Pushing for a higher speed isn’t just for athletes. Researchers, too, can achieve such feats with their discoveries. This is the case for Jinyang Liang, Professor at the Institut national de la recherche scientifique (INRS), and his team, whose research results have recently been published in Nature Communications.
The group based at INRS’ Énergie Matériaux Télécommunications Research Centre has developed a new ultrafast camera system that can capture up to 156.3 trillion frames per second with astonishing precision. For the first time, 2D optical imaging of ultrafast demagnetization in a single shot is possible. This new device called SCARF (for swept-coded aperture real-time femtophotography) can capture transient absorption in a semiconductor and ultrafast demagnetization of a metal alloy. This new method will help push forward the frontiers of knowledge in a wide range of fields, including modern physics, biology, chemistry, materials science, and engineering.
Improving on past advances
Professor Liang is known around the world as a pioneer of ultrafast imaging. Already, in 2018, he was the principal developer of a major breakthrough in the field, which laid the groundwork for the development of SCARF.
Until now, ultrafast camera systems have mainly used an approach involving sequentially capturing frames one by one. They would acquire data through brief, repeated measurements, then put everything together to create a movie that reconstructed the observed movement.
“However, this approach can only be applied to inert samples or to phenomena that happen the exact same way each time. Fragile samples, not to mention non-repeatable phenomena or phenomena with ultrafast speeds, cannot be observed with this method.”
Professor Jinyang Liang, expert in ultra-fast and biophotonic imaging said, “For example, phenomena such as femtosecond laser ablation, shock-wave interaction with living cells, and optical chaos cannot be studied this way.”
The first tool developed by Professor Liang helped fill this gap. The T-CUP (Trillion-frame-per-second compressed ultrafast photography) system was based on passive femtosecond imaging capable of acquiring ten trillion (1013) frames per second. This was a major first step towards ultrafast, single-shot real-time imaging.

Yet challenges still remained.
“Many systems based on compressed ultrafast photography have to cope with degraded data quality and have to trade the sequence depth of the field of view. These limitations are attributable to the operating principle, which requires simultaneously shearing the scene and the coded aperture.”
Miguel Marquez, postdoctoral fellow and co-first author of the study said, “SCARF overcomes these challenges. Its imaging modality enables ultrafast sweeping of a static coded aperture while not shearing the ultrafast phenomenon. This provides full-sequence encoding rates of up to 156.3 THz to individual pixels on a camera with a charge-coupled device (CCD). These results can be obtained in a single shot at tunable frame rates and spatial scales in both reflection and transmission modes.”
A range of applications
SCARF makes it possible to observe unique phenomena that are ultrafast, non-repeatable, or difficult to reproduce, such as shock wave mechanics in living cells or matter. These advances could potentially be used to develop better pharmaceutics and medical treatments.
What’s more, SCARF promises very appealing economic spin-offs. Two companies, Axis Photonique and Few-Cycle, are already working with Professor Liang’s team to produce a marketable version of their patent-pending discovery. This represents a great opportunity for Quebec to strengthen its already enviable position as a leader in photonics.
The work was carried out in the Advanced Laser Light Source (ALLS) Laboratory in collaboration with Professor François Légaré, Director of the Énergie Matériaux Télécommunications Research Centre, and international colleagues Michel Hehn, Stéphane Mangin and Grégory Malinowski of the Institut Jean Lamour at the Université de Lorraine (France) and Zhengyan Li of Huazhong University of Science and Technology (China).
This research was funded by the Natural Sciences and Engineering Research Council of Canada, the Canada Research Chairs Program, the Canada Foundation for Innovation, the Ministère de l’Économie et de l’Innovation du Québec, the Canadian Cancer Society, the Government of Canada’s New Frontiers in Research Fund, as well as the Fonds de recherche du Québec-Nature et Technologies and the Fonds de recherche du Québec -Santé.

A team of researchers from the Case Western Reserve University School of Medicine has provided fresh insight into the dangers some common household chemicals pose to brain health. They suggest that chemicals found in a wide range of items, from furniture to hair products, may be linked to neurological conditions like multiple sclerosis and autism spectrum disorders.
Neurological problems impact millions of people, but only a fraction of cases can be attributed to genetics alone, indicating that unknown environmental factors are important contributors.
The new study published today in the journal Nature Neuroscience, discovered that some common home chemicals specifically affect the brain’s oligodendrocytes, a specialized cell type that generates the protective insulation around nerve cells.
“Loss of oligodendrocytes underlies multiple sclerosis and other neurological diseases,” said the study’s principal investigator, Paul Tesar, the Dr. Donald and Ruth Weber Goodman Professor of Innovative Therapeutics and director of the Institute for Glial Sciences at the School of Medicine. “We now show that specific chemicals in consumer products can directly harm oligodendrocytes, representing a previously unrecognized risk factor for neurological disease.”
On the premise that not enough thorough research has been done on the impact of chemicals on brain health, the researchers analyzed over 1,800 chemicals that may be exposed to humans. They identified chemicals that selectively damaged oligodendrocytes belong to two classes: organophosphate flame retardants and quaternary ammonium compounds. Since quaternary ammonium compounds are present in many personal-care products and disinfectants, which are being used more frequently since the COVID-19 pandemic began, humans are regularly exposed to these chemicals. And many electronics and furniture include organophosphate flame retardants.
The researchers used cellular and organoid systems in the laboratory to show that quaternary ammonium compounds cause oligodendrocytes to die, while organophosphate flame retardants prevented the maturation of oligodendrocytes.
They demonstrated how the same chemicals damage oligodendrocytes in the developing brains of mice. The researchers also linked exposure to one of the chemicals to poor neurological outcomes in children nationally.

“We found that oligodendrocytes — but not other brain cells — are surprisingly vulnerable to quaternary ammonium compounds and organophosphate flame retardants,” said Erin Cohn, lead author and graduate student in the School of Medicine’s Medical Scientist Training Program. “Understanding human exposure to these chemicals may help explain a missing link in how some neurological diseases arise.”
The association between human exposure to these chemicals and effects on brain health requires further investigation, the experts warned. Future research must track the chemical levels in the brains of adults and children to determine the amount and length of exposure needed to cause or worsen disease.
“Our findings suggest that more comprehensive scrutiny of the impacts of these common household chemicals on brain health is necessary,” Tesar said. “We hope our work will contribute to informed decisions regarding regulatory measures or behavioral interventions to minimize chemical exposure and protect human health.”
Additional contributing researchers from Case Western Reserve School of Medicine and from the U.S. Environmental Protection Agency included Benjamin Clayton, Mayur Madhavan, Kristin Lee, Sara Yacoub, Yuriy Fedorov, Marissa Scavuzzo, Katie Paul Friedman and Timothy Shafer.
The research was supported by grants from the National Institutes of Health, National Multiple Sclerosis Society, Howard Hughes Medical Institute and New York Stem Cell Foundation, and philanthropic support by sTF5 Care and the Long, Walter, Peterson, Goodman and Geller families.

Researchers at the Francis Crick Institute have shed light on the proteins controlling the development of ovaries in mice before and after birth. This could lead to a better understanding of how female infertility develops.
Following their research identifying the gene responsible for initiating the development of ovaries in the mouse embryo, the scientists aimed to understand which genes maintain the functions of the ovaries, including producing eggs, after birth.
Previous experiments have shown that removing a gene called Foxl2 in female (XX) mice at different points in development has different effects depending on the timing. If removed from embryos, ovaries become abnormal and the adult mice are infertile. If removed from adult mice, their ovaries begin to resemble testes1.
In research published today in Science Advances, the team found that, while FOXL2 does play a role during embryonic development, it has the most impact after birth, where the protein regulates the activity of many more genes, including some involved in functions critical for the ovary such as egg development.
FOXL2 is a type of protein that physically sits on top of specific regions in DNA (‘enhancers’) and influences whether and how other (target) genes are read.
The researchers used a technique called chromatin proteomics to ‘fish out’ all of the other proteins that interact with FOXL2 when it is bound to DNA. They found that the number of protein interactions drastically increased in ovaries after birth compared to during embryonic development.
Among many others, they identified a protein called USP7, which binds to FOXL2 when it interacts with its DNA targets. Until now, researchers weren’t aware of USP7 and FOXL2 interaction or what role USP7 was playing in ovary development.

When the researchers removed the Usp7 gene from female mice, they found that the mice couldn’t develop ovaries beyond puberty, so were infertile. The team believe USP7 might be needed to stabilise FOXL2 on top of DNA.
FOXL2 and USP7 share some common roles in humans. People lacking one copy of the FOXL2 gene can start making eggs but don’t develop full ovaries, so have problems with fertility. USP7 mutations can also lead to infertility in people, as well as neurodevelopmental disorders.
Genetic testing is key to diagnose problems with sexual development, so researchers hope to find the major genetic causes of infertility and consider how gene editing techniques could help with future treatments.
Robin Lovell-Badge, Group Leader of the Stem Cell Biology and Developmental Genetics Laboratory at the Crick, said: “In our research, we’ve come closer to answers for two major questions regarding development — what drives ovary development, and how the function of the ovary is maintained. We’ve found that FOXL2 has very different roles throughout development, and identified another crucial protein, USP7.
“The genetic factors underlying female development haven’t been as well studied as male development, because many female developmental pathways happen at the same time rather than in an easy-to-follow sequence. Infertility is a big problem worldwide, so shedding light on the key genes and proteins responsible at each stage is vital.”
Roberta Migale, Postdoctoral Fellow at the Crick and first and co-senior author on the study, said: “This is the first time we’ve been able to use these approaches to see the interactions that FOXL2, a factor critical for female fertility, establishes with other proteins whilst they are bound to DNA in mouse ovaries. Factors that actively bind to the DNA are more likely to have an impact on the regulation of genes important for the development and function of the ovary. We’ve identified USP7 through this method and the hope is that many more proteins responsible for ovary development can be found using our approach.”
A Crick-wide effort, Robin and Roberta worked with several specialist teams, including the Genetic Modification Service, Bioinformatics and Biostatistics, Proteomics, Flow Cytometry, Experimental Histopathology, Light Microscopy, and the Biological Research Facility.
The researchers will continue to study the role of the USP7 protein in sexual development.

The prevalence of overweight and obesity in the group of 3- and 4-year-olds in Sweden has decreased after the pandemic. The increase during the pandemic thus appears to have been temporary. These are the findings of a study conducted at the University of Gothenburg and Uppsala University.
The study, published in the journal JAMA Pediatrics, is based on data on 50,833 children aged 3-5 years. Healthcare data about the children are sourced from regular check-ups at pediatric healthcare centers, BVC. Participating regions were Dalarna, Jönköping County and Sörmland.
The researchers have previously been able to demonstrate increased overweight and obesity during the pandemic among 3- and 4-year-olds in Sweden. According to the current study, today’s 3- and 4-year-olds are at about the same levels as 3- and 4-year-olds before the pandemic. The group of 5-year-olds has not had similar weight changes.
The studied time periods are before the COVID-19 pandemic (up to and including April 2020), early pandemic (May 2020-May 2021), late pandemic (June 2021-March 2022) and post-pandemic (from April 2022).
Increasing and decreasing BMI
In the group of 3-year-olds, the proportion with obesity increased from 2.4 percent before the pandemic to 3.4 percent during the early pandemic, and then decreased to 2.3 percent during the late pandemic. After the pandemic, the proportion of 3-year-olds with obesity was 2.6 percent.
The development of overweight in 3-year-olds follows the same pattern. The proportion of overweight children went from 11.6 to 13.2 percent, followed by a decline to 11.3 during the late pandemic. After the pandemic, the proportion of overweight 3-year-olds was 11.9 percent.

In the group of 4-year-olds, BMI (body mass index) also changed significantly. The obesity rate increased from 2.6 percent before the pandemic to 3.7 percent during the early pandemic, then declined to 3.1 percent during the late pandemic and to 2.5 percent after the pandemic.
The proportion of overweight in the group of 4-year-olds rose from 10.3 percent before the pandemic to 11.7 percent during the early pandemic, and then decreased to 9.9 percent during the late pandemic and after the pandemic.
Unhealthy weight can regress
Globally, weight gain in young children during the pandemic has been explained by changes in dietary habits and reduced physical activity as a result of social restrictions and closed preschools. In Sweden, preschools were up and running, but the weight trend remained the same as in other countries, which, according to the researchers, may be due to the fact that many children missed out on nutritious food and regular outdoor activity.
The fact that the weight trend has now been broken is also of great importance in the long term. Childhood obesity increases the likelihood of continued obesity in adulthood, with an increased risk of cardiovascular disease, cancer, and lower quality of life.
Responsible for the study are Anton Holmgren, Pediatrician at Halland Hospital, who conducts research in pediatrics at Sahlgrenska Academy, University of Gothenburg, and Anna Fäldt, Researcher at Uppsala University within pediatric health and parenthood.
“The fact that the proportion of overweight and obese 3- and 4-year-olds has decreased indicates that the weight gains were related to the pandemic, and that an unhealthy weight status can be reversed. This also applies at the individual level, a significant proportion of the children where we had repeated measurements dropped to a lower BMI class after the pandemic,” says Anton Holmgren.

A team of scientists led by Prof Guillermo Bazan from NUS Institute for Functional Intelligent Materials (I-FIM) has developed a novel antibiotic named COE-PNH2 that is capable of combating hard-to-treat mycobacterial lung infections. Such infections, which are notorious for resisting conventional treatment, pose a serious health threat, especially to the elderly and those with underlying conditions. COE-PNH2 disrupts bacterial defences, eliminates the bacteria more thoroughly, and exhibits low frequency of resistance, offering potentially safer and more effective treatment.
Antibiotic resistance is casting an increasingly long shadow over today’s healthcare landscape, undermining the ability to combat infections that were once readily manageable. Among these, nontuberculous mycobacteria infections are notorious for their stubborn resistance to conventional medication and their penchant for afflicting those with existing lung diseases such as bronchiectasis, chronic obstructive pulmonary disease and cystic fibrosis. The elderly and those with underlying conditions are particularly vulnerable, with the incidence of infection doubling in these demographics and contributing to a significant rise in public health costs.
Researchers from the Institute for Functional Intelligent Materials (I-FIM) at the National University of Singapore (NUS) have innovated a conjugated oligoelectrolyte (COE)-based compound that has the potential to turn the tide on the disease. Called COE-PNH2, this novel agent not only demonstrates high efficacy against Mycobacterium abscessus (Mab), one of the most prevalent mycobacteria species, but also shows a blend of potency and safety that could reshape the treatment paradigm for persistent lung infections.
The researchers’ interdisciplinary study, partly funded by NUS Yong Loo Lin School of Medicine’s (NUS Medicine) Kickstart Initiative, was published in scientific journal Science Translational Medicine on 21 February 2024. Kickstart Initiative is a translational medicine programme aimed at bringing NUS Medicine’s promising biomedical research projects to market.
This study is led by Professor Guillermo Bazan, a principal investigator at I-FIM, and Department of Pharmacology at NUS Medicine, in collaboration with Associate Professor Kevin Pethe, Provost’s Chair in Infectious Disease, Nanyang Technological University, Singapore’s Lee Kong Chian School of Medicine (LKCMedicine).
A new frontier in antibiotic therapy
Individuals afflicted with nontuberculous mycobacteria infections often stumble upon many hurdles when it comes to treatment. Regimens are arduous, cure rates are unsatisfactory, and side effects are difficult to bear. Even when the infection appears to be successfully reined in, the threat of relapse is not off the table.

Conventional antibiotics often falter — the bacteria’s uncharacteristically thick and impermeable cell envelope, as well as a shrewd evolutionary sleight of hand, have made the pathogens especially resistant towards common treatments. Additionally, the ability of the bacteria to enter a dormant state — forming what is referred to as persisters, poses a daunting challenge in antibiotic therapy, as these persisters often survive traditional treatments only to cause relapse.
Here is where COEs shake things up. A class of antimicrobial compounds with a modular molecular framework, COEs can be engineered into a panoply of therapeutic agents to fight a broad spectrum of infections. “COEs represent a fundamentally different approach to antibiotic design,” noted Prof Bazan, a corresponding author of the study. “Their unique structure, which facilitates the spontaneous interaction with lipid bilayers, allows them to breach the bacterial defences that so often thwart existing drugs.”
COE-PNH2, the molecule designed and crafted by the I-FIM researchers, is optimised to target Mab, employing a dual mechanism that disrupts the bacterial membrane and obstructs vital bioenergetic pathways — a one-two punch that leaves the bacteria with little room to hide. In particular, the molecule attacks both replicating and dormant forms of Mab, exhibiting robust bactericidal activity that leads to a more comprehensive eradication of the bacteria, leaving no refuge for resistance to crop up while reducing the likelihood of relapse.
“Resistance development is often the Achilles’ heel of new antibiotics,” said Prof Bazan. “COE-PNH2 exhibited a low frequency of resistance in our study, which suggests that it may remain effective longer than existing treatments, providing patients with a more durable solution.”
Safety is also a cornerstone of the new antibiotic. It demonstrated low toxicity in mammalian cells and did not induce the destruction of red blood cells (haemolysis) at concentrations far exceeding those required for antibacterial activity. This noncytotoxic nature underscores COE-PNH2’s potential as a therapeutic agent with a wide margin of safety.
This safety is also reinforced through in vivo studies. When tested in a preclinical model of acute lung infection, the novel compound was well-tolerated, while its therapeutic effect was pronounced, achieving a substantial reduction in bacterial load without the emergence of resistant strains.

Navigating the path to clinical use
“As COE is a relatively new antibiotic platform, the subsequent phase of this study requires us to understand the mechanism of action of the drug in greater detail,” highlighted corresponding author of the study Assoc Prof Pethe, noting that moving the novel compound along its journey from petri dish and in vivo studies to patient is very much a work in progress.
For starters, unravelling the molecular interaction between COE-PNH2 and mammalian and bacterial cell membranes is crucial. Furthermore, there is a need to dissect various mechanisms through which the compound functions. For instance, it is unclear to the researchers whether the hydrogen-bonding moieties of the compound contribute to its enhanced potency against nutrient-starved persisters. Uncovering the precise manner in which COE-PNH2 compromises these resilient forms could shine new light on more effective strategies for combating dormant bacterial strains.
Intriguingly, the researchers have also discovered the presence of intracellular vesicles in Mab treated with COE-PNH2. Are these vesicles by-products of disrupted bioenergetics, or do they form as a result of physical interactions between the compound and the membrane lipids? The answers may provide vital insights into how COE-PNH2 exerts its antimicrobial action and inform the development of interventions for other hard-to-treat pathogens.
“Mycobacterium abscessus infections are notoriously difficult to treat as the organism is resistant to multiple classes of antibiotics, hence a new class of antibiotics will add to our armamentarium to fight the infection,” said Dr Catherine Ong, Senior Consultant at the Division of Infectious Diseases, Department of Medicine, National University Hospital.
The combined efforts by researchers at I-FIM, NUS Medicine, and LKCMedicine is one step in the right direction where a range of microbial maladies can be dealt with by harnessing the therapeutic potential of COEs.

The famous work ethic of honey bees might spell disaster for these busy crop pollinators as the climate warms, new research indicates.
Flying shortens the lives of bees, and worker honey bees will fly to find flowers whenever the weather is right, regardless of how much honey is already in the hive. Using climate and bee population models, researchers found that increasingly long autumns with good flying weather for bees raises the likelihood of colony collapse in the spring.
The study, published in Scientific Reports, focused on the Pacific Northwest but holds implications for hives across the U.S. The researchers also modeled a promising mitigation: putting colonies into indoor cold storage, so honey bees will cluster in their hive before too many workers wear out.
“This is a case where a small amount of warming, even in the near future, will make a big impact on honey bees,” said lead author Kirti Rajagopalan, a Washington State University climate researcher. “It’s not like this is something that can be expected 80 years from now. It is a more immediate impact that needs to be planned for.”
For this study, researchers ran simulations through a honey bee population dynamics model using climate projections for 2050 and the end of the century at 2100. They found that honey bee colonies that spend the winter outside in many areas of the Pacific Northwest would likely experience spring colony collapses in both the near- and long-term scenarios. This also occurred under a simulation where climate change continued as it is progressing now and one where greenhouse gas emissions were reduced in the near future.
Worker honey bees will forage for food whenever temperatures rise above about 50 degrees Fahrenheit. When it gets colder, they cluster in the hive, huddling with other bees, eating honey reserves and shivering, which helps keep the bees warm. In the spring, the adult worker bees start flying again. That means they also start dying. If too many older worker bees die before their replacements emerge ready to forage, the whole colony can collapse. Scientists have estimated this happens when there are fewer than 5,000 to 9,000 adult bees in the hive.
This study found that colonies wintering outside in colder areas like Omak in the far north of Washington state might still do all right under climate change. But for honey bee colonies in many other places, like Richland, Washington near the border of Oregon, staying outside in the winter would mean the spring hive population would plummet to fewer than 9,000 adults by 2050 and less than 5,000 by the end of the century.

The authors note that the simulations just looked at seasonal factors like temperature, wind and the amount of daylight, making them fairly conservative models.
“Our simulations are showing that even if there is no nutritional stress, no pathogens, no pesticides — just the conditions in fall and winter are enough to compromise the age structure of a colony. So when the hive comes out of winter, the bees are dying faster than they’re being born,” said co-author Gloria DeGrandi-Hoffman, a research leader at the U.S. Department of Agriculture’s Carl Hayden Bee Research Center.
The researchers also simulated a potential mitigation, placing honey bee hive boxes in cold storage so the bees start to cluster earlier and save workers. For instance, in the Richland scenarios, by the end of the century, having bees in cold storage from October to April would boost the spring hive population to over 15,000 compared to around 5,000 to 8,000 if they were kept outside.
A relatively new practice, cold storage is gaining popularity among commercial beekeepers to help manage bee health and for the logistics involved in moving hives to California to pollinate almond trees in February, an event that draws more than two million hives from across the country.
“A lot of beekeepers are already practicing this management technique of storing bees indoors because it has a lot of immediate potential to help in a number of ways,” said co-author Brandon Hopkins, a WSU entomologist. “These findings demonstrate that there are additional benefits to this practice for the survival of colonies in a changing climate.”
This research received support from the Washington Department of Agriculture’s Specialty Crop Block Grant.

Humans pass on more viruses to domestic and wild animals than we catch from them, according to a major new analysis of viral genomes by UCL researchers.
For the new paper published in Nature Ecology & Evolution, the team analysed all publicly available viral genome sequences, to reconstruct where viruses have jumped from one host to infect another vertebrate species.
Most emerging and re-emerging infectious diseases are caused by viruses circulating in animals. When these viruses cross over from animals into humans, a process known as zoonosis, they can cause disease outbreaks, epidemics and pandemics such as Ebola, flu or Covid-19. Given the enormous impact of zoonotic diseases on public health, humans have generally been considered as a sink for viruses rather than a source, with human-to-animal transmission of viruses receiving far less attention.
For the study, the research team developed and applied methodological tools to analyse the nearly 12 million viral genomes that have been deposited on public databases to date. Leveraging this data, they reconstructed the evolutionary histories and past host jumps of viruses across 32 viral families, and looked for which parts of the viral genomes acquired mutations during host jumps.
The scientists found that roughly twice as many host jumps were inferred to be from humans to other animals (known as anthroponosis) rather than the other way round. This pattern was consistent throughout most viral families considered. Additionally, they found even more animal-to-animal host jumps, that did not involve humans.
The team’s work highlights the high and largely underappreciated fact that human viruses frequently spread from humans into wild and domestic animals.
Co-author Professor Francois Balloux (UCL Genetics Institute) said: “We should consider humans just as one node in a vast network of hosts endlessly exchanging pathogens, rather than a sink for zoonotic bugs.

“By surveying and monitoring transmission of viruses between animals and humans, in either direction, we can better understand viral evolution and hopefully be more prepared for future outbreaks and epidemics of novel illnesses, while also aiding conservation efforts.”
The findings also show that, on average, viral host jumps are associated with an increase in genetic changes, or mutations in viruses, relative to their continued evolution alongside just one host animal, reflecting how viruses must adapt to better exploit their new hosts.
Further, viruses that already infect many different animals show weaker signals of this adaptive process, suggesting that viruses with broader host ranges may possess traits that make them inherently more capable of infecting a diverse range of hosts, whereas other viruses may require more extensive adaptations to infect a new host species.
Lead author, PhD student Cedric Tan (UCL Genetics Institute and Francis Crick Institute) said: “When animals catch viruses from humans, this can not only harm the animal and potentially pose a conservation threat to the species, but it may also cause new problems for humans by impacting food security if large numbers of livestock need to be culled to prevent an epidemic, as has been happening over recent years with the H5N1 bird flu strain.
“Additionally, if a virus carried by humans infects a new animal species, the virus might continue to thrive even if eradicated among humans, or even evolve new adaptations before it winds up infecting humans again.
“Understanding how and why viruses evolve to jump into different hosts across the wider tree of life may help us figure out how new viral diseases emerge in humans and animals.”
Cell entry is generally seen as the first step for a virus to infect a host. However, the team found that many of the adaptations associated with host jumps were not found in the viral proteins that enable them to attach to and enter host cells, which points to viral host adaptation being a complex process that remains to be fully understood.
Co-author Dr Lucy van Dorp (UCL Genetics Institute) said: “Our research was made possible only by the countless research teams that have openly shared their data via public databases. The key challenge, moving forward, is to integrate the knowledge and tools from diverse disciplines including genomics, epidemiology, and ecology to enhance our understanding of host jumps.”

Scientists from The Australian National University (ANU) have discovered a gene mutation is responsible for causing psoriasis — a chronic inflammatory skin disease that causes patients to develop red, scaly and itchy patches across their body.
According to ANU researcher Dr Chelisa Cardinez, if two copies of this mutated gene (known as IKBKB) are present, patients with psoriasis may go on to develop psoriatic arthritis, leaving them with joint pain, stiffness and swelling. Thanks to the world-first discovery from ANU, scientists now know what causes the progression from a skin-only disease to a skin and joint disease.
It’s hoped the findings will lead to improved diagnosis and treatment for patients with psoriasis and psoriatic arthritis — conditions that patients say carry stigma in the community.
“Using a mouse model, we identified that this mutation led to an abnormal function in a group of immune cells known as regulatory T cells,” Dr Cardinez, from the ANU John Curtin School of Medical Research (JCSMR), said.
“These cells are normally considered gatekeepers of the immune system. However, we found that this mutation alters the function of these cells, causing them to contribute to inflammation and promote the onset of disease.”
Rebecca Davey is one of at least 500,000 Australians that live with psoriasis. She also happens to have psoriatic arthritis and says the stiffness and pain she feels when she gets out of bed in the morning can be extreme.
“People don’t understand the debilitating effects these conditions can have on the individual and in fact a whole family when someone is in constant pain, has poor sleep from pain, and feels constantly fatigued,” Ms Davey said.

“My psoriatic arthritis drugs have largely reduced the larger outbreaks on my skin, but you do have to consider everything you put on your skin and the fabrics you wear. As a former nurse, even the constant hand washing that was required for work would cause my skin to flare up. It’s one of the reasons why I no longer work in the hospital system.”
Psoriasis and psoriatic arthritis are forms of autoimmune disease. These types of diseases occur when the immune system attacks healthy cells after wrongly perceiving them as a threat. According to Arthritis Australia, three out of every 10 Australians with psoriasis develop psoriatic arthritis.
Although there is no cure for psoriasis, there are treatments that can help manage the condition. In October 2023, the Pharmaceutical Benefits Scheme (PBS) listed a new, subsidised drug for Australians living with severe psoriasis.
Ms Davey, who is also CEO of Arthritis ACT, says it’s important to break down the stigma associated with these conditions. She says psoriasis is very misunderstood in the community.
“So many people are accused of having poor hygiene due to the plaques or even just minor skin lesions as they erupt. It’s not the individual’s fault that their skin is in the condition it’s in; psoriasis is a painful, debilitating condition,” she said.
“I had no idea what was causing my hands to flare up all the time. Our poor GPs often don’t recognise these conditions early.

“In regional and rural areas there is a drastic shortage of specialists both in dermatology and rheumatology to diagnose and treat these conditions, and people can wait over a year for an appointment if their symptoms are less dramatic.
“We must raise greater awareness of invisible disabilities such as those created by these conditions. A person might look ok from the outside, but in reality they are struggling on a daily basis.”
Dr Cardinez said: “Studies have shown that delays in psoriatic arthritis diagnosis is linked to worse clinical outcomes for patients. Therefore, earlier detection and treatment of these immune diseases is key to improving health outcomes.
“By developing a better understanding of the IKBKB gene and the role it plays in promoting the onset of these diseases, it could bring us a step closer to one day finding a cure, which would offer new hope for hundreds of thousands of Australians.”

The NewsOn the eve of oral arguments in a Supreme Court case that could affect future access to abortion pills, new research shows the fast-growing use of medication abortion nationally and the many ways women have obtained access to the method since Roe v. Wade was overturned in June 2022.The DetailsPackages of abortion pills being prepared to send to patients.Sophie Park for The New York TimesA study, published on Monday in the medical journal JAMA, found that the number of abortions using pills obtained outside the formal health system soared in the six months after the national right to abortion was overturned. Another report, published last week by the Guttmacher Institute, a research organization that supports abortion rights, found that medication abortions now account for nearly two-thirds of all abortions provided by the country’s formal health system, which includes clinics and telemedicine abortion services.The JAMA study evaluated data from overseas telemedicine organizations, online vendors and networks of community volunteers that generally obtain pills from outside the United States. Before Roe was overturned, these avenues provided abortion pills to about 1,400 women per month, but in the six months afterward, the average jumped to 5,900 per month, the study reported.Overall, the study found that while abortions in the formal health care system declined by about 32,000 from July through December 2022, much of that decline was offset by about 26,000 medication abortions from pills provided by sources outside the formal health system.“We see what we see elsewhere in the world in the U.S. — that when anti-abortion laws go into effect, oftentimes outside of the formal health care setting is where people look, and the locus of care gets shifted,” said Dr. Abigail Aiken, who is an associate professor at the University of Texas at Austin and the lead author of the JAMA study. The co-authors were a statistics professor at the university; the founder of Aid Access, a Europe-based organization that helped pioneer telemedicine abortion in the United States; and a leader of Plan C, an organization that provides consumers with information about medication abortion. Before publication, the study went through the rigorous peer review process required by a major medical journal.The telemedicine organizations in the study evaluated prospective patients using written medical questionnaires, issued prescriptions from doctors who were typically in Europe and had pills shipped from pharmacies in India, generally charging about $100. Community networks typically asked for some information about the pregnancy and either delivered or mailed pills with detailed instructions, often for free.Online vendors, which supplied a small percentage of the pills in the study and charged between $39 and $470, generally did not ask for women’s medical history and shipped the pills with the least detailed instructions. Vendors in the study were vetted by Plan C and found to be providing genuine abortion pills, Dr. Aiken said.We are having trouble retrieving the article content.Please enable JavaScript in your browser settings.Thank you for your patience while we verify access. If you are in Reader mode please exit and log into your Times account, or subscribe for all of The Times.Thank you for your patience while we verify access.Already a subscriber? Log in.Want all of The Times? Subscribe.

Published26 minutes agoShareclose panelShare pageCopy linkAbout sharingBy Hugh PymHealth editorMore than 27,000 healthcare workers in England are set to receive one-off payments of at least £1,600 in their April pay packets. The money will go to staff such as community nurses, physiotherapists and cleaners who do NHS work, but are employed by non-NHS organisations. It follows a campaign for these workers to get the same pay award already made to NHS staff last year in England.That was a lump sum of at least £1,655 and a 5% pay rise.Health Secretary Victoria Atkins said the move would ensure “hardworking staff” and the organisations they work for can fully benefit from the NHS pay deal. “I hugely value the hard work of all our healthcare staff, and those working in non-NHS organisations offer vital support to patients.”I want to ensure that eligible staff receive these payments, which is why we chose to deliver this funding and why we have taken the decision to relax the financial eligibility criteria employers must meet,” she said.But one employers’ group said the process was unfair, and some would still not get the money.What’s happening?The pay award to NHS staff was made last May. But staff working in frontline NHS settings who are employed by other organisations did not get the one-off payment, even though they are on similar contracts to their NHS counterparts under a system agreed with unions, known as Agenda For Change. These include not-for-profit community groups known as social enterprises, founded to take on outsourced services. In November 2023, the Government said it would pay out the money but employers, who had previously threatened legal action, were told to apply and demonstrate that they could not afford to make the payments from their own resources. In February 2024, an employers’ organisation – Social Enterprise UK – told BBC News it was concerned about delays.Some organisations with staff on Agenda for Change contracts have now been told the funding will be transferred in time for April pay packets. One of them, CSH Surrey, which provides community nursing and therapy services to adults and children, welcomed the announcement. Steve Flanagan, its chief executive, said: “We have all fought hard for this and I really appreciate the support from partners across the NHS with this campaign”. Physiotherapist Julie Tollit told BBC News in October she felt “completely demoralised” when she was told she would not receive the payment. Following the latest announcement, she said: “As a healthcare worker at a social enterprise who provides vital NHS community services, receiving this payment recognises how I am – and have always been – part of the NHS family.” NHS pay: Health staff to begin legal fight over Covid bonusBut employers whose staff do NHS work but not on Agenda for Change contracts will not get the government funding. Dan Gregory, director of Social Enterprise UK, said: “While we’re relieved to see some of our members receive this long-awaited funding, the process itself is fundamentally unfair, failing to recognise their crucial role in delivering frontline care. Some social enterprises have not received funding, while many did.”Other health staff who didn’t get the lump sum payment include some “bank staff” who provide temporary cover for hospital trusts to fill rota gaps. The Royal College of Nursing has also been campaigning on behalf of members in GP practices.And some members of the Unite union have staged industrial action when employers have failed to make the payments. These include cleaners, porters and other NHS facilities staff. Separate pay deals have been agreed in Scotland, Wales and Northern Ireland. More on this storyHealth staff win Covid bonus after legal threatPublished6 November 2023Health staff to begin legal fight over Covid bonusPublished26 October 2023Some NHS temporary staff miss out on full pay dealPublished21 July 2023