For years, many women have faced a confusing message about menopause hormone therapy. It can be extremely effective for hot flashes and night sweats, yet older research created fears that the same treatment might harm the heart. A new U.S. study offers a more detailed picture. Researchers found that women with menopause symptoms who started […]
A person being treated for heart disease may also have a hidden problem in the kidneys. New European guidelines say doctors should look for that connection much earlier, because damage to the heart and kidneys can feed into each other and increase the risk of serious illness. The European Society of Cardiology developed the new […]
Fatty liver disease is extremely common, and many people have it without knowing. For years, it was often treated as a problem mainly involving the liver, especially when patients had no obvious symptoms. A new scientific review argues that this view may be too narrow. Researchers led by the University of Manchester and Northern Care […]
Stretching from West Africa to the Gulf of Mexico, a massive bloom of sargassum seaweed is swamping beaches and killing coastal wildlife. But scientists have discovered the floating algae also shelters a vast array of ocean creatures, and some are now calling for its protection.
Air pollution is often discussed as a long-term health threat, but new research suggests the body may begin responding after only a few hours. Scientists at the University of Louisville found that about three hours of exposure to polluted air was linked to a small but measurable change in the way the nervous system controls […]
For years, Perdue Agribusiness has been embroiled lawsuits over claims it polluted local groundwater with PFAS, the cancer-causing "forever chemical." So neighbors were skeptical when Perdue asked to increase the treated wastewater it pours in a local stream.
Former federal environmental officials are sounding an alarm in a new report about potential health impacts from data center pollution amidst what they see as a breakdown in oversight.
Scientists in Brazil have demonstrated that a combination of three non-destructive imaging techniques, visible-spectrum (RGB) photography, X-ray radiography, and three-dimensional magnetic resonance imaging (MRI), can detect and characterize hidden damage in soybean seeds that conventional quality tests frequently miss. The study, published in Smart Agricultural Technology, comes at a critical moment: Brazil is the world’s largest soybean producer and exporter, with an estimated harvest of 166 million tons for the 2024/2025 growing season, and seed quality is increasingly under threat from the very climate extremes that help drive the country’s agricultural productivity.
The research, led by Rafael Mateus Alves and colleagues at institutions including the Seed Technology Center of Embrapa Soybean and the University of São Paulo, was funded by the São Paulo Research Foundation (FAPESP). Its central premise is deceptively simple: because seed quality is largely determined in the field, before harvest even begins, researchers and seed companies need tools that can look inside a seed without killing it. Destructive assays such as the tetrazolium viability test, which stains metabolically active tissue red, are the industry standard, but they end the life of the sample. That is a particular problem for breeding programs, where each seed represents a unique genetic combination that must survive analysis if it is to be planted.
The seed itself is a small miracle of engineering. A protective coat, derived from the ovule integuments and marked by a scar called the hilum, regulates water uptake and shields the embryo within. The embryo contains the plumule, which gives rise to the plant’s first true leaves; the apical meristem, precursor of the aerial plant; and the hypocotyl–radicle axis, which breaks through the soil and forms the primary root. Flanking this axis are the cotyledons, storage organs packed with macromolecules that are metabolized and shipped to the growing axis during germination. Damage to any of these structures, from insects, fungi, drought, heat, or rough handling during harvest, can silently reduce a seed lot’s vigor, the capacity for rapid, uniform germination that underpins successful crop establishment.
To interrogate this architecture non-invasively, the team assembled ten representative seeds from production fields, commercial lots, and storage samples, each embodying a distinct damage category: stink bug injury, purple seed stain caused by fungi, green seeds from incomplete maturation, wrinkled seeds from heat and drought stress, weathering-related coat ruptures, severe structural failure, mechanical harvest damage, and internal galleries bored by the cigarette beetle (Lasioderma serricorne) during storage. Every seed was imaged sequentially with each of the three modalities and then subjected to the tetrazolium test as a qualitative reference standard.
The technical pipeline was meticulously standardized. For visible-light imaging, seeds were mounted on acetate sheets and photographed with a Leica DMLB microscope equipped with a DFC 310FX digital camera, oriented in four standardized positions with the hilum consistently to the right. X-ray radiographs were acquired on a Faxitron MX-20 DC-12 system operating at 34 kilovolts, with a nine-second exposure and an object-to-source distance of 11.4 centimeters; uniform contrast settings were applied to all images to make damaged tissues directly comparable. The MRI work used a horizontal 2 Tesla superconducting magnet coupled to a Bruker Avance III spectrometer operating at 85.24 megahertz for proton nuclei. Before scanning, seeds were conditioned to raise their moisture content from roughly 8–10 percent (wet basis) by incubation on moistened germination paper for three hours at 25 °C, a step that ensured sufficient hydrogen signal for imaging. A three-dimensional FLASH pulse sequence, with a 3-millisecond echo time and 75-millisecond repetition time, collected data on a 128×128×128 matrix over a 12.8-millimeter field of view, yielding isotropic voxels of 100 micrometers per side. Datasets were zero-padded to 256³ before Fourier transformation and rendered in three dimensions using ImageJ with the 3Dscript plugin.
The resulting image galleries are striking. On seeds punctured by stink bugs, the dominant pest of Brazilian soybean fields, RGB images revealed darkened patches on the cotyledons and near the plumule, the visible legacy of insect feeding that lacerates tissue and injects yeasts that degrade it from within. X-ray images flagged zones of reduced radiation absorption in the same darkened regions, while MRI cross-sections exposed the depth of tissue destruction with unusual clarity, precisely because degraded tissue no longer absorbs water and therefore produces no magnetic resonance signal. The tetrazolium test confirmed that these zones lacked respiratory activity, meaning they were metabolically dead.
Not every symptom tells the same story, however, and the multimodal approach proved especially powerful at distinguishing superficial from structural damage. Seeds with purple seed stain, caused by Cercospora fungi that secrete the toxin cercosporin, showed internal structures that appeared entirely normal in both X-ray and MRI. Yet the tetrazolium test produced an unusually intense red coloration at the stained coat, indicating that fungal activity had compromised the seed coat’s ability to regulate water uptake, allowing the staining solution to penetrate more deeply into the embryo. Similarly, green seeds, which retain chlorophyll because heat and drought interrupted maturation, showed no structural anomalies under X-ray or MRI, but their membranes proved unusually permeable to the tetrazolium solution, hinting at the physiological deterioration typical of immature tissue.
Where MRI truly distinguished itself was in detecting damage invisible to every other method. One seed that appeared flawless in visible light and radiographically normal in X-ray images revealed, in its three-dimensional MRI reconstruction, internal ruptures running through the central cotyledons, the likely consequence of rapid, uneven drying that forces differential cellular expansion and eventual tissue collapse. In mechanically damaged seeds, the X-ray images showed a crack in the hypocotyl–radicle axis that the camera could not see, but MRI went further, revealing the full extent of the fissure and the displacement of the axis relative to the cotyledons. The team also documented a dramatic structural failure nicknamed the “popcorn effect,” in which alternating wetting and rapid drying cycles tear the seed coat and force the cotyledons apart, a phenomenon increasingly reported in Brazilian seed lots as late-season weather grows more erratic.
To move beyond qualitative observation, the researchers extracted grayscale histograms from each X-ray image, normalizing pixel frequencies across the full 0–255 intensity range. Two statistical descriptors, mean gray level and Shannon entropy, were then compared across damage categories using one-way ANOVA followed by Tukey’s honest significance test. The analysis yielded clear separation: undamaged seeds showed the narrowest distributions with peaks at high grayscale values, while beetle-infested seeds and wrinkled seeds displayed the broadest distributions with heavy weight in the lower gray ranges, reflecting hollowed-out tissues and sparse, deformed structures. Mean gray level differed significantly across categories, peaking in undamaged seeds and bottoming out in wrinkled ones, while Shannon entropy, a measure of histogram complexity, was highest in beetle-damaged seeds and lowest in healthy ones. Because each damage category produced a characteristic radiographic fingerprint, the authors suggest these histogram metrics could support automated, quantitative screening in commercial seed laboratories.
Each modality, the authors stress, occupies a distinct niche. RGB imaging is fast, cheap, and ideal for surface screening but blind to anything beneath the coat. X-ray radiography, already a mainstay of seed testing labs, reveals internal voids, malformations, and cavities rapidly and non-destructively, though it cannot report on metabolic viability and demands careful standardization. MRI, with its superb soft-tissue contrast and genuine three-dimensional resolution, excels at detecting subtle physiological and structural alterations, latent mechanical injury, hydration-induced ruptures, and moisture redistribution, but its cost and acquisition time currently confine it to research settings. The tetrazolium test remains valuable as a reference but is destructive and subject to interpreter bias.
The authors argue the techniques should be viewed as complementary rather than competing, and they sketch a future in which RGB and X-ray screening handle high-throughput commercial quality control while MRI resolves ambiguous or high-stakes cases, such as breeding lines and seed physiology studies. Advances in imaging hardware, automation, and artificial intelligence-based analysis, they note, could eventually fuse these modalities into scalable phenotyping workflows. For now, the message is clear: in an era when a single season of heat, drought, and hungry insects can undermine an entire seed lot, the ability to see damage in all three dimensions, without sacrificing the seed itself, may prove as transformative for agriculture as it has been for medicine.
Subject of Research: Non-destructive multimodal imaging (RGB, X-ray, and MRI) for detecting abiotic- and biotic-stress-induced damage in soybean seeds
Article Title: When damage goes deep: a multi-technique approach including 3D for soybean seed damage assessment
Article References: Alves, R. M., Teixeira, J. M., Marassi, A. G., Henning, F. A., Umburanas, R. C., Gomes-Junior, F. G., & Tannús, A. (2026). When damage goes deep: a multi-technique approach including 3D for soybean seed damage assessment. Smart Agricultural Technology, 15, Article 102523. https://doi.org/10.1016/j.atech.2026.102523
North Carolina has secured $455 million in payments from Chemours, DuPont and Corteva over PFAS pollution, along with a separate $135 million reserve intended to protect future drinking water and cleanup work.
The US Environmental Protection Agency (EPA) worked directly with pesticide maker Bayer in approving the controversial herbicide dicamba earlier this year, presenting the company with different options for how to reduce drift and runoff and then aligning on those options in the final decision, according to internal agency records.
Beneath every step we take, soils hold one of the planet’s largest reservoirs of carbon, a vast, slow-moving bank of organic matter that quietly regulates how much of the world’s carbon stays locked away and how much escapes into the atmosphere as greenhouse gas. Now a sweeping new review warns that climate-driven extremes, droughts, floods, and wildfires, are rewriting the rules of that subterranean economy in ways that conventional models and land-management practices have not yet caught up with. The analysis, led by environmental scientist Nanthi Bolan of the University of Western Australia and colleagues, including a corresponding authorship by Bolan himself, synthesizes a substantial body of global evidence on how extreme weather reshapes carbon inputs to soil, microbial processing, erosion, and the sequestration of carbon that underpins soil health, water retention, nutrient cycling, and agricultural productivity.
The work, published in the journal Carbon Research, is notable for the scale of its underlying evidence base. On 14 January 2026, the authors searched Google Scholar, PubMed, and Web of Science using terms spanning climate change, extreme weather, soil carbon, microbial activity, decomposition, erosion, dissolved organic matter, and leaching. The initial sweep returned 14,218 records; after removing duplicates and screening for eligibility, 3,754 articles remained for bibliometric and qualitative analysis. From those, 187 publications were selected for detailed synthesis based on relevance, methodological rigor, and the substantive quality of their findings. Keyword co-occurrence patterns were mapped with VOSviewer, a bibliometric tool that reveals the intellectual architecture of a research field. The result is a critical review grounded in structured literature screening rather than new experimental data, but its synthesis offers one of the most comprehensive maps yet of how extremes rearrange the soil carbon cycle.
The review’s central finding is that no two extremes act alike. Drought, the most widespread disturbance, operates largely through the plant side of the equation. When rainfall fails, photosynthesis slows, plant biomass production falls, and the total flux of carbon entering soils through roots, residues, and litter declines. There is a nuance here: under moderate water stress, plants may temporarily shift a greater proportion of their fixed carbon belowground, investing in roots to chase moisture. But prolonged drought overwhelms that compensatory response. Microbial biomass shrinks, litter decomposition stalls, and the living engine of the soil carbon cycle idles. Then comes the deceptive twist: when rain finally returns, rewetting triggers a rapid pulse of carbon dioxide as starved soil microbes seize upon the accumulated substrates left behind by months of suspended activity. That post-drought CO₂ flush, the review emphasizes, can erase much of the apparent “savings” that accumulated during the dry period. Across the assembled evidence, repeated and multi-year drought was consistently associated with declining soil organic carbon, with grasslands and arable croplands showing particularly pronounced losses, ecosystems that happen to anchor much of the world’s food production.
Flooding tells the opposite story, but it ends in many of the same places. Water saturation chokes off oxygen diffusion through soil pores, forcing microbial metabolism into anaerobic pathways. That shift changes everything downstream. Prolonged waterlogging can drive the chemical reduction of iron oxyhydroxides, minerals that in oxygenated conditions act as microscopic glues binding organic carbon to soil particles. When those minerals dissolve, the carbon they held is released as dissolved organic carbon, which can then be stripped away by erosion and leaching and exported to rivers, lakes, and ultimately the ocean. The review stresses, however, that flooding is not unambiguously a carbon loss story. Wetlands and other periodically inundated ecosystems can accumulate and retain enormous carbon stocks precisely because water constrains decomposition. Whether a flood event releases carbon or banks it depends on the interplay between plant inputs, oxygen availability, and hydrological transport, a delicate balance that shifting rainfall regimes are actively destabilizing.
Wildfire is the most dramatic and immediately visible of the three forces, and its effects cascade on multiple timescales. Combustion directly strips vegetation, litter, and soil organic matter, transferring carbon to the atmosphere in hours. But fire also rearranges the physical and biological landscape of the soil in subtler ways: it can increase erosion by removing protective ground cover, alter soil wettability in ways that change hydrological behavior, restructure microbial communities, and expose previously protected carbon, once shielded inside aggregates or mineral associations, to fresh decomposition. There is a paradoxical bright spot. Pyrogenic carbon, the charcoal-like residue of incomplete combustion, is chemically recalcitrant and can persist in soils for centuries or millennia, functioning as a long-term carbon sink. Whether a fire leaves a landscape as a net carbon source or stabilizes some of its carbon in pyrogenic form depends on fire severity, soil moisture, fuel load, ecosystem type, and the trajectory of post-fire recovery. The review is clear that this balance cannot be predicted from fire alone; it is contingent, site by site, on conditions that vary widely across the globe.
Perhaps the most consequential theme running through the synthesis is that carbon responses cannot be inferred from the type of extreme event alone. Land use, soil mineralogy, hydrology, salinity, vegetation composition, microbial community makeup, and the timing of events within a season all determine whether carbon ends up stored, mobilized, or released. Iron and aluminum oxyhydroxides and clay minerals, for instance, provide mineral protection that can shield organic matter even under stress, while sandy or low-clay soils offer little such refuge. Managed croplands respond differently from native grasslands; saline coastal soils behave differently from acidic forest soils. And compound events, drought followed by wildfire, or alternating drought and flooding in rapid succession, may produce effects that are qualitatively different from those of isolated disturbances, as when a dried landscape burns more intensely, or when post-fire soils, stripped of vegetation, wash away in the first heavy rain. The review argues that the climate science and soil science communities have largely studied these disturbances one at a time, while the real world increasingly delivers them in combination.
The implications for climate mitigation and adaptation are substantial. Soil organic carbon is frequently invoked in national climate pledges and voluntary carbon markets as a bankable sink, yet the review suggests that the security of that bank depends heavily on how often and how severely extremes strike. If multi-year droughts steadily drain carbon from grasslands and croplands, or if fires repeatedly reset accumulation cycles, the effective permanence of soil carbon storage becomes far more fragile than many accounting frameworks assume. Conversely, protecting and rebuilding soil carbon delivers benefits well beyond climate: it improves water retention in drought-prone regions, supports nutrient cycling, stabilizes soil structure against erosion, and sustains the microbial diversity on which fertility depends. Carbon stewardship, in other words, is not separable from food security or ecosystem resilience; it is the same problem viewed from different angles.
The authors are candid about the limits of the current evidence base. The article does not report newly generated datasets and does not present a dedicated limitations section, and its conclusions rest on a qualitative synthesis of selected publications. Consequently, they call for improved and more consistent evidence across soil types, land uses, and both terrestrial and aquatic environments, and across multiple temporal scales, from the instantaneous CO₂ pulse after rewetting to the multi-decadal trajectory of carbon storage. Standardizing measurements of carbon pools, microbial functions, and event intensity, they argue, would make results comparable across ecosystems and enable more confident generalization, something the field currently struggles to achieve given heterogeneous methods and site-specific reporting.
Looking forward, the review sketches a research agenda that is as technologically ambitious as it is mechanistically focused. The authors recommend integrating high-resolution remote sensing with ground observations, advanced spectroscopy, molecular analyses, and integrated modeling to track carbon as it moves through soils and into waterways. They single out several priorities: characterizing microbial genomic and functional diversity as it responds to stress, quantifying carbon stoichiometry, probing the interactions between organic matter and iron and aluminum oxyhydroxides, understanding clay-mineral protection mechanisms, tracking long-term storage outcomes, and systematically studying the sequencing of compound extreme events. Each of these threads addresses a gap in the mechanistic chain that links a weather event in the atmosphere to a molecule of carbon, stabilized or released, in the soil.
What emerges from the review is a picture of the soil carbon cycle not as a stable background process but as a dynamic, contested system whose behavior under climate extremes is far less predictable than once assumed. The same storm that floods a rice paddy and exports carbon to a river delta may, a few hundred kilometers away, end a drought and briefly green a grassland, with opposite consequences for the atmosphere. As extremes grow more frequent and more compound, the review makes the case that understanding, and safeguarding, the carbon held beneath our feet will require science that is as interconnected and as restless as the weather itself.
Subject of Research: Impacts of climate change-induced extreme weather events (drought, flooding, wildfire) on carbon dynamics in soil
Article Title: Impacts of climate change-induced extreme weather events on carbon dynamics in soil
Article References: Bolan, N., Messiga, A. J., Sharma, S., Mukherjee, S., Bolan, S., Salehin, S. M. U., Rupngam, T., Rajan, N., Zhang, T., Yang, Y., Jagadesh, M., & Siddique, K. H. M. (2026). Impacts of climate change-induced extreme weather events on carbon dynamics in soil. Carbon Research, 5(1), Article 58. https://doi.org/10.1007/s44246-026-00300-5
Keywords: adaptation of land management practices to climate extremes, challenges to conventional soil carbon models, Climate change impacts on soil carbon storage, effects of droughts and floods on soil microbial activity, global evidence on soil carbon dynamics, implications for greenhouse gas emissions, influence of extreme weather on nutrient cycling and water retention, resilience of soil carbon reservoirs to climate, review of climate-driven soil carbon processes, soil erosion and carbon loss due to extreme weather, soil health and agricultural productivity under climate stress, wildfire influence on soil organic matter
Twenty-five years after the September 11 terrorist attacks, researchers at the Icahn School of Medicine at Mount Sinai have uncovered evidence that the environments in which World Trade Center responders live today may be quietly shaping their risk of frailty, post-traumatic stress disorder, and depression. The study, published in Nature Communications, is the first to examine how neighborhood-level environmental exposures later in life may interact with the chemical and psychological injuries sustained during the disaster response, adding a new dimension to one of the most intensively studied disaster health cohorts in the world.
The research team analyzed data from 18,734 responders who both live in New York City and receive care through one of the World Trade Center Health Program Clinical Centers of Excellence. These responders represent a population that experienced an extraordinary confluence of toxic exposures—dust, combustion products, airborne particulates, and a cocktail of known and suspected carcinogens—alongside severe psychological trauma. While decades of prior research have documented elevated rates of respiratory disease, cancer, and mental illness in this group, far less attention had been paid to whether the everyday conditions of their neighborhoods might compound or buffer those effects as responders age.
To answer that question, the researchers linked each responder’s residential address to annual estimates of three environmental factors: air pollution, high ambient temperatures, and neighborhood greenness, the last typically quantified through satellite-derived vegetation indices. This exposure-assessment approach, common in the field of environmental epidemiology, allowed the team to characterize the conditions each participant encountered where they lived year after year, rather than relying on broad regional averages. The researchers then examined whether those exposures were associated with the probability of being classified as frail, and with diagnosed PTSD and depression.
The results were striking in their consistency. Responders living in hotter neighborhoods—areas that experience more extreme heat days, a burden that falls disproportionately on densely built urban districts with impervious surfaces and little tree canopy—showed an elevated risk of frailty, a geriatric syndrome marked by diminished physiological reserve and heightened vulnerability to stressors. Elevated concentrations of air pollution were likewise associated with increased risks of both frailty and adverse mental health outcomes. Frailty itself is increasingly understood as a whole-body phenomenon, involving chronic inflammation, immune dysregulation, and cumulative cellular wear, all of which are plausible biological pathways through which heat and pollution could accelerate aging.
The mental health findings carried equal weight. Higher pollution and heat exposure were associated with increased odds of PTSD and depression, while responders living in greener surroundings—those with more parks, trees, and vegetated land near their homes—showed lower risks of all three conditions. This inverse association with greenness aligns with a substantial body of literature suggesting that access to green space can reduce psychological stress, encourage physical activity, dampen inflammation, and moderate urban heat, though the observational design of the study means that causation cannot be definitively established.
Perhaps the most provocative finding concerned interaction effects. The researchers found that responders who had experienced higher levels of World Trade Center–related chemical and psychological exposure appeared more vulnerable to the effects of environmental stressors in their current neighborhoods. In other words, the disaster and the decades that followed may not be independent chapters in these individuals’ health histories. Instead, responders already carrying the biological imprint of trauma and toxic dust—including altered inflammatory profiles, epigenetic changes, and persistent hypothalamic-pituitary-adrenal axis dysregulation—may enter later life with less reserve to absorb additional environmental insults. Everyday exposures that might be merely uncomfortable for a healthy middle-aged adult could, for these individuals, translate into measurable acceleration of physical decline and psychological deterioration.
“Twenty-five years after 9/11, we are still learning about the factors that influence the health of those who responded to the attacks,” said Helena Furman Krasnov, PhD, postdoctoral researcher at the Icahn School of Medicine and the study’s first author. “Our findings suggest that everyday exposures, including heat, air pollution, and access to green space, may contribute to responders’ long-term physical and psychological well-being. Understanding these factors could help identify new opportunities to support healthy aging in this population.”
The study’s senior and corresponding author, Maayan Yitshak-Sade, MPH, PhD, Associate Professor of Environmental Medicine at Mount Sinai and a member of the Institute for Exposomic Research, framed the work within the broader exposome paradigm—the effort to capture the totality of environmental exposures an individual accumulates over a lifetime. “Our findings suggest that the health consequences of 9/11 may not end with the disaster itself,” she said. “For responders already carrying the biological effects of trauma and toxic exposures, everyday environmental conditions may represent an additional source of stress on the body and mind. These findings highlight the importance of considering where people live, not just what they experienced during the disaster.”
That framing underscores a conceptual shift in disaster medicine. Traditional models tend to treat a catastrophic event as a discrete exposure with a defined aftermath. The Mount Sinai findings instead suggest that disaster-related health effects may unfold across an entire life course, modified by conditions that have no obvious connection to the original event. A responder’s risk of frailty in 2026 may reflect not only the hours spent at Ground Zero, but also the temperature of the summers they have endured since, the particulate matter drifting through their streets, and whether a leafy park sits within walking distance of their apartment.
The study arrives at a moment when urban environmental health has become a pressing policy concern. Extreme heat now kills more Americans annually than any other weather phenomenon, and cities including New York have launched ambitious initiatives to expand tree canopy, create cool corridors, and retrofit public housing with resilient cooling infrastructure. Air pollution, even at levels within regulatory limits, continues to be linked to cardiovascular, respiratory, and neurocognitive harm. If the associations identified in this cohort hold up under further scrutiny, they could strengthen the case for targeted environmental interventions—not as amenities, but as clinical supports for a vulnerable population.
The implications also extend well beyond the World Trade Center community. The researchers point out that survivors and responders from other disasters—wildfires that blanket entire regions in smoke and ash, industrial accidents that release toxic plumes, building collapses that bury rescue workers in dust—may face the same dual burden of physical and psychological exposures that continues to shape health long after the initial event. Climate change is intensifying heat waves and wildfire seasons simultaneously, meaning that disaster-affected populations may increasingly find themselves living in precisely the kinds of hostile urban microclimates the study identifies as risky. The framework developed here could inform how health surveillance programs for disaster cohorts are designed, prompting them to collect residential and environmental data alongside clinical outcomes.
The authors are careful to note the study’s observational nature. Associations between neighborhood environment and health can be confounded by socioeconomic status, housing quality, access to care, and the self-selection of healthier individuals into greener, quieter neighborhoods. The investigators controlled for available covariates, and the sheer size of the cohort lends statistical power, but randomized evidence on green space exposure is practically impossible to generate, and residual confounding remains an inherent limitation of the design. Longitudinal follow-up, and ideally natural-experiment analyses—such as the addition of new parks or major infrastructure changes—will be needed to firm up causal inference.
That work is already on the horizon. The team plans to investigate whether beneficial environmental factors, including green space and access to healthy food, can actively reduce the long-term health effects associated with World Trade Center–related exposures—a question that shifts the framing from risk identification to potential intervention. If confirmatory studies support the protective role of greenness, the findings could justify clinical guidance for responders, and potentially for other disaster-exposed populations, that goes beyond medication and monitoring to encompass the places where patients live.
For a population that has already given so much and borne so much, the idea that healing might partly depend on the landscape outside the front door is both sobering and hopeful. It suggests that some of the damage inflicted on September 11, 2001 may not be fixed, but modifiable—and that the next chapter of care for responders could be written not only in clinics, but in city planning offices, park commissions, and the slow, patient work of greening the neighborhoods where aging heroes live out their lives.
Subject of Research: People
Article Title: Urban Exposures, Frailty, and Mental Illness in World Trade Center Health Program Responders
Article References: Krasnov, H., Hung, W., Knobel, P., Kloog, I., Ko, F., Thompson, H., Colicino, E., Teitelbaum, S. L., Just, A. C., & Yitshak-Sade, M. (2026). Urban exposures, frailty, and mental illness in World Trade Center Health Program responders. Nature Communications, 17(1), Article 9449. https://doi.org/10.1038/s41467-026-77401-7
Keywords: World Trade Center responders, 9/11 health, frailty, PTSD, depression, air pollution, extreme heat, green space, exposome, environmental health, Nature Communications, Mount Sinai
Every year, MIT Technology Review puts together a list of some of the brightest and best young minds working across science and technology. Our 35 Innovators Under 35 are the ones to watch—people whose research and technical work stands to shape the future of their fields.
This year, the list includes nine people who are transforming biotech. And this week, I’m going to give you a taste of some of the very cool stuff five of them are working on, which includes lifesaving innovations and groundbreaking “age reversal” tech.
1. Preventing maternal deaths
Let’s start with Paschal Kija, a 28-year-old who has developed a device to treat postpartum hemorrhage—a dangerous birth complication that contributes to around 29% of maternal deaths in his home country, Tanzania. The Mkanda Salama (“Safe Wrap” in Swahili) is easy to use and costs just $70. A study found that it stopped postpartum bleeding in 73% of women within 20 minutes.
2. Making brain electrodes inspired by Japanese art
For decades, scientists have been developing, testing, and implanting brain electrodes. These devices are literally inserted into people’s brains, so while they can help us understand brain activity and treat various neurological disorders, it’s not totally surprising that they can also cause a bit of damage. Xiao Yang, 34, is working on ultra-small electrodes, which she hopes will have less of an impact on surrounding brain tissue. Her electrodes are flexible, too—in fact, they look a lot like actual neurons.
Yang is also creating sheets of electrodes to study brain cells in the lab. Inspired by kirigami—the traditional Japanese art of cutting paper to form three-dimensional shapes—she’s created a sheet of electrodes with a honeycombed structure shaped like a spiral basket. And she’s already using it to study brain cells.
3. Developing an all-new treatment for baby KJ
In 2024, Kyle “KJ” Muldoon Jr. was born with a rare and potentially fatal genetic disorder. Sarah Grandinette was a member of a team that developed an entirely new, personalized treatment for him—a gene-editing therapy essentially designed to correct a genetic misspelling.
Grandinette, who is now 26, created cells with KJ’s genetic variant and used them to screen gene-editing approaches; then she tested potential medicines in mice and monkeys. KJ ultimately got his first dose of the resulting treatment when he was about seven months old. He responded well and was eventually discharged from hospital. He’s “doing pretty great,” she says.
4. Reversing the aging process to treat eye disease
The buzziest tech in longevity right now centers on reprogramming—attempts to rewind the age of cells by resetting them to a more embryonic-like state. In a study published in 2020, Yuancheng (Ryan) Lu (now 34) and his colleagues showed that a reprogramming therapy reversed vision loss in aged, blind mice. Now an almost identical version of that therapy is being tested in people with eye disease. Life Biosciences, the company developing the drug, dosed its first volunteer in June.
5. Using AI to design new viruses
Last year, Samuel King used a generative AI model to come up with new genetic blueprints for bacteriophages—teeny viruses that can infect bacteria. Once he had those blueprints, he printed them out as strands of DNA. In experiments, he found that those AI-designed viruses could create new copies of themselves, burst out of bacterial cells, and infect other nearby bacteria. Viruses aren’t alive, but King, 27, hopes that AI-designed life forms might one day be used to make drugs or soak up pollution.
You can read more about these innovators, and the others on the biotech list, here.
This article first appeared in The Checkup, MIT Technology Review’s weekly biotech newsletter. To receive it in your inbox every Thursday, and read articles like this first, sign up here.
Many people are familiar with melatonin, a hormone that helps ready the body for sleep. But there's another, lesser-known chemical in the brain, called orexin, that tips the scale in the other direction: waking the body up.
In 1999, two scientists independently uncovered the function of orexin and published papers about it. Dr. Masashi Yanagisawa, a molecular biologist and physician now at the University of Tsukuba in Japan, came across orexin while studying the interaction of receptors and chemicals in the brain. Dr. Emmanuel Mignot, now the director of the Stanford Center for Narcolepsy, homed in on orexin while studying narcoleptic dogs. (His Chihuahua, named Watson, has narcolepsy, and he previously had another dog with the condition, named Bear.)
This year, the pair of researchers won the coveted Albert Lasker Basic Medical Research Award for this fundamental finding that helped reshape our understanding of sleep. Their work has since led to the development of drugs for insomnia and narcolepsy.
Yanagisawa told Live Science that, at the start of his research career, he didn't expect to end up studying sleep. Mignot, on the other hand, had an early interest in understanding narcolepsy so that better treatments for the neurological disorder could be developed. Live Science spoke with Mignot about the discovery of orexin and how the field might progress in the future.
Nicoletta Lanese: What initially drew you to studying narcolepsy?
Dr. Emmanuel Mignot: There were three things that attracted me to narcolepsy: Number one, it was a human problem. It was already known [at the time] that it was not super rare. I'm not saying it's super common, but 1 person per 3,000, 0.03% — it's reasonably common. And nobody cared about it. I would talk to neurologists and they'd say, "Oh, I've never seen one case in my entire life." So I would say, "Yes, of course; you miss them all." That was the state of the play at the time.
Number two, was what this was a quintessential sleep disorder [in which sleep itself is disrupted]. I thought that if we found the cause of this disease, we could potentially discover something totally new about sleep — a fantastic entry point to a mystery.
The third thing that made me ready to go there was that it was tractable. A lot of problems are not tractable.
NL: Why did you start working with the dogs with narcolepsy?
EM: I studied the pharmacological basis because I was trained in pharmacology, and as a psychiatrist, and I discovered how this drug modafinil [a stimulant-based narcolepsy treatment] was working. But quickly, I realized I'm not going to find the cause by doing pharmacology. I'm only going to explore what's known.
That's when I started to fall in love with genetics, even though I was not trained as a geneticist. I said, "We have to find this gene in the dogs." It looks like they have all the symptoms. It was a huge bet, and it took me 10 years because I was definitely … overoptimistic. But it was worth the price at the end.
After narcolepsy was described — the dog gene — suddenly narcolepsy became much more famous.
NL: And scientists already knew about narcolepsy in dogs at that time?
EM: The guy at Stanford that started the sleep program was called Dr. [William] Dement. He was a graduate student in Chicago in the 1950s, when [Eugene] Aserinsky and [Nathaniel] Kleitman discovered REM sleep. He had the foresight to understand that this was an important discovery.
[Later], he discovered that narcolepsy was really a disorder where people go into REM sleep and have this very abnormal dreaming. He came in 1970 to Stanford, and the first thing he did after his medical school was to start a clinic to see patients with narcolepsy. Around then, he spoke at an American Medical Association conference in San Francisco, and he discussed different sleep disorders, including narcolepsy. And then there was someone in the audience that said, "Oh my god; I have a dog with your disease. Every time it gets excited — boom — it collapses. And it sleeps all the time."
That dog had already been euthanized, but it still gave him the idea that these dogs have narcolepsy — maybe we should try to get some. So he went to a lot of veterinarians to talk to them about it, and they identified a whole series of dogs, including the first poodle, Monique, who had narcolepsy. And they started this little colony of dogs. Initially, they tried to breed them, but most cases of narcolepsy are actually not genetic. Then, in 1977, they got a whole litter of Dobermans, and then Labradors, that had some form that was genetic.
So when I arrived, it was in 1987. They already had the dog colony. I came to study the pharmacology, to try to find a better treatment for narcolepsy. But I did stand on the shoulders of giants.
NL: At that time, it's not like you had a complete dog genome. Did that make studying their genetics challenging?
EM: It was crazy. A couple of human genes had been isolated, and mouse genes, but it was a handful. We didn't even have the full genome map in humans. And meanwhile, dogs — no pun intended — were in no man's land. Very little was known.
It took me 10 years. I had times where some people didn't believe that the dogs had narcolepsy. There were a few depressing moments, but I was convinced that was the right thing to do.
Orexin (pictured) is a peptide in the brain that promotes wakefulness. (Image credit: theasis via Getty Images)
NL: When you ultimately found the receptor for orexin, did it surprise you? It strikes me as surprising that there would be a discrete "switch" in the brain that controls wakefulness.
EM: I was lucky. Honestly, I had no idea. I got enamored with genetics because what I love [about it] is you can find something without any hypothesis. You just search for it, and what you find tells you what it is. You have no prerequisite for knowing what you would find.
I could have found something much less significant. That was a dream, to find a GPCR [G-protein coupled receptor, a protein on the outside of cells]. Can you imagine? A drug target.
Then, it turned out to be immediately applicable to humans. That, too, was a lot of luck; let's be honest. I was just trying to find the cause of one thing and one step at a time; it could have been something very complicated. It turned out to be simple.
Was I surprised? No, because I was not expecting one or another.
NL: Do you recall what the reception was like when the initial finding was published?
EM: It had an immediate effect, for several reasons. For example, I was seeing a lot of patients with narcolepsy at the time, but they were all old folks that had had narcolepsy forever. A lot of people would tell me, "I think I had it from when I was born, because I don't remember." We were never seeing children.
But after narcolepsy was described — the dog gene — suddenly narcolepsy became much more famous. And what happened is that people started to pay attention to narcolepsy, and we started to see kids. In kids, the picture is so much different. They gain an enormous amount of weight; it's very abrupt. It's a little bit different than what you see in adults, where they have adapted to it.
That was, I think, a practical consequence of the discovery. It really put narcolepsy on the map.
The second thing that happened is, all the drug companies started to develop hypnotics [sleeping pills], trying to block the orexin. They developed hypnotics relatively quickly, and they are very effective. They are probably safer than benzos [benzodiazepines] and so forth.
NL: Is it considered safer because the orexin blockers better replicate natural sleep?
EM: We know that the orexin definitely drops during sleep, so blocking it is definitely a way to recapitulate that drop; that's true. It's an awake-promoting system, so if you remove something that makes you more awake, it's safer than inducing sleep by shutting down the brain.
NL: As you moved to studying narcolepsy in humans, you found evidence that there might be an autoimmune response involved; it's been suggested that such a response may be harming the cells that make orexin in the brain. Was there suspicion that the condition had an autoimmune element previously?
EM: It's not something I 100% discovered. In 1983, before I came to study narcolepsy, there was a guy in Japan who I met, called Yutaka Honda. [Editor's note: Honda's research linked narcolepsy to the human leukocyte antigen (HLA) region of the genome, which helps regulate immune responses.]
The HLA is the way the immune system sees the world. That had just been discovered as very important for transplantation, because it's very polymorphic [takes on different forms] from one person to the next. They [Honda's group] found that all narcoleptics had a particular genetic variant, called HLA-DR2. This was a total surprise.
When I came, that was already known. But then people really looked and tried to see if the disease was autoimmune, but they couldn't find anything — no autoantibody, nothing. It was all negative.
I did a study with African Americans, and in African Americans, I found that this DR2 marker was not the best marker for narcolepsy. It was a gene just next to it that was called DQB1*06:02. [Editor's note: That HLA variant is now recognized as a strong risk factor for narcolepsy, particularly for narcolepsy type 1 (which involves a symptom called cataplexy).]
I'm very proud of that study because I think it's the first time that people used human diversity to actually map down a genetic factor more precisely, which now is used commonly. It's called transethnic mapping.
NL: New treatments that target orexin have just been approved. Do you see those therapies as an extension of your earlier findings?
EM: Of course. I was trained as a pharmacologist originally, so obviously, I do a lot of clinical trials. I see my patients totally transformed by this medication. It's just amazing. I'm so fortunate. How could you get a better reward than seeing your patients totally transformed by this medication?
It's going to have a lot of other applications [beyond narcolepsy]. Some people think it's going to be very helpful for ADHD; some people think it could be very helpful for depressed people with excessive sleepiness. We don't know, really; there's a lot of possibilities.
Another thing I'm excited about is that I have a few patients with [both] narcolepsy and schizophrenia. You cannot give them stimulants. If you give them modafinil or another dopamine stimulant [for narcolepsy], they have even more hallucinations. Often, they are sedated by their medication, and we are very poor at making people more motivated and active. These [orexin-activating] drugs seem to have effects beyond just waking people up. They seem to increase motivation.
You don't know until you try, but I'm sure it's going to have other applications.
This interview has been condensed and edited lightly for clarity. It is for informational purposes only and is not meant to offer medical advice.
Fears that modern electronic devices may harm children are nothing new. Gadgets with screens of any size have long been allegedly melting, rotting, and/or corrupting the brains of youths for decades. However, a medical case report published this week offers a new and alarming way our digital doodads may cause physical harm.
In BMJ Case Reports, two UK doctors, Mara Znagoveanu and Edward Artley, report the case of a boy who came to an emergency department with alarming marks on his abdomen. The marks were described as being in a patch about 15 centimeters (six inches) wide, made of flat, reddish-brown "interlacing lines forming irregular circles and a lace-like morphology." A picture of the marks is here.
Mysterious marks
The boy, whom they described only as being in "mid-childhood," was not in any pain, and the rash was not warm to the touch or tender. He and his parents said they couldn't think of any recent injuries or trauma that might explain the marks. He was otherwise healthy, hadn't recently been ill, and had no systemic symptoms, such as fever or fatigue. Everything about the boy's health, growth, and medical history looked normal.
Grounding mats and bed sheets sold by Terra Wellness do not provide a genuine ground connection due to a high value electrical resistor intentionally used in their product. All such grounding products are fraudulent making this a scam. I recommend directly grounding yourself by standing on the earth with bare feet.
Login
