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A study of children and adolescents who received a COVID-19 vaccination following multisystem inflammatory syndrome (MIS-C) found that there were no reports of serious complications including myocarditis or MIS-C reoccurrence. About half of participants experienced mild and typical reactions, including arm soreness and fatigue. The study, funded by the National Institutes of Health, demonstrates that it is safe to get a vaccine after having MIS-C. The findings will publish today in JAMA Network Open.
The multicenter, observational study, the largest of its kind to examine COVID vaccination in this group, helps resolve a lingering question about whether the COVID vaccine can increase the risk of health problems in young people who have had MIS-C, a rare and potentially fatal immunological reaction that can occur following infection with SARS-CoV-2, the virus that causes COVID-19.
MIS-C is a poorly understood condition that affects 1 in about 3,000 to 4,000 children and adolescents who had COVID-19, according to the Centers for Disease Control and Prevention (CDC). It occurs a few weeks after COVID infection and can lead to organ failure. Symptoms can range from stomach pain, fever, and rash to inflammation of the heart muscle, a serious condition called myocarditis. The exact causes of MIS-C are unknown, but medications can be given to decrease the inflammation that can damage organs.
Some families and healthcare professionals have questioned whether COVID vaccines could lead to more serious adverse reactions in those with a history of MIS-C, including a recurrence of the disease, but data on this topic were lacking.
The cross-sectional study included 22 medical centers (21 in the United States and 1 in Canada) participating in the NHLBI’s Long-Term Outcomes After the Multisystem Inflammatory Syndrome in Children (MUSIC) study. It enrolled 385 patients aged 5 years or older with prior MIS-C who were eligible for COVID-19 vaccination. Of this group,185 (48.1%) received at least one vaccine dose. The median age was 12.2 years and 73.5% were male. The participants were racially diverse — 24.3% were Black, 31.9% were Hispanic, and 28.6% were white. The median length of time from their MIS-C diagnosis to their first vaccine dose was 9 months.
Of those who received a COVID vaccination following MIS-C, mild adverse reactions — mostly arm soreness and fatigue — occurred in 49% of them, similar to the general population. There were no reports of serious complications, including myocarditis or recurrence of MIS-C, the researchers said.

“We are very reassured by the results and this safety data should be comforting to families and healthcare professionals when considering and recommending vaccination,” said study co-leader Matthew D. Elias, M.D., a pediatric cardiologist at Children’s Hospital of Philadelphia and clinical assistant professor of pediatrics at the University of Pennsylvania, Philadelphia. Audrey Dionne, M.D., a pediatric cardiologist at Boston Children’s Hospital and assistant professor of pediatrics at Harvard Medical School, Boston, also served as the study’s co-leader. The researchers have routinely treated children with MIS-C throughout the pandemic.
Dionne added that the findings provide support for the CDC’s recommendation that patients with a history of MIS-C receive a COVID vaccine at least 90 days after diagnosis and that it is safe to do so.
“In light of the acute and long-term consequences of COVID-19 it is vital to continue the development, testing, and deployment of preventive as well as therapeutic agents in at-risk groups as well as the general population,” said Gary H. Gibbons, M.D., director of the National Heart, Lung, and Blood Institute (NHLBI), part of NIH.
To date, more than 9,000 patients have been diagnosed with MIS-C in the United States, and 74 have died, according to data from the CDC (https://covid.cdc.gov/covid-data-tracker/#mis-national-surveillance). However, the disease appears to be on the decline, according to studies by others.
“A big part of that decline is that COVID vaccination has been protective against this rare condition in those who have received it,” Dionne said.
While many patients with MIS-C make a full clinical recovery, some studies suggest chronic symptoms linger after MIS-C, which is why long-term outcome studies will be beneficial, the researchers said. The MUSIC study is part of an NIH collaborative research effort called CARING for Children with COVID, which aims to better understand how COVID affects children, who account for roughly 13% of the total cases in the United States.
Research reported in this study was funded by the NHLBI’s MUSIC study, which was supported by grants HL135680, HL135685, HL135683, HL135689, HL135646, HL135665, HL135678, HL135682, HL135666, HL135691, and HL068270. The study uses the research infrastructure of the Pediatric Heart Network, a pediatric cardiology research consortium funded by the NHLBI, and its data coordinating center, HealthCore Inc.

Obesity and metabolic diseases, such as diabetes, are extremely common in the United States. Tiny proteins called microproteins have long been overlooked in research, but new evidence demonstrates that they have an important role in metabolism. Salk scientists have discovered that both brown and white fat is filled with thousands of previously unknown microproteins, and show that one of these microproteins, called Gm8773, can increase appetite in mice.
These findings, published in Cell Metabolism on January 3, 2023, could lead to the development of a therapeutic to help people gain weight in certain disease situations, such as during chemotherapy for cancer. Furthermore, by establishing the existence of these microproteins, the team provides a valuable resource for the scientific community to study microproteins as well.
“It is vital to better understand the processes that regulate obesity and metabolic health in order to provide improved therapies for the future,” says Salk Professor Alan Saghatelian, co-corresponding author of the study and holder of the Dr. Frederik Paulsen Chair. “Having this list of microproteins will aid the field of metabolism in identifying new players in a variety of metabolic diseases. And we’ve demonstrated one biologically active microprotein that promotes feeding, as well as other microproteins that are involved in fat metabolism.”
Fat tissue secretes many different proteins to regulate feeding, energy balance, and the production of heat. White fat, known as “bad fat,” is often found just beneath the skin and in the abdominal region. This type of fat acts as an energy storage depot and is related to obesity and other diseases caused by excess weight. In contrast, brown fat or “good fat” is located around the shoulders and along the spinal cord. Brown fat is associated with proper nutrition, exercise, and health.
In this study, the scientists used innovative genomics technologies to examine the brown, white, and beige fat (another type of fat with features similar to both white and brown fat) in mouse cells. They discovered 3,877 genes that produce microproteins in both white and brown fat. Additionally, they explored the levels of these genes in mice fed a high-fat Western diet, and linked hundreds of microproteins to changes in fat tissue metabolism. Overall, the analysis highlights many likely metabolically relevant microproteins for the first time.
“We’ve provided a roadmap on how to best use our data to link and eventually characterize the roles of microproteins in fundamental metabolic pathways,” says first author Thomas Martinez, a former postdoctoral fellow in Saghatelian’s lab who is now an assistant professor at UC Irvine.
The team also focused in on a microprotein called Gm8773, located in the feeding center of the brain, called the hypothalamus. The location of the microprotein in the brain suggested it may play a role in appetite. Indeed, when the scientists administered Gm8773 to obese mice, the mice consumed more food. There is also a human gene similar to Gm8773 called FAM237B, and this gene could act similarly in humans to promote eating. According to the researchers, this microprotein could eventually be developed into a therapeutic to promote weight gain in those experiencing extreme weight loss.
“The new microproteins presented in our study are exciting discoveries for the field of metabolism and for the study of fat biology,” says co-corresponding author Chris Barnes, formerly of Novo Nordisk Research Center Seattle, Inc., now head of proteomics at Velia Therapeutics. “We hope that this resource will be used to generate numerous new experimental hypotheses for the scientific community to test in their own labs, and that this work leads to the identification of novel mechanisms in biology.”
In the future, the scientists plan to develop tools to investigate the roles of Gm8773 and FAM237B with the goal of eventually developing a therapeutic that can increase appetite in humans.
Other authors include Cynthia Donaldson, Joan M. Vaughan, Calvin Lau, and Maxim N. Shokhirev of Salk; Brian C. Searle of Ohio State University; Lindsay K. Pino and Michael J. MacCoss of the University of Washington; Eduardo V. De Souza, and Cristiano V. Bizarro of the Pontifcia Universidade Catolica do Rio Grande do Sul in Brazil; and Sally Lyons-Abbott, Angie L. Bookout, Ariel Abramov, Arian F. Baquero, Karalee Baquero, Dave Friedrich, Justin Huard, Ray Davis, Bong Kim, Ty Koch, Aaron J. Mercer, Ayesha Misquith, Sara A. Murray, Sakara Perry, Christina Sanford, Alex Simon, Yu Zhang, Garrett Zipp, and Andrew J. Whittle of Novo Nordisk Research Center Seattle, Inc.
The work was supported by the National Institutes of Health (R01 GM133981, P41 GM103533, R24

Numerous studies have shown health benefits of time-restricted eating including increase in life span in laboratory studies, making practices like intermittent fasting a hot topic in the wellness industry. However, exactly how it affects the body on the molecular level, and how those changes interact across multiple organ systems, has not been well understood. Now, Salk scientists show in mice how time-restricted eating influences gene expression across more than 22 regions of the body and brain. Gene expression is the process through which genes are activated and respond to their environment by creating proteins.
The findings, published in Cell Metabolism on January 3, 2023, have implications for a wide range of health conditions where time-restricted eating has shown potential benefits, including diabetes, heart disease, hypertension, and cancer.
“We found that there is a system-wide, molecular impact of time-restricted eating in mice,” says Professor Satchidananda Panda, senior author and holder of the Rita and Richard Atkinson Chair at Salk. “Our results open the door for looking more closely at how this nutritional intervention activates genes involved in specific diseases, such as cancer.”
For the study, two groups of mice were fed the same high-calorie diet. One group was given free access to the food. The other group was restricted to eating within a feeding window of nine hours each day. After seven weeks, tissue samples were collected from 22 organ groups and the brain at different times of the day or night and analyzed for genetic changes. Samples included tissues from the liver, stomach, lungs, heart, adrenal gland, hypothalamus, different parts of the kidney and intestine, and different areas of the brain.
The authors found that 70 percent of mouse genes respond to time-restricted eating.
“By changing the timing of food, we were able to change the gene expression not just in the gut or in the liver, but also in thousands of genes in the brain,” says Panda.

Nearly 40 percent of genes in the adrenal gland, hypothalamus, and pancreas were affected by time-restricted eating. These organs are important for hormonal regulation. Hormones coordinate functions in different parts of the body and brain, and hormonal imbalance is implicated in many diseases from diabetes to stress disorders. The results offer guidance to how time-restricted eating may help manage these diseases.
Interestingly, not all sections of the digestive tract were affected equally. While genes involved in the upper two portions of the small intestine — the duodenum and jejunum — were activated by time-restricted eating, the ileum, at the lower end of the small intestine, was not. This finding could open a new line of research to study how jobs with shiftwork, which disrupts our 24-hour biological clock (called the circadian rhythm) impact digestive diseases and cancers. Previous research by Panda’s team showed that time-restricted eating improved the health of firefighters, who are typically shift workers.
The researchers also found that time-restricted eating aligned the circadian rhythms of multiple organs of the body.
“Circadian rhythms are everywhere in every cell,” says Panda. “We found that time-restricted eating synchronized the circadian rhythms to have two major waves: one during fasting, and another just after eating. We suspect this allows the body to coordinate different processes.”
Next, Panda’s team will take a closer look at the effects of time-restricted eating on specific conditions or systems implicated in the study, such as atherosclerosis, which is a hardening of the arteries that is often a precursor to heart disease and stroke, as well as chronic kidney disease.
Other authors include Shaunak Deota, Terry Lin, April Williams, Hiep Le, Hugo Calligaro, Ramesh Ramasamy, and Ling Huang of Salk; and Amandine Chaix of the University of Utah.
The research was supported by the National Institutes of Health (grants CA258221, DK115214, CA014195, and AG065993) and the Wu-Tsai Human Performance Alliance.

If your alertness and reaction time is see-sawing more than usual, you may be more at risk of a viral illness.
That’s the key finding of an experiment led by University of Michigan researchers working in close collaboration with researchers at the Duke University School of Medicine and the University of Virginia.
“We all know that if we’re stressed, or haven’t slept enough, that predisposes us to have a less resilient immune system,” said Alfred Hero, the John H. Holland Distinguished University Professor of Electrical Engineering and Computer Science at U-M and corresponding author of the study in Scientific Reports.
“This is the first exposure study in humans to show that one’s cognitive performance before exposure to a respiratory virus can predict the severity of the infection,” he said.
Subtle variations in every day cognitive performance can signal changes in brain states that are known to increase the risk of illness such as stress, fatigue and poor sleep. The team wanted to measure cognitive function and explore whether it was predictive of immune performance after exposure to a respiratory virus. Cognitive variability, measured with an at-home, digital self-test, turned out to be very predictive.
The team studied a cohort of 18 healthy volunteers who took brain performance tests three times per day for three days and then were exposed to a cold virus known as human rhinovirus. The software provided 18 measures of cognitive function including reaction time, attention and rapid switching between numbers and symbols, which were combined to derive an index of variability.

“In the beginning, we didn’t find that cognitive function had a significant association with susceptibility to illness because we used the raw scores. But later, when we looked at change over time, we found that variation in cognitive function is closely related to immunity and susceptibility,” said Yaya Zhai, a recent Ph.D. graduate in bioinformatics at U-M and first author of the study. She and Hero led the development of the cognitive variability index.
The team assessed viral shedding by using a saline solution to wash out the nasal passages of participants. They determined the presence of viral infection and the quantity of virus in the fluid by growing the virus in a cell culture. As for symptoms, the team used the Jackson score, in which participants rated themselves from one to three on eight common cold symptoms.
“This is an interesting observation in a relatively small study. I hope that there will be a chance to confirm these findings in a larger, more definitive study,” said Ronald Turner, professor emeritus of pediatrics at the University of Virginia, who ran the experiment.
The team is optimistic that smartphone use could eventually help identify times of heightened susceptibility to illness, monitoring cognitive indicators like typing speed and accuracy as well as how much time the user spends sleeping.
“Traditional clinical cognitive assessments that look at raw scores in a single time point often do not provide a true picture of brain health,” said P. Murali Doraiswamy, director of the Neurocognitive Disorders Program at the Duke University School of Medicine, who designed the neurocognitive testing portion of the study.

“At home, periodic cognitive monitoring, through self-test digital platforms, is the future of brain health assessment,” said Doraiswamy.
The study was part of a project funded by the Defense Advanced Research Projects Agency to discover whether it was possible to predict susceptibility to illness in soldiers. That project was led by Geoffrey Ginsburg, then a professor at the Duke Center for Applied Genomics and Precision Medicine, and he led the contingent of the team analyzing blood samples for biomarkers that could indicate susceptibility to illness.
The experiment also discovered a few genetic markers that may indicate reduced immune function, which the team may explore further in future studies.
Lumos Labs provided access to their online Neurocognitive Performance Tests but was not involved in the process of conducting the study or the publication of the report.
Hero is also the R. Jamison and Betty Williams Professor of Engineering, professor of biomedical engineering and professor of statistics at U-M. Zhai is now a data scientist at VivoSense Inc. Ginsburg is now the chief medical and scientific officer of the All of Us research program at the National Institutes of Health. Doraiswamy is also a professor of psychiatry and medicine at the Duke University School of Medicine and an adviser to Lumos Labs.
U-M and Duke have filed for patent protection for the cognitive variability index.

Radiation, used to treat half of all cancer patients, can be measured during treatment for the first time with precise 3D imaging developed at the University of Michigan.
By capturing and amplifying tiny sound waves created when X-rays heat tissues in the body, medical professionals can map the radiation dose within the body, giving them new data to guide treatments in real time. It’s a first-of-its-kind view of an interaction doctors have previously been unable to “see.”
“Once you start delivering radiation, the body is pretty much a black box,” said Xueding Wang, the Jonathan Rubin Collegiate Professor of Biomedical Engineering, professor of radiology and corresponding author of the study in Nature Biotechnology. He also leads U-M’s Optical Imaging Laboratory.
“We don’t know exactly where the X-rays are hitting inside the body, and we don’t know how much radiation we’re delivering to the target. And each body is different, so making predictions for both aspects is tricky.”
Radiation is used in treatment for hundreds of thousands of cancer patients each year, bombarding an area of the body with high energy waves and particles, usually X-rays. The radiation can kill cancer cells outright or damage them so that they can’t spread.
These benefits are undermined by a lack of precision, as radiation treatment often kills and damages healthy cells in the areas surrounding a tumor. It can also raise the risk of developing new cancers.

With real-time 3D imaging, doctors can more accurately direct the radiation toward cancerous cells and limit the exposure of adjacent tissues. To do that, they simply need to “listen.”
When X-rays are absorbed by tissues in the body, they are turned into thermal energy. That heating causes the tissue to expand rapidly, and that expansion creates a sound wave.
The acoustic wave is weak and usually undetectable by typical ultrasound technology. U-M’s new ionizing radiation acoustic imaging system detects the wave with an array of ultrasonic transducers positioned on the patient’s side. The signal is amplified and then transferred into an ultrasound device for image reconstruction.
With the images in-hand, an oncology clinic can alter the level or trajectory of radiation during the process to ensure safer and more effective treatments.
“In the future, we could use the imaging information to compensate for uncertainties that arise from positioning, organ motion and anatomical variation during radiation therapy,” said Wei Zhang, a research investigator in biomedical engineering and the study’s first author. “That would allow us to deliver the dose to the cancer tumor with pinpoint accuracy.”
Another benefit of U-M’s technology is it can be easily added to current radiation therapy equipment without drastically changing the processes that clinicians are used to.
“In future applications, this technology can be used to personalize and adapt each radiation treatment to assure normal tissues are kept to a safe dose and that the tumor receives the dose intended,” said Kyle Cuneo, associate professor of radiation oncology at Michigan Medicine. “This technology would be especially beneficial in situations where the target is adjacent to radiation sensitive organs such as the small bowel or stomach.”
The research team is led by U-M, including Wang, Cuneo and Issam El Naqa, adjunct professor of radiation oncology at the U-M Medical School. The team works with partners at the Moffitt Cancer Center.
The University of Michigan has applied for patent protection and is seeking partners to help bring the technology to market. The research was supported by the National Cancer Institute and the Michigan Institute for Clinical and Health Research.
Story Source:
Materials provided by University of Michigan. Original written by Jim Lynch. Note: Content may be edited for style and length.

To recognize a famous voice, human brains use the same center that lights up when the speaker’s face is presented, finds a clever neuroscience study where participants were asked to identify U.S. presidents.
The new study, published last week in the Journal of Neurophysiology, suggests that voice and face recognition are linked even more intimately than previously thought. It offers an intriguing possibility that visual and auditory information relevant to identifying someone feeds into a common brain center, allowing for more robust, well-rounded recognition by integrating separate modes of sensation.
“From behavioral research, we know that people can identify a familiar voice faster and more accurately when they can associate it with the speaker’s face, but we never had a good explanation of why that happens,” said senior author Taylor Abel, M.D., associate professor of neurological surgery at the University of Pittsburgh School of Medicine. “In the visual cortex, specifically in the part that typically processes faces, we also see electrical activity in response to famous people’s voices, highlighting how deeply the two systems are interlinked.”
Even though the interplay between the auditory and the visual brain processing systems has been widely acknowledged and investigated by various teams of neuroscientists all over the world, those systems were traditionally thought to be structurally and spatially distinct.
Until recently, few studies attempted to directly measure activity from the brain center — the primary role of which is to consolidate and process visual information — to determine whether this center is also engaged when participants are exposed to famous voice stimuli.
Researchers at Pitt had a unique opportunity to study that interaction in patients with epilepsy who, as part of their medical care, were temporarily implanted with electrodes measuring brain activity to determine the source of their seizures.
Five adult patients consented to participate in the study, where Abel and his team showed participants photographs of three U.S. presidents — Bill Clinton, George W. Bush and Barack Obama — or played short recordings of their voices, and asked participants to identify them.
Recordings of the electrical activity from the region of the brain responsible for processing visual cues — called the fusiform gyri, or FG — showed that the same region became active when participants heard familiar voices, though that response was lower in magnitude and slightly delayed.
“This is important because it shows that auditory and visual areas interact very early when we identify people, and that they don’t work in isolation,” said Abel. “In addition to enriching our understanding of the basic functioning of the brain, our study explains the mechanisms behind disorders where voice or face recognition is compromised, such as in some dementias or related disorders.”
Ariane Rhone, Ph.D., of the University of Iowa, and Kyle Rupp, Ph.D., of Pitt, are co-first authors. Additional authors of the study are Dan Tranel, Ph.D., and Matthew Howard, III, Ph.D., both of the University of Iowa; and Jasmine Hect, Ph.D., and Emily Harford, Ph.D., both of Pitt.
This work was supported by National Institutes of Health grants R01 DC004290 and R21 DC019217.

After decades of fundamental scientific and drug discovery research, Alzheimer’s disease has remained inscrutable and incurable, with a bare minimum of therapeutic progress. But in a new review article in Nature Neuroscience, MIT scientists write that by employing the new research capability of single-cell profiling, the field has rapidly achieved long-sought insights with strong potential for both explaining Alzheimer’s disease and doing something meaningful about it. By analyzing this new evidence, for instance, the authors show that the disease’s disruptions converge on five main areas of cellular function, or “pathways,” in each of five major brain cell types.
Single-cell profiling technologies produce comprehensive measurements of genetic activity in individual cells, such as levels of RNA which is transcribed from DNA, so that the cell’s functions and roles of in the biology of the brain, and the pathology of disease, can be assessed. Single-cell profiling technologies go beyond genome sequencing, which catalogs the DNA present in most every cell of a person, by revealing how each cell is uniquely making use of that common set of instructions. In studying Alzheimer’s disease, scientists have been using single-cell profiling to see how various brain cells, such as distinct types of neurons and microglia and astrocytes act differently in disease compared to how they behave in a healthy brain.
In the article, MIT Brain and Cognitive Sciences doctoral student Mitch Murdock and Picower Professor Li-Huei Tsai, Director of MIT’s Picower Institute for Learning and Memory and Aging Brain Initiative, write that while the findings of single-cell profiling studies confirm that the disease’s terrible effects are complex and far-reaching, there appear to also be five pathways that become perturbed in each of five major cell types. Investigating these pathways, they write, could produce valuable biomarkers of disease and yield meaningful targets for therapeutic intervention: Inflammation and immune response Lipid (fat molecule) signaling and metabolism Metabolic stress and protein folding DNA damage and cellular senescence (aging) Interactions with brain vasculature (blood vessels)For each of these pathways in neurons, microglia, astrocytes, oligodendrocytes and oligodendrocyte precursor cells, Tsai and Murdock identify specific differences in gene regulation, found in single-cell studies, that significantly occur in brains of Alzheimer’s patients or mouse models compared to healthy control samples.
For example, Tsai and Murdock highlight more than a dozen genes all intimately involved in lipid processing whose expression is altered in various ways in various cells in the brain’s prefrontal cortex. For another example they show that all five cell types show impairments in DNA repair, albeit by changed expression of different genes in each.
“By identifying vulnerable cell types and the molecular programs that give rise to them, therapeutic interventions might reverse aberrant cellular trajectories,” Murdock and Tsai wrote in Nature Neuroscience. “While many transcriptional alterations are cell-type specific, these changes ultimately might converge on shared signaling pathways across cell types that might represent targets for new therapeutic strategies.”
To be sure, the authors note, there is still plenty of work to be done, both in refining and improving on single-cell techniques and also exploiting newer related opportunities. The paper notes a number of issues that must be carefully considered in producing valid single-cell profiling results, including where cells are sampled in the brain for sequencing, from whom, and in what condition. Moreover, it’s not always straightforward to show how changes in gene expression necessarily affect biology and it’s even harder to know whether any particular intervention, for instance to target altered inflammation pathways, will prove safe and effective as a therapy.
Future directions, meanwhile could include making greater use of “spatial transcriptomics,” which measures gene transcription in cells where they are situated within the brain, rather than removing them for analysis. Studies should be expanded to incorporate more human samples so that varying disease and demographic differences can be fully accounted for. Datasets should be shared and integrated, the authors write, and better comparisons between human and mouse samples are necessary to better understand how well, or not, they overlap.
“Single-cell profiling facilitates a nuanced portrait of the diverse cellular processes perturbed in the AD brain,” Tsai and Murdock conclude. “These varied molecular programs help explain the divergence between healthy aging and cognitive decline, and highlight cell-type-specific molecular programs involved in AD. Core signaling modules are disrupted across multiple cell types, and manipulating disrupted cellular states will pave the way for new therapeutic opportunities.”

Teens who frequently checked social media showed an increasing sensitivity to peer feedback, although the cause of the changes was not clear.The effect of social media use on children is a fraught area of research, as parents and policymakers try to ascertain the results of a vast experiment already in full swing. Successive studies have added pieces to the puzzle, fleshing out the implications of a nearly constant stream of virtual interactions beginning in childhood.A new study by neuroscientists at the University of North Carolina tries something new, conducting successive brain scans of middle schoolers between the ages of 12 and 15, a period of especially rapid brain development.The researchers found that children who habitually checked their social media feeds at around age 12 showed a distinct trajectory, with their sensitivity to social rewards from peers heightening over time. Teenagers with less engagement in social media followed the opposite path, with a declining interest in social rewards.The study, published on Tuesday in JAMA Pediatrics, is among the first attempts to capture changes to brain function correlated with social media use over a period of years.The study has important limitations, the authors acknowledge. Because adolescence is a period of expanding social relationships, the brain differences could reflect a natural pivot toward peers, which could be driving more frequent social media use.“We can’t make causal claims that social media is changing the brain,” said Eva H. Telzer, an associate professor of psychology and neuroscience at the University of North Carolina, Chapel Hill, and one of the authors of the study.But, she added, “teens who are habitually checking their social media are showing these pretty dramatic changes in the way their brains are responding, which could potentially have long-term consequences well into adulthood, sort of setting the stage for brain development over time.”A team of researchers studied an ethnically diverse group of 169 students in the sixth and seventh grades from a middle school in rural North Carolina, splitting them into groups according to how often they reported checking Facebook, Instagram and Snapchat feeds.At around age 12, the students already showed distinct patterns of behavior. Habitual users reported checking their feeds 15 or more times a day; moderate users checked between one and 14 times; nonhabitual users checked less than once a day.The subjects received full brain scans three times, at approximately one-year intervals, as they played a computerized game that delivered rewards and punishment in the form of smiling or scowling peers.While carrying out the task, the frequent checkers showed increasing activation of three brain areas: reward-processing circuits, which also respond to experiences like winning money or risk-taking behavior; brain regions that determine salience, picking out what stands out in the environment; and the prefrontal cortex, which helps with regulation and control.The results showed that “teens who grow up checking social media more often are becoming hypersensitive to feedback from their peers,” Dr. Telzer said.The findings do not capture the magnitude of the brain changes, only their trajectory. And it is unclear, authors said, whether the changes are beneficial or harmful. Social sensitivity could be adaptive, showing that the teenagers are learning to connect with others; or it could lead to social anxiety and depression if social needs are not met.Researchers in the field of social media warned against drawing sweeping conclusions based on the findings.“They are showing that the way you use it at one point in your life does influence the way your brain develops, but we don’t know by how much, or whether it’s good or bad,” said Jeff Hancock, the founding director of the Stanford Social Media Lab, who was not involved in the study. He said that many other variables could have contributed to these changes.“What if these people joined a new team — a hockey team or a volleyball team — so started getting a lot more social interaction?” he said. It could be, he added, that the researchers are “picking up on the development of extroversion, and extroverts are more likely to check their social media.”He described the paper as “a very sophisticated piece of work,” contributing to research that has emerged recently showing that sensitivity to social media varies from person to person.“There are people who have a neurological state that means they are more likely to be attracted to checking frequently,” he said. “We’re not all the same, and we should stop thinking that social media is the same for everyone.”Over the last decade, social media has remapped the central experiences of adolescence, a period of rapid brain development.Nearly all American teenagers engage through social media, with 97 percent going online every day and 46 percent reporting that they are online “almost constantly,” according to the Pew Research Center. Black and Latino adolescents spend more hours on social media than their white counterparts, research has shown.Researchers have documented a range of effects on children’s mental health. Some studies have linked use of social media with depression and anxiety, while others found little connection. A 2018 study of lesbian, gay and bisexual teenagers found that social media provided them validation and support, but also exposed them to hate speech.Experts who reviewed the study said that because the researchers measured students’ social media use only once, around age 12, it was impossible to know how it changed over time, or to rule out other factors that might also affect brain development.Without more information about other aspects of the students’ lives, “it is challenging to discern how specific differences in brain development are to social media checking,” said Adriana Galvan, a specialist in adolescent brain development at the University of California Los Angeles, who was not involved in the study.Jennifer Pfeifer, a professor of psychology at the University of Oregon and co-director of the National Scientific Council on Adolescence, said, “All experience accumulates and is reflected in the brain.”“I think you want to put it into this context,” she said. “So many other experiences that adolescents have will also be changing the brain. So we don’t want to get into some kind of moral panic about the idea that social media is use is changing adolescents’ brains.”Dr. Telzer, one of the study’s authors, described the rising sensitivity to social feedback as “neither good nor bad.”“It’s helping them connect to others and obtain rewards from the things that are common in their social world, which is engaging in social interactions online,” she said.“This is the new norm,” she added. “Understanding how this new digital world is influencing teens is important. It may be associated with changes in the brain, but that may be for good or for bad. We don’t necessarily know the long-term implications yet.”

Published20 minutes agoShareclose panelShare pageCopy linkAbout sharingImage source, Getty ImagesBy Michelle RobertsDigital health editorAmerican football star Damar Hamlin is the latest athlete to encounter heart problems during competitive play. The 24-year-old fell to the ground after colliding with an opponent during the primetime game. Medics confirmed he had gone into cardiac arrest – meaning his heart had stopped beating properly and was unable to do its job of pumping blood around the body. Urgent resuscitation was required on the pitch to help save his life. He is now in a critical condition in hospital. Doctors treating him have not yet described the exact underlying cause. NFL player in critical condition after cardiac arrestBlunt trauma is one possibility, triggering something called commotio cordis. In this rare scenario, a direct hit to the chest can result in cardiac arrest by making the heart go into an abnormal, life-threatening rhythm. It’s different to a heart attack, which happens when blood supply to the heart muscle is cut off.Another possibility with blunt trauma is major structural damage to the heart from force of the blow. It’s not yet known what internal injuries Hamlin may have sustained from the incident and whether there has been any significant damage to his heart.Another potentially lethal heart condition affecting some young athletes is a genetic disorder known as hypertrophic cardiomyopathy. This video can not be playedTo play this video you need to enable JavaScript in your browser.Individuals who have this can appear extremely fit and well, with no obvious warning signs that there is a such a serious underlying problem. It is a condition in which the heart muscle becomes overgrown or “hypertrophied”. The thickened heart muscle can make it harder for the heart to pump blood. And there may be related life-threatening heart rhythm problems too. Danish footballer Christian Eriksen had a cardiac arrest at a Euro 2020 match and was close to death on the pitch. Doctors used a defibrillator to shock his heart and get it working again. He’s since had a small device, called an ICD, fitted to keep his heart on track. This video can not be playedTo play this video you need to enable JavaScript in your browser.Eriksen has said there was no history of a heart condition in his family and, like other top-flight footballers, he was tested regularly throughout his career.In 2012, another footballer, Fabrice Muamba, collapsed on the pitch when his heart stopped beating correctly. He needed 15 defibrillator shocks in all. Muamba was ‘dead’ for 78 minutesHow tiny device led to Eriksen’s ‘miracle’ football returnRapid medical intervention can work, but it’s not always possible to save every life.Sudden death syndrome (SDS) is an umbrella term used for the many different causes of cardiac arrest in young people. They are very rare.According to the charity Cardiac Risk in the Young (CRY), every week in the UK, 12 people aged under 35 die from sudden cardiac arrest.In about 1 in every 20 cases of sudden cardiac death and up to 1 in 5 young sudden cardiac deaths, no definite cause of death can be found, even after an expert cardiac pathologist has examined the heart for structural abnormalitiesA simple way to diagnose many cardiac abnormalities is by having an ECG (electrocardiogram) test. It can reveal if the electrical impulses are awry. Dangerous arrhythmias can then be treated, before they cause a major issue. You can read more about the topic here.When to do CPROnly do it if someone is:unconscious and not breathingunconscious and not breathing properlyIf someone is unconscious but they’re breathing normally, call the emergency services and put them in the recovery position.Don’t waste time checking for a pulse – if someone is unresponsive and not breathing or not breathing normally then call and start CPR.How to do CPRThis video can not be playedTo play this video you need to enable JavaScript in your browser.More on this storyNFL player in critical condition after cardiac arrest2 hours agoRelated Internet LinksBritish Heart foundationThe BBC is not responsible for the content of external sites.

People with a condition known as dry eye disease are more likely than those with healthy eyes to suffer injuries to their corneas. Studying mice, researchers at Washington University School of Medicine in St. Louis have found that proteins made by stem cells that regenerate the cornea may be new targets for treating and preventing such injuries.
The study is published online Jan. 2 in the Proceedings of the National Academy of Sciences.
Dry eye disease occurs when the eye can’t provide adequate lubrication with natural tears. People with the common disorder use various types of drops to replace missing natural tears and keep the eyes lubricated, but when eyes are dry, the cornea is more susceptible to injury.
“We have drugs, but they only work well in about 10% to 15% of patients,” said senior investigator Rajendra S. Apte, MD, PhD, the Paul A. Cibis Distinguished Professor in the John F. Hardesty, MD, Department of Ophthalmology & Visual Sciences. “In this study involving genes that are key to eye health, we identified potential targets for treatment that appear different in dry eyes than in healthy eyes. Tens of millions of people around the world — with an estimated 15 million in the United States alone — endure eye pain and blurred vision as a result of complications and injury associated with dry eye disease, and by targeting these proteins, we may be able to more successfully treat or even prevent those injuries.”
The researchers analyzed genes expressed by the cornea in several mouse models — not only of dry eye disease, but also of diabetes and other conditions. They found that in mice with dry eye disease, the cornea activated expression of the gene SPARC. They also found that higher levels of SPARC protein were associated with better healing.
“We conducted single-cell RNA sequencing to identify genes important to maintaining the health of the cornea, and we believe that a few of them, particularly SPARC, may provide potential therapeutic targets for treating dry eye disease and corneal injury,” said first author Joseph B. Lin, an MD/PhD student in Apte’s lab.
“These stem cells are important and resilient and a key reason corneal transplantation works so well,” Apte explained. “If the proteins we’ve identified don’t pan out as therapies to activate these cells in people with dry eye syndrome, we may even be able to transplant engineered limbal stem cells to prevent corneal injury in patients with dry eyes.”
Lin JB, Shen X, Pfeifer CW, Shiau F, Santeford A, Ruzycki PA, Clark BS, Liu Q, Huang AJW, Apte RS. Dry eye disease in mice activates adaptive corneal epithelial regeneration distinct from constitutive renewal in homeostasis. Proceedings of the National Academy of Sciences, Jan. 2, 2023.
The study was funded with support from the National Eye Institute, the National Institute of Diabetes and Digestive and Kidney Diseases and the National Institute of General Medical Sciences of the National Institutes of Health (NIH). Grant numbers: R01 EY019287, R01 EY027844, R01 EY024704, P30 EY02687, F30 DK130282, T32 GM07200 Additional funding provided by the Jeffrey T. Fort Innovation Fund, a Centene Corp. contract for the Washington University-Centene ARCH Personalized Medicine Initiative and Research to Prevent Blindness.
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Materials provided by Washington University School of Medicine. Original written by Jim Dryden. Note: Content may be edited for style and length.