Publisher Health

Ultrasound imaging is a safe and noninvasive window into the body’s workings, providing clinicians with live images of a patient’s internal organs. To capture these images, trained technicians manipulate ultrasound wands and probes to direct sound waves into the body. These waves reflect back out to produce high-resolution images of a patient’s heart, lungs, and other deep organs.
Currently, ultrasound imaging requires bulky and specialized equipment available only in hospitals and doctor’s offices. But a new design by MIT engineers might make the technology as wearable and accessible as buying Band-Aids at the pharmacy.
In a paper appearing today in Science, the engineers present the design for a new ultrasound sticker — a stamp-sized device that sticks to skin and can provide continuous ultrasound imaging of internal organs for 48 hours.
The researchers applied the stickers to volunteers and showed the devices produced live, high-resolution images of major blood vessels and deeper organs such as the heart, lungs, and stomach. The stickers maintained a strong adhesion and captured changes in underlying organs as volunteers performed various activities, including sitting, standing, jogging, and biking.
The current design requires connecting the stickers to instruments that translate the reflected sound waves into images. The researchers point out that even in their current form, the stickers could have immediate applications: For instance, the devices could be applied to patients in the hospital, similar to heart-monitoring EKG stickers, and could continuously image internal organs without requiring a technician to hold a probe in place for long periods of time.
If the devices can be made to operate wirelessly — a goal the team is currently working toward — the ultrasound stickers could be made into wearable imaging products that patients could take home from a doctor’s office or even buy at a pharmacy.

New research from VCU Massey Cancer Center — published Thursday in Cell Reports — demonstrated that a novel targeted therapy could be an effective treatment option for a deadly pediatric cancer known as neuroblastoma.
Neuroblastoma is a type of cancer that develops in nerve tissue, most commonly in the glands around the kidneys. Despite multiple medical advancements that have improved outcomes for the disease, high-risk neuroblastoma remains responsible for the most cancer-related deaths in children five years and younger.
Previous research has demonstrated that the activation of a specific group of proteins — MEK/ERK — helps neuroblastoma cells survive and grow. However, a class of drugs used to prohibit the function of these proteins called MEK inhibitors have proven ineffective in treating the disease because high doses are associated with a substantial level of toxicity.
“Breakthroughs significantly altering the fate of high-risk neuroblastomas have been elusive,” said study author Anthony Faber, Ph.D., co-leader of the Developmental Therapeutics research program and Natalie N. and John R. Congdon, Sr. Endowed Chair in Cancer Research at VCU Massey Cancer Center.
To address the lack of effective treatment options for neuroblastoma, Faber’s laboratory along with his collaborators performed high-throughput drug screening with SHP099. This compound belongs to a new class of drugs that target and block an enzyme called SHP2, which is along the same genetic pathway as MEK/ERK.
High-throughput screening is an important method in drug discovery and design that allows researchers to automate thousands to millions of tests on chemical or biological compounds.
Repeatedly, Faber and his research team found that neuroblastoma tumors in mice were sensitive to SHP099, and the tumors shrank considerably in some of the models. SHP099 had a particularly effective impact in tumor cells that had limited or no expression of the neurofibromin 1 (NF1) protein. Additionally, they determined that NF1 expression is much lower in advanced or relapsed neuroblastoma cells, and the protein is more readily deactivated in high-risk neuroblastoma.
“We found variable yet consistently positive effects across all models of low NF1, high-risk neuroblastoma, revealing a new drug target in relapsed disease,” said Faber, who is also an associate professor in the Philips Institute for Oral Health Research at the VCU School of Dentistry.
Faber said one of the most important findings in the study — made by first authors Jinyang Cai, Ph.D., and Sheeba Jacob, Ph.D., — was that SHP2 inhibitors were ineffective at blocking the function of MEK/ERK in healthy cells and therefore were not toxic to them.
“These findings suggest that, unlike MEK inhibitors, SHP2 inhibitors may be dosed high enough to inhibit MEK/ERK signaling in neuroblastoma tumors,” said Faber, who credited the high efficiency and capabilities of the Cancer Mouse Models Core at Massey for allowing his team to comprehensively test SHP099.
As there are a large number of SHP2 inhibitors now in clinical testing, Faber will work with collaborator John Glod, M.D., Ph.D., to hopefully bring one of these inhibitors into clinical testing at the National Cancer Institute. Currently, Faber’s group is also planning to test SHP2 inhibitors in combination with anti-GD2 therapy, an approved immunotherapy for neuroblastoma.
In addition to neuroblastoma, Faber’s team also found SHP099 to be effective in head and neck squamous cell carcinoma (HNSCC). Separate findings will be published soon, and the team is planning further testing of a combination therapy in HNSCC with SHP2 and EGFR inhibitors.
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Materials provided by Virginia Commonwealth University. Original written by Blake Belden. Note: Content may be edited for style and length.

Early exposure to antibiotics kills healthy bacteria in the digestive tract and can cause asthma and allergies, a new study demonstrates.
The study, published in Mucosal Immunology, has provided the strongest evidence so far that the long-observed connection between antibiotic exposure in early childhood and later development of asthma and allergies is causal.
“The practical implication is simple: Avoid antibiotic use in young children whenever you can because it may elevate the risk of significant, long-term problems with allergy and/or asthma,” said senior author Martin Blaser, director of the Center for Advanced Biotechnology and Medicine at Rutgers.
In the study, the researchers, who came from Rutgers, New York University and the University of Zurich, noted that antibiotics, “among the most used medications in children, affect gut microbiome communities and metabolic functions. These changes in microbiota structure can impact host immunity.”
In the first part of the experiment, five-day-old mice received water, azithromycin or amoxicillin. After the mice matured, researchers exposed them to a common allergen derived from house dust mites. Mice that had received either of the antibiotics, especially azithromycin, exhibited elevated rates of immune responses — i.e., allergies.
The second and third parts of the experiment tested the hypothesis that early exposure to antibiotics (but not later exposure) causes allergies and asthma by killing some healthy gut bacteria that support proper immune system development.
Lead author Timothy Borbet first transferred bacteria-rich fecal samples from the first set of mice to a second set of adult mice with no previous exposure to any bacteria or germs. Some received samples from mice given azithromycin or amoxicillin in infancy. Others received normal samples from mice that had received water.
Mice that received antibiotic-altered samples were no more likely than other mice to develop immune responses to house dust mites, just as people who receive antibiotics in adulthood are no more likely to develop asthma or allergies than those who don’t.
Things were different, however, for the next generation. Offspring of mice that received antibiotic-altered samples reacted more to house dust mites than those whose parents received samples unaltered by antibiotics, just as mice that originally received antibiotics as babies reacted more to the allergen than those that received water.
“This was a carefully controlled experiment,” said Blaser. “The only variable in the first part was antibiotic exposure. The only variable in the second two parts was whether the mixture of gut bacteria had been affected by antibiotics. Everything else about the mice was identical.
Blaser added that “these experiments provide strong evidence that antibiotics cause unwanted immune responses to develop via their effect on gut bacteria, but only if gut bacteria are altered in early childhood.”
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Materials provided by Rutgers University. Original written by Andrew Smith. Note: Content may be edited for style and length.

Of the roughly 20,000 people in the U.S. diagnosed with esophageal cancer this year, just 4,000 are likely to still be alive in 2027.
Such dire data has long driven researchers to try to understand the roots of the disease, but they have discovered little — until now.
A team of researchers at the Case Western Reserve University School of Medicine and Case Comprehensive Cancer Center believe they have identified a cell signaling pathway responsible for the development of esophageal adenocarcinomas, an aggressive form of esophageal cancer that has gradually become more common, even in younger people.
“The incidence of esophageal cancers has increased several fold over the last few decades, making it the most common esophageal malignancy in the U.S.,” said Kishore Guda, associate professor at the School of Medicine and member of the Case Comprehensive Cancer Center. “Like gastric and pancreatic cancers, these are highly aggressive malignancies that can be resistant to treatment, with dismal survival rates and with lack of effective targeted therapies.”
New research published this month in Gastroenterologyexplains how an important molecular signal, known to scientists as the “Ephrin B2 (EphB2) Tyrosine kinase pathway,” is activated during the development of esophageal adenocarcinomas and contributes to cancer growth. The findings also show that the EphB2 pathway appears to control the growth of cancer cells while also regulating the behavior of normal esophageal cells.
“From a molecular standpoint, EphB2 induces the levels of a well-recognized pro-cancer gene, called c-MYC. One mechanism by which EphB2 seems to affect MYC levels is through its direct interaction with a protein known as MYCBP2, which is a suppressor of MYC activity,” Guda said. “This is the first discovery to our knowledge that demonstrates EphB2 regulation of MYC and its physical interaction with MYCBP2.”
By analyzing normal, pre-cancer, and cancerous biopsy samples with RNA sequencing, the researchers found that EphB2 signaling is hyperactivated in nearly all instances of esophageal adenocarcinomas as well as a condition called Barrett’s esophagus.
Barrett’s esophagus occurs when the lining of the esophagus becomes damaged by acid reflux, resulting in the replacement of esophageal cells with intestinal-type cells. This condition is linked to an increased risk of developing esophageal cancer, according to the National Institutes of Health (NIH).
The scientists believe the EphB2 pathway is an attractive therapeutic target and suppressing its activity in cancer could be a beneficial treatment strategy for these cancers.
“Our immediate goal is to explore and develop EphB2 chemical inhibitors and/or EphB2-targeting immune-cell based strategies, and to test their efficacy in preclinical esophageal as well as gastric cancer models, followed by transitioning to human trials,” said Guda.
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Materials provided by Case Western Reserve University. Note: Content may be edited for style and length.

Research at the University of Wisconsin-Madison’s Center for Healthy Minds has isolated the changes in pain-related brain activity that follow mindfulness training — pointing a way toward more targeted and precise pain treatment.
The study, published today (July 27) in The American Journal of Psychiatry, identified pathways in the brain specific to pain regulation on which activity is altered by the center’s eight-week Mindfulness Based Stress Reduction course.
These changes were not seen in participants who took a similar course without the mindfulness instruction — important new evidence that the brain changes are due to the mindfulness training itself, according to Joseph Wielgosz, who led the work while he was a graduate student at UW-Madison and is now a postdoctoral researcher at Stanford University. The study is the first to demonstrate pain-related brain changes from a standardized mindfulness course that is widely offered in clinical settings.
Around one-third of Americans experience pain-related problems, but common treatments — like medications and invasive procedures — don’t work for everyone and, according to Wielgosz, have contributed to an epidemic of addiction to prescription and illicit drugs.
Popular with patients and promising in its clinical outcomes, mindfulness training courses like MBSR have taken a central place in the drive for a more effective approach to pain management. By practicing nonjudgmental, “present-centered” awareness of mind and body, participants can learn to respond to pain with less distress and more psychological flexibility — which can ultimately lead to reductions in pain itself.
To measure neural pain response, study participants had their brains scanned while receiving a carefully controlled heat-based stimulus on their forearm. The researchers recorded two brain-wide signatures of pain-related activity, developed by collaborator Tor Wager, a professor of neuroscience at Dartmouth College. This innovative technique dramatically improves the ability to detect pain-related signals in the brain’s complex activity. Changes in signatures can also be more easily interpreted in psychological terms.

Being exposed to work requirements in order to receive nutrition benefits from the U.S. government significantly increased mental health care use for depression and anxiety, a new Northwestern University study has found. The policy’s negative effects occurred much sooner for women than men.
This is the first study to look at how work requirements associated with the Supplemental Nutrition Assistance Program (SNAP) — sometimes referred to as food stamps — affect mental health.
The study was published July 28 in the journal Health Services Research.
SNAP improves food security, health and economic wellbeing for low-income individuals and families and is provided by the U.S. Department of Agriculture’s Food and Nutrition Service.
“We’ve known for a while that food insecurity is associated with poor mental health outcomes because of the fear, stigma, depression, anxiety and stress around it,” said corresponding author Lindsey Allen, assistant professor of emergency medicine at Northwestern University Feinberg School of Medicine. “So it’s no wonder peoples’ stress increased when they realized they were going to lose their access to food unless they met these requirements.”
Background on SNAP, how the study worked
While SNAP work requirements are federally mandated, states can get exemptions incounties where there isn’t much economic opportunity. With rising employment rates and job availability over the past decade, these waivers are being eliminated, exposing hundreds of thousands of SNAP enrollees to the requirements.

Researchers at the University of Colorado Anschutz Medical Campus have shown a direct link between vagus nerve stimulation and its connection to the learning centers of the brain. The discovery may lead to treatments that will improve cognitive retention in both healthy and injured nervous systems.
The study was published last week in the journal Neuron.
“We concluded that there is a direct connection between the vagus nerve, the cholinergic system that regulates certain aspects of brain function, and motor cortex neurons that are essential in learning new skills,” said Cristin Welle, PhD, senior author of the paper and the vice chair of research for the Department of Neurosurgery at the University of Colorado School of Medicine. “This could provide hope to patients with a variety of motor and cognitive impairments, and someday help healthy individuals learn new skills faster.”
Researchers taught healthy mice a task that’s normally difficult to see if it could help improve learning. They discovered that stimulating the vagus nerve during the process helped them learn the task much faster and achieve a higher performance level. This showed that vagus nerve stimulation can increase learning in a healthy nervous system.
The vagus nerve is critical because it regulates internal organ functions like digestion, heart rate and respiration. It also helps control reflex actions like coughing, swallowing and sneezing.
The study also revealed a direct connection between the vagus nerve and the cholinergic system that’s essential for learning and attention. Each time the vagus nerve was stimulated, researchers could observe the neurons that control learning activated within the cholinergic system. Damage to this system has been linked to Alzheimer’s disease, Parkinson’s disease and other motor and cognitive conditions. Now that this connection has been established in healthy nervous systems, Welle said it could lead to better treatment options for those whose systems have been damaged.
“The idea of being able to move the brain into a state where it’s able to learn new things is important for any disorders that have motor or cognitive impairments,” she said. “Our hope is that vagus nerve stimulation can be paired with ongoing rehabilitation in disorders for patients who are recovering from a stroke, traumatic brain injury, PTSD or a number of other conditions.”
In addition to the study, Welle and her team have applied for a grant that would allow them to use a non-invasive device to stimulate the vagus nerve to treat patients with multiple sclerosis who have developed movement deficits. She’s also hoping this device could eventually help healthy people learn new skills faster.
“I think there’s a huge untapped potential for using vagus nerve stimulation to help the brain heal itself,” she said. “By continuing to investigate it, we can ultimately optimize patient recovery and open new doors for learning.”
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Materials provided by University of Colorado Anschutz Medical Campus. Original written by Laura Kelley. Note: Content may be edited for style and length.

A gene that UVA Health researchers discovered is responsible for the deadliest type of brain tumor is also responsible for two forms of childhood cancer, the scientists have found.
The new discovery may open the door to the first targeted treatments for two types of rhabdomyosarcoma, a cancer of the soft tissue that primarily strikes young children.
The gene may also play an important role in other cancers that form in muscle, fat, nerves and other connective tissues in both children and adults, the research suggests.
“We accumulated multiple lines of evidence supporting [the gene] AVIL is powerful driver for both major types of rhabdomyosarcoma,” said researcher Hui Li, PhD, of the University of Virginia School of Medicine’s Department of Pathology and UVA Cancer Center. “The tumors are oncogene addicted to AVIL, which supports the rationale to design therapeutic interventions to target AVIL in this childhood cancer.”
Rhabdomyosarcoma Oncogene
Li and his team discovered in 2020 that the gene AVIL is the oncogene (cancer-causing gene) responsible for glioblastoma, the most lethal form of brain cancer. Less than 7% of patients with glioblastoma survive five years after diagnosis.

What are the chances you will contract Covid-19 on a plane flight? A study led by MIT scholars offers a calculation of that for the period from June 2020 through February 2021. While the conditions that applied at that stage of the Covid-19 pandemic differ from those of today, the study offers a method that could be adapted as the pandemic evolves.
The study estimates that from mid-2020 through early 2021, the probability of getting Covid-19 on an airplane surpassed 1 in 1,000 on a totally full flight lasting two hours at the height of the early pandemic, roughly December 2020 and January 2021. It dropped to about 1 in 6,000 on a half-full two-hour flight when the pandemic was at its least severe, in the summer of 2020. The overall risk of transmission from June 2020 through February 2021 was about 1 in 2,000, with a mean of 1 in 1,400 and a median of 1 in 2,250.
To be clear, current conditions differ from the study’s setting. Masks are no longer required for U.S. domestic passengers; in the study’s time period, airlines were commonly leaving middle seats open, which they are no longer doing; and newer Covid-19 variants are more contagious than the virus was during the study period. While those factors may increase the current risk, most people have received Covid-19 vaccinations since February 2021, which could serve to lower today’s risk — though the precise impact of those vaccines against new variants is uncertain.
Still, the study does provide a general estimate about air travel safety with regard to Covid-19 transmission, and a methodology that can be applied to future studies. Some U.S. carriers at the time stated that onboard transmission was “virtually nonexistent” and “nearly nonexistent,” but as the research shows, there was a discernible risk. On the other hand, passengers were not exactly facing coin-flip odds of catching the virus in flight, either.
“The aim is to set out the facts,” says Arnold Barnett, a management professor at MIT and aviation risk expert, who is co-author of a recent paper detailing the study’s results. “Some people might say, ‘Oh, that doesn’t sound like very much.’ But if we at least tell people what the risk is, they can make judgments.”
As Barnett also observes, a round-trip flight with a change of planes and two two-hour segments in each direction counts as four flights in this accounting, so a 1 in 1,000 probability, per flight, would lead to approximately a 1 in 250 chance for such a trip as a whole.

The enzymes found in living organisms have impressive catalytic power. Thanks to enzymes the chemical reactions that sustain life happen millions of times faster than they would occur without them. Enzymes speed up reactions by helping to lower the activation energy needed to start them, but for more than 70 years how enzymes achieve this has been the subject of intense debate.
Dr. Tor Savidge, professor of pathology and immunology at Baylor College of Medicine and Texas Children’s Microbiome Center, and his colleagues are changing the way to look at this old argument. In their work published in Chemical Science, they investigated the similarities and differences between the two mechanisms currently under debate by characterizing catalytic reactions at a detailed molecular level.
“At present time, two major different reaction mechanisms are proposed to explain enzymatic catalytic power,” Savidge said. “One proposes that enzymes lower the reaction’s activation energy via stabilization of transition states (TS) and the other that they do it by destabilizing the ground state (GS) of enzymes. The current idea is that these mechanisms are mutually exclusive.”
First author Dr. Deliang Chen at Gannan Normal University in China and his colleagues took a theoretical approach, taking into consideration previous findings from the Savidge lab showing that the noncovalent interactions of substrates and enzymes with water are important in terms of the mechanism of the enzymatic reactions.
“In a biological environment you have to consider the water — that it is going to interfere with the very complex atomic interactions occurring in the enzyme’s active site. We need to consider all of them to understand where exactly you need to have electrostatic interactions that are going to favor that enzymatic process,” Savidge said. “When you take that into consideration, you can understand how these mechanisms are operating.”
Their analyses led the team to propose something new, that TS and GS are not that different after all. They use a similar atomic mechanism to boost the enzymatic reaction forward. The mechanism involves water in altering the charge of important residues within the catalytic site in a way that favors the formation of an energetically favorable state that drives the enzymatic reaction to occur.
“The important, new point here is not how this is achieved but when it is achieved,” Savidge said. “We have shown that in stabilization of transition states, the charges that drive the reaction forward are formed before the substrate enters the active site. While in the destabilization ground state this also occurs but after the substrate enters the active site.”
The researchers also proposed that the common mechanism between TS and GS is universal, it can be applied to many enzymatic reactions.
“Our findings have important implications not only to better understand the catalytic power of enzymes, but also for practical drug design applications. “We use our findings to more deeply explore microbial enzymatic catalysis in different environments and to design artificial enzymes.”
Yibao Li, Xun Li, Xiaolin Fan, at Gannan Normal University, and Xuechuan Hong at Wuhan University School of Pharmaceutical Sciences also contributed to this work.
This work is supported by grants from the National Natural Science Foundation of China (21763002), the Natural Science Foundation of Jiangxi Province (20202ACBL203008) and the National Institute of Allergy and Infectious Diseases (U01-AI24290 and P01-AI152999).
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Materials provided by Baylor College of Medicine. Original written by Ana María Rodríguez, Ph.D.. Note: Content may be edited for style and length.