Publisher Health

New substances that activate adrenalin receptors instead of opioid receptors have a similar pain relieving effect to opiates, but without the negative aspects such as respiratory depression and addiction. This is the result of research carried out by an international team of researchers led by the Chair of Pharmaceutical Chemistry at Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU). Their findings, which have now been published in the  scientific journal Science, are a milestone in the development of non-opioid pain relief.
Opiates cause addiction, new substances do not
They are a blessing for patients suffering from severe pain, but they also have serious side effects: Opioids, and above all morphine, can cause nausea, dizziness and constipation and can also often cause slowed breathing that can even result in respiratory failure. In addition, opiates are addictive — a high percentage of the drug problem in the USA is caused by pain medication, for example.
In order to tackle the unwanted medical and social effects of opioids, researchers all over the world are searching for alternative analgesics. Prof. Dr. Peter Gmeiner, Chair of Pharmaceutical Chemistry is one of these researchers. “We are focusing particularly on the molecular structures of the receptors that dock onto the pharmaceutical substances,” says Gmeiner. “It is only when we understand these on the atomic level that we can develop effective and safe active substances.” Collaborating with an international team of researchers, Prof. Gmeiner discovered an active substance in 2016 that bonds to known opioid receptors and that offers the same level of pain relief as morphine, even though it has no chemical similarity to opiates.
New approach: Adrenaline receptors instead of opioid receptors
Peter Gmeiner is currently following a lead that seems very promising: “Many non-opioid receptors are involved in pain processing, but only a small number of these alternatives have as yet been validated for use in therapies,” he explains. Gmeiner and a team of researchers from Erlangen, China, Canada and the USA have now turned their attention to a new receptor that is responsible for binding adrenaline — the alpha 2A adrenergic receptor. There are already some analgesics that target this receptor such as brimonidine, clonidine and dexmedetomidine. Gmeiner: “Dexmedetomidine relieves pain, but has a strong sedative effect, which means its use is restricted to intensive care in hospital settings and is not suitable for broader patient groups.”
The aim of the research consortium is to find a chemical compound that activates the receptor in the central nervous system without a sedative effect. In a virtual library of more than 300 million different and easily accessible molecules, the researchers looked for compounds that physically match the receptor but are not chemically related to known medication. After a series of complex virtual docking simulations, around 50 molecules were selected for synthesis and testing and two of these fulfilled the desired criteria. They had good bonding characteristics, activated only certain protein sub-types and thus a very selective set of cellular signal pathways, whereas dexmedetomidine responds to a significantly wider range of proteins.
Pain relief without sedation in animal models
By further optimizing the identified molecules, for which extremely high-resolution cryo-electron microscopic imaging was used, the researchers were able to synthesize agonists that produced high concentrations in the brain and reduced the sensation of pain effectively in investigations with animal models. “Various tests confirmed that docking on the receptor was responsible for the analgesic effect,” explains Gmeiner. “We are particularly pleased about the fact that none of the new compounds caused sedation, even at considerably higher doses than those that would be required for pain relief.”
The successful separation of analgesic properties and sedation is a milestone in the development of non-opioid pain medication, especially as the newly-identified agonists are comparatively easy to manufacture and administer orally to patients. However, Prof. Gmeiner has to dampen any hopes of rapid widespread use in human medicine: “We are currently still talking about basic research. The development of medication is subject to strict controls and in addition to significant amounts of funding, it takes a long time. However, these results still make us very optimistic.”

Endothelial cells — the cells that line blood vessels — grown alongside leukemia cells become corrupted and rescue the cancer cells from many chemotherapy drugs, a study by Weill Cornell Medicine investigators found.
A growing body of evidence suggests that genetic mutations are not enough to cause cancer; tumor cells also need the right environment to grow. The new study, published in Blood on Aug. 18, found that endothelial cells can protect T-cell acute lymphoblastic leukemia (T-ALL) cells, which cause an aggressive type of blood cancer, from chemotherapy drugs that would otherwise kill the cancer cells. The discovery and the platform they used could improve the way scientists find and test new drugs for the condition.
“We have identified endothelial cells as a new player in T-ALL,” said co-senior author Dr. Giorgio Inghirami, professor of pathology and laboratory medicine and a member of the Sandra and Edward Meyer Cancer Center at Weill Cornell Medicine. “Our platform may lead to more effective drug discovery programs and better clinical trials.”
About 30 percent of patients with T-ALL don’t respond to chemotherapy, and some successfully treated patients will have a recurrence years later, Dr. Inghirami said. It can create a very difficult experience for patients and their families.
Previous studies had suggested the stromal cells in the bone marrow might play a role in blood cancers, but no one had looked at the cells lining the blood vessels. So, Dr. Inghirami teamed up with study co-senior author Dr. Shahin Rafii, chief of the Division of Regenerative Medicine and director of the Hartman Institute for Organ Regeneration at Weill Cornell Medicine, to develop a way to study the effects of chemotherapies on T-ALL and endothelial cells growing together. They developed a preclinical model with tumor cells from patients with T-ALL. Study co-senior author Dr. Leandro Cerchietti, associate professor of medicine in the Division of Hematology and Medical Oncology and a member of the Meyer Cancer Center at Weill Cornell Medicine, helped them build and test a library of 433 drug compounds on the tumor cells alone. They used a high-volume automated platform to test the drugs.
Next, they tested the drugs again on T-ALL cells grown with an endothelial cell line engineered in Dr. Rafii’s laboratory. They found that these tumor cells were resistant to many chemotherapies, and they became more aggressive. Single-cell RNA sequencing showed changes in gene expression affecting multiple gene pathways in both endothelial and cancer cells grown together. The endothelial cells became corrupted and expressed genes that promote cancer growth. Endothelial cells extracted from T-ALL tumors expressed the same genes, suggesting the model recreates what happens in the body.
“This is a groundbreaking discovery that shows T-ALL is dependent on growth factors from the endothelial cells to respond to many treatments,” said Dr. Rafii, who is also the Arthur B. Belfer Professor in Genetic Medicine and a member of the Meyer Cancer Center at Weill Cornell Medicine. “When the blood vessels are corrupted, the chemotherapy doesn’t work.”
During the drug screening process, they found five chemotherapies that remain effective in the presence of corrupted endothelial cells. The drugs also slowed tumor growth and spread and extended survival in mice with T-ALL. One of the drugs is irinotecan, a drug long used to treat gynecological and colon cancers. Dr. Inghirami noted that the drug was previously tested for treating blood cancer and was abandoned. But the new evidence suggests revisiting the drug. He said altering the drug and applying what clinicians have learned about managing its side effects might lead to better results.
The “Ferrari-like” platform the team developed for the study may have an even more significant impact than the individual drug discoveries, said Dr. Inghirami, who is also a hematopathologist at NewYork-Presbyterian/Weill Cornell Medical Center. He explained that despite promising pre-clinical studies, most drug candidates fail in clinical trials.
“There is tremendous attrition because we may be using poorly informative pre-clinical systems to study drugs,” he said. “It is naïve to think that results of drugs tested on a single cell type in the laboratory would accurately reflect what happens in the body.”
Instead, Dr. Inghirami suggested using the team’s platform to screen drugs in progressively more complex systems including multicellular samples, organoids and patient-derived mouse models. Drug candidates screened this way might have a better chance of success in clinical trials.
“This stepwise approach could revolutionize the way we study drug candidates in the laboratory and lead to more successful clinical trials,” he said.
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Materials provided by Weill Cornell Medicine. Note: Content may be edited for style and length.

A team of scientists from the Krembil Brain Institute, part of the University Health Network in Toronto, and Duke University in Durham, North Carolina, has developed the first computer model predicting the role of cortical glial cells in cognition.
The paper was published today in the journal Proceedings of the National Academy of Sciences (PNAS).
“The role of neurons is well documented, but neurons are interspersed with glial cells and many synapses in the brain have glia nearby,” says Dr. Maurizio De Pittà, a scientist at the Krembil Brain Institute and the first author of the study. “We currently do not understand how neurons and glia work together, or how glial dysfunction contributes to cognitive deficits.”
Glial cells are abundant throughout the brain and play several important roles. These cells have long been thought to be passive bystanders — physically supporting neurons and synapses, bringing nutrients to neurons, and removing toxins and waste products. However, scientists have recently discovered that glia interact with neurons in a fashion similar to the way that neurons communicate with one another through chemical signals.
This paper presents the first theory of the role glia play in cognitive processing, in the brain. “The type of glial cells that we study — known as astrocytes — can modify the activity of our brain circuits and influence the way we behave,” says Dr. De Pittà.
The study looked at the role of astrocytes in working memory, which is the ability to store information for ongoing tasks, such as following the storyline of a movie or counting to ten.

In a series of experiments using functional magnetic resonance imaging (fMRI) to measure brain activity across networks in the brain, Johns Hopkins Medicine researchers looked at how stress might increase appetite in obese and lean adults. The researchers found that stress impacts the brain’s responses to food, and that both lean and obese adults react to food cues in areas of the brain associated with reward and cognitive control.
The findings of the study were published Sept. 28 in PLOS ONE.
For the study, the researchers analyzed data from 29 adults (16 women and 13 men), 17 of whom had obesity and 12 of whom were lean. Participants completed two fMRI scans, one following a combined social and physiological stress test.
Participants were given a food word reactivity test during both scans. This test involved looking at how people’s brains reacted to food words, such as menu items on a chalkboard. To maximize the appetitive response in the brain, the researchers asked participants to imagine how each food looked, smelled and tasted, and how it would feel to eat it at that moment. They were also asked how much they wanted each food, and if they felt they should not eat that food, to see how they approached decision-making related to each food.
“The experiments showed that obese and lean adults differ somewhat in their brain responses, with obese adults showing less activation of cognitive control regions to food words, especially to high-calorie foods, like for example, grilled cheese,” says lead researcher Susan Carnell, Ph.D., associate professor of psychiatry and behavioral sciences at the Johns Hopkins University School of Medicine.
The study also showed that stress impacts brain responses to food. For example, obese individuals showed greater activation of the orbitofrontal cortex, a brain reward region, after the stress test. “We also found evidence for links between the subjective stress experienced and brain responses in both groups. For example, lean individuals who reported higher stress following the test showed lower activation of the dorsolateral prefrontal cortex, a key brain area for cognitive control,” says Carnell.
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Materials provided by Johns Hopkins Medicine. Note: Content may be edited for style and length.

Viruses are tiny packets of destruction and there are more of them than any other biological entity on the planet.
Luckily, only a few hundred are known to make people sick, and figuring out what makes those viruses tick can help prevent illness. What’s more, examining the way viruses have evolved to infect mammals can perhaps even answer basic questions about human health.
A study from a team at U-M Medical School takes a closer look at a virus that causes tumors in monkeys, called SV40. SV40 is a DNA virus that, in order to make more of itself, burrows into a cell and then into its nucleus, thereby infecting it.
“SV40 is used as a tool for understanding how viruses that cause cancer in humans work,” said Chelsey Spriggs, Ph.D., assistant professor, Cell & Developmental Biology and Microbiology & Immunology at U-M Medical School, Research Assistant Professor at the U-M Life Sciences Institute, and first author of the study. Several viruses have been tied to cancer in people, including human papillomavirus, Kaposi Sarcoma-associated Herpesvirus and Epstein-Barr virus.
The study team wanted to more fully understand how this infection process happens inside the cell. An earlier study from Spriggs (at the time a postdoctoral fellow in the lab of Billy Tsai, Ph.D., the Corydon Ford Collegiate Professor of Cell & Developmental Biology), and their team found that SV40 travels from the surface of the cell, through the endosome, the endoplasmic reticulum and then to the cytosol where it is partially disassembled. The latest study illuminates the final and most important step for infection, entry into the nucleus.
The virus itself is bigger than the portal it uses to gain entry into a cell’s nucleus, explained Spriggs, called the nuclear pore complex. The nuclear pore complex is a major port in the membrane of the nucleus, regulating the transport of proteins, RNA and other cellular cargo from the nucleus into the cell’s cytoplasm and back again. Many viruses exploit this passageway to sneak into the nucleus.
The new study found that SV40 uses the nuclear pore complex and another protein complex called LINC, which connects the inner and outer membranes of the nucleus, first disassembling itself into a smaller package made up of two proteins and the virus’ genome. Unlike many other viruses that grab onto fingerlike projections sticking out from the nuclear pore complex, SV40 interacts with LINC first before entering it.
This difference in technique might underlie SV40’s ability to cause cancer, Spriggs notes. Further research into how SV40 exploits LINC and the nuclear pore complex could even help scientists understand how the two important cellular membrane complexes interact with each other, which so far is somewhat of a mystery.
“Viruses use a lot of the same pathways that are disrupted in cancers and other diseases,” said Spriggs. “Studying them is good for understanding human biology.”
Spriggs recently opened her own independent research lab at the University of Michigan studying the entry mechanism of human oncogenic viruses.
Additional authors on this paper include Grace Cha and Jiaqian Li.
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Materials provided by Michigan Medicine – University of Michigan. Original written by Kelly Malcom. Note: Content may be edited for style and length.

Locked fingers, known as trigger finger, are more common among people with diabetes than in the general population. A study led by Lund University in Sweden shows that the risk of being affected increases in the case of high blood sugar. The study has been published in Diabetes Care.
Trigger finger means that one or more fingers, often the ring finger or thumb, ends up in a bent position that is difficult to straighten out. It is due to the thickening of tendons, which bend the finger, and their connective tissue sheath, which means that the finger becomes fixed in a bent position towards the palm. It is a painful condition that can often be treated with cortisone injections, but sometimes requires surgery.
“At the hand surgery clinic, we have noted for a long time that people with diabetes, both type 1 and type 2, are more often affected by trigger finger. Over 20 percent of those who require surgery for this condition are patients who have, or will develop, diabetes,” says Mattias Rydberg, doctoral student at Lund University, resident physician at Skåne University Hospital and first author of the study.
To study whether high blood sugar (blood sugar dysregulation) increases the risk of trigger finger, the researchers examined two registers: Region Skåne’s healthcare database, which includes all diagnoses, and the Swedish national diabetes register. Between 1 and 1.5 per cent of the population are affected by trigger finger, but the diagnosis arises among 10-15 per cent of those who have diabetes, and the phenomenon appears most in the group with type 1 diabetes.
The newly published study strengthens the pattern of blood sugar being a crucial factor for an increased risk of being affected by trigger finger. High blood sugar increased the risk of being affected by trigger finger among both men and women in the groups with type 1 diabetes and type 2 diabetes. Blood sugar is measured in HbA1C, also referred to as long-term blood sugar, and when regulated, is under 48. The group of men with the worst regulated blood sugar (HbA1C > 64) had up to 5 times as high a risk of being affected than men with well-regulated (HbA1< 48) blood sugar. "However, we can't know for certain if any of the groups seek healthcare more often than others which could be a factor that affects the results," says Mattias Rydberg. The mechanism, or mechanisms, behind the increased risk are unknown, but there are theories that high blood sugar makes both the flexor tendons and their connective tissue sheaths thicker, thus causing them to lock more easily. It was previously known that those with unregulated blood sugar are more prone to nerve entrapments in the hand. "It is important to draw attention to the complications from diabetes and how they can arise in order to discover them early, which enables faster treatment and thus a better outcome. In addition to nerve compressions and trigger finger, there may also be a link with thickening of the connective tissue in the palm (Dupuytren's contracture), impairment of joint movement and the risk of arthritis at the base of the thumb. The mechanisms behind these complications probably differ in the case of diabetes. The results of this study are interesting, as we can show that blood sugar dysregulation has a connection with the development of trigger finger," says Lars B. Dahlin, professor at Lund University and consultant in hand surgery at Skåne University Hospital. The next step in the research will be to chart how effective it is to operate on patients with diabetes who are affected by trigger finger. "From our experience at the clinic, surgery goes well and there are few complications, but it takes a little longer for patients with type 1 and type 2 diabetes to regain full movement and function. We want to investigate this hypothesis further. Another interesting idea is to see if trigger finger could be a warning signal for type 2 diabetes. It is far from all who are affected by trigger finger that have diabetes, but it would be interesting to see if by using modern registers we can discover those who are in the risk zone for developing diabetes," concludes Mattias Rydberg. Story Source: Materials provided by Lund University. Note: Content may be edited for style and length.

What exactly are the molecular interactions between the virus causing COVID-19 and its human host? How might our genetic differences cause different disease courses? And how do still-emerging virus variants differ in their host-virus interactions? To get to the bottom of these questions, an international team of researchers has generated a systematic map of molecular contacts between the SARS-CoV-2 virus and its human host.
The contact map, published in the journal Nature Biotechnology, reveals more than 200 direct protein-protein contacts, or protein interactions. The international consortium of scientists, led by Pascal Falter-Braun, Director at the Helmholtz Munich Institute of Network Biology (INET) and Professor at the Faculty of Biology, Ludwig-Maximilians-University (LMU) Munich, Germany, included teams in Canada, USA, France, Spain and Belgium.
In contrast to previous large-scale studies on protein-protein associations, now the direct protein contacts between virus and host could be precisely identified. “To really understand the mechanistic connections between virus and host, we need to know how the parts fit together,” says Frederick Roth, Professor at the University of Toronto’s Donnelly Centre and Sinai Health (Toronto, Canada).
Taking a closer look at this newly-revealed set of direct protein interactions (or ‘contactome’), the team found chains of connections between viral proteins and infection-relevant human genes. For example, they were able to trace connections between certain SARS-CoV-2 proteins and human proteins encoded by the genes that have been linked to an increased likelihood of severe COVID-19 in other studies. They also found connections between the viral proteins and genes involved in, for example, metabolic disorders like obesity and diabetes.
“We already know that genetic differences in humans have an important role in the course and severity of a COVID-19 infection,” says Pascal Falter-Braun, and he continues, “thanks to identification of the molecular contact points, it is now possible to examine the underlying mechanisms.”
Initial insights included a demonstration that important inflammatory signalling pathways are directly activated by the virus. These contacts may help explain the exaggerated inflammatory reaction, that plays a major role in severe cases of COVID-19.
However, the protein-protein contacts not only point to impacts on the function of human cells and the human immune system, but also impact the function of SARS-CoV-2, including the rate at which the virus replicates.
According to Falter-Braun, the interaction of virus and human cells can be thought of as a visit of the virus to a restaurant: The guest — the virus — initially only has contact with the waiter, but subsequently the waiter goes to the kitchen, communicates the order to the chef, and the virus again gets an answer, in this example the meal, which in turn affects the virus. Depending on which proteins in the human cells — that is: waiter, chef, kitchen assistant, etc — encounter which proteins of the virus, the infection and immune reaction can turn out differently.
“Because of this mutual influence of protein-protein connections, our systematic contact map points to many potential drug targets,” says Falter-Braun. The scientists have already been able to confirm, for example, that the human protein USP25 is recruited to help certain viral process and that its inhibition significantly reduces the multiplication of the virus.
“Many of the technologies and collaborations in this study were developed for other purposes, then quickly ‘pivoted’ to the COVID-19 pandemic, highlighting the value of fundamental research investments” says Dr. Dae-Kyum Kim, a lead author who began this work at Sinai Health (Toronto) and continued it as an Assistant Professor at the Roswell Park Comprehensive Cancer Center. To this end, they first had to put in some effort and use the latest technology, because charting the contact map was at times like solving a huge puzzle for the international team of researchers: The scientists systematically examined and displayed the interactions of around 30 viral proteins, each with ~17,500 human proteins in so-called assays, interrogating 450,000 protein pairs. By hand, one would never have managed this in such a short time. “We resorted to robotics when testing the individual plates each with multiple assays so that each protein type was automatically paired with another. And we had artificial intelligence methods do the initial evaluation of whether interactions occurred or not,” Falter-Braun says.
Such a mammoth project required a team effort. “From molecular biology methods to computational analysis of networks and protein domains, to expertise in virology and innate immunity, we collaborated across disciplines,” says Falter-Braun. “Our expertise in virus-host interactomics combined with RNA viruses biology, enabled assessing the virus’ dependence on host direct partners” specifies Caroline Demeret from the Institut Pasteur.
The effort, researchers believe, was worth it: The contactome map will serve as a platform for the scientific community to study individual interactions in more detail and to understand their impact on molecular mechanisms and clinical progression, and thus uncover starting points for new therapeutic possibilities.

When and why does type 1 diabetes manifest in children? For the first time, researchers conducted a long-term study on infants and young children with increased genetic risk of type 1 diabetes. The results have now been published in the Journal of Clinical Investigation. The authors provide a unique picture of the dynamics of blood sugar regulation during early childhood and its relationship to the development of autoimmunity.
The POInT study is uniquely poised to study blood sugar levels during the development of autoimmunity
Within the framework of the Global Platform for the Prevention of Autoimmune Diabetes (GPPAD), the clinical primary prevention study POInT (Primary Oral Insulin Trial) is conducted multicentrically at seven clinical sites in five countries. POInT aims to prevent the formation of islet autoantibodies, and thus the induction of type 1 diabetes. As a result of a misdirected immune reaction, the insulin-producing beta cells of the pancreas are destroyed in people with type 1 diabetes. It was previously thought that metabolic changes occur close to the onset of clinical disease and that the pancreatic beta cells are destroyed by the autoimmunity. However, no-one had looked closely at what happens when the autoimmunity starts. Therefore, the POInT study conducted a frequent follow-up in the first years of life — starting at four months of age — in over 1,000 children with a genetically determined 10 percent risk to develop type 1 diabetes. This enabled the researchers to precisely correlate changes in blood glucose with the timing of islet autoantibody development.
“Our results change our understanding of the development of type 1 diabetes. We show that metabolic changes occur in an earlier phase of the disease than previously anticipated,” explains Anette-Gabriele Ziegler, Director at the Helmholtz Munich Institute of Diabetes Research (IDF). Together with an international team of researchers, she conducted the POInT study. The team examined the pre- and post-prandial blood sugar levels together with islet autoantibodies in the participating children.
Results provide new approaches for research
First, and in contrast to the previous assumption, the results showed that the blood sugar concentrations shortly after birth are not stable. Instead they decrease in the first year of life, and then increase again at around 1.5 years of age. “The dynamic changes in glucose metabolism in the first years of life were a surprise to us. They very likely reflect changes in the pancreatic islets and signal that we need to study glucose metabolism and the pancreas in early life more intensely” says Katharina Warncke, Chief Physician for Paediatric Endocrinology / Diabetology at the Department of Pediatrics and scientist at the IDF. Importantly, the scientists found that in the children who developed autoimmunity compared to children who did not, blood sugar levels after meals were already higher two months before the formation of islet antibodies. This difference persisted and was also followed by increases in pre-meal values after the autoimmunity.
Puzzle around the key event inducing the autoimmune reaction
The researchers were able to determine that blood sugar levels of infants and young children behave dynamically and reflect the concentration peak of islet autoantibodies — this indicates a phase of activity and susceptibility of islet cells. “The change in post-meal blood sugar levels shortly before the initial detection of autoantibodies points to the likelihood that there is an event impairing the function of the islets preceding and contributing to the autoimmune reaction. As glucose values further increase after seroconversion, the impairment or damage seems to be sustained leading to further glucose instability,” explains Warncke.
“The observed changes in blood sugar levels in relation to autoantibody formation are exciting. Now we know that the start of the disease process is likely to be acting at the pancreatic islets and we can focus our research to find the cause of this chronic illness,” says Ezio Bonifacio, Professor at the Center for Regenerative Therapies Dresden at the Technische Universität Dresden.
In summary, the scientists discovered that metabolic alterations occur in a much earlier stage of the disease than previously assumed: changes can occur in parallel to autoimmunity or even precede it. The researchers suggest that the excess increase in blood sugar levels after eating and shortly before the formation of antibodies is connected to a change in islet cell function.
The goal: prevention of new cases
“Changes in glucose levels could thus serve as an indicator of islet cell dysfunction and a potential onset of autoimmunity against beta cells in the future,” summarizes Ziegler. However, this requires intensive further research of glucose metabolism and additional biomarkers in early childhood. The scientists ultimately strive to reduce the number of new cases of type 1 diabetes. Four out of every 1,000 children in Western, industrialised nations are currently affected.
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Materials provided by Helmholtz Munich. Note: Content may be edited for style and length.

A government-funded study on the potential for cross-contaminating kitchen surfaces with pathogens during food preparation has pointed to an unlikely culprit for spreading sickness: spice containers.
Detailing findings in the Journal of Food Protection, Donald Schaffner, a Distinguished Professor in the Department of Food Science at the Rutgers School of Environmental and Biological Sciences who co-authored the study in collaboration with North Carolina State University colleagues, concluded that when consumers are preparing meals, spice containers can easily become cross-contaminated with health-threatening microorganisms. Cross-contamination is the process by which microbes are transferred from one substance or object to another, often with harmful effects.
The study was commissioned by the U.S. Department of Agriculture’s (USDA) Food Safety and Inspection Service.
“In addition to more obvious surfaces like cutting boards, garbage can lids and refrigerator handles, here’s something else that you need to pay attention to when you’re trying to be clean and sanitary in your kitchen,” Schaffner said. “Our research shows that any spice container you touch when you’re preparing raw meat might get cross-contaminated. You’ll want to be conscious of that during or after meal preparation.”
Foodborne illnesses such as non-typhoidal Salmonella and Campylobacter account for nearly 2 million infections per year in the U.S., according to studies by the U.S. Centers for Disease Control and Prevention (CDC). A significant portion of those illnesses are derived from USDA-regulated food products, including chicken, turkey, beef, pork and game, according to the Interagency Food Safety Analytics Collaboration, a group formed in 2011 by the CDC, the USDA’s Food Safety and Inspection Service and the U.S. Food and Drug Administration. Scientists said they believe proper handling of food — including adequate cooking, consistent handwashing and sanitizing of kitchen surfaces and utensils — can combat cross-contamination.
“The purpose of this study was to determine the prevalence and degree of cross-contamination across a variety of kitchen surfaces during a consumer meal preparation event,” said Schaffner, who also is the Rutgers Agricultural Experiment Station’s Extension Specialist in Food Science.
Researchers monitored the behavior of 371 adults cooking an identical turkey burger recipe in several kitchens of various sizes, ranging from small apartment-style kitchens to larger teaching kitchens, in extension centers and food banks. Participants prepared a meal consisting of raw ground turkey patties with a seasoning recipe, along with a prepackaged salad. To simulate the movement of a pathogen across a kitchen, researchers inoculated the meat ahead of time with a bacteriophage known as “MS2” to serve as a safe tracer. Bacteriophages are viruses that infect bacteria and have no effect on humans.
Participants weren’t informed that researchers would be examining their food safety behaviors until after they had prepared the meal. Once the meal had been prepared, researchers swabbed kitchen utensils, cleaning areas and kitchen surfaces to test for the presence of the MS2 tracer. Based on observations of participants’ behavior during cooking, researchers decided to take samples from some new categories of surfaces, such as spice containers and sink faucet handles.
The researchers found the most frequently contaminated objects were spice containers, with about 48 percent of the samples showing evidence of MS2 contamination. This prevalence of contamination was significantly different from many other surfaces sampled. Cutting boards and trash can lids were the second and third most contaminated. Faucet handles were the least contaminated object studied.
“We were surprised because we had not seen evidence of spice container contamination before,” Schaffner said. “Most research on the cross-contamination of kitchen surfaces due to handling of raw meat or poultry products has focused on kitchen cutting boards or faucet handles and has neglected surfaces like spice containers, trash bin lids and other kitchen utensils. This makes this study and similar studies from members of this group more comprehensive than previous studies.”
Researchers involved included Benjamin Chapman, professor and department head, Agricultural and Human Sciences, and Lee-Ann Jaykus, the William Neal Reynolds Distinguished Professor, Food, Bioprocessing and Nutrition Sciences, Margaret Kirchner, Savana Everhart, Lindsey Doring, Caitlin Smits, Jeremy Faircloth, Minh Duong, Rebecca Goulter, Lydia Goodson, Lisa Shelley and Ellen Thomas Shumaker, all of North Carolina State University; Sheryl Cates of RTI International; Christopher Bernstein of the Consumer Financial Protection Bureau; and Aaron Lavallee of the U.S. Department of Agriculture.
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Materials provided by Rutgers University. Original written by Kitta Macpherson. Note: Content may be edited for style and length.

New research from pediatricians at UT Southwestern and Children’s Health reveals the impact of COVID-19 on mental health in children. Separately, a study funded by a $2.5 million grant from the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) will investigate the ideal way to use oxygen during resuscitation of infants born preterm.
COVID-19 and mental health
A study led by Jacqueline Bolt, M.D., a UTSW Pediatric Emergency Medicine Fellow, examined how the patterns and outcomes of pediatric mental and behavioral health (MBH) visits to the Emergency Department (ED) at Children’s Medical Center Dallas changed before the pandemic and after it began. Dr. Bolt and her colleagues collected information from electronic medical records on patients who visited the ED from March through September between 2017 and 2019 to study trends before the pandemic, then compared the same span between 2019 and 2020.
The researchers report in Pediatric Emergency Care that ED visits for pediatric MBH gradually increased in the years before the pandemic, reflecting nationwide trends. Although overall ED visits for MBH decreased in 2020, the proportion of total visits jumped 42.8%. Demographic groups with the highest increase in MBH visits included females, adolescents between ages 15 and 17, and non-Hispanic patients. Pediatric patients who came to the ED in 2020 for MBH treatment were significantly more likely to be admitted or transferred for inpatient psychiatric care than in previous years.
“These findings highlight specific areas in pediatric MBH care that may benefit from targeted interventions,” Dr. Bolt said. “Future research is needed to investigate longer-term trends as well as effective prevention and intervention strategies.”
Other UTSW and Children’s Health researchers who contributed to the study include Faisalmohemed Patel, Laura Stone, Divya Pandian, Matthias Manuel, and Nakia Gaines.