NASA has announced a new commercial partnership for the next satellite headed to the Red Planet.
California-based Relativity Space will design, build and launch the spacecraft that carries NASA's Aeolus instrument suite to orbit around Mars, where the probe will be the first to provide daily measurements of the planet's global environment. Aeolus will collect data on Martian dust and cloud cover, winds and temperatures, according to a NASA release.
"Public-private partnerships like this are a force multiplier for science," NASA Administrator Jared Isaacman said in a statement on Wednesday (June 17).
The newly announced relationship, and others between NASA and private industry, is designed to allow the agency to concentrate its resources on important science discovery. "By pairing NASA’s world‑class instruments with commercial innovation and investment, we can deliver more science, more often, and reduce the time it takes to get essential data into the hands of researchers preparing for future human missions to Mars," Isaacman said.
Aeolus consists of four instruments, designed to work in tandem to create a complete picture of the Martian atmosphere and its behavior. In addition to refining scientific models for the Martian environment, NASA plans to use the data to reduce risks to future robotic and crewed missions landing on Mars' surface.
The science suite includes the Doppler Wind and Temperature Sounder (DWTS‑Ozone), in collaboration with GATS, designed to measure wind speeds and temperatures present up to 37 miles (60 kilometers) above the ground. The Thermal Limb Sounder (TLS), designed with Xiomas Technologies, will create vertical temperature profiles and provide data on atmospheric dust and cloud cover, while the Surface Radiometric Sensor Package (SuRSeP) collects compositional data on those clouds and dust, and tracks how the Martian surface absorbs, stores and releases energy, like heat. Finally, Aeolus' Wide‑Field Context Camera (WFCC) will take daily images to assess atmospheric activity across the whole of Mars.
NASA is targeting 2028 for the launch of the Aeolus mission, which will be designed and built at NASA's Ames Research Center in California, where it will also be integrated on Relativity's spacecraft for testing ahead of launch. NASA has committed to support Aeolus' scientific operations for at least one Martian year (approximately 687 Earth days). However, the agency has historically extended its missions to Mars, when able.
NASA was recently forced to end operations of its MAVEN (Mars Atmosphere and Volatile Evolution) probe around Mars, after an anomaly led to a loss of communications with the satellite, but the spacecraft ran for more than a decade beyond its original one-year mission. The agency's only two active satellites orbiting the Red Planet are the Mars Reconnaissance Orbiter (MRO) and Mars Odyssey, which are both operating nearly two decades or more, respectively, beyond their initial mission timelines.
For its part, Relativity will be in charge of designing the Mars-bound spacecraft and will also be responsible for launch and for satellite operations in space. The company's pathfinder launch vehicle, the Terran 1 rocket, lifted off for the first and only time in March 2023, but it failed to reach orbit. The company then pivoted to development of the bigger, partially reusable Terran R rocket, which is expected to debut sometime later this year. Eric Schmidt, who served as Google CEO from 2001 to 2011, was appointed to lead Relativity in March 2025.
In a groundbreaking study shedding light on the molecular intricacies of arousal regulation, researchers from Pompeu Fabra University (UPF) and the Centre for Genomic Regulation (CRG) have unveiled the profound influence of neuronal microexons on behavioral states in zebrafish. This study elucidates how subtle alterations in these tiny genetic fragments can trigger hyperarousal—a state marked by heightened neural excitability and pronounced insomnia-like symptoms—which echoes the pathophysiological features observed in various neurodevelopmental disorders. The implications extend far beyond aquatic models, offering a window into the conserved mechanisms of arousal that potentially inform conditions such as autism spectrum disorder and schizophrenia in humans.
Arousal represents a fundamental neurophysiological process essential for survival, enabling organisms to respond to external and internal stimuli with appropriate behavioral and neural adaptations. This highly conserved mechanism across species ensures a meticulously balanced state, modulating responsiveness between lethargy and sensory hypersensitivity. Dysregulation of this balance manifests clinically as either diminished responsiveness or excessive wakefulness and sensory overload, typical hallmarks of stress and various neurodevelopmental pathologies.
Fundamental to this regulatory system is the diversity of proteins synthesized during development and adulthood through alternative splicing—a sophisticated post-transcriptional gene editing process. Alternative splicing enables the generation of multiple functionally distinct protein isoforms from a single gene, often mediated by the inclusion or exclusion of microexons. Microexons are exceptionally short exonic sequences within neuronal genes that profoundly influence protein function and neuronal circuit dynamics despite their minuscule size.
The investigative team employed zebrafish larvae, leveraging their optical transparency and genetic tractability to scrutinize the behavioral consequences of neural microexon misregulation. Larvae exhibiting abnormal microexon patterns demonstrated conspicuous hyperarousal behaviors including disrupted swim patterns and shortened sleep duration. “These larvae not only sleep less frequently but also take considerably longer to initiate sleep,” remarks first author Tahnee Mackensen. This behavioral hyperactivity parallels neural hyperexcitability, suggesting microexon regulation as a pivotal determinant of neurobehavioral states.
At the cellular signaling level, the researchers identified dysregulated cyclic adenosine monophosphate (cAMP) cascades as a key mediator of the observed hyperactive state. cAMP is a ubiquitous second messenger involved in modulating neuronal excitability and synaptic plasticity. The altered splicing of microexons modulates cAMP synthesis and degradation pathways, leading to an aberrant excitation of forebrain neurons in hyperaroused larvae. Notably, this altered cAMP signaling manifests as heightened cAMP-dependent protein kinase A (PKA) activity and subsequent phosphorylation of the transcription factor CREB, implicating the canonical cAMP-PKA-CREB pathway in the regulation of arousal.
The study’s pharmacological interventions underscore the centrality of cAMP regulation in arousal control. Application of cAMP inhibitors normalized the elevated neural activity and behavioral hyperarousal in mutant fish, whereas artificially elevating cAMP in wild-type fish recapitulated the hyperactive phenotype. This bidirectional modulation fortifies the concept that neuronal cAMP levels function as a ‘thermostat’ for arousal states, fine-tuning neuronal excitability and behavioral responsiveness.
Beyond the immediate findings in zebrafish, this research builds upon prior observations in drosophila models demonstrating that microexon disruption similarly impairs sleep and elevates arousal. “The parallel between species indicates an evolutionarily conserved arousal mechanism,” explains Manuel Irimia, senior author. This conservation implies that microexon misregulation, while mechanistically nuanced, may contribute to the neuropsychiatric symptomatology observed in mammals, including humans.
Human neurological disorders such as autism and schizophrenia are often accompanied by sleep disruption and sensory processing anomalies attributed, in part, to aberrant microexon splicing. While microexon alterations are unlikely to be sole causative factors, they may exacerbate or modulate disease phenotypes by disturbing neural excitability homeostasis. These insights prompt a reevaluation of therapeutic strategies aimed at restoring microexon splicing fidelity or modulating cAMP signaling pathways to alleviate neurodevelopmental symptomatology.
Moreover, the link between this microexon-cAMP pathway and mood disorders such as anxiety and depression opens compelling avenues for future research. The cAMP-PKA-CREB axis has well-documented roles in synaptic plasticity and mood regulation, suggesting that microexon-associated dysregulation could contribute to broader neuropsychiatric conditions. “This discovery might just scratch the surface of a complex regulatory network influencing brain function,” notes Mackensen.
The transparency and genetic accessibility of the zebrafish model provided unparalleled opportunities to visualize and quantify internal states through behavioral readouts. Advanced imaging of larval swimming patterns and direct measurement of neurochemical parameters furnished robust correlative evidence linking genetic alterations to functional outcomes. These technical advancements highlight the integrative power of model organisms in neuroscience.
Importantly, this research received support from an array of prestigious funding bodies, including the Horizon 2020 Framework Programme, the Marie Sklodowska-Curie Actions, and the Wellcome Trust, emphasizing the global significance and collaborative nature of this work. The study’s publication in Science Advances confirms its high impact and relevance to the scientific community.
As the team pursues translational studies, the prospect of correcting arousal imbalances by manipulating cAMP pathways or restoring microexon expression presents a promising frontier. This is especially critical given that aberrant arousal and sleep disturbances profoundly impair quality of life in neurodevelopmental disorders. The findings pave the way for multidisciplinary approaches integrating molecular genetics, neurobiology, and pharmacology to develop targeted interventions.
In summation, the identification of neuronal microexons as key modulators of arousal states via the cAMP-PKA-CREB pathway in zebrafish represents a seminal advance in our understanding of the molecular substrates governing complex behavioral phenotypes. This research not only deciphers fundamental biological mechanisms but also holds translational potential to inform therapeutic avenues for neuropsychiatric conditions marked by disrupted arousal and sleep.
Subject of Research: Animals
Article Title: Neuronal microexons modulate arousal via the cAMP-PKA-CREB pathway in zebrafish
News Publication Date: 19-Jun-2026
Web References: 10.1126/sciadv.ady8291
Image Credits: UPF – CRG
Keywords: Exons, Gene splicing, Developmental neuroscience, Anxiety, Sleep disorders, cAMP signaling, Zebrafish
In early 2024, a baffling outbreak of H5N1 avian influenza emerged among dairy cattle in the Texas Panhandle, presenting a new and unexpected clinical manifestation of the virus. Unlike the typical respiratory illness caused by H5N1 in other mammals, affected cows exhibited severe necrotizing mastitis, an inflammatory condition predominantly targeting the mammary glands. This atypical tissue tropism challenged existing paradigms and delayed the accurate diagnosis, as initial veterinary investigations focused mainly on bacterial pathogens common to mastitis. The revelation that H5N1 was the etiological agent marked a critical moment in understanding how influenza viruses can adapt to novel hosts and tissues.
The study, recently published in Science Advances by researchers at the University of Pittsburgh School of Public Health, provides pioneering mechanistic insights into this unusual manifestation. The research team, led by Dr. Suresh Kuchipudi, elucidated the molecular basis for the H5N1 virus’s propensity to infect bovine mammary tissue rather than respiratory organs. This phenomenon, now observed in over 100 avian and mammalian species globally, underscores the remarkable plasticity of the H5N1 virus and its ability to exploit unique receptor architectures in different host species.
Traditionally, H5N1 and related influenza viruses target sialic acid glycan receptors present in the respiratory tract, facilitating viral entry primarily via respiratory epithelial cells. However, in bovines, the absence of clinical respiratory disease despite the presence of these glycans suggested a more nuanced receptor interaction paradigm. Kuchipudi’s group hypothesized that not just the presence but the precise molecular subtype and distribution of influenza receptors could dictate tissue tropism. Their investigation focused on delineating the receptor landscape across bovine tissues using cutting-edge glycomic methods combined with binding assays and ultra-high-resolution microscopy.
The team employed glycomics—a comprehensive approach to cataloging glycan structures—collaborating with expert Dr. Lauren E. Pepi from Harvard Medical School. They identified that among various glycan receptors, only a particular subclass known as N-linked sialic acid receptors demonstrated a high affinity for the H5N1 virus. Crucially, these receptors were found to be prevalent and densely expressed in the mammary epithelial cells of the udder but conspicuously scarce in bovine airway tissues. This spatial receptor distribution offers a molecular explanation for the virus’s unusual targeting of the mammary gland, enabling productive viral replication and resulting clinical mastitis.
The discovery sheds light on the critical role of receptor architecture in species-specific influenza virus infection. Prior reports indicated the presence of flu-related glycans in bovine respiratory tissues, but those receptors did not support significant viral binding or replication. The differential receptor expression patterns in respiratory versus mammary tissues effectively reprogrammed the virus’s tissue tropism. This specialization allows H5N1 to hijack the bovine mammary environment as a niche, explaining why infected cattle shed the virus in milk rather than displaying respiratory symptoms.
Beyond animal health, this finding carries important public health implications. The intense viral shedding into milk poses a risk to farm workers exposed to raw milk and raises concerns regarding zoonotic transmission routes. Dr. Kuchipudi points out that while pasteurization effectively neutralizes the virus, the common practice of feeding raw milk to domestic pets, notably cats, can facilitate cross-species transmission. Indeed, previous studies documented feline fatalities linked to H5N1 infection. This highlights the hidden dangers of viral reservoirs in dairy cattle and underscores the need for enhanced surveillance and biosecurity protocols within agricultural settings.
Methodologically, the study stands out for its innovative multimodal approach. The integration of high-precision receptor mapping with functional binding experiments allowed researchers to move beyond conventional histochemical staining. This enabled a granular understanding of the receptor types mediating viral entry, paving the way for predictive models of viral host and tissue susceptibility. By decoding the receptor landscape at this molecular scale, the research team demonstrated an unprecedented ability to identify viral tropism determinants, which could serve as early warning indicators for emergent influenza strains.
Looking forward, these insights form the foundation for a new paradigm in influenza research and surveillance. Scientists can now preemptively screen various animal species—not just for the presence of virus-compatible receptors but for specific tissue vulnerabilities within those hosts. This capability is transformative for anticipating how H5N1 and related viruses might manifest clinically, whether through respiratory symptoms, mastitis-like conditions, or neurological involvement, as previously seen in felines. Such proactive screening could revolutionize public health responses, affording precious time to deploy targeted interventions and prevent widespread outbreaks.
The implications of receptor-based viral tropism extend beyond livestock to potential future zoonoses affecting humans. Understanding the molecular basis of host adaptation provides critical clues into viral evolution and spillover risk. This knowledge also informs vaccine development and therapeutic strategies by highlighting tissue-specific pathways of viral entry and replication. As zoonotic influenza viruses continue to adapt, harnessing receptor glycomics will be vital for staying ahead of viral evolution and protecting both animal and human health.
The study was a collaborative effort involving multiple institutions and experts, including contributors from Pennsylvania State University, Harvard University, and North Dakota State University. Their combined expertise spanned infectious diseases, glycomics, virology, and veterinary medicine, enabling a comprehensive and multidisciplinary approach. Supported by the U.S. Department of Agriculture’s National Institute of Food and Agriculture and Pitt Public Health, this research exemplifies how fundamental science can directly inform and improve agricultural biosecurity and zoonotic disease preparedness.
Ultimately, this investigation marks a significant milestone in understanding influenza virus host adaptation. By revealing the receptor basis for the bovine-specific tissue tropism of H5N1, the study not only clarifies an enigmatic veterinary health issue but also establishes a versatile scientific framework for future viral threat assessment. As influenza viruses continue to evolve in complex ecological contexts, such mechanistic insights will be indispensable tools to foresee their next unexpected moves and mitigate their impact on global health.
Subject of Research: Animals
Article Title: Receptor Basis of Unusual Tissue Tropism of Avian Influenza H5N1 Clade 2.3.4.4b Virus in Cattle
News Publication Date: 19-Jun-2026
Web References: https://doi.org/10.1126/sciadv.aea2068
Image Credits: Department of Infectious Diseases and Microbiology, School of Public Health, University of Pittsburgh
Keywords: Avian influenza, Glycomics, Public health, Viruses
In a groundbreaking stride toward the future of quantum technology, researchers have unlocked a new mechanism to control quantum emitters embedded in hexagonal boron nitride (hBN), a layered two-dimensional material. This breakthrough could serve as a critical leap forward in integrating quantum emitters into practical devices, bringing quantum computing, secure quantum communications, and ultra-sensitive quantum sensors closer to reality. This promising development emerged from meticulous experimental studies demonstrating the ability to reversibly tune the color and wavelength of light emitted by quantum defects in hBN simply by twisting its atomic layers.
Quantum emitters are nanoscopic sources of light that emit photons with quantum characteristics, pivotal for next-generation technologies reliant on quantum information processing. However, a formidable challenge in utilizing these emitters has been the difficulty in precisely controlling their optical properties post-fabrication. Dr. Angus Gale, the lead scientist behind this research, elucidated how their work provides an innovative “lever” by exploiting the intrinsic layered nature of hBN to adjust the quantum emission properties dynamically. Unlike traditional solid-state hosts such as diamond or silicon carbide, whose structures are rigid and three-dimensional, hBN’s atomically thin layers can be mechanically manipulated, lending itself to an unprecedented degree of tunability.
The team’s experiments demonstrated that by picking up, stacking, twisting, and restacking these ultra-thin hBN slices at varied angles, they could modulate the quantum emitters’ light emission dramatically. These shifts in wavelength were not minor perturbations but substantial changes far exceeding what has been typically achievable in similar solid-state quantum systems. This finding challenges the traditional paradigm which often seeks to stabilize quantum defect behavior within rigid host materials. Instead, the researchers embraced the inherent flexibility and twistability of hBN to realize a new class of quantum control.
Professor Igor Aharonovich, the supervising author, emphasized the broader implications of this twist-controlled modulation approach. He noted that coupling two-dimensional materials at specific twist angles opens up an entirely fresh set of physical phenomena that were previously inaccessible. By assembling layers with precision angular misalignment, new quantum states can emerge, potentially transforming the landscape of material engineering for quantum applications. This strategic layering and twisting, known as “twistronics,” has already inspired revolutionary advances in graphene-based systems, yet this study extends the concept into the realm of quantum emitters embedded in hBN.
One key advantage of using hBN is that its layered crystal structure allows researchers to systematically alter the interaction between layers, effectively tuning the electronic environment surrounding the defects responsible for quantum light emission. As Dr. Gale metaphorically illustrated, far from being a solid block, hBN behaves more like a stack of cheese slices. Just as peeling and recombining slices of cheese can change how flavors intermingle, twisting hBN slices changes the interaction between atomic planes, which in turn alters quantum emitter characteristics. This mechanical engineering at the nanoscale provides a versatile platform for on-demand tuning of quantum light sources.
This technology breakthrough is fundamentally experimental but holds widespread implications. Adjustable quantum emitters could accelerate the development of quantum computing hardware, where precise photon control is essential for encoding and manipulating qubits. Similarly, secure quantum communication protocols rely on tailored quantum light sources to guarantee the generation and distribution of entangled photons immune to interception. Moreover, quantum sensing that exploits the extreme sensitivity of quantum states to environmental changes stands to benefit significantly from tunable quantum emitters, pushing the boundaries of detection limits in fields ranging from medicine to navigation.
Another remarkable facet of the research is the ability to repeatedly pick up, twist, and restack hBN layers without degrading the quantum emitter properties. This reversibility enables iterative fine-tuning of device characteristics and might yield adaptable quantum systems reconfigurable post-production, a feature highly desirable from a technological deployment perspective. This contrasts sharply with permanent structural modifications used in conventional quantum emitter fabrication, which restrict adjustable control and device flexibility.
The team’s methodology involved sophisticated nanofabrication techniques and high-resolution optical spectroscopy to probe the quantum emitters’ response to twist-induced modifications. By correlating the angular misalignment with spectral shifts in emitted light, they constructed a detailed understanding of the underlying physics governing emission control. These insights provide a blueprint for engineering tailored quantum emitters with bespoke characteristics suitable for specific applications.
The research findings have been detailed in a paper published in the eminent journal Science Advances, signaling the scientific community’s enthusiasm for the potential unlocked by twistable quantum systems. Importantly, the authors have declared no competing interests, affirming the independent and foundational nature of this inquiry. Funded by the Australian Research Council and the Air Force Office of Scientific Research, the work highlights the vibrant collaboration between academic institutions and funding bodies committed to propelling quantum technologies.
This discovery heralds a new era in quantum material science, where layered two-dimensional crystals are no longer passive hosts but active tunable platforms. By harnessing the mechanical and electronic versatility of materials like hBN, researchers are gradually unlocking complex quantum phenomena with precision control previously deemed unachievable. The implications extend well beyond fundamental research, marking exciting progress toward quantum devices that could redefine computational power, information security, and sensory precision globally.
In summary, the twist-controlled modulation of quantum emitters in hexagonal boron nitride exemplifies the convergence of cutting-edge experimental physics and materials science innovation. By capitalizing on the unique layered architecture of hBN and the emerging discipline of twistronics, this research pioneers functional tunability in quantum light sources. As the scientific community continues to develop and refine these approaches, we edge closer to the practical implementation of quantum technologies that promise profound societal and technological transformation.
Subject of Research: Not applicable
Article Title: Twist-controlled modulation of quantum emitters in hexagonal boron nitride
News Publication Date: 19-Jun-2026
Web References: 10.1126/sciadv.aec0101
References:
Keywords:
Quantum mechanics, Hexagonal boron nitride, Two-dimensional materials, Quantum emitters, Twistronics, Quantum light sources, Quantum computing, Quantum communication, Quantum sensing, Layered materials, Nanofabrication, Photonic modulation
Scientists identified an autoimmune mechanism linked to a major IBD risk gene, opening the door to targeted diagnosis and personalized therapies for thousands of patients. For decades, inflammatory bowel disease (IBD) has been treated as a single disorder, even though patients often experience dramatically different symptoms, disease courses, and responses to therapy. A new study [...]Swimming matched running for fitness gains but delivered greater heart growth and more favorable molecular changes, making it potentially more beneficial for cardiovascular health. For decades, swimming and running have been considered two of the best forms of aerobic exercise for cardiovascular health. But new research suggests they may not strengthen the heart in exactly [...]Lower vitamin C levels were linked to reduced brain volume and weaker neural connectivity in older adults, suggesting a potential connection between nutrition and brain health. Could a common vitamin help preserve the brain as we age? A new study of more than 2,000 older adults in Japan found that people with lower levels of [...]Atherosclerosis remains the foremost cause of cardiovascular disease-related morbidity and mortality globally, posing a substantial challenge to healthcare systems. Although traditional risk factors such as diet, lifestyle, and genetics have been extensively studied, recent advances have illuminated the pivotal role played by epigenetic mechanisms in shaping the onset and progression of atherosclerotic disease. Epigenetics, the reversible modulation of gene expression without alterations to the DNA sequence, encompasses DNA methylation, histone modifications, and non-coding RNAs, all of which intricately orchestrate cellular behavior within vascular tissues.
Emerging research reveals that DNA methylation patterns, both globally across the genome and in gene-specific loci, critically regulate cellular proliferation and inflammatory responses integral to atherogenesis. Hypomethylation or hypermethylation at particular sites can drastically affect the transcriptional activity of genes responsible for maintaining vascular homeostasis. This phenomenon underscores a dynamic regulatory system where environmental cues and pathological stimuli can induce lasting epigenomic changes that propagate vascular dysfunction and inflammation.
Histone post-translational modifications add another sophisticated layer to this epigenetic landscape. Primarily involving acetylation and methylation of histone proteins, these modifications influence chromatin structure and, consequently, gene accessibility. Within atherosclerotic plaques, histone modifications have been shown to govern networks of genes related to lipid metabolism, cellular plasticity, and inflammatory signaling. Such modifications enable vascular cells to adapt to inflammatory and metabolic stress by modulating transcriptional programs essential for plaque development and instability.
Non-coding RNAs have further expanded the complexity of epigenetic regulation within the vascular milieu. Long non-coding RNAs (lncRNAs) shape the transcriptomic profiles of specific cell types and exert control over the localization and activity of epigenetic enzymes. This targeting ensures that epigenetic remodeling is not only precise but also tailored to cellular needs in the context of vascular remodeling. Concurrently, microRNAs (miRNAs), small regulatory RNAs, predominantly mediate post-transcriptional gene silencing but have been identified to participate in non-canonical functions that influence vascular cell phenotype and immune responses.
The integration of multi-omics approaches, combining epigenomics, transcriptomics, and proteomics, has revolutionized our understanding of the cell-specific epigenetic contributions in atherosclerosis. These technological advancements enable the dissection of complex intercellular interactions within plaques and facilitate the mapping of genetically associated loci to discrete epigenetic modifications. This multidimensional insight is vital to unraveling the heterogeneity of atherosclerotic lesions and their diverse clinical manifestations.
In vascular endothelial cells, epigenetic alterations modulate barrier function, inflammation, and response to shear stress, all of which are critical in the initial stages of atherogenesis. Endothelial dysfunction triggered by epigenetic dysregulation sets the stage for immune cell recruitment and plaque formation. Meanwhile, vascular smooth muscle cells (VSMCs) exhibit remarkable plasticity through epigenetic reprogramming that drives their phenotypic switch from a contractile to a synthetic state, facilitating extracellular matrix remodeling and plaque stability or vulnerability.
Immune cells within the atherosclerotic microenvironment are also subject to profound epigenetic modulation. Macrophages, T cells, and other leukocytes display distinct epigenetic signatures that influence their activation states and inflammatory profiles. Epigenetic memory within these immune populations can perpetuate chronic vascular inflammation, underscoring the need for targeted interventions that modulate immune cell epigenomes to mitigate atherosclerotic progression.
Preclinical studies have leveraged these mechanistic insights to explore epigenetic drug candidates capable of attenuating plaque burden and vascular inflammation. Histone deacetylase inhibitors, DNA methylation modulators, and RNA-based therapeutics have demonstrated efficacy in experimental models, highlighting their potential to recalibrate aberrant gene expression patterns driving disease. However, challenges remain in achieving cell-type specificity, minimizing off-target effects, and ensuring the durability and safety of such interventions in humans.
A critical hurdle for translational success lies in the delivery mechanisms for epigenetic therapies. Nanoparticle-based systems and ligand-targeted delivery platforms are under investigation to enhance precision targeting of vascular and immune cells within plaques. These delivery technologies aim to maximize therapeutic benefit while circumventing systemic toxicity, thereby advancing the clinical applicability of epigenetic modulators.
Long-term safety is another paramount consideration as epigenetic drugs inherently affect gene regulation, potentially leading to unforeseen consequences. Rigorous preclinical evaluation and carefully designed clinical trials are imperative to balance efficacy with safety, ensuring that epigenetic therapies can be integrated into cardiovascular medicine without triggering deleterious off-target effects.
The prospect of leveraging epigenetic regulation heralds a transformative shift in cardiovascular therapeutics, enabling precision medicine tailored to an individual’s unique epigenomic landscape. By elucidating the dynamic and reversible nature of epigenetic modifications in vascular cells and immune populations, researchers are charting new pathways to mitigate atherosclerosis beyond conventional lipid-lowering and anti-inflammatory strategies.
Continued exploration into the interplay between genetic predisposition and environmental influences mediated by epigenetic mechanisms promises to deepen our understanding of atherosclerosis pathobiology. This holistic view integrates molecular, cellular, and systemic insights, empowering the development of sophisticated therapeutics capable of interrupting the disease process at its regulatory roots.
In summary, the frontier of atherosclerosis research lies at the intersection of epigenetics and vascular biology. The potential to manipulate gene expression programs with high specificity and reversibility offers an unprecedented opportunity to combat the global burden of cardiovascular disease. As the field advances, collaboration across disciplines and innovative technological approaches will be essential to realize the therapeutic promise of epigenetic modulation in clinical practice.
With ongoing efforts focused on unraveling cell-specific epigenetic mechanisms, refining drug delivery technologies, and ensuring long-term treatment safety, the era of epigenetics-driven precision cardiology is on the horizon. This paradigm shift not only holds the key to diminishing the impact of atherosclerosis but also exemplifies the broader potential of epigenetic therapies across complex diseases.
Subject of Research: Epigenetic regulation mechanisms in atherosclerosis and their potential for therapeutic intervention.
Article Title: Epigenetic regulation in atherosclerosis and its therapeutic potential
Article References:
Santovito, D., Atzler, D. & Weber, C. Epigenetic regulation in atherosclerosis and its therapeutic potential. Nat Rev Cardiol (2026). https://doi.org/10.1038/s41569-026-01313-8
Image Credits: AI Generated
Norway is preparing to move ahead with the construction of the world’s first ship tunnel after securing funding in the revised national budget, and completing the evaluation of contractor bids for the project.
The Norwegian Coastal Administration (Kystverket) announced that it is ready to sign a contract with the winning contractor for the Stad Ship Tunnel project. The government agency expects construction to begin in early 2027.
The decision follows after Norway’s center-left parties reached an agreement to include funding for the project in the revised national budget. Final approval by the Norwegian Parliament is expected by June 19.
“We have received the news regarding the ship tunnel,” Einar Vik Arset, Kystverket General Director, said. “We are ready to initiate the processes needed to facilitate a construction start in the beginning of 2027.”
First mentioned in an article in the Nordre Bergenhus Amtstidende newspaper, in 1874, the Stad Ship Tunnel will be the world’s largest ship tunnel. Located on the Stadlandet Peninsula, it is expected to stretch 1.1 miles (1.7 kilometers) through solid rock, or 1.37 miles (2.2 kilometers) when entrance sections are included.
The tunnel will measure 164 feet (50 meters) in height and 118 feet (36 meters) in width. Officials noted that it will be excavated through the narrowest part of the peninsula, connecting Moldefjord and Kjødepollen in the Vanylvsfjord region. The dimensions are large enough to accommodate vessels up to the size of Norway’s famous Coastal Route ships, including the Hurtigruten fleet.
It will allow large cargo vessels, ferries, and cruise ships to bypass the Stadhavet Sea. The waters are considered among the most hazardous along Norway’s coast, with rough weather, powerful currents, and high waves contributing to more than 30 maritime deaths since World War II.
“This is a major project, but we have prepared thoroughly over several years,” Arset pointed out. “We are ready as soon as we receive instructions from the Ministry of Trade, Industry and Fisheries.”
According to Kystverket, about 81 percent of today’s ship traffic will be able to use the tunnel. Cruise ships will reportedly be limited to a speed of eight knots inside it. This will allow them to complete the passage in about 10 minutes.
For its construction, Norway will excavate roughly three million cubic meters of rock. This is equivalent to around 750,000 truckloads of material. The project will rely on conventional drill-and-blast methods to carve the tunnel through hard gneiss rock beneath the peninsula.
Kystverket said that it has completed its review of bids from three consortiums competing for the project’s main construction contract. The final contenders include Norway’s AF Gruppen, France’s Eiffage Génie Civil, and a joint venture between Sweden’s Skanska and Norway’s Vassbakk & Stol.
“The evaluation has been completed,” Harald Inge Johnsen, one of the project’s manager, concluded in a press release. “Once the contract award is announced, there will be a standstill period for any complaints before the contract can be signed as planned.”
Additional contracts covering demolition work and new water infrastructure near the tunnel site are also ready to be tendered. The Stad Ship Tunnel is expected to improve navigational safety and reliability for maritime traffic along Norway’s rugged western coast.
Researchers built Sashimi-Bot to master one of robotics’ slipperiest challenges.
WALLOPS ISLAND, Va. — For over 20 years, NASA's Swift space observatory has been conducting prolific science in orbit, hunting for signs of gamma-ray bursts — the most powerful explosions in the universe. Now, it's falling to Earth, doomed to a fiery death by the end of the year as its orbit decays.
But maybe not.
NASA, it turns out, has a daring rescue mission in the works, something never before attempted in space: the Swift Boost mission. The endeavor calls for an untested spacecraft built by the Arizona company Katalyst Space Technologies to rendezvous and dock with Swift — something the observatory was never designed to do — before the observatory falls back to Earth.
If all goes well, Katalyst's space tug (it's called Link) will lift the Swift observatory into a higher, safer orbit — one that will add years of life to the aging space telescope's mission. Liftoff is officially set for June 27, with Link launching on the last-ever Pegasus XL rocket, an air-launched booster built by Northrop Grumman.
"Frankly, I have to be honest: No one thought it was going to be possible," Shawn Domagal-Goldman, NASA's Astrophysics Division director, told reporters here on Wednesday (June 17). "No one thought we would get as far as we've already gotten today."
What stands out most is how quickly the mission came together.
It was just in September 2025 that NASA picked Katalyst to build a spacecraft capable of boosting Swift on a budget of $30 million. That was nine months ago. And now, the finished Link spacecraft — with its three robotic arms, three main Hall thrusters and a suite of other instruments — is packed aboard its Pegasus XL rocket and tucked on the belly of its L-1011 Stargazer carrier plane for a trip to its launch site in the South Pacific's Kwajalein Atoll.
"In the last nine months, we have gone from a clean sheet to a spacecraft that is currently integrated on a rocket on an airplane, ready to go to Kwaj for launch," said Kieran Wilson, Link's principal investigator at Katalyst Space, on Wednesday. "This is an absolutely unprecedented development timeline for this program."
Yet that "swift" timeline, if you will, is essential if NASA is to rescue the Swift space observatory.
NASA originally launched Swift (its full name is the Neil Gehrels Swift Observatory, after its late principal investigator) in 2004 on a $250 million mission to search the sky for gamma-ray bursts and other high-energy astrophysics phenomena in the cosmos. From its original orbit about 375 miles (600 kilometers) above Earth, Swift was a silent sentinel, ready to quickly pivot to new targets with unprecedented speed.
"Swift was designed to study gamma-ray bursts, short-lived flashes of high-energy light that release more energy in just a few seconds than the sun will in its entire lifetime," Swift principal investigator Brad Cenko told reporters Wednesday. "It's been extremely successful in this regard, detecting over 2,000 of these sources all the way out to the edge of the visible universe."
It was Swift that helped scientists confirm without a doubt that the heaviest elements we know of, including the shiny gold and platinum in the jewelry you're wearing right now, were forged by these explosive cosmic events, Cenko said. Swift was expected to last two years in orbit. It's well into its second decade now, and still in good health — well, except for that "falling out of space" part.
You see, Swift doesn't have thrusters, or a propulsion system of any kind. And over the years, an increase in solar activity — space weather from the sun — has puffed up Earth's atmosphere to create more drag on Swift than expected, pulling it down from its initial orbit.
Last year, the Swift mission team realized the space telescope was falling faster than expected. Without a rescue mission, Swift would crash to Earth by the end of this summer.
"It was okay for a generic spacecraft to come out of orbit," Domagal-Goldman said. "But this was not just any spacecraft. This is an observatory with unique capabilities for astrophysics … It is a swift observatory that can quickly pivot across the night sky to find things that go boom in the night."
"So we decided, yeah, we want to go save this one this time because of how special it is," he added.
A lot has to go right for Katalyst's Link spacecraft to rescue Swift.
The 937-pound (425-kilogram) spacecraft will launch into an initial testing orbit on June 27 and perform a series of checkouts to ensure that its basic systems (three main engines, 16 reaction control thrusters, solar arrays, robotic arms) are all working properly.
"We'll have a commissioning period of a few weeks, after which we will begin maneuvers in order to approach Swift," Wilson said.
Once Link reaches Swift's orbit, it will perform a series of proximity operations, dock, and then raise the space observatory to its initial orbit over the period of a several months. If that goes to plan, Swift could be back to performing science by this fall, Cenko said. (The telescope has been in a low-power mode to preserve what orbit it can since February.)
If Link is successful, Swift could get another five or more years of life in space. Link, meanwhile, will detach and be intentionally deorbited (meaning it will fall to Earth on purpose) to end its mission.
"All this is challenging and risky," Wilson said. "There's a lot of spacecraft that have had far longer development cycles with far more funding behind them that have failed for mundane reasons."
A lot of simple things can go wrong.
For example, the solar arrays on Link might malfunction, Wilson said. Swift has been in orbit for so long, its protective insulation blankets may be as brittle as glass and break when Link's robotic arms grab on, he added.
And then there's the sun. It was increased solar activity that put Swift in its perilous situation. That activity is ongoing. In fact, Swift may be one big solar storm away from doom if the sun fires off a major storm before Katalyst's Link can reach it.
Swift is on track to fall below an altitude of 186 miles (300 km) by October. At that point, it may be too low for Link to reach the observatory. A surprise solar storm could accelerate that fall, but NASA remains hopeful.
"At the moment, we think we have several months where Swift will be at a sufficiently high altitude to give Katalyst folks a great chance to capture and boost us," Cenko said.
Katalyst is banking on the future need for spacecraft servicing and life extension in space. This week, the company raised $12 million in funding to develop an even more capable spacecraft called Nexus, which it plans to "expand satellite servicing to multi-orbit, multi-mission operations."
"Over the last decade or so, we've gotten very good at launching things into space," said Robert Lamontagne, Katalyst's vice president for strategic partnerships. "Katalyst is here really to kind of demark the end of that throwaway model, and the start of a new model."
The first test flight of a Nexus mission could launch in 2027. Its target: a U.S. Space Force satellite called Rooster in geostationary orbit 22,236 miles (35,786 km) above Earth, much higher than the Swift observatory. That Nexus-1 mission will launch atop an Ariane 6 rocket next year.
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An airplane carrying a rocket loaded with a robotic spacecraft designed to raise NASA’s Neil Gehrels Swift Observatory departed the agency’s Wallops Flight Facility in Virginia on Thursday, June 18.
Stargazer, a modified L-1011 operated by Northrop Grumman, took off for Kwajalein Atoll, part of the Republic of the Marshall Islands in the South Pacific Ocean. Attached to the belly of the aircraft was one of the company’s Pegasus XL rockets with LINK inside.
NASA contracted Katalyst Space to design and build LINK to rendezvous and dock with Swift and lift it back to a higher altitude.
Spacecraft in low Earth orbit experience drag caused by our planet’s atmosphere, which gradually reduces their altitude if they do not have propulsion systems to counteract the effect.
Recent solar activity magnified this effect on Swift, which began to sink faster than anticipated.
Katalyst selected Northrop Grumman’s Pegasus XL launch vehicle as the best means of reaching Swift on a short timeline based on orbital and programmatic needs.
Later this month, Stargazer will carry the rocket to an altitude of around 40,000 feet before releasing it.
After several seconds in free-fall, Pegasus XL will fire the first of its three-stage rocket motors, delivering LINK into orbit in about 10 minutes.
Learn more about the Swift mission at:
https://science.nasa.gov/mission/swift/swift-boost-mission/
By Jeanette Kazmierczak
Goddard Space Flight Center, Greenbelt, Md.
The post Aircraft Carrying Swift Boost Satellite Takes off From NASA Wallops appeared first on NASA Science.
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