Publisher Health

From fizzy drinks to cereals and packaged snacks to processed meat, ultra-processed foods are packed with additives. Oil, fat, sugar, starch and sodium, as well as emulsifiers such as carrageenan, mono- and diglycerides, carboxymethylcellulose, polysorbate and soy lecithin continue to strip food of healthy nutrients while introducing other ingredients that could also be detrimental to human health.
Hundreds of novel ingredients never encountered by human physiology are now found in nearly 60 percent of the average adult’s diet and nearly 70 percent of children’s diets in the United States.
While obesity and lack of physical activity are well recognized contributors to avoidable morbidity and mortality in the U.S., another emerging hazard is the unprecedented consumption of these ultra-processed foods in the standard American diet. This may be the new “silent” killer, as was unrecognized high blood pressure in previous decades.
Physicians from Florida Atlantic University’s Schmidt College of Medicine explored this hypothesis and provide important insights to health care providers in a battle where the entertainment industry, the food industry and public policy do not align with their patients’ needs. Their findings are published in a commentary in The American Journal of Medicine.
“Those of us practicing medicine in the U.S. today find ourselves in an ignominious and unique position — we are the first cohort of health care professionals to have presided over a decline in life expectancy in 100 years,” said Dawn H. Sherling, M.D., corresponding author, associate program director for the internal medicine residency and an associate professor of medicine, FAU Schmidt College of Medicine. “Our life expectancy is lower than other economically comparable countries. When we look at increasing rates of non-communicable diseases in less developed nations, we can see a tracking of this increase along with increasing consumption of ultra-processed foods in their diets.”
Although professional organizations such as the American College of Cardiology cautions patients to “choose minimally processed foods instead of ultra-processed foods” in their 2021 dietary guidelines, there is a caveat that “there is no commonly accepted definition for ultra-processed foods, and some healthy foods may exist within the ultra-processed food category.”
“When the components of a food are contained within a natural, whole food matrix, they are digested more slowly and more inefficiently, resulting in less calorie extraction, lower glycemic loads in general, and lower rise in triglyceride-rich lipoproteins after eating, which could result in atherosclerotic plaque,” said Allison H. Ferris, M.D., senior author, an associate professor and chair, Department of Medicine, and director of the internal medicine residency program, FAU Schmidt College of Medicine. “Therefore, even if the troublesome additives were removed from the ultra-processed food, there would still be concern for an over-consumption of these products possibly leading to obesity, diabetes and heart disease.”
The authors add that public health organizations are increasingly making use of the NOVA classification system, which divides foods into four categories — whole foods, culinary ingredients (items like butter, oil and salt), traditionally processed foods (such as bread and yogurt made with few ingredients), and ultra-processed foods — or those foods that are industrially made and use ingredients not normally found in a domestic kitchen.

According to the authors, one plausible mechanism to explain the hazards is that ultra-processed foods contain emulsifiers and other additives that the mammalian gastrointestinal tract mostly does not digest. They may act as a food source for our microbiota, and as such may be creating a dysbiotic microbiome that can, in the right host, promote disease.
“Additives, such as maltodextrin, may promote a mucous layer that is friendly to certain species of bacteria that are found in greater abundance in patients with inflammatory bowel disease,” said Sherling. “When the mucous layer is not properly maintained, the epithelial cell layer may become vulnerable to injury, as has been shown in feeding studies using carrageenan in humans and other studies in mice models, using polysorbate-80 and cellulose gum, triggering immunologic responses in the host.”
The authors add that there have been marked increases in colorectal cancer in the U.S., especially among younger adults. They opine that increased ultra-processed food consumption may be a contributor as well as to several other gastrointestinal diseases.
“Whether ultra-processed foods contribute to our currently rising rates of non-communicable disease requires direct testing in analytic studies designed a priori to do so,” said Charles H. Hennekens, M.D., FACPM, co-author, the First Sir Richard Doll Professor of Medicine and senior academic advisor, FAU Schmidt College of Medicine. “In the meantime, we believe it is incumbent upon all health care professionals to discuss the benefits of increasing consumption of whole foods and reducing consumption of ultra-processed foods with their patients.”
The authors also opine that just as the dangers of tobacco began to emerge during the middle of the prior century, decades passed before the preponderance of the evidence and the efforts of forward-thinking health officials prompted policy change to discourage the use of cigarettes. They say there is likely to be a similar path for ultra-processed foods.
“The multinational companies that produce ultra-processed foods are just as, if not more, powerful than tobacco companies were in the last century, and it is unlikely that governments will be able to move quickly on policies that will promote whole foods and discourage the consumption of ultra-processed foods,” said Sherling. “Importantly, health care providers also should remain cognizant of the difficulties that many of our patients have in being able to afford and find healthier options, which calls for a broader public health response.”

The vast majority of positron emission tomography (PET) imaging systems map out how the body uses a radioactive form of glucose for energy. Since many cancers use glucose as metabolic fuel, they light up on glucose PET scans. However, not all cancers use glucose as fuel, and some normal organs, like the brain and heart, use high amounts of glucose too, making it difficult to identify some diseases from this type of diagnostic scan.
Now, scientists at the University of Ottawa (uOttawa) have developed a new radiotracer (called [18F]4-FDF) that can map how cells use fructose for energy. Fructose is a different type of metabolic fuel that is increasingly being recognized as a fuel for disease. Fructose, a monosaccharide known as “fruit sugar,” is a common dietary sugar found naturally in fruit, honey, and processed foods. Unlike glucose, fructose is not normally used for fuel by the healthy brain and heart, appearing mostly in healthy liver and kidneys. By identifying where fructose is being used in the body, [18F]4-FDF will allow for earlier detection of a wide range of diseases, including cancers, as well as inflammation of the heart and brain.
The research was conducted in the Molecular Medicine Lab at uOttawa under Associate Professor Adam Shuhendler from uOttawa’s Faculty of Science, who is also a scientist at the University of Ottawa Heart Institute, in collaboration with uOttawa professors Robert Ben and Christina Addison. Lead author Alexia Kirby, who is a doctoral student in biology, was responsible for validating and testing the radiotracer across various cell and animal models, while Nicholas Calvert, a doctoral student in chemistry and biomolecular sciences, used carbon isotope labeling to determine the metabolic pathway of the radiotracer in cells. The synthetic chemistry was developed by colleagues Rob Ben, Thomas Charlton, and Mojmir Suchy, while Dominic Graf and Mojmir Suchy handled the radiochemistry.
“For the first time, we can see where fructose, a common dietary sugar, is used in the body. Outside of the kidneys and the liver, fructose metabolism in any other organs may point to a sinister problem including cancer and inflammation,” explains Professor Shuhendler.
The [18F]4-FDF compound is made of a carefully modified form of fructose that incorporates a radioactive fluorine atom at a key chemical position, allowing researchers to track where and how much fructose is metabolized in our bodies. Through imaging with a PET camera, a tool that is routinely used in diagnostic imaging, observers can see the increased fructose used by malfunctioning organs and tissues, providing early indications of inflammation.
This discovery opens up new avenues for the earlier detection and care of cancers, as well as brain and heart conditions.

An Emory University study published Feb. 15 in Nature Mental Health shows wildfires lead to an increase of anxiety-related emergency department visits in the western United States, amplifying the concerning parallel trajectory of two escalating public health crises — mental health and climate change.
The National Institutes of Health-funded study — conducted by researchers at Emory’s Rollins School of Public Health — is among the largest and most comprehensive research ever undertaken on the association between wildfire-related exposures and anxiety disorders.
Analyzing satellite-driven data and nearly 1.9 million emergency department visits across five states (California, Arizona, Nevada, Oregon and Utah) from 2007-18, the researchers showed wildfire smoke events — which is when wildfires become the main source of ambient pollution within a ZIP code — were associated with a 6.3% increase in mental health-related emergency department visits.
In addition to this startling data, the study shows: Women, girls and older adults are more susceptible to severe anxiety disorders associated with wildfire exposures. Men and boys also experienced an increase in anxiety disorders but only when linked to major smoke events. Evidence for enhanced disaster risk reduction and climate risk management strategies, including climate awareness and risk communication tailored for vulnerable populations.What the researchers say:
“The scary thing about climate change is it doesn’t have a clear boundary; you fear a lot about the unknown. Now we can use the knowledge we’ve gained to tell people there is no need to panic. When you receive a wildfire smoke alert, close your windows, limit your outdoor activities and don’t panic. Those sorts of preventative measures can potentially benefit the entire population,” says study co-author Yang Liu, PhD, chair and Gangarosa Distinguished Professor in the Gangarosa Department of Environmental Health at Rollins.
“Mental health is one of the most prevalent health conditions in the U.S. and our study found multiple pathways between wildfires and an association with severe anxiety disorders. Many people are already dealing with some mild or moderate mental health symptoms. Now imagine they wake up and see the sky covered in smoke, they’re likely going to feel even more anxious,” says the study’s lead author Qingyang Zhu, PhD, a postdoctoral fellow in the Gangarosa Department of Environmental Health.
Why it matters: Rising temperatures and shifting drying patterns substantially escalated the potential for wildfires globally over the past 20 years, resulting in expanded burned areas and prolonged fire seasons. The western United States is notoriously a major fire-prone region, due to the recurrent presence of fire weather conditions, increasing droughts and the abundance of fuel resources. Climate change has been linked to a variety of psychological disorders such as anxiety, depression, post-traumatic stress disorder and eating disorders. Mental health disorders, including anxiety disorders, have been an increasing threat to global public health in the past three decades. According to the most recent Global Burden of Disease study released in 2020, anxiety disorder was the 24th leading contributor — out of 369 diseases — to the global burden of disease.This research was supported by the National Institute of Environmental Health Sciences of the NIH (ES034175 and ES027892). The NIH has established an NIH Climate Change and Health Initiative to reduce health threats from climate change, including mental health.

Annual breast cancer screening beginning at age 40 and continuing to at least age 79 results in the highest reduction in mortality with minimal risks, according to a new study published today in Radiology, a journal of the Radiological Society of North America (RSNA).
Breast cancer is the second most common cause of cancer death for women in the U.S. Despite research demonstrating that consistent participation in screening mammography can reduce breast cancer deaths by 40%, only 50% or less of eligible women actually participate in annual screening.
“There is an ongoing debate over the recommendations for breast cancer screening, specifically about when to start and the frequency of screening,” said lead researcher Debra L. Monticciolo, M.D., professor of radiology at Dartmouth Geisel School of Medicine in Hanover, New Hampshire.
Dr. Monticciolo said a recommendation by the U.S. Preventive Services Task Force (USPSTF) in 2009 to screen every other year, or biennially, beginning at age 50 resulted in a nationwide decline in screening participation. The USPSTF drafted new recommendations in 2023, suggesting women participate in biennial screening between 40 and 74. The American College of Radiology, the Society of Breast Imaging and the National Comprehensive Cancer Network recommend annual screening for women at average risk for breast cancer beginning at age 40 and continuing as long as the woman is in good health.
In the study, Dr. Monticciolo and colleagues performed a secondary analysis of Cancer Intervention and Surveillance Modeling Network (CISNET) 2023 median estimates of breast cancer screening outcomes. CISNET modeling data gives researchers the opportunity to estimate the outcomes of screening at various frequencies and starting ages using U.S. data.
The researchers compared the benefits of screening, including mortality reduction, life years gained, breast cancer deaths averted, and its risks — including benign, or unnecessary, biopsies and recall rates — for four different scenarios: biennial screening of women 50-74 (the longstanding USPSTF recommendation), biennial screening of women 40-74 (the task force’s new draft recommendation), annual screening 40-74, and annual screening 40-79. CISNET does not offer modeling past age 79.
The review of CISNET estimates showed that annual screening of women 40-79 with either digital mammography or tomosynthesis showed a mortality reduction of 41.7%. Biennial screening of women 50-74 and 40-74 showed mortality reduction of 25.4% and 30%, respectively. Annual screening of women 40-79 years showed the lowest per mammogram false-positive screens (6.5%) and benign biopsies (0.88%) compared to other screening scenarios.

“The biggest takeaway point of our study is that annual screening beginning at 40 and continuing to at least age 79 gives the highest mortality reduction, the most cancer deaths averted, and the most years of life gained,” Dr. Monticciolo said. “There’s a huge benefit to screening annually until at least 79 and even more benefit if women are screened past 79.”
Dr. Monticciolo said that although the USPSTF uses CISNET modeling to formulate its recommendations, it refers to recall rates and benign biopsies as harms, rather than risks.
“To balance the harms and benefits of screening mammography, they’re willing to give up some mortality benefit to avoid women being recalled for additional imaging and benign biopsies,” she said.
According to the researchers’ analyses, the chance of a woman having a benign biopsy following annual screening is less than 1%, and all recall rates for screening mammography are under 10%. When screening is performed annually with tomosynthesis, the recall rate decreases to 6.5%.
“The risks of screening are non-lethal and manageable for most women,” she said. “But advanced breast cancer is often lethal. Breast cancer is easier to treat if it’s found earlier; we’re able to spare women extra surgeries and chemotherapy. It’s just a better idea to shift to early detection, and that’s what screening does.”
Dr. Monticciolo said she hopes that her study will add to the body of literature that supports annual screening beginning at age 40 as the best way to diagnose cancer early.
“This paper is important because it shows once again that there’s a tremendous increase in mortality benefit by screening annually between the ages of 40-79, and that the chances of experiencing harm are low on a per-exam basis,” she said. “It comes down to valuing women’s lives. I am hoping that primary care physicians see that risks of screening are manageable, and the benefits are tremendous. We need to do this for women.”

Researchers have discovered more than 275 million previously unreported genetic variants, identified from data shared by nearly 250,000 participants of the National Institutes of Health’s All of Us Research Program. Half of the genomic data are from participants of non-European genetic ancestry. The unexplored cache of variants provides researchers new pathways to better understand the genetic influences on health and disease, especially in communities who have been left out of research in the past. The findings are detailed in Nature, alongside three other articles in Nature journals.
Nearly 4 million of the newly identified variants are in areas that may be tied to disease risk. The genomic data detailed in the study are available to registered researchers in the Researcher Workbench, the program’s platform for data analysis.
“As a physician, I’ve seen the impact the lack of diversity in genomic research has had in deepening health disparities and limiting care for patients,” said Josh Denny, M.D., M.S., chief executive officer of the All of Us Research Program and an author of the study. “The All of Us dataset has already led researchers to findings that expand what we know about health — many that may not have been possible without our participants’ contributions of DNA and other health information. Their participation is setting a course for a future where scientific discovery is more inclusive, with broader benefits for all.”
To date, more than 90% of participants in large genomics studies have been of European genetic ancestry. NIH Institute and Center directors noted in an accompanying commentary article in Nature Medicine that this has led to a narrow understanding of the biology of diseases, and impeded the development of new treatments and prevention strategies for all populations. They emphasize that many researchers are now utilizing the All of Us dataset to advance precision medicine for all.
For example, in a companion study published in Communications Biology, a research team led by Baylor College of Medicine, Houston, reviewed the frequency of genes and variants recommended by the American College of Medical Genetics and Genomics across different genetic ancestry groups in the All of Us dataset. These genes and variants mirror those in the program’s Hereditary Disease Risk research results offered to participants. The authors found significant variability in the frequency of variants associated with disease risk between different genetic ancestry groups and compared with other large genomic datasets.
While more research is needed before these findings can be used to tailor genetic testing recommendations for specific populations, researchers believe the difference in the number of these variants may be influenced by past studies’ limited diversity and their disease-focused approach to participant enrollment, rather than a difference in the prevalence of the variants.
In a separate study, investigators with the eMERGE program tapped the All of Us dataset to calibrate and implement 10 polygenic risk scores for common diseases across diverse genetic ancestry groups. These scores calculate an individual’s risk of disease by taking into account genetic and family history factors. Without accounting for diversity, polygenic risk scores could cause false results that misrepresent a person’s risk for disease and create inequitable genetic tools. Without the diversity of the All of Us data, these polygenic risk scores would have only been applicable to some of the population.
“All of Us values intentional community engagement to ensure that populations historically underrepresented in biomedical research can also benefit from future scientific discoveries,” said Karriem Watson, D.H.Sc., M.S., M.P.H., chief engagement officer of the All of Us Research Program. “This starts with building awareness and improving access to medical research so that everyone has the opportunity to participate.”
More than 750,000 people have enrolled in All of Us to date. Ultimately, the program plans to engage at least one million people who reflect the diversity of the United States and contribute data from DNA, electronic health records, wearable devices, surveys, and more over time.

Researchers at the University of Colorado Anschutz Medical Campus have found that inhibiting a key protein can stop the destruction of synapses and dendritic spines commonly seen in Alzheimer’s disease.
The study, whose first author is Tyler Martinez, a student in the Pharmacology and Molecular Medicine PhD program at the University of Colorado School of Medicine, was published recently in the journal eNeuro.
The researchers, using rodent neurons, found that targeting a protein called Mdm2 with an experimental cancer drug known as nutlin, stopped neurotoxic amyloid-b peptides that accumulate in Alzheimer’s disease (AD) from overly pruning synapses.
“Cognitive impairments associated with AD correlate with dendritic spine and excitatory synapse loss, particularly within the hippocampus,” said the study’s senior author Professor Mark Dell’Acqua, PhD, vice-chair of the Department of Pharmacology at the CU School of Medicine.
Dell’Acqua said trimming excess dendritic spine synapses is normal in the post-natal brain but can be abnormally accelerated in AD causing loss of memory and learning.
“When this protein Mdm2 is turned on inappropriately it leads to pruning of the synapses when amyloid-b is present,” he said. Amyloid-b is the main component of amyloid plaques found in the brain of those with AD. “When we used the drug that inhibits Mdm2 on the neurons it completely blocked dendritic spine loss triggered by amyloid-b. So inhibiting this protein is clearly working.”
Dendritic spines protrude from dendrites, a component of neurons, and receive synaptic signals that are critical in learning and memory.

Dell’Acqua, director of the Neurotechnology Center at the CU School of Medicine, noted that much of the research into AD therapies tends to focus on eradicating amyloid plaques in the brain.
“There are questions if anti-amyloid therapy is the be all and end all of AD therapy,” he said. “Even if you could tolerate the high cost, the effectiveness is questionable. We are saying that it may also be possible to intervene in the process by blocking some of the impacts of amyloid-b. And you could intervene by targeting Mdm2.”
The next step is determining whether they can block AD progression in an animal model. If so, human trials could happen in the future. Drugs that target Mdm2 are already developed and in clinical trials for cancer but still need FDA approval.
“This is an encouraging first step that gives us a new lead to pursue,” Dell’Acqua said.

Oocytes are immature egg cells that develop in almost all female mammals before birth. The propagation of future generations depends on this finite reserve of cells surviving for many years without incurring damage. In mice, this can be a period of up to eighteen months, while in humans it can last almost half a century, the average time between birth and menopause. How the cells accomplish this remarkable feat of longevity has been a longstanding question.
Researchers at the Centre for Genomic Regulation (CRG) in Barcelona have discovered a new mechanism which explains how oocytes remain in pristine conditions for decades without succumbing to the wear and tear that would cause other cell types to fail. The findings, reported today in the journal Cell, represent a new frontier to explore unexplained causes of infertility.
The researchers looked at protein aggregates, which are clumps of misfolded or damaged proteins. If left unchecked, these harmful substances accumulate in the cytoplasm and have highly toxic effects. Protein aggregates are known to accumulate in neurons and their effects have been linked to several neurodegenerative diseases. Cells usually manage aggregates by breaking them down with specialized enzymes. They can also divide into two new cells, concentrating aggregates in one of the cells and sparing the other.
But oocytes are not like the other cells. Their long life means they cannot dissipate toxic substances through cell division. Constantly breaking down protein aggregates is an inviable strategy, as it requires using a high amount of energy that may not be available. Oocytes also have the job of donating their entire cytoplasm to an embryo after fusing with a sperm, and so prefer to reduce their metabolic activity, a strategy which avoids generating by-products which can damage the maternal DNA and compromise future reproductive success. This makes oocytes particularly sensitive to the effects of misfolded or damaged proteins.
However, “in contrast to the tens of thousands of papers on protein aggregation in neurons, how mammalian oocytes cope with protein aggregation is essentially unstudied, despite having the same problem of being long-lived and non-dividing,” explains Dr. Elvan Böke, Group Leader of the Oocyte Biology & Cellular Dormancy programme at the Centre for Genomic Regulation and author of the study. “We wanted to explore how oocytes deal with these misfolded or damaged proteins,” adds Dr. Böke.
Patrolling ‘clean-up crews’
Dr. Böke’s team, led by Dr. Gabriele Zaffagnini, started by collecting thousands of immature oocytes, mature eggs, and early embryos from adult mice. Using special dyes, they observed how the protein aggregates behave in real-time using a technique called live-cell imaging. They also used electron microscopy to get a closer look and see nanoscopic details inside cells, work that took five and a half years to complete.

The researchers discovered special structures in the oocytes which they named EndoLysosomal Vesicular Assemblies — or ELVAs for short. These structures — there are about 50 per each oocyte — roam the cytoplasm, where they capture and hold onto protein aggregates, rendering them harmless. Cells have many subcellular structures known as organelles, which perform jobs much like an organ does in the body. The researchers conceptualise ELVAs as a “superorganelle” because it is a network of many different types of cellular components working together as a single unit.
The study revealed a crucial moment during the oocyte maturation stage, which is when an oocyte converts into a mature egg, preparing for ovulation and possible fertilisation. During this stage, the researchers observed ELVAs moving towards the cell’s surface and breaking down the protein aggregates, essentially deep-cleaning the cytoplasm. This is the first observation of the unique strategy oocytes employ to get rid of protein aggregates.
“An oocyte must donate all its cytoplasm to the embryo at fertilisation, so it cannot afford for garbage to accumulate, which would pose an existential risk for its function. In that sense, ELVAs are like a sophisticated waste disposal network or clean-up crew, patrolling the cytoplasm to ensure no aggregates are freely floating. ELVAs keep these aggregates in a confined environment until the oocyte is ready to dispose of them in one fell swoop. It’s an effective and energy-efficient strategy,” says Dr. Zaffagnini, postdoctoral researcher at the Centre for Genomic Regulation.
Protein aggregates may contribute to infertility
Fertility declines with age, and poor oocyte quality is the major cause of female infertility. Global infertility rates are also on the rise, with delayed motherhood being one of the contributing factors. Understanding how oocytes remain healthy, and what causes these strategies to fail with age, is critical for understanding unexplained causes of infertility and open up new avenues for treatment.
The findings of the study suggest that the presence of protein aggregates could interfere with both egg and embryo quality. When the researchers experimentally prevented the ability of ELVAs to degrade protein aggregates during the oocyte maturation process, it led to the formation of defective eggs. When the researchers intervened and “forced” the embryos to inherit aggregated proteins, 3 in 5 (60%) failed to complete very early stages of development.
“A lot of studies have historically focused on one small aspect of why oocyte quality declines, which are meiosis and euploidy. However, a recent review of eleven thousand embryo transfers has shown that the decline in female fertility with age are heavily influenced by other, yet unknown factors. Our research opens a fascinating future direction to explore whether protein degradation, and problems with how they are regulated in oocytes, could explain the age-related decline in embryo health,” concludes Dr. Böke.
Another type of long-lived cell which do not divide yet have to deal with protein aggregates are neurons. The accumulation of the harmful substances in these cells is linked to the development of several types of neurodegenerative diseases including Alzheimer’s. Could ELVA-like compartments also exist in neurons and other cell types? The study opens the door for future research avenues beyond the field of reproduction.

The freshness of animal meat is an essential property determining its quality and safety. With advanced technology capable of preserving food for extended periods of time, meat can be shipped around the globe and consumed long after an animal dies. As global meat consumption rates increase, so too does the demand for effective measures for its age.
Despite the technological advances keeping meat fresh for as long as possible, certain aging processes are unavoidable. Adenosine triphosphate (ATP) is a molecule produced by breathing and responsible for providing energy to cells. When an animal stops breathing, ATP synthesis also stops, and the existing molecules decompose into acid, diminishing first flavor and then safety. Hypoxanthine (HXA) and xanthine are intermediate steps in this transition. Assessing their prevalence in meat indicates its freshness.
In AIP Advances, from AIP Publishing, researchers from the Vietnam Academy of Science and Technology, VNU University of Science, Hanoi University of Science and Technology, and the Russian Academy of Sciences developed a biosensor using graphene electrodes modified by zinc oxide nanoparticles to measure HXA. The team demonstrated the sensor’s efficacy on pork meat.
While many HXA sensing methods currently exist, they can be costly and time-consuming and require specialists.
“In comparison to modern food-testing methods, like high-performance liquid chromatography, gas chromatography, mass spectrometry, atomic and molecular spectroscopy, and nuclear magnetic resonance spectroscopy, biosensors like our sensor offer superior advantages in time, portability, high sensitivity, and selectivity,” said author Ngo Thi Hong Le.
The sensor is produced using a polyimide film, which is converted into porous graphene using a pulsed laser. The added zinc oxide nanoparticles attract the HXA molecules to the electrode surface. When HXA interacts with the electrode, it oxidizes and transfers its electrons, spiking the electrode’s voltage. The linear relationship between HXA and voltage increase enables easy determination of HXA content.
To assess the sensor’s ability, the researchers tested solutions with known quantities of HXA. After the outstanding performance, the researchers measured the biosensor’s practicality using pork tenderloins purchased from a supermarket. The sensor performed with over 98% accuracy, favorable detection range, and low detection limit.
“In Vietnam, pork is the most consumed meat,” said Le. “Therefore, pork quality monitoring is one of the important requirements in the food industry in our country, which is why we prioritized it.”
More than just pork, any meat product can be evaluated by this biosensor.

A flurry of recent studies has found that microplastics are present in virtually everything we consume, from bottled water to meat and plant-based food. Now, University of New Mexico Health Sciences researchers have used a new analytical tool to measure the microplastics present in human placentas.
In a study published February 17 in the journal Toxicological Sciences, a team led by Matthew Campen, PhD, Regents’ Professor in the UNM Department of Pharmaceutical Sciences, reported finding microplastics in all 62 of the placenta samples tested, with concentrations ranging from 6.5 to 790 micrograms per gram of tissue.
Although those numbers may seem small (a microgram is a millionth of a gram), Campen is worried about the health effects of a steadily rising volume of microplastics in the environment.
For toxicologists, “dose makes the poison,” he said. “If the dose keeps going up, we start to worry. If we’re seeing effects on placentas, then all mammalian life on this plant could be impacted. That’s not good.”
In the study, Campen and his team, partnering with colleagues at the Baylor College of Medicine and Oklahoma State University, analyzed donated placenta tissue. In a process called saponification, they chemically treated the samples to “digest” the fat and proteins into a kind of soap.
Then, they spun each sample in an ultracentrifuge, which left a small nugget of plastic at the bottom of a tube. Next, using a technique called pyrolysis, they put the plastic pellet in a metal cup and heated it to 600 degrees Celsius, then captured gas emissions as different types of plastic combusted at specific temperatures.
“The gas emission goes into a mass spectrometer and gives you a specific fingerprint,” Campen said. “It’s really cool.”
The researchers found the most prevalent polymer in placental tissue was polyethylene, which is used to make plastic bags and bottles. It accounted for 54% of the total plastics. Polyvinyl chloride (better known as PVC) and nylon each represented about 10% of the total, with the remainder consisting of nine other polymers.

Marcus Garcia, PharmD, a postdoctoral fellow in Campen’s lab who performed many of the experiments, said that until now, it has been difficult to quantify how much microplastic was present in human tissue. Typically, researchers would simply count the number of particles visible under a microscope, even though some particles are too small to be seen.
With the new analytical method, he said, “We can take it to that next step to be able to adequately quantify it and say, ‘This is how many micrograms or milligrams,’ depending on the plastics that we have.”
Plastic use worldwide has grown exponentially since the early 1950s, producing a metric ton of plastic waste for every person on the planet. About a third of the plastic that has been produced is still in use, but most of the rest has been discarded or sent to landfills, where it starts to break down from exposure to ultraviolet radiation present in sunlight.
“That ends up in groundwater, and sometimes it aerosolizes and ends up in our environment,” Garcia said. “We’re not only getting it from ingestion but also through inhalation as well. It not only affects us as humans, but all off our animals — chickens, livestock — and all of our plants. We’re seeing it in everything.”
Campen points out that many plastics have a long half-life — the amount of time needed for half of a sample to degrade. “So, the half-life of some things is 300 years and the half-life of others is 50 years, but between now and 300 years some of that plastic gets degraded,” he said. “Those microplastics that we’re seeing in the environment are probably 40 or 50 years old.”
While microplastics are already present in our bodies, it is unclear what health effects they might have, if any. Traditionally, plastics have been assumed to be biologically inert, but some microplastics so small they are measured in nanometers — a billionth of a meter — and are capable of crossing cell membranes, he said.

Campen said the growing concentration of microplastics in human tissue might explain puzzling increases in some types of health problems, such as inflammatory bowel disease and colon cancer in people under 50, as well as declining sperm counts.
The concentration of microplastics in placentas is particularly troubling, he said, because the tissue has only been growing for eight months (it starts to form about a month into a pregnancy). “Other organs of your body are accumulating over much longer periods of time.”
Campen and his colleagues are planning further research to answer some of these questions, but in the meantime he is deeply concerned by the growing production of plastics worldwide.
“It’s only getting worse, and the trajectory is it will double every 10 to 15 years,” he said. “So, even if we were to stop it today, in 2050 there will be three times as much plastic in the background as there is now. And we’re not going to stop it today.”

Surveys show most men in the United States are interested in using male contraceptives, yet their options remain limited to unreliable condoms or invasive vasectomies. Recent attempts to develop drugs that block sperm production, maturation, or fertilization have had limited success, providing incomplete protection or severe side effects. New approaches to male contraception are needed, but because sperm development is so complex, researchers have struggled to identify parts of the process that can be safely and effectively tinkered with.
Now, scientists at the Salk Institute have found a new method of interrupting sperm production, which is both non-hormonal and reversible. The study, published in Proceedings of the National Academy of Sciences (PNAS) on February 20, 2024, implicates a new protein complex in regulating gene expression during sperm production. The researchers demonstrate that treating male mice with an existing class of drugs, called HDAC (histone deacetylase) inhibitors, can interrupt the function of this protein complex and block fertility without affecting libido.
“Most experimental male birth control drugs use a hammer approach to blocking sperm production, but ours is much more subtle,” says senior author Ronald Evans, professor, director of the Gene Expression Laboratory, and March of Dimes Chair in Molecular and Developmental Biology at Salk. “This makes it a promising therapeutic approach, which we hope to see in development for human clinical trials soon.”
The human body produces several million new sperm per day. To do this, sperm stem cells in the testes continuously make more of themselves, until a signal tells them it’s time to turn into sperm — a process called spermatogenesis. This signal comes in the form of retinoic acid, a product of vitamin A. Pulses of retinoic acid bind to retinoic acid receptors in the cells, and when the system is aligned just right, this initiates a complex genetic program that turns the stem cells into mature sperm.
Salk scientists found that for this to work, retinoic acid receptors must bind with a protein called SMRT (silencing mediator of retinoid and thyroid hormone receptors). SMRT then recruits HDACs, and this complex of proteins goes on to synchronize the expression of genes that produce sperm.
Previous groups have tried to stop sperm production by directly blocking retinoic acid or its receptor. But retinoic acid is important to multiple organ systems, so interrupting it throughout the body can lead to various side effects — a reason many previous studies and trials have failed to produce a viable drug. Evans and his colleagues instead asked whether they could modulate one of the molecules downstream of retinoic acid to produce a more targeted effect.
The researchers first looked at a line of genetically engineered mice that had previously been developed in the lab, in which the SMRT protein was mutated and could no longer bind to retinoic acid receptors. Without this SMRT-retinoic acid receptor interaction, the mice were not able to produce mature sperm. However, they displayed normal testosterone levels and mounting behavior, indicating that their desire to mate was not affected.

To see whether they could replicate these genetic results with pharmacological intervention, the researchers treated normal mice with MS-275, an oral HDAC inhibitor with FDA breakthrough status. By blocking the activity of the SMRT-retinoic acid receptor-HDAC complex, the drug successfully stopped sperm production without producing obvious side effects.
Another remarkable thing also happened once the treatment was stopped: Within 60 days of going off the pill, the animals’ fertility was completely restored, and all subsequent offspring were developmentally healthy.
The authors say their strategy of inhibiting molecules downstream of retinoic acid is key to achieving this reversibility.
Think of retinoic acid and the sperm-producing genes as two dancers in a waltz. Their rhythm and steps need to be coordinated with each other for the dance to work. But if you throw something in that makes the genes miss a step, the two are suddenly out of sync and the dance falls apart. In this case, the HDAC inhibitor causes the genes’ misstep, halting the dance of sperm production.
However, if the dancer can find its footing and get back in step with its partner, the waltz can resume. In the same way, the authors say that removing the HDAC inhibitor allows the sperm-producing genes to get back in sync with the pulses of retinoic acid, turning sperm production back on as desired.
“It’s all about timing,” says co-author Michael Downes, a senior staff scientist in Evans’ lab. “When we add the drug, the stem cells fall out of sync with the pulses of retinoic acid, and sperm production is halted, but as soon as we take the drug away, the stem cells can reestablish their coordination with retinoic acid and sperm production will start up again.”
The authors say the drug doesn’t damage the sperm stem cells or their genomic integrity. While the drug was present, the sperm stem cells simply continued regenerating as stem cells, and when the drug was later removed, the cells could regain their ability to differentiate into mature sperm.

“We weren’t necessarily looking to develop male contraceptives when we discovered SMRT and generated this mouse line, but when we saw that their fertility was interrupted, we were able to follow the science and discover a potential therapeutic,” says first author Suk-Hyun Hong, a staff researcher in Evans’ lab. “It’s a great example of how Salk’s foundational biological research can lead to major translational impact.”
Other authors include Glenda Castro, Dan Wang, Russell Nofsinger, Annette R. Atkins, and Ruth T. Yu of Salk, Maureen Kane, Alexandra Folias, and Joseph L. Napoli of UC Berkeley, Paolo Sassone-Corsiof UC Irvine, Dirk G. de Rooij of Utrecht University, and Christopher Liddle of the University of Sydney.
The work was supported by the National Institutes of Health (grants CA265762 and CA220468) and the Next Generation Sequencing and Flow Cytometry Cores at Salk, funded by the Salk Cancer Center (NCI grant NIH-NCI CCSG: P30 014195).