications of the technology could impact stem cell, cancer and neuroscience research.
“In the conventional ultrasound stimulation experiments, a cell culture dish is placed in a water bath, and a bulky ultrasound transducer directs the ultrasound waves to the cells through the water medium,” said Sri-Rajasekhar “Raj” Kothapalli, principal investigator and assistant professor of biomedical engineering at Penn State. “This was a complex setup that didn’t provide reproducible results: The results that one group saw another did not, even while using the same parameters, because there are several things that could affect the cells’ survival and stimulation while they are in water, as well as how we visualize them.”
Kothapalli and his collaborators miniaturized the ultrasound stimulation setup by creating a transparent transducer platform made of a piezoelectric lithium niobate material. Piezoelectric materials generate mechanical energy when electric voltage is applied. The chip’s biocompatible surface allows the cells to be cultured directly on the transducer and used for repeated stimulation experiments over several weeks.
When connected to a power supply, the transducer emits ultrasound waves, which pulse the cells and trigger ion influx and outflux.

Many COVID-19 patients newly diagnosed with diabetes during hospital admission may in fact have a temporary form of the disease related to the acute stress of the viral infection and may return to normal blood sugar levels soon after discharge, a study by Massachusetts General Hospital (MGH) has found. These patients are more likely to be younger, non-white, and on Medicaid or uninsured compared to individuals with previously diagnosed diabetes, suggesting many of these “new-onset” cases may simply be pre-existing but undiagnosed diabetes in individuals with limited access to healthcare services, according to the study published in Journal of Diabetes and Its Complications.
High rates of newly diagnosed diabetes mellitus (NDDM) have been reported in COVID-19 hospital admissions around the world. It is still unclear, however, if this phenomenon represents truly new diabetes or previously undiagnosed cases, what the cause of these elevated blood sugars may be, and whether patients’ blood sugars improve after resolution of COVID-19 infection. Pre-existing diabetes in people with COVID-19 has been associated with higher rates of hospitalization, intensive care unit (ICU) admission, mechanical ventilation, and death.
“We believe that the inflammatory stress caused by COVID-19 may be a leading contributor to ‘new-onset’ or newly diagnosed diabetes,” says lead author Sara Cromer, MD, an investigator with the Department of Medicine-Endocrinology, Diabetes and Metabolism at MGH. “Instead of directly causing diabetes, COVID-19 may push patients with pre-existing but undiagnosed diabetes to see a physician for the first time, where their blood sugar disorder can be clinically diagnosed. Our study showed these individuals had higher inflammatory markers and more frequently required admission to hospital ICUs than COVID-19 patients with pre-existing diabetes.”
For its study, the MGH team looked at 594 individuals who exhibited signs of diabetes mellitus when admitted to MGH at the height of the pandemic in the spring of 2020. Of that group, 78 had no known diagnosis of diabetes prior to admission. Researchers learned that many of these newly diagnosed patients — versus those with pre-existing diabetes — had less severe blood sugar levels but more severe COVID-19. Follow-up with this cohort after hospital discharge revealed that roughly half its members reverted to normal blood sugar levels and that only eight percent required insulin after one year.
“This suggests to us that newly diagnosed diabetes may be a transitory condition related to the acute stress of COVID-19 infection,” explains Cromer. Indeed, this key finding supports the clinical argument that newly diagnosed diabetes is likely caused by insulin resistance — the inability of cells to properly absorb blood sugar in response to insulin, resulting in higher-than- normal build-up of glucose in the blood — rather than by insulin deficiency, caused by direct and permanent injury to the beta cells which manufacture insulin.
“Our results suggest that acute insulin resistance is the major mechanism underlying newly diagnosed diabetes in most patients with COVID-19, and that insulin deficiency, if it occurs at all, is generally not permanent,” says Cromer. “These patients may only need insulin or other medications for a short time, and it’s therefore critical that physicians closely follow them to see if and when their conditions improve.”
Cromer is an instructor in Medicine at Harvard Medical School (HMS). Senior author Deborah Wexler, MD, is an associate professor of Medicine at HMS, associate clinical chief of the MGH Diabetes Unit, and clinical director of the MGH Diabetes Center. Co-author Melissa Putman, MD, is assistant professor of Pediatrics at HMS and an attending physician in Endocrinology at MGH.
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Though the risk to humans is low, scientists warn that outbreaks among farmed birds increase the potential for the virus to mutate and pose a threat to humans.A highly contagious and deadly form of avian influenza has been barreling across the eastern half of the United States in recent weeks, killing both wild birds and farmed poultry and raising fears that an unchecked outbreak could prove calamitous for an industry that was devastated by a similar virus seven years ago.Since early January, when it began killing chickens in northeast Canada, the virus has been identified in migratory waterfowl from Florida to Maine, and has infected backyard chickens in Virginia and New York and sickened thousands of turkeys in Kentucky and Indiana, prompting mass cullings and import bans.On Wednesday, federal officials announced that the virus, a so-called highly pathogenic avian influenza, had been found in a Delaware commercial chicken farm on the Delmarva Peninsula, home to one of the country’s largest concentrations of poultry farms.Experts suspect wild birds returning from winter feeding grounds are spreading the virus, most likely through contaminated droppings. With the peak springtime migration still weeks away, many fear the worst is yet to come.“It’s very concerning given how quickly this thing is accelerating,” said Henry Niman, a biochemist in Pittsburgh who studies the genetic evolution of viruses and has been tracking the outbreak’s spread across the country. “I think we could see historic levels of infections.”Federal officials have been urging poultry growers to report sick or dying birds and to tighten their farms’ biosecurity measures, which includes preventing contact between wild birds and domestic animals.“It’s important to note that avian influenza is not considered to be a risk to public health and it’s not a food-safety risk,” Mike Stepien, a spokesman for the Department of Agriculture’s Animal and Plant Health Inspection Service, said in an email.Although the danger to humans is low, scientists are keeping a close eye on the virus, the Eurasian H5N1, which is closely related to an Asian strain that has infected hundreds of people since 2003, mostly those who had worked with infected poultry. That virus does not spread efficiently among humans, but it is extremely deadly, with a fatality rate of 60 percent, according to the Centers for Disease Control and Prevention.The strain currently spreading across the United States has not jumped to humans, but virologists and epidemiologists say the mounting infections among birds is worrisome because it increases the possibility that the virus could mutate in ways that make it more infectious to people.Dr. Gail Hansen, a public health veterinarian who is the former state epidemiologist for Kansas, noted that influenza viruses have historically been behind the pandemics that affect humans. Some medical historians have traced the deadly influenza pandemic of 1918 to Army recruits in Kansas who may have caught the pathogen from farm animals and then spread it to military camps in Europe.“Scientists always assumed the next pandemic would be a respiratory influenza,” she said. “We were wrong with Covid, but it’s these kinds of viruses that keep us awake at night.”Young turkeys at an Iowa barn in 2015, after a devastating avian influenza outbreak that year. The avian flu circulating now has sickened thousands of turkeys in Kentucky and Indiana.Charlie Neibergall/Associated PressThe virus has also been coursing through Asia, the Middle East and Europe. In recent weeks, 300 outbreaks have been reported in 29 European countries. In Israel, an outbreak at a nature reserve killed thousands of cranes.At the moment turkey farmers, especially those in Indiana and Kentucky, are most worried. Over the past two weeks, several farms in those states have been shuttered after officials discovered the virus among birds that spend their entire lives crammed into massive sheds. Farmers say they have been stunned by how efficiently the virus kills, with animals dying hours after the initial infection.In Indiana, state officials have moved quickly, euthanizing more than 100,000 birds and throwing a six-mile cordon around affected farms — a containment area within which exports are halted and birds are tested daily.“Everyone is on super-high alert and trying to be as prepared as possible because we all remember the devastation of 2014 and 2015,” said Dr. Denise Heard, a veterinarian with the U.S. Poultry & Egg Association.The 2014-15 outbreak is considered the most destructive in the nation’s history. It sent poultry and egg prices soaring and cost the industry more than $3 billion — though the federal government compensated farmers for lost flocks. In the end, nearly 50 million birds were killed by the virus or destroyed to prevent its spread, a vast majority of them in Iowa and Minnesota.John Burkel, 54, a fourth-generation turkey grower in northern Minnesota, has been watching the spread with trepidation. In 2015, the virus tore through his farm in a matter of days, leaving just 70 survivors in a shed that had held 7,000 birds. The weeks that followed were spent culling, composting the dead and then repeatedly disinfecting the barns.As a precaution, health officials also advised that he and his son take a course of the antiviral drug Tamiflu. “We’ve never seen a virus that virulent,” said Mr. Burkel, a state legislator who works the farm with his wife and two children. “It was just horrible.”Since then, agriculture officials across the country have pushed farmers to embrace an array of biosecurity measures aimed at preventing outbreaks. They include sealing up tiny holes that might allow mice or sparrows to enter barns, disinfecting the tires of feed-delivery trucks before they enter a farm and creating “clean” and “dirty” zones where workers can change into fresh footwear and coveralls before stepping inside an animal containment shed.At the same time, experts say that federal officials have strengthened the nationwide system of surveillance that allows researchers to track, in almost real time, an avian flu’s spread within wild bird populations. “I think the crisis of 2015 made us realize it takes a village to prevent an outbreak and has left us much better prepared,” said Dr. Yuko Sato, a poultry veterinarian at Iowa State University who advises local farmers about improving their biosecurity practices.But hypervigilance has its limits, especially against a microscopic pathogen that can infiltrate a barn on the leg of a single housefly. For a growing number of scientists, the real threat is the nation’s industrialized system of meat and dairy production, with its reliance on genetically identical creatures packed by the thousands inside huge confinement sheds.Nearly all the nine billion chickens raised and slaughtered in the United States each year can trace their lineage to a handful of breeds that have been manipulated to favor fast growth and plump breasts. The birds are also exceptionally vulnerable to outbreaks of disease. “They all have the same immune system, or lack of an immune system, so once a virus gets inside a barn, it’s going to spread like wildfire,” said Dr. Hansen, the public health veterinarian.Andrew deCoriolis, the executive director of Farm Forward, a sustainable agriculture advocacy group, said the lack of genetic diversity isn’t just a threat to the nation’s food supply; it is also a potential threat to public health. More than half the 22 strains of novel influenza virus that the C.D.C. has identified as “of special concern” to human health are avian influenza viruses, he said, noting that a 2018 study examining the emergence of 39 highly pathogenic avian viruses found that all two of them had emerged on industrial poultry farms.He said the sector’s emphasis on biosecurity and infection containment obscures a larger, thornier issue that requires a fundamental rethinking of meat and egg production in the United States.“Instead of asking how factory farms can prevent infections that originate in the environment, which is how they frame it now, we should be asking how they can prevent infections that originate on factory farms,” he said. “If we keep raising more and more animals in these conditions, we should expect the exact outcome we’re getting because that’s how the system is set up.”

An anti-tumor drug promotes weight loss in mice at low doses by activating a natural hunger-suppressing pathway, according to a new study publishing Feb. 24 in the open-access journal PLOS Biology by Jiang Wei Wu and colleagues at Northwest A&F University in Shaanxi, China. The results provide a promising new avenue for development of anti-obesity treatments.
Growth differentiation factor 15 (GDF15) is a hormone that circulates in response to a wide variety of stimuli, including stress. Previous work has shown that elevation of GDF15 leads to a drop in body weight, while suppression of it leads to obesity.
To search for drugs that could increase GDF15 production, the authors turned to the “Connectivity Map,” a database of gene expression profiles of human cells in response to drug exposure. They found that cells exposed to a drug called camptothecin increased their expression of GDF15. Camptothecin is derived from the Asian tree Camptotheca acuminata, and is a known inhibitor of a DNA repair enzyme (hence its use as an anti-tumor drug).
In obese mice, the authors showed that oral administration of camptothecin rapidly elevated the level of GDF15 in the blood, and over the course of 30 days, reduced food intake by about 12% and body weight by about 11%. In contrast, in lean mice, camptothecin did not elevate GDF15 and there was no effect on either food intake or body weight.
Camptothecin’s effect was specific to GDF15, and GDF15 exerted its effect through its receptor, called GFRAL, the team showed, since an antibody against GDF15 prevented the weight loss, as did knocking down GFRAL expression.
Camptothecin has been studied in anti-cancer trials, but was ultimately set aside due to safety concerns. Its safety as an anti-obesity drug has yet to be determined, Wu said, but noted that the dose used in this study, if scaled up to a human, would be about one-thirtieth of the lowest dose used in human anti-cancer trials. Additionally, the anti-obesity mechanism appears to be separate from the anti-cancer mechanism, which involves blocking the function of the DNA-repair enzyme topoisomerase, and to function at a much lower drug concentration.
“We believe our results convincingly argue that camptothecin may have therapeutic benefits for obesity and its associated metabolic disorders,” Wu says. “Further study is needed to evaluate its efficacy and safety in advanced models to increase the translational impact.”
Wu adds, “In this study, by using in silico drug-screening approach, we discovered that Camptothecin (CPT), a previously identified anti-tumor drug by the US National Cancer Institute, is a GDF15 inducer. CPT elevates circulating GDF15 via activation of hepatic ISR pathway, this activates the GDF15 receptor GFRAL in the hindbrain AP, which subsequently suppresses food intake and reduces body weight in obese mice.”
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Scintillators are materials that emit light when bombarded with high-energy particles or X-rays. In medical or dental X-ray systems, they convert incoming X-ray radiation into visible light that can then be captured using film or photosensors. They’re also used for night-vision systems and for research, such as in particle detectors or electron microscopes.
Researchers at MIT have now shown how one could improve the efficiency of scintillators by at least tenfold, and perhaps even a hundredfold, by changing the material’s surface to create certain nanoscale configurations, such as arrays of wave-like ridges. While past attempts to develop more efficient scintillators have focused on finding new materials, the new approach could in principle work with any of the existing materials.
Though it will require more time and effort to integrate their scintillators into existing X-ray machines, the team believes that this method might lead to improvements in medical diagnostic X-rays or CT scans, to reduce dose exposure and improve image quality. In other applications, such as X-ray inspection of manufactured parts for quality control, the new scintillators could enable inspections with higher accuracy or at faster speeds.
The findings are described in the journal Science, in a paper by MIT doctoral students Charles Roques-Carmes and Nicholas Rivera; MIT professors Marin Soljacic, Steven Johnson, and John Joannopoulos; and 10 others.
While scintillators have been in use for some 70 years, much of the research in the field has focused on developing new materials that produce brighter or faster light emissions. The new approach instead applies advances in nanotechnology to existing materials. By creating patterns in scintillator materials at a length scale comparable to the wavelengths of the light being emitted, the team found that it was possible to dramatically change the material’s optical properties.
To make what they coined “nanophotonic scintillators,” Roques-Carmes says, “you can directly make patterns inside the scintillators, or you can glue on another material that would have holes on the nanoscale. The specifics depend on the exact structure and material.” For this research, the team took a scintillator and made holes spaced apart by roughly one optical wavelength, or about 500 nanometers (billionths of a meter).

Chemists at MIT have developed a novel way to synthesize himastatin, a natural compound that has shown potential as an antibiotic.
Using their new synthesis, the researchers were able not only to produce himastatin but also to generate variants of the molecule, some of which also showed antimicrobial activity. They also discovered that the compound appears to kill bacteria by disrupting their cell membranes. The researchers now hope to design other molecules that could have even stronger antibiotic activity.
“What we want to do right now is learn the molecular details about how it works, so we can design structural motifs that could better support that mechanism of action. A lot of our effort right now is to learn more about the physicochemical properties of this molecule and how it interacts with the membrane,” says Mohammad Movassaghi, an MIT professor of chemistry and one of the senior authors of the study.
Brad Pentelute, an MIT professor of chemistry, is also a senior author of the study, which appears today in Science. MIT graduate student Kyan D’Angelo is the lead author of the study, and graduate student Carly Schissel is also an author.
Mimicking nature
Himastatin, which is produced by a species of soil bacteria, was first discovered in the 1990s. In animal studies, it was found to have anticancer activity, but the required doses had toxic side effects. The compound also showed potential antimicrobial activity, but that potential hasn’t been explored in detail, Movassaghi says.