Publisher Health

Discoveries by West Virginia University forensic scientists about how gunshot residue behaves on skin, hair and fabric will allow crime scene investigators to catch up to the proliferation of new, eco-friendly types of ammunition and make faster, more informed decisions at crime scenes and in forensic laboratories.
Lead and other toxic components of ammunition are crucial in establishing the presence of gunshot residue, or GSR, at crime scenes. However, heavy metals like lead aren’t present in new “green” ammunitions that are changing the rules for GSR analysis, according to Tatiana Trejos, associate professor in the Eberly College of Arts and Sciences Department of Forensic and Investigative Science.
“A major forensics discovery was that, when you fire a gun, a cloud of particles is produced by the primer, the material that explodes and causes a bullet to eject. The primer contains, among other things, inorganic compounds, heavy metals like lead, barium, antimony,” Trejos said.
“When this cloud touches our skin, tiny particles remain there. The composition of those particles is specific to firearm discharge — we don’t commonly find that combination of metals in other conditions. That realization was a big help to forensic scientists in firearms-related investigations.”
But over the years, ammunition has changed. More primers are manufactured without metals harmful to the environment and human health. That’s a challenge for GSR analysis and the reason forensic science — a field that uses scientific methods to help solve crimes and examine trial evidence — is looking beyond inorganic compounds like metals to organic compounds like nitroglycerine that are also released when a gun fires.
“If we combine information about organic and inorganic compounds in GSR, we can have more confidence in our results,” Luis Arroyo, an analytical chemist and associate professor, said. “For over a decade, scientific groups have said we need to know more about organic gunshot residue. We’re missing opportunities to confirm the presence of GSR, and this research funded by the National Institute of Justice is helping to narrow that gap.”
The research establishes how organic and inorganic compounds in GSR differ in the ways they each persist on surfaces and transfer to other surfaces during activities like running, hand shaking or washing.

Trejos and Arroyo published the results of the studies in a Forensic Chemistry paper co-authored with WVU graduate students Courtney Vander Pyl, Kourtney Dalzell, Korina Menking-Hoggatt and Thomas Ledergerber.
To gather data, the team created new and improved organic and inorganic GSR “reference standards” or methodologies for creating standardized mixes of particles that accurately mirror real-world gunshot residue, allowing different labs to meaningfully compare results.
They applied those particles to fabrics, to the skin and hair of real human volunteers and to an artificial skin product called Strat-M. Then they subjected those surfaces to real and simulated activities like running, struggling, washing and rubbing, before measuring the remaining particles.
Trejos said the experiments established Strat-M as a viable substitute for human skin.
“Artificial skin has been used by fields like pharmaceuticals, cosmetics, health sciences. Now we have proved it can provide a consistent forensic standard while allowing us to test conditions that wouldn’t be feasible or safe for a person’s skin.”
The researchers found inorganic GSR particles persist longer on a surface — a palm, a sweatshirt — than organic compounds, but they’re more susceptible to being lost or transferred by common activities. A shooter who washes their hands with soap and water, then dries them with a paper towel, will likely prevent crime scene investigators from identifying GSR based on analysis of lead, barium and antimony particles on their hands.

The fact that inorganic particles persist over time and are significantly lost only due to outside forces can be critical to questions about whether someone is the victim of a suicide or homicide, Trejos said.
Organic compounds, conversely, may be lost from clothing if a suspect struggles during arrest, but they are less likely to transfer to someone else, like the arresting officer.
Up to 100 characteristic inorganic particles could transfer from one person to another during a handshake, compared to no transfer at all for organic compounds. But unlike inorganic particles, organic particles are lost over time due to factors like evaporation from the skin.
Trejos said the next step is to put the findings to use in combination with another methodology the group recently developed, which allows field CSIs to immediately analyze possible GSR at a crime scene.
As enthusiastic as Trejos is about the research, she emphasizes that real-life CSIs don’t have as many answers as the ones on television.
“Right now, we can do a pretty good job answering the question, ‘Is GSR present or not?’ But the next and more interesting question is, ‘Did this person fire the gun?’ Forensics is not always able to answer that with high certainty. This research opens new avenues to answer questions relevant to a judge or jury.
“By providing faster and more informative investigative tools, we’re helping to apprehend offenders with more solid evidence, and we’re minimizing the potential for false incarcerations.”

Cancer cells with extra chromosomes depend on those chromosomes for tumor growth, a new Yale study reveals, and eliminating them prevents the cells from forming tumors. The findings, said the researchers, suggest that selectively targeting extra chromosomes may offer a new route for treating cancer.
The study was published July 6 in the journal Science.
Human cells typically have 23 pairs of chromosomes; extra chromosomes are an anomaly known as aneuploidy.
“If you look at normal skin or normal lung tissue, for example, 99.9% of the cells will have the right number of chromosomes,” said Jason Sheltzer, assistant professor of surgery at Yale School of Medicine and senior author of the study. “But we’ve known for over 100 years that nearly all cancers are aneuploid.”
However, it was unclear what role extra chromosomes played in cancer — for instance, whether they cause cancer or are caused by it.
“For a long time, we could observe aneuploidy but not manipulate it. We just didn’t have the right tools,” said Sheltzer, who is also a researcher at Yale Cancer Center. “But in this study, we used the gene-engineering technique CRISPR to develop a new approach to eliminate entire chromosomes from cancer cells, which is an important technical advance. Being able to manipulate aneuploid chromosomes in this way will lead to a greater understanding of how they function.”
The study was co-led by former lab members Vishruth Girish, now an M.D.-Ph.D. student at Johns Hopkins School of Medicine, and Asad Lakhani, now a postdoctoral researcher at Cold Spring Harbor Laboratory.

Using their newly developed approach — which they dubbed Restoring Disomy in Aneuploid cells using CRISPR Targeting, or ReDACT — the researchers targeted aneuploidy in melanoma, gastric cancer, and ovarian cell lines. Specifically, they removed an aberrant third copy of the long portion — also known as the “q arm” — of chromosome 1, which is found in several types of cancer, is linked to disease progression, and occurs early in cancer development.
“When we eliminated aneuploidy from the genomes of these cancer cells, it compromised the malignant potential of those cells and they lost their ability to form tumors,” said Sheltzer.
Based on this finding, the researchers proposed cancer cells may have an “aneuploidy addiction” — a name referencing earlier research that discovered that eliminating oncogenes, which can turn a cell into a cancer cell, disrupts cancers’ tumor-forming abilities. This finding led to a model of cancer growth called “oncogene addiction.”
When investigating how an extra copy of chromosome 1q might promote cancer, the researchers found that multiple genes stimulated cancer cell growth when they were overrepresented — because they were encoded on three chromosomes instead of the typical two.
This overexpression of certain genes also pointed the researchers to a vulnerability that might be exploited to target cancers with aneuploidy.

Previous research has shown that a gene encoded on chromosome 1, known as UCK2, is required to activate certain drugs. In the new study, Sheltzer and his colleagues found that cells with an extra copy of chromosome 1 were more sensitive to those drugs than were cells with just two copies, because of the overexpression of UCK2.
Further, they observed that this sensitivity meant that the drugs could redirect cellular evolution away from aneuploidy, allowing for a cell population with normal chromosome numbers and, therefore, less potential to become cancerous. When researchers created a mixture with 20% aneuploid cells and 80% normal cells, aneuploid cells took over: after nine days, they made up 75% of the mixture. But when the researchers exposed the 20% aneuploid mixture to one of the UCK2-dependent drugs, the aneuploid cells comprised just 4% of the mix nine days later.
“This told us that aneuploidy can potentially function as a therapeutic target for cancer,” said Sheltzer. “Almost all cancers are aneuploid, so if you have some way of selectively targeting those aneuploid cells, that could, theoretically, be a good way to target cancer while having minimal effect on normal, non-cancerous tissue.”
More research needs to be done before this approach can be tested in a clinical trial. But Sheltzer aims to move this work into animal models, evaluate additional drugs and other aneuploidies, and team up with pharmaceutical companies to advance toward clinical trials.
“We’re very interested in clinical translation,” said Sheltzer. “So we’re thinking about how to expand our discoveries in a therapeutic direction.”

Many Americans can trace some lines of their family tree back to the 1600s. However, African Americans descended from enslaved Africans, who began arriving in North America in 1619, lack ancestral information spanning several centuries.
A new USC and Stanford study, recently published in Genetics, provides insight into who occupies these missing branches of family trees — and gives a glimpse of how many branches there are.
“Slavery was not that many generations ago, so my family still tells stories about our enslaved ancestors, like who they were and, in my case, how we ended up as light as we are,” said first author Jazlyn Mooney, the Gabilan Assistant Professor of Quantitative and Computational Biology at the USC Dornsife College of Letters, Arts and Sciences. “But these are just stories and that is what most African Americans have left. We don’t have any records or numbers. There’s no tangible data.”
For Mooney, the study sheds light on her personal ancestry. “It’s fairly easy to trace my mother’s side of the family all the way back to the early 1500s,” Mooney said, noting that her mother’s family traces to the medieval Jewish expulsion from Spain and is part of a community that came to New Mexico in the 1600s. “But my father is African American. And in that case, very quickly, we are no longer able to trace anything because of the lack of genealogical records.”
That’s because enslaved African Americans were rarely included in any official records. The 1870 federal census recorded formerly enslaved African Americans by name, and though it is a vital tool for genealogical research, many African Americans are still not able trace their family members to or beyond this document.
This study helps fill in those blank spaces along a typical African American’s family tree. Using computational methods informed by genetic data, researchers estimate that a random African American born between 1960 and 1965 is descended from, on average, 314 African and 51 European ancestors reaching back to 1619. “The rough outline of African-American family trees is well-known. There are many enslaved Africans, as well as some Europeans. But how many? The study asks a new question and gives some estimates,” Mooney said.

Although the research doesn’t reveal precisely who the African and European individuals were, the historical record can provide a general storyline. For example, many of the European ancestors appear in the family tree during the time of slavery, a period marked by prevalent sexual violence and exploitation of enslaved women. What’s more, many of the African ancestors — untraceable through written records — are people who survived the deadly Middle Passage of the Transatlantic Slave Trade, imprisoned and packed into slave ships for trips lasting as long as 80 days.
To conduct the study, researchers created a 14-generation model divided into three time periods: The first period, 1619-1808, includes the founding of the African American population, with the population formed by Africans and Europeans. The second period, 1808-1865, is marked by the end of legal importation of enslaved African captives into the United States. The number of new African ancestors declines sharply, and the African American population continues to grow with contributions from Europeans and European Americans continuing. The third period, 1865-1965, begins with the end of legal enslavement and continues to many African Americans living today. With the end of legal slavery comes reduced contributions from the European and European-American sources; contributions from African sources remain low due to low immigration.”It’s a powerful method,” said co-author Noah Rosenberg of Stanford. “Genetic ancestry studies usually focus on clustering the genomes of living people. The approach here is different. The ancestry is modeled with an explicit sense of genealogical descent over time.”
The study also notes that some of the famous African Americans whose genealogies have been publicly reported, such as Michelle Obama, were born during the 1960-1965 period.
“It was helpful to think about these well-known people,” Mooney said.
Mooney said that she and her colleagues are working on a computational model that will break the numbers down into their male and female components, which could add more context to African American population history.
“We could also explore adding in different ancestry components,” Mooney said. “For example, some African American individuals have Native American ancestry. This could be studied as well.”

A study conducted by researchers from the Department of Neurology at MedUni Vienna and University Hospital Vienna has demonstrated for the first time that diagnosis of multiple sclerosis (MS) can be significantly improved by additionally measuring the thickness of retinal layers in the eye. Use of the procedure, which is already available at the Departments of MedUni Vienna and University Hospital Vienna, helps to detect the condition at an earlier stage and predict its progression more accurately. This can lead to a decisive increase in the chance of improved patient outcomes. The findings have been published in the journal Neurology.
As part of their investigation, the research team headed by Gabriel Bsteh and Thomas Berger of the Department of Neurology at MedUni Vienna and University Hospital Vienna collaborated with colleagues from MedUni Vienna and University Hospital Vienna’s Department of Ophthalmology and Optometrics to examine 267 MS patients over a period of five years. Their research built on study results published in 2022, which showed that MS relapse-related damage to the retina reflects the degree of damage caused to the patient’s brain. The previous study also demonstrated that a 5 micrometre (µm) reduction in the thickness of the retinal layer following optic neuritis indicated a doubling of the risk of permanent disability after the next relapse. Thanks to the latest research with the large cohort of MS patients, the research team has confirmed that the thickness of the retinal layer can be used as a precise biomarker to assist early diagnosis.
Diagnostic procedure already available
The researchers used a procedure known as optical coherence tomography (OCT) to measure the thickness of the retinal layer. An imaging method that uses infrared light, OCT allows for the generation of high-resolution, three-dimensional images of extremely thin layers of tissue measuring just a few micrometres (1 µm is 1/1,000th of a millimetre). OCT is also a tool for diagnosing and evaluating the progression of eye diseases such as glaucoma. “So we already have this procedure at our disposal,” commented Gabriel Bsteh, first author of the study. He added: “If we use optical coherence tomography alongside the current criteria to diagnose MS, we obtain significantly more accurate results at a much earlier stage. This means we can initiate treatment measures sooner, which considerably improves the long-term prognosis for patients.”
Retina as a window on the brain
Multiple sclerosis is an autoimmune, chronic inflammatory disease that causes inflammation and loss of nerve cells throughout the nervous system. For the most part, patients are unable to feel the consequences of this damage to begin with, so the condition often goes undiagnosed until a late stage, meaning that valuable time is lost during which effective treatment could have been administered. Given that early detection and prognosis of the disease’s progression play a decisive role in MS cases, medical researchers have been trying to find improved detection methods for some time now to help avert serious consequences such as impaired mobility and blindness as far as possible. “We have identified a new biomarker for MS diagnosis, namely the retinal layer thickness, which can be likened to a window to the brain,” said Gabriel Bsteh, summing up the study’s key finding. In the next phases of research, the focus will turn to the importance of retinal layer thickness in measuring responses to MS treatment.

Researchers from the University of St Andrews have developed peptides that can help combat bacteria growing in biofilms, which occur in up to 80% of human infections.
Treating infections becomes significantly more challenging when biofilms are present, as they not only reduce the effectiveness of antibiotics but also give rise to several medical complications. These complications include infections following joint replacements, prosthetic devices, as well as contamination in catheters and other medical equipment. The lack of specific treatments makes the management and treatment of biofilms exceptionally difficult.
Published in Nature Chemical Biology (Thursday 29th June), the team of researchers, led by Dr Clarissa Melo Czekster and Dr Christopher Harding from the School of Biology at St Andrews, in collaboration with researchers at University of Dundee, developed antimicrobial peptides that can target the harmful bacteria growing in biofilms.
The team determined how a key enzyme (PaAP) in biofilms work and developed a revolutionary new strategy to inhibit the protein. Their inhibitor is potent and targets cells from the human pathogen Pseudomonas aeruginosa in biofilms. Pseudomonas aeruginosa is one of the top pathogens of concern by the World Health Organisation, causing chronic infections in patients with cystic fibrosis and other conditions, which means a biofilm inhibitor is urgently needed.
Dr Czekster and the team are currently working in collaboration with the University of St Andrews Technology Transfer Centre and industry partner Locate Bio, a biomedicine spinout of the University of Nottingham, to commercialise the technology. The Locate Bio team are trialling the peptides to see how they work with the company’s Programmed Drug Release technology to develop new orthobiologic solutions and products. The Technology Transfer Centre has filed a UK priority patent application.
Dr Czekster said: “Our research reveals how designed inhibitors can target a key enzyme in bacterial virulence, offering molecular insights applicable to aminopeptidases in diverse organisms.
“This remarkable new research presents an innovative strategy to target bacterial biofilms and pave the way for better treatment of bacterial infection.”

Potentially harmful chemicals generated by the Marshall Fire in late 2021 may have lingered inside some Boulder County homes for weeks after the disaster — hiding in small particles of dust that residents could have mixed back into the air when they vacuumed carpets or turned on fans, according to recent research.
The study, led by researchers from the University of Colorado Boulder, is the latest to look at the long-lasting impacts of this devastating event. The Marshall Fire ignited in the morning on Dec. 30, 2021, and within hours destroyed more than 1,000 homes and buildings.
Engineers and chemists at CU Boulder wanted to take a particularly close look at those homes that survived the blaze but still faced the towering walls of smoke.
Through late January and early February 2022, the scientists collected meticulous samples of particles of dust in the air and on surfaces in a sample of homes from the fire zone. They discovered that burning from the blaze may have left a mark on these buildings. Dust samples, for example, revealed elevated concentrations of potentially harmful materials like polycyclic aromatic hydrocarbons (PAHs), which the Environmental Protection Agency considers carcinogens.
The team can’t be sure what risk, if any, the particles posed to the health of people living in these neighborhoods. But the researchers hope that their results could one day help the survivors of future wildfires make informed decisions about when they can move back into their homes.
“This is going to happen again, unfortunately,” said Jonathan Silberstein, a doctoral student in the Paul M. Rady Department of Mechanical Engineering at CU Boulder. “Maybe not in Boulder, but somewhere in the United States. We hope this research will help inform best practices for recovering after the next fire.”
The study is one of several that CU Boulder researchers carried out across Boulder County in the wake of the disaster. The same team, for example, is also studying the toxic gases that may have seeped into homes from the fire to build out a more complete picture of the possible health risks.

“This was a really tragic event, but it was rewarding to have the opportunity to quickly address the concerns of the community many of us live in,” said Michael Hannigan, co-author of the study and a professor of mechanical engineering. “The community members couldn’t have been more receptive, helpful and gracious.”
Returning home
Christine Wiedinmyer is one of those community members. She’s also a co-author of the new study.
On Dec. 30, 2021, the CU Boulder air quality scientist was working from the basement of her home in the Rock Creek area of Boulder County when she started receiving texts from her friends: Authorities had just evacuated the Costco in the nearby town of Superior. Wiedinmyer and her teenage son left not long after, grabbing their laptops, some important documents and a few items of clothing.
“I really didn’t appreciate the extent of the fire until I got to my brother’s house in Denver, and I saw the news,” said Wiedinmyer, associate director of science for the Cooperative Institute for Research in Environmental Sciences (CIRES). “I thought: We’re not going back today.”
When she did return to her home on New Year’s Eve, Wiedinmyer found it still standing. But the flames, which had spread to within a few hundred yards from her house, had left a fingerprint on the structure.

“It smelled like the day after a campfire,” she said. “Below the doors and windowsills, you could see this black dust.”
At the same time, Wiedinmyer’s neighbors came to her with questions she couldn’t answer: Was it safe for them to move back home? What kind of cleaning should they do?
An eye on dust
To begin to answer those questions, Wiedinmyer joined a dream team of scientists from across CU Boulder. They included Hannigan; Marina Vance, assistant professor of mechanical engineering; Joost de Gouw, a chemist and professor at CIRES; and Colleen Reid, assistant professor of geography.
In a first-of-its-kind study, the team visited several homes in the burn area, a region spanning more than 6,000 acres in Superior, Louisville and unincorporated Boulder County — then picked four houses to study in-depth for this study, including Wiedinmyer’s. The team scraped dust from windowsills and installed monitors to track particles in the air on a minute-by-minute basis.
The group’s results revealed what may be the most detailed story to date of what happens to homes that survive this kind of fire.
The floating particles of ash produced by the fire seemed to settle out of the air in these houses within a day or two. But the dust that Wiedinmyer had seen on her windowsills lingered, and didn’t stay put. In February, the researchers took measurements as a six-person cleaning crew entered one of the homes to vacuum and mop. The concentrations of particles in the air nearly doubled during that time. Overnight in the same house, the team saw airborne particles spike about once every 20 minutes — likely due to the home’s HVAC system switching on and off.
Silberstein noted that the concentrations of contaminants like PAHs and some heavy metals were higher in those samples of dust that in Boulder County homes outside of the burn zone. But levels weren’t above the typical range for many urban areas in the U.S.
“Human activity, like cleaning, seemed to cause resuspension,” Silberstein said. “If there are compounds in that dust that are potentially bad for human health, that’s when you might see the greatest health risks.”
Wear a mask
Wiedinmyer noted that the team’s results represent just the first step in understanding how disasters like the Marshall Fire may affect nearby homes.
“I found it really frustrating because I couldn’t tell my neighbors what to do,” Wiedinmyer said. “I couldn’t tell them if it safe to move back in, only what I had done in my own house.”
For her part, the scientist cleaned her floors and windowsills and aired out her home for a week. She and her family didn’t move back in until the burning smell had gone away. Silberstein noted that anyone cleaning up a house after a fire should be diligent about wearing a mask to avoid breathing in potentially harmful dust.
He appreciated the chance to see his scientific knowledge help his community in a time of need.
“Often, our kind of research can feel removed from people’s everyday lives,” Silberstein said. “But this project felt like we were making a tangible difference.”

Wearable sensors are becoming a promising tool in personalized healthcare and exercise monitoring. In a recent study, researchers from Japan develop a novel wearable chemical sensor capable of measuring the concentration of chloride ions in sweat. By using a heat-transfer printing technique, the proposed sensor can be applied to the outer surface of common textiles to prevent skin irritation and allergies, and could also be useful in the early detection of heat stroke and dehydration.
The remarkable level of miniaturization possible in modern electronics has paved the way for realizing healthcare devices previously confined to the realm of science fiction. Wearable sensors are a prominent example of this. As the name suggests, these devices are worn on the body, usually directly on the skin. They can monitor important bodily parameters, including heart rate, blood pressure, and muscle activity.
Some wearable sensors can also detect chemicals in bodily fluids. For instance, sweat biosensors can measure the concentration of ions in sweat, providing information on their levels in blood. However, designing such chemical sensors is more complex than physical sensors. Direct contact between a wearable chemical sensor and skin can cause irritation and allergies. In contrast, if the sensor is fabricated directly on a wearable textile, its accuracy decreases due to surface irregularities.
In a recent study, a research team, led by Associate Professor Isao Shitanda of the Tokyo University of Science (TUS) in Japan, has developed an innovative sweat biosensor that addresses the aforementioned problems. Their work,published online in ACS Sensors on June 15, 2023, describes the use of a technique called “heat-transfer printing” to fix a thin, flexible chloride ion sensor onto a textile substrate. The study was co-authored by Dr. Masahiro Motosuke, Dr. Tatsunori Suzuki, Dr. Shinya Yanagita, and Dr. Takahiro Mukaimoto of TUS.
“The proposed sensor can be transferred to fiber substrates, and thus can be incorporated into textiles such as T-shirts, wristbands, and insoles,” explains Dr. Shitanda. “Further, health indicators such as chloride ion concentration in sweat can be measured by simply wearing them.”
The heat-transfer printing approach offers several advantages. For one thing, the sensor is transferred outside of the piece of clothing, which prevents skin irritation. In addition, the wicking effect of the textile helps spread the sweat evenly between the electrodes of the sensor, creating a stable electrical contact. Moreover, printing the sensor on a flat surface and then transferring it prevents the formation of blurred edges that commonly occur when printing directly onto a textile.
The researchers carefully selected the materials and electrochemical mechanisms of the sensor to avoid risking an allergic reaction for the wearer. After developing the sensor, they conducted various experiments using artificial sweat to verify its accuracy in measuring chloride ion concentration. The change in the electromotive force of the sensor was −59.5 mTV/log CCl−. Additionally, it displayed a Nernst response and a linear relationship with the concentration range of chloride ions in human sweat. Moreover, no other ions or substances typically present in sweat were found to interfere with the measurements.
Lastly, the team tested the sensor on a volunteer who exercised on a static bicycle for 30 minutes, by measuring their perspiration rate, chloride ion levels in blood, and saliva osmolality every five minutes to compare with the data previously gathered by the sensor. The proposed wearable sensor could reliably measure the concentration of chloride ions in sweat.
The sensor can also transmit data wirelessly, making it useful for real-time health monitoring. “Since chloride is the most abundant electrolyte in human sweat, measuring its concentration provides an excellent indicator of the body’s electrolyte balance and a useful tool for the diagnosis and prevention of heat stroke,” remarks Dr. Shitanda.
This research thus demonstrates the potential of using wearable ion sensors for the real-time monitoring of sweat biomarkers, facilitating personalized healthcare development and athlete training management.

Obesity risk genes make people feel hungrier and lose control over their eating, but practicing dietary restraint could counteract this.
New research by University of Exeter, Exeter Clinical Research Facility, and University of Bristol — funded by the Medical Research Council Doctoral Training Partnership and published in the International Journal of Epidemiology — found that those with higher genetic risk of obesity can reduce the effects that are transmitted via hunger and uncontrolled eating by up to half through dietary restraint.
Psychology PhD student, Shahina Begum, from the University of Exeter is lead author and said: “At a time when high calorie foods are aggressively marketed to us, it’s more important than ever to understand how genes influence BMI. We already know that these genes impact traits and behaviours such as hunger and emotional eating, but what makes this study different is that we tested the influence of two types of dietary restraint — rigid and flexible — on the effect of these behaviours. What we discovered for the first time was that increasing both types of restraint could potentially improve BMI in people genetically at risk; meaning that restraint-based interventions could be useful to target the problem.”
Genes linked to obesity increase BMI, with up to a quarter of this effect explained by increases in hunger and uncontrolled (including emotional) eating. There are over 900 genes that have so far been identified by researchers as being associated with BMI and several studies suggest these risk genes influence feelings of hunger and loss of control towards food.
This study examined 3,780 adults aged between 22 and 92 years old from two UK cohorts: the Genetics of Appetite Study, and Avon Longitudinal Study of Parents and Children. Their weight and height were measured, and they provided a DNA sample via their blood to calculate an overall score for their genetic risk of obesity. They then completed questionnaires to measure 13 different eating behaviours, including disinhibition (a tendency to engage in binge or emotional eating) and over-eating due to hunger.
As expected, researchers found that a higher genetic risk score was associated with a higher BMI, partly due to increased disinhibition and hunger. However, results also found that those who had high levels of dietary restraint reduced those effects by almost half for disinhibition and a third for hunger — suggesting that restraint may counteract some of the effects of genetic risk.
There are different types of dietary restraint, including flexible strategies — such as being conscious about what you eat and deliberately taking small servings — to rigid strategies, like calorie counting. The study tested the influence of both types of restraint for the first time and found both could potentially improve BMI in people genetically at risk.
Interventions to facilitate dietary restraint could include changing the food environment (reducing the calorie content or portion size of food) or supporting individuals — and members of the research team have developed a Food Trainer app (https://www.exeter.ac.uk/research/foodt/) to help achieve that. The app works as a game that trains people to repeatedly stop to high calorie food and research suggests this training may be particularly beneficial for those with a higher BMI.
The paper is entitled “Mediation and moderation of genetic risk to obesity through eating behaviours in two UK cohorts” and is published in the International Journal of Epidemiology.

Viruses in human-made environments cause public health concerns, but they are generally less studied than bacteria. A recent study led by environmental scientists from City University of Hong Kong (CityU) provided the first evidence of frequent interactions between viruses and bacteria in human-made environments. It found that viruses can potentially help host bacteria adapt and survive in nutrient-depleted human-made environments through a unique gene insertion.
By understanding these virus-bacteria interactions and identifying the possible spread of antibiotic resistance genes, the research team hopes its latest findings can help derive effective control strategies to minimize human exposure to harmful microorganisms.
Virus-host interactions are central to the ecology and evolution of microbial communities in diverse ecosystems. However, the immune mechanisms of infection and the virus-host interactions that occur in human-made environments, including buildings, public space, transportation and infrastructure, have been poorly understood.
“As more and more of the global population are living in urban areas, the importance of hygiene in human-made environments is growing, particularly indoor ones, as occupants inside are constantly exposed to diverse microorganisms, which have public health implications. However, most previous studies of human-made environments overlooked viruses,” said Professor Patrick Lee Kwan-Hon in the School of Energy and Environment (SEE) at CityU, who led the study.
“Therefore, in our study, we comprehensively investigated viruses in human-made environments, and we identified many novel molecular mechanisms in which viruses and bacteria interact with each other. These findings are important not only for basic microbial science, but also the management of human-made environments to protect residents’ health,” added Professor Lee.
In the study, researchers collected 738 samples from different types of human-made environments, including public facilities and residences, in Hong Kong. They collected the samples mainly from the surfaces of handrails, bollards, floors, poles, doorknobs and skin of residents. Then they used the metagenomic sequencing technique for analysis.
The analysis resulted in many interesting discoveries. First, the data showed that viruses are integral members of microbial communities in human-made environments. Among them, bacteriophages, a kind of virus that infects and replicates within bacteria, are all over various surfaces in human-made environments. The team also identified many viruses that are distinct from those in other ecosystems.
Second, the team found evidence of viruses inserting genes that control a specific step in a metabolic pathway and even the entire metabolic pathway into bacteria hosts. This suggests that viruses could help bacteria adapt and coevolve to survive in nutrient-depleted human-made environments.
The study also found diverse and novel immune systems against viruses in bacteria, and small proteins in viruses that can evade bacteria immune systems. These results suggest that viruses and bacteria hosts frequently interact with each other in human-made environments and that they each have mechanisms to defend against each other.
They also detected antibiotic resistance genes (ARGs) in viruses on human skin and frequently touched indoor surfaces. These ARG-carrying viruses might infect bacterial hosts, and ARGs might be horizontally transferred between bacterial species. Therefore, the role played by viruses in human-made environments in the development of antibiotic resistance in bacteria is crucial and warrants further investigation.
“Our study shows that the diversity, composition, metabolic functions and lifestyle of viruses vary, depending on the conditions of each human-made environment,” said Professor Lee. “Therefore, it is important to develop customized control strategies to minimize human exposure to harmful microorganisms and to better protect residents’ health. Our findings can contribute to this goal by enhancing the fundamental understanding of complex virus-bacteria interactions in human-made environments.”

For the first time, scientists have shown that gut bacteria differences are associated with later development of juvenile idiopathic arthritis, a debilitating rheumatic childhood disease, and that these differences are present years before the disease is diagnosed.
The research team, which includes scientists from the University of Florida and researchers in Sweden, made this discovery by analyzing stool samples from one-year-old children in a long-term study called All Babies in Southeast Sweden. The scientists compared bacteria found in children who went on to develop juvenile idiopathic arthritis with those who did not.
“Our work suggests that an imbalance in microbes, especially the increased prevalence of several proinflammatory bacterial species, could serve as a potential indicator of future disease risk,” said Angelica Ahrens, co-first author of the study and a postdoctoral associate in the UF/IFAS department of microbiology and cell science.
Juvenile idiopathic arthritis, or JIA, which is also called childhood arthritis and pediatric rheumatic disease, is an autoimmune disease marked by inflammation of the joints and sometimes other parts of the body. Children with JIA experience pain, swelling, stiffness and other symptoms that make daily activities challenging. Current treatments for JIA include anti-inflammatory drugs and steroid injections.
“These treatments can help control inflammation and reduce symptoms, but they are not without their drawbacks and they do not cure the disease. There is a need to find alternative approaches, and the bacteria found in gastrointestinal tract may be a promising place to start,” said Dr. Erik Kindgren, co-first author of the study and a pediatrician at Skaraborg Hospital in Sweden who treats children with JIA.
While other studies have shown microbial differences in children already diagnosed with JIA, this study is the first to demonstrate that these differences are present years before children first show symptoms of the disease.

The study found that children with gut bacteria known to cause inflammation were nearly seven times more likely to develop JIA. The researchers also found that bacteria known to promote a healthy gut lining were absent or reduced in children who later developed the disease. These trends held true even when the researchers controlled for factors already associated with the disease, such as being breastfed for shorter periods or early exposure to antibiotics.
The scientists say the findings are a first step toward understanding what causes JIA — the term “idiopathic” in the name means the cause of the condition is unknown.
“Looking ahead, this line of discovery could lead to the development of screening tools in early pediatric wellness visits. By constructing risk profiles and implementing targeted interventions and preventative measures to reduce those risks, we may be able to prevent disease onset in some people,” Ahrens said.
First, though, researchers will need to understand how the bacteria identified in the study contribute to the disease.
“Functionally, what are these bacteria doing in the body that leads to this disease? That’s what we need to investigate next,” Ahrens said.
The current study only looked at a snapshot of the gut microbiome at one year of age, so future work may investigate how the gut microbiome of children with JIA progresses over time.
The study’s authors — which also include Eric Triplett, chair of the UF/IFAS department of microbiology and cell science, and Dr. Johnny Ludvigsson, senior professor at Linköping University and both founder and leader of the All Babies in Southeast Sweden study — plan to continue their trans-Atlantic collaboration by examining microbial differences associated with other conditions that appear in childhood.