Publisher Health

Nearly 3 percent of Americans suffer from binge-eating disorder at some point their lifetimes, and of them, more than eight in 10 survived childhood abuse, neglect, or other trauma.
Now, a Virginia Tech scientist has identified how early life trauma may change the brain to increase the risk of binge eating later in life.
Research led by principal investigator Sora Shin, an assistant professor with the Fralin Biomedical Research Institute at VTC, revealed how a pathway in the brain that typically provides signals to stop eating may be altered by early life trauma.
The discovery, obtained from studies in mice, in Nature Neuroscience on Dec. 12 adds new perspective to behaviors such as binge eating and obesity.
“We wanted to know the mechanism underlying how early life trauma induces these eating disorders,” said Shin, who is also an assistant professor in the Department of Human Nutrition, Foods and Exercise in the College of Agriculture and Life Sciences. “What we found is a specific brain circuit that is vulnerable to stress, causing it to become dysfunctional.”
“This finding speaks to a set of broader health questions, which is how life’s health course is set based on certain early experiences,” said Michael Friedlander, executive director of the Fralin Biomedical Research Institute at VTC and Virginia Tech’s vice president for Health Sciences and Technology. “We are increasingly aware that early experiences and exposures ranging from those that occur even pre-conception in future parents through those that the fetus experiences in utero and to those that the child experiences throughout postnatal life can have dramatic impact on our health course throughout life. Dr. Shin’s latest discovery in this one particular case shines an important new mechanistic light on this process. Like all innovative research, the study also raises additional important questions such as whether and how these effects can be changed. Dr. Shin’s research can empower such lines of inquiry since a neural substrate and mechanism have been identified.”
Stress symptoms can affect our body, thoughts and feelings, and behavior. In Shin’s finding, the stress on mice who were separated from their litter mates may trigger life-long eating behavior changes.

It’s a scene many parents have experienced — just as they’re trying to cook dinner, take a phone call or run an errand, their child has a meltdown.
And sometimes, handing a fussy preschooler a digital device seems to offer a quick fix. But this calming strategy could be linked to worse behavior challenges down the road, new findings suggest.
Frequent use of devices like smartphones and tablets to calm upset children ages 3-5 was associated with increased emotional dysregulation in kids, particularly in boys, according to a Michigan Medicine study in JAMA Pediatrics.
“Using mobile devices to settle down a young child may seem like a harmless, temporary tool to reduce stress in the household, but there may be long term consequences if it’s a regular go-to soothing strategy,” said lead author Jenny Radesky, M.D., a developmental behavioral pediatrician at University of Michigan Health C.S. Mott Children’s Hospital.
“Particularly in early childhood, devices may displace opportunities for development of independent and alternative methods to self-regulate.”
The study included 422 parents and 422 children ages 3-5 who participated between August 2018 and January 2020, before the COVID-19 pandemic started. Researchers analyzed parent and caregiver responses to how often they used devices as a calming tool and associations to symptoms of emotional reactivity or dysregulation over a six-month period.

The nanomaterial graphene oxide — which is used in everything from electronics to sensors for biomolecules — can indirectly affect the immune system via the gut microbiome, as shown in a new study on zebrafish by researchers at Karolinska Institutet in Sweden. The findings are reported in the journal Nature Nanotechnology.
“This shows that we must factor the gut microbiome into our understanding of how nanomaterials affect the immune system,” says the paper’s corresponding author Bengt Fadeel, professor at the Institute of Environmental Medicine, Karolinska Institutet. “Our results are important for identifying the potential adverse effects of nanomaterial and mitigating or preventing such effects in new materials.”
Graphene is an extremely thin material, a million times thinner than a human hair. It comprises a single layer of carbon atoms and is stronger than steel yet flexible, transparent, and electrically conductive. This makes it extremely useful in a multitude of applications, including in “smart” textiles equipped with wearable electronics and as a component of composite materials, to enhance the strength and conductivity of existing materials.
With the increased use of graphene-based nanomaterials comes a need to examine how these new materials affect the body. Nanomaterials are already known to impact on the immune system, and a few studies in recent years have shown that they can also affect the gut microbiome, the bacteria that naturally occur in the gastrointestinal tract.
The relationship between nanomaterial, gut microbiome and immunity has been the subject of the present study performed using zebrafish. The nanomaterial investigated was graphene oxide, which can be described as a relative of graphene that consists of carbon atoms along with atoms of oxygen. Unlike graphene, graphene oxide is soluble in water and of interest to medical research as, for example, a means of delivering drugs in the body.
In the study, the researchers exposed adult zebrafish to graphene oxide via the water and analysed how it affects the composition of the microbiome. They used both normal fish and fish lacking a receptor molecule in their intestinal cells called the aryl hydrocarbon receptor, commonly abbreviated as AhR, a receptor for various endogenous and bacterial metabolites.

Tech companies have developed many devices that work outside the body, such as cell phones, smart watches, tablets and hundreds of others. Inside the body, though? That’s obviously trickier for several reasons, but power for a device is a big one.
Biobattery researchers at Binghamton University, State University of New York have a solution for the hard-to-reach small intestine, which winds around the human gut for an average of 22 feet.
“There are some regions in the small intestine that are not reachable, and that is why ingestible cameras have been developed to solve this issue,” said Professor Seokheun “Sean” Choi, lead researcher and faculty member in the Department of Electrical and Computer Engineering. “They can do many things, such as imaging and physical sensing, even drug delivery. The problem is power. So far, the electronics are using primary batteries that have a finite energy budget and cannot function for the long term.
The Watson team’s solution builds on findings that Choi has made over the past decade about utilizing bacteria to create low levels of electricity that can power sensors and Wi-Fi connections as part of the Internet of Things.
Other options inside the small intestine are less viable: Traditional batteries are potentially harmful, wireless power transfer from outside the body is inefficient, temperature differences aren’t enough to harness thermal energy and intestinal movement is too slow for mechanical energy. Instead, Choi’s biobatteries utilize microbial fuel cells with spore-forming Bacillus subtilis bacteria that remain inert until they reach the small intestine.
“How do you make your micro-fuel cell selectively work in the small intestine? We use a pH-sensitive membrane that requires certain conditions to activate,” Choi said. “When you look at our gastrointestinal tract, the esophagus has a neutral pH, the same as the small intestine, but the transit time is only 10 seconds. It will not activate in this area, and it will never work in the stomach because the stomach has a very low pH. It only works in the small intestine.”
Choi knows that some people might balk at ingesting bacteria, but our bodies are filled with nontoxic microbes that help with digestion and other functions.
“We use these spores as a dormant, storable biocatalyst,” he said. “The spores can be germinated when the nutrients are available, and they can resume vegetative life and generate the power.”
Although this research has just been published, Choi and his students already are looking ahead to improving the capsule-sized biobatteries. Once the fuel cell reaches the small intestine, it takes up to an hour to germinate completely — faster would be better. The cell generates around 100 microwatts per square centimeter of power density — enough for wireless transmission, but 10 times more would offer many more options for use. The batteries also would require animal and human testing as well as biocompatibility studies.
Choi can foresee several uses that low-level microbial fuel cells could power, including biological and chemical sensors, drug-delivery systems and electrical stimulation devices.
“I believe that our micro-fuel cell has a huge potential, but we have a long way to go,” he said.
The research team included PhD students Maryam Rezaie and Zahra Rafiee.
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Materials provided by Binghamton University. Original written by Chris Kocher. Note: Content may be edited for style and length.

Iron is a critical micronutrient for the survival of plants and humans, yet too much iron can also be toxic. An interdisciplinary research team from Heinrich Heine University Düsseldorf (HHU) has discovered that the protein PATELLIN2 is not only involved in regulating iron levels in plants. PATELLIN2 is one of a group of proteins that are also involved in the transport of vitamin E in humans. The researchers are now presenting the results, which are also important for supplying people with iron via plant foods, in the journal Plant Physiology.
Iron is an essential micronutrient for humans. Iron and zinc deficiencies in a person’s diet cause severe damage to health, above all in unborn and young children. To secure world food supplies and fight malnutrition, particularly in the poorest countries, it is therefore necessary to ensure the supply of iron primarily from plant sources and improve it through targeted breeding.
Plants need iron for fundamental metabolic reactions such as their photosynthesis and respiration. However, iron is a double-edged sword for them: Unfavourable environmental conditions such as drought can put plants under stress, which is exacerbated by the presence of reactive metal ions — including iron. Being rooted, plants obviously cannot move away from local stress conditions, so land plants have needed to evolve other ways to deal with stress factors.
These include iron regulation. For research and application it is important to understand how plants manage their nutrition with micronutrients during their growth with the potentially risky consequences of oxidative stress. If we know these processes, we can influence them in a targeted way to improve plant productivity and food quality, in particular in light of climate change — which increases the chances of drought.
A team comprising representatives from biology, chemistry and medicine at HHU, headed by Professor Dr Petra Bauer and Dr Rumen Ivanov from the Chair of Botany, has examined iron uptake mechanisms in plants using Arabidopsis thaliana (thale cress) as a model plant. The iron-regulated transporter IRT1 plays an important role in iron uptake in plant roots.
Root cells control the activity of IRT1, enabling plants to limit the toxicity and oxidative stress caused by metal ions. The HHU researchers were able to show that IRT1 binds the so-called SEC14 domain lipid transfer protein PATELLIN2. This in turn changes the protein environment of IRT1 depending on iron supply.
Another lipid transfer protein with an SEC14 domain plays a key role in vitamin E homoeostasis in humans and the transport of vitamin E from the intestine through the liver to the various organs in the body. The body obtains vitamin E from plant foods, primarily leaves and seeds.
PATELLIN2 can bind the molecule alpha-tocopherol, one of the most important vitamin E compounds in leaves and roots. Jannik Hornbergs, who conducted the studies during his PhD at HHU in cooperation with Dr Karolin Montag, says: “We have established that the SEC14 lipid transfer protein PATELLIN2 and tocopherols are critical for iron mobilisation in the root and antioxidative activities as a reaction to iron.”
The link between iron transport and SEC14 lipid transfer protein enables new working models for how cells can use vitamin E to control the extent of oxidative stress caused by iron. Dr Rumen Ivanov and Professor Bauer on the importance of the results: “Ultimately, these links that we now know can be used to identify new breeding targets for crop plants that can achieve stress resistance and maximise iron content in the plants.”
The research programme was conducted within the framework of the Collaborative Research Centre (CRC) 1208 “Identity and dynamics of membrane systems — from molecules to cellular functions,” which is based at HHU. In addition to the team headed by Professor Bauer, the working groups headed by Professor Dr Kai Stühler (Molecular Proteomics Laboratory), Professor Dr Birgit Strodel (Computational Biochemistry Group), Professor Dr Laura Hartmann (Chair of Macromolecular Chemistry) and Professor Dr Jürgen Zeier (Molecular Ecophysiology of Plants) were also involved.
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Materials provided by Heinrich-Heine University Duesseldorf. Original written by Arne Claussen. Note: Content may be edited for style and length.

Huntington’s disease (HD) is a neurological disorder that causes progressive loss of movement, coordination and cognitive function. It is caused by a mutation in a single gene called huntingtin or HTT. More than 200,000 people worldwide live with the genetic condition, approximately 30,000 in the United States. More than a quarter of a million Americans are at risk of inheriting HD from an affected parent. There is no cure.
But in a new study, published December 12, 2022 in Nature Neuroscience, researchers at University of California San Diego School of Medicine, with colleagues elsewhere, describe using RNA-targeting CRISPR/Cas13d technology to develop a new therapeutic strategy that specifically eliminates toxic RNA that causes HD.
CRISPR is known as a genome-editing tool that allows scientists to add, remove or alter genetic material at specific locations in the genome. It is based on a naturally occurring immune-defense system used by bacteria. However, current strategies run the risk of off-target edits at unintended sites that may cause permanent and inheritable chromosomal insertions or genome alterations. Because of this, significant efforts have focused on identifying CRISPR systems that target RNA directly without altering the genome.
In the case of HD, the condition is caused by repetitive and damaging sequences in the HTT gene.
Our cells have a hard time copying repetitive DNA, and these copying errors can cause repetitive sequences to grow longer with each generation,” said senior study author Gene Yeo, PhD, professor of cellular and molecular medicine at UC San Diego School of Medicine.
“In the Huntingtin gene, these repeats can sometimes grow to many times their normal length, with the resulting repeat-expanded protein tending to aggregate and form toxic clumps in a part of the brain called the striatum that is important for regulating movement. The loss of functional neurons in the striatum ultimately leads to HD symptoms.”
With colleagues at UC Irvine and Johns Hopkins University, Yeo and his team investigated whether recently described RNA-targeting CRISPR technology could be used to affect RNA (a chemical intermediate between DNA instructions and protein production) accumulation associated with HD.

Researchers at The University of Texas at Dallas have identified specific bacteria in the bladder that may indicate which postmenopausal women are more susceptible to recurrent urinary tract infections (UTIs), and they found that estrogen may play a role in reducing that susceptibility.
“We found a very strong association between beneficial bacteria in the bladder and the use of estrogen hormone therapy in postmenopausal women,” said Dr. Nicole De Nisco, assistant professor of biological sciences in the School of Natural Sciences and Mathematics. “Estrogen is important not just in regulating reproductive processes, but also in shaping the chemical environment of the entire body. When you lose that hormone, you lose all the benefits that it provides.”
De Nisco is the corresponding author of a study published online Sept. 30 and in the Oct. 18 print edition of Cell Reports Medicine. The researchers found robust correlations between so-called “good” bacteria and urinary estrogens in postmenopausal women without a history of UTIs.
Urinary tract infections are among the most common adult bacterial infections and impart a particularly significant medical burden on women, with more than 50% of women suffering a UTI in their lifetimes. Age is one of the strongest associated risk factors for UTIs.
Working with Dr. Philippe Zimmern, a professor of urology at UT Southwestern Medical Center, the UTD research team tested 75 postmenopausal women who fell into three groups: Those who did not have a history of UTIs. Those who have recurrent UTIs and were experiencing one at the time of testing. Those who have recurrent UTIs but were not experiencing one at the time of testing.Michael Neugent BS’13, MS’19, PhD’20, a postdoctoral fellow in De Nisco’s lab and first author of the article, said the research suggests that UTIs and estrogen shape the group of all microbes — called the microbiome — found in the urinary and genital tracts of postmenopausal women.

Multiple Sclerosis (MS) is almost always accompanied by fatigue, a massive tiredness that is described by the vast majority of patients as the most distressing symptom. In a recent scientific study, a research group led by Stefan Seidel from the Department of Neurology at MedUni Vienna and AKH Vienna identified light therapy as a promising non-drug treatment option: patients included in the study showed a measurable improvement after just 14 days of use. The study results were recently published in the Multiple Sclerosis Journal — Experimental, Translational and Clinical.
For the first time, Stefan Seidel’s research team relied not only on surveys but also on objective measurements when selecting the test persons. For example, sleep-wake disorders were ruled out in the 26 participating MS patients, particularly with the assistance of various sleep medicine examinations. “In this manner, for example, we ensured that MS patients with fatigue do not suffer from sleep apnea or periodic leg movements during sleep. Both are sleep disorders that can lead to fatigue in everyday life,” elaborated study leader Stefan Seidel.
Performance improvement
The test persons — all patients of the Neurology Department at MedUni Vienna and AKH Vienna — were equipped with commercially available light sources for self-testing at home: Half of the participants received a daylight lamp with a brightness of 10,000 lux, while the other half received an identical lamp that emitted a red light with an intensity of

Researchers at UC San Francisco (UCSF) have engineered molecules that act like “cellular glue,” allowing them to direct in precise fashion how cells bond with each other. The discovery represents a major step toward building tissues and organs, a long-sought goal of regenerative medicine.
Adhesive molecules are found naturally throughout the body, holding its tens of trillions of cells together in highly organized patterns. They form structures, create neuronal circuits and guide immune cells to their targets. Adhesion also facilitates communication between cells to keep the body functioning as a self-regulating whole.
In a new study, published in the Dec. 12, 2022, issue of Nature, researchers engineered cells containing customized adhesion molecules that bound with specific partner cells in predictable ways to form complex multicellular ensembles.
“We were able to engineer cells in a manner that allows us to control which cells they interact with, and also to control the nature of that interaction,” said senior author Wendell Lim, PhD, the Byers Distinguished Professor of Cellular and Molecular Pharmacology and director of UCSF’s Cell Design Institute. “This opens the door to building novel structures like tissues and organs.”
Regenerating Connections Between Cells
Bodily tissues and organs begin to form in utero and continue developing through childhood. By adulthood, many of the molecular instructions that guide these generative processes have disappeared, and some tissues, like nerves, cannot heal from injury or disease.

The potent opioid increasingly is afflicting people of color in American cities. “I’ve seen a lot of terrible drugs,” said a veteran drug counselor. “This is the worst.”MILWAUKEE — Glenda O. Hampton doesn’t need to look far to witness the devastation of the fentanyl epidemic in her neighborhood on Milwaukee’s north side.She has found men lying on the curb, barely conscious, their legs splaying into the street as cars whiz by. She can count at least three people in recent months who sought treatment at the storefront rehabilitation center she runs, then relapsed and died from using fentanyl.“I’ve seen a lot of terrible drugs,” said Ms. Hampton, 68, a tiny figure seated behind her crowded desk, as a group counseling session was underway down the hall. “This is the worst.”The synthetic opioid fentanyl has swept across the United States in recent years, the latest wave of a drug crisis that began with opioid painkillers and was followed by heroin. Fentanyl is a startlingly potent drug, 100 times more powerful than morphine, that was linked to the deaths of more than 70,000 Americans in 2021. They included first-time users who ingested more fentanyl than their bodies could handle, unsuspecting college students taking party drugs like cocaine that were laced with fentanyl, and people with longstanding addictions searching for cheap and plentiful highs.Desilynn Smith, left, an addiction counselor, leading a group session at Gateway to Change in Milwaukee. Milwaukee is seeing a surge in deaths from fentanyl, especially in Black and Latino communities.Todd Heisler/The New York TimesIn cities like Milwaukee, fentanyl is increasingly a crisis in heavily Black and Latino neighborhoods. It is spreading within communities that are already straining under the weight of poverty, disinvestment and violent crime, and are now struggling to control a drug whose reach grows every year.A federal report released in July said that drug overdose deaths in the United States — which are largely driven by fentanyl — hit people of color the hardest, with rates among young Black people during the coronavirus pandemic rising the most sharply. Data from Milwaukee County showed that from 2020 to 2021, fatal overdoses increased by 6 percent among white people, but 55 percent among Black people.In 2021, more than 500 drug-related deaths in Milwaukee County were tied to fentanyl, officials said, and this year’s death toll is expected to be even higher.“Unfortunately, this epidemic is affecting communities of color really hard,” Cavalier Johnson, the mayor of Milwaukee, said in an interview. “The number of fentanyl-related deaths has continued to grow, and so too has the share of people of color who have succumbed to fentanyl-related deaths.”Mayor Johnson, a native of the predominantly Black north side of Milwaukee, has faced a cascade of crises since becoming mayor in 2021. The city budget is strained, with rising pension costs leading officials to consider cuts to libraries, the city’s police force and fire departments. The number of homicides in Milwaukee, a city with a population of 577,000, nearly doubled from 2019 to 2021.Fentanyl Overdoses: What to KnowCard 1 of 5Devastating losses.