He diagnosed dozens of patients with what he said were suppressed memories of being tortured by cults. He later lost his license.Bennett Braun, a Chicago psychiatrist whose diagnoses of repressed memories involving horrific abuse by devil worshipers helped to fuel what became known as the “satanic panic” of the 1980s and ’90s, died on March 20 in Lauderhill, Fla., north of Miami. He was 83.Jane Braun, one of his ex-wives, said the death, in a hospital, was from complications of a fall. Dr. Braun lived in Butte, Mont., but had been in Lauderhill on vacation.Dr. Braun gained renown in the early 1980s as an expert in two of the most popular and controversial areas of psychiatric treatment: repressed memories and multiple personality disorder, now known as dissociative identity disorder.He claimed that he could help patients uncover memories of childhood trauma — the existence of which, he and others said, were responsible for the splintering of a person’s self into many distinct personalities.He created a unit dedicated to dissociative disorders at Rush-Presbyterian-St. Luke’s Medical Center in Chicago (now Rush University Medical Center); became a frequently quoted expert in the news media; and helped to found the what is now the International Society for the Study of Trauma and Dissociation, a professional organization of over 2,000 members today.It was from that sizable platform that Dr. Braun publicized his most explosive findings: that in dozens of cases, his patients discovered memories of being tortured by satanic cults and, in some cases, of having participated in the torture themselves.We are having trouble retrieving the article content.Please enable JavaScript in your browser settings.Thank you for your patience while we verify access. If you are in Reader mode please exit and log into your Times account, or subscribe for all of The Times.Thank you for your patience while we verify access.Already a subscriber? Log in.Want all of The Times? Subscribe.

Rice University engineers have developed the smallest implantable brain stimulator demonstrated in a human patient. Thanks to pioneering magnetoelectric power transfer technology, the pea-sized device developed in the Rice lab of Jacob Robinson in collaboration with Motif Neurotech and clinicians Dr. Sameer Sheth and Dr. Sunil Sheth can be powered wirelessly via an external transmitter and used to stimulate the brain through the dura — the protective membrane attached to the bottom of the skull.
The device, known as the Digitally programmable Over-brain Therapeutic (DOT), could revolutionize treatment for drug-resistant depression and other psychiatric or neurological disorders by providing a therapeutic alternative that offers greater patient autonomy and accessibility than current neurostimulation-based therapies and is less invasive than other brain-computer interfaces (BCIs).
“In this paper we show that our device, the size of a pea, can activate the motor cortex, which results in the patient moving their hand,” said Robinson, a professor of electrical and computer engineering and of bioengineering at Rice. “In the future, we can place the implant above other parts of the brain, like the prefrontal cortex, where we expect to improve executive functioning in people with depression or other disorders.”
Existing implantable technologies for brain stimulation are powered by relatively large batteries that need to be placed under the skin elsewhere in the body and connected to the stimulating device via long wires. Such design limitations require more surgery and subject the individual to a greater burden of hardware implantation, risks of wire breakage or failure and the need for future battery replacement surgeries.
“We eliminated the need for a battery by wirelessly powering the device using an external transmitter,” explained Joshua Woods, an electrical engineering graduate student in the Robinson lab and lead author on the study published in Science Advances. Amanda Singer, a former graduate student in Rice’s applied physics program who is now at Motif Neurotech, is also a lead author.
The technology relies on a material that converts magnetic fields into electrical pulses. This conversion process is very efficient at small scales and has good misalignment tolerance, meaning it does not require complex or minute maneuvering to activate and control. The device has a width of 9 millimeters and can deliver 14.5 volts of stimulation.
“Our implant gets all of its energy through this magnetoelectric effect,” said Robinson, who is founder and CEO of Motif, a startup working to bring the device to market. “The physics of that power transfer makes this much more efficient than any other wireless power transfer technologies under these conditions.”
Motif is one of several neurotech companies that are probing the potential of BCIs to revolutionize treatments for neurological disorders.

“Neurostimulation is key to enabling therapies in the mental health space where drug side effects and a lack of efficacy leave many people without adequate treatment options,” Robinson said.
The researchers tested the device temporarily in a human patient, using it to stimulate the motor cortex — the part of the brain responsible for movement — and generating a hand movement response. They next showed the device interfaces with the brain stably for a 30-day duration in pigs.
“This has not been done before because the quality and strength of the signal needed to stimulate the brain through the dura were previously impossible with wireless power transfer for implants this small,” Woods said.
Robinson envisions the technology being used from the comfort of one’s home. A physician would prescribe the treatment and provide guidelines for using the device, but patients would retain complete control over how the treatment is administered.
“Back home, the patient would put on their hat or wearable to power and communicate with the implant, push ‘go’ on their iPhone or their smartwatch and then the electrical stimulation from that implant would activate a neuronal network inside the brain,” Robinson said.
Implantation would require a minimally invasive 30-minute procedure that would place the device in the bone over the brain. Both the implant and the incision would be virtually invisible, and the patient would go home the same day.

“When you think about a pacemaker, it’s a very routine part of cardiac care,” said Sheth, professor and vice-chair of research, McNair Scholar and Cullen Foundation Endowed Chair of Neurosurgery at the Baylor College of Medicine. “In neurological and psychiatric disorders, the equivalent is deep brain stimulation (DBS), which sounds scary and invasive. DBS is actually quite a safe procedure, but it’s still brain surgery, and its perceived risk will place a very low ceiling on the number of people who are willing to accept it and may benefit from it. Here’s where technologies like this come in. A 30-minute minor procedure that is little more than skin surgery, done in an outpatient surgery center, is much more likely to be tolerated than DBS. So if we can show that it is about as effective as more invasive alternatives, this therapy will likely make a much larger impact on mental health.”
For some conditions, epilepsy for example, the device may need to be on permanently or most of the time, but for disorders such as depression and OCD, a regimen of just a few minutes of stimulation per day could suffice to bring about the desired changes in the functioning of the targeted neuronal network.
In terms of next steps, Robinson said that on the research side he is “really interested in the idea of creating networks of implants and creating implants that can stimulate and record, so that they can provide adaptive personalized therapies based on your own brain signatures.” From the therapeutic development standpoint, Motif Neurotech is in the process of seeking FDA approval for a long-term clinical trial in humans. Patients and caregivers can sign up on the Motif Neurotech website to learn when and where these trials will begin.
The work was supported in part by The Robert and Janice McNair Foundation, the McNair Medical Institute, DARPA and the National Science Foundation.

A third of the nearly 20 million women who participated in a national health survey report migraines during menstruation, and of them, 11.8 million, or 52.5%, were premenopausal. The analysis was conducted by researchers at Georgetown University Medical Center and Pfizer, Inc., which makes a migraine medication.
Because of the underuse of medications to help treat or prevent menstrual migraines, investigators wanted to understand how common menstrual migraines were and which groups of women could most benefit from potential therapies. The study will be presented April 16, at the American Academy of Neurology 2024 Annual Meeting in Denver.
“The first step in helping a woman with menstrual migraine is making a diagnosis; the second part is prescribing a treatment; and the third part is finding treatments patients are satisfied with and remain on to reduce disability and improve quality of life,” says the study author, Jessica Ailani, MD, professor of clinical neurology at Georgetown University School of Medicine and director of the MedStar Georgetown Headache Center at Medstar Georgetown University Hospital.
The researchers used the 2021 U.S. National Health and Wellness Survey, conducted by the National Center for Health Statistics, to analyze responses from women who reported their current migraine treatments, frequency and disabilities via the Migraine Disability Assessment Test (MIDAS), a five-question survey. A migraine headache can cause severe throbbing pain or a pulsing sensation, usually on one side of the head. It’s often accompanied by nausea, vomiting, and extreme sensitivity to light and sound.
“Discrepancies in the incidence of who gets migraine attacks associated with menses is likely due to premenopausal women having more regular menstrual cycles and thus more menstrual-related migraines,” says Ailani. “Additionally, as women move into their 40’s and become peri-menopausal, there tends to be a greater shift through the month in hormone levels also leading to frequent migraine attacks.”
The survey found that for all women during their menstrual periods, migraine attacks occurred as frequently as 4.5 times and that monthly only migraine headaches lasted 8.4 days, on average; 56.2 % of women had moderate-to-severe migraine-specific disabilities that ranked highest on the MIDAS scale.
When looking at treatments women in the survey used to help control their migraine symptoms, 42.4% used over-the-counter medications while 48.6% used prescription medications. Of the 63.9 % of women who used migraine treatments for acute symptoms, the most commonly used were triptans, a class of drugs developed in the 1990s to quiet overactive nerves associated with migraines and cluster headaches.

Sara’s story
Sara, a 38 year old mother of two, says her migraines are predictably and consistently worse during her period.
“It definitely disrupts my ability to go about my normal activities including at work,” Sara says. “I’m pretty lucky that I’m generally responsive to prescription medication, but I often still have to lie down for an hour or so while the medicine kicks in.”
Sara is being treated preventatively for migraines with Botox. She says over the past couple of months, she’s had a couple of migraines outside of when she gets her period, but that the headaches are definitely worse during menstruation.
“While I had my last period, I had a migraine every day for a week,” Sara says. “It’s starkly different [during menstruation].”
Prevention Possibilities
Non-steroidal anti-inflammatory drugs (NSAIDs), such as naproxen or ibuprofen, are sometimes used as preventive medications for women with regular menstrual periods. In this study, 21.1% of women reported use of any migraine prevention medications or therapies.

“Preventive treatments are used less frequently than acute treatment for migraine,” Alaini said. “In my opinion, this is because preventive therapy is a long-term commitment by both a woman and her clinician to improving the disease process. Migraine is a life-long brain disease without a cure, and the goal of preventive therapy is to reduce disease burden and improve quality of life. Unfortunately, newer disease-specific treatments are costly, so generic older treatments are often used and come with greater side effects.”
Next Steps
The researcher’s next steps involve looking at larger databases to see if they can mimic findings on a global scale. They want to determine if women with menstrual-related migraine are frequently turning to non-migraine treatments as was seen in around 53% of their current study group.
“As a headache specialist in the U.S., I know I can do better for women in my clinic, but what can be done for the millions of women who don’t get into a headache clinic? That is our true next step,” says Ailani. “If you have migraines related to your menstrual cycle, discuss this with your gynecologist or neurologist. There are treatments that can help and if the first treatment tried does not work, do not give up.”
In addition to Ailani, co-authors include Joshua Brown, Motomori Lewis, Aaron Jenkins, Jessica Cirillo, Karin Hygge Blakeman, Jiyue Yang, Lucy Abraham from Pfizer, Inc, New York.
This work was supported by Pfizer.

he most common type of lung fibrosis — scarring of the lungs — is idiopathic, meaning of unknown cause.
Researchers are urgently trying to find ways to prevent or slow idiopathic pulmonary fibrosis (IPF) and related lung conditions, which can cause worsening shortness of breath, dry cough, and extreme fatigue. Average survival following diagnosis of IPF is just three to five years, and the disease has no cure.
A recent U-M study from a team led by Sean Fortier, M.D. and Marc Peters-Golden, M.D. of the Division of Pulmonary and Critical Care Medicine at U-M Medical School uncovers a pathway used during normal wound healing that has the potential to reverse IPF.
Using a mouse model, they simulated IPF by administering bleomycin, a chemotherapy agent that causes cell injury and confirmed that the resulting lung scarring resolved itself over the span of about six weeks.
Because of this, “studying fibrosis is kind of tough,” said Fortier. “If we’re going to give experimental drugs to try and resolve fibrosis, we have to do it before it resolves on its own.
Otherwise, we will not be able to tell if the resolution was the action of the drug or natural repair mechanisms of the body.”
However, he said, “there’s actually a lot to learn about how the mouse gets better on its own. If we can learn the molecular mechanisms by which this occurs, we may uncover new targets for IPF.”
The process by which lung injury either leads to healing or fibrosis relies in part on what happens to a cell called a fibroblast, which forms connective tissue.

During injury or illness, fibroblasts are activated, becoming myofibroblasts that form scar tissue by secreting collagen. When the job is done, these fibroblasts must be deactivated, or de-differentiated, to go back to their quiet state or undergo programmed cell death and be cleared.
“This is the major distinction between normal wound healing and fibrosis — the persistence of activated myofibroblasts,” explained Fortier. That deactivation is controlled by molecular brakes. The study examined one of these brakes, called MKP1 — which the team found was expressed at lower levels in fibroblasts from patients with IPF.
By genetically eliminating MKP1 in fibroblasts of mice after establishing lung injury, the team saw that fibrosis continued uncontrolled.
“Instead of at day 63, seeing that nice resolution, you still see fibrosis,” said Fortier.
“We argued by contradiction: when you knock out this brake, fibrosis that would otherwise naturally disappear, persists and therefore MKP1 is necessary for spontaneous resolution of fibrosis.”
They performed several additional studies using CRISPR techniques to demonstrate how MKP1 applies the brakes, mainly by deactivating the enzyme p38α, which is implicated in a cell’s reaction to stress.

Furthermore, they demonstrated that neither of the two current FDA approved drugs for lung fibrosis, pirfenidone and nintedanib, are able to turn off myofibroblasts.
“That’s totally in keeping with the fact that they do slow the progression, but they don’t halt or reverse disease,” said Fortier.
Fortier hopes the discovery that this pathway reverses fibrosis leads to exploration of additional brakes on fibrosis.
“So much work on fibrosis has focused on how we can prevent it, but when a patient presents to my clinic with a dry cough, shortness of breath, and low oxygen as a result of underlying IPF, the scarring is already present. Of course, we’d love a way to prevent the scarring from getting worse, but the Holy Grail is to reverse it.”

A study conducted at the Faculty of Sport and Health Sciences at the University of Jyväskylä showed that a genetic predisposition for higher muscle strength predicts a longer lifespan and a lower risk for developing common diseases. This is the most comprehensive international study to date on hereditary muscle strength and its relationship to morbidity. The genome and health data of more than 340,000 Finns was used in the research.
Muscle strength, especially hand grip strength, can indicate an individual’s physiological resources to protect against age-related diseases and disabilities, as well as their ability to cope with them. Age-related loss of muscle strength is individual and influenced not only by lifestyle but also by genetics.
The study revealed that individuals with a genetic predisposition for higher muscle strength have a slightly lower risk for common noncommunicable diseases and premature mortality. However, it did not predict better survival after acute adverse health events compared to the time before illness onset.
“It seems that a genetic predisposition for higher muscle strength reflects more on an individual’s intrinsic ability to resist and protect oneself against pathological changes that occur during aging than the ability to recover or completely bounce back after severe adversity,” says doctoral researcher Päivi Herranen from the Faculty of Sport and Health Sciences.
The research utilized a unique study population
Muscle strength is a multifactorial trait influenced by lifestyle and environmental factors but also by numerous genetic variants, each with a very small effect on muscle strength. In this study, the genetic predisposition for muscle strength was defined by constructing a polygenic score for muscle strength, which summarizes the effects of hundreds of thousands of genetic variants into a single score. The polygenic score makes it possible to compare participants with an exceptionally high or low genetic predisposition for muscle strength, and to investigate associations with inherited muscle strength and other phenotypes, in this case, common diseases.
“In this study, we were able to utilize both genetic information and health outcomes from over 340,000 Finnish men and women,” Herranen explains.

“To our knowledge, this is the first study to investigate the association between a genetic predisposition for muscle strength and various diseases on this scale.”
Further research on the effects of lifestyles is still needed
Information about the genetic predisposition for muscle strength could be used alongside traditional risk assessment in identifying individuals who are at particularly high risk of common diseases and health adversities. However, further research on the topic is still needed.
“Based on these results, we cannot say how lifestyle factors, such as physical activity, modify an individual’s intrinsic ability to resist diseases and whether their impact on health differs among individuals due to genetics,” Herranen notes.
The study utilized the internationally unique FinnGen dataset, compiled through the collaboration of Finnish biobanks. The dataset consisted of 342,443 Finns who had given their consent and provided a biobank sample. The participants were aged 40 to 108 years, and 53% of them were women. The diagnoses selected for the study were based on the leading causes of death and the most significant noncommunicable diseases in Finland. Selected diagnoses included the most common cardiometabolic and pulmonary diseases, musculoskeletal and connective tissue diseases, falls and fractures, mental health and cognitive disorders, cancers, as well as overall mortality and mortality from cardiovascular diseases.
The study is the second publication of Päivi Herranen’s doctoral thesis, which investigates how genetics and environmental factors affect biological aging, particularly the weakening of muscle strength and functional capacity with age. The research is part of the GenActive project, funded by the Research Council of Finland and the Juho Vainio and Päivikki and Sakari Sohlberg foundations. The project is led by Assistant Professor and Academy Research Fellow Elina Sillanpää. The research was conducted in collaboration with the Gerontology Research Center (GEREC), the Institute for Molecular Medicine Finland (FIMM), and the FinnGen research project.

Machine learning (ML) enables the accurate and efficient computation of fundamental electronic properties of binary and ternary oxide surfaces, as shown by scientists. Their ML-based model could be extended to other compounds and properties. The present research findings can aid in the screening of surface properties of materials as well as in the development of functional materials.
The design and development of novel materials with superior properties demands a comprehensive analysis of their atomic and electronic structures. Electron energy parameters such as ionization potential (IP), the energy needed to remove an electron from the valence band maximum, and electron affinity (EA), the amount of energy released upon the attachment of an electron to the conduction band minimum, reveal important information about the electronic band structure of surfaces of semiconductors, insulators, and dielectrics. The accurate estimation of IPs and EAs in such nonmetallic materials can indicate their applicability for use as functional surfaces and interfaces in photosensitive equipment and optoelectronic devices.
Additionally, IPs and EAs depend significantly on the surface structures, which adds another dimension to the complex procedure of their quantification. Traditional computation of IPs and EAs involves the use of accurate first-principles calculations, where the bulk and surface systems are separately quantified. This time-consuming process prevents quantifying IPs and EAs for many surfaces, which necessitates the use of computationally efficient approaches.
To address the wide-ranging issues affecting the quantification of IPs and EAs of nonmetallic solids, a team of scientists from Tokyo Institute of Technology (Tokyo Tech), led by Professor Fumiyasu Oba, have turned their focus towards machine learning (ML). Their research findings have been published in theJournal of the American Chemical Society.
Prof. Oba shares the motivation behind the present research, “In recent years, ML has gained a lot of attention in materials science research. The ability to virtually screen materials based on ML technology is a very efficient way to explore novel materials with superior properties. Also, the ability to train large datasets using accurate theoretical calculations allows for the successful prediction of important surface characteristics and their functional implications.”
The researchers employed an artificial neural network to develop a regression model, incorporating the smooth overlap of atom positions (SOAPs) as numerical input data. Their model accurately and efficiently predicted the IPs and EAs of binary oxide surfaces by using the information on bulk crystal structures and surface termination planes.
Moreover, the ML-based prediction model could ‘transfer learning,’ a scenario where a model developed for a particular purpose can be made to incorporate newer datasets and reapplied for additional tasks. The scientists included the effects of multiple cations in their model by developing ‘learnable’ SOAPs and predicted the IPs and EAs of ternary oxides using transfer learning.
Prof. Oba concludes by saying, “Our model is not restricted to the prediction of surface properties of oxides but can be extended to study other compounds and their properties.”

A research team from the National University of Singapore (NUS) has unearthed new findings which may help explain the connection between cancer risk and poor diet, as well as common diseases like diabetes, which arise from poor diet. The insights gained from this study hold promise for advancing cancer prevention strategies aimed at promoting healthy ageing.
Led by Professor Ashok Venkitaraman, this ground-breaking study was conducted by scientists from the Cancer Science Institute of Singapore (CSI Singapore) at NUS and NUS Centre for Cancer Research (N2CR) under the Yong Loo Lin School of Medicine, with colleagues from the Agency for Science, Technology and Research (A*STAR).
Prof Venkitaraman, Director of CSI Singapore, explained, “Cancer is caused by the interaction between our genes and factors in our environment, such as diet, exercise, and pollution. How such environmental factors increase cancer risk is not yet very clear, but it is vital to understand the connection if we are to take preventive measures that help us stay healthy longer.”
A chemical linked to diabetes, obesity, and poor diet can heighten cancer risk
The research team first studied patients who are at a high risk of developing breast or ovarian cancers because they inherit a faulty copy of the cancer gene — BRCA2 — from their parents. They demonstrated that cells from such patients were particularly sensitive to the effects of methylglyoxal, which is a chemical produced when our cells break down glucose to create energy. The study showed that this chemical can cause faults in our DNA that are early warning signs of cancer development.
The team’s research also suggested that people who do not inherit a faulty copy of BRCA2 but could experience higher-than-normal levels of methylglyoxal — such as patients with diabetes or pre-diabetes, which are connected with obesity or poor diet — can accumulate similar warning signs indicating a higher risk of developing cancer.
Prof Venkitaraman elaborated, “Our research suggests that patients with high methylglyoxal levels may have higher cancer risk. Methylglyoxal can be easily detected by a blood test for HbA1C, which could potentially be used as a marker. Furthermore, high methylglyoxal levels can usually be controlled with medicines and a good diet, creating avenues for proactive measures against the initiation of cancer.”
The study’s first author, Dr Li Ren Kong, Lee Kuan Yew Fellow from N2CR, added, “We started the study aiming to understand what factors elevate risk in families susceptible to cancer, but ended up discovering a deeper mechanism linking an essential energy consumption pathway to cancer development. These findings raise awareness of the impact of diet and weight control in the management of cancer risks.”

Novel mechanism for tumour formation
Interestingly, the research team’s work also revised a longstanding theory about certain cancer-preventing genes. This theory — called the Knudson’s ‘two-hit’ paradigm — was first formulated in 1971, and it was proposed that these genes must be inactivated permanently in our cells before cancer can arise. The NUS team has now found that methylglyoxal can temporarily inactivate such cancer-preventing genes, suggesting that repeated episodes of poor diet or uncontrolled diabetes can ‘add up’ over time to increase cancer risk. This new knowledge is likely to be influential in changing the direction of future research in this area.
Next phase of research
Building on their novel discoveries, the researchers aim to conduct further studies to understand if metabolic disorders, such as diabetes or poor diets, affect cancer risk in Singapore and other Asian countries.
The research team also hopes to identify new mechanisms underlying the connection between metabolism, diet and cancer that they have discovered, to develop more effective approaches to prevent or delay the onset of cancer.

In cellular biology, unraveling the complexities of cellular function at the molecular level remains a paramount endeavor. Significant scientific focus has been placed on understanding the interactions at organelle contact sites, especially between mitochondria and the endoplasmic reticulum (ER). These sites are critical hubs for the exchange of essential biomolecules, such as lipids and calcium, which are vital for maintaining cellular homeostasis. Disruptions in this inter-organelle communication are implicated in the onset of various diseases, including neurodegenerative disorders, emphasizing the need to elucidate the mechanisms governing organelle interactions. However, the study of these dynamic complexes presents significant challenges due to the lack of available tools, complicating the quest to understand ER-mitochondria contact sites.
Emerging from this need, a novel strategy called “OrthoID” has been developed through the collaborative efforts of scientists from POSTECH, Daegu Catholic University School of Medicine, and Seoul National University. Featured in Nature Communications, OrthoID addresses this challenge by refining our ability to identify proteins that act as mediators in these critical conversations.
Traditional methods relied heavily on the streptavidin-biotin (SA-BT) binding pair system, derived from nature, for tagging and isolating these mediator proteins. However, this approach has its limitations, particularly in capturing the full spectrum of protein interactions between two different organelles. OrthoID overcomes these limitations by introducing an additional synthetic binding pair, cucurbit[7]uril-adamantane (CB[7]-Ad), to work alongside SA-BT. The combination of mutually orthogonal binding pair systems allowed a more precise identification and analysis of the mediator proteins that freely translocate between the ER and mitochondria, facilitating a deeper exploration of the proteins involved in the organelle contact sites and uncovering their roles in cellular functions and disease mechanisms.
Through meticulous experiments, the researchers have demonstrated the efficacy of OrthoID in rapidly and accurately labeling proteins involved in the dynamic processes of organelle communication. By leveraging proximity labeling techniques (APEX2 and TurboID) with orthogonal binding pair systems, the method effectively labeled and isolated proteins facilitating the critical interactions between mitochondria and ER. This approach not only identifies known proteins involved in ER-mitochondria contacts but also uncovers new protein candidates, including LRC59, whose roles at the contact site were previously unknown. Moreover, they also successfully pinpointed the multiple protein sets undergoing structural and locational changes at the ER-mitochondria junction during critical cellular process such as mitophagy, where damaged mitochondria are targeted for degradation.
“The flexibility and modularity of OrthoID are among its greates strengths.” states Prof. Kimoon Kim who led the research from POSTECH. This adaptability not only allows for the study of various organelle contact sites but also opens new avenues for exploring complex cellular communications, overcoming the technical limitations of existing methods.”
Prof. Kyeng Min Park from Daegu Catholic University School of Medicine adds, “OrthoID stands as a versatile and useful research tool, aimed to decode the complex language of cellular communication. It is expected to facilitate discoveries that will have profound implications for understanding cellular health, elucidating disease mechanisms, and fostering the development of new therapeutic strategies.”
The collaborative team included Prof. Kimoon Kim and Dr. Ara Lee from the Department of Chemistry, Dr. Gihyun Sung from the Division of Advanced Materials Science at Pohang University of Science and Technology (POSTECH), Prof. Kyeng Min Park from Daegu Catholic University School of Medicine, Professor Hyun-Woo Rhee from the Department of Chemistry and Professor Jong-Seo Kim from the School of Biological Sciences at Seoul National University.
This work was supported by the National Research Foundation of Korea (NRF) and Institute for Basic Science (IBS).

A Dartmouth-led study suggests that people who frequently consume seafood may face an increased risk of exposure to PFAS, the family of ubiquitous and resilient human-made toxins known as “forever chemicals.”
The findings stress the need for more stringent public health guidelines that establish the amount of seafood people can safely consume to limit their exposure to perfluoroalkyl and polyfluoroalkyl substances, the researchers report in the journal Exposure and Health. This need is especially urgent for coastal regions such as New England where a legacy of industry and PFAS pollution bumps up against a cultural predilection for fish, the authors write.
“Our recommendation isn’t to not eat seafood — seafood is a great source of lean protein and omega fatty acids. But it also is a potentially underestimated source of PFAS exposure in humans,” said Megan Romano, the study’s corresponding author and an associate professor of epidemiology at Dartmouth’s Geisel School of Medicine.
“Understanding this risk-benefit trade-off for seafood consumption is important for people making decisions about diet, especially for vulnerable populations such as pregnant people and children,” Romano said.
The study paired an analysis of PFAS concentrations in fresh seafood with a statewide survey of eating habits in New Hampshire. National data indicate that New Hampshire — along with all of New England — is among the country’s top consumers of seafood, which made the state ideal for understanding the extent of people’s exposure to PFAS through fish and shellfish.
“Most existing research focuses on PFAS levels in freshwater species, which are not what people primarily eat,” said Romano, who studies the effects of PFAS and other endocrine-disrupting chemicals in drinking water on New England communities. “We saw that as a knowledge gap in the literature, especially for a New England state where we know people love their seafood.”
The study also drew on New Hampshire’s extensive data on the sources and effects of PFAS, which are a staple of consumer products such as plastics and nonstick coatings. The molecular stability that makes PFAS versatile also makes them nearly indestructible, leading them to be called forever chemicals.

In humans, PFAS are associated with cancer, fetal abnormalities, high cholesterol, and thyroid, liver, and reproductive disorders. The chemicals have accumulated in soil, water, and wildlife, and studies have shown that nearly all Americans have measurable amounts in their blood.
“PFAS are not limited to manufacturing, fire-fighting foams, or municipal waste streams — they are a decades-long global challenge,” said study co-author Jonathan Petali, a toxicologist with the New Hampshire Department of Environmental Services. “New Hampshire was among the first states to identify PFAS in drinking water. We’re a data-rich state due to years spent investigating the impacts of PFAS and trying to mitigate exposure.”
The researchers measured the levels of 26 varieties of PFAS in samples of the most consumed marine species: cod, haddock, lobster, salmon, scallop, shrimp, and tuna. The seafood studied was purchased fresh from a market in coastal New Hampshire and originated from various regions.
Shrimp and lobster clocked the highest concentrations with averages ranging as high as 1.74 and 3.30 nanograms per gram of flesh, respectively, for certain PFAS compounds, the researchers report. Concentrations of individual PFAS in other fish and seafood measured generally less than one nanogram per gram.
The prevalence of PFAS in the environment makes it difficult to know exactly where and how the chemicals enter the marine food chain, the researchers report. Some shellfish may be especially vulnerable to the buildup of PFAS in their flesh due to feeding and living on the seafloor, as well as their proximity to sources of PFAS that are near the coast. Larger marine species may ingest PFAS by eating smaller species that, like shellfish, are prone to having the compounds accumulate in their systems.
Buttressing the study is a survey of 1,829 New Hampshire residents the researchers conducted to gauge how much seafood Granite Staters eat — and it’s a lot.

The survey found that men in New Hampshire eat just over one ounce of seafood per day and women eat just under one ounce. Both are higher than what the National Health and Nutrition Examination Survey found for men and women in the Northeast, and more than 1.5 times the national average for both. Daily intake for New Hampshire children aged 2 to 11 years old was about 0.2 ounces, the highest end of the range for children nationwide.
About 95% of adults the researchers surveyed reported they ate seafood within the past year, and 94% of that group consumed fish or shellfish within the previous month. More than two-thirds of those respondents ate seafood within the past week.
But people in New Hampshire do not eat seafood uniformly. More than half of the people who ate seafood in the week before the survey lived on the state’s coast or near the border with Massachusetts. More than 60% of people with a household income below $45,000 per year reported consuming seafood at least once per week, whereas people with higher household incomes reported eating seafood less often.
Of the species the researchers tested for PFAS, shrimp, haddock, and salmon were consumed by more than 70% of the adults who ate seafood once a month or more. Lobster was eaten by just over 54% of these adults. Salmon, canned tuna, shrimp, and haddock were the most commonly consumed species among children.
Federal guidelines for safe seafood consumption exist for mercury and other contaminants, but there are none for PFAS, said Celia Chen, a co-author of the study and a research professor in the Department of Biological Sciences at Dartmouth.
“Top predator species such as tuna and sharks are known to contain high concentrations of mercury, so we can use that knowledge to limit exposure. But it’s less clear for PFAS, especially if you start looking at how the different compounds behave in the environment,” said Chen, who leads several federally funded projects examining how and where PFAS accumulate in aquatic food webs in New Hampshire and Vermont.
The establishment of safety guidelines would help protect people who are especially susceptible to pollutants, said Kathryn Crawford, the study’s first author and an assistant professor of environmental studies at Middlebury College.
“Seafood consumption advisories often provide advice for those individuals that is more conservative than for the rest of the population,” said Crawford, who began the project as a postdoctoral researcher in the Romano Lab at Dartmouth. “People who eat a balanced diet with more typical, moderate amounts of seafood should be able to enjoy the health benefits of seafood without excessive risk of PFAS exposure.”

Consuming sugar-sweetened drinks in the first few years of childhood can be linked to poor diet patterns that increase the risk of obesity in later life, according to a new study by the School of Psychology at Swansea University.
Published in the European Journal of Clinical Nutrition, the study tracked the influence of diet on 14,000 British children from birth to adulthood and is believed to be the longest of its kind ever reported.
Using the Avon Longitudinal Study of Parents and Children, the research team found: Children who drank fizzy drinks such as cola or sugar-sweetened fruit cordials before the age of two gained more weight when they were 24 years old. Girls who had pure fruit juice gained less weight, while the weight of boys remained the same. At three years of age, toddlers who drank cola consumed more calories, fat, protein, and sugar but less fibre. In contrast, those given pure apple juice consumed less fat and sugar but higher amounts of fibre.The study also highlighted corresponding differences in food choices. Children who consumed pure apple juice often followed a diet with more fish, fruit, green vegetables, and salad, whereas those drinking cola ate more burgers, sausages, pizza, french fries, meat, chocolate, and sweets.
Additionally, the team discovered a link between sugar-sweetened drinks and social deprivation, with children from affluent backgrounds more likely to have access to pure fruit juice.
Lead researcher Professor David Benton said: “The early diet establishes a food pattern that influences, throughout life, whether weight increases. The important challenge is to ensure that a child develops a good dietary habit: one that offers less fat and sugar, although pure fruit juice, one of your five a day, adds vitamin C, potassium, folate, and plant polyphenols.”
Dr Hayley Young added: “Obesity is a serious health concern, one that increases the risk of many other conditions. Our study shows thatthe dietary causes of adult obesity begin in early childhood and that if we are to control it, more attention needs to be given to our diet in the first years of life.”