Publisher Health

A new analysis describes how U.K. residents shifted the amount of time they spent on various activities over the course of the pandemic and whether they participated online or in-person. Lan Li of University College London, Centre for Digital Health in Emergencies (dPHE), U.K., and colleagues present these findings in the open-access journal PLOS ONE on July 13, 2022.
When the COVID-19 pandemic began, the U.K. joined many countries in introducing restrictions on people’s movement and social activities to mitigate viral spread. A growing body of research reveals how such restrictions have affected people’s lifestyles worldwide. However, it has been less clear how behavioral patterns of U.K. residents changed over time as different restrictions were implemented and lifted.
To help clarify, Li and colleagues conducted six online surveys of U.K. residents between April 2020 and July 2021 and were ultimately able to follow 203 people who responded to multiple surveys. The surveys included questions about 16 different types of activities respondents participated in during different phases of the pandemic, such as journaling, shopping, and getting active, and whether they participated online or in person.
Statistical analysis of the responses showed that the biggest changes in terms of amount of time spent — as well as the biggest changes in online versus in-person participation — occurred for cultural activities, spending time with others, and travelling. Changes were most pronounced in March to June 2020, corresponding with the first lockdown period, when participation in all 16 activities decreased. The biggest shift from in-person to online participation occurred from March to October 2020, which included the first lockdown followed by relaxation of restrictions.
On July 19, 2021, all restrictions were eliminated in the U.K. However, this analysis found, participation in cultural and group activities remained lower than before the pandemic. The majority of respondents also continued to participate in many activities online.
These findings could help U.K. policymakers understand the impact of their pandemic restrictions. In the future, the researchers plan to investigate how demographic factors, such as age and employment, may have affected the results, as well as long-term mental health implications of the lifestyle changes.
Prof. Patty Kostova, director of UCL dPHE and the lead of the study, adds: “This longitudinal research study illustrated citizens’ resilience throughout the stages of the pandemic.”
Lan Li adds: “This longitudinal study determines the frequency and way of people doing activities from Spring 2020 to Summer 2021 during different phases of the COVID-19 pandemic in the UK. The findings provide an invaluable insight into understanding how people in the UK changed their lifestyle, including what activities they do, and how they accessed those activities in light of the COVID-19 pandemic and related public health policy implemented to address the pandemic.”
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Most vaccines, from measles to Covid-19, require a series of multiple shots before the recipient is considered fully vaccinated. To make that easier to achieve, MIT researchers have developed microparticles that can be tuned to deliver theiir payload at different time points, which could be used to create “self-boosting” vaccines.
In a new study, the researchers describe how these particles degrade over time, and how they can be tuned to release their contents at different time points. The study also offers insights into how the contents can be protected from losing their stability as they wait to be released.
Using these particles, which resemble tiny coffee cups sealed with a lid, researchers could design vaccines that would need to be given just once, and would then “self-boost” at a specified point in the future. The particles can remain under the skin until the vaccine is released and then break down, just like resorbable sutures.
This type of vaccine delivery could be particularly useful for administering childhood vaccinations in regions where people don’t have frequent access to medical care, the researchers say.
“This is a platform that can be broadly applicable to all types of vaccines, including recombinant protein-based vaccines, DNA-based vaccines, even RNA-based vaccines,” says Ana Jaklenec, a research scientist at MIT’s Koch Institute for Integrative Cancer Research. “Understanding the process of how the vaccines are released, which is what we described in this paper, has allowed us to work on formulations that address some of the instability that could be induced over time.”
This approach could also be used to deliver a range of other therapeutics, including cancer drugs, hormone therapy, and biologic drugs, the researchers say.

Researchers at the Salk Institute and King Abdullah University of Science and Technology (KAUST) in Saudi Arabia have discovered a new underlying cause of Wiskott-Aldrich syndrome, a rare genetic disease that leads to bleeding and immune deficiencies in babies. Their findings, published in the journal Nature Communications on June 25, 2022, revolve around how cells cut and paste strands of RNA in a process called RNA splicing. The genetic mutations associated with Wiskott-Aldrich syndrome, they found, disrupt this process which, in turn, prevents numerous immune and anti-inflammatory proteins from being made correctly.
“This study not only suggests new targets for treating Wiskott-Aldrich syndrome with small molecule drugs, but also sheds new light on the basic biology of RNA splicing, an important and not fully understood process,” says co-corresponding author Juan Carlos Izpisua Belmonte, a professor in Salk’s Gene Expression Laboratory and holder of the Roger Guillemin Chair.
Babies with Wiskott-Aldrich syndrome begin to develop symptoms quickly after birth: itchy, scaly rashes, frequent bruises and nose bleeds are some of the first signs. Over time, they become prone to infections and are more likely than other children to develop autoimmune diseases and cancers. The only potential cure is a bone marrow transplant, which carries a host of complications and only works in some children.
Scientists have long known that Wiskott-Aldrich syndrome is caused by mutations in a gene on the X chromosome; the gene and the protein it encodes were named WASP after the syndrome. The WASP protein is found throughout cells in the blood and immune system, and one of its functions is to maintain these cells’ cytoskeletons, the microscopic networks of proteins that give cells their shape and organization. But changes to the cytoskeleton couldn’t explain all the symptoms.
Former Salk Postdoctoral Fellow Mo Li, now the head of KAUST’s Laboratory of Stem Cell and Regeneration, and Izpisua Belmonte wondered if WASP plays other roles — particularly in the nuclei of blood and immune cells, where genetic material is stored and processed.
To find out, they removed the WASP gene from stem cells and coaxed the cells to become macrophages or B cells, two types of immune cells impacted by the disease. They also collected cells from two patients with Wiskott-Aldrich syndrome and generated induced pluripotent stem cells (iPSCs) containing the disease-associated mutations in WASP. Then they compared the altered cells to normal macrophages and B cells.

When researchers working on the Human Genome Project completely mapped the genetic blueprint of humans in 2001, they were surprised to find only around 20,000 genes that produce proteins. Could it be that humans have only about twice as many genes as a common fly? Scientists had expected considerably more.
Now, researchers from 20 institutions worldwide bring together more than 7,200 unrecognized gene segments that potentially code for new proteins. For the first time, the study makes use of a new technology to find possible proteins in humans — looking in detail at the protein-producing machinery in cells. The new study suggests the gene discovery efforts of the Human Genome Project were just the beginning, and the research consortium aims to encourage the scientific community to integrate the data into the major human genome databases.
The study recently published story in Nature Biotechnology, was co-led by Dr. Jorge Ruiz- Orera from Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC) in Germany, Dr. Sebastiaan van Heesch from the Princess Máxima Center for pediatric oncology in the Netherlands, Dr. Jonathan Mudge from the European Molecular Biology Laboratory — European Bioinformatics Institute (EMBL-EBI) in the United Kingdom, and Dr. John Prensner from the Broad Institute of MIT and Harvard in the United States.
New gene sequences remained out of reach
In the past few years, thousands of frequently very small open reading frames (ORFs) have been discovered in the human genome. These are spans of DNA sequence that may contain instructions for building proteins. Several authors of the current study have previously found ORFs and described them in scientific journals: Van Heesch, together with MDC-Professors Norbert Hübner and Uwe Ohler described new mini-proteins in the human heart and reported on them in “Cell” in 2019; Prensner also published on ORFs in “Nature Biotechnology” in 2021. Yet none of these previously virtually unexplored segments were included afterwards in reference databases. Other sequences were reported in journals such as “Science” or “Nature Chemical Biology,” but remained largely out of reach for most members of the scientific community — despite evidence that they produce RNA molecules that subsequently bind to ribosomes, the cell’s protein factories.
Traditionally, protein-coding regions in genes have been identified by comparing DNA sequences from multiple species: the most important coding regions have been preserved during animal evolution. But this method has a drawback: coding regions that are relatively young, i.e., that arose during the evolution of primates, fall through the cracks and are therefore missing from the databases.

Researchers have warned the long-term effects of coronavirus will have a significant impact on the UK workforce for some time.
Of those who have been infected with Covid-19, 5.5 per cent of people will develop life-changing chronic illness, in particular heart and lung conditions. Others have also experienced long lasting symptoms, including shortness of breath, fatigue, fever, headaches, brain fog and other neurological problems.
A new collaborative study by the Universities of Portsmouth and Southampton, published in Applied Economics Letters, estimates that 80,000 people had left employment due to Long Covid by early March this year.
Donald Houston, Professor of Economic Geography at the University of Portsmouth and co-author of the paper, said: “Continued waves of coronavirus infections, which may go on for a number of years, will keep people off work while sick with Long Covid. Many will lose their jobs and some will remain out of the workforce for a long time or permanently.”
At the peak of the Omicron wave in February, 2.9 million people of working-age (7 per cent of the total) had experienced persistent Covid-19 symptoms for more than 12 weeks. This figure is expected to rise following the current wave of infections, given that vaccination only gives modest protection against Long Covid.
“The effects of this is what we can feel now in the economy,” said Dr Darja Reuschke, Associate Professor of Economic Geography at the University of Southampton and co-author of the paper.

Researchers at the Centre for Genomic Regulation (CRG) in Barcelona reveal that Srrm3 is a master regulator gene crucial for the development of photoreceptors, cells in the back of the retina which capture and process light, sending signals to the brain that enable vision. Knocking the gene out in zebrafish resulted in severe visual impairment.
The research found that, in vertebrates, Srrm3 works by regulating alternative splicing, a process that allows cells to make more than one type of protein from a single gene and is particularly prominent in neuronal cells. The misregulation of alternative splicing can have a devastating impact on human health, for example in cancer or neurological disorders.
Srrm3 was found to specifically regulate the splicing of microexons, tiny fragments of DNA that are just 3-27 letters long. Despite their small size, the regulation of microexons has been shown to play a critical role in protein and cellular function.
The researchers identified dozens of different microexons that are mainly present in photoreceptors but not in other neurons. A large proportion of these microexons affect the function of around 70 genes important for the development of a photoreceptor’s outer segment, the part of the cell that absorbs light. The findings are published in the Proceedings of the National Academy of Sciences.
The study reveals a new layer of cellular specialisation required for the unique cellular shape and function of retinal cells, one of the most complex and specialised cells in the human body. Because of this complexity, retinal cells depend on many unique genes for their development, any which of can have a disease-causing mutation and result in vision loss.
One of the most common causes of inherited vision loss is retinitis pigmentosa, a genetic disorder for which the molecular mechanisms involved are poorly understood. Between 40 to 50 percent of cases of retinitis pigmentosa have no explanation, meaning they carry mutations in genes yet to be identified. The authors of the study plan on carrying out future studies to assess whether Srrm3 or the microexons involved could explain some of these cases.
“The Srrm3 gene has neither been associated with the development of photoreceptor cells nor with the pathogenesis of retinal diseases before. We are already exploring the gene’s role in patients without a genetic diagnosis. If we find cases with mutations in this specific gene, or on any retinal microexons, it could lead to potential new therapeutic strategies to manage the condition,” says Ludovica Ciampi, PhD student at the CRG and first author of the study.
According to ICREA Research Professor Manuel Irimia, understanding microexon regulation in specific cell types is key for identifying new therapeutic targets. “Photoreceptors have unique properties thanks to the regulation of alternative splicing and microexons. This helps make the cell more specialised but also perhaps more susceptible to genetic diseases. Modulating splicing activity is now possible, so the more intricate biology we uncover, the more likely we are to find therapeutic targets to treat retinal diseases,” concludes Dr. Irimia.
The study is a result of a collaboration between ICREA Research Professors Luis Serrano and Manuel Irimia at the CRG, as well as the Telethon Institute of Genetics and Medicine of Naples, Italy and the University of Zurich in Switzerland. The work is funded by the European Research Council, Spanish Ministry of Science and Innovation and the Generalitat de Catalunya.
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Individuals with no dementia risk factors, such as smoking, diabetes or hearing loss, have similar brain health as people who are 10 to 20 years younger than them, according to a new Baycrest study. The study found that a single dementia risk factor could reduce cognition by the equivalent of up to three years of aging.
“Our results suggest lifestyle factors may be more important than age in determining someone’s level of cognitive functioning. This is great news, since there’s a lot you can do to modify these factors, such as managing diabetes, addressing hearing loss, and getting the support you need to quit smoking,” says Dr. Annalise LaPlume, Postdoctoral Fellow at Baycrest’s Rotman Research Institute (RRI) and the study’s lead author.
The study is one of the first to look at lifestyle risk factors for dementia across the entire lifespan.
“While most studies of this nature look at mid- and older-adulthood, we also included data from participants as young as 18, and we found that risk factors had a negative impact on cognitive performance across all ages. This is crucial as it means risk factors can and should be addressed as early as possible,” says Dr. Nicole Anderson, Senior Scientist at the RRI, Associate Scientific Director of Baycrest’s Kimel Family Centre for Brain Health and Wellness, and senior author of this study.
The study, published today in the journal Alzheimer’s & Dementia: Diagnosis, Assessment, and Disease Monitoring, a journal of the Alzheimer’s Association, included data from 22,117 people aged 18 to 89 who completed the Cogniciti Brain Health Assessment, developed by Baycrest. Participants took the test in their own homes by going to the Cogniciti website (https://cogniciti.com/). The test takes around 20 minutes to complete and consists of a background questionnaire and four cognitive tasks.
The researchers looked at participants’ performance on memory and attention tests, and how this was impacted by eight modifiable risk factors for dementia: low education (less than a high school diploma), hearing loss, traumatic brain injury, alcohol or substance abuse, hypertension, smoking (currently or in the past four years), diabetes and depression.
Each factor led to a decrease in cognitive performance by as much as three years of aging, with each additional factor contributing the same amount of decline. For example, having three risk factors could lead to a decrease in cognitive performance equivalent to as much as nine years of aging. The effects of the risk factors increased with age, as did the number of risk factors people had.
“All in all, our research shows that you have the power to decrease your risk of cognitive decline and dementia,” says Dr. LaPlume. “Start addressing any risk factors you have now, whether you’re 18 or 90, and you’ll support your brain health to help yourself age fearlessly.”
This research was supported by the Alzheimer Society of Canada, and the Natural Sciences and Engineering Research Council of Canada.
With additional funding, the researchers could look further into the differences between normal agers and “super agers” — people who have identical cognitive performance to those several decades younger than them.
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Researchers have developed a noninvasive method to identify a potential cause of hypertension with a drastic reduction in radiation exposure, a study shows.
Around 10-15% cases of hypertension, or high blood pressure, are believed to be caused by excessive production of the hormone aldosterone, which affects the body’s salt-water balance. This can be due to an adrenal adenoma, a tumor that causes irregular aldosterone production.
The current testing for an adrenal adenoma is invasive, sampling the blood leaving the adrenal gland. For years, radiologists had used an iodine agent for measuring cholesterol uptake, the precursor to aldosterone, as a noninvasive alternative. This test was complicated by requiring patients to take steroids for a week prior to imaging and exposed them to high amounts of radiation.
A Michigan Medicine team led by Allen Brooks, Ph.D., an assistant research scientist, developed a new reagent that replaced the iodine with fluorine-18, a radioisotope commonly used in PET scans. They found that the method resulted in significantly less radiation exposure and could allow screening for hypertension-linked aldosterone adenomas. The paper is published in the Journal of Nuclear Medicine.
“This agent gives us a noninvasive way to find out if aldosterone is being produced abnormally, one that significantly limits the potential harm to our patients through decreased exposure to radiation and limiting of steroid use,” said Benjamin Viglianti, M.D., Ph.D., senior author of the paper and associate professor of radiology at University of Michigan Medical School.
“Adrenal adenoma, if identified, can be removed surgically, which can cure people of their hypertension. This can help people with the disease by being deployed as a screening tool.”
The original iodine agent used for imaging patients with adrenal aldosteronism was developed at University of Michigan in the 1970s. It was discontinued in the late 2000s due to federal regulations.
Researchers tested the fluorine-18 reagent in nine healthy subjects, finding it safe to use and effective at detecting stimulated hormone production through increased cholesterol uptake. The next step, they say, is to conduct a larger clinical trial analyzing patients with hypertension caused by excessive aldosterone production.
However, given cholesterol is found in other diseases, particularly the cardiovascular system, there is hope that this agent could have broader clinical applications.
“This work is a modern improvement of one of the imaging agents developed 50 years ago by Raymond Counsell, William Beierwaltes and a team here at the university,” Brooks said. “The continued close collaboration between physician scientists and research chemists have enabled the translation of new diagnostic agents to improve our understanding of disease and hopefully improve patient outcomes.”
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Materials provided by Michigan Medicine – University of Michigan. Original written by Noah Fromson. Note: Content may be edited for style and length.

The incidence of inflammatory bowel disease (IBD) — an intractable disease characterized by chronic inflammation of the gastrointestinal (GI) tract — has increased significantly in Japan. Chronic inflammation associated with IBD often leads to the development of cancer in the colorectal region.
For patients who have visible or low-grade dysplasia (abnormal cell growth which may not be malignant), endoscopic resection, a technique used to remove cancerous lesions, and colonoscopy are usually employed. However, for patients with a high rate of neoplasia (severe cell growth which is malignant), a total proctocolectomy, i.e., complete removal of the colon and rectum is the standard treatment, which is highly detrimental to their quality of lives.
Hence, identifying the severity and grade of the neoplasia during diagnosis is essential before proceeding with treatment. Unfortunately, the presence of inflammation in the colorectal region makes it difficult for endoscopists to classify the type of IBD neoplasia (IBDN). This leaves biopsy as the only viable option, which is associated with high risks and often leads to inaccurate diagnoses, highlighting the need for a simpler diagnostic technique with high accuracy.
To this end, a team of researchers from Okayama University Graduate School of Medicine, including Assistant Professor Hideaki Kinugasa, Doctor Shumpei Yamamoto, Professor Sakiko Hiraoka, and Professor Yoshiro Kawahara conducted a pilot study to develop an artificial intelligence (AI) system that classifies IBDN lesions accurately. In addition, as part of this study, which was published in Gastroenterology and Hepatology first on May 29, 2022, they compared the diagnostic ability of endoscopists with that of the new AI system.
First, the team used a conventional neural network (CNN) — a type of neural network used for the analysis of visual imagery — known as Efficient-Net-B3, to develop the AI-system’s prototype. They trained this system using 862 endoscopic images of 99 IBDN lesions from patients with IBD derived from two hospitals between 2003 and 2021, and validated it using a deep-learning framework. Next, they asked endoscopists with over 8 years of experience in gastrointestinal endoscopy to analyse the images and classify the lesions into two types based on the need for proctocolectomy, and compared their classification to that of the AI-system.
As a result of data-augmentation, the AI-system generated approximately six million images from the original data set, which were then used to analyse clinicopathological characteristics of patients and the lesions.
Based on these analyses, the team found that most patients had ulcerative colitis — a type of IBD, with more than 95% of them presenting pancolitis and left-sided colitis. Moreover, the AI-system displayed an image-based diagnostic ability with 64.5% sensitivity, 89.5% specificity, and 80.6% accuracy, and a lesion-based diagnostic ability with 74.4% sensitivity, 85% specificity, and 80.8% accuracy. What’s interesting is that the correct diagnosis rate of the AI system was 79.0, while that of endoscopists was 77.8.
What do these findings imply? “Our AI-system prototype proved successful in determining the degree of malignancy of IBD-tumors and is valuable enough to contribute to clinical practice in the coming years,” said Assistant Prof. Kinugasa in response.
The team also highlighted that combining this AI-based automatic diagnosis of neoplastic lesions with existing endoscopic diagnostic techniques might provide superior diagnostic results in real-time.
While discussing the system’s additional advantages and real-life applications, Assistant Prof. Kinugasa added, “Using this AI-system can ensure that endoscopists do not misdiagnose IBD neoplastic lesions, patients receive prompt treatment, and more appropriate treatment strategies are developed and applied for early as well as advanced stages of IBD.”
Here’s hoping that this AI-system revolutionizes the diagnosis of IBD-associated neoplasia and improves the lives of patients with IBD in Japan and the rest of the world!

Medicinal microrobots could help physicians better treat and prevent diseases. But most of these devices are made with synthetic materials that trigger immune responses in vivo. Now, for the first time, researchers reporting in ACS Central Science have used lasers to precisely control neutrophils — a type of white blood cell — as a natural, biocompatible microrobot in living fish. The “neutrobots” performed multiple tasks, showing they could someday deliver drugs to precise locations in the body.
Microrobots currently in development for medical applications would require injections or the consumption of capsules to get them inside an animal or person. But researchers have found that these microscopic objects often trigger immune reactions in small animals, resulting in the removal of microrobots from the body before they can perform their jobs. Using cells already present in the body, such as neutrophils, could be a less invasive alternative for drug delivery that wouldn’t set off the immune system. These white blood cells already naturally pick up nanoparticles and dead red blood cells and can migrate through blood vessels into adjacent tissues, so they are good candidates for becoming microrobots. Previously, researchers have guided neutrophils with lasers in lab dishes, moving them around as “neutrobots.” However, information on whether this approach will work in living animals was lacking. So, Xianchuang Zheng, Baojun Li and colleagues wanted to demonstrate the feasibility of light-driven neutrobots in animals using live zebrafish.
The researchers manipulated and maneuvered neutrophils in zebrafish tails, using focused laser beams as remote optical tweezers. The light-driven microrobot could be moved up to a velocity of 1.3 µm/s, which is three times faster than a neutrophil naturally moves. In their experiments, the researchers used the optical tweezers to precisely and actively control the functions that neutrophils conduct as part of the immune system. For instance, a neutrobot was moved through a blood vessel wall into the surrounding tissue. Another one picked up and transported a plastic nanoparticle, showing its potential for carrying medicine. And when a neutrobot was pushed toward red blood cell debris, it engulfed the pieces. Surprisingly, at the same time, a different neutrophil, which wasn’t controlled by a laser, tried to naturally remove the cellular debris. Because they successfully controlled neutrobots in vivo, the researchers say this study advances the possibilities for targeted drug delivery and precise treatment of diseases.
The authors acknowledge funding from the National Natural Science Foundation of China, the Basic and Applied Basic Research Foundation of Guangdong Province, and the Science and Technology Program of Guangzhou.
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