Scientists discover new T cells and genes related to immune disorders

Researchers led by Yasuhiro Murakawa at the RIKEN Center for Integrative Medical Sciences (IMS) and Kyoto University in Japan and IFOM ETS in Italy have discovered several rare types of helper T cells that are associated with immune disorders such as multiple sclerosis, rheumatoid arthritis, and even asthma. Published July 4 in Science, the discoveries were made possible by a newly developed technology they call ReapTEC, which identified genetic enhancers in rare T cell subtypes that are linked to specific immune disorders. The new T cell atlas is publicly available and should help in the development of new drug therapies for immune-mediated diseases.

Helper T cells are kind of white blood cell that make up a large part of the immune system. They recognize pathogens and regulate the immune response. Many immune-mediated disease are caused by abnormal T cell function. In autoimmune diseases like multiple sclerosis, they mistakenly attack parts of the body as if they were pathogens. In the case of allergies, T cells overreact to harmless substances in the environment like pollen. We know of several common T cells, but recent studies have shown that rare and specialized types of T cells exist, and they might be related to immune-mediated diseases.

Within all cells, including T cells, there are regions of DNA called “enhancers”. This DNA does not code for proteins. Instead, it codes for small pieces of RNA, and enhances the expression of other genes. Variations in T cell enhancer DNA therefore lead to differences in gene expression, and this can affect how T cells function. Some enhancers are bidirectional, which means that both strands of the DNA are used as templates for enhancer RNA. The researchers from several different laboratories at RIKEN IMS, as well as colleagues at other institutes, teamed up to develop the new ReapTEC technology and look for connections between bidirectional T cell enhancers and immune diseases.

After analyzing about a million human T cells, they found several groups of rare T cell types, accounting for less than 5% of the total. Applying ReapTEC to these cells identified almost 63,000 active bidirectional enhancers. To figure out if any of these enhancers are related to immune diseases, they turned to genome-wide association studies (GWAS), which have reported numerous genetic variants, called single-nucleotide polymorphisms, that are related to various immune diseases.

When the researchers combined the GWAS data with the results of their ReapTEC analysis, they found that genetic variants for immune-mediated diseases were often located within the bidirectional enhancer DNA of the rare T cells that they had identified. In contrast, genetic variants for neurological diseases did not show a similar pattern, meaning that the bidirectional enhancers in these rare T cells are related specifically to immune-mediated diseases.

Going even deeper into the data, the researchers were able to show that individual enhancers in certain rare T cells are related to specific immune diseases. Overall, among the 63,000 bidirectional enhancers, they were able to identify 606 that included single-nucleotide polymorphisms related to 18 immune-mediated diseases. Lastly, the researchers were able to identify some of the genes that are the targets of these disease-related enhancers. For example, when they activated an enhancer that contained a genetic variant related to inflammatory bowel disease, the resulting enhancer RNA triggered upregulation of the IL7R gene.

“In the short-term, we have developed a new genomics method that can be used by researchers around the world,” says Murakawa. “Using this method, we discovered new types of helper T cells as well as genes related to immune disorders. We hope that this knowledge will lead to a better understanding of the genetic mechanisms underlying human immune-mediated diseases.”

In the long-term, the researchers believe follow-up experiments will be able to identify new molecules that can be used to treat immune-mediated diseases.

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The dawn of the Antarctic ice sheets

In recent years global warming has left its mark on the Antarctic ice sheets. The “eternal” ice in Antarctica is melting faster than previously assumed, particularly in West Antarctica more than East Antarctica. The root for this could lie in its formation, as an international research team led by the Alfred Wegener Institute has now discovered: sediment samples from drill cores combined with complex climate and ice-sheet modelling show that permanent glaciation of Antarctica began around 34 million years ago — but did not encompass the entire continent as previously assumed, but rather was confined to the eastern region of the continent (East Antarctica). It was not until at least 7 million years later that ice was able to advance towards West Antarctic coasts. The results of the new study show how substantially differently East and West Antarctica react to external forcing, as the researchers describe in the journal Science.

Around 34 million years ago, our planet underwent one of the most fundamental climate shifts that still influences global climate conditions today: the transition from a greenhouse world, with no or very little accumulation of continental ice, to an icehouse world, with large permanently glaciated areas. During this time, the Antarctic ice sheet built up. How, when and, above all, where, was not yet known due to a lack of reliable data and samples from key regions, especially from West Antarctica, that document the changes in the past. Researchers from the Alfred Wegener Institute, Helmholtz Centre for Polar and Marine Research (AWI) have now been able to close this knowledge gap, together with colleagues from the British Antarctic Survey, Heidelberg University, Northumbria University (UK), and the MARUM — Center for Marine Environmental Sciences at the University of Bremen, in addition to collaborators from the Universities in Aachen, Leipzig, Hamburg, Bremen, and Kiel, as well as the University of Tasmania (Australia), Imperial College London (UK), Université de Fribourg (Switzerland), Universidad de Granada (Spain), Leicester University (UK), Texas A&M University (USA), Senckenberg am Meer, and the Federal Institute for Geosciences and Natural Resources in Hanover, Germany.

Based on a drill core that the researchers retrieved using the MARUM-MeBo70 seafloor drill rig in a location offshore the Pine Island and Thwaites glaciers on the Amundsen Sea coast of West Antarctica, they were able to establish the history of the dawn of the icy Antarctic continent for the first time. Surprisingly, no signs of the presence of ice can be found in this region during the first major phase of Antarctic glaciation. “This means that a large-scale, permanent first glaciation must have begun somewhere in East Antarctica,” says Dr Johann Klages, geologist at the AWI who led the research team. This is because West Antarctica remained ice-free during this first glacial maximum. At this time, it was still largely covered by dense broadleaf forests and a cool-temperate climate that prevented ice from forming in West Antarctica.

East and West Antarctica react very different to external conditions

In order to better understand where the first permanent ice formed in Antarctica, the AWI paleoclimate modelers combined the newly available data together with existing data on air and water temperatures and the occurrence of ice. “The simulation has supported the results of the geologists’ unique core,” says Prof Dr Gerrit Lohmann, paleoclimate modeler at the AWI. “This completely changes what we know about the first Antarctic glaciation.” According to the study, the basic climatic conditions for the formation of permanent ice only prevailed in the coastal regions of the East Antarctic Northern Victoria Land. Here, moist air masses reached the strongly rising Transantarctic Mountains — ideal conditions for permanent snow and subsequent formation of ice caps. From there, the ice sheet spread rapidly into the East Antarctic hinterland. However, it took some time before it reached West Antarctica: “It wasn’t until about seven million years later that conditions allowed for advance of an ice sheet to the West Antarctic coast,” explains Hanna Knahl, a paleoclimate modeler at the AWI. “Our results clearly show how cold it had to get before the ice could advance to cover West Antarctica that, at that time, was already below sea level in many parts.” What the investigations also impressively show is how different the two regions of the Antarctic ice sheet react to external influences and fundamental climatic changes. “Even a slight warming is enough to cause the ice in West Antarctica to melt again — and that’s exactly where we are right now,” adds Johann Klages.

The findings of the international research team are critical for understanding the extreme climate transition from the greenhouse climate to our current icehouse climate. Importantly, the study also provides new insight that allows climate models to simulate more accurately how permanently glaciated areas affect global climate dynamics, that is the interactions between ice, ocean and atmosphere. This is of crucial importance, as Johann Klages says: “Especially in light of the fact that we could be facing such a fundamental climate change again in the near future.”

Using new technology to gain unique insights

The researchers were able to close this knowledge gap with the help of a unique drill core that they retrieved during the expedition PS104 on the research vessel Polarstern in West Antarctica in 2017. The MARUM-MeBo70 drill rig developed at MARUM in Bremen was used for the first time in Antarctica. The seabed off the West Antarctic Pine Island and Thwaites glaciers is so hard that it was previously impossible to reach deep sediments using conventional drilling methods. The MARUM-MeBo70 has a rotating cutterhead, which made it possible to drill about 10 meters into the seabed and retrieve the samples.

The research project, and the Polarstern expedition PS104 in particular, was funded by the AWI, MARUM, the British Antarctic Survey, and the NERC UK-IODP Programme.

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Not so selfish after all: Viruses use freeloading genes as weapons

Curious bits of DNA tucked inside genomes across all kingdoms of life historically have been disregarded since they don’t seem to have a role to play in the competition for survival. Or so researchers thought.

These DNA pieces came to be known as “selfish genetic elements” because they exist, as far as scientists could tell, to simply reproduce and propagate themselves, without any benefit to their host organisms. They were seen as genetic hitchhikers that have been inconsequentially passed from one generation to the next.

Research conducted by scientists at the University of California San Diego has provided fresh evidence that such DNA elements might not be so selfish after all. Instead, they now appear to factor considerably into the dynamics between competing organisms.

Publishing in the journal Science, researchers in the School of Biological Sciences studied selfish genetic elements in bacteriophages (phages), viruses that are considered the most abundant organisms on Earth. To their surprise, researchers found that selfish genetic elements known as “mobile introns” provide their virus hosts with a clear advantage when competing with other viruses: phages have weaponized mobile introns to disrupt the ability of competing phage viruses to reproduce.

“This is the first time a selfish genetic element has been demonstrated to confer a competitive advantage to the host organism it has invaded,” said study co-first author Erica Birkholz, a postdoctoral scholar in the Department of Molecular Biology. “Understanding that selfish genetic elements are not always purely ‘selfish’ has wide implications for better understanding the evolution of genomes in all kingdoms of life.”

Decades ago biologists noted the existence of selfish genetic elements but were unable to characterize any role they play in helping the host organism survive and reproduce. In the new study, which focused on investigating “jumbo” phages, the researchers analyzed the dynamics as two phages co-infect a single bacterial cell and compete against each other.

They looked closely at the endonuclease, an enzyme that serves as a DNA cutting tool. The endonuclease from one phage’s mobile intron, the studies showed, interferes with the genome of the competing phage. The endonuclease therefore is now regarded as a combat tool since it has been documented cutting an essential gene in the competing phage’s genome. This sabotages the competitor’s ability to appropriately assemble its own progeny and reproduce.

“This weaponized intron endonuclease gives a competitive advantage to the phage carrying it,” said Birkholz.

The researchers say the finding is especially important in the evolutionary arms race between viruses due to the constant competition in co-infection.

“We were able to clearly delineate the mechanism that gives an advantage and how that happens at the molecular level,” said Biological Sciences graduate student Chase Morgan, the paper’s co-first author. “This incompatibility between selfish genetic elements becomes molecular warfare.”

The results of the study are important as phage viruses emerge as therapeutic tools in the fight against antibiotic resistant bacteria. Since doctors have been deploying “cocktails” of phage to combat infections in this growing crisis, the new information is likely to come into play when multiple phage are implemented. Knowing that certain phage are using selfish genetic elements as weapons against other phage could help researchers understand why certain combinations of phage may not reach their full therapeutic potential.

“The phages in this study can be used to treat patients with bacterial infections associated with cystic fibrosis,” said Biological Sciences Professor Joe Pogliano. “Understanding how they compete with one another will allow us to make better cocktails for phage therapy.”

The authors of the paper are: Erica Birkholz, Chase Morgan, Thomas Laughlin, Rebecca Lau, Amy Prichard, Sahana Rangarajan, Gabrielle Meza, Jina Lee, Emily Armbruster, Sergey Suslov, Kit Pogliano, Justin Meyer, Elizabeth Villa, Kevin Corbett and Joe Pogliano.

The research detailed in the Science study was funded by an Emerging Pathogens Initiative grant from the Howard Hughes Medical institute, the National Institutes of Health (R01- GM129245 and R35 GM144121) and the National Science Foundation (MRI grant NSF DBI 1920374).

Competing interest disclosure: Professors Kit and Joe Pogliano have an equity interest in Linnaeus Bioscience Inc. and receive income.

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How dust pollution from shrinking Great Salt Lake affects communities disproportionately

New research from the University of Utah demonstrates how wind-carried dust from the exposed bed of Great Salt Lake is disproportionately affecting disadvantaged communities in the Salt Lake metro area.

The findings suggest restoring the lake to a healthy water level would reduce disparities in harmful dust exposure experienced by different racial/ethnic and socioeconomic groups, along with delivering other ecological and economic benefits.

Exposure to particulate pollution arising from dry portions of the playa is highest among Pacific Islanders and Hispanics and lowest among white people compared to other racial/ethnic groups, according to the findings reported June 21 in the journal One Earth. It was also higher for individuals without a high school diploma. 

This is likely because Salt Lake City’s lower-income neighborhoods are more likely to lie in the path of windblown dust from Great Salt Lake, which has shrunk to less than half its historical size, leaving about 800 square miles of lakebed exposed.

More than two decades of drought and unrelenting upstream diversions have contributed to the decline of the saline terminal lake located immediately west and north of Utah’s main population corridor along the Wasatch Front.

“People here in Utah are concerned about the lake for a variety of reasons — the ski industry, the brine shrimp, the migratory birds, recreation — and this study adds environmental justice and the equity implications of the drying lake to the conversation,” said lead author Sara Grineski, a professor of sociology and environmental studies.

Grineski led an interdisciplinary team of U faculty, largely associated with the Wilkes Center for Climate Science and Policy, from both the College of Social and Behavioral Science (CSBS) and the College of Science. Co-authors are Timothy Collins and Malcolm Araos (geography); John Lin, Derek Mallia and Kevin Perry (atmospheric sciences); and William Anderegg (biology).

The study analyzed data from the Utah Department of Environmental Quality’s air-quality monitoring network, which screens for fine particulate matter, or PM2.5. Comprised of ultra tiny particles that can penetrate lung tissue, this pollution is linked to myriad health problems, including cardiovascular disease and asthma.

During dust storms, current levels expose residents to 26 micrograms per cubic meter, or μg/m3, of PM2.5 on average, according to the study, significantly higher than the World Health Organization’s threshold of 15 μg/m3. Were the lake to dry up completely, exposure could rise to 32 μg/m3, while restoring the lake could reduce exposure to 24 μg/m3 during these wind events, according to the study.

The study examined four such events in 2022 on April 19, 20 and 21 and May 7, when spikes of recorded PM2.5 coincided with high winds.

For the study, which was funded by the National Science Foundation, researcher Derek Mallia developed a model for predicting exposure levels for the three counties abutting the lake’s east and south shores — Salt Lake, Davis and Weber, home to 1.8 million residents — under four different lake level scenarios. It uses a weather model that simulates wind direction and speed, and includes a wind-blown dust model, which measures how much dust is emitted from an erodible surface, such as the Great Salt Lake playa, and is primarily based on the wind speed and soil texture and characteristics.

“We have to use weather models, since we cannot physically go out to the lake and remove/add water to see how much more/less dust it would emit,” Mallia said. “Models like the one that I developed let us run these hypothetical scenarios.”

The study’s scenarios range from a totally dry lake, to very low lake level, to current lake, to ‘healthy’ lake level designated as 4,200 feet above sea level. The lake’s South Arm currently sits at 4,194.4 feet, almost 6 feet higher than the historic low of 4,188.7 registered at the end of 2022.

According to the model, neighborhood disparities in exposure levels would increase when the lake level drops.

“We frame it the converse. Lake levels rise, overall levels of dust go down during the dust events and the gap, especially between Hispanic and Pacific Islander people, narrows with respect to the level of dust exposure for non-Hispanic white people,” Grineski said. “So if we can take better care of the lake, the dust for everyone goes down and the gap in exposure between these groups goes down too.”

Her team’s prior research has previously documented disparities of PM2.5 exposure generally in the Salt Lake Valley

“There is a really strong pattern of inequality with respect to race and ethnicity,” she added. “It’s sort of a hopeful finding that if we can raise the lake to a ‘healthy’ level we can at least with respect to lake dust we can reduce some of that inequality.”

Most dust from the playa is PM10, pollution comprised of much larger particles that are only measured at a few of Utah’s air quality monitoring stations. Without a robust PM10 monitoring network, researchers and regulators are deprived of a key data source that could give a more complete assessment of the lakebed dust threat, according to co-author Kevin Perry. He said the study points to the need for Utah to expand its network of PM10 monitors since windblown lakebed dust contains about six times more PM10 than PM2.5.

“We have to use the PM2.5 data because that’s the network that we have available. It’s not what I would design and not what I would like to do,” he said. “Because of the network being so sparse, I can’t even answer a really basic question, like how many dust events do we have a year that are impacting these communities. And that’s super frustrating.”

A professor of atmospheric science, Perry is known as “Dr. Dust” thanks to his tireless bicycle forays across the vast lakebed gathering sediment samples. These sediments were found to be contaminated with heavy metals in some places.

He noted that potentially harmful dust events typically occur in the spring and fall when cold fronts pass through the Wasatch Front.

“Before a cold front gets here, we have really strong winds from the south that will last for 12 or 18 hours,” Perry said. “And where’s it pushing that dust? It’s pushing it to Layton, Syracuse, Ogden, Brigham City where we have almost no PM10 monitors at all, and then the wind reverses and we’ll get three to four or five hours of stuff coming into Salt Lake Valley where we do have monitors.”

Because of its ability to infiltrate living tissue, PM2.5 is considered more harmful to human health than PM10, which is also classified as a criteria pollutant under the federal Clean Air Act.

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Scientists map how deadly bacteria evolved to become epidemic

Pseudomonas aeruginosa — an environmental bacteria that can cause devastating multidrug-resistant infections, particularly in people with underlying lung conditions — evolved rapidly and then spread globally over the last 200 years, probably driven by changes in human behaviour, a new study has found.

P. aeruginosa is responsible for over 500,000 deaths per year around the world, of which over 300,000 are associated with antimicrobial resistance (AMR). People with conditions such as COPD (smoking-related lung damage), cystic fibrosis (CF), and non-CF bronchiectasis, are particularly susceptible.

How P. aeruginosa evolved from an environmental organism into a specialised human pathogen was not previously known. To investigate this, an international team led by scientists at the University of Cambridge examined DNA data from almost 10,000 samples taken from infected individuals, animals, and environments around the world. Their results are published today in Science

By mapping the data, the team was able to create phylogenetic trees — ‘family trees’ — that show how the bacteria from the samples are related to each other. Remarkably, they found that almost seven in ten infections are caused by just 21 genetic clones, or ‘branches’ of the family tree, that have rapidly evolved (by acquiring new genes from neighbouring bacteria) and then spread globally over the last 200 years. This spread occurred most likely as a result of people beginning to live in densely-populated areas, where air pollution made our lungs more susceptible to infection and where there were more opportunities for infections to spread.

These epidemic clones have an intrinsic preference for infecting particular types of patients, with some favouring CF patients and other non-CF individuals. It turns out that the bacteria can exploit a previously unknown immune defect in people with CF, allowing them to survive within macrophages. Macrophages are cells that ‘eat’ invading organisms, breaking them down and preventing the infection from spreading. But a previously-unknown flaw in the immune systems of CF patients means that once the macrophage ‘swallows’ P. aeruginosa, it is unable to get rid of it.

Having infected the lungs, these bacteria then evolve in different ways to become even more specialised for a particular lung environment. The result is that certain clones can be transmitted within CF patients and other clones within non-CF patients, but almost never between CF and non-CF patient groups.

Professor Andres Floto, Director of the UK Cystic Fibrosis Innovation Hub at the University of Cambridge and Royal Papworth Hospital NHS Foundation Trust, and senior author of the study said: “Our research on Pseudomonas has taught us new things about the biology of cystic fibrosis and revealed important ways we might be able to improve immunity against invading bacteria in this and potentially other conditions.

“From a clinical perspective, this study has revealed important information about Pseudomonas. The focus has always been on how easily this infection can spread between CF patients, but we’ve shown that it can spread with worrying ease between other patients, too. This has very important consequences for infection control in hospitals, where it’s not uncommon for an infected individual to be on an open ward with someone potentially very vulnerable.

“We are incredibly lucky at Royal Papworth Hospital where we have single rooms and have developed and evaluated a new air-handling system to reduce the amount of airborne bacteria and protect all patients.”

Dr Aaron Weimann from the Victor Phillip Dahdaleh Heart & Lung Research Institute at the University of Cambridge, and first author on the study, said: “It’s remarkable to see the speed with which these bacteria evolve and can become epidemic and how they can specialise for a particular lung environment. We really need systematic, pro-active screening of all at risk patient groups to detect and hopefully prevent the emergence of more epidemic clones.”

The research was funded by Wellcome and the UK Cystic Fibrosis Trust.

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Clever pupils don’t need to attend academically selective schools to thrive, study finds

Findings published in a new peer-reviewed paper in the British Journal of Educational Studies challenges the idea that academically selective schools are necessary for clever pupils to achieve good outcomes.

Selective schools are government-funded schools that enrol only the highest performing students. Pupils take a standardized entrance exam, from which the best-scoring are enrolled.

Some argue that selective schools are necessary for bright pupils to reach their full academic potential. Selective schools can outperform or perform just as well as elite schools in final year exams, but without the high fees charged to parents. Hence, selective schools can offer a means for children from low socioeconomic backgrounds to receive a first-class education.

However, others argue that selective schools disproportionately benefit high socioeconomic children whose parents can afford private tutoring to prepare them for the entrance exams.

“Studies show that parents wish to enrol their children into selective schools, because they believe it will increase the chances of their children getting into a prestigious university, and securing a well-paid and high-status job,” says Melissa Tham, a research fellow at the Mitchell Institute at Victoria University, Melbourne, Australia.

To find out whether there are benefits associated with selective schools, Tham and her colleagues Shuyan Huo, and Andrew Wade tracked almost 3000 pupils from the Longitudinal Surveys of Australian Youth (LSAY), a nationally representative survey program that follows young Australians over an 11-year period. The survey started when respondents were aged 15 in 2009.

As expected, the selective schools featured in the study had a higher proportion of academically high-achieving students, as measured by mathematics and reading scores.

However, at ages 19 and 25 there was little difference between the educational and employment outcomes of children who attended selective schools versus non-selective schools. For example, the study found that while 81% of selective school students went on to secure a job or university place at 19 compared to 77.6% of pupils from non-selective schools, this difference disappeared when the students were matched on key characteristics, including socioeconomic background, gender, and geographical location.

At age 25, all outcomes between selective and non-selective school students were not significant, except general life satisfaction. Attending a selective school increased a student’s general life satisfaction score by just 0.19 points. Meanwhile, students who attended non-selective school were just as likely to go on to study at university or secure a job as their peers who attended selective schools.

“These very modest findings indicate that attending an academically selective school does not appear to pay off in large benefits for individuals,” says Andrew Wade, co-author of the study.

“We argue that academically selective schools in the government sector therefore contradicts the principles of inclusive and equitable education which underpin Australia’s school system.”

According to the authors, the findings suggest that more research is needed to determine whether selective schools offer any benefit to academically able students.

“Rather than tweak some aspects of the enrolment processes, we see greater value in conducting a thorough and critical examination of fully and partially selective schools, and scaling back selectivity if the supposed benefits are not found,” says Huo.

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NI records sharp rise in measles cases

There have been 11 cases of measles in Northern Ireland in 2024 and 68 in the Republic of Ireland.

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Banksy Responds After James Cleverly Brands His Glastonbury Stunt ‘Vile And Unacceptable’

Banksy has issued a response to home secretary James Cleverly’s claim that his recent stunt at Glastonbury was “vile and unacceptable”.

During a performance by Idles at the music event on Friday night, an inflatable boat filled with dummies wearing orange life jackets, intended to represent refugees trying to pass through treacherous seas, was passed out to the crowd.

The band had initially been unaware of the stunt that was carried out during their song Danny Nedelko, which opens with the lines: “My blood brother is an immigrant. A beautiful immigrant.”

An Idles spokesperson later confirmed the boat was, indeed, a Banksy piece.

According to a photo shared on X by Glastonbury Live, the boat also returned to the crowd for Little Simz’s set on the Pyramid Stage the following day.

The stunt was met with condemnation from the Home Secretary, who told Sky News: “People die in the Mediterranean, they die on the Channel. This is not funny. It is vile. This is a celebration of the loss of life in the Channel.”

He added: “To joke about it, to celebrate it at a pop festival when there have been children dying in the Channel, is completely unacceptable.”

James Cleverly
James Cleverly

Wiktor Szymanowicz via Getty Images

Now, the anonymous street artist has responded to Cleverly’s comments on Instagram.

“The home secretary called my Glastonbury boat vile and unacceptable’ which seemed a bit over the top,” Banksy wrote.

“The real boat I fund, the MV Louise Michel rescued 17 unaccompanied children from the central Med on Monday night.

“As punishment the Italian authorities have detained it – which seems vile and unacceptable to me.”

The MV Louise Michel, provides life-saving support to those in distress crossing the Mediterranean, and was purchased with the proceeds from the sale of Banksy artwork.

Banksy’s Glastonbury stunt comes after he returned with his first art instalment of 2024 back in March.

The mural featured a stencil of a woman who had sprayed green paint over a white wall behind a pollarded tree, which gave the illusion of leaves.

Last year, he also unveiled a divisive new piece of street artwork centring around domestic violence against women.

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The Simple Reason Why You’ve Been Storing Your Cheese Wrong

Have you found that no matter how well you seal plastic food bags, cheese always tends to go off inside of them very quickly?

Yes, me too. I find myself reaching for the cheese a couple of days later, only to see that it’s suddenly inedible.

Well, it’s not because we haven’t sealed them effectively, according to one medical expert. It’s much more simple than that and in part comes down to the types of cheese we’re having.

Dr Karan Rajan explained in a recent TikTok video that if you’ve been wrapping your cheese in food bags, you’ve been setting yourself up for failure.

How to properly store cheese

So if, like me, you thought that most foods could be refrigerated in the same way, this will be a cold awakening. (Sorry.)

Dr Rajan explained: “Once you finish gobbling your cheese like a hungry little rat, try and avoid putting your cheese in a plastic bag. Especially softer cheeses which have a higher water content.”

These include Havati, Mozzarella, and Gouda.

He said: “This is because moisture can get trapped in the plastic bag and cover the cheese surface. This provides a breeding ground for bacteria and mould — and not the tasty kind.”

Instead, Dr Rajan recommends using cheese paper, which actually is a thing, yes. Alternatively, parchment paper is a good choice, too.

If you are still keen to use plastic bags, Dr Rajan recommends first wrapping the cheese in wax, parchment or cheese paper before placing it inside of the bag.

Fortunately, harder cheeses like Parmigiano can withstand plastic bags no problem.

He did also point out that you could just eat the food very quickly, ‘for science, of course’ and to reduce food waste.

Of course.

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Man Found Guilty Of Plotting To Kidnap, Rape And Murder Holly Willoughby

This article contains discussions of violence and sexual assault.

A man facing trial for plotting to kidnap, rape and murder the TV personality Holly Willoughy has been found guilty.

Back in October of last year, it was first reported by The Sun that the former This Morning host was “under police guard” after “sinister” messages were found on a man’s phone reportedly threatening to “seriously harm” the daytime TV presenter.

Security guard Gavin Plumb – who did not know the presenter personally – was subsequently charged with soliciting to commit murder and incitement to commit kidnap, with his trial getting underway on Monday 24 June.

Following eight days of trial, Plumb – who had denied the allegations made against him – was found guilty of three charges at Chelmsford Crown Court on Thursday. He will be sentenced on Friday 12 July.

Prosecution Alison Morgan KC previously told the court that Plumb had developed an “obsession with Holly Willoughby that had developed over a number of years” and had a serious and “real intention” to kidnap the daytime star from her home and take her to “a location where she would be raped repeatedly”, before murdering her.

“It was not just the ramblings of a fantasist; the defendant had carefully planned what he would do,” Morgan said on the first day of the trial.

Plumb had two previous convictions for attempted kidnap and false imprisonment, dating back to 2006 and 2008.

It was previously noted that Plumb’s alleged plans only came to light after he shared them with an undercover police officer based in the US, with whom he’d been speaking online.

Greg Wood of Essex Police told BBC News: “If the American officer hadn’t have contacted us… I’ve got no doubt that Gavin Plumb could’ve gone on to commit some really horrific crimes.”

Holly Willoughby at the NTAs last year
Holly Willoughby at the NTAs last year

Jeff Spicer via Getty Images

According to The Guardian, Nicola Rice of the Crown Prosecution Service, said: “Gavin Plumb is a dangerous man who plotted unspeakable violence against one of the nation’s most familiar faces.

“Despite his attempts to pass himself off as a harmless fantasist, the prosecution persuaded the jury that Plumb posed a very real threat.

“The chilling details of his plans were laid bare with the help of an undercover officer from the US who alerted the FBI to the threat, and the seriousness of Plumb’s scheme was exposed when the prosecution successfully applied to tell the jury about Plumb’s previous convictions.

“I hope his conviction brings some comfort to Holly Willoughby and her family and shows others that the Crown Prosecution Service will always seek the strongest possible charges against those who plot violence against women.”

When details of the kidnap plot were first made public last year, it was reported that Holly was “under police guard at her home”.

She subsequently made the decision to step down from This Morning after 14 years at the helm, which she said was “for me and my family”.

Holly then took an extended break from the media spotlight, before making her return to TV in January, when she and new co-host Stephen Mulhern presented the latest series of Dancing On Ice.

Help and support:

  • Rape Crisis services for women and girls who have been raped or have experienced sexual violence – 0808 802 9999
  • Survivors UK offers support for men and boys – 0203 598 3898
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