Publishing their findings in the academic journal Nature Scientific Reports, the team behind the study shows how beginners who undertook piano lessons for just one hour a week over 11 weeks reported significant improvements in recognising audio-visual changes in the environment and reported less depression, stress and anxiety.

In the randomised control study, 31 adults were assigned into either a music training, music listening, or a control group. Individuals with no prior musical experiences or training were instructed to complete weekly one-hour sessions. Whilst the intervention groups played music, the control groups either listened to music or used the time to complete homework.

The researchers found that within just a few weeks of starting lessons*, people’s ability to process multisensory information — i.e., sight and sound — was enhanced. Improved ‘multisensory process’ has benefits for almost every activity we participate in — from driving a car and crossing a road, to finding someone in a crowd or watching TV.

These multisensory improvements extended beyond musical abilities. With musical training, people’s audio-visual processing became more accurate across other tasks. Those who received piano lessons showed greater accuracy in tests where participants were asked to determine whether sound and vision ‘events’ occurred at the same time.

This was true both for simple displays presenting flashes and beeps, and for more complex displays showing a person talking. Such fine-tuning of individuals’ cognitive abilities was not present for the music listening group (where participants listened to the same music as played by the music group), or for the non-music group (where members studied or read).

In addition, the findings went beyond improvements in cognitive abilities, showing that participants also had reduced depression, anxiety and stress scores after the training compared to before it. The authors suggest that music training could be beneficial for people with mental health difficulties, and further research is currently underway to test this.

Cognitive psychologist and music specialist Dr Karin Petrini from the University of Bath’s Department of Psychology, explained: “We know that playing and listening to music often brings joy to our lives, but with this study we were interested in learning more about the direct effects a short period of music learning can have on our cognitive abilities.

“Learning to play an instrument like the piano is a complex task: it requires a musician to read a score, generate movements and monitor the auditory and tactile feedback to adjust their further actions. In scientific terms, the process couples visual with auditory cues and results in a multisensory training for individuals.

“The findings from our study suggest that this has a significant, positive impact on how the brain processes audio-visual information even in adulthood when brain plasticity is reduced.”

Notes

• Each music training session included two segments. The first 20-minute segment was dedicated to finger exercise. The second segment consisted of learning songs from the ABRSM 2017-2018 piano grade one exam list for 40 minutes. All training sessions were carried out on a one-to-one basis. Participants learned these pieces in the order presented below. They proceeded to the next song once they could play the former one correctly and fluently:

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  William Gillock A Stately Sarabande. Classic Piano Repertoire (Elementary).

• Johann Christian Bach Aria in F, BWV Anh. II 131.

• Giuseppe Verdi La donna è mobile (from Rigoletto).

• Bryan Kelly Gypsy Song: No. 6 from A Baker’s Dozen.

• Traditional American Folk Song: When the saints go marching in.

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Researchers at The University of Texas at Austin and Texas A&M University have applied emerging electronic tattoo (e-tattoo) technology to this type of monitoring, known as electrodermal activity or EDA sensing. In a new paper published recently in Nature Communications, the researchers created a graphene-based e-tattoo that attaches to the palm, is nearly invisible and connects to a smart watch.

“It’s so unobstructive that people sometimes forget they had them on, and it also reduces the social stigma of wearing these devices in such prominent places on the body,” said Nanshu Lu, professor in the Department of Aerospace Engineering and Engineering Mechanics and leader of the project.

Lu and her collaborators have been advancing wearable e-tattoo technology for many years. Graphene has been a favorite material because of how thin it is and how well it measures electrical potential from human body, leading to very accurate readings.

But, such ultra-thin materials can’t handle much, if any strain. So that makes applying them to parts of the body that include a lot of movement, such as the palm/wrist, challenging.

The secret sauce of this discovery is how the e-tattoo on the palm is able to successfully transfer data to a rigid circuit — in this case a commercially available smart watch, in out-of-lab, ambulatory settings. They used a serpentine ribbon that has two layers of graphene and gold partially overlapped. By snaking the ribbon back and forth, it can handle the strain that comes with movements of the hand for everyday activities like holding the steering wheel while driving, opening doors, running etc.

Current palm monitoring tech uses bulky electrodes that fall off and are very visible, or EDA sensors applied to other parts of the body, which gives a less accurate reading.

Other researchers have tried similar methods using nanometer-thick straight-line ribbons to connect the tattoo to a reader, but they couldn’t handle the strain of constant movement.

Lu said the researchers were inspired by virtual reality (VR), gaming and the incoming metaverse for this research. VR is used in some cases to treat mental illness; however, the human-aware capability in VR remains lacking in many ways.

“You want to know whether people are responding to this treatment,” Lu said. “Is it helping them? Right now, that’s hard to tell.”

Other members of the team include Hongwoo Jang and Eunbin Kim from the Texas Materials Institute; Sangjun Kim and Kyoung-Ho Ha from the Walker Department of Mechanical Engineering; Xiangxing Yang from the Chandra Family Department of Electrical and Computer Engineering; and Kaan Sel and Roozbeh Jafari from Texas A&M’s Department of Electrical and Computer Engineering.

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In the first study of its kind, researchers found that people who reported trouble sleeping were on average more likely to have indicators of poor cardiometabolic health — inflammatory markers, cholesterol and body weight — which can contribute to type 2 diabetes.

In Australia, almost one million adults have type 2 diabetes. Globally, type 2 diabetes affects more than 422 million people.

UniSA researcher Dr Lisa Matricciani says different aspects of sleep are associated with risk factors for diabetes.

“Everyone knows that sleep is important. But when we think about sleep, we mainly focus on how many hours of sleep we get, when we should also be looking at our sleep experience as a whole,” Dr Matricciani says.

“How soundly we sleep, when we go to bed and get up, and how regular our sleep habits are, may be just as important as sleep duration.”

“In this study, we examined the association of different aspects of sleep, and risk factors for diabetes, and found a connection between those who had troubled sleep and those who were at risk of type 2 diabetes.”

The study assessed more than 1000 Australian adults* with a median age of 44.8 years. Researchers examined a range of sleep characteristics: self-report trouble sleeping, duration, timing, efficiency, and day-to-day sleep length variability.

“People who reported having trouble sleeping were also more likely to have a higher body mass index, as well as blood markers of cholesterol and inflammation,” Dr Matricciani says.

“When it comes down to the crunch, we know we must prioritise our sleep to help stay in good health. More research is needed, but as this study shows, it’s important to think about sleep as a whole, not just as one aspect.”

Notes

• *Most participants (87 per cent) were mothers.
• Approximately half of all participants (48 per cent) reported that they never had troubled sleep.

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Led by researchers from Institute of Psychiatry, Psychology & Neuroscience (IoPPN), King’s College London, this is the largest study worldwide to examine whether air pollution exposure is linked with the occurrence of multiple long-term health conditions.

Multimorbidity is defined as having two or more physical or mental health conditions and affects 27 per cent of adults in UK primary care. It increases the use of healthcare services and the costs of primary and secondary care, but its association with air pollution has not been studied in the UK until now.

Published in Frontiers in Public Health the study showed that high levels of traffic-related air pollution — fine particulate matter 2.5 (PM_2.5) and nitrogen dioxide (NO₂) — were associated with an increased risk of having at least two long term health conditions. The strongest associations were observed for co-occurring neurological, respiratory, cardiovascular and common mental health conditions such as depression and anxiety.

This research was funded by National Institute for Health and Care Research (NIHR) Maudsley Biomedical Research Centre and NIHR Applied Research Collaboration (ARC) South London.

Dr Amy Ronaldson, Research Associate at Institute of Psychiatry, Psychology & Neuroscience (IoPPN), King’s College London and first author on the study said: “People with more than one long-term health condition have a lower quality of life and greater dependence on the healthcare system. Our NIHR funded research has indicated that those people that live in areas of higher traffic-related air pollution are at greater risk of having multiple health conditions. The study does not prove that air pollution causes multimorbidity, but it does warrant further research in this area. It could be that simple measures to reduce traffic levels could potentially improve lives and lessen the pressure on our healthcare systems.”

Researchers analysed data from UK Biobank — a large-scale biomedical database and research resource containing anonymised genetic, lifestyle and health information from half a million UK participants. aged between 40 and 69 years. Participants were assessed for 36 physical and five mental health chronic conditions. Multimorbidity was defined as having two or more of these conditions.

Physical and mental health data from UK Biobank in 2010 were linked with the estimated concentration of air pollution at the residential address of the participants.

The study found that those participants exposed to higher concentrations (above 10µg/m³) of fine particulate matter had a 21 per cent increased risk of two or more co-occurring conditions compared to those exposed to concentrations below 10µg/m³.

For participants exposed to above 30µg/m³ of NO₂ the research showed a 20 per cent increased risk of having two or more co-occurring conditions compared to those participants that were exposed to concentrations of NO₂ below 20µg/m³.

Amongst those with multiple conditions, increased exposure to both PM_2.5 and NO₂ was linked to a greater severity of the co-occurring conditions.

Dr Ioannis Bakolis, Reader at IoPPN, King’s College London and senior author on the study said: “How air pollution affects multiple organs and systems at the same time is not yet fully understood, but there is some evidence that mechanisms such as inflammation, oxidative stress and immune activation could be triggered by air particulates, which can cause damage to the brain, heart, blood, lungs and gut.

“Our study suggests that it could be through shared mechanisms that air pollution negatively impacts several body systems and increases the likelihood of people developing multiple long term health conditions. More research is needed to understand just how air pollution affects the different bodily systems, but it may be that tackling air pollution could help prevent and alleviate the debilitating impact of multiple long-term health conditions.”

Researchers identified several patterns in the associations: the strongest links were primarily between conditions relating to the respiratory system (asthma, chronic obstructive pulmonary disease) as well as the cardiovascular system (atrial fibrillation, coronary heart disease, heart failure) but also to neurological and common mental conditions (stroke, substance abuse, depression, anxiety).

The study, ‘Associations between air pollution and multimorbidity in the UK Biobank: A cross-sectional study’ was published in Frontiers in Public Health.

This study has been funded by the National Institute for Health and Care Research (NIHR) Biomedical Research Centre at South London and Maudsley NHS Foundation Trust and King’s College London and the NIHR Applied Research Collaboration South London.

Now a follow-up study by the same group, published in Science Translational Medicine, has found that the 2-dose vaccines still provide protection against lung disease in rhesus macaques one year after they had been vaccinated as infants.

The co-senior authors of the paper are Kristina De Paris, PhD, professor of microbiology and immunology at the UNC School of Medicine, Sallie Permar, MD, PhD, chair of the Department of Pediatrics at Weill Cornell Medicine, and Koen K.A. Van Rompay, DVM, PhD, leader of the Infectious Disease Unit at the California National Primate Research at the University of California, Davis. Co-first authors are Emma C. Milligan at the Children’s Research Institute in the UNC School of Medicine and Katherine Olstad at the California National Primate Research Center.

To evaluate SARS-CoV-2 infant vaccination, the researchers immunized two groups of eight infant rhesus macaques at the California National Primate Research Center at 2 months of age and again four weeks later. Each animal received one of two vaccine types: a preclinical version of the Moderna mRNA vaccine or a vaccine combining a protein developed by the Vaccine Research Center of the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health with a potent adjuvant formulation. Consisting of 3M’s molecular adjuvant 3M-052 formulated in a squalene emulsion by the Access to Advanced Health Institute (AAHI), the adjuvant formulation stimulates immune responses by engaging receptors on immune cells.

“Following up on our SARS-CoV-2 infant rhesus macaque study, we gave the animals a high-dose challenge with a SARS-CoV-2 variant one year later to assess durability of vaccine-induced immune responses and their efficacy,” Dr. De Paris said. “We found that both vaccines protected against lung disease, despite the fact that the challenge SARS-CoV-2 variants acquired numerous mutations in their spike protein that differed from the vaccine immunogen.”

Overall, the adjuvanted protein vaccine candidate maintained higher levels of neutralizing antibodies and provided superior protection compared to the mRNA vaccine, Dr. De Paris said. These data imply that these vaccines are safe and highly effective when given to young infant macaques. Furthermore, the results inform the optimization and development of SARS-CoV-2 vaccines in a way that may reduce the need for frequent boosters and protect special populations that don’t have fully developed immune systems, such as young children.

“With COVID-19, young infants are one of the most vulnerable pediatric populations. This fall, we are seeing a sharp rise in hospitalizations due to respiratory virus disease in infants as the result of a confluence of SARS-CoV-2, flu, and RSV circulation,” said Dr. Permar, who is also the Nancy C. Paduano Professor in Pediatrics at Weill Cornell Medicine and pediatrician-in-chief at NewYork-Presbyterian Komansky Children’s Hospital. “We should take every opportunity to provide safe and effective vaccine immunity to our youngest patients, including considering COVID-19 vaccination earlier than the currently recommended 6 months of age.”

“This study emphasizes the need to get human infants immunized against SARS-CoV-2 as much as possible, as the benefits are clear and long-lasting. It also highlights the value of animal models in infectious disease research,” Dr. Van Rompay said. “The lessons we learned and the resources and tools that were developed in the current study will be very valuable for future pandemic preparedness, to more effectively combat outbreaks with novel coronaviruses or other respiratory viruses in pediatric populations.”

This research was funded through grants from the National Institutes of Health (P01AI117915-06S1), (U54 CA260543), (P510D11107), (UM1 AI068618-15: HVTN/HPTN, CoVPN), (P30AI050410: UNC Center for AIDS Research), and (P30 CA016086: UNC-LCCC Flow Cytometry Core Facility).

Other authors are Caitlin A. Williams, Michael Mallory, Patricia Cano, Kaitlyn A. Cross, Jennifer E. Munt, Carolina Garrido, Lisa Lindesmith, Jennifer Watanabe, Jodie L. Usachenko, Lincoln Hopkins, Ramya Immareddy, Yashavanth Shaan Lakshmanappa, Sonny R. Elizaldi, Jamin W. Roh, Rebecca L. Sammak, JoAnn L. Yee, Savannah Herbek, Trover Scobey, Dieter Miehlke, Genevieve Fouda, Guido Ferrari, Hongmei Gao, Xiaoying Shen, Pamela A. Kozlowski, David Montefiori, Michael Hudgens, Darin K. Edwards, Andrea Carfi, Kizzmekia S. Corbett, Barney S. Graham, Christopher B. Fox, Mark Tomai, Smita S. Iyer, Ralph Baric, Rachel Reader, and Dirk P. Dittmer.

Since the beginning of the pandemic, the coronavirus has been constantly changing. The biggest leap seen in the evolution of SARS-CoV-2 to date was observed by researchers a year ago, when a variant was discovered that differed from the genome of the original virus by more than 50 mutations. First detected in a patient in South Africa in mid-November 2021, the variant later named Omicron BA.1 spread to 87 countries around the world within just a few weeks. By the end of December, it had replaced the previously dominant Delta variant worldwide.

Since then, speculations about the origin of this highly transmissible variant have centered around two main theories: Either the coronavirus jumped from a human to an animal where it evolved before infecting a human again as Omicron, or the virus survived in a person with a compromised immune system for a longer period of time and that’s where the mutations occurred. A new analysis of COVID-19 samples collected in Africa before the first detection of Omicron now casts doubt on both these hypotheses.

The analysis was carried out by an international research team led by Prof. Jan Felix Drexler, a scientist at the Institute of Virology at Charité and the German Center for Infection Research (DZIF). Other key partners in the European-African network included Stellenbosch University in South Africa and the Laboratory of Viral Hemorrhagic Fever (LFHB) in Benin. The scientists started by developing a special PCR test to specifically detect the Omicron variant BA.1. They then tested more than 13,000 respiratory samples from COVID-19 patients that had been taken in 22 African countries between mid-2021 and early 2022. In doing so, the research team found viruses with Omicron-specific mutations in 25 people from six different countries who contracted COVID-19 in August and September 2021 – two months before the variant was first detected in South Africa.

To learn more about Omicron’s origins, the researchers also decoded, or “sequenced,” the viral genome of some 670 samples. Such sequencing makes it possible to detect new mutations and identify novel viral lineages. The team discovered several viruses that showed varying degrees of similarity to Omicron, but they were not identical. “Our data show that Omicron had different ancestors that interacted with each other and circulated in Africa, sometimes concurrently, for months,” explains Prof. Drexler. “This suggests that the BA.1 Omicron variant evolved gradually, during which time the virus increasingly adapted to existing human immunity.” In addition, the PCR data led the researchers to conclude that although Omicron did not originate solely in South Africa, it first dominated infection rates there before spreading from south to north across the African continent within only a few weeks.

“This means Omicron’s sudden rise cannot be attributed to a jump from the animal kingdom or the emergence in a single immunocompromised person, although these two scenarios may have also played a role in the evolution of the virus,” says Prof. Drexler. “The fact that Omicron caught us by surprise is instead due to the diagnostic blind spot that exists in large parts of Africa, where presumably only a small fraction of SARS-CoV-2 infections are even recorded. Omicron’s gradual evolution was therefore simply overlooked. So it is important that we now significantly strengthen diagnostic surveillance systems on the African continent and in comparable regions of the Global South, while also facilitating global data sharing. Only good data can prevent policymakers from implementing potentially effective containment measures, such as travel restrictions, at the wrong time, which can end up causing more economic and social harm than good.”

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