Publisher Health

Post-traumatic stress disorder (PTSD) is a difficult-to-cure mental health condition that is caused by experiencing a traumatizing event, such as interpersonal violence or disaster. While sufferers of PTSD have existed across all of human history and the condition is even observed in animals, the diagnosis of this condition only appeared in the 1970s after the Vietnam War. PTSD patients are widely known to suffer from various symptoms from recurring flashbacks, anxiety, and negative alteration in cognition.
Currently, various treatment options, such as antidepressants or cognitive behavioral therapy, are used to treat PTSD. Selective serotonin reuptake inhibitors (SSRIs) are the only class of antidepressants that are approved for the treatment of PTSD. However, the medications have drawbacks of delayed action and are not effective in some patients.
Cognitive-behavioral therapies, such as eye movement desensitization and reprocessing (EMDR), are also frequently used to treat PTSD. However, such fear extinction therapies are not effective in half of the patients. Moreover, even when the therapy is successful, PTSD is notorious for the recurrence of symptoms. Such relapse of previously treated PTSD is called “spontaneous recovery,” which is a subject of many studies.
In the past, studies have pointed out that activities in glutamatergic neurons are an important part of the pathophysiology of PTSD. Particular interest is in the effects of the N-methyl-D-aspartate receptor (NMDAR) on these neurons, which is responsible for controlling synaptic plasticity related to learning and memory.
To tackle PTSD by its roots, the researchers from the Center for Cognition and Sociality within the Institute for Basic Science (IBS) in conjunction with Yale University explored the molecular mechanism of PTSD treatment. In their latest research, published in Molecular Psychiatry, the IBS team tested a PTSD trial drug called NYX-783 in mice and examined the molecular mechanism of its actions. NYX-783 is a newly discovered drug that is known to modulate the NMDAR functions in neurons.
There are two established rodent models of PTSD: auditory fear conditioning (AFC) and single-prolonged stress (SPS) models. For auditory fear conditioning, the mice were habituated to an environment and subjected to a combination of a tone and electric shock for fear conditioning to induce PTSD. To induce single prolonged stress, some of the mice were exposed to multiple stressors to induce single prolonged stress before the fear conditioning. It should be noted that stressful experience before fear conditioning is well known to cause further difficulties in PTSD treatment later on.

T cells are immune cells that help our bodies fight disease by seeking and destroying unhealthy cells.
Regulatory T cells, or Treg cells, put the brakes on T cells, preventing them from misbehaving and attacking the body’s healthy tissues.
Researchers have now discovered a way to release the “handbrake” hold that Treg cells have over normal T cells and intentionally put them into overdrive.
Lifting this restraint could supercharge the response of T cells and lead to better treatment options for cancers and infections, where patients would benefit from rapid clearance of the unhealthy cells.
The research, led by Dr Charis Teh, Simon Preston, Associate Professor Daniel Gray and Professor Marc Pellegrini, is published in Science Immunology.
At a glance Researchers have found a way to supercharge T cell responses, which could be used to clear some infections and cancers faster. By taking the regulatory “handbrake” off, the T cells were able to go into overdrive and boost the immune response. The findings offer a better understanding of how T cells can be manipulated to fight diseases like cancer and infections, while avoiding the risk of autoimmune conditions like diabetes and multiple sclerosis.Boosted response

A new study has demonstrated that maternal exercise during pregnancy improves the metabolic health of offspring, even when the mother is obese or on a high-fat diet. Physical exercise by the mother induces the placenta to secrete the key protein SOD3, resulting in a lowered risk of diabetes for the offspring. The findings in the paper identified the mechanisms behind this process.
The results were published in the Journal Diabetes on March 15, 2022.
A worrying trend
Maternal obesity and type 2 diabetes are on the rise. Over 30% of women of childbearing age in Western and Asian countries are classified as obese. Meanwhile, 630 million people are expected to be living with type 2 diabetes by 2045. Children born to obese mothers or mothers with type 2 diabetes have an increased risk of diabetes, even after going on to live healthy lives.
“With the growth of maternal obesity, a worrying cycle is forming where the risks of diabetes gets passed down from generation to generation,” says assistant professor Joji Kusuyama from Tohoku University’s Interdisciplinary Institute for Frontier Sciences (FRIS), and lead author of the study. “Stopping this cycle is a critical and pressing medical problem.”
In the research group with Kusuyama was Laurie Goodyear, Nathan Makarewicz, Brent Albertson, Ana Alves-Wagner, Royce Conlin, Noah Prince, Christiano Alves, Krithika Ramachandran, and Michael Hirshman from the Joslin Diabetes Center; Chisayo Kozuka from RIKEN’s Center for Integrative Medical Sciences; Toshihisa Hatta from Kanazawa’s Medical University; Yang Xiudong and Yang Xia from the University of Texas at Houston; and Ryoichi Nagatomi from Tohoku University’s Graduate School of Biomedical Engineering.

Measuring the viral load of people infected with SARS-CoV-2 is one of the main factors in evaluating the infectiousness of COVID-19 patients. Viral load can be influenced by the infecting SARS-CoV-2 variant as well as the vaccination status of the patient.
A research team from the University of Geneva (UNIGE) and the University Hospitals of Geneva (HUG) measured the infectious viral load of nearly 600 symptomatic patients to detect possible differences between the original virus, Delta and Omicron sublineage BA.1, as well as according to vaccination status. They discovered that Delta causes a higher viral load than the original virus and the Omicron variant. For Delta and Omicron breakthrough infections, vaccination drastically reduces the viral load. In the case of Omicron, however, the decrease was only observed after three doses of vaccine. Furthermore, Omicron’s very high infectiousness is seemingly related to factors other than viral load alone. These results, to be read in the journal Nature Medicine, highlight the benefit of vaccination for public health in addition to individual protection against the severe form of the disease, and remind us that variants of the virus must be closely monitored to prevent further massive outbreaks.
The diagnosis of COVID-19 consists of a PCR test performed on a nasopharyngeal or salivary swab. “This test is very effective in identifying infected people, but does not indicate whether they are infectious, that is, capable of transmitting the virus to other people,” says Isabella Eckerle, professor in the Department of Medicine at UNIGE Faculty of Medicine and head of the HUG-UNIGE Centre for Emerging Viral Diseases, who led this work. “However, the notion of contagiousness is essential for deciding on collective prevention measures, such as periods of isolation.”
PCR tests can only detect the presence of viral RNA, but do not indicate whether the virus is still intact and able to spread. The measurement of the infectious viral load necessarily involves culturing the virus for several days in a biosafety level 3 laboratory, a procedure impossible to perform routinely.
Lower viral load due to vaccination
Since the beginning of the pandemic, samples taken at the HUG screening centre have been kept for research purposes, with the authorisation of the persons concerned. “We were able to reanalyze samples from previous waves of the disease,” explains Benjamin Meyer, a researcher at the Centre for Vaccinology in the Department of Pathology and Immunology at UNIGE Faculty of Medicine. “We measured the infectious viral load of 3 cohorts of patients during the first 5 symptomatic days to compare the viral load caused by the original virus (118 samples, spring 2020), the Delta variant (293 samples, fall 2021) and the Omicron variant sublineage BA.1 (154 samples, winter 2022), as well as, for the last two cohorts, whether a significant difference could be detected in vaccinated and unvaccinated individuals.”
Overall, the infectious viral load for the Delta cohort was significantly higher than that of the cohort with the original virus. However, people infected by Delta who received two doses of mRNA vaccine had a significantly lower infectious viral load than unvaccinated people. “For the Omicron cohort, contrary to what can be assumed given its rapid spread, the infectious viral load was overall lower than that of the Delta cohort,” says Isabella Eckerle. In contrast, only people who were boosted (that is, having received three doses of the vaccine) had their viral load decreased; people who received two doses only had no benefit in this regard compared to unvaccinated people. “This is immunologically consistent: many vaccines require 3 doses spaced several months apart to induce a sustained immune response, such as that against Hepatitis B virus,” explains Isabella Eckerle.
Omicron: a variant far away from the previous ones
Why is the Omicron variant so contagious, if the viral load it induces is lower than its predecessors? “We still don’t know, but our data suggest that other infectious mechanisms are at play,” explains Pauline Vetter, clinic director at the HUG-UNIGE Center for Emerging Diseases. “It is now clear that the mutations of Omicron strongly differentiate it from other variants, allowing it to partially escape the vaccine, and diminish the effectiveness of some antiviral treatments used so far.” However, vaccination has been shown to be useful in limiting the occurrence of severe symptoms and most likely also the transmission of the virus. Indeed, in countries where the population, especially the elderly, is poorly vaccinated, Omicron has proven to be just as deadly.
The Geneva study also shows that the knowledge acquired for previous variants must be updated every time a new variant emerges to be able to adapt the means of combating COVID-19. “In view of our results, the greatest caution should be exercised in the face of a virus whose evolution is not fully understood, and against which currently existing treatments lose some of their effectiveness,” conclude the authors.
This work was carried out thanks to grants from the Swiss National Science Foundation (SNSF), the Pictet Group’s Fondation Ancrage bienfaisance and the HUG Private Foundation.

Why do human mothers have a much harder time giving birth compared to our evolutionary cousins, the chimpanzees and macaques?
The differences are a big head and wide shoulders. But it has made all the difference for safer births.
“The question is actually two-fold, ” says study author Naoki Morimoto of Kyoto University. “What also makes childbirth difficult for women is the relatively narrow pelvis.”
Morimoto’s team discovered two central aspects of the female human skeletal anatomy that deserve attention when discussing the evolution of childbirth.
The first comes with its own set of points: initially, the growth of human shoulders slows down just before birth and speeds up thereafter; next, this phenomenon alleviates the problem of shoulder dystocia, where the shoulders interfere with safe passage of the fetus through the birth canal.
“It is important to note that the second point reconciles the incompatibility of wide shoulders with the narrow birth canal. The shoulders show an ‘intelligent’ modification in fetal development,” notes lead author PhD candidate Mikaze Kawada.
What makes a human skeletal makeup ‘human’ in terms of the head and shoulders is size proportionality to the pelvis. Our largely developed brains have resulted in large heads, and our wide shoulders explain bipedal stability and an ability to throw objects far.
On the other hand, the need to make walking more efficient reduced the size of the pelvis as our ancestors treaded farther and more frequently.
Morimoto and his team used computed tomography to obtain cross-sectional representations of the clavicle in humans, chimpanzees, and Japanese macaques from fetal to adult samples.
The team then looked at different shoulder-width to birth-risk correlations between humans and the two other primates. Chimpanzees have proportionally large shoulders and yet, like macaques, fewer shoulder-related birth complications. Since chimpanzees move about less frequently on two feet, their pelvis — and therefore their birth canal — is larger than that of their human counterparts.
“We surmise that the wide shoulders, relative to the pelvis of our ancestors, emerged simultaneously with the narrower pelvis as we became fully bipedal,” says Morimoto, “but before the brain evolved to today’s size.”
Morimoto concludes, “This study motivates us to further examine the extent to which obstetric and metabolic constraints in our ancestors have influenced human ontogeny in relation to evolutionary adaptations.”
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A decision-support framework developed by management science researchers from The University of Texas at Dallas could help clinicians objectively identify and estimate harms and benefits of opioid use for pain management.
In a study published online Feb. 3 in the INFORMS journal Decision Analysis, Naveen Jindal School of Management researchers explored how clinicians make decisions when prescribing opioids and developed a quantitative model of the process that incorporates multiple factors.
“The ongoing opioid epidemic has been a serious public health problem, and prescription opioids play a role in this problem,” said Dr. Metin Cakanyildirim, professor of operations management and one of the study’s authors. “Opioid drugs are initially prescribed to treat pain, but their use can potentially lead to adverse effects of drug tolerance, increased sensitivity to pain, dependence, addiction and overdose.”
According to the Centers for Disease Control and Prevention (CDC), more than 14,000 people died in 2019 from overdoses involving prescription opioids.
Cakanyildirim and first author Abdullah Gokcinar, a doctoral student in operations management, were motivated by the opportunity to use management science tools to manage a nonmonetary process — pain — occurring outside business contexts.
To provide an analytical framework for evidence-based opioid prescribing, they collaborated with pain researchers Dr. Ted Price BS’97, Ashbel Smith Professor of neuroscience in the School of Behavioral and Brain Sciences and director of the Center for Advanced Pain Studies, and Dr. Meredith Adams, assistant professor of anesthesiology at Wake Forest School of Medicine.

It is estimated that about one in four adults worldwide has a liver condition that is a risk factor for heart disease, according to a new American Heart Association scientific statement published today in the Association’s peer-reviewed journal Arteriosclerosis, Thrombosis, and Vascular Biology. The condition, called nonalcoholic fatty liver disease (NAFLD), occurs when abnormally elevated amounts of fat are deposited in the liver, sometimes resulting in inflammation and scarring. The prevalence of NAFLD is an estimate, given the challenges in diagnosing the condition, which are detailed in the statement.
An American Heart Association scientific statement is an expert analysis of current research and may inform future guidelines. Professional organizations specializing in gastroenterology have previously published statements on the condition, however, they focus on liver toxicity (including scarring, cirrhosis and liver cancer) rather than heart disease risk. This is the Association’s first statement about NAFLD.
“Nonalcoholic fatty liver disease (NAFLD) is a common condition that is often hidden or missed in routine medical care. It is important to know about the condition and treat it early because it is a risk factor for chronic liver damage and cardiovascular disease,” said P. Barton Duell, M.D., FAHA, chair of the statement writing committee and professor of medicine in the Knight Cardiovascular Institute and Division of Endocrinology, Diabetes and Clinical Nutrition at Oregon Health & Science University in Portland, Oregon.
There are two types of NAFLD: one when only fat is present in the liver (called non-alcoholic fatty liver), and the other when inflammation and scarring are also present (called non-alcoholic steatohepatitis, or NASH). Excess alcohol intake can cause similar fat deposits and liver dysfunction, so the term NAFLD is used to differentiate between disease caused by excess alcohol intake vs. disease without alcohol as the underlying cause.
NAFLD may go undiagnosed for years, thus, the statement emphasizes the need for awareness and monitoring for NAFLD, access to improved screening tools and treatment and highlights the lifestyle changes to help prevent and treat the disorder.
NAFLD raises heart disease risk
Heart disease is the leading cause of death in people with NAFLD. The diseases share many of the same risk factors, including metabolic syndrome (elevated blood sugar and blood triglycerides, increased abdominal fat and high blood pressure); Type 2 diabetes; impaired glucose tolerance (prediabetes); and obesity. However, people with NAFLD are at higher risk of heart disease than people who have the same heart disease risk factors without the liver condition.

Scientists at Trinity College Dublin have announced a significant advance in our understanding of epilepsy, as they have identified a potential method of preventing damaging seizure activity.
Epilepsy is a chronic central nervous system (CNS) disorder affecting approximately 1% of the population and 50 million people worldwide. It is characterised by recurrent, spontaneous seizures caused by disrupted electrical activity in the brain.
While the brain accounts for just 2% of human body mass, it expends almost 20% of the body’s daily energy production. In order to maintain this high energy demand brain cells are nourished by an intricate network of capillaries that forms the so-called blood-brain barrier (BBB). Such is the extent of these capillaries, we estimate that every brain cell is essentially nourished by its own capillary.
Fundamentally, it is disruption to the integrity of these capillaries and the BBB that the Trinity scientists believe is a key driver of seizure activity in humans. Promisingly though, their new research shows that restoring that integrity can prevent seizures.
“Our findings suggest that designing medicines aimed at stabilising the integrity of blood vessels in the brain may hold promise in treating patients who are currently non-responsive to anti-seizure medications,” said Dr Matthew Campbell, Associate Professor in Trinity’s School of Genetics and Microbiology.
“This work represents one of the first conclusive studies that pinpoints a key feature of seizures that has to date not been studied in great molecular detail.”
Importantly, the work was translational in nature and included both basic and clinical research arms involving patients diagnosed with epilepsy. Using similar techniques in humans and in pre-clinical models, the scientists were able to show that BBB disruption was a key driver of seizure activity.

Organic aerosols — such as those released in cooking — may stay in the atmosphere for several days, because of nanostructures formed by fatty acids as they are released into the air.
By identifying the processes which control how these aerosols are transformed in the atmosphere, scientists will be able to better understand and predict their impact on the environment and the climate.
Experts at the Universities of Birmingham and Bath have used instruments at the Diamond Light Source and the Central Laser Facility, both based at the Harwell Campus in Oxford, to probe the behaviour of thin films of oleic acid — an unsaturated fatty acid commonly released when cooking.
In the study, published in Atmospheric Chemistry and Physics, they were able to analyse the particular molecular properties that control how rapidly aerosol emissions can be broken down in the atmosphere.
Then, using a theoretical model combined with experimental data the team was able to predict the amount of time aerosols generated from cooking may hang around in the environment.
These types of aerosols have long been associated with poor air quality in urban areas, but their impact on human-made climate change is hard to gauge. That’s because of the diverse range of molecules found within aerosols, and their varying interactions with the environment.
By identifying the nanostructure of molecules emitted during cooking that slows down the break-up of organic aerosols, it becomes possible to model how they are transported and dispersed into the atmosphere.
Lead author Dr Christian Pfrang, of the University of Birmingham’s School of Geography, Earth and Environmental Sciences, said: “Cooking aerosols account for up to 10 per cent of particulate matter (PM) emissions in the UK. Finding accurate ways to predict their behaviour will give us much more precise ways to also assess their contribution to climate change.”
Co-author Dr Adam Squires, of the University of Bath, said: “We’re increasingly finding out how molecules like these fatty acids from cooking can organise themselves into bilayers and other regular shapes and stacks within aerosol droplets that float in the air, and how this completely changes how fast they degrade, how long they persist in the atmosphere, and how they affect pollution and weather.”
The research was funded by the Natural Environment Research Council and the data was produced and analysed using the University of Birmingham’s BlueBEAR high performance and high throughput computing service. BlueBEAR employs some of the latest technology to deliver fast and efficient processing capacity for researchers while minimizing energy consumption by using direct, on-chip, water cooling.
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Photocatalyst made using a combination of titanium dioxide (TiO2) and copper oxide (CuxO) nanoclusters inactivates various variant types of novel coronavirus SARS-CoV-2. Scientists in Nara Medical University, Kanagawa Institute of Industrial Science and Technology, and Tokyo Institute of Technology have developed this antiviral photocatalyst, in a recent breakthrough, which has been proven to be effective under both darkness and indoor light.
The novel coronavirus (SARS-CoV-2), responsible for the ongoing COVID-19 pandemic, has affected millions of people worldwide. The main transmission pathway of the virus is through droplets released by infected people into the air. Additionally, these droplets exist on various surfaces as well. Viral infections mainly occur in indoor environments where many people gather, Antiviral chemicals, such as alcohol and hydrogen peroxide, are often used to decontaminate regularly touched surfaces. These chemicals essentially render the virus inactive by breaking down their proteins. However, these chemicals are volatile in nature and, therefore evaporate away. As a result, the disinfection process has to be carried out regularly.
Now in a study published in Scientific Reports, a research team of Nara Medical University, Kanagawa Institute of Industrial Science and Technology, and Tokyo Institute of Technology has developed a solid-state photocatalyst as an alternative defense against the virus. Unlike chemical disinfectants, solid-state coatings remain for a long time, and since the viral outbreak, have been the subject of intensive research around the world. Solid-state antiviral coatings have the advantage of being non-toxic, abundant, and chemically and thermally stable.
Many of these solid-state coatings use TiO2 photocatalysts that, when exposed to ultraviolet (UV) light, cause oxidation reaction that can destroy organic matter like the spike proteins found on the surfaces of coronaviruses. However, these coatings are activated only when exposed to UV light, which is not present in typical indoor environments. In most of indoor environments, lightings are usually turned off in the night time, thus the antiviral material under dark condition is desired.
To get the coating to work under visible light as well dark conditions, the team has developed a composite consisting of TiO2 and CuxO nanoclusters. CuxO nanoclusters are composed of a mixed valence number oxide, in which Cu(I) and Cu(II) species are present. The Cu(II) species in CuxO contributes to the visible-light-driven photocatalysis reaction, whereas the Cu(I) species plays a crucial role in denaturing virus proteins, thereby causing their inactivation under dark conditions.
By coating the CuxO/TiO2 powder on a glass, the team showed that it could inactivate even the highly virulent Delta variant of SARS-CoV-2. The team has also confirmed the inactivation of Alfa, Beta, and Gamma variants by CuxO/TiO2 in addition to the wild type strain.
The team carefully investigated the antiviral mechanism using sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE), ELISA assay, and RT-qPCR analysis. These analyses strongly suggest that the Cu(I) species in CuxO denaturalises spike proteins and also causes RNA fragmentation of SARS-CoV-2, even under dark condition. Furthermore, white light irradiation causes the photocatalytic oxidation of the organic molecules of SARS-CoV-2. Based on this antiviral mechanism, the present antiviral material is not limited to a specific variant of the virus and will be effective to inactivate various types of a potential mutant strain.
White light illumination in the present study is usually used as an indoor light apparatus. This can make the CuxO/TiO2 photocatalyst very effective in reducing the risk of COVID-19 infection in indoor environments, which are usually subjected to both light and darkness periodically.
Hopefully, this study will take us one step closer to protecting ourselves better against the coronavirus, and adjusting to the post-COVID era.
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