How to inactivate common cold viruses

Every year, respiratory syncytial viruses (RSV) cause countless respiratory infections worldwide. For infants, young children and people with preexisting conditions, the virus can be life-threatening. The team from the Department for Molecular and Medical Virology at Ruhr University Bochum has explored ways to reduce the risk of infection. Their findings show that — when used correctly — alcohol-based hand sanitizers and commercially available surface disinfectants provide good protection against transmission of the virus via surfaces.
Some viruses are known to remain infectious for a long time on surfaces. To determine this period for RSV, the Bochum-based virology team examined how long the virus persists on stainless steel plates at room temperature. “Even though the amount of infectious virus decreased over time, we still detected infectious viral particles after seven days,” says Dr. Toni Luise Meister. “In hospitals and medical practices in particular, it is therefore essential to disinfect surfaces on a regular basis.” A test of five surface disinfectants containing alcohol, aldehyde and hydrogen peroxide showed that all cleaning agents inactivated the virus effectively on surfaces.
RSV is easier to render harmless than some other viruses
Likewise, hand sanitizers recommended by the WHO showed the desired effect. “An alcohol content of 30 percent was sufficient: we no longer detected any infectious virus after hand disinfection,” points out Toni Luise Meister. RSV is thus easier to render harmless than some other viruses, such as monkeypox virus or hepatitis B virus.
Still, most infections with RSV are transmitted from one person to another, via droplets from the air we breathe. The risk of contracting the virus from an infected person decreases if that person rinses their mouth for 30 seconds with a commercial mouthwash. The lab tests showed that three mouthwashes for adults and three of four mouthwashes designed specifically for children reduced the amount of virus in the sample to the point that the virus could no longer be detected.
“If we assume that these results from the lab can be transferred to everyday life, we are not at the mercy of seasonal flu and common cold, but can actively prevent infection,” concludes Toni Luise Meister. “In addition to disinfection, people should wash their hands regularly, maintain a proper sneezing and coughing etiquette, and keep their distance from others when they’re experiencing any symptoms.”

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Bird flu is undergoing changes that could increase the risk of widespread human transmission

A new study from researchers in China and Nottingham has discovered that a subtype of avian flu virus, endemic in poultry farms in China, is undergoing mutational changes, which could increase the risk of the disease being passed on to humans.
Researchers also say that the findings raise concerns of a potential epidemic or pandemic in the making and that concerted research is necessary to closely monitor such viruses in poultry and humans.
The results, which have been published in Cell, report on the characterisation of a human isolate — from a human patient — of the H3N8 avian influenza virus (AIV). Using laboratory mice and ferrets as models for human infection, the study found that virus has undergone several adaptive changes to cause severe animal infections and making it transmissible by the airborne route between animals.
In humans, the avian H3N8 virus infection has been found to cause acute respiratory distress syndrome and can even be fatal. The virus is widespread in chicken flocks; however previously, the features of how it might be transmitted from animals to humans is poorly understood.
“We demonstrate that an avian H3N8 virus isolated from a patient with severe pneumonia replicated efficiently in human bronchial and lung epithelial cells, was extremely harmful in its effects in laboratory mammalian hosts and could be passed on through respiratory droplets,” says Professor Kin-Chow Chang,at the University of Nottingham.
“Importantly, we discovered that the virus had acquired human receptor binding preference and amino acid substitution PB2-E627K, which are necessary for airborne transmission. Human populations, even when vaccinated against human H3N2 virus, appear immunologically naïve to emerging mammalian adapted H3N8 AIVs and could be vulnerable to infection at epidemic or pandemic proportion.
“Acid resistance of influenza virus is also an important barrier for avian influenza virus to overcome to acquire the adaptability and transmissibility in new mammals or humans. The current novel H3N8 virus has not acquired the acid resistance yet. So, we should pay attention to the change on acid resistance of the novel H3N8 virus.”
The study, titled ‘Airborne transmission of human-isolated avian H3N8 influenza virus between ferrets’ was a collaboration between the University of Nottingham, China Agricultural University in Beijing, the Chinese Academy of Sciences and the Chinese Center for Disease Control and Prevention.

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Deciphering the 'highway code' of our cells

Cancers, degenerative diseases: deregulation of our cells’ internal communication pathways is at the root of many conditions. Microtubules — microscopic protein filaments — play a crucial role in controlling these exchanges. However, their mechanisms remain poorly understood. A team from the University of Geneva (UNIGE) has identified a new mechanism, involving two proteins, that governs their growth. The discovery opens up unprecedented prospects for the development of new treatments that can act at the very heart of cells. These results are published in the Proceedings of the National Academy of Sciences (PNAS).
As a city needs fluid transport networks for its exchange and development, so cells need internal microscopic ”roads” to supply themselves, grow and divide. These ”roads” are called ”microtubules”. They are long protein filaments that form the backbone of the cell. Problems with their regulation can cause diseases such as cancer and neurodegenerative disorders.
Understanding how they work — and in particular the mechanisms that control and regulate their growth — is therefore crucial. Although significant advances have been made in this field over the last forty years, the complexity of this system continues to require intense research.
Two key proteins
Recent work by Charlotte Aumeier, assistant professor in the Biochemistry Department at the UNIGE Faculty of Science, provides new insights into the functioning of the microtubule. It shows how two specific proteins, CLIP-170 and EB3, undergo liquid-liquid phase separation at the tip of the microtubule during its growth. In other words, these two proteins separate from the cellular liquid medium to form a second liquid phase at the tip of the microtubule, like a drop of oil in water.
Microtubules are dynamic structures that continually build and deconstruct themselves. ”This phenomenon of phase separation, at the level of the microtubule, increases the concentration of proteins, including tubulin, and significantly stimulates the growth rate of microtubules while reducing depolymerisation events, i.e. microtubule decay events,” explains Charlotte Aumeier, the last author of the study. This mechanism therefore seems to control the dynamics of cellular microtubules in a very concrete way.
Joint Action
Julie Miesch, a PhD student in Charlotte Aumeier’s laboratory and first author of the study, explains that ”it is the synergy between CLIP-170 and EB3 that ensures the regulation of microtubule growth, thanks to a liquid-liquid phase separation mechanism”. Taken individually, CLIP-170 has no interaction with tubulin. As for EB3, although it is capable of interacting with tubulin, it only forms tiny aggregates on the surface. The combination of these two proteins makes it possible to regulate the speed of microtubule growth locally.
The role of these two proteins was observed by in vitro and then in cellulo measurements using a combination of two methods, total internal reflection fluorescence microscopy and high-throughput confocal microscopy, available at the UNIGE within the ACCESS GENEVA platform.
These results highlight a new level of regulation in the control of microtubule dynamics. This opens up the possibility of new targets in the development of new anti-cancer therapies. This breakthrough promises to further broaden our understanding and our ability to act at the very heart of cellular processes.

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New study shows effectiveness of mpox vaccine

A new international study led by Queen Mary University of London has shown mpox (formerly known as monkeypox) infections to be less severe among those who are vaccinated or had a previous infection in 2022, underlining the importance and effectiveness of vaccination.
The research, published in The Lancet Infectious Diseases, was delivered by the SHARE-net collaborative and looked at 38 mpox infections in 37 gay and bisexual men. Eight of the 38 were reinfections, and 30 infections occurred after a complete vaccination course. In the people who had been vaccinated, the results showed that the patients had fewer lesions (abnormal tissue such as a wound or rash), less mucosal disease (diseases of the mucous membranes of the mouth and genitals), and a minimal need for pain medication or hospitalisation.
The severity of symptoms was observed and assessed using the Mpox-SSS score, which was developed during the 2022 multi-country outbreak. The Mpox-SSS score is a numerical score given considering seven different factors including the number of lesions, the level of care required for the patient, the amount of pain medication needed, the extent of mucosal areas affected, and whether there is any bacterial superinfection — i.e., additional infections.
Using this scoring system it was possible to demonstrate and measure severity. In those who had been reinfected, the disease was less severe with a lesser requirement for pain medication compared to their first bout, and fewer areas of the body were affected while recovery was also faster. The first infection lasted 21 days (median) whereas the second infection lasted 15 days (median).
The study is the largest and only case series to examine both reinfections and infections after a complete vaccine course of Modified Vaccinia Ankara-Bavarian Nordic (MVA-BN).
Since May 2022, there have been more than 87,000 cases of human mpox across 112 countries. Transmissions have primarily affected sexually active gay and bisexual men and been caused by skin-to-skin and bodily fluid contact. As evidenced by the two previous SHARE-net global case series published in The NEJM and The Lancet, infection often causes rashes, fevers, and blisters. It can also lead to brain inflammation and seizures. In people with advanced HIV disease, it carries a mortality of up to 27% in the most immunosuppressed group.
Neither natural immunity from a prior mpox infection nor post-vaccination immunity can prevent someone from getting the virus. However, the study shows that the immunity from both reduces severity.
Research lead author Chloe Orkin, Professor of HIV Medicine at Queen Mary University of London and Director of the SHARE collaborative, said: “This is good news and shows that post-vaccination infections are less severe and the need for hospitalisation is lower. This is clear evidence that vaccination is an important tool in reducing morbidity and controlling further outbreaks.
“We have to ensure global access to vaccinations and treatments if we want to curb this global outbreak, especially in the African regions that have been historically worst affected and are still without access to vaccines or treatment for mpox.”

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Active children are more resilient

The school year has hardly begun and the first exams are already approaching. According to findings by researchers from the University of Basel, school children cope better with the stress if they get plenty of daily exercise.
“Get some exercise!” It’s one suggestion adults frequently hear when they complain about stress in their lives. Exercise helps relieve stress. But does this also apply to children? Does exercise help them manage the pressures to achieve at school? A research team led by Dr. Manuel Hanke and Dr. Sebastian Ludyga from the Department of Sport, Exercise and Health recently examined the effect of physical activity on children’s stress levels. Their findings appear in the Journal of Science and Medicine in Sport.
For their study, they had 110 children between the ages of 10 and 13 wear a sensor tracking their daily movement over the course of a week. They then brought the participants into the lab on two separate occasions to complete a stressful task and a non-stressful control task (see the box). The researchers tested the children’s physical stress reaction via the concentration of the stress hormone cortisol in their saliva.
Less cortisol in active children
“We wanted to determine whether physical activity makes children more resilient under laboratory-controlled circumstances,” explains project director Sebastian Ludyga. The results showed that the participants who got more than an hour of exercise per day, as the World Health Organization (WHO) recommends, did in fact produce less cortisol in the stress task than the children who were less active.
“Regularly active children seem to have a reduced physiological stress reaction in general,” notes Manuel Hanke, lead author of the study. Even in the control task, which involved an unfamiliar situation, making it still somewhat unsettling for the participants, there was a difference in cortisol levels between more and less active children — though overall cortisol levels were lower than in the stress task.
Stress hormone levels increase during exercise
One possible explanation for this finding could be that cortisol levels also increase during exercise, says Sebastian Ludyga. “When children regularly run, swim, climb, etc., the brain learns to associate a rise in cortisol with something positive. The body’s reaction always has a cognitive component as well: this positive association helps to prevent the concentration of cortisol from rising to too high a level in exam situations as well.”

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AI performs comparably to human readers of mammograms

Using a standardized assessment, researchers in the UK compared the performance of a commercially available artificial intelligence (AI) algorithm with human readers of screening mammograms. Results of their findings were published in Radiology, a journal of the Radiological Society of North America (RSNA).
Mammographic screening does not detect every breast cancer. False-positive interpretations can result in women without cancer undergoing unnecessary imaging and biopsy. To improve the sensitivity and specificity of screening mammography, one solution is to have two readers interpret every mammogram.
According to the researchers, double reading increases cancer detection rates by 6 to 15% and keeps recall rates low. However, this strategy is labor-intensive and difficult to achieve during reader shortages.
“There is a lot of pressure to deploy AI quickly to solve these problems, but we need to get it right to protect women’s health,” said Yan Chen, Ph.D., professor of digital screening at the University of Nottingham, United Kingdom.
Prof. Chen and her research team used test sets from the Personal Performance in Mammographic Screening, or PERFORMS, quality assurance assessment utilized by the UK’s National Health Service Breast Screening Program (NHSBSP), to compare the performance of human readers with AI. A single PERFORMS test consists of 60 challenging exams from the NHSBSP with abnormal, benign and normal findings. For each test mammogram, the reader’s score is compared to the ground truth of the AI results.
“It’s really important that human readers working in breast cancer screening demonstrate satisfactory performance,” she said. “The same will be true for AI once it enters clinical practice.”
The research team used data from two consecutive PERFORMS test sets, or 120 screening mammograms, and the same two sets to evaluate the performance of the AI algorithm. The researchers compared the AI test scores with the scores of the 552 human readers, including 315 (57%) board-certified radiologists and 237 non-radiologist readers consisting of 206 radiographers and 31 breast clinicians.

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Resistant starch supplement reduces liver triglycerides in people with fatty liver disease

Resistant starch is a nondigestible fiber that ferments in the large intestine, and consumption of it has previously been shown to have a positive effect on metabolism in animal studies. Now, a 4-month randomized controlled trial in people with non-alcoholic fatty liver disease (NAFLD) indicates that daily intake of resistant starch can alter gut bacteria composition and lower liver triglycerides and liver enzymes associated with liver injury and inflammation. This research appears in the journal Cell Metabolism on September 5.
NAFLD, caused by a buildup of fat in the liver, affects about 30% of the population worldwide. It can lead to severe liver diseases and contribute to other conditions, such as type 2 diabetes and cardiovascular disease. Currently, there is no approved medicine available to treat NAFLD. Doctors usually recommend dietary changes and exercise to alleviate the conditions.
“We think it would be very meaningful if we can find an effective approach, maybe through identifying new therapeutic targets, to manage NAFLD,” says Huating Li, the paper’s co-corresponding author at Shanghai Sixth People’s Hospital.
Previous research has suggested that NAFLD is associated with perturbed gut microbiota. For example, people with early-stage NAFLD already have an altered gut bacteria profile. So, Li and her team wanted to investigate if resistant starch — a type of fiber known to encourage the growth of beneficial gut bacteria — can help treat NAFLD.
The team recruited 200 NAFLD patients and provided them with a balanced dietary plan designed by a nutritionist. Among them, 100 patients also received a resistant starch powder derived from maize while the other 100 received calorie-matched non-resistant corn starch as a control. They were instructed to drink 20 grams of the starch mixed with 300 mL water (1 ¼ cups) before meals twice a day for 4 months.
After the 4-month experiment, participants who received the resistant starch treatment had nearly 40% lower liver triglyceride levels compared to patients in the control group. In addition, patients who had the resistant starch treatment also saw reductions in liver enzymes and inflammatory factors associated with NAFLD. Importantly, these benefits were still apparent even when statistically adjusted for weight loss.
“Our study shows resistant starch’s impact in improving patients’ liver conditions is independent of body weight changes,” says Yueqiong Ni, the paper’s co-first author at Shanghai Sixth People’s Hospital and Leibniz Institute for Natural Product Research and Infection Biology — Hans-Knöll-Institute (HKI) in Germany.
By analyzing patients’ fecal samples, the team found the resistant starch group had a different microbiota composition and functionality compared with the control. In particular, the treatment-group patients had a lower level of Bacteroides stercoris, a key bacterial species that can affect fat metabolism in the liver through its metabolites. The reduction in B. stercoris is stronglylinked to the decrease in liver triglyceride content, liver enzymes, and metabolites observed.
When the team transplanted fecal microbiota from resistant starch-treatment patients to mice fed with a high-fat high-cholesterol diet, the mice saw a significant reduction in liver weight and liver triglyceride levels and improved liver tissue grading compared with mice that received microbiota from the control group.
“We are able to identify a new intervention for NAFLD, and the approach is effective, affordable and sustainable. Compared with strenuous exercise or weight loss treatment, adding resistant starch to a normal and balanced diet is much easier for people to follow through,” Li says.

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Synchronizing your internal clocks may help mitigate jet lag, effects of aging

Traveling to faraway places is a great way to seek out new experiences, but jet lag can be an unpleasant side effect. Adjusting to a new time zone is often accompanied by fatigue, difficulty sleeping, and a host of other problems that can turn an otherwise exciting adventure into a miserable trip.
Jet lag is caused by a difference between the circadian system — the body’s internal clock — and the surrounding environment. Around the turn of the century, scientists began to recognize that the body has multiple internal clocks, calibrated in different ways, and that jet lag-like symptoms can result when these clocks drift out of sync with each other. This can happen in several ways and grows more prevalent with age.
In Chaos, from AIP Publishing, a team of scientists from Northwestern University and the Santa Fe Institute developed a theoretical model to study the interactions between multiple internal clocks under the effects of aging and disruptions like jet lag.
Modern research has shown that circadian clocks are present in almost every cell and tissue in the body. Each relies on its own set of cues to calibrate; the brain’s clock depends on sunlight, for instance, while the peripheral organs calibrate at mealtime.
“Conflicting signals, such as warm weather during a short photoperiod or nighttime eating — eating when your brain is about to rest — can confuse internal clocks and cause desynchrony,” said author Yitong Huang.
At this point, little is known about how the body’s various internal clocks affect each other. The added complexity of accounting for multiple clocks means researchers tend to use simplified models.
“Most studies primarily focus on one particular time cue or a single clock,” said Huang. “Important gaps remain in our understanding of the synchronization of multiple clocks under conflicting time cues.”
Huang and her colleagues took a different approach, building a mathematical framework that accounts for this complex interplay between systems. Their model features two populations of coupled oscillators that mimic the natural rhythms of circadian cycles. Each oscillator influences the others while simultaneously adjusting based on unique external cues.

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Linking two solar technologies is a win-win for efficiency and stability

While conventional silicon-based solar cells have had an unmistakable impact on the buildout of renewable energy resources around the world, additional performance improvements have become increasingly difficult to make as the devices approach their practical efficiency limits. This constraint has prompted scientists to seek out new technologies that can be combined with silicon cells to unlock higher efficiencies.
Solar cells made with crystals called perovskites are one such technology that have rapidly emerged as an appealing low-cost add-on, but perovskite cells are notoriously susceptible to voltage-induced changes — the shade cast from an overhanging tree branch or nearby plant can zap an entire module within minutes.
Now, researchers from Princeton University and the King Abdullah University of Science and Technology (KAUST) have connected the well-established silicon solar cell with the up-and-coming perovskite in a tandem solar cell to not only boost overall efficiency, but also to strengthen stability. The results, reported in Joule on Sep. 5, illustrate that the connection protects the frail perovskite solar cell from voltage-induced breakdown while attaining greater efficiencies than either cell can achieve on their own.
“Tandem solar cells have already demonstrated power conversion efficiencies that are greater than either silicon or perovskite solar cells alone,” said Barry Rand, research leader and professor of electrical and computer engineering and the Andlinger Center for Energy and the Environment. “We thought that in addition to their higher efficiencies, tandem solar cells could also solve some of the stability challenges facing perovskites by linking them with silicon cells, which are much more stable.”
To test their hypothesis, the researchers built three strings of solar cells: one containing only silicon solar cells, one with only perovskites, and one composed of tandem solar cells, with the two technologies connected in a series. The researchers then shaded one of the cells in the string to simulate the partial shading conditions that a solar array may encounter at least once in its decades-long lifespan.
Such partial shading usually spells doom for perovskites, as the still-illuminated cells force charge to flow through the now-shaded and inactive cell, quickly degrading both it and the entire module. Silicon solar cells, on the other hand, are much more resilient to voltage fluxes, and can endure periods of partial shading with fewer issues.
As expected, the perovskite-only solar module quickly deteriorated after partial shading, while the silicon solar module was only minimally impacted. Interestingly, however, the tandem solar module was just as resilient as the silicon-only module, implying that by connecting the two solar technologies, the silicon cell was able to mask the frailty of the perovskite.

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Why are male kidneys more vulnerable to disease than female kidneys? Mouse study points to testosterone

Female kidneys are known to be more resilient to disease and injury, but males need not despair. A new USC Stem Cell-led study published in Developmental Cell describes not only how sex hormones drive differences in male and female mouse kidneys, but also how lowering testosterone can “feminize” this organ and improve its resilience.
“By exploring how differences emerge in male and female kidneys during development, we can better understand how to address sex-related health disparities for patients with kidney diseases,” said Professor Andy McMahon, the study’s corresponding author, and the director of the Eli and Edythe Broad Center for Regenerative Medicine and Stem Cell Research at the Keck School of Medicine of USC.
First authors Lingyun “Ivy” Xiong and Jing Liu from the McMahon Lab and their collaborators identified more than 1,000 genes with different levels of activity in male and female mouse kidneys, in a study supported by the National Institutes of Health. The differences were most evident in the section of the kidney’s filtering unit known as the proximal tubule, responsible for reabsorbing most of the nutrients such as glucose and amino acids back into the blood stream. Most of these sex differences in gene activity emerged as the mice entered puberty and became even more pronounced as they reached sexual maturity.
Because female kidneys tend to fare better in the face of disease or injury, the researchers were interested how the gene activity of kidneys becomes “feminized” or “masculinized” — and testosterone appeared to be the biggest culprit.
To feminize the kidneys of male mice, two strategies worked equally well: castrating males before puberty and thus lowering their natural testosterone levels, or removing the cellular sensors known as androgen receptors that respond to male sex hormones.
Intriguingly, three months of calorie restriction — which is an indirect way to lower testosterone — produced a similar effect. Accordingly, calorie restriction has already been shown to mitigate certain types of kidney injuries in mice.
To re-masculinize the kidneys of the castrated males, the researchers only needed to inject testosterone. Similarly, testosterone injection masculinized the kidneys of females who had their ovaries removed before puberty.

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