Publisher Health

When it comes to preventing tick bites — especially in light of the dramatic, decade-long rise in tick-borne diseases — bug sprays help but are less than optimal.
For example, DEET was designed to keep quick-moving mosquitoes from landing on their host, where they bite and fly off in seconds. Ticks, on the other hand, don’t fly but rather ambush and then climb slowly up their host until they embed, feed and may remain for days.
“Unfortunately most repellants were developed for mosquitoes 75-plus years ago and not for ticks,” says vector-borne disease expert Stephen Rich, professor of microbiology at the University of Massachusetts Amherst and executive director of the UMass Amherst-based New England Center of Excellence in Vector-Borne Diseases (NEWVEC). “DEET, the gold standard, works fairly well, but a holy grail would be to have another repellency tool — not a contact repellent like DEET but a spatial repellent — that works as good as or better than DEET against ticks.”
Experiments at Rich’s Laboratory of Medical Zoology used a new controlled-release device developed by scientist-entrepreneur Noel Elman with funding from the Department of Defense’s medical research programs. Rich and colleagues tested the effects on ticks after releasing the synthetic pyrethroids transfluthrin and metofluthrin into a small, transparent chamber equipped with three vertical climbing sticks. Ticks don’t come in direct contact with the repellents but rather the active ingredients create more of a “force field” that alters and slows the ticks’ progress toward their target.
The results, published today, Nov. 8, in the journal PLOS ONE, found that the two spatial repellents were effective at changing the behavior of ticks, making them less likely to climb vertically and more likely to detach or fall off the stick.
“While we still have much work to do, these innovative findings prove the principle that these spatial repellents alter the behavior in ticks in a way we hope will lead to fewer tick bites,” says Rich, senior author.

While the physical differences between humans and non-human primates are quite distinct, a new study reveals their brains may be remarkably similar. And yet, the smallest changes may make big differences in developmental and psychiatric disorders.
Understanding the molecular differences that make the human brain distinct can help researchers study disruptions in its development. A new study, published recently in the journal Science by a team including University of Wisconsin-Madison neuroscience professor Andre Sousa, investigates the differences and similarities of cells in the prefrontal cortex — the frontmost region of the brain, an area that plays a central role in higher cognitive functions — between humans and non-human primates such as chimpanzees, Rhesus macaques and marmosets.
The cellular differences between these species may illuminate steps in their evolution and how those differences can be implicated in disorders, such as autism and intellectual disabilities, seen in humans. Sousa, who studies the developmental biology of the brain at UW-Madison’s Waisman Center, decided to start by studying and categorizing the cells in the prefrontal cortex in partnership with the Yale University lab where he worked as a postdoctoral researcher.
“We are profiling the dorsolateral prefrontal cortex because it is particularly interesting. This cortical area only exists in primates. It doesn’t exist in other species,” Sousa says. “It has been associated with several relevant functions in terms of high cognition, like working memory. It has also been implicated in several neuropsychiatric disorders. So, we decided to do this study to understand what is unique about humans in this brain region.”
Sousa and his lab collected genetic information from more than 600,000 prefrontal cortex cells from tissue samples from humans, chimpanzees, macaques and marmosets. They analyzed that data to categorize the cells into types and determine the differences in similar cells across species. Unsurprisingly, the vast majority of the cells were fairly comparable.
“Most of the cells are actually very similar because these species are relatively close evolutionarily,” Sousa says.
Sousa and his collaborators found five cell types in the prefrontal cortex that were not present in all four of the species. They also found differences in the abundancies of certain cell types as well as diversity among similar cell populations across species. When comparing a chimpanzee to a human the differences seem huge — from their physical appearances down to the capabilities of their brains. But at the cellular and genetic level, at least in the prefrontal cortex, the similarities are many and the dissimilarities sparing.
“Our lab really wants to know what is unique about the human brain. Obviously from this study and our previous work, most of it is actually the same, at least among primates,” Sousa says.
The slight differences the researchers found may be the beginning of determining some of those unique factors, and that information could lead to revelations about development and developmental disorders at a molecular level.
“We want to know what happened after the evolutionary split between humans and other primates,” Sousa says. “The idea is you have a mutation in a gene or in several genes and those genes now have slightly different functions. But if these genes are relevant for brain development, for example, how many of a certain cell is produced, or how cells are connecting to other cells, how is it affecting the neuronal circuitry and their physiological properties? We want to understand how these differences lead to differences in the brain and then lead to differences we can observe in adults.”
The study’s observations were made in the brains of adults, after much of the development is complete. This means that the differences may be occurring during the brain’s development. So, the researchers’ next step is to study samples from developing brains and extend their area of investigation past the prefrontal cortex to potentially find where and when these differences originate. The hope is that this information will lead to a more robust foundation to lay developmental disorder research on top of.
“We are able to do extraordinary things, right? We are studying life itself, the universe, and so much more. And this is really unique when you look around,” says Sousa, whose team included graduate students Ryan Risgaards and Zachary Gomez-Sanchez, research intern Danielle Schmidt, and undergraduate students Ashwin Debnath and Cade Hottman. “If we have these unique abilities, it has to be something in the brain, right? There is something in the brain that allows us to do all of that and we are really interested in knowing what it is.”
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Materials provided by University of Wisconsin-Madison. Original written by Emily Leclerc. Note: Content may be edited for style and length.

MACHETE is a new CRISPR-based technique developed by researchers at the Sloan Kettering Institute (SKI) to study large-scale genetic deletions efficiently in laboratory models.
People are already calling it the Machete Paper.
Still, lead authors Francisco “Pancho” Barriga and Kaloyan Tsanov of the Sloan Kettering Institute don’t want the name of their new research technique to overshadow their findings — which shed new light on a genetic change that contributes to about 15% of all cancers, and which might help identify patients likely to respond to immunotherapies.
MACHETE is what the duo call the CRISPR-based method they developed to study copy number alterations, or CNAs, which are large-scale genetic changes that frequently happen in cancer.
The MACHETE acronym stands for Molecular Alteration of Chromosomes with Engineered Tandem Elements. It’s a new way of slicing out significant targeted sections of genetic code to mirror changes that arise in cancer and other human diseases.
This means that, for the first time, there’s a straightforward and efficient way to study CNA deletions in laboratory models — such as the mouse models of pancreatic cancer and melanoma used in their study, which was published in Nature Cancer on November 7, 2022.

An experiment carried out across ten workplace cafeterias found no significant change in the overall number of calories purchased when food and drink labels showed the amount of physical activity required to burn off their calories.
More than three in five UK adults are overweight or obese, increasing their risk of diseases such as type 2 diabetes and cancer. A major factor that contributes to this is excess energy intake — in other words, eating too many calories. Measures that can help reduce energy intake could help tackle the obesity problem.
In the UK, adults eat as many as a third of their meals out of home, including in workplace cafeterias, and these meals are often much higher in calories than meals eaten at home. Since April 2022 calorie labelling is now required on food and drink served out of the home in businesses employing 250 or more people. While many people welcome this information, evidence for its effectiveness in reducing calories purchased or consumed is limited in quantity and quality. For example, two previous studies conducted by the authors in nine worksite cafeterias found no evidence for an effect of simple calorie labelling (kcal) on calories purchased.
Another option is to show the amount of exercise required to burn off these calories — so-called PACE (physical activity calorie-equivalent) labels — for example, a 1014kcal ‘large battered haddock’ portion would take upwards of five hours walking (278 minutes) to burn off. A recent systematic review — a type of study that brings together existing evidence — concluded that PACE labels may reduce energy selected from menus and decrease the energy consumed when compared with simple calorie labels or no labels, but only one of the 15 studies reviewed was in a ‘real world’ setting.
To explore whether PACE levels can make a difference in real world settings, researchers from the University of Cambridge’s Behaviour and Health Research Unit carried out an experiment across 10 workplace cafeterias in England over a 12 week period in 2021. Their results are published today in PLOS Medicine.
The team collected baseline sales data for a period of business-as-usual for the cafeterias ahead of the experiment. During this period, most labels and menus featured only the product name and price, though some products included standardised front-of-pack nutrition labels on branded and in-house products. During the intervention period the ten cafeterias included calorie information and PACE labels alongside food and drinks items and on items including hot meals, sandwiches, cold drinks and desserts. These labels displayed the minutes of walking that would be needed to burn off the calories in the product.
The team found no evidence that including PACE labels resulted in an overall change in energy purchased from labelled items. However, there was a great deal of variability, with one cafeteria reporting a fall per transaction of 161kcal and another an increase of 69kcal, while five of the cafeterias reported no significant change.
First author Dr James Reynolds from the School of Psychology, Aston University, who carried out the research while at Cambridge, said: “Although we found that showing the amount of exercise required to burn off calories made little difference to the number of calories purchased — and, we can assume, eaten and drunk — there was considerable variability between cafeterias. This suggests that other factors may have influenced the effectiveness of these labels, such as the type of food sold in the cafeteria or the characteristics of those using them.”
The number of calories purchased from items that did not feature the PACE labels did not change and the labels made little difference to the revenue for the cafeterias — just a small increase of 3p per transaction.
Senior author Professor Dame Theresa Marteau, Director of the Behaviour and Health Research Unit at the University of Cambridge, said: “This is the largest study in a real world setting to look at the impact of PACE labels on food and drink purchases, examining 250,000 transactions across 10 worksite cafeterias. The findings suggest that PACE labels, contrary to expectations, may have little or no impact on the food people buy in worksite cafeterias.”
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Materials provided by University of Cambridge. Note: Content may be edited for style and length.

The type of virus used as a model to study the efficacy of non-neutralizing antibodies against the virus responsible for AIDS has a crucial role to play, according to a new study led by Andrés Finzi, Université de Montréal professor and researcher at the CHUM Research Centre.
Published in Cell Reports, the study shows for the first time in humanized mice that the expression of the viral protein Vpu is essential in allowing infected cells to evade the elimination mechanism known as antibody-dependent cell-mediated cytotoxicity (ADCC).
Among other things, this mechanism, well documented in the scientific literature, is used by non-neutralizing antibodies to get rid of cells infected by the virus.
To develop a vaccine against the human immunodeficiency virus, or HIV-1, many laboratories study the generation of this same category of antibodies to prevent infection.
Today, millions of people live with HIV-1 and have non-neutralizing antibodies. Still, the disease has yet to be eradicated. If the antibodies are so effective, why don’t they appear to work?
This conundrum was all it took to spark the curiosity of UdeM doctoral student Jérémie Prévost, the first author of the study and a team member under Finzi, the study’s lead author and a Canada Research Chair in Retroviral Entry.

The costliness of drug development and the limitations of studying physiological processes in the lab are two separate scientific issues that may share the same solution.
Microphysical systems (MPSs) are in vitro platforms made up of cells in a microenvironment that closely mimics that found in the body, allowing scientists to recreate the conditions of tissues found within the body for both further elucidation of biological conditions and systems and for applications such as testing drugs in a more precise model than animal testing allows. However, the advancements that MPSs could provide have been limited up to this point by an inability to accurately record exactly what is happening at a cellular level. Now, a team of scientists has developed an electrochemical sensing platform that could solve this issue.
The results were published in Biosensors and Bioelectronics on October 29, 2022.
“Recent bioengineering techniques have realized a construction of tissue model integrated with a perfusable vascular network,” said corresponding author Yuji Nashimoto, formally of the Frontier Research Institute for Interdisciplinary Sciences at Tohoku University, now at Tokyo Medical and Dental University. “However, to utilize the models as drug screening tools, we need biosensors to monitor their functions in real-time, which until now were lacking. This study developed new electrochemical sensing platform to monitor the vascularized tissue model.”
The team identified electrochemical sensors as ideal for cell functionality readouts because of their low invasiveness, real-time detection and high sensitivity for in vitro culture platforms. Integrating electrochemical sensors into MPSs, however, has been difficult because of their incompatibility with microfluidic devices, according to the researchers.
The researchers were able to integrate their sensing platform for 3D cultured cells with a perfusable vascular network — an engineered vascular system that includes the passage of fluids through it — to measure oxygen metabolism in 3D tissues with vascular flow that mimics that in the human body in real-time.
This successful integration was achieved in part by designing the system to have an open top and a lower layer with five channels for culturing the vascular network and an upper layer that was used for both culturing 3D cultured cells and for oxygen metabolism analysis. The two layers were separated by a thin membrane.
The researchers tested the platform with human lung fibroblast spheroids. They then applied it to a cancer organoid and evaluated the oxygen metabolism changes during drug administration through the vascular network. The results showed that their sensors were successfully integrated into the system to provide the desired accurate measurements.
“We found that the platform could integrate a perfusable vascular network with 3D cultured cells, and the electrochemical sensor could detect the change in oxygen metabolism in a quantitative, non-invasive and real-time manner,” said corresponding author Hitoshi Shiku of the Graduate School of Engineering and of the Graduate School of Environmental Studies, both at Tohoku University. “Biosensors are very important tools to realize more physiological drug screening. Our research group has developed various sensors for the purpose. We continue to expand the detectable molecules and to develop more robust and high-throughput sensors.”
According to the researchers, future studies should include ways to address the changes of the spheroid and organoid during device culture as well as the development of a perfusable vascular network in an even more controlled environment than currently possible. While the researchers identified the next steps for future studies, the results of this study hold promise for monitoring perfusable vascular networks for drug testing purposes in a way that was not previously achieved.
“This study developed oxygen metabolism analysis for the vascularized tissue model,” Shiku said. “In the future, the detectable molecules should be expanded, and the signal-to-noise ratio should be improved.”
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Materials provided by Tohoku University. Note: Content may be edited for style and length.

“Breathe in… Breathe out…” Or: “take a deep breath and count to ten.” The calming effect of breathing in stressful situations, is a concept most of us have met before. Now Professor Micah Allen from the Department of Clinical Medicine at Aarhus University has come a step closer to understanding how the very act of breathing shapes our brain.
The researchers synthesized results from more than a dozen studies with rodent, monkey, and human brain imaging, and used it to propose a new computational model that explains how our breathing influences the brain’s expectations.
“What we found is that, across many different types of tasks and animals, brain rhythms are closely tied to the rhythm of our breath. We are more sensitive to the outside world when we are breathing in, whereas the brain tunes out more when we breathe out. This also aligns with how some extreme sports use breathing, for example professional marksmen are trained to pull the trigger at the end of exhalation,” explains Professor Micah Allen.
The study suggest that breathing is more than just something we do to stay alive, explains Micah Allen.
“It suggests that the brain and breathing are closely intertwined in a way that goes far beyond survival, to actually impact our emotions, our attention, and how we process the outside world. Our model suggests there is a common mechanism in the brain which links the rhythm of breathing to these events.”
Breathing can affect our mental health
Understanding how breathing shapes our brain, and by extension, our mood, thoughts, and behaviours, is an important goal in order to better prevent and treat mental illness.

Researchers at Ruhr University Bochum, Germany, have started investigating whether there might be faster and more efficient ways to develop and improve mental health interventions. In the journal Psychological Medicine, they present the “leapfrog design” as a means to efficiently test new interventions without having to conduct several clinical trials one after the other. The Bochum-based team headed by Dr. Simon Blackwell describes the method together with a colleague from the Ludwig Maximilian University of Munich in the journal Psychological Medicine, published online on 4 November 2022.
Method adapted from cancer research
“Clinical trials tend to be time-consuming and inefficient,” says Blackwell from the Mental Health Research and Treatment Center at Ruhr University. “They can take years and require hundreds of participants — and at the end of all that, it may turn out that the intervention that’s being tested is not effective after all. And even if the new intervention was effective, we’d probably soon want to improve it, for example because of new research that had been published in the meantime. This, in turn, means that we’d have to plan and conduct another clinical trial — on an even bigger scale and requiring even more time.”
In order to find an alternative to traditional psychological treatment research, the team of psychologists adapted methods from cancer research. In their leapfrog design, interventions that prove ineffective are abandoned at an early stage and replaced directly with new interventions. In addition, new findings from basic research can be seamlessly integrated into an ongoing clinical trial so that they can be tested for their clinical utility straight away. Another important aspect of the leapfrog design is that an effective intervention is not only more quickly identified — it is also then set as the new benchmark for other interventions to beat. This leapfrog process allows continuous and systematic optimisation of new and existing interventions.
Non-effective interventions are quickly discarded
In the current publication, the researchers showed that the method is feasible. They compared different versions of an online training for people who feel depressed. The severity of depressive symptoms was assessed at different timepoints using questionnaires. As part of the online training, participants practised imagining positive everyday situations. A total of 188 participants took part and four different versions of the training were tested. At the end, the researchers identified one training version that was the most effective at alleviating symptoms. The training focused in particular on reducing the anhedonic symptoms of depression, i.e. the loss of the ability to look forward to and enjoy activities. These are precisely the symptoms that are a key target for new interventions, as they often do not respond to currently available interventions.
“We were able to quickly identify which training versions were less effective than others and replace them with new training versions while the study was still ongoing,” explains Simon Blackwell, who received the 2022 Early Career Scientist-Practitioner Award from the European Association for Behavioural and Cognitive Therapies. “Compared to a study using a classic trial design, the leapfrog method required significantly fewer participants to identify the most effective training version.”
The researchers have published all materials for the implementation of the leapfrog design — from planning to data analysis — in an open-access format. “We hope that other researchers will use the design to develop the psychological interventions we urgently need at a faster pace than before,” concludes the Bochum researcher. “Something has to change in the way we research mental health interventions. We believe that the leapfrog design provides a promising way forwards.”
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Materials provided by Ruhr-University Bochum. Original written by Julia Weiler. Note: Content may be edited for style and length.

Parkinson’s disease affects 3% of population over 65 years old, and the average age of onset is 60. Regarding juvenile Parkinson, which represents the of all Parkison’s cases, the disease begins before 40 years old. Now, a group of researchers of the Faculty of Medicine and Health Sciences, the Institute of Neurosciences of the University of Barcelona (UBNeuro) and the Bellvitge Biomedical Research Institute (IDIBELL), has deciphered, for the first time, the molecular mechanism by which a mutation of the adenosine type 1 receptor gene is associated with juvenile Parkinson’s.
The team, led by Professor Francisco Ciruela (UB-IDIBELL-UBNeuro), focused on the study of the mechanistic field of the mutation of the brain receptor, previously defined as the potential cause for the early disease. The results, presented in the journal Biomedicine and Pharmacotherapy, reveal that the mutation reduced this receptor’s ability to interact with other adenosine receptors — with the type 2receptor — , which would cause an increase in the neuronal circuits’ excitability in the brain region called the striatum.
“We propose that the inability of both adenosine receptors to interact would generate glutamatergic hyperexcitability in the neuronal circuits of the striatum, a key mechanism in the pathogenesis of juvenile Parkinson’s,” notes Francisco Ciruela, professor of the Department of Pathology and Experimental Therapeutics of the UB and head of the IDIBELL Research Group on Neuropharmacology and Pain.
An imbalance in the excitability of the neuronal circuit
The adenosine receptors are brain receptors assembled to G proteins and involved in motor functions. Previously, their involvement in neurodegenerative pathologies such as Parkinson’s disease had already been suggested.
The studied mutation affects the type 1 adenosine receptor, which has an inhibitory effect on its counterpart — the type 2 adenosine receptor — through which it facilitates the glutamate release and the circuit’s excitability. According to the conclusions, the mutation would prevent the molecular and functional interaction of both adenosine receptors and, as a result, it would facilitate glutamate release, which would cause hyperexcitability in the striatum neuronal circuits.
The study includes the participation of research teams from the Autonomous University of Barcelona (UAB), the Luxembourg Institute of Health (LIH) and the National Institutes of Health (NIH) in Baltimore (United States).
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Materials provided by University of Barcelona. Note: Content may be edited for style and length.

Patients with nasopharyngeal cancer are often treated with drugs that activate their immune system against the tumor. Until now, it was feared that vaccination against Covid-19 could reduce the success of cancer treatment or cause severe side effects. A recent study by the Universities of Bonn and Shanxi in the People’s Republic of China now gives the all-clear in this regard. According to the study, the cancer drugs actually worked better after vaccination with the Chinese vaccine SinoVac than in unvaccinated patients.
The results are published as a “Letter to the editor” in the journal Annals of Oncology, but are already available online.
Many cancer cells are capable of subverting the body’s immune response. They do this by pushing a kind of button on the immune cells, the PD-1 receptor. In this way, they effectively shut down these endogenous defense forces. Drugs can be used to block PD-1 receptors. This enables the immune system to fight the tumor more effectively.
Vaccination against Covid also stimulates the immune response, involving the PD-1 receptor. “It was feared that the vaccine would not be compatible with anti-PD-1 therapy,” explains Dr. Jian Li of the Institute of Molecular Medicine and Experimental Immunology (IMMEI) at the University Hospital Bonn. “This risk is especially true for nasopharyngeal cancer, which, like the SARS Cov-2 virus, affects the upper respiratory tract.”
Together with cooperation partners from the People’s Republic of China, the bioinformatician has now investigated whether this concern is justified. More than 1,500 patients treated in 23 hospitals from all over China participated in the analysis. Such multi-center studies are considered to be particularly informative because the participants are very diverse and, moreover, the results are not distorted by regional characteristics.
Vaccinated patients responded better to cancer therapy
A subset of 373 affected individuals had been vaccinated with the Chinese Covid vaccine SinoVac. “Surprisingly, they responded significantly better to anti-PD-1 therapy than the unvaccinated patients,” explains Prof. Dr. Christian Kurts, Director of IMMEI and member of the Transdisciplinary Research Area “Life & Health” and the Cluster of Excellence ImmunoSensation. “Furthermore, they did not experience severe side effects more often.” The researchers cannot say why the treatment was more successful after vaccination. “We assume that vaccination activates certain immune cells, which then attack the tumor,” says Prof. Dr. Qi Mei of Shanxi University Hospital. “We will now investigate this hypothesis further.”
Nasopharyngeal cancer is quite rare in this country. In southern China and other countries in Southeast Asia, however, the disease is widespread. One of the suspected reasons for this is the frequent use of air conditioning in the hot and humid regions. Nutritional factors also appear to play an important role. In Taiwan, nasopharyngeal cancer is now considered one of the leading causes of death among young men.
Participating institutions and funding
In addition to the University of Bonn and the University Hospital, Shanxi Medical University and Tongji Medical College were involved in the work. The researchers also collaborated with a number of clinics throughout China. The study was funded by the Sino-German Center for Research Promotion (SGC), the DFG Cluster of Excellence ImmunoSensation², and the German Federal Ministry of Education and Research (BMBF).
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Materials provided by University of Bonn. Note: Content may be edited for style and length.