Publisher Health

A new systematic review by researchers at UCL and Wingate University has highlighted the importance of identifying childhood verbal abuse by adults as a standalone subtype of child maltreatment, to ensure targeted prevention and address the lasting harm it can inflict.
Child maltreatment is currently classified into four subtypes: physical abuse, sexual abuse, emotional abuse, and neglect. These classifications guide the creation of interventions and the monitoring of affected populations.
The study, published in Child Abuse & Neglect: The International Journal and commissioned by charity, Words Matter, examines a total of 149 quantitative and 17 qualitative studies to assess how child verbal abuse is currently defined and measured.
Researchers found that there needs to be a more consistent way of defining childhood verbal abuse, as it currently varies between parents and other authorities, with it being normalised in some cultures as a form of discipline.
The nature of childhood verbal abuse involves behaviours that can be detrimental to a child’s wellbeing, such as belittling, shouting, and threatening language.
It was found that these actions could have a lasting impact throughout the child’s life, creating underlying emotional and psychological repercussions, including increased risks of anger, depression, substance abuse, self-harm and obesity.
However, the team noted that there was a noticeable void in acknowledging childhood verbal abuse by adults as a distinct maltreatment subtype and that doing so would be a starting point for its identification and prevention.

People looking to reduce their cholesterol and trim fat from around their waist could try swapping meat for Quorn protein, according to the findings from a new study by Northumbria University, Newcastle, published in the European Journal of Nutrition, which saw positive effects in both areas in just two weeks.
Researchers from the University found that participants who ate Quorn products — the popular mycoprotein-based meat substitute — over just a two-week period, saw a significant 12% drop in ‘bad’ LDL cholesterol and a 7% fall in total cholesterol, compared to those who ate similar products made from red and processed meat. In addition, they also reduced their waist circumference by close to 1cm (0.95cm) on average over the 14 days.
Such a drop in total cholesterol levels could, according to medical research, reduce a person’s risk of dying from a cardiovascular disease, such as a stroke or coronary heart disease, by as much as 9% . Waist circumference is a good measure of abdominal fat and a key marker of cardiovascular health, with a near 1cm reduction in the mycoprotein group, achieved within a short period, suggesting potential benefits for heart health and body composition.
The investigator-blind trial — which involved 20 healthy male adults who were randomly assigned to consume 240 grams per day of red and processed meat or an equivalent amount of Quorn over two 14-day periods — also revealed further heart health benefits from consuming mycoprotein, the unique ingredient in all Quorn products. Researchers identified a clinically meaningful trend toward lower systolic and diastolic blood pressure in the mycoprotein group, potentially contributing to improved cardiovascular health.
The findings come after the latest annual Health Survey for England estimated that well over half (59%) of adults suffer from raised cholesterol , almost two-thirds (64%) are overweight or living with obesity and almost a third (30%) have high blood pressure . All three are known to cause cardiovascular disease — meaning millions of people could be at risk of a potentially fatal heart attack or stroke.
High cholesterol is mainly caused by diets high in saturated fat, carrying excess fat around your waist and not exercising enough, and is described, alongside high blood pressure, as one of the ‘silent killers’ that are often symptomless and only identified through a medical emergency.
Elevated levels of low-density lipoprotein (LDL) cholesterol, often referred to as ‘bad’ cholesterol, can lead to the build-up of fatty plaques in a person’s arteries, which restrict blood flow and increase their risk of a heart attack or stroke. Currently, high LDL cholesterol is associated with a quarter (115) of the 460 heart and circulatory disease deaths recorded in the UK every day.

A breakthrough study, jointly led by Professor Jang Hyun Choi and Professor Sung Ho Park from the Department of Biological Sciences at UNIST has identified an important factor involved in the development of non-alcoholic fatty liver disease (NAFLD) caused by obesity. The research team discovered that Thrap3, a protein associated with thyroid hormone receptors, plays a significant role in exacerbating NAFLD by inhibiting the activity of adenosine monophosphate-activated protein kinase (AMPK), a key regulator of fat metabolism in the liver.
NAFLD encompasses various metabolic diseases such as fatty hepatitis and cirrhosis resulting from excessive fat accumulation. Despite its prevalence, effective treatments for NAFLD have been limited. However, this groundbreaking research sheds light on potential therapeutic approaches.
Through animal experiments conducted on rats, the research team demonstrated that Thrap3 directly binds to AMPK within the liver. This interaction prevents AMPK from translocating from the nucleus to the cytoplasm and impairs autophagy — a process crucial for breaking down triglycerides and reducing cholesterol levels. In essence, inhibiting Thrap3 expression presents a promising avenue for effectively treating NAFLD.
“We have encountered significant challenges while developing treatment strategies for non-alcoholic fatty liver disease. However, our discovery of the Thrap3 gene provides us with an effective method to tackle this condition,” commented Professor Choi.
Additionally, it was confirmed that suppressing Thrap3 expression effectively improves non-alcoholic steatohepatitis — an inflammatory disease stemming from fatty liver.
Supported by funding from Korea Research Foundation under the Ministry of Science and ICT, National Mouse Phenotype Analysis Group (KMPC), and UNIST Future Lead Project; this research was published online on August 1st in Experimental and Molecular Medicine. Professor Jang Hyun Choi, alongside Professor Sung Ho Park, served as corresponding authors of the paper, with Dr. Hyun-Jun Jang and Dr. Yo Han Lee from the Department of Biological Sciences at UNIST participating as co-authors.

UVA Health researchers have developed a powerful new tool to understand how medications affect men and women differently, and that will help lead to safer, more effective drugs in the future.
Women are known to suffer a disproportionate number of liver problems from medications. At the same time, they are typically underrepresented in drug testing. To address this, the UVA scientists have developed sophisticated computer simulations of male and female livers and used them to reveal sex-specific differences in how the tissues are affected by drugs.
The new model has already provided unprecedented insights into the biological processes that take place in the liver, the organ responsible for detoxifying the body, in both men and women. But the model also represents a powerful new tool for drug development, helping ensure that new medications will not cause harmful side effects.
“There are incredibly complex networks of genes and proteins that control how cells respond to drugs,” said UVA researcher Jason Papin, PhD, one of the model’s creators. “We knew that a computer model would be required to try to answer these important clinical questions, and we’re hopeful these models will continue to provide insights that can improve healthcare.”
Harmful Effects From Drugs
Papin, of UVA’s Department of Biomedical Engineering, developed the model in collaboration with Connor Moore, a PhD student, and Christopher Holstege, MD, a UVA emergency medicine physician and director of UVA Health’s Blue Ridge Poison Center. “It is exceedingly important that both men and women receive the appropriate dose of recommended medications,” Holstege noted. “Drug therapy is complex and toxicity can occur with subtle changes in dose for specific individuals.”
Before developing their model, the researchers first looked at the federal Food and Drug Administration’s Adverse Event Reporing System to evaluate the frequency of reported liver problems in men and women. The scientists found that women consistently reported liver-related adverse events more often than did men.

Like fingerprints, a firearm’s discarded shell casings have unique markings. This allows forensic experts to compare casings from a crime scene with those from a suspect’s gun. Finding and reporting a mismatch can help free the innocent, just as a match can incriminate the guilty.
But a new study from Iowa State University researchers reveals mismatches are more likely than matches to be reported as “inconclusive” in cartridge-case comparisons.
“Firearms experts are failing to report evidence that’s favorable to the defense, and it has to be addressed and corrected. This is a terrible injustice to innocent people who are counting on expert examiners to issue a report showing that their gun was not involved but instead are left defenseless by a report that says the result was inconclusive,” says Gary Wells, an internationally recognized pioneer and scholar in eyewitness memory research.
The Distinguished Professor Emeritus co-authored the paper with Andrew Smith, associate professor of quantitative psychology. Smith studies memory, judgment and decision-making and is affiliated with both the Cognitive Psychology Program and the Psychology and Law Research group at Iowa State.
The two researchers pulled a dataset from a previously published experiment involving 228 firearms examiners and 1,811 cartridge-case comparisons. Overall, the participants were highly accurate in determining whether casings from a common firearm matched or mismatched. But when Smith and Wells applied a well-established mathematical model to the data, they found 32% of actual mismatch trials were reported as inconclusive compared to 1% of actual match trials.
“If the 16% of inconclusive reports lined up more evenly across actual matches and non-matches, we could chalk it up to human error. But the asymmetry, combined with the near-perfect performance of examiners, indicated something else was going on. They almost certainly knew that most of the cases they called inconclusive were actual mismatches,” says Smith.
Asking the wrong question
The researchers say a flawed response scale could help explain the dissociation between what examiners know and what they report.

People frequently exposed to racial or ethnic discrimination may be more susceptible to obesity and related health risks in part because of a stress response that changes biological processes and how we process food cues. These are findings from UCLA researchers conducting what is believed to be the first study directly examining effects of discrimination on responses to different types of food as influenced by the brain-gut-microbiome (BGM) system.
The changes appear to increase activation in regions of the brain associated with reward and self-indulgence — like seeking “feel-good” sensations from “comfort foods” — while decreasing activity in areas involved in decision making and self-control.
“We examined complex relationships between self-reported discrimination exposure and poor food choices, and we can see these processes lead to increased cravings for unhealthy foods, especially sweet foods, but also manifested as alterations in the bidirectional communication between the brain and the gut microbiome,” said Arpana Gupta, PhD, a researcher and co-director of the UCLA Goodman-Luskin Microbiome Center and the UCLA G. Oppenheimer Center for Neurobiology of Stress and Resilience.
“Our results show that a person’s brain-gut crosstalk may change in response to ongoing experiences of discrimination — affecting food choices, cravings, brain function, and contributing to alterations in gut chemistry that have been implicated in stress and inflammation. It appears that in response to stressful discrimination experiences, we seek comfort in food, manifested as increased cravings, and increased desire for highly palatable foods, such as high-calorie foods and, especially, sweet foods. These alterations may ultimately cause people exposed to discrimination to be more vulnerable to obesity and obesity-related disorders,” said Gupta, senior author of the paper, which appears in Nature Mental Health.
Previous studies have looked into many factors — genetics, diet, exercise, and others — that could contribute to disproportionately high rates of obesity and related disorders occurring in African Americans and others in communities of color. Few studies have addressed the potential role of discrimination in obesity, and this is the first known study providing direct evidence of possible brain-gut interactions linking discrimination to eating behaviors.
The findings are based on results of functional MRI brain scans, sophisticated statistical modeling techniques, and analyses of metabolites of the glutamate pathway in the digestive tract.
Participants included 107 people — 87 women and 20 men — of diverse racial and ethnic backgrounds who completed a validated and widely used questionnaire that measures chronic experiences of unfair treatment. Based on their scores, participants’ responses were divided into “high discrimination exposure” and “low discrimination exposure” groups.

Mount Sinai investigators have developed a new approach for treating invasive bladder cancer without the need for surgical removal of the bladder, according to a study published in Nature Medicine in September. Removing the bladder is currently a standard approach when cancer has invaded the muscle layer of the bladder.
In a phase 2 clinical trial that was the first of its kind, doctors found that some patients could be treated with a combination of chemotherapy and immunotherapy without the need to remove their bladder. Surgical removal of the bladder can be curative in muscle-invasive bladder cancer, but the procedure can have profound effects on a patient’s quality of life.
“Treatment for muscle-invasive bladder cancer is in need of major improvements from both a quality-of-life and an effectiveness standpoint,” said Matthew Galsky, MD, Co-Director of the Center of Excellence for Bladder Cancer at The Tisch Cancer Institute, a part of the Tisch Cancer Center at Mount Sinai. “If additional research confirms our findings, this may lead to a new paradigm in the treatment of muscle-invasive bladder cancer.”
Seventy-six patients participated in this clinical trial, and approximately 43 percent achieved a complete response — no detectable cancer — when treated with the combination of chemotherapy and immunotherapy. Patients with a clinical complete response were offered the opportunity to proceed with additional immunotherapy, without surgical removal of the bladder. Among patients opting to proceed without surgical removal of the bladder, about 70 percent had no evidence of recurrent cancer after two years. Based on the results of this trial, two follow-up studies were launched to build on this approach; one is ongoing, and another will open in the next six months.
Colleagues at City of Hope, the University of Pennsylvania, the University of Wisconsin, the University of Southern California, the University of Utah, and Oregon Health and Sciences University also participated in this research. This study was funded by Bristol Myers-Squibb, the Foundation for the NIH/Partnership for Accelerating Cancer Therapies, and the V Foundation.

Researchers at the University of Cologne’s CECAD Cluster of Excellence for Aging Research and the CEPLAS Cluster of Excellence for Plant Sciences have found a promising synthetic plant biology approach for the development of a therapy to treat human neurodegenerative diseases, especially Huntington’s disease. In their publication “In-planta expression of human polyQ-expanded huntingtin fragment reveals mechanisms to prevent disease-related protein aggregation” in Nature Aging, they showed that a synthetic enzyme derived from plants — stromal processing peptidase (SPP) — reduces the clumping of proteins responsible for the pathological changes in models of Huntington’s disease in human cells and the nematode Caenorhabditis elegans.
Huntington’s disease is among the so called polyglutamine (polyQ) diseases, a group of neurodegenerative disorders caused by multiple repetitions of glutamine amino acids in specific proteins. An excessive number of polyQ repeats can cause proteins to aggregate or accumulate in harmful and damaging protein deposits, leading to cellular dysfunction and death. To date, nine polyQ disorders have been described in humans. They all remain incurable. Among them, Huntington’s disease is an inherited condition that causes widespread deterioration in the brain and disrupts thinking, behavior, emotion and movement.
Plants are immune to harmful protein aggregation
In their recent study, Professor Dr David Vilchez (CECAD) and Dr Ernesto Llamas (CEPLAS) followed an unconventional approach to find potential drugs to treat polyQ diseases like Huntington’s. Plants are constantly challenged by the environment, but they cannot move to escape from these conditions. However, plants possess a striking resilience to stress that allows them to live long. Unlike humans who suffer from proteinopathies caused by the toxic aggregation or cluster of proteins, plants do not experience these kinds of diseases. They express hundreds of proteins containing polyQ repeats, but no pathologies from these factors have been reported. To explore how plants deal with toxic protein aggregation, Dr Ernesto Llamas, first author of the study, and colleagues introduced the toxic mutant protein huntingtin in plants, which causes cell death in human neurons. In contrast to animal and human models, they found that Arabidopsis thaliana plants actively removed huntingtin protein clumps and avoid harmful effects.
By means of synthetic biology, the scientists then transferred the plants’ ability to avoid aggregation into human cultivated cells and animal models of Huntington’s disease. Their hope is that the use of plant proteins could lead to new therapeutic approaches for treating Huntington’s disease and other neurodegenerative diseases.
“We were surprised to see plants completely healthy, even though they were genetically producing the toxic human protein. The expression of mutant huntingtin in other models of research like human cultured cells, mice and nematode worms induce detrimental effects and symptoms of disease,” said David Vilchez.
Plant protein alleviates symptoms in human cells and nematodes
The next step was to discover how plants avoided the toxic aggregation of mutant huntingtin. Indeed, the scientists discovered that the chloroplasts, the plant-specific organelles that perform photosynthesis, were the reason why plants do not show toxic protein deposits. Llamas said: “Unlike humans, plants have chloroplasts, an extra cellular type of organelle that could provide an expanded molecular machinery to get rid of toxic protein aggregates.”

A strategy for cellular reprogramming involves using targeted genetic interventions to engineer a cell into a new state. The technique holds great promise in immunotherapy, for instance, where researchers could reprogram a patient’s T-cells so they are more potent cancer killers. Someday, the approach could also help identify life-saving cancer treatments or regenerative therapies that repair disease-ravaged organs.
But the human body has about 20,000 genes, and a genetic perturbation could be on a combination of genes or on any of the over 1,000 transcription factors that regulate the genes. Because the search space is vast and genetic experiments are costly, scientists often struggle to find the ideal perturbation for their particular application.
Researchers from MIT and Harvard University developed a new, computational approach that can efficiently identify optimal genetic perturbations based on a much smaller number of experiments than traditional methods.
Their algorithmic technique leverages the cause-and-effect relationship between factors in a complex system, such as genome regulation, to prioritize the best intervention in each round of sequential experiments.
The researchers conducted a rigorous theoretical analysis to determine that their technique did, indeed, identify optimal interventions. With that theoretical framework in place, they applied the algorithms to real biological data designed to mimic a cellular reprogramming experiment. Their algorithms were the most efficient and effective.
“Too often, large-scale experiments are designed empirically. A careful causal framework for sequential experimentation may allow identifying optimal interventions with fewer trials, thereby reducing experimental costs,” says co-senior author Caroline Uhler, a professor in the Department of Electrical Engineering and Computer Science (EECS) who is also co-director of the Eric and Wendy Schmidt Center at the Broad Institute of MIT and Harvard, and a researcher at MIT’s Laboratory for Information and Decision Systems (LIDS) and Institute for Data, Systems and Society (IDSS).
Joining Uhler on the paper, which appears today in Nature Machine Intelligence, are lead author Jiaqi Zhang, a graduate student and Eric and Wendy Schmidt Center Fellow; co-senior author Themistoklis P. Sapsis, professor of mechanical and ocean engineering at MIT and a member of IDSS; and others at Harvard and MIT.

By genetically testing nearly one thousand embryos, scientists have provided the most detailed analysis of embryo fate following human in vitro fertilization.
Nearly half the embryos studied underwent developmental arrest because of genetic mishaps in early development — a revealing insight that suggests more IVF babies could come to term with changes in the fertility treatment process. The unique combination of data from arrested embryos also sheds new light on the still largely mysterious earliest stages of pregnancy through natural means.
“We think this also happens in natural conception, and it’s why it takes on average several or more months to get pregnant,” said author Rajiv McCoy, an assistant professor of biology at Johns Hopkins University. “It is very surprising that most of these embryo arrests are coming not from errors in egg formation, but from errors happening in cell divisions after fertilization. The fact that these errors don’t come from the egg suggests that maybe they could be mitigated by changing the way IVF is done.”
The research is set to publishin Genome Medicine.
Johns Hopkins and London Women’s Clinic researchers in the UK compared IVF embryos that failed to develop within a few days of fertilization with embryos that survived, looking for genetic differences.
“Genetic testing is typically only done on IVF embryos that survive in order to decide which embryo to transfer to the uterus,” McCoy said. “But from a biology standpoint, if we want to understand what’s allowing these embryos to survive, then we have to test all other embryos too.”
The findings reveal how some embryos start growing properly while the maternal genetic material pre-loaded into the egg control cell division, only to falter and stall when the embryo’s genes take over.