A 2D device for quantum cooling

To perform quantum computations, quantum bits (qubits) must be cooled down to temperatures in the millikelvin range (close to -273 Celsius), to slow down atomic motion and minimize noise. However, the electronics used to manage these quantum circuits generate heat, which is difficult to remove at such low temperatures. Most current technologies must therefore separate quantum circuits from their electronic components, causing noise and inefficiencies that hinder the realization of larger quantum systems beyond the lab.

Researchers in EPFL’s Laboratory of Nanoscale Electronics and Structures (LANES), led by Andras Kis, in the School of Engineering have now fabricated a device that not only operates at extremely low temperatures, but does so with efficiency comparable to current technologies at room temperature.

“We are the first to create a device that matches the conversion efficiency of current technologies, but that operates at the low magnetic fields and ultra-low temperatures required for quantum systems. This work is truly a step ahead,” says LANES PhD student Gabriele Pasquale.

The innovative device combines the excellent electrical conductivity of graphene with the semiconductor properties of indium selenide. Only a few atoms thick, it behaves as a two-dimensional object, and this novel combination of materials and structure yields its unprecedented performance. The achievement has been published in Nature Nanotechnology.

Harnessing the Nernst effect

The device exploits the Nernst effect: a complex thermoelectric phenomenon that generates an electrical voltage when a magnetic field is applied perpendicular to an object with a varying temperature. The two-dimensional nature of the lab’s device allows the efficiency of this mechanism to be controlled electrically.

The 2D structure was fabricated at the EPFL Center for MicroNanoTechnology and the LANES lab. Experiments involved using a laser as a heat source, and a specialized dilution refrigerator to reach 100 millikelvin — a temperature even colder than outer space. Converting heat to voltage at such low temperatures is usually extremely challenging, but the novel device and its harnessing of the Nernst effect make this possible, filling a critical gap in quantum technology.

“If you think of a laptop in a cold office, the laptop will still heat up as it operates, causing the temperature of the room to increase as well. In quantum computing systems, there is currently no mechanism to prevent this heat from disturbing the qubits. Our device could provide this necessary cooling,” Pasquale says.

A physicist by training, Pasquale emphasizes that this research is significant because it sheds light on thermopower conversion at low temperatures — an underexplored phenomenon until now. Given the high conversion efficiency and the use of potentially manufacturable electronic components, the LANES team also believes their device could already be integrated into existing low-temperature quantum circuits.

“These findings represent a major advancement in nanotechnology and hold promise for developing advanced cooling technologies essential for quantum computing at millikelvin temperatures,” Pasquale says. “We believe this achievement could revolutionize cooling systems for future technologies.”

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Lucy Letby sentenced to 15th whole life term

The former nurse, 34, attempted to murder the premature baby by dislodging her breathing tube.

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Maternity staff faced racism from colleagues – CQC

Overseas staff brought in to tackle midwife shortages say they experienced discrimination.

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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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