Conditions: Williams Syndrome; Autism Disorder
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Sponsors: Qilu Hospital of Shandong University
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Low Birthweight Increases Risk of Early Stroke
Research led by the University of Gothenburg in Sweden suggests that low birthweight is a risk factor for having a stroke in younger adulthood.
In a study including just under 800,000 people, the investigators found that risk for early stroke events was 18-23% higher in men and women who had a birth weight under the median level than those with a higher birth weight.
Around 795,000 people in the U.S. have a stroke each year. Although it can affect people of any age, it is much more common in older individuals with estimates of prevalence suggesting that 0.9% of 18–44 year olds have strokes versus 3.8% of those in the 45–64 year age group and 7.7% of people aged 65 and over.
Low birth weight has been previously linked to an increased risk for stroke in several studies. Researchers think that low birth weight is an indicator of exposure to an adverse environment in the womb that may adversely affect the cardiovascular system of the fetus in a way that increases stroke risk—for example, by increasing the risk of high blood pressure.
Over the last 10-15 years, stroke prevalence has stayed the same in older adults but has gone up by 14-16% in 18-64 year-olds. Lina Lilja, a doctoral student at the University of Gothenburg, and colleagues aimed to investigate whether low birth weight increased the risk of stroke in younger adults.
They included 420,173 men and 348,758 women from Sweden who were born between 1973 and 1982 and followed up from birth until 2022. The researchers collected data on birth weight, gestational age, and body mass index in young adulthood, as well as information on first stroke and the type of stroke.
Overall, 2252 first stroke events were recorded at an average age of 36 years. Of these, 1624 were ischemic stroke (average age 37 years) and 588 were intracerebral hemorrhage (average age 33 years).
The results, which will be presented at the European Congress on Obesity in Istanbul later this year, showed that birth weight below the median (3.5kg) increased the risk for all stroke by 21%. The rates of stroke were slightly higher in men with a low birthweight at 23% versus women with a low birthweight at 18%.
Notably, gestational age at birth and young adult body mass index were not linked to stroke risk in this study.
The post Low Birthweight Increases Risk of Early Stroke appeared first on Inside Precision Medicine.
Pancreatic Cancer Development Driven by NADPH Disruption
Researchers at the University of Michigan have uncovered metabolic pathways that explain how pancreatic cells transition from acinar-to-ductal metaplasia to pancreatic ductal adenocarcinoma (PDAC). The study, published in Nature Metabolism, detailed on how reduced production of a molecule central to biosynthesis and oxidative stress control called NADPH alters cellular conditions to favor cancer progression. By examining precancerous pancreatic lesions, the team found that disruptions in enzymes responsible for NADPH production increase oxidative stress, accelerating the formation of lesions and, in some cases, the progression to PDAC.
“We know a lot about how pancreatic tumors behave and look, but we don’t know how they become cancerous,” said lead author Megan Radyk, PhD, a former postdoc in the lab of Costas Lyssiotis, PhD, at the University of Michigan and now an assistant professor at Roswell Park Comprehensive Cancer Center. “We wanted to learn about what metabolic changes happen before you get an established tumor.”
PDAC is the most common form of pancreatic cancer and has a low five-year survival rate. The disease develops through a stepwise process that begins with acinar-to-ductal metaplasia (ADM), a reversible state in which pancreatic cells respond to injury or inflammation by adopting a duct-like phenotype. Under normal conditions, these cells can revert to their original state. However, in the presence of oncogenic KRAS mutations, this process is disrupted, leading to persistent ADM and progression to pancreatic intraepithelial neoplasia (PanIN), which can ultimately become PDAC.
NADPH’s normal role is in maintaining cellular homeostasis. It supports the synthesis of lipids, cholesterol, and nucleotides, and it aids antioxidant systems that regulate reactive oxygen species (ROS). Under normal conditions, NADPH helps neutralize ROS, preventing cellular damage. The current study, however, demonstrated that lower levels of NADPH impair antioxidant defenses, leading to increased ROS and lipid peroxidation, which in turn promote the formation of precancerous lesions.
The researchers identified two NADPH-producing enzymes for their work: glucose-6-phosphate dehydrogenase (G6PD) and malic enzyme 1 (ME1). Both enzymes support the production of the appropriate levels of NADPH needed for biosynthesis and ROS regulation.
Using a multimodal approach involving RNA sequencing, metabolomics, and mouse models with oncogenic KRAS mutations, the Michigan team studied how the loss of these two enzymes affects pancreatic tissue. They observed that deficiency in either G6PD or ME1 increased ROS levels and accelerated the formation of ADM and pancreatic intraepithelial neoplasia (PanIN) lesions. Antioxidant treatments, including glutathione and N-acetyl cysteine, reduced lesion formation, further bolstering the current understanding of the role of oxidative stress in early tumorigenesis. The team achieved similar results when these methods were applied to human pancreatic tissue samples.
But results from later in the study showed that the two enzymes played distinct roles in the later stages of PDAC. While they both contributed to early lesion formation, only the loss of ME1 promoted progression to PDAC. This suggests that although both enzymes regulate NADPH and oxidative stress, they have distinct roles in later metabolic demands of cancer cells.
The study builds on prior research showing that KRAS mutations drive metabolic reprogramming and ROS production in pancreatic cells. Previous work has also indicated that antioxidant pathways, including those regulated by NRF2, are activated during tumor initiation.
Clinically, these findings suggest that targeting metabolic pathways involved in NADPH production could provide a strategy to intercept pancreatic cancer before it fully develops. Measuring levels of G6PD, ME1, or related metabolites could also serve as biomarkers to identify patients at higher risk of lesions progressing to cancer.
“Our study can help the search for new biomarkers that can intercept pancreatic cancer before it progresses,” the researchers wrote.
Future research will focus on identifying additional enzymes that regulate NADPH levels and determining how these pathways can be targeted safely. The researchers also plan to study whether patients with mutations in G6PD, ME1, or related pathways have an increased risk of pancreatic disease.
The post Pancreatic Cancer Development Driven by NADPH Disruption appeared first on Inside Precision Medicine.
Injectable Microgel Developed to Reduce Bleeding in Infants Undergoing Surgery
Biomedical researchers headed by a team at the Lampe Joint Department of Biomedical Engineering, University of North Carolina at Chapel Hill/North Carolina State University, have developed an injectable microgel to help reduce bleeding in infants who require surgical care. Tests in an animal model showed that the hemostatic microgels, known as B-knob-triggered microgels (BK-TriGs), reduced bleeding by at least 50%.
Research lead Ashley Brown, PhD, who is the Lampe Distinguished Professor of Biomedical Engineering, is co-corresponding author of the team’s published paper in Science Advances, titled “Hemostatic B-knob-triggered microgels (BK-TriGs) to address bleeding in neonates.” In their paper the team concluded “This study highlights the potential of BK-TriGs, designed for neonatal-specific clotting mechanisms, to address the heightened bleeding and thrombosis risks in neonates, who face 4.4 times higher postsurgery mortality … Our findings support BK-TriGs as a promising approach for improving hemostasis in neonates, offering a tailored, effective solution for this vulnerable patient population.”
When adults cut themselves, a multi-step process called hemostasis stops the bleeding from the injured blood vessel. But hemostasis in infants is different from hemostasis in adults. This difference can be problematic if infants require surgery to address significant medical problems. In surgeries, neonatal patients normally receive blood from adult donors to compensate for blood lost during the operation. “Current treatments rely on transfusing adult blood products, which may cause complications resulting from structural and functional differences between neonatal and adult fibrinogen,” the authors wrote. “… these transfusions pose serious safety concerns by increasing morbidity, prolonging intensive care unit stays, and elevating posttransfusion thrombosis risks in neonates.”
Brown noted, “… if you give adult blood to an infant, the difference in adult hemostasis versus infant hemostasis can lead to too much clotting. That can increase the likelihood of thrombosis, where blood clots form in the lungs or elsewhere and put the baby at risk … “My research team has done a lot of work on surgery-related bleeding in newborns, and we wanted to develop a therapeutic intervention that would reduce bleeding and—by extension—reduce the need for infants to receive adult blood transfusions during surgery.”
The scientists have now reported on their development of a material called B-knob triggered microgels (BK-TriGs). “Fibrin is the main clotting protein in human blood,” Brown explains. “There is a short amino acid sequence called a ‘B peptide’ that links together fibrin molecules to create blood clots where they are needed—and these B peptides play a particularly important role in hemostasis for infants. The BK-TriGs are engineered particles that are studded with those B peptides.”
The particles can absorb water and become squishy hydrogels, which mimic the mechanical properties of natural platelets in a way that maximizes the ability of the B peptides to create fibrin networks and stanch bleeding. “Functionalized with a fibrin hole b–specific peptide, BK-TriGs enhance clot density and resistance to degradation,” the team noted.
The researchers first tested the BK-TriGs by using microfluidic devices that allowed them to conduct in vitro testing to see how the microgels affected clotting in blood plasma from human adults and infants. “In vitro studies using neonatal platelet-poor plasma (PPP) showed that at an optimal concentration, BK-TriGs increased clot density by more than 100% and improved stability by reducing fibrinolysis,” they wrote in summary. “Under flow conditions BK-TriGs promoted robust clot formation compared to plasma-only controls.” Brown noted, “We found that BK-TriGs worked better at improving blood clotting in infant plasma than in adult plasma, which was what we expected to see.”
To further test the efficacy of the BK-TriGs, the researchers worked with lab mice that were genetically engineered to not make fibrinogen, the precursor to fibrin. This allowed the researchers to first introduce infant fibrinogen into the lab mice so that the mice exhibit a form of hemostasis similar to infants. “This innovative model enabled the evaluation of BK-TriGs in a setting that replicates key aspects of neonatal fibrinogen polymerization and fibrinolytic sensitivity, providing preliminary insights into their potential clinical utility.”
Brown added, “We found that the BK-TriGs outperformed any of the other options we tested at reducing blood loss. Specifically, the BK-TriGs reduced blood loss by 50-60% compared to the control group.”
The authors further stated, “The findings highlight the potential of BK-TriGs as a promising synthetic platelet-mimetic approach for enhancing clot density and stability, particularly in neonatal plasma where traditional blood products may pose risks … A fibrin-targeted approach like BK-TriGs, which enhances clot formation without introducing systemic thrombotic risk, may offer a safer alternative to adult fibrinogen transfusions.”
Next steps for the work are to see how BK-TriGs compare to other hemostatic therapeutics that are on the market, either on their own or when used in conjunction with BK-TriGs. “The results we’re reporting here are exciting, but we are still far removed from clinical use,” Brown, acknowledged. “We need to make sure there are no unforeseen risks associated with blood clotting.” The team also commented, “Expanding this research to include different clinical bleeding scenarios will be essential to advancing these materials toward therapeutic applications.”
“This is particularly relevant in neonates, where the most severe bleeding complications often arise in critical sites such as the gastrointestinal tract and the brain,” Brown continued, “But if we do find BK-TriGs are safe and effective, we’re optimistic this could be a cost-effective way to make surgery safer for infants. Manufacturing the BK-TriG particles would be relatively inexpensive—certainly in comparison to blood products.”
The post Injectable Microgel Developed to Reduce Bleeding in Infants Undergoing Surgery appeared first on GEN – Genetic Engineering and Biotechnology News.
How an Alzheimer’s Risk Gene Rewires the Brain Decades Before Symptoms
For millions of people worldwide, carrying the APOE4 gene variant means a significantly higher risk of developing Alzheimer’s disease. Yet one of the biggest unanswered questions has been when, and how, that risk begins to take hold in the brain.
New research from the Gladstone Institutes, published in Nature Aging, suggests that the effects of APOE4 emerge far earlier than previously understood. The study shows that subtle but important changes in brain activity occur long before memory loss begins, offering a potential window for early intervention.
Early changes in a seemingly healthy brain
Alzheimer’s disease is typically diagnosed after cognitive symptoms appear, but growing evidence suggests that the disease process begins decades earlier. The new study adds to this picture by demonstrating that brain circuits in young individuals carrying APOE4 are already functioning differently.
We found fundamental changes in brain circuits occurring in young mice that still had normal learning and memory, and importantly, that those changes predicted the development of cognitive deficits at older ages, ” said Misha Zilberter, PhD, principal staff research scientist at Gladstone and senior author of the study.
The researchers observed increased neuronal activity in the hippocampus, a brain region essential for learning and memory. Similar patterns of hyperactivity have been reported in human APOE4 carriers, even before clinical symptoms arise.
According to the scientists, this suggests that Alzheimer’s risk is not simply a matter of late-stage degeneration, but may instead involve long-term changes in how brain circuits are wired and function.
Smaller neurons, stronger signals
To understand what drives this early hyperactivity, the team examined individual brain cells. They found that neurons in key regions of the hippocampus were physically smaller in APOE4 carriers compared to those with the more common, lower-risk APOE3 variant.
While this might seem like a minor structural difference, it has functional consequences. Smaller neurons are more easily activated, meaning they fire more readily in response to stimuli. This heightened sensitivity can lead to persistent hyperactivity within neural circuits.
Over time, this imbalance may place stress on the brain and contribute to the gradual decline seen in Alzheimer’s disease.
A surprising source of dysfunction
For years, researchers believed that APOE4’s effects were primarily driven by astrocytes, support cells in the brain that produce most of the APOE protein. However, the new findings challenge this assumption.
The team discovered that the disruptive effects on brain activity were instead linked to APOE4 produced directly by neurons themselves. When APOE4 was removed from neurons, their size and activity returned to normal. Removing it from astrocytes, by contrast, had little effect.
This shift in understanding refocuses attention on neurons as key drivers of early disease processes, rather than passive victims of surrounding dysfunction.
A reversible pathway—and a new target
Perhaps the most striking finding of the study is that these early changes may not be permanent.
The researchers identified a protein called Nell2 as a central player in the process. Levels of Nell2 were elevated in APOE4 neurons and appeared to drive both the reduction in cell size and the increase in neuronal activity.
By reducing Nell2 levels in adult mice, the team was able to restore normal neuron structure and function—even after the changes had already occurred.
“What’s exciting about Nell2 is that we were able to reverse the disease manifestations in adult mice by lowering its level,” said Yadong Huang, co-senior author of the study. “That tells us the damage is not irreversible […].”
This raises the possibility of developing therapies that target Nell2, potentially slowing or preventing disease progression in individuals at high genetic risk.
Implications for early intervention
APOE4 is present in roughly one in four people and in the majority of Alzheimer’s patients. Despite this, current treatments largely focus on late-stage symptoms rather than early prevention.
The new findings suggest that intervening earlier, before cognitive decline begins, could be key. If brain circuit changes can be detected and corrected at an early stage, it may be possible to delay or even prevent the onset of Alzheimer’s disease.
The study also highlights the importance of understanding how genetic risk translates into functional changes in the brain. Rather than acting as a simple risk marker, APOE4 appears to actively reshape neural activity over time.
A shift in perspective
More broadly, the work reflects a growing shift in Alzheimer’s research, from focusing solely on hallmark features such as amyloid plaques and tau tangles to examining earlier, subtler changes in brain function.
By identifying a concrete pathway linking genetic risk to altered brain activity, the study provides a clearer framework for understanding how the disease develops.
“This study is a big breakthrough for the field of Alzheimer’s research,” Huang said. “It opens the door to a better understanding of how APOE4 alters the function of neurons at a young age to increase risk of cognitive decline, and to the development of therapies that could block the detrimental effects of APOE4 early on.”
While the findings are based on mouse models, they align closely with observations in humans and offer a strong foundation for future research. The next steps will involve determining whether targeting Nell2 or similar pathways can produce similar benefits in human patients.
If successful, such approaches could transform how Alzheimer’s disease is treated, not as an inevitable consequence of aging, but as a process that can be detected early and potentially reversed.
The post How an Alzheimer’s Risk Gene Rewires the Brain Decades Before Symptoms appeared first on Inside Precision Medicine.
Epigenetic Strategy Restores Tumor Suppressor in Acute Myeloid Leukemia Models
Scientists from The Jackson Laboratory (JAX) and their collaborators elsewhere have found a potential way to treat cases of acute myeloid leukemia that involves turning a key cancer fighting gene back on. Besides potentially treating AML without harsh chemotherapy regimens, their work also highlights a promising strategy for studying gene-silencing mechanisms in other diseases. Full details of the study, which was done in mice, are available in a paper published in Science Translational Medicine titled “Epigenetic reactivation of the tumor suppressor ZBTB7A by KDM4 inhibition in human acute myeloid leukemia.”
Normally, tumor suppressor genes work to prevent cells from becoming cancerous. But in cancers like AML, some of these genes are switched off epigenetically. These changes to gene activity are difficult to track because standard DNA sequencing technologies are designed to find mutated DNA. “If we can identify which genes have been silenced and understand how to turn them back on, that could open up entirely new therapeutic possibilities,” said Eric Wang, PhD, an assistant professor JAX who led the research. “Instead of only trying to kill these cells, we may be able to restore the mechanisms that normally keep them under control.”
Though scientists have made great strides in developing therapies for AML, prognosis for the disease is still relatively poor. Part of the challenge is that AML cells remain in an immature, stem cell-like state. According to the paper, Wang and his team developed a tool that combines fluorescence in situ hybridization and flow cytometry with CRISPR gene editing technology to map gene activity in cells. They used the tool, called FISHnCRISP, to identify a tumor-suppressing gene called ZBTB7A that is silenced in AML patients. By restoring ZBTB7A expression, the scientists forced the cancer cells into a state where they grew less aggressively.
Digging into the details, AML cells produce a longer version of ZBTB7A’s regulatory tail, that contains sites that attract a protein called ZFP36L2, which reduces the gene’s activity. Additionally, a family of enzymes known as KDM4 modify how DNA is packaged inside AML cells, which effectively silences ZBTB7A expression. Data from experiments in mice with AML showed that when KDM4 enzymes were blocked, ZBTB7A regained its expression, reducing leukemia burden while leaving normal blood formation largely unaffected.
Importantly, “there are drug candidates out there to inhibit KDM4, and in our study we just repurposed one of them to treat AML cells,” Wang said. “We won’t know unless we test it in clinical trials, but this approach could be better than chemotherapy, because we showed it’s not toxic at all to normal blood cells.”
Future studies will focus on refining the approach and determining whether it might be combined with existing treatments. The team plans to test an experimental drug that targets KDM4, which is currently being tested in a clinical trial for solid tumors.
“We demonstrated that downregulating ZBTB7A causes this hyperinflammatory state that promotes cancer growth” and “now, we’re proposing this epigenetic approach to force AML cells to differentiate into white blood cells that eventually undergo cell death,” Wang said. “We could potentially translate our research into an early phase clinical trial more readily than developing a whole new compound from scratch.”
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STAT+: NIH would get $5 billion cut under Trump’s 2027 budget, but Congress unlikely to go along
The White House is asking Congress to cut $5 billion from the National Institutes of Health and to downsize the number of its institutes and centers from 27 to 22 — a plan that is expected to receive a chilly reception from lawmakers from both parties.
The president’s fiscal year 2027 budget request, released Friday, asks for $41 billion for the NIH and eliminates the National Center for Complementary and Integrative Health, the Fogarty International Center, and the National Institute on Minority Health and Health Disparities. The 2027 budget also proposes consolidating two institutes focused on research on drug and alcohol abuse into a new entity called the National Institute of Substance Use and Addiction Research, as well as relocating the National Institute of Environmental Health Sciences into the Centers for Disease Control and Prevention.
The White House proposal also asks Congress to slash the budget for the Advanced Research Projects (ARPA-H), which funds cutting-edge science, from its current $1.5 billion to $945 million.
Four things we’d need to put data centers in space
MIT Technology Review Explains: Let our writers untangle the complex, messy world of technology to help you understand what’s coming next. You can read more from the series here.
In January, Elon Musk’s SpaceX filed an application with the US Federal Communications Commission to launch up to one million data centers into Earth’s orbit. The goal? To fully unleash the potential of AI without triggering an environmental crisis on Earth. But could it work?
SpaceX is the latest in a string of high-tech companies extolling the potential of orbital computing infrastructure. Last year, Amazon founder Jeff Bezos said that the tech industry will move toward large-scale computing in space. Google has plans to loft data-crunching satellites, aiming to launch a test constellation of 80 as early as next year. And last November Starcloud, a startup based in Washington State, launched a satellite fitted with a high-performance Nvidia H100 GPU, marking the first orbital test of an advanced AI chip. The company envisions orbiting data centers as large as those on Earth by 2030.
Proponents believe that putting data centers in space makes sense. The current AI boom is straining energy grids and adding to the demand for water, which is needed to cool the computers. Communities in the vicinity of large-scale data centers worry about increasing prices for those resources as a result of the growing demand, among other issues.
In space, advocates say, the water and energy problems would be solved. In constantly illuminated sun-synchronous orbits, space-borne data centers would have uninterrupted access to solar power. At the same time, the excess heat they produce would be easily expelled into the cold vacuum of space. And with the cost of space launches decreasing, and mega-rockets such as SpaceX’s Starship promising to push prices even lower, there could be a point at which moving the world’s data centers into space makes sound business sense. Detractors, on the other hand, tell a different story and point to a variety of technological hurdles, though some say it’s possible they may be surmountable in the not-so-distant future. Here are four of the must-haves we’d need to make space-based data centers a reality.
A way to carry away heat
AI data centers produce a lot of heat. Space might seem like a great place to dispel that heat without using up massive amounts of water. But it’s not so simple. To get the power needed to run 24-7, a space-based data center would have to be in a constantly illuminated orbit, circling the planet from pole to pole, and never hide in Earth’s shadow. And in that orbit, the temperature of the equipment would never drop below 80 °C, which is way too hot for electronics to operate safely in the long term.
Getting the heat out of such a system is surprisingly challenging. “Thermal management and cooling in space is generally a huge problem,” says Lilly Eichinger, CEO of the Austrian space tech startup Satellives.
On Earth, heat dissipates mostly through the natural process of convection, which relies on the movement of gases and liquids like air and water. In the vacuum of space, heat has to be removed through the far less efficient process of radiation. Safely removing the heat produced by the computers, as well as what’s absorbed from the sun, requires large radiative surfaces. The bulkier the satellite, the harder it is to send all the heat inside it out into space.
But Yves Durand, former director of technology at the European aerospace giant Thales Alenia Space, says that technology already exists to tackle the problem.
The company previously developed a system for large telecommunications satellites that can pipe refrigerant fluid through a network of tubing using a mechanical pump, ultimately transferring heat from within a spacecraft to radiators on the exterior. Durand led a 2024 feasibility study on space-based data centers, which found that although challenges exist, it should be possible for Europe to put gigawatt-scale data centers (on par with the largest Earthbound facilities) into orbit before 2050. These would be considerably larger than those envisioned by SpaceX, featuring solar arrays hundreds of meters in size—larger than the International Space Station.
Computer chips that can withstand a radiation onslaught
The space around Earth is constantly battered by cosmic particles and lashed by solar radiation. On Earth’s surface, humans and their electronic devices are protected from this corrosive soup of charged particles by the planet’s atmosphere and magnetosphere. But the farther away from Earth you venture, the weaker that protection becomes. Studies show that aircraft crews have a higher risk of developing cancer because of their frequent exposure to high radiation at cruising altitude, where the atmosphere is thin and less protective.
Electronics in space are at risk of three types of problems caused by high radiation levels, says Ken Mai, a principal systems scientist in electrical and computer engineering at Carnegie Mellon University. Phenomena known as single-event upsets can cause bit flips and corrupt stored data when charged particles hit chips and memory devices. Over time, electronics in space accumulate damage from ionizing radiation that degrades their performance. And sometimes a charged particle can strike the component in a way that physically displaces atoms on the chip, creating permanent damage, Mai explains.
Traditionally, computers launched to space had to undergo years of testing and were specifically designed to withstand the intense radiation present in Earth’s orbit. These space-hardened electronics are much more expensive, though, and their performance is also years behind the state-of-the-art devices for Earth-based computing. Launching conventional chips is a gamble. But Durand says cutting-edge computer chips use technologies that are by default more resistant to radiation than past systems. And in mid-March, Nvidia touted hardware, including a new GPU, that is “bringing AI compute to orbital data centers.”
Nvidia’s head of edge AI marketing, Chen Su, told MIT Technology Review, that “Nvidia systems are inherently commercial off the shelf, with radiation resilience achieved at the system level rather than through radiation‑hardened silicon alone.” He added that satellite makers increase the chips’ resiliency with the help of shielding, advanced software for error detection, and architectures that combine the consumer-grade devices with bespoke, hardened technologies.
Still, Mai says that the data-crunching chips are only one issue. The data centers would also need memory and storage devices, both of which are vulnerable to damage by excessive radiation. And operators would need the ability to swap things out or adapt when issues arise. The feasibility and affordability of using robots or astronaut missions for maintenance is a major question mark hanging over the idea of large-scale orbiting data centers.
“You not only need to throw up a data center to space that meets your current needs; you need redundancy, extra parts, and reconfigurability, so when stuff breaks, you can just change your configuration and continue working,” says Mai. “It’s a very challenging problem because on one hand you have free energy and power in space, but there are a lot of disadvantages. It’s quite possible that those problems will outweigh the advantages that you get from putting a data center into space.”
In addition to the need for regular maintenance, there’s also the potential for catastrophic loss. During periods of intense space weather, satellites can be flooded with enough radiation to kill all their electronics. The sun has just passed the most active phase of its 11-year cycle with relatively little impact on satellites. Still, experts warn that since the space age began, the planet has not experienced the worst the sun is capable of. Many doubt whether the low-cost new space systems that dominate Earth’s orbits today are prepared for that.
A plan to dodge space debris
Both large-scale orbiting data centers such as those envisioned by Thales Alenia Space and the mega-constellations of smaller satellites as proposed by SpaceX give a headache to space sustainability experts. The space around Earth is already quite crowded with satellites. Starlink satellites alone perform hundreds of thousands of collision avoidance maneuvers every year to dodge debris and other spacecraft. The more stuff in space, the higher the likelihood of a devastating collision that would clutter the orbit with thousands of dangerous fragments.
Large structures with hundreds of square meters of solar arrays would quickly suffer damage from small pieces of space debris and meteorites, which would over time degrade the performance of their solar panels and create more debris in orbit. Operating one million satellites in low Earth orbit, the region of space at the altitude of up to 2,000 kilometers, might be impossible to do safely unless all satellites in that area are part of the same network so they can communicate effectively to maneuver around each other, Greg Vialle, the founder of the orbital recycling startup Lunexus Space, told MIT Technology Review.
“You can fit roughly four to five thousand satellites in one orbital shell,” Vialle says. “If you count all the shells in low Earth orbit, you get to a number of around 240,000 satellites maximum.”
And spacecraft must be able to pass each other at a safe distance to avoid collisions, he says.
“You also need to be able to get stuff up to higher orbits and back down to de-orbit,” he adds. “So you need to have gaps of at least 10 kilometers between the satellites to do that safely. Mega-constellations like Starlink can be packed more tightly because the satellites communicate with each other. But you can’t have one million satellites around Earth unless it’s a monopoly.”
On top of that, Starlink would likely want to regularly upgrade its orbiting data centers with more modern technology. Replacing a million satellites perhaps every five years would mean even more orbital traffic—and it could increase the rate of debris reentry into Earth’s atmosphere from around three or four pieces of junk a day to about one every three minutes, according to a group of astronomers who filed objections against SpaceX’s FCC application. Some scientists are concerned that reentering debris could damage the ozone layer and alter Earth’s thermal balance.
Economical launch and assembly
The longer hardware survives in orbit, the better the return on investment. But for orbital data centers to make economic sense, companies will have to find a relatively cheap way to get that hardware in orbit. SpaceX is betting on its upcoming Starship mega-rocket, which will be able to carry up to six times as much payload as the current workhorse, Falcon 9. The Thales Alenia Space study concluded that if Europe were to build its own orbital data centers, it would have to develop a similarly potent launcher.
But launch is only part of the equation. A large-scale orbital data center won’t fit in a rocket—even a mega-rocket. It will need to be assembled in orbit. And that will likely require advanced robotic systems that do not exist yet. Various companies have conducted Earth-based tests with precursors of such systems, but they are still far from real-world use.
Durand says that in the short term, smaller-scale data centers are likely to establish themselves as an integral part of the orbital infrastructure, by processing images from Earth-observing satellites directly in space without having to send them to Earth. That would be a huge help for companies selling insights from space, as many of these data sets are extremely large, and competition for opportunities to downlink them to Earth for processing via ground stations is growing.
“The good thing with orbital data centers is that you can start with small servers and gradually increase and build up larger data centers,” says Durand. “You can use modularity. You can learn little by little and gradually develop industrial capacity in space. We have all the technology, and the demand for space-based data processing infrastructure is huge, so it makes sense to think about it.”
Smaller facilities probably won’t do much to offset the strain that terrestrial data centers are placing on the planet’s water and electricity, though. That vision of the future might take decades to come to fruition, some critics think—if it even gets off the ground at all.
STAT+: White House proposes 12% cut to federal health agencies in 2027 budget request
WASHINGTON — The White House wants Congress to cut spending on the Department of Health and Human Services by more than 12%, according to its proposed 2027 federal budget, released Friday.
The budget is broadly similar to what the Trump administration proposed last year. That includes deep cuts to the National Institutes of Health, the elimination of a health research agency, and the creation of a new agency devoted to chronic diseases called the Administration for a Healthy America.
The president’s budget is as an agenda-setting document, offering a sense of what the administration hopes to focus on in the coming year. Congress, however, is ultimately responsible for passing laws that set federal spending.
The Unspoken Toll: Why Exam Pressure Must Be Part of the Youth Mental Health Discussion
A Conversation with Tatum Redmond and Amanda van der Vyver-Anderson from Community Keepers, South Africa
By Mai El Shoush, Partnerships Campaign Manager, Stavros Niarchos Foundation (SNF) Global Center for Child and Adolescent Mental Health at the Child Mind Institute
Community Keepers is an award-winning organization based in Stellenbosch, South Africa, which works to improve the social and emotional well-being of learners and their caregivers. The SNF Global Center at the Child Mind Institute works with the organization to further advance the comprehensive mission of transforming schools into safe spaces where student well-being is prioritized alongside academic achievement. This includes strengthening the workforce to expand evidence-based support and brief interventions through low-intensity psychological therapy approaches.
While addressing the workforce gaps, the partnership has yielded valuable insight into the essential competencies front line workers require to effectively support young people experiencing mental health challenges. Together with other NGOs, Community Keepers has also been instrumental in strengthening the process of developing context-sensitive and culturally appropriate training materials scheduled for pilot implementation in South Africa later this year – representing an important step towards strengthening mental health care systems for underserved communities. The partnership also extends beyond training development, as the SNF Global Center at the Child Mind Institute continues to collaborate closely with Community Keepers on an upcoming randomized control trial (RCT). The scientific evaluation will assess both the feasibility of establishing a virtual clinic for young people and the effectiveness of remotely delivered cognitive behavioral therapy (CBT) interventions via video consultations. The research is intended to expand access to equitable and quality mental health care for young people across South Africa. Tatum Redmond has been a care facilitator in one of the Community Keepers’ high school-based offices, while Amanda van der Vyver-Anderson is an educational psychologist and heads the training and development of Mental Health First Aiders for internal and external staff.
How important is it to approach issues such as academic pressure within the wider conversation around youth mental health in South Africa, and beyond?
It is critical to integrate discussions of exam stress into the broader dialogue surrounding youth mental health, both here in South Africa and internationally. We see countless students under immense pressure to not only pass, but also secure their future prospects and meet family expectations. This is unfortunately often dismissed as “just school” or a “normal” experience. However, it impacts a substantial number of young people, often more severely than we acknowledge. And the level of support available is not equitable across the board. Addressing this is crucial because of the detrimental effects on core cognitive functions — and ultimately, academic performance — as well as the significant toll on mental health. This can manifest as anxiety, burnout, and even depression.
In what ways can exam-related stress connect to broader mental health challenges?
While a certain level of stress can serve as a beneficial motivator, severe distress can lead to cognitive shutdown. This specifically impacts the executive functions — planning, organizing, prioritizing, working memory, focus, and concentration — that are fundamental to preparing for exams. This shutdown can then create a detrimental, ongoing cycle of heightened stress about exams or the future, coupled with a decline in the ability to take effective action.
It’s vital to recognize that exam stress does not merely stay in the exam room — it can be a gateway to larger mental health challenges. Constant stress regarding school performance, marks, or the fear of failure can escalate into conditions like anxiety, chronic overwhelm, or depression. Students may experience sleep disruption, poor nutrition, and feelings of inadequacy. And these symptoms often persist long after the test is over. Compounding this is the reluctance of most students to seek help because they believe their feelings are normal or fear appearing weak. Yet, if left unaddressed, sustained pressure along with these symptoms can profoundly affect their psychological well-being.
What role do community-focused organizations such as Community Keepers play in linking academic stress to systematic youth mental health support and improvement?
Organizations like Community Keepers play a truly pivotal role — not merely as emergency responders but as an integrated support system within educational institutions as well. Crucially, they move beyond immediate crisis response by collaborating with schools to develop long-term support and to provide safe spaces to engage in dialogue. They offer genuine attention and care when learners are struggling with school demands, exams, and family pressures.
The approach is not just “addressing stress today” but asking, “How can we create an enduring environment where young people feel safe, supported, and connected?” Doing this requires collaboration with the learners themselves, educators and school staff, as well as parents, caregivers, and community leaders.
What factors make schools uniquely positioned to be safe and supportive spaces?
Schools are exceptionally well-positioned to serve as safe and supportive spaces for students for several key reasons:
- Learners spend a substantial portion of their day at school, making it a primary setting where adults can observe signs of distress, anxiety, or coping difficulties.
- Schools have the opportunity to house critical personnel — teachers, counselors, and external partners like Community Keepers — who are on hand to offer support or a listening ear.
- The curriculum can extend beyond academic skills and learning. It can include mental health and emotional literacy, stress management, and peer support.
- When a school actively fosters an environment of safety, respect, and validation, it fundamentally alters how learners navigate pressure, stress, or complex personal problems. Having a guaranteed safe space at school is deeply stabilizing for the mind.
How can the goal of securing mental health support as a pillar of education be reached?
Achieving the goal of establishing mental health support as a solid, non-negotiable pillar of education requires several strategic commitments:
- Schools must actively allocate resources for it, ensuring adequate numbers of support staff, rather than relying on minimal provision. Teachers need training to recognize signs of distress and respond helpfully and appropriately.
- Mental health literacy must be integrated into the curriculum. Instead of only focusing on academic subjects, topics like stress management, emotional intelligence, and maintaining healthy relationships should be covered.
- The government must demonstrate a serious commitment, including mental health support in education budgets, developing clear policies, and ensuring rigorous follow-through.
How have your practices and initiatives in promoting and supporting schools as safe spaces made meaningful change?
We’ve observed tangible change in the learners’ attitudes; those who feel comfortable expressing their emotions are generally happier and more resilient because they have established a safe, non-judgmental space where trust is built.
What role can teachers and school leadership play as partners in creating an evidence-based supportive learning environment? Where are the gaps in building capacity and how can they be better supported?
Educators and school leadership are essential partners in establishing an environment that successfully supports learner mental health and cultivates a culture of well-being. They can do so by:
- Prioritizing both the physical space and curriculum time necessary for learners to engage with support services.
- Serving as role models who embody and encourage emotional regulation and actively normalize help-seeking behaviour.
- Remaining deeply cognisant of factors that contribute to learner distress so as to not inadvertently exacerbate it.
Investing in staff wellness and support, capacity building, and policy reform is not merely beneficial, but a foundational requirement to capacitate educators effectively. This allows them to sustainably support the mental health of their entire school community.
The SNF Global Center’s work in South Africa is carried out through the Child and Adolescent Mental Health Initiative (CAMHI South Africa). We are proud to expand the partnership with Community Keepers and value their collaboration towards co-creating scalable, school-centered mental health approaches that authentically respond to the diverse lived-experiences of young people.
The post The Unspoken Toll: Why Exam Pressure Must Be Part of the Youth Mental Health Discussion appeared first on Child Mind Institute.