Publisher Health

Nearly half of parents who relied on formula to feed their babies during the infant formula shortage last year resorted to potentially harmful feeding methods, according to a survey from researchers at the University of California, Davis. The study was published in the journal BMC Pediatrics.
In an online anonymous survey of U.S. parents, the number of individuals that used at least one unsafe feeding practice increased from 8% before the formula shortage to nearly 50% during the shortage. Unsafe practices included watering down formula, using expired or homemade formula, or using human milk from informal sharing.
The percentage of parents who shared human milk increased from 5% to 26%, and the percentage using watered-down formula increased from 2% to 29% during the shortage.
“These are alarming statistics. The infant formula shortage increased food insecurity and threatened the nutrition of millions of American infants,” said lead author Jennifer Smilowitz, a faculty affiliate with the UC Davis Department of Food Science and Technology. “Our survey found that parents were not offered many safe alternatives and resorted to unsafe methods in an attempt to feed their infants.”
The study also sought to understand what parents experienced during the crisis to find ways to prevent future infant feeding crises in the future.
Too few formula manufacturers, milk banks
In 2022, the U.S. had a severe shortage of infant formula due to a recall by Abbott Nutrition and the voluntary shutdown of its Michigan manufacturing plant. Abbott is the largest formula maker in the U.S. and provides over 40% of the country’s infant formula. This shortage was made worse by trade policies that made it harder to import formula. By the end of May 2022, some states had an out-of-stock rate as high as 90%.

The Special Supplemental Nutrition Program for Women, Infants, and Children, or WIC, serves more than 40% of U.S. infants and accounts for more than half of infant formula consumption. Abbott Nutrition had dominated most of the WIC contracts in the U.S.
“Ninety percent of the infant formula sold in the U.S. is sold by four companies,” Smilowitz said. “This has resulted in systemic failures that inequitably impact low-income communities.”
The survey found that parents also used pasteurized human donor milk from milk banks, an alternative and safe method. Smilowitz said that alternative is limited by the small number of milk banks in the U.S. and by the expense. Donor milk costs from $3 to $5 per ounce. During the shortage, parents who turned to milk banks increased from 2% to 26%.
Limited options for lower-income parents
Smilowitz said the study points to the need for policy changes within the regulatory and healthcare systems to provide families with clinical prenatal and postnatal lactation support, access to banked donor milk and access to more commercially available products.

Additionally, workplace policies need to change to support the needs of breastfeeding women. Inadequate family leave can result in earlier formula feeding. Some workplace policies don’t support the privacy and time needed for pumping. These policies disproportionately affect low-income parents.
“We should not forget what happened during this formula shortage,” Smilowitz said. “Another crisis is looming if healthcare, workplace and regulatory policies in the U.S. do not systemically change.”
Smilowitz said she hopes the infant formula shortage will not have health consequences for infants.
“We have this generation of children affected by the formula shortage and we won’t know for maybe a decade if there was an impact on brain development,” Smilowitz said. “We can only hope that the shortage resulted in only acute effects and that infants will be robust enough to overcome any potential long-term problems.”
Karina Cernioglo, a fourth-year medical student at UC Davis, co-authored the study. The funding for the study was supported by the 2020 UC Davis Chancellor’s Innovation Award.

Two to three weeks after conception, an embryo faces a critical point in its development. In the stage known as gastrulation, the transformation of embryonic cells into specialized cells begins. This initiates an explosion of cellular diversity in which the embryonic cells later become the precursors of future blood, tissue, muscle, and more types of cells, and the primitive body axes start to form. Studying this process in the human-specific context has posed significant challenges to biologists, but new research offers an unprecedented window into this point in time in human development.
A recent strategy to combat these challenges is to model embryo development using stem cell technologies, with many valuable approaches emerging from research groups across the globe. But embryos don’t grow in isolation and most previous developmental models have lacked crucial supporting tissues for embryonic growth. A groundbreaking model that includes both embryonic and extraembryonic components will allow researchers to study how these two parts interact around gastrulation stages — providing a unique look at the molecular and cellular processes that occur, and offering potential new insights into why pregnancies can fail as well as the origins of congenital disorders. The team, including Berna Sozen, PhD, and Zachary Smith, PhD, both assistant professors of genetics at Yale School of Medicine (YSM), published its findings in Nature on [tk].
“This work is extremely important as it provides an ethical approach to understand the earliest stages of human growth,” says Valentina Greco, PhD, the Carolyn Walch Slayman Professor of Genetics at YSM and incoming president-elect of the International Society for Stem Cell Research (ISSCR), who was not involved in the study. “This stem cell model provides an excellent alternative to start to understand aspects of our own early development that is normally hidden within the mother’s body.”
“The Sozen and Smith groups have achieved a milestone in developing in vitro models to study the earliest stages of human development that are unfeasible yet so important for understanding health and disease,” says Haifan Lin, PhD, the Eugene Higgins Professor of Cell Biology, director of the Yale Stem Cell Center, and president of ISSCR. “I commend their exceptional accomplishment as well as their sensitivity to ethical issues by limiting the model’s ability to develop further”
The ethical questions are profound, including whether these models have the potential to develop into human beings. Sozen, the principal investigator of the study, emphasizes that they do not. The published paper demonstrates that this model lacks trophectodermal cells, which are required for an embryo to implant in the uterus. Sozen says this model also represents a developmental stage beyond the time frame in which embryos can implant. “It is very important to focus on the fact that our model cannot grow further or implant and therefore is not considered a human embryo,” she says. But as a reductionist strategy to mimic and study aspects of natural development, its potential is immense, especially where universal guidelines severely limit scientists’ ability to study actual embryos.
New Model Contains Embryonic and Extraembryonic Tissues
All embryos have two components — embryonic and extraembryonic. The tissues we have now in our adult bodies grew from the embryonic component. The extraembryonic component includes the tissues that offer nutritional and other support, such as the placenta and yolk sac. The majority of previous embryo models of developmental stages around gastrulation were single-tissue models that only contained the embryonic component.
In the new study, the Yale-led team grew embryonic stem cells in vitro in the lab to generate their new model. They transferred these cells into a 3D culture system and exposed them to a conditions which stimulated the cells to spontaneously self-organize and differentiate. The cells diverged into two lineages — embryonic and extraembryonic precursors. The extraembryonic cells in this model were precursors for the yolk sac. The researchers grew these cellular lineages in the culture for approximately one week and analyzed how they guided each other as they developed. “We started looking into very mechanistic details, such as what signals they are giving each other and how specific genes are impacting one another,” says Sozen. “This has been limited in the literature previously.”
The Need for Models of Human Development
While researchers have learned a great deal from embryos of other species such as mouse, the lack of accessibility to human embryos has left significant knowledge gaps about our development. “If you want to understand human development, you need to look at the human system,” says Sozen. “This work is really important because it’s giving us direct information about our own species.” Not only does this model give access into the human gastrulation window, but will also allow for a greater quantity of research. The ability to generate as many as thousands of these models will allow for mass analysis that is not possible with human embryos. “I’m one scientist with one vision,” says Sozen. “But thinking about what other scientists are envisioning globally and what we can all accomplish is just really, really exciting to me.”
The new model has over 70% efficiency — in other words, the stem cells aggregate correctly over roughly 70% of the time. As noted by the authors, there are some limitations to the strategy, and it is challenging to benchmark some findings against the natural embryo itself. Sozen hopes to continue to work on the models so that they become more standardized in the future.
The team believes the models will transform scientists’ knowledge around human developmental biology. In their latest publication, the team explored some of the molecular paths underlying human gastrulation onset. In future studies, they hope to delve even deeper into the developmental pathways, including whether pregnancy loss and congenital disorders may stem from failures during gastrulation stages. Sozen believes her model can be used to look at some of these disorders and learn more about what is going awry. “Previous model systems have been able to look at this, but our model is unique because it has this extra tissue that allows us to analyze a bit deeper,” she says.

For the first two weeks of life, mice with a hereditary form of deafness have nearly normal neural activity in the auditory system, according to a new study by Johns Hopkins Medicine scientists. Their previous studies indicate that this early auditory activity — before the onset of hearing — provides a kind of training to prepare the brain to process sound when hearing begins.
The findings are published June 27 in PLOS Biology.
Mutations in Gjb2 cause more than a quarter of all hereditary forms of hearing loss at birth in people, according to some estimates. The connexin 26 protein coded by the gene is in a family of proteins known as GAP junctions, because these proteins span the tiny gap between cells and form a kind of tube that connects two cells to trade ions, metabolites and other molecules that communicate or maintain an equilibrium.
This unexpected finding, according to investigators, suggests a molecular mechanism for the observation that people with this hereditary mutation respond well to cochlear implants, the electronic devices that are designed to mimic sound conduction in the inner ear and can improve hearing in those with severe hearing loss. According to the National Institutes of Health, about 118,100 cochlear implants were implanted in adults and 65,000 in children between December 2019 and March 2021.
The connexin 26 protein in the cochlea, the spiral-like structure in the inner ear, is highly enriched in supportive cells, which, like their name implies, provide structural and nutritional help to surrounding hair cells and auditory neurons.
Previous studies have shown that, without connexin 26, the cochlea fails to develop its normal shape and is incapable of amplifying sound-induced vibrations necessary for efficient sound detection. Despite this disruption to the cochlear structure, this research shows the cochlea is still capable of producing the “spontaneous” activity needed to shape brain development.

“Supportive cells are extremely important for tissues and organs,” says neuroscientist Dwight Bergles, Ph.D., the Diana Sylvestre and Charles Homcy Professor at the Johns Hopkins University School of Medicine. “The new study shows how critical they are for training the auditory system and getting it ready to process sound.”
For the study, Bergles and Calvin Kersbergen, an M.D./Ph.D. candidate in Johns Hopkins’ Medical Scientist Training Program, created a mouse model that lacked connexin 26 specifically in supportive cells in the cochlea.
By using external electrodes to measure electrical responses in the auditory nerve in response to tones or clicks, they found that mice lacking connexin 26 only in supportive cells of the cochlea were, indeed, deaf, demonstrating the crucial role of these intercellular channels in hearing.
However, Bergles and Kersbergen wondered if this change in supportive cells and shape of the cochlea would also disrupt spontaneous activity in younger mice, less than 2 weeks old, before their ear canal opens.
The researchers found that mice without connexin 26 still exhibit bursts of electrical activity in auditory neurons at nearly the same levels as young mice with intact connexin 26. Further investigation revealed that spontaneous activity in supportive cells was able to activate sensory hair cells in the inner ear, leading to normal neuronal activity in sound-processing areas of the brain.

“Even in the absence of connexin 26, we still find robust spontaneous activity in the cochlea in these young mice,” says Bergles.
Bergles says there is now evidence that the role of supportive cells in this early period is to “train” the auditory system to respond to sound at certain frequencies. Since the ear canal isn’t open yet, supportive cells generate their own activity spontaneously to stimulate the mechanically sensitive hair cells in the fluid-filled cochlea.
“It’s as if the cochlea is producing its own ‘sounds’ at this stage of development,” Bergles says. “This practice may help the auditory neurons and circuits in the brain mature before the ear canal opens.”
“It’s like a baseball player in a batting cage, learning the basics of their swing and preparing to face the unpredictability of a real pitcher,” says Bergles.
Finally, the researchers found that spontaneous activity in supportive cells of deaf mice halts once the ear canal opens. At the same time, because the mice can’t process sound, their auditory neurons actually increase their sensitivity to sound.
This hypersensitivity to sound is similar to the phenomenon of hyperacusis, in which normal levels of sound can be painful. In humans, this hearing loss-induced hypersensitivity can also lead to constant ringing of the ears, called tinnitus.
Bergles says the research also suggests a molecular mechanism for why people with this hereditary mutation who receive cochlear implants early on tend to do better than those who receive them later.
“Spontaneous activity in supportive cells in the cochlea may provide the molecular evidence for empirical data showing better outcomes among people who have cochlear implants placed earlier in life,” says Bergles.
The research team plans to study whether they can tap into the spontaneous activity pathway in supportive cells to treat tinnitus and other auditory conditions.
Scientists Travis Babola and Patrick Kanold also contributed to this research.
Funding was provided by the National Institutes of Health (F30DC018711, F32DC019842, U19NS107464, R01DC009607, R01DC008860, P30NS050274).

Published27 JuneShareclose panelShare pageCopy linkAbout sharingThis video can not be playedTo play this video you need to enable JavaScript in your browser.By Jim Reed and Michelle RobertsBBC NewsEx-health secretary Matt Hancock has criticised the UK’s pandemic planning before Covid hit, saying it was “completely wrong”.He told the Covid Inquiry that planning was focused on the provision of body bags and how to bury the dead, rather than stopping the virus taking hold.He said he was “profoundly sorry” for each death.After giving evidence he approached some of the bereaved families, but they turned their backs on him as he left.The former health secretary, who answered questions from the inquiry on Tuesday, said he understood his apology might be difficult for families to accept, even though it was “honest and heartfelt”.He added it was a “colossal” failure to assume the virus spreading could not be stopped.Under questioning from Hugo Keith KC, lead counsel to the Covid Inquiry, Mr Hancock stressed that the “attitude, the doctrine of the UK was to plan for the consequences of a disaster”.He said the government was focused on different questions, such as “can we buy enough body bags?” and “where are we going to bury the dead?””That was completely wrong,” he added. Covid: How many people died?What is the Covid Inquiry and how long will it take?Ex-medical officer close to tears over Covid deathsUK public services were depleted when Covid hitMr Keith asked Mr Hancock why, if he was so critical of the UK’s approach to pandemic planning, it was not changed while he was health secretary. Mr Hancock said: “The only answer I can give is because I was assured that we had the best system in place in the world. “In hindsight, I wish I’d spent that short period of time [before the pandemic] changing the entire attitude to how we respond to a pandemic.”When Mr Hancock praised workers across health and social care during the pandemic, Hugo Keith made the analogy: “Lions led by structural donkeys, Mr Hancock. Personally, everyone gave their all but the system was not fit for purpose, was it?”Mr Hancock replied: “That’s absolutely right.”The former health secretary added: “I bear responsibility for all the things that happened, not only in my department, but also the agencies that reported to me as secretary of state.”What else did we learn?The inquiry also heard from the former health secretary that medicines for intensive care were “within hours” of running out at the peak of the pandemic. He added that the only reason they did not was because of work done in 2019 in preparation for a no-deal Brexit.Mr Hancock said he had to overrule initial advice not to quarantine people being brought back from Wuhan early in the pandemic, and that everybody in the Western world missed that lockdowns would be necessary.He also criticised the World Health Organization (WHO) for giving advice which “stated that we should not have lockdowns”.He said it was “madness” but he had to “overrule” initial advice not to quarantine people coming in from China. He also blamed the WHO for having “written into the international health regulations that you shouldn’t close borders”.Because there was “no such thing” as mass contact tracing systems as the pandemic took hold, Mr Hancock said the inability to test people in large numbers was “terrible”.He also used the word terrible to describe the government having no idea whether care homes had the right protections in place. He said the government didn’t even know how many care home residents there were at the start of the pandemic.Image source, ReutersHowever, he said the responsibility for ensuring the social care sector was prepared for a pandemic fell to local authorities, and he “didn’t have the levers to act”. The former health secretary was also repeatedly asked about the recommendations from Exercise Cygnus, a three-day test run in October 2016 to find out how prepared the UK was for a influenza pandemic. It concluded that the UK’s plan was not sufficient to “cope with the extreme demands of a severe pandemic”.The inquiry has seen evidence that only eight of the 22 recommendations made after that exercise had been fully addressed by the time Covid hit, with work on the other 14, including preparing the social care sector, still ongoing. He described Exercise Cygnus as “flawed in its central assumption” that a pandemic was a disaster that needed to be “cleaned up” rather than something that needed to be stopped or contained in the first place. He said: “The doctrinal flaw was the biggest by a long way because if we’d had a flu pandemic, we still would have had the problem of no plan in place for lockdown, no prep for how to do one, no work on what, how best to lock down with the least damage.”I understand deeply the consequences of lockdown and the negative consequences for many, many people – many of which persist to this day.”Mr Hancock said that some of that work on the Exercise Cygnus had been paused because of the need to prepare the country for a no-deal Brexit. But he said that he was “not convinced” that, even if all those recommendations had been addressed, the country would have been in a better place to deal with Covid. As a result, the UK was “better prepared in terms of supply chains,” but the “overall impact” was hard to judge.”I’m afraid it’s impossible to know,” he added. Bereaved relatives demand answersWhen Mr Hancock first arrived at the inquiry, a widow showed him images of her husband, who died from Covid.Lorelei King, 69, was holding two A4 posters, which she showed to the former health secretary as he stepped out of a black Jaguar.One poster displayed an image of Mr Hancock with Mrs King’s husband, Vincent Marzello, who died in a care home in March 2020, aged 72.”You shook my husband’s hand for your photo op,” the photo was captioned. The other picture showed Mr Marzello’s coffin.Image source, ReutersMr Hancock didn’t respond as he walked in to the building.Mrs King told journalists: “Care homes became charnel houses because there was no testing, there was insufficient PPE, but, most disastrously, it’s because they discharged people from hospitals without testing them.”She called on Mr Hancock to “tell the truth” to the inquiry, adding: “The bereaved families deserve that much.”What is the Covid Inquiry?It is about going through what happened and learning lessonsNo-one will be found guilty or innocentAny recommendations made do not have to be adopted by governmentsThe inquiry has no formal deadline but is due to hold public hearings until 2026Scotland is holding a separate inquiry in addition to the wider UK oneSign up for our morning newsletter and get BBC News in your inbox.More on this storyEx-medical officer close to tears over Covid deathsPublished20 JuneWhat is the UK Covid inquiry and how does it work?Published1 hour agoRelated Internet LinksUK Covid-19 InquiryThe BBC is not responsible for the content of external sites.

A new study led by scientists from TUD Dresden University of Technology reveals that the cells in the fruit fly brain possess a remarkable ability to shift their energy production to fats and send signals to the body’s other organs, prompting them to start delivering lipids from fat stores to the brain during periods of starvation. The findings were published in the journal Nature Communications.
The brain, being one of the body’s most energy-demanding organs, typically relies on sugar as its primary fuel source. However, during starvation, the brain can adapt and utilize alternative fuels, such as ketone bodies derived from stored fat. The question of whether brain cells can solely rely on externally obtained fuel or directly utilize fat has long puzzled scientists.
Metabolic Switch
Led by Prof. Stefanie Schirmeier from the Faculty of Biology and Dr. Marko Brankatschk from the Biotechnology Center (BIOTEC) at TU Dresden, the research team used a comprehensive range of methods, including genetic manipulation, molecular biology, lipid analysis, and behavioral studies, to demonstrate how fruit fly brain cells can switch to fats to generate alternative neuronal fuel and safeguard against neurodegeneration.
“While neurons often come to mind when we think of the brain, there are other cells in the brain, called glia. They play vital roles in supporting and maintaining neurons. Our study shows that these glial cells respond to sugar shortage by activating fat utilization. In fruit flies, these cells utilize fats stored in lipid droplets or absorb lipids from circulation to produce ketones for the neurons to consume. This switch is crucial for the fly’s survival,” explains Dr. Marko Brankatschk, research group leader at BIOTEC.
Metabolic Sensor
The study also revealed that glial cells act as messengers, signaling the body about the brain’s energy shortage. “Our findings suggest that the metabolic switch in glial cells acts as a trigger, initiating a communication cascade that alerts the rest of the body to the challenging metabolic situation in the brain. As a result, the body’s fat-storing organs mobilize reserves to sustain the brain’s energy supply. It remains to be seen if a similar mechanism exists in the human brain,” explains Prof. Schirmeier.
“Our work relies on Drosophila melanogaster, the common fruit fly, which has long served as a valuable model organism for studying development and disease. Our study demonstrates its potential to unlock insights into complex metabolic changes and their biological consequences,” concludes Prof. Schirmeier.
The research conducted by TU Dresden scientists holds the potential to expand our understanding of brain metabolism and highlights the significance of studying simple model organisms to discover the intricate mechanisms underlying complex biological processes.

In the midst of a global opioid epidemic, a team of scientists is exploring natural killer (NK) cells as an alternative treatment for neuropathic pain. In an Opinion piece published June 27th in the journal Trends in Neurosciences, the researchers gather existing evidence for the impact of NK cells in pain, pointing to their ability to prune the damaged nerve cells that may cause it. They urge the scientific community to explore biological mechanisms underlying NK cell activity to move towards a realistic pain therapy that is both effective and safe.
Neuropathic pain is a chronic condition experienced as a recurring shooting or stabbing sensation. It is caused by nerve damage, which may occur because of trauma, a disease such as diabetes, or after chemotherapy.
“The prevalence of neuropathic pain is unfortunately only likely to increase over time,” says co-author Alexander Davies, a neurophysiologist with the Neural Injury Group at Oxford University. “As we get better at treating diseases like cancer, we have survivors who may be left with pain from either the cancer treatment or the surgery that was used to remove it.”
While therapies such as opioids and antidepressants are currently used to address these pain symptoms, they do not treat the underlying cause of pain and have their own risks and side effects. The authors point out that 564,000 people overdosed on opioids in the United States between 1999 and 2020.
“The main approach is silencing the neurons,” Davies says. “While we certainly need anesthetics to deal with pain in the short term, if we use them in the long term, we can become addicted to the sensation of removing pain, which is in itself pleasurable.”
Alongside T cells and B cells, NK cells are a type of white blood cell called lymphocytes. Their existing role in the body includes attacking tumors or viruses. NK cells increase activity during acute pain. However, they appear to decline in frequency or potency in people who experience chronic pain. Not having a fully functional NK cell population may therefore prevent people from resolving neuropathic pain in the long term.
“We first became interested in this idea when one of my colleagues found a T cell response after nerve injury, but I noticed that NK cells were also involved,” says senior author Seog Bae Oh, a neurobiologist at Seoul National University. “NK cells are typically explored in the context of cancer, but I thought it was worth looking at them in pain as well.”
NK cells may resolve pain because they are involved in the process by which neurons are pruned. Injury and disease can cause neurons to become incorrectly wired or to stop functioning as intended, resulting in pain symptoms. Introducing NK cells could help to remove these anomalies. Experiments in mice have shown that if a neuron is in distress, its axon, the segment responsible for transmitting messages, displays a molecule called the RAE1 stress ligand. This could alert the NK cells to their need for pruning. A similar ligand, belonging to what is known as the ULBP family, is also seen in sensory neurons in humans with pain.
Conversely, NK cells may have a negative effect in the central nervous system, such as the brain and spinal cord, where neurons cannot regenerate so easily if they are removed. Their impact here should be considered carefully in the design of any possible therapies.
The authors stress that our understanding of the processes by which NK cells support pain relief is still limited, and their potential viability as a future treatment depends on further research. Both Davies and Oh are continuing to explore their NK cells in pain. Oh and his colleagues are investigating the therapeutic potential of NK cells in a range of preclinical models as well as their activity in patients who experience pain, while Davies is working to identify the cellular targets of NK cells following nerve injury.
“We need to have a better mechanistic understanding of how NK cells work and what they can target before we can develop realistic therapies, and we need to minimize their side effects,” Davies says. “However, the more prongs we have to treat neuropathic pain, the more likely we are ultimately to be able to address it.”

Using nanomagnets composites and conductive yarn, scientists have invented a smart textile that can sense and measure body movements — from muscles flexing to veins pulsing. The device, presented on June 27 in the journal Matter, is self-powered, stretchy, durable, waterproof, and can be made with a sewing machine for a few dollars. It may one day aid clinicians in assessing muscle injuries and support patients’ recovery.
The smart textile is not technically made of fabric but has a cloth-like texture. It’s made of a nanomagnet-filled rubber patch that is roughly the size of two stamps. Using a sewing machine, the researchers stitched silver-coated conductive yarn onto the patch in a coil design. Mechanical forces, such as a finger tap, can deform the pattern of magnetic fields within the rubber, thus creating an electric current through the yarn. The two phenomena where forces change magnetic fields and magnetic flux variations generate electricity are known as the magnetoelastic effect and electromagnetic induction.
“Our device is very sensitive to biomechanical pressure,” says senior author Jun Chen  of the Department of Engineering, University of California, Los Angeles. “The device converts muscle activities into quantifiable, high-fidelity electrical signals that are sent wirelessly to phone apps. This demonstrates the potential for personalized physical therapies and improving the rehabilitation of muscle injuries.”
The device is not only sensitive, but it’s also precise, detailing body movements down to each muscle group. Attaching the device to different body parts, researchers distinctly measured throat movements while drinking water, ankle movements while walking, and even monitored a person’s pulse from their wrist. When affixed to a person’s bicep, the device can show whether they are bending their arm or gripping their fist and to what degree or force. Based on these types of information, a clinician can find the Goldilocks zones to prevent over-excursion and encourage moderate activities, tailoring recovery goals for their patients.
Chen and his team also put the device’s functionality to the test. To mimic real-world conditions such as excessive sweating and heavy rain the team wet the device with a water spray and tested its signal output. The signals remained strong. Besides being waterproof, the device is also stretchy and durable, extending 3.5 times its length and withstanding 100,000 cycles of deformation. From a production standpoint, Chen notes that the device is easy to fabricate and highly scalable, and each patch is estimated to cost less than $3.
“Another highlight of the device is its self-powering properties,” says Chen. “The ability to convert biomechanical force to electricity means the device is also a generator. This eliminates the need for bulky, heavy, and rigid battery packs usually needed in wearable electronic designs.”
Next, the team wants to make the smart textile thinner and lighter to optimize the wearer’s experience. Chen and his team, who discovered the magnetoelastic effect in soft systems in 2021, also plan to explore new ways to incorporate his findings into other wearable or implantable bioelectronics.
“We’ve tested the device for cardiovascular monitoring and respiration monitoring as well,” says Chen. “One day, we may be able to reinvent or replace current systems, such as EKGs, that require external power sources, and make them less bulky and more wearable.”
This work was supported by the University of California, Los Angeles; the Hellman Fellows Research Grant; the Brain & Behavior Research Foundation Young Investigator Grant; and the Children’s Hospital Los Angeles.

A new study from Washington University School of Medicine in St. Louis suggests that growing up in poverty may influence the wiring of a child’s brain.
The study, published June 27 in JAMA Network Open, indicates a link between both neighborhood and household poverty and the brain’s white matter tracts, which allow for communication between brain regions. White matter plays a critical role in helping the brain process information.
The findings stem from the largest long-term study of brain development and child health conducted in the U.S. — the Adolescent Brain Cognitive Development (ABCD) Study, which was launched by the National Institutes of Health (NIH) in 2015. Washington University is a national leader in studies of the developing brain and is one of 21 study sites around the country participating in the ABCD Study, which is following nearly 12,000 children, beginning at ages 9 to 10, for at least a decade.
“White matter integrity is very important in brain development,” said first author Zhaolong (Adrian) Li, a neuroimaging research technician in the Department of Psychiatry. “For example, weaknesses in white matter are linked to visuospatial and mental health challenges in children. If we can capture how socioeconomic status affects white matter early on in a child’s life, the hope is we can, one day, translate these findings to preventive measures.”
The researchers also found that childhood obesity and lower cognitive function may explain, at least partially, poverty’s influence on white matter differences. Generally, children who grow up in poverty have a higher risk of obesity and score lower on tests of cognitive function than their peers in higher income neighborhoods and households. The latter could be due, in part, to limited access to enriching sensory, social and cognitive stimulation.
“Our finding that obesity and cognitive enrichment may be relevant mediators, if confirmed, would provide strong support for managing healthy weight and encouraging cognitively stimulating activities to support brain health in disadvantaged children,” said Tamara Hershey, PhD, the James S. McDonnell Professor of Cognitive Neuroscience and a professor of psychiatry and of radiology.

The research was conducted in the Neuroimaging Labs Research Center in the university’s Mallinckrodt Institute of Radiology.
White matter, the densely packed nerve fibers deep in the brain, gets its white color from the fatty substance that surrounds nerve fibers. The fatty coating is responsible for the rapid transmission of information along nerve cell tracts. The organization and connectivity between these tracts support learning and proper communication across brain regions. Disruption in these communication pathways has been linked to physical challenges as well as worse mental health outcomes.
The scientists used the publicly available ABCD Study database, through which they were able to model water movement as an indicator of white matter integrity in the brain scans of 8,842 children ages 9 to 11. Just like rocks, pebbles and boulders impact the flow of water in a river, diverse brain cell structures create barriers that hinder water diffusion. The researchers found less directional movement of water molecules in the brains of children living in poverty, signifying structural changes in white matter regions. They also found higher water content in spherical spaces in the brain, which hinted at possible neuroinflammation in children who live in poverty.
A child’s environment is complex, involving both neighborhood and family influences. Disadvantaged neighborhoods suffer disproportionately from unemployment, poverty, and income disparity. Single-parent homes are more common, and residents are typically less educated, earn a lower income, and own less property.
“Our analysis revealed that neighborhood poverty is linked to white matter differences and putative immune cell presence. We found a similar link when looking at household socioeconomic status, taking into account annual income and parental education,” Li said.
“Wealth and income inequality are accelerating in the U.S.,” said co-corresponding author Scott Marek, PhD, an assistant professor of radiology and of psychiatry. “We and others are starting to scratch the surface of how inequality may harm the developing brain and affect mental health outcomes. Our findings emphasize shifting away from the thinking that socioeconomics is a unitary construct. It’s not schools or parenting alone that matter for brain health. It’s likely the collection of many neighborhood and familial life factors.”
Hershey, who directs the Neuroimaging Labs Research Center and is a co-corresponding author, cautioned that the study only looked at one time point. Therefore, it is too soon to know if poverty triggered the brain differences seen in the study, she said. However, the ABCD Study continues to track enrolled children through brain scans and cognitive testing with the potential for future long-term brain development studies in disadvantaged children.
“We hope this work encourages future studies to examine modifiable health risk factors in large and longitudinal samples that would one day translate to intervention,” Hershey said.

Cambridge scientists have created a stem cell-derived model of the human embryo in the lab by reprogramming human stem cells. The breakthrough could help research into genetic disorders and in understanding why and how pregnancies fail.
Published today in the journal Nature, this embryo model is an organised three-dimensional structure derived from pluripotent stem cells that replicate some developmental processes that occur in early human embryos.
Use of such models allows experimental modelling of embryonic development during the second week of pregnancy. They can help researchers gain basic knowledge of the developmental origins of organs and specialised cells such as sperm and eggs, and facilitate understanding of early pregnancy loss.
“Our human embryo-like model, created entirely from human stem cells, gives us access to the developing structure at a stage that is normally hidden from us due to the implantation of the tiny embryo into the mother’s womb,” said Professor Magdalena Zernicka-Goetz in the University of Cambridge’s Department of Physiology, Development and Neuroscience, who led the work.
She added: “This exciting development allows us to manipulate genes to understand their developmental roles in a model system. This will let us test the function of specific factors, which is difficult to do in the natural embryo.”
In natural human development, the second week of development is an important time when the embryo implants into the uterus. This is the time when many pregnancies are lost.

The new advance enables scientists to peer into the mysterious ‘black box’ period of human development — usually following implantation of the embryo in the uterus — to observe processes never directly observed before.
Understanding these early developmental processes holds the potential to reveal some of the causes of human birth defects and diseases, and to develop tests for these in pregnant women.
Until now, the processes could only be observed in animal models, using cells from zebrafish and mice, for example.
Legal restrictions in the UK currently prevent the culture of natural human embryos in the lab beyond day 14 of development: this time limit was set to correspond to the stage where the embryo can no longer form a twin.
Until now, scientists have only been able to study this period of human development using donated human embryos. This advance could reduce the need for donated human embryos in research.

Zernicka-Goetz says the while these models can mimic aspects of the development of human embryos, they cannot and will not develop to the equivalent of postnatal stage humans.
Over the past decade, Zernicka-Goetz’s group in Cambridge has been studying the earliest stages of pregnancy, in order to understand why some pregnancies fail and some succeed.
In 2021 and then in 2022 her team announced in Developmental Cell, Nature and Cell Stem Cell journals that they had finally created model embryos from mouse stem cells that can develop to form a brain-like structure, a beating heart, and the foundations of all other organs of the body.
The new models derived from human stem cells do not have a brain or beating heart, but they include cells that would typically go on to form the embryo, placenta and yolk sac, and develop to form the precursors of germ cells (that will form sperm and eggs).
Many pregnancies fail at the point when these three types of cells orchestrate implantation into the uterus begin to send mechanical and chemical signals to each other, which tell the embryo how to develop properly.
There are clear regulations governing stem cell-based models of human embryos and all researchers doing embryo modelling work must first be approved by ethics committees. Journals require proof of this ethics review before they accept scientific papers for publication. Zernicka-Goetz’s laboratory holds these approvals.
“It is against the law and FDA regulations to transfer any embryo-like models into a woman for reproductive aims. These are highly manipulated human cells and their attempted reproductive use would be extremely dangerous,” said Dr Insoo Hyun, Director of the Center for Life Sciences and Public Learning at Boston’s Museum of Science and a member of Harvard Medical School’s Center for Bioethics.
Zernicka-Goetz also holds position at the California Institute of Technology and is NOMIS Distinguished Scientist and Scholar Awardee.
The research was funded by the Wellcome Trust and Open Philanthropy.

Molecular imaging with 18F-flubatine PET/MRI has shown that neuroreceptors in the brains of individuals with obesity respond differently to food cues than those in normal-weight individuals, making the neuroreceptors a prime target for obesity treatments and therapy. This research, presented at the Society of Nuclear Medicine and Molecular Imaging 2023 Annual Meeting, contributes to the understanding of the fundamental mechanisms underlying obesity and offers valuable insights into potential medical interventions.
Worldwide, more than one billion people are obese. The global obesity epidemic poses a major challenge for health care systems worldwide, and the search for interventions to achieve sustainable weight loss is a high priority. By investigating biological and behavioral mechanisms in individuals with obesity, scientists are seeking to identify potential pathways for treatments and interventions.
“The brain’s cholinergic system is a unique area of interest when it comes to studying obesity,” said Swen Hesse, MD, clinical scientist and professor in the Department of Nuclear Medicine at the University of Leipzig in Leipzig, Germany. “Cholinergic changes in the brain’s reward and attentional networks seem to play an important role in how people decide what foods are most desirable, or salient. In our study, we aimed to measure changes in α4β2* nicotinic acetylcholine receptors found in the cholinergic system in response to high-caloric food cues.”
In the study, 15 individuals with obesity and 16 normal-weight controls underwent PET/MRI with 18F-flubatine twice on separate days, once while in a resting state and once while viewing food pictures. Total distribution volume of 18F-flubatine was estimated, and a visual analog scale was used to assess states of hunger/satiety, appetite, disinhibition, craving and taste. Eating behavior was also measured using the Three-Factor Eating Questionnaire (TFEQ).
In the resting state, no significant difference in total distribution volume of 18F-flubatine was noted between the participants with obesity and normal-weight controls. While viewing photos of food, however, the total distribution volume of 18F-flubatine was higher in the obese compared with normal-weight controls in the thalamus of the brain, particularly in those with a higher TFEQ score.
For normal-weight controls there was a stronger connectivity to the dorsal attention network of the brain when viewing food cues, whereas for participants with obesity, a stronger connectivity was found with the salience network. Finally, analyses of the total volume distribution and different behavioral measures showed significant correlation between total volume distribution in the hypothalamus and measure for satiety in normal-weight controls. In participants with obesity there was a significant correlation with measures of disinhibition and the nucleus accumbens.
“We anticipate that the results of our study will pave the way for novel drug treatments and behavioral interventions to effectively combat obesity worldwide,” noted, Osama Sabri, MD, PhD, professor, director, and chairman of the Department of Nuclear Medicine at the University of Leipzig. “In addition, the imaging technology utilized in this study holds promise for identifying biomarkers that can aid in patient stratification and facilitate personalized medicine approaches in the near future.”