Publisher Health

New research associates the presence of Caudovirales in gut microbiota to an improvement in cognitive functions and memory in humans, mice and flies. The article, published in the journal Cell Host & Microbe, was led by Dr. Jordi Mayneris-Perxachs and Dr. José Manuel Fernández-Real, of the Nutrition, Eumetabolism and Health group of the Girona Biomedical Research Institute (IDIBGI) Dr. Josep Trueta and CIBEROBN, and has been carried out in collaboration with the Neuropharmacology research group led by Dr. Rafael Maldonado of Pompeu Fabra University and attached to the Hospital del Mar Medical Research Institute (IMIM); the FISABIO Foundation, the University of Valencia (UV) and the University of Alicante (UA). The results show that bacteriophages present in the gut microbiota influence the relationship between the microbiome and the brain.
In a sample of 114 people, which was later expanded to 942 subjects (participants in the IDIBGI’s Ageing Imagenoma Project), the researchers found that “individuals with more Caudovirales performed better at executive processes and verbal memory, while the presence of higher levels of Microviridae, on the other hand, was associated with a greater deterioration in the brain’s executive abilities,” states Dr. Fernández-Real, head of the Nutrition, Eumetabolism and Health group of the IDIBGI and CIBEROBN, who is also Head of the Endocrinology Section at Hospital Dr. Josep Trueta in Girona and director of the Department of Medical Sciences at the University of Girona.
Dairy products, a possible means of acquiring Caudovirales
Bacteriophages, a type of virus that replicates within bacteria, represent one of the largest gaps in the knowledge of the human microbiome. This research has focused on the study of two types of bacteriophages that are prevalent in our gut microbiota: Caudovirales and Microviridae.
To find out how people can access these viruses, the researchers conducted food surveys on the participants to find out about their diet. Interestingly, individuals who had more Caudovirales in their gut microbiota consumed more dairy products on a regular basis. This finding is supported by the scientific literature in this area: some previous research indicated that people who ate more dairy produce had better cognitive functions.
In order to further reinforce the result, an experiment was performed in mice, using the microbiota present in the different samples of human faeces, transplanting it into the intestine of the rodents. “Mice that received a microbiota rich in Caudovirales performed better cognitively than other mice, with significant improvements in spatial memory and emotional memory,” asserts Dr. Rafael Maldonado.
A second confirmatory experiment was conducted in fruit flies (Drosophila melanogaster) as an animal model. First, one group of flies was fed whey powder, and it was seen to have greater memory capacity than the other group of Drosophila that ingested sterilized, therefore virus-free, whey powder. The experiment was repeated, but in this case the feeding of the flies was supplemented with isolated bacteriophages. The results were replicated again. Observing a group of genes in the fly’s brain, the authors found that the presence of Caudovirales upregulated the genes associated with memory.
The results of this study reinforce the consideration of bacteriophage viruses as influential actors in the relationship between the human microbiome and the brain. In addition, the work opens the way to new lines of research, such as the study of possible dietary supplements with this virus in isolation to improve people’s cognitive abilities.
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Materials provided by Universitat Pompeu Fabra – Barcelona. Note: Content may be edited for style and length.

The next generation of mosquito control might target the pests’ reproductive genes.
Researchers at the University of Cincinnati examined genetic material of three species of mosquito responsible for killing millions of people around the world each year. In a collaboration between UC’s chemistry and biology departments, researchers revealed the surprising genetic modifications female mosquitoes undergo, in part to create the next generation.
Using tools called liquid chromatography-tandem mass spectrometry, researchers found as many as 33 genetic modifications in the transfer RNA of female mosquitoes. Like DNA, transfer RNA serves as the building blocks of life, communicating the genetic code from DNA to build new proteins that regulate the body’s tissues and organs.
“That’s important because it means there are different requirements for making proteins in males and females,” said Melissa Kelley, lead author and a postdoctoral researcher in UC’s College of Arts and Sciences.
“Proteins do a bunch of things: they do the housekeeping needed to keep an organism alive. And there are specialized ones that are created like when females are getting ready to lay eggs,” Kelley said.
By better understanding these modifications at the molecular level, scientists might be able to find a new weapon to control mosquito populations.

Physical distancing policies and particularly stay-at-home work mandates have proven highly effective at slowing the spread of the COVID-19 virus. But these measures have had numerous unwanted consequences, including dramatic reductions in economic productivity. Are there alternative methods that have the potential to simultaneously contain pandemic spread while also minimizing negative economic effects? Researchers at the Max Planck Institute for Human Development examined this question using data and methods commonly excluded from pandemic-control policy design. Their findings were published in Scientific Reports.
Throughout the COVID-19 pandemic, the chief non-pharmaceutical intervention has been physical distancing, including widespread closure of shared workspaces and a concomitant shift to remote work where possible. These measures are not only disruptive to workers, workplaces and economies, but also likely to cause long-term shifts in working patterns. Their economic costs have been significant, including losses in working hours and a drop in global Gross domestic product (GDP), the full magnitude of which will not be known until the pandemic is over.
Researchers at the Max Planck Institute for Human Development investigated the efficacy of various pandemic containment measures through data-based simulations. By focusing on occupational interventions, and using detailed data on the distribution of the workforce across occupations, wage and workplace proximity, they were able to model the economic impact of particular containment strategies alongside each intervention’s epidemiological impact.
“We conducted simulations of how diseases such as COVID-19 spread primarily through a workforce, rather than just through an indistinguishable population of people, which is a simplification that people often make,” explains Alex Rutherford, senior research scientist and principal investigator at the Center for Humans and Machines at the Max Planck Institute for Human Development and co-lead author of the study. “We saw that the nature of one’s job had strongly affected the outcome of the pandemic.”
The team used public data on jobs to assign a ‘proximity score’ to each occupation. This reflected how many people a given worker was likely to be in contact with. From this they built a ‘contact network’ showing how an infectious disease such as COVID-19 spreads from person to person.
The data was from New York City, treated as a paradigmatic urban setting, and include both occupational information and data from public databases, such as the “Occupational Information Network” (O*NET), which collects occupational data and statistical and economic information from the United States. Such categories of data rarely figure in the design of pandemic control policies. Using data on salaries, the number of people doing each job in NYC and whether they can work from home, the team measured the social and economic effects an epidemic has specifically due to the actions taken to try to stop it. The social effects are based on how many people get infected and the economic costs are based on how many people are furloughed and have their salary covered because they can’t work from home.
The researchers compared how effective various contact reduction interventions were on lessening the impact of the epidemic; socially and economically. These ranged from no intervention to very complex measures based on the structure of the contact network of the respective professional group.
“Our findings demonstrate that the structure of the contact network heavily influences disease dynamics in non-trivial ways,” explains Demetris Avraam, first author of the study and postdoctoral researcher at the Center for Humans and Machines at the Max-Planck-Institute for Human Development. For example, furloughing a small proportion of workers can lead to pruning of the network in such a way that the epidemic persists for a long time, albeit at low levels, leading to a long and costly furlough. Intuitive strategies such as furloughing workers based on the essentialness of their job, by wage or at random all perform poorly on this basis. In contrast, network-based metrics such as degree and centrality are able to reduce the peak of the infection (flattening the curve) and also reduce the epidemic duration.
The researchers found that the basic strategy of worker removal according to the number of close personal contacts that worker has, performs approximately the same as more complex metrics based on complete network structure or other occupational characteristics.
“In practice, the number of contacts could be estimated simply using a smartphone app that estimates Bluetooth proximity to other terminals without tracking IDs,” says study co-lead author Manuel Cebrian, Leader of the Digital Mobilization Group at the Center for Humans and Machines at the Max Planck Institute for Human Development. His research has included how smartphone data and tracing apps can be used for pandemic response.
The COVID-19 pandemic has caused many profound societal changes that are unlikely to be reversed even once the disease abates. This includes vast changes in demand across sectors, the large-scale adoption of remote working and challenging deeply ingrained understandings of workplaces. This has also implications for future automation of jobs. Automation processes are increasingly used in occupations with a high degree of contact with others. For example, online consultations with doctors or online trainings in sports and education are on the rise.

Barbara Han, a disease ecologist at the Cary Institute of Ecosystem Studies, knew it was a question of when, not if, the coronavirus would spread to animals. As the first reports of infected animals appeared in 2020, she began working on an artificial intelligence model that would predict which creatures might be next.“We had a pretty lofty goal of being able to predict exactly which species we should be keeping an eye on, given that we think it’s going to spill back,” Dr. Han said. As her team worked, the trickle of cases in new species became a flood: cats and dogs in homes and mink on farms. The virus infiltrated zoos, infecting the usual suspects (tigers and lions) as well as more surprising species (the coatimundi, which is native to the Americas and resembles a raccoon crossed with a lemur, and the binturong, which is native to Southeast Asia and resembles a raccoon crossed with an elderly man).Dr. Han and her colleagues ultimately identified 540 mammalian species that were most likely to host and spread the coronavirus. She had been especially worried that the red fox, which ranked high on her list of at-risk creatures, and is widespread in Europe and North America, would be susceptible to the virus. “We’re just waiting for somebody to report it,” she said.Just days earlier, in fact, researchers in Colorado had announced that the virus had proved capable of infecting red foxes in the lab. “Oh no!” Dr. Han exclaimed when informed of the finding. “It really sucks to be right in my line of work.”Last fall, scientists analyzing tissue samples from dead white-tailed deer in Iowa found that the virus was widespread in that species. The discovery intensified concerns that the virus might establish itself in an animal reservoir, mutate and spread to other species, including back to humans. It also opened a rabbit hole: If deer can silently spread the coronavirus, what else could? And what else will?Experts say there is no need to panic, and emphasize that animals are not to blame. “Really, humans are infecting the animals, and now animals are sick and some of them are dying,” Dr. Han said.But identifying the species at risk is crucial for protecting both human and animal health. It is also a formidable scientific problem, with a wide array of potentially vulnerable species. Scientists must analyze a constant, chaotic stream of computational predictions, laboratory data and confirmed infections in zoos, homes and the wild.In an ideal world, scientists would monitor every potentially susceptible population. But in the real one, they are trying to strike a delicate balance between identifying the species of highest concern and casting a wide net as the virus mutates and variants emerge. “It wouldn’t surprise me if you would find an animal species or an animal reservoir that nobody has thought about,” Dr. Diego Diel, a virologist at Cornell University, said.The basics of infectionScientists use a variety of tools to identify susceptible species. Each approach has limitations, but together they paint a fuller picture of which animals are at risk.Some research teams are focusing on the ACE2 receptor, a protein found on the surface of the cells of many species. The coronavirus’s spiky protrusions allow it to bind to these receptors, like a key in a lock, and enter cells.In 2020, a group of scientists compared the ACE2 receptors of hundreds of vertebrates, mostly mammals, with those of humans to determine which species the virus might infect. (The ACE2 receptors of birds, reptiles, fish and amphibians are not similar enough to ours to raise concern.)“The predictions have been very good so far,” Harris A. Lewin, a biologist at the University of California, Davis, and an author of the study, said in an email. The scientists predicted, for instance, that white-tailed deer were at high risk for infection.But some predictions proved entirely wrong: The paper identified farmed mink as a species of “very low” concern — and then in April 2020 the virus raged through mink farms.Indeed, ACE2 offers only a snapshot of susceptibility. “Viral infection and immunity is much more complex than just a virus binding to a cell,” Kaitlin Sawatzki, a virologist at Tufts University, said in an email.And of the world’s nearly 6,000 mammalian species, scientists have sequenced the ACE2 receptors of just a few hundred of them, creating a biased data set. These sequenced species include model organisms used in experiments, species that carry other diseases, and charismatic zoo denizens, not necessarily the animals that people are most likely to encounter.“If a pandemic were to have arisen from a squirrel, we would be like, ‘God, what’s wrong with us? We didn’t even measure the basic biology of a squirrel,’” Dr. Han said. So scientists have to find creative ways to make predictions for animals whose ACE2 sequences remain unknown. ACE2 sequences play a crucial role in basic biological functions, such as regulating blood pressure. By collecting a species’ basic life history details — such as what it eats and whether it is nocturnal — Dr. Han’s team trained a machine learning algorithm to identify those that appeared likely to bind to and transmit the virus, allowing them to predict susceptibility across many more mammals.Scientists can test these computational predictions in the lab by trying to infect animal cells or live animals with the virus. Such experiments can differentiate species that may seem similar; one study found that deer mice could be infected with — and shed — the original version of the virus, while house mice could not.But what happens in a collection of cells does not always occur in real animals, and what happens in a lab, where animals typically receive high doses of the virus, may not reflect real life. For instance, although the original virus can replicate in pig cell lines, actual pigs do not appear to be highly susceptible, researchers found.To learn whether animals have been infected by the virus in the real world, scientists can perform what are known as serology studies, looking for coronavirus antibodies in their blood. “Serology helps us to look at the historical exposure,” Dr. Suresh Kuchipudi, a veterinary microbiologist at Penn State, said.The discovery of widespread antibodies in white-tailed deer set off scientific alarm bells because it indicated that many of the animals had already been infected by the virus. It prompted researchers to look for active infections in the cervids, which they soon found.But sampling and swabbing free-ranging animals can be difficult and time-consuming. So the U.S. Department of Agriculture, which received $300 million under the American Rescue Plan to conduct disease surveillance in animals, is now asking zoos, aquariums and wildlife facilities to send in blood samples, which will be analyzed for coronavirus antibodies.And researchers at Tufts, including Dr. Sawatzki, have enlisted wildlife rehabilitation specialists to swab an eclectic collection of creatures, including black bears, bobcats and hundreds of bats. (Bat rehabilitators often submit guano samples instead of oral swabs, which can be difficult to obtain from the animals. “They have very tiny little mouths,” Dr. Sawatzki said.) So far, all have been negative.Bats have been a source of concern because they are reservoirs for other coronaviruses, and many scientists believe that SARS-CoV-2 initially emerged from bats. But bat species are incredibly diverse, and not all of them appear to be susceptible to the virus — a reminder that animals of highest concern may not be intuitive, scientists said.Complicating matters, the virus is not static, and animals that resisted infection with past variants might be vulnerable to new ones. For example, lab mice that were not susceptible to the original coronavirus or to the Delta variant were susceptible to Beta and Gamma.“That’s the problem with emerging diseases,” said Dr. Scott Weese, an infectious diseases veterinarian at the University of Guelph in Ontario. “You have to keep resetting your knowledge every time something changes,” he added.Marine BuffardA shortlist of speciesBiological susceptibility is just one piece of the puzzle; whether or not a species becomes a reservoir depends on a constellation of factors. “It depends on their social behavior, the immune response that’s mounted by the animals, the population size, the kind of connection with different populations of animals,” said Dr. Keith Hamilton, head of the preparedness and resilience department at the World Organization for Animal Health.For a virus that is overwhelmingly transmitted by humans, a species’s relationship with us matters tremendously. Although narwhals’ ACE2 receptors technically place them at “high risk” for infection, they are not likely to run into us. Still, risk isn’t zero for marine mammals, especially captive ones: In 2006, a human likely transmitted MRSA to a bottlenose dolphin in a marine park in North America.And the risk to pets is manifest.“We’ve heard stories of dogs getting infected from people sharing food and letting them lick off their plates when they were sick,” said Dr. Casey Barton Behravesh, who directs the One Health Office at the Centers for Disease Control and Prevention, which created a national repository for data on coronavirus cases in animals. “Or even drinking out of toilets.”Pet dogs, cats and hamsters can all be infected by the virus. Hamsters in a Hong Kong pet store most likely infected two people, leading to a contentious hamster cull.But we are far more likely to infect our pets than they are to infect us, and many of these infections will be dead ends, scientists predicted. Infectious pets can also be isolated. “Your hamster at home that you may have bought some time ago is not a high risk to you,” Dr. Hamilton said.A larger concern, scientists said, are the “peridomestic” species that live alongside us but roam freely; in North America, these include deer mice, red foxes and feral cats. These animals may act as a bridge between humans and wild populations, spreading the virus to species we may not encounter. And rodents, which are reservoirs for other pathogens, “should be definitely on the top of the list,” Dr. Kuchipudi said.To monitor this potential threat, officials from the U.S.D.A. and other agencies are looking for signs of the virus in some of these animals — including rodents, skunks, foxes and opossums — that live in and around zoos, wildlife facilities and mink farms.Globally, certain threatened species are also a top concern. Three snow leopards in a Nebraska zoo died after contracting the coronavirus, and a wild leopard cub in India was found to be infected.And great apes, which frequently encounter tourists and researchers, are vulnerable to other respiratory viruses. “Great apes are uniquely susceptible to human pathogens, because we’re closely genetically related,” said Dr. Kirsten Gilardi, a wildlife veterinarian at the University of California, Davis.So far, no coronavirus infections have been reported in wild apes, but researchers are monitoring the animals closely, collecting fecal samples from those with respiratory illnesses.‘A long game’Animal surveillance is “a long-game question,” said Dr. Andrew Bowman, a veterinary epidemiologist at Ohio State University. “How do we get ahead of the virus and try to understand what might be coming down the line, potentially years from now?”To keep tabs on mutations in animals, and whether they are transmitted across species, federal researchers are conducting genomic surveillance, comparing virus samples from infected animals with those from humans in close contact with them.Some researchers are analyzing potential variants. Dr. Kuchipudi and his colleagues created a computational model that virtually generates novel patterns of mutations and then assesses whether they might make the virus more likely to infect, say, cows. Scientists can then watch for those mutations in databases — and observe cattle more closely if the sequences appear. ​​“This will give us a way to make sense of the sequencing data and proactively screen,” Dr. Kuchipudi said.Scientists also worry about the longer-term threat of viral recombination, in which an animal is simultaneously infected by two coronaviruses that swap genetic material, generating a new virus. Researchers at the University of Liverpool created a model predicting potential hosts in which coronaviruses, including SARS-CoV-2, could recombine.Staying ahead of the virus will require long-term funding and commitment. But scientists say making these investments now could result in better systems for monitoring pathogens in other species and an expanded understanding of how animal health is linked to ours. It may even help experts catch the next looming health threat before it spills over from animals.“There’s no harm in understanding better the world around us,” Dr. Han said. “There can only be harm in not understanding and not investing in that knowledge, which is really obvious now.”

Researchers and clinicians have been working to use focused ultrasound combined with microbubbles to open the blood-brain barrier (BBB) for both noninvasive diagnostic use as well as to deliver treatments to the brain for tumors and neurodegenerative diseases. However, the few existing devices for preclinical research are expensive, bulky and lack the precision needed for small animal research.
Hong Chen, associate professor of biomedical engineering at the McKelvey School of Engineering and of radiation oncology at the School of Medicine at Washington University in St. Louis, and her team have developed a low-cost, easy-to-use and highly precise focused ultrasound (FUS) device that can be used on small animal models in preclinical research.
The FUS transducer, created in-house using a 3D printer, costs about $80 to fabricate. It can be integrated with a commercially available stereotactic frame to precisely target a mouse brain. Results of the work were published online in IEEE Transactions on Biomedical Engineering Feb. 15
The device had several benefits, Chen said, including achieving sub-millimeter targeting accuracy and having a tunable drug-delivery outcome. In addition, using higher frequency FUS transducers decreased the BBB opening volume and improved the precision of FUS-BBB opening in targeting individual structures in the mouse brain.
“We showed that under the same pressure level, a higher-frequency FUS transducer achieved a small drug delivery volume, improving the spatial precision of BBB opening compared with what has been achieved with lower-frequency transducers,” Chen said.
To create the transducer, the team only needed to connect wires to the electrodes on the elements. The rest of the parts were made on a 3D printer. With the use of a stereotactic frame, her team was able to target the exact location they wanted in the brain, which eliminated one of the barriers to more widespread use of the FUS technique. Chen’s team has made the design available on Github.
“We expect this device could be manufactured by research groups without ultrasound background and used in various applications in preclinical research with minimal training needed,” Chen said.
The team used contrast-enhanced MRI to measure the BBB opening volume at different acoustic pressures and evaluated the drug delivery outcome using a model drug. The device was shown to be very safe, with a microhemorrhage found in two mice at the highest tested acoustic pressures and no tissue damage found in other groups.
Focused ultrasound uses ultrasonic energy to target tumors or tissue in the brain. Once located, the researchers inject microbubbles into the blood that travel to the targeted tissue then pop, causing small tears of the blood-brain barrier. The ruptures allow drugs to be delivered or biomarkers from a tumor to pass through the blood-brain barrier and release into the blood. Chen and her lab have been perfecting the technique in preclinical models for the past several years.
Chen said she hopes this device can reduce the barriers to the adoption of the FUS technique by the broad research community.
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Materials provided by Washington University in St. Louis. Original written by Beth Miller. Note: Content may be edited for style and length.

Tendons are tissues that connect muscles to bones and are important for movement and locomotion. Injuries to tendons are quite common, with millions of people — particularly athletes — affected worldwide, and can often take many months to recover from, significantly impacting quality of life. Furthermore, while many options for treatment exist, none of them are perfect cures and many result in pain, immunogenicity, or long-term treatment failure. Therefore, a novel therapeutic strategy for tendon repair is needed.
In a study published in the Journal of Tissue Engineering in January 2022, researchers from Tokyo Medical and Dental University (TMDU) have successfully induced human stem cells to create artificial tendon-like tissue that mimics tendon properties and offers significantly improved tendon reconstruction in a mouse tendon-rupture model.
Human induced pluripotent stem cells, or hiPSCs, are special stem cells that can be derived from any adult cells and can be differentiated into any specialized cell-type. “Using hiPSCs with Mohawk (Mkx), we could produce artificial tendon tissue.” explains Hiroki Tsutsumi, lead author of the study. Mohawk is a transcription factor that promotes the expression of genes involved in tendon-formation and thus drives differentiation of stem cells into tendon cells. These Mohawk-expressing stem cells were then put in a specialized 3D culture system that exerts mechanical force on the cells while they are growing. This simulates the conditions for tendon development and enhances the cell alignment and organization, allowing them to create tendon-like tissues.
Next, the research team tested the artificial tendon in a mouse model of tendon rupture. The results were exciting. Six weeks after the implantation, the artificial tendon had similar mechanical properties to a normal undamaged mouse tendon. In addition, the implanted tendon-like tissue was able to recruit and mobilize tendon cells from the host that can further participate in the repair process. This confirmed a good integration of the tissue.
“We demonstrated that the bio-tendons derived from human induced pluripotent stem cells have similar mechanical and biological properties to normal tendons and can be fully integrated relatively quickly after a transplant surgery in a mouse model, making them an attractive strategy for clinical application in tendon injuries. The next step towards clinical translation would be to test them in large animal models to assess their capacity as a biomaterial on a larger scale,” concludes Hiroshi Asahara, lead author of the study. These promising results suggest that a novel medical strategy for tendon repair may be clinically available in the future.
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The COVID-19 pandemic has presented both challenges and opportunities for medical training. Remote learning technology has become increasingly important in several fields. A new study finds that in a remote environment, an artificial intelligence (AI) tutoring system can outperform expert human instructors.
The Neurosurgical Simulation and Artificial Intelligence Learning Centre at The Neuro (Montreal Neurological Institute-Hospital) recruited seventy medical students to perform virtual brain tumour removals on a neurosurgical simulator. Students were randomly assigned to receive instruction and feedback by either an AI tutor or a remote expert instructor, with a third control group receiving no instruction.
An AI-powered tutor called the Virtual Operative Assistant (VOA) used a machine learning algorithm to teach safe and efficient surgical technique and provided personalized feedback, while a deep learning Intelligent Continuous Expertise Monitoring System (ICEMS) and a panel of experts assessed student performance.
In the other group, remote instructors watched a live feed of the surgical simulations and provided feedback based on the student’s performance.
The researchers found that students who received VOA instruction and feedback learned surgical skills 2.6 times faster and achieved 36 per cent better performance compared to those who received instruction and feedback from remote instructors. And while researchers expected students instructed by VOA to experience greater stress and negative emotion, they found no significant difference between the two groups.
Surgical skill plays an important role in patient outcomes both during and after brain surgery. VOA may be an effective way to increase neurosurgeon performance, improving patient safety while reducing the burden on human instructors.
“Artificially intelligent tutors like the VOA may become a valuable tool in the training of the next generation of neurosurgeons,” says Dr. Rolando Del Maestro, the study’s senior author. “The VOA significantly improved expertise while fostering an excellent learning environment. Ongoing studies are assessing how in-person instructors and AI-powered intelligent tutors can most effectively be used together to improve the mastery of neurosurgical skills.”
“Intelligent tutoring systems can use a variety of simulation platforms to provide almost unlimited chances for repetitive practice without the constraints imposed by the availability of supervision,” says Ali Fazlollahi, the study’s first author. “With continued research, increased development, and dissemination of intelligent tutoring systems, we can be better prepared for ever-evolving future challenges.”
This study, published in the Journal of the American Medical Association (JAMA Network Open) on Feb. 22, 2022, was funded by the Franco Di Giovanni Foundation, the Royal College of Physicians and Surgeons of Canada, and the Brain Tumour Foundation of Canada Tumour Research Grant along with The Neuro. Cognitive assessment was led by Dr. Jason Harley at McGill University’s Department of Surgery.
The Neuro
The Neuro – The Montreal Neurological Institute-Hospital – is a bilingual, world-leading destination for brain research and advanced patient care. Since its founding in 1934 by renowned neurosurgeon Dr. Wilder Penfield, The Neuro has grown to be the largest specialized neuroscience research and clinical center in Canada, and one of the largest in the world. The seamless integration of research, patient care, and training of the world’s top minds make The Neuro uniquely positioned to have a significant impact on the understanding and treatment of nervous system disorders. In 2016, The Neuro became the first institute in the world to fully embrace the Open Science philosophy, creating the Tanenbaum Open Science Institute. The Montreal Neurological Institute is a McGill University research and teaching institute. The Montreal Neurological Hospital is part of the Neuroscience Mission of the McGill University Health Centre. For more information, please visit www.theneuro.ca
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Leading health care organizations recommend exclusive breastfeeding for six months after birth, yet some mothers report stopping due to a perceived lack of milk supply. Penn State College of Medicine researchers found in a recent study that women who stopped breastfeeding because they believed they had inadequate milk supply — a condition called perceived inadequate milk supply (PIMS) — are more likely to have a specific mutation in a gene found in mammary tissue. These women were also more likely to have babies who gained less weight. The researchers said that screening for this mutation, when combined with maternal characteristics like age and body mass index, could be useful in identifying mothers at risk for stopping breastfeeding prematurely due to a perceived lack of milk supply.
“The World Health Organization, the American Academy of Pediatrics and the American College of Obstetricians and Gynecologists recommend exclusive breastfeeding for at least six months because it provides developing infants with optimum nutrition and is associated with improved health outcomes,” said Dr. Steven Hicks, lead researcher and pediatrician at Penn State Health Children’s Hospital. “While 83% of women initiate breastfeeding, only a reported 57% continue to six months. Socioeconomic and environmental factors may contribute to early cessation, but milk supply is also an often-cited reason. Identifying women who are more likely to have low milk supply could help get them resources to continue breastfeeding such as lactation consultation services.”
Previous research has linked maternal genetics with nutrients in breast milk, but few studies have explored how genetics may relate to supply. The researchers studied 18 genes highly expressed in mammary, or milk-producing, tissue in women. They looked for mutations in those genes to see whether mutations were associated with mothers’ perceived milk supply.
The study team followed 88 women between 19 and 42 years old for the first year of their baby’s life. The mothers completed surveys about their infant’s feeding habits at one, four, six and twelve months of age that asked questions about perceived milk supply, whether women supplemented their child’s diet with formula and reasons why they did so. Decreased or low milk production, signs of allergies from breastfeeding and other personal reasons such as work, day care or time constraints were included as possible reasons for why women began to supplement with formula. Mothers also provided a DNA sample by having saliva collected.
Using responses from the surveys, the researchers classified the mothers as having either PIMS or perceived adequate milk supply (PAMS). They found that the 45 mothers with PIMS were more likely to breastfeed for shorter periods, report lower milk supply and have infants who were not gaining adequate weight.
The researchers analyzed the mothers’ DNA samples and looked for mutations among 18 genes that are involved in the secretion of breast milk. Although modifications in 10 of the genes studied were found among some women, the team found that only one, a variant in the milk fat globule EGF and factor V/VIII domain containing gene (MFGE8), occurred more frequently in women with PIMS. Those without the mutation were more likely to have adequate milk supply and report a longer duration of breastfeeding.
Using statistical modeling, the researchers found that maternal characteristics like age, previous breastfeeding duration and body mass index alone could not differentiate between mothers with PIMS and PAMS. However, when adding in MFGE8 mutation status into the model, it strongly predicted which women reported adequate or inadequate milk supplies. The researchers published their results in the journal Breastfeeding Medicine.
“Identifying risk of PIMS at the outset of breastfeeding could provide opportunities for early, targeted interventions such as guidance from a trained lactation support professional,” Hicks said. He noted that current assessment of PIMS is guided by subjective reports and that counseling may help identify foods and medications that help or hinder milk production.
Hicks said that the study’s findings will need to be validated in a larger study that includes more mothers. He also said that more research is needed to uncover the biological processes that determine how this particular gene affects milk supply in moms in order to better understand its association with PIMS status.
“Moms with this mutation still produce milk, even if it may be less than women without the mutation, but challenges like poor diet, hydration or sleep could be enough to hinder the supply that they do have,” Hicks said. “Screening for this variant and combining that with maternal reports and characteristics could help identify moms and babies that may need additional support.”
Desirae Chandran, Alexandra Confair, Kaitlyn Warren and Yuka Imamura Kawasawa of Penn State College of Medicine also contributed to this research. 
This research was supported by the Gerber Foundation and the Center for Research on Women and Newborns. The research team also cites the use and support of the genome sciences facility of the Institute for Personalized Medicine at Penn State College of Medicine.
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Traces of the SARS-CoV-2 coronavirus that causes COVID-19 can be detected in microscopically small fluid droplets exhaled during a very short time span. This is the finding of a new study from the University of Gothenburg. The measurement was carried out primarily with an advanced research instrument developed by the publishing research team.
The findings have now been published in the journal Influenza and Other Respiratory Viruses. The measurements were made with the research instrument Particles in Exhaled Air (PExA), developed at Occupational and Environmental Medicine at Sahlgrenska Academy, and with a smaller handheld instrument called the Breath Explor (BE).
Infection spread with exhaled air is well known, but now the researchers show that a few breaths are sufficient for detecting traces of viruses in microscopically small fluid droplets (i.e. particles) exhaled from small airways, at least early in the course of COVID-19.
“We show that aerosol particles with the ribonucleic acid (RNA) virus can be found early in the course of COVID-19. The particles we can detect are very small-less than five micrometers in diameter-and we have here managed to capture particles with RNA virus in just a few breaths,” said Emilia Viklund, a doctoral student in occupational and environmental medicine and lead author of the study.
Affects in the small airways
Of course, this immediately leads to conjecture about possibly replacing unpleasant nasal swab tests with convenient and easy breath tests. However, according to Professor Anna-Carin Olin, the inventor of PExA, that would be extrapolating the findings too far.

As organisms grow, older cells can undergo a phenomenon called senescence. This process defines a cell state where cells permanently stop dividing but do not die. Senescent cells secrete toxic pro-inflammatory factors contributing to the development of many diseases.
Researchers from Boston University School of Medicine (BUSM) have shown that obesity in experimental models led to senescence of macrophages, an immune cell subtype within fat or adipose tissue.
According to the researchers, the fact that macrophages can become senescent is an unexpected finding. Many of the macrophages within obese tissue were senescent and those senescent cells may be a significant driver of fat tissue fibrosis. These findings suggest that obesity accelerates cellular or biological immune aging in fat.
“In healthy individuals, those cells contribute to cleaning the tissue from dead adipocytes (cells specialized for the storage of fat) and help in the cellular turnover. We demonstrated that macrophages lost this capacity when they become senescent,” explained first and co-corresponding author Nabil Rabhi, PhD, an instructor of biochemistry at BUSM.
The researchers also found that senescent macrophages secrete a variety of factors, one of which is a molecule called osteopontin which they found is responsible for adipose tissue fibrosis. “Our finding suggests that macrophages ages faster in obese animals. This accelerated senescence may contribute to the pathological thickness or fibrosis of fat tissue observed in obese individuals with type 2 diabetes,” said Rabhi. The researchers believe understanding new regulatory pathways that control adipose tissue responses to obesity may help identify new targets for obesity treatment. “Our finding indicates that targeting the senescent macrophages population or using osteopontin inhibition may represent a promising approach for obesity treatment and its adverse complication including type 2 diabetes,” added Rabhi.
Collaborators from BUSM included co-corresponding authors Matthew D. Layne, PhD, associate professor of biochemistry and assistant dean for research and Stephen R. Farmer, PhD, professor of biochemistry.
These findings appear online in the journal Life Science Alliance.
Funding for this study was provided by the National Institutes of Health/National Institute of Diabetes and Digestive and Kidney Diseases (DK117161 and DK117163 to SRF), the American Heart Association (AHA) fellowship (17POST33660875 to NR) and The Evans Center for Interdisciplinary Biomedical Research ARC on “Connecting Tissues and Investigators, Fibrosis in Pathology” at Boston University.
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Materials provided by Boston University School of Medicine. Note: Content may be edited for style and length.