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Patients with mild Covid-19 infections experience a significantly increased longer lasting reduced sense of taste and smell. This is also the case for long-term shortness of breath, although relatively few people are affected. And women and the elderly are particularly affected. This is shown by new research findings from Aarhus University Aarhus University Hospital and Regional Hospital West Jutland.
The last 14 months have taught us that there are different symptoms and outcomes of Covid-19. However, the vast majority of people who fall ill with Covid-19 experience mild symptoms and get over the disease in two to three weeks.
These are precisely some of the people who have been the subject of a new study from AUH, HEV and AU. In the study, researchers have compared symptoms on a daily basis for up to 90 days in 210 healthcare workers who had tested positive and 630 with a negative test.
Each day, the participants received a link to a questionnaire on whether they had experienced one of the following symptoms within the last 24 hours: coughing, sore throat, headaches, fever, muscle pain, shortness of breath and reduced sense of taste and smell.
“We saw that the prevalence of a longer lasting reduced taste and smell is significantly increased in patients with mild Covid-19 disease who did not require hospitalisation. This pattern is also seen for shortness of breath, but far fewer people were affected,” says Henrik Kolstad, who is behind the study.
Women and the elderly experience more symptoms
Thirty per cent of those who had tested positive and almost none of the participants with a negative test reported a reduced sense of taste and smell over the full ninety days. At the beginning of the project, shortness of breath was reported by twenty per cent of those who had tested positive, with the figure falling to five per cent after thirty days, though without ever reaching the level of the participants who had tested negative.

Scientists explored a technique called ‘neurofeedback,’ which enables ADHD patients to train their attention, based on instant feedback from the level of their brain activity. The team of neuroscientists found that not only did the training have a positive effect on patients’ concentration abilities, but also that the attention improvement was closely linked to an enhanced response from the brain — the P3 wave — which is known to reflect integration of information in the brain.
Attention Deficit Hyperactivity Disorder (ADHD) affects about 7% of children, with a two out of three chance of persisting into adulthood. This neurodevelopmental disorder is characterised by concentration difficulties, increased distractibility, impulsivity and hyperactivity. Today, ADHD is treated with pharmaceutical drugs that may have unwanted side effects. This is why scientists from the University of Geneva (UNIGE) and the University Hospitals of Geneva (HUG), Switzerland, explored a new technique called ‘neurofeedback’, which enables ADHD patients to train their attention, based on instant feedback from the level of their brain activity. The team of neuroscientists found that not only did the training have a positive effect on patients’ concentration abilities, but also that the attention improvement was closely linked to an enhanced response from the brain- the P3 wave — which is known to reflect integration of information in the brain, with higher P3 amplitudes indicating greater attention towards detected targets. The findings are open-access and have been published in the journal Clinical Neurophysiology.
Attention Deficit Hyperactivity Disorder (ADHD) develops in childhood and leads to numerous difficulties with attention, concentration and impulsiveness. It has genetic associated with environmental causes, and is characterised by a deficit in dopamine, a neurotransmitter involved in executive functions. “These disorders persist for the most part into adulthood and lead to problems in relational and socio-professional functioning, making it easier for people with this disorder to turn to alcohol or drugs,” notes Marie-Pierre Deiber, a researcher in the Department of Psychiatry at UNIGE Faculty of Medicine and at the HUG Division of Psychiatric Specialties.
Today, ADHD is treated with medications that increase the concentration of dopamine, which improves the patient’s attention. As the disorder is often accompanied by depression, anxiety or even bipolar disorders, treatment is generally combined with psychotherapy. “However, pharmaceutical treatments can be accompanied by significant side effects, such as nervousness, sleep disturbance, but also an increased risk of developing other psychiatric disorders or cardiovascular diseases,” explains Roland Hasler, a researcher in the HUG Division of Psychiatric Specialties. “This is why we wanted to investigate a completely non-pharmacological and non-invasive treatment based on the principle of ‘neurofeedback’.”
Sending the brain its own signals
Neurofeedback is a type of neurocognitive intervention based on the training of “real-time” brain signals. Using an electroencephalogram (EEG) with 64 sensors, the scientists capture the electrical activity of cortical neurons and focus their analysis on the spontaneous Alpha rhythm (with frequency around 10 Hertz), coupling its amplitude fluctuation to a video game that the patients can control with the power of their attention. “The aim of neurofeedback is to make the patients aware of the moments when they are no longer attentive. With practice, brain networks then “learn” to reduce attentional lapses through neuroplasticity,” explains Tomas Ros, researcher in the Department of Basic Neurosciences at UNIGE Faculty of Medicine and at the Centre for Biomedical Imaging (CIBM). To do this, the patient’s EEG is connected to a computer that displays the image of a space shuttle. When the patient is in an attentive brain state (low Alpha rhythm), this makes the space shuttle move forward. But as soon as the patient is distracted or loses attention (high Alpha rhythm), this stops the space-shuttle movement instantly. Faced with the stopping of the space shuttle, the patient realizes that he/she was no longer paying attention and refocuses to restart the shuttle.
Training the brain to focus without medication?
To measure the effects of neurofeedback training, the Geneva team administered an attention test to 25 adults with ADHD, and 22 neurotypical adults. The results showed that, at baseline, ADHD patients made more mistakes and had a more variable reaction time than the control participants, in line with a signature of impaired attention. After 30 minutes of neurofeedback training, the participants took the attention test again.
“The first finding was that stimulus detection and response variability were improved, indicating attentional enhancement,” says Marie-Pierre Deiber. “But what interested us most was the impact of the neurofeedback training on the P3 component, which has previously been shown to be reduced in ADHD, and directly linked to the neurocognitive processing of the stimulus.” The higher the amplitude of the P3, the more efficient the processing of the stimulus is, and the more accurate the response to the attention task. “The amplitude of the P3 increased significantly after neurofeedback training, and was directly associated with a reduction in the number of errors made by the patients,” reports Tomas Ros.
This study firstly shows that a single 30-minute session of neurofeedback can induce short-term plasticity in the brain and encourages attentional improvements in ADHD patients. Secondly, it supports the existence of an electro-physiological marker of attentional processing in ADHD. “Thus, the P3 could be a cerebral signature that would allow us to better understand the neurocognitive mechanisms of ADHD,” continues Nader Perroud, professor in the Department of Psychiatry at UNIGE Faculty of Medicine and at the HUG Division of Psychiatric Specialties. Finally, as the effects are evident in the short term, the scientists plan to carry out a neurofeedback treatment based on multiple training sessions, in order to observe whether the brain’s plasticity is strengthened over time. “The ultimate goal is to enable patients to learn to concentrate without medication and to be able to train their brain in the comfort of their home,” concludes Tomas Ros.

A stimulating environment keeps the “hippocampus” — which is the brain’s memory control center — young, so to speak. Causes of this are molecular mechanisms that affect gene regulation. These current findings from studies in mice provide clues as to why an active, varied life can help preserve mental fitness in old age. Researchers from the DZNE and the Center for Regenerative Therapies Dresden (CRTD) at the Technische Universität Dresden report on this in the journal Nature Communications.
Human DNA — and this also applies to mice — contains thousands of genes. However, it is not only the genetic blueprint that is decisive for the function of a cell and whether it is healthy or not, but above all which genes can be switched on or off. Aging, living conditions and behavior are known to influence this ability to activate genes. The phenomenon, referred to as “epigenetics,” was the focus of the current study. For this, researchers including Dr. Sara Zocher and Prof. Gerd Kempermann examined mice that had grown up in different environments: One group of animals experienced, from a young age, an “enriched” environment with toys and tunnel tubes. The rodents of a second group did not have such occupational opportunities.
Attachments to the DNA
When the scientists examined the genome, they found that in those mice that grew up in the stimulating environment, there was, with age, only a relatively small change in certain chemical tags of the DNA. In mice from the low-stimulus environment, these changes were much more pronounced — in comparison between young and older animals. “We registered so-called methyl groups, which stick to the DNA,” explains Gerd Kempermann, speaker for the DZNE’s Dresden site, DZNE research group leader and also a scientist at the CRTD. “These chemical attachments do not alter the genetic information per se. Rather, they influence whether individual genes can be activated or not.”
Malleable Brains
Such “epigenetic markings” tend to diminish with age, but in the animals with stimulating living conditions, the decrease in methyl groups was comparatively small. Thus, in old mice raised in a varied environment, gene activity had, in a sense, remained young. In particular, this affected a series of genes relevant to growing new neurons and cellular connections in the hippocampus. “Epigenetically, these animals retained a younger hippocampus,” Kempermann says. Therefore, the brains of these mice were more malleable — experts speak of greater “neuroplasticity” — than in conspecifics of the same age that had grown up in a low-stimulus environment.
The current study did not include behavioral experiments. However, Kempermann points out that many other studies have shown that mice raised in high-stimulus settings perform better on memory tests than those from low-stimulus environments. “It is fair to assume that this mental fitness is due to the stabilization of methylation patterns that we observed,” the neuroscientist says. “Of course, the question is to what extent our findings also apply to humans. Here, the situation is likely to be more complicated. After all, it is about how living conditions influence behavior and the way humans react to external stimuli is much more complex than in mice. However, we have good reasons to believe that the basic epigenetic principles are the same in humans as in mice.”
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Mice are an important animal model of human vision due to the powerful genetic tools available in this species. However, mouse vision was thought to be different to that of humans because humans have a region of the retina specialized for fine details called the ‘fovea’ whereas mice do not. Researchers from the Netherlands Institute of Neuroscience (NIN) have shown that the visual cortex of mice does contain a region of enhanced visual sensitivity dubbed the ‘focea’, making the mouse a better model of human vision than previously expected. The findings were published in Nature Communications on the 29th June.
A specialization for high resolution vision
The fovea is a region in the human retina in which the light-sensitive cells are more closely packed together yielding higher resolution vision. It is used for reading and recognizing faces. Humans move their eyes three times per second to point the fovea at interesting parts of the world. Mice do not have this specialization and it was thought that they have no reason to move their eyes to ‘scan the world’ in more detail.
While studying how the retina of the mouse was mapped in cortical regions of the brain, the researchers found that the map of visual space in the cortex has a better visual resolution at a location that represents a region directly in front of and slightly above the mouse in space. They named this cortical location the ‘focea’ as it is reminiscent of the fovea of humans.
A better organized map of space.
To determine the source of the better resolution the researchers measured the responses from individual brain cells using electrodes. The cells at the focea did not appear to the differ from other cells. “Initially we were puzzled” explains Matthew Self, lead researcher on the project, “we were seeing a very clear focea in the map, but nothing when we measured the data from single-neurons. We realized that the focea could originate from regions of the cortex where the maps are better organized across cells.”
To study this, the researchers measured maps of space across thousands of cells using a two-photon microscope. The results confirmed their hypothesis; maps of space in the focea were well-organized with neighboring cells responding to neighboring parts of space. In contrast, the maps outside the focea were more scattered. The results suggested that mice might have better vision in the focea than elsewhere.
The focea in natural behaviors
The fact that mice have a focea could mean that they also move their eyes to point their focea at interesting parts of world, analogous to the human fovea. The findings have important consequences for the use of mice as a model of human vision. Dr Self stated: “The fact that mice have a focea opens up the possibility of understanding the neural circuits underlying high-detail vision and studying the neural basis of attention and eye-movements in this species.”
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Researchers at the UAB and the UniZar have identified a human peptide found in the brain that blocks the α-synuclein aggregates involved in Parkinson’s disease and prevents their neurotoxicity. The study, published in Nature Communications, suggests that this could be one of the organism’s natural mechanisms with which to fight aggregation. The discovery may help to develop new therapeutic and diagnosis strategies for Parkinson’s disease and other synuclein pathologies.
The death of neurons specialised in the synthesis of dopamine, one of the brain’s main neurotransmissors, deteriorates the motor and cognitive capacities of those with Parkinson’s disease. The loss of these neurons is related to alpha-synuclein aggregation. Recent studies show that oligomers, the initial aggregates of this protein, are the most pathogenic forms of α-synuclein and are responsible for the spreading of the disease in the brain.
Therefore, one of the more promising approaches in fighting this disorder consists in neutralising these oligomers and, thus, slow down the pathological progression. However, the fact that these aggregates do not present a defined structure and that they are transitory by nature makes it extremely difficult to identify molecules that bind with enough strength as to explore any clinical application.
A scientific collaboration between researchers from the Institute for Biotechnology and Biomedicine (IBB) at the Universitat Autònoma de Barcelona (UAB) and from the Instituto de Biocomputación y Física de Sistemas Complejos (BIFI) of the Universidad de Zaragoza (UniZar) now has been able to identify a human endogenous peptide which strongly and specifically attaches to the α-synuclein oligomers, thus avoiding their aggregation and blocking their neurotoxicity, two processes closely related to the neurodegenerative decline of Parkinson’s disease. The identification and study of the peptide, called LL-37, was recently published in Nature Communications.
“LL-37 interacts with the toxic alpha-synuclein oligomers in a selective manner and with a strength superior to that of any peptide previously described, equivalent to the strength exhibited by antibodies. It inhibits aggregation at very low concentrations and protects neuronal cells from being damaged,” researchers point out.
They add that, “LL-37 is found naturally in the human organism, both in the brain and in the intestine, organs in which α-synuclein aggregation takes place in Parkinson’s disease. This suggests that LL-37’s activity might respond to a mechanism developed by the body itself as a means to naturally fight this disease.”
Encouraged by this idea, researchers now want to study how its expression can be regulated and if this strategy can become a safe therapy with the potential of influencing the course of the disease. “There is a possibility that a therapy for Parkinson’s disease already lies in our interior and that it only needs to be activated correctly,” states Salvador Ventura, researcher at the IBB and coordinator of the study.
The identification of LL-37 was conducted under the framework of a research analysing the structure and characteristics of pathogenic oligomers with the aim of neutralising them in a specific manner. The analyses conducted demonstrate that helical peptides with a hydrophobic side and another positively charged side are ideal for this type of activity. The trials allowed researchers to identify three molecules with anti-aggregation activity: in addition to the human molecule, a second peptide present in bacteria and a third artificially made molecule were identified.
In addition to representing a possible therapeutic route for Parkinson’s disease and other synuclein pathologies, the molecules identified in the study are promising tools for its diagnosis, given that they discriminate between functional and toxic α-synuclein species.
“Until now there were no molecules capable of selectively and efficiently identifying toxic α-synuclein aggregates; the peptides we present on these issues are unique and, therefore, have great potential as diagnostic and prognostic tools,” says study co-coordinator Nunilo Cremades, researcher at BIFI-UniZar.
In the study, over 25,000 human peptides were computationally analysed, and single molecule spectroscopy methods, as well as protein engineering, were applied, in addition to cell cultures in vitro using toxic oligomers.
Participating in the study were researchers from the IBB-UAB and the Department of Biochemistry and Molecular Biology at the UAB Jaime Santos (first author of the article), Irantzu Pallarès and Salvador Ventura (co-coordinators of the study), members of the “Protein Folding and Conformational Diseases” group; and BIFI-UniZar researchers Pablo Gracia (second author of the article) and Nunilo Cremades (co-coordinator of the study, predoctoral researcher and lead researcher, respectively, of the “Amyloid Protein Misfolding and Aggregation” NEUROMOL group from the BIFI-Unizar.

Tel Aviv University’s groundbreaking technology may revolutionize the treatment of cancer and a wide range of diseases and medical conditions. In the framework of this study, the researchers were able to create a new method of transporting RNA-based drugs to a subpopulation of immune cells involved in the inflammation process, and target the disease-inflamed cell without causing damage to other cells.
The study was led by Prof. Dan Peer, a global pioneer in the development of RNA-based therapeutic delivery. He is Tel Aviv University’s Vice President for Research and Development, head of the Center for Translational Medicine and a member of both the Shmunis School of Biomedicine and Cancer Research, George S. Wise Faculty of Life Sciences, and the Center for Nanoscience and Nanotechnology. The study was published in Nature Nanotechnology.
Prof. Peer: “Our development actually changes the world of therapeutic antibodies. Today we flood the body with antibodies that, although selective, damage all the cells that express a specific receptor, regardless of their current form. We have now taken out of the equation healthy cells that can help us, that is, uninflamed cells, and via a simple injection into the bloodstream can silence, express or edit a particular gene exclusively in the cells that are inflamed at that given moment.”
As part of the study, Prof. Peer and his team were able to demonstrate this groundbreaking development in animal models of inflammatory bowel diseases such as Crohn’s disease and colitis, and improve all inflammatory symptoms, without performing any manipulation on about 85% of the immune system cells. Behind the innovative development stands a simple concept, targeting to a specific receptor conformation.
“On every cell envelope in the body, that is, on the cell membrane, there are receptors that select which substances enter the cell,” explains Prof. Peer. “If we want to inject a drug, we have to adapt it to the specific receptors on the target cells, otherwise it will circulate in the bloodstream and do nothing. But some of these receptors are dynamic — they change shape on the membrane according to external or internal signals. We are the first in the world to succeed in creating a drug delivery system that knows how to bind to receptors only in a certain situation, and to skip over the other identical cells, that is, to deliver the drug exclusively to cells that are currently relevant to the disease.”
Previously, Prof. Peer and his team developed delivery systems based on fatty nanoparticles — the most advanced system of its kind; this system has already received clinical approval for the delivery of RNA-based drugs to cells. Now, they are trying to make the delivery system even more selective.
According to Prof. Peer, the new breakthrough has possible implications for a wide range of diseases and medical conditions. “Our development has implications for many types of blood cancers and various types of solid cancers, different inflammatory diseases, and viral diseases such as the coronavirus. We now know how to wrap RNA in fat-based particles so that it binds to specific receptors on target cells,” he says. “But the target cells are constantly changing. They switch from ‘binding’ to ‘non-binding’ mode in accordance with the circumstances. If we get a cut, for example, not all of our immune system cells go into a ‘binding’ state, because we do not need them all in order to treat a small incision. That is why we have developed a unified protein that knows how to bind only to the active state of the receptors of the immune system cells. We tested the protein we developed in animal models of inflammatory bowel disease, both acute and chronic.”
Prof. Peer adds, “We were able to organize the delivery system in such a way that we target to only 14.9% of the cells that were involved in the inflammatory condition of the disease, without adversely affecting the other, non-involved, cells, which are actually completely healthy cells. Through specific binding to the cell sub-population, while delivering the RNA payload we were able to improve all indices of inflammation, from the animal’s weight to pro-inflammatory cytokines. We compared our results with those of antibodies that are currently on the market for Crohn’s and colitis patients, and found that our results were the same or better, without causing most of the side effects that accompany the introduction of antibodies into the entire cell population. In other words, we were able to deliver the drug ‘door-to-door,’ directly to the diseased cells.”
The study was led by Prof. Peer, together with Dr. Niels Dammes, a postdoctoral fellow from the Netherlands, with the collaboration of Dr. Srinivas Ramishetti, Dr. Meir Goldsmith and Dr. Nuphar Veiga, from Prof. Dan Peer’s lab. Professors Jason Darling and Alan Packard of Harvard University in the United States also participated. The study was funded by the European Union, in the framework of the European Research Council (ERC).
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Immunologists at McMaster University have discovered a previously unknown mechanism which acts like a spider web, trapping and killing pathogens such as influenza or SARS-CoV-2, the virus responsible for COVID-19.
The researchers have found that neutrophils, the most abundant white blood cells in the human body, explode when they bind to such pathogens coated in antibodies and release DNA outside of the cell, creating a sticky tangle which acts as a trap.
The findings, published online in the Proceedings of the National Academy of Science, are significant because little is understood about how antibodies neutralize viruses in the respiratory tract.
The discovery has implications for vaccine design and delivery, including aerosol and nasal spray technologies that could help the body head off infections before they have a chance to take hold.
“Vaccines can produce these antibodies that are present in our lungs, which are the first type of antibody to see viruses like flu or COVID-19, which infect our lungs and respiratory tracts,” says the study’s lead author Matthew Miller, an associate professor at McMaster’s Michael G. DeGroote Institute for Infectious Disease Research and Canada’s Global Nexus for Pandemics and Biological Threats. “Mechanisms that can stop the infection at the site where it enters our body can prevent the spread and serious complications.”
By comparison, injectable vaccines are designed to bolster antibodies in the blood, but those antibodies are not as prevalent at the sites where infection begins.
“We should be thinking carefully about next generation COVID-19 vaccines that could be administered in the respiratory tract to stimulate antibodies. We don’t have many candidates right now that are focused on raising the mucosal response,” says Hannah Stacey, a graduate student in the Miller Lab and lead author of the paper, who recently won a major national scholarship from the Canadian Society for Virology for her work on COVID-19.
“If you want a lot of these antibodies that are really abundant in blood, then injections make the most sense, but if you want antibodies that are abundant in the respiratory tract, then a spray or an aerosol makes sense,” she says.
Researchers caution that while the body’s spider-web mechanism has the potential to be hugely beneficial, it can cause harm too, including inflammation and further illness when the web formation is uncontrollable.
They point to the early waves of the pandemic, prior to vaccinations, when these NETs, or neutrophil extracellular traps, were found in some patients’ lungs, and had made their breathing more difficult.
“An immune response that is meant to protect you can end up harming you if it’s not properly controlled,” says Miller. “It’s important to understand the balance of the immune system. If you have a lot of these antibodies before you get infected, they are likely going to protect you, but if the infection itself stimulates a lot of those antibodies it might be harmful.”
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Materials provided by McMaster University. Original written by Michelle Donovan. Note: Content may be edited for style and length.

COVID-19’s socio-economic effects will likely cause another severe production crisis in the coffee industry, according to a Rutgers University-led study.
The study, which appears in the journal Proceedings of the National Academy of Sciences, included researchers from the University of Arizona, University of Hawaii at Hilo, CIRAD, Santa Clara University, Purdue University West Lafayette and University of Exeter.
“Any major impacts in the global coffee industry will have serious implications for millions of people across the globe, including the coffee retail market here in the United States,” said lead author Kevon Rhiney, an assistant professor in the Department of Geography at Rutgers-New Brunswick.
Coffee is one of the most widely traded agricultural commodities in the world, supporting the livelihoods of about 100 million people globally, especially in low income countries. But the industry has long struggled with many stresses, including institutional reforms, market price volatilities, extreme climate and plant diseases and pests. And over the past year, COVID-19 has become a new threat to the coffee industry by acting as potential trigger for renewed epidemics of coffee leaf rust, the most severe coffee plant disease in the world.
The researchers drew on recent studies of the fungal disease, which has severely impacted several countries across Latin America and the Caribbean over the last decade. They looked at how past outbreaks have been linked to poor crops and investment in coffee farms, and how COVID-19’s impacts on labor, unemployment, stay-at-home orders and international border policies could affect investments in coffee plants and in turn create conditions favorable for future shocks.
The researchers concluded that COVID-19’s socio-economic disruptions are likely to drive the coffee industry into another severe production crisis.
“Our paper shows that coffee leaf rust outbreaks are complex socio-economic phenomena, and that managing the disease also involves a blend of scientific and social solutions,” Rhiney said. “There is no ‘magic bullet’ that will simply make this problem disappear. Addressing coffee leaf rust involves more than just getting outbreaks under control; it also involves safeguarding farmers’ livelihoods in order to build resilience to future shocks.”
The researchers said the challenges from coffee leaf rust reflect a trend in disease-driven collapses in recent years in major global commodity markets such as banana and cocoa, where large-scale farming of single crops and homogenization of plant traits make it easy for diseases to emerge and spread.
They conclude that the COVID-19 pandemic highlights the interconnectedness of the global coffee system as both a vulnerability and a source of strength.
“The spread of COVID-19 and coffee leaf rust both reveal the systemic weaknesses and inequalities of our social and economic systems,” Rhiney said. According to the team, “We can thus only have a healthy coffee system by building up the well-being of the most vulnerable. It is critical to recognize the key roles of labor and healthy functioning ecosystems in producing and sustaining profits. This means challenging the status quo and the current coffee value chains to better recognize the value produced by small-scale producers, while at the same time uplifting essential but under-recognized parts of the production process, such as human health, food security and sustainability.”
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A conclusive narrative review has found physical punishment of children is not effective in preventing child behavior problems or promoting positive outcomes and instead predicts increases in behavior problems and other poor outcomes over time. The study by an international group of scientists including a researcher from The University of Texas at Austin was published today in The Lancet.
Caregivers in many parts of the world use physical punishment as a response to children’s perceived misbehavior: 63% of children between the ages of 2 and 4 worldwide — approximately 250 million children — are regularly subjected to physical punishment by caregivers.
Sixty-two countries have banned the practice, which is increasingly seen as a form of violence.
The team looked at studies involving physical punishment such as spanking and excluded any behaviors that could constitute child physical abuse. The researchers found ample evidence to support a United Nations statement from the Committee on the Rights of the Child that recommended countries end the use of all types of physical punishment on children.
“There is no evidence that physical punishment is good for children,” said Elizabeth Gershoff, the Amy Johnson McLaughlin Centennial Professor in Human Development and Family Sciences at The University of Texas at Austin and senior author of the paper. “All the evidence indicates that physical punishment is harmful to children’s development and well-being.”
The review looked at 69 studies, most of which were from the United States, with eight from other countries. Scientists found that physical punishment was not associated with any positive outcomes for children and increased the risk that children would experience severe violence or neglect. The paper points out that negative outcomes associated with physical punishment, such as behavior problems, occurred no matter the child’s sex, race, or ethnicity and regardless of the overall parenting styles of the caregivers. The authors also found evidence that the magnitude of negative outcomes for children increased the more frequently physical punishment was used.
“Parents hit their children because they think doing so will improve their behavior,” Gershoff said. “Unfortunately for parents who hit, our research found clear and compelling evidence that physical punishment does not improve children’s behavior and instead makes it worse.”
In the U.S., it is legal in all 50 states for parents to use physical punishment. It is also legal in 19 states for schools to use physical punishment against children. The paper was intended as a resource for policymakers and people who work with families, such as medical and mental health providers.
“This is a public health issue,” said Anja Heilmann, lead author of the paper who is an associate professor at University College London. “Given the strength of the evidence that physical punishment has the potential to cause harm to children, policymakers have a responsibility to protect children and legislate to end the use of physical punishment in all settings.”
Gershoff previously authored a landmark 2016 meta-analysis of dozens of studies and found that physical punishment was not associated with any positive outcomes for children and was heavily associated with a variety of negative outcomes. Gershoff’s work was cited by former Secretary of Education John B. King Jr. in a 2016 federal letter urging states to consider ending the use of physical punishment in schools. Gershoff also helped to inform policy statements from the American Academy of Pediatrics and the American Psychological Association that use research on the harmful effects of physical punishment as a basis for recommending that caregivers no longer use it.
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A microfilter device that can easily separate and capture trace amounts of cancer cells in blood has been developed by a Kumamoto University research group. The palm-sized device is expected to contribute to the development of new cancer diagnostic technologies based on cancer cells in the blood, such as early detection by blood test, postoperative management, and recurrence monitoring.
The blood of people with cancer contains trace amounts of cancer cells (CTCs) that have detached from the primary cancer site. However, the amount of these cells is only a few per milliliter, whereas red or white blood cells number in the billions, making it very difficult to separate and detect them. Although devices for detecting CTCs have been developed in the past, they require expensive equipment and reagents, which has been a bottleneck for their practical application.
The unique microfilter device developed by the Kumamoto University research group can easily and inexpensively separate and capture CTCs without any large equipment. The device is dynamically and three-dimensionally deformed by the fluid force when blood is pumped through it. It also utilizes nucleic acid aptamers, which bind specifically and firmly to target molecules. This enables both size-selective and affinity-selective separation and capture of tiny cancer cells.
While evaluating the device, researchers demonstrated that it could capture cancer cells even at a concentration of just five cancer cells in one mL of healthy blood. Since there are about five billion (red and white) blood cells in a mL of blood, the device proved to have a very high detection capability. Researchers also found that almost no blood cells were adsorbed by the microfilter, achieving a blood cell removal rate of more than 98%. It also had a high selective detection capability. Furthermore, in a comparative evaluation, they proved that the device was able to detect cancer cells with higher accuracy than existing devices.
“This work demonstrates that our micro-filter device can accurately detect trace amounts of cancer cells in blood,” said Associate Professor Yuta Nakashima, who led the study. “We expect it will be adopted for cancer diagnosis and treatment, including for early diagnosis of cancers that cannot be detected by imaging like CT and PET scans, postoperative follow-up, recurrence monitoring, and tailor-made treatments. In the future, we plan to use blood samples donated by cancer patients to verify the practical and clinical application of the method.”
This research was posted online in Talanta on 1 June 2021.
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