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.

Keywords

soil organic carbon, extreme weather, drought, flooding, wildfire, carbon sequestration, microbial activity, dissolved organic carbon, erosion, pyrogenic carbon, climate change, soil health

Agua, aire, humo o sangre obedecen a unas ecuaciones fundamentales de la física. Durante casi 90 años, sin embargo, nadie había logrado demostrar qué les ocurre bajo determinadas condiciones extremas.

En un rincón de Villa Adriana, entre el llamado Anfiteatro y un banco de toba, hay una losa de mármol de apenas 40 por 35 centímetros que sigue exactamente donde la dejaron hace unos 1.900 años. Dos líneas de letras capitales bastan para explicar por qué el hallazgo interesa tanto a los arqueólogos: FVLGVR SVBMANIVM, […]

Microsoft has entered the final phase of retiring Azure SQL Data Sync, blocking new deployments in subscriptions that have never used the service. The restriction took effect on September 9, ahead of the service's shutdown on September 30, 2027. Subscriptions that already use the service can continue creating, modifying, and managing sync groups and member databases until retirement. Other subscriptions can no longer adopt it. The service uses a hub-and-spoke model, with an Azure SQL database serving as the hub and other databases joining its synchronization group. Members can be other Azure SQL databases or on-premises SQL Server databases, which require a sync agent. A conflict resolution policy determines whether the hub or member database takes precedence when changes clash. SQL Data Sync supports scenarios including hybrid environments, in which applications and databases are split between local infrastructure and Azure, as well as geographically distributed applications. Microsoft acknowledged that customers will need to choose among several possible replacements. It offered little technical explanation for the retirement, referring only to evolving "operational, security, and compliance requirements." Microsoft announced the retirement two years ago, but blocking first-time deployments gives customers another reason to begin planning their transition. Microsoft lists alternatives including Azure Data Factory, Azure Functions, read replicas, linked servers, database mirroring, availability groups, and transactional replication. However, it noted that "there is no single replacement that maps to every SQL Data Sync configuration." Existing users have just over a year to migrate before the final cutoff. Those without a migration plan will need one before the service shuts down. ®

A new virus emerges in rural China. Although those who contract it initially display moderate, flu-like symptoms, their health quickly declines. The mortality rate is unclear, but one aspect is immediately obvious—it’s very contagious. Within three months, nations around the world are planning lockdown protocols and quarantine measures. Politicians seem completely out of their league and ill-equipped. 

The world eventually recovers from the ordeal, but consequences of the virus linger for decades.While society pushes forward, there’s no promise that an even deadlier virus isn’t already lurking out of sight.

This isn’t about COVID-19, by the way. It’s the plot to the novel World War Z—arguably the most realistic depiction of a zombie apocalypse ever created. Released 20 years ago this week, the horror novel by Max Brooks quickly became one of the undisputed cornerstones of walking dead canon. Readers and critics devoured the book (no pun intended), but their responses often worry Brooks. Much like the reception to his first book, The Zombie Survival Guide, many fans seem to misunderstand his intentions. These projects weren’t simply intended to entertain. Max Brooks was trying to warn everyone about the looming threats we would prefer to ignore.

While the 54-year-old writer ostensibly writes books about zombies, Sasquatch, and (soon) an alien invasion, his attention to disaster details and hyperrealism has earned him a parallel career as a security and threat analyst for some of the world’s most respected geopolitical think tanks.

To celebrate World War Z’s 20th anniversary, Popular Science recently spoke with Brooks about the book’s massive impact.

This interview has been edited for length and clarity.

Andrew Paul: Did you anticipate World War Z attaining the legacy it now has in popular culture?

Max Brooks: Oh, God no. Of course not. Especially because I’m never tapped into pop culture. I don’t know what anybody else is doing—even when it was my job writing for Saturday Night Live! I’m good at thinking about what I think about.

AP: Before World War Z, you wrote an actual preparedness handbook called The Zombie Survival Guide. What prompted you to take a hyperreal approach to such a seemingly outlandish subject?

MB: The reason I wrote [them] was because all the zombie stories, even to this day, tend to focus around small groups. To me, it’s like trying to understand World War II from watching Saving Private Ryan. I had big picture questions nobody was answering.

I think the best zombie movie ever made was Dawn of the Dead. To me, the most interesting part was when they’re holed up in the mall watching the news. That window into the wider world was so fascinating, and I wanted more.

AP: But there was a time when World War Z almost never happened, right?

MB: [The publisher] didn’t know what to do with The Zombie Survival Guide. Their marketing strategy almost killed my career before it even launched. They thought, “Well, no one is clearly that much of a loser that he’s actually spent this much time thinking about [zombies]. Clearly, he’s a cool guy making fun of those losers. And because he’s Mel Brooks’ son and he’s coming off SNL, we’re gonna position him as Mel Brooks, Jr. writing Younger Frankenstein.”

But The Zombie Survival Guide really is a disaster preparedness manual. It’s why [soldiers] took it to Afghanistan; people told me it saved their lives when they were lost in the woods. I didn’t make anything up. It’s not Hollywood stuff—it’s all about dehydration and dry socks and shelter.

But [these books were] legitimately the product of years of thinking, “If I was in a zombie world, how would I survive?” It really set me on this path of asking, “What happens when the grown-ups drop the ball?”

AP: And now it’s your job to worry professionally.

MB: I’ve now been part of three military and national security think tanks—the Atlantic Council, the Center for Strategic and International Studies, and the Modern War Institute at West Point. I’m a non-resident senior fellow at all three of them, and it’s my job to study real threats.

For some reason, I was not blessed with the wall of denial. Like, I can’t just say, “That would never happen and I’m just going to go about my merry way.” I’m already terrified! And the way to reduce my anxiety is to study the threat so that it’s not nebulous.

AP: What was the most difficult part in preparing to write World War Z?

MB: You don’t know what you don’t know, so you don’t know what you’re missing. There’s always a fear of groping around in the dark; of not even knowing who to talk to. That was a real struggle, because I’m an insular guy. I’m not a social guy. Part of it was talking to experts, but part of it was reading books—and I’m fully dyslexic. So that was a real slog.

It was also about never trusting the internet. I used it once or twice, like, to research laser weaponry. I literally went to a company’s website, saw their demonstration video, and was like, “Yeah, okay. That is not a practical weapon for hunting zombies. I see how long it takes to burn through something.”

AP: Obviously humanity’s most terrifying challenge in the last 20 years was the COVID-19 pandemic. How do you view that real-world horror in the context of World War Z? 

MB: COVID was scary because I knew it was coming thanks to my friends in the military and biodefense community. I was part of what was called the Blue Ribbon Biodefense Panel for germ attacks way before COVID. So I already had at my fingertips the ability to tell the difference between panic porn in the media and the real deal. I also had to study diseases enough to write about a zombie plague. But also, it came from being on the receiving end of a bioterror attack. When I worked at SNL [from 2001 to 2003], we had the anthrax letters delivered to our building [in October 2001].

So, I knew this was coming, but the question was how to warn people. I had people laughing at me. Ironically, the people who are the worst minds to reach are the smarty-smarts because they think they know everything.

AP: Were you expecting COVID to be much worse than it was?

MB: Oh, much worse. It got me into trouble, because I was prepping for, like, tanks on the street, you know? I was ready for that. I stocked my home with food that would last the longest as opposed to food that my wife would actually eat. 

But the irony is, had it been worse, we might have actually done better. Studying diseases over the years—it’s sort of like the slow zombie versus the fast zombie. The fast zombie is so scary you have to react. The slow zombie gives you the false sense of security. Like, “Oh, I can take ‘em out.” COVID was the slow zombie. It allowed us to be arrogant and dismiss it: “Oh, it’s no worse than the flu.”

AP: How did you see that play out during the quarantine?

MB: It goes back to when COVID hit New York City. I had written a book called The Harlem Hellfighters, which was a true story of African American soldiers in World War I. They’re still an active unit in the National Guard, and I’m friends with their chief medical officer. Their job was to pick up the dead bodies around New York.

He said to me, “If those bodies had been stacked up on the street for everyone to see them, there would have been no argument about masking or distancing or taking the vaccine.” The hiding of it is what allowed naysayers to get way more people killed.

AP: Where did the grown-ups “drop the ball,” as you say?

MB: I think the greatest failure on the part of leadership at every level was not publicizing the dead. Maybe they were afraid of angry letters and backlash and didn’t want to cause a panic, but that’s exactly what they should have done.

A doctor in Los Angeles told me they converted hospital rooms into morgues. He said, “You don’t believe the amount of bodies. We’ve got pyramids of body bags.” And I’m like, “Well, then why is this not on the news every night?”

AP: After experiencing an actual global plague, how do you feel about World War Z’s overall accuracy?

MB: I think it was accurate for the time. I would still have the plague coming from China, 100 percent. I would love to say that was my genius futuristic prediction, but no. I based it on SARS. And this is why it’s unforgivable that it happened again. If I wrote it today, I would really highlight why it was allowed to be [downplayed]—and the reason is our greed. All of our stuff is made in China.

I would also really change the politicization of information. We’re living in a time where all facts have become tribalized. We’ve had 20 years of such dumbing down that I think it would be a central tenant of the book.

AP: Would you change how the United States responded to a zombie outbreak?

MB: I still firmly believe we are a moderate country, but I don’t know how brave we are. In order for a crime to be committed, you don’t need 100 bullies. You just need one bully and 99 cowards.

The psycho fanatics have a microphone now, which was inconceivable 20 years ago. They are hate merchants, and the erosion of our education system has created a demand that the merchants supply.

AP: So you think we would have handled COVID differently in 2006?

MB: If COVID happened 20 years earlier, we would all have gotten vaccinated, because of all the grandmas and grandpas who grew up before the polio vaccine.

AP: What else has changed?

MB: When I talk to people in power, I try to educate them about what I call “uphill influence” versus “downhill influence.” Downhill influence is when there’s a pre-existing bias that you just need to hijack and ride downhill. There’s gravity already there, and that’s not necessarily a bad thing. It was an established fact 20 or 30 years ago that vaccines kept you safe. So, if you were rolling out a vaccine, you could already just ride that existence acceptance downhill. The gravity was with you.

Uphill is when you have to educate before you can even start to persuade. You first have to educate people about just the world that you’re trying to explain. Vaccines have gone from downhill to uphill. The [subjects] we all had to try to stay awake through in seventh grade science class aren’t even there anymore.

I understand [MAHA supporters] want a clean planet, food, and water, and all of that will make you healthier. However, in 1491, the people who lived on this continent had all that, right? The moment the first Javier Bardem-looking Spaniard coughed on them, whole civilizations died.

AP: Both of your zombie books hinge on public education, and that’s now a major aspect of your threat analysis work. Do you know why you keep returning to this theme?

MB: I think one of the reasons I’m so obsessed with education is because I was not a good student. I have such ferocious learning disabilities. I never felt instantly comfortable learning, and I’ve always had to find workarounds. My mother had to help me find workarounds so I could learn. So when I research, it takes so much time and effort and [there’s] so much insecurity. I understand how hard it is to teach something to someone who doesn’t naturally pick it up.

I’m very lucky that I come from two parents who had no formal education, but were both very smart. Most importantly, they were very curious. I became very comfortable with the idea of approaching something as an absolute beginner.

AP: It took 14 years between World War Z and your follow-up sci-fi novel, Devolution. Your next book, The First Hundred Hours: A Story of Alien Invasion, comes out in 2027. Is there a reason for such long pauses between these projects?

MB: I’m not a natural scientist. The amount I’ve had to study for this new book has been excruciating. But it’s very humbling having to talk to the experts and say things like, “Please talk to me like I’m a third grader—and not a smart third grader.”

AP: Would you end World War Z the same if it was set in 2026?

MB: I would still end it on a positive note, and I think that has to do with being an American. We don’t have the luxury of abandoning our ideals, because that’s all we are. We’re not a nation-state—the ideals in America are all that hold this mutt [of a] nation together. We all come from different places and tribes, and we all agree to live under a certain set of guidelines. It’s really critical that we fight for those guidelines.

If there is one takeaway, it’s the central reason I wrote the book in the first place. We’re all stuck on the same planet together, and that planet is not that big anymore. What affects some of us could potentially affect all of us. I think America has some amazing cultural strengths, but one of our weaknesses is our isolationism. That’s built on an outdated notion that we are somehow protected by two oceans and our geography. That’s not true anymore.

The post Max Brooks reflects on 20 years of ‘World War Z’ appeared first on Popular Science.

Endometriosis, a chronic inflammatory condition affecting an estimated one in ten women of reproductive age, has long frustrated clinicians with its stubborn tendency to recur despite surgery and hormone therapy. A new review published in Reproductive Sciences argues that the answer to this therapeutic failure may lie in a single transcription factor: ZEB1, or Zinc Finger E-Box Binding Homeobox 1. Written by Gaurav Doshi and Sanket Shirodkar of SVKM’s Dr. Bhanuben Nanavati College of Pharmacy in Mumbai, the review synthesises evidence from across the field to position ZEB1 as a master molecular integrator—converging hormonal, inflammatory and epigenetic signals into a single programme that drives lesion establishment, invasiveness and drug resistance.

The biological centrepiece of the review is epithelial–mesenchymal transition, or EMT, the process by which epithelial cells lose their adhesive, stationary character and acquire the migratory, invasive traits of mesenchymal cells. In endometriosis, EMT is thought to be essential for the survival of endometrial cells that reflux into the pelvic cavity during menstruation and subsequently implant on peritoneal surfaces, ovaries and other ectopic sites. ZEB1 sits at the apex of this programme. It suppresses CDH1, the gene encoding E-cadherin, the principal adhesion molecule holding epithelial sheets together, and in doing so dismantles the cell–cell junctions that would otherwise keep ectopic cells anchored and vulnerable. The review details how ZEB1 accomplishes this repression by recruiting chromatin-remodelling machinery, notably the SWI/SNF ATPase subunit BRG1, to the E-cadherin promoter, effectively silencing it epigenetically. The result is a stabilised mesenchymal differentiation that permits attachment, invasion and, ultimately, the vascularisation required for a lesion to persist.

Crucially, the authors argue that ZEB1 is not merely one EMT factor among many, such as SNAI1, SNAI2 or its paralog ZEB2, but a systems-level hub. Immunohistochemical and molecular studies have repeatedly shown selective upregulation of ZEB1 in ectopic endometriotic lesions compared with matched eutopic endometrium, and its expression is particularly pronounced in deep infiltrating disease. One frequently cited clinical study found ZEB1 expression to be a potential indicator of invasive endometriosis, while a pilot investigation of different disease phenotypes has extended these observations across superficial, ovarian and deep infiltrating subtypes. Measurable ZEB levels have even been detected in plasma and peritoneal fluid of patients with endometriosis and infertility, raising the prospect of ZEB-family proteins as circulating biomarkers.

Perhaps the most consequential section of the review concerns the bidirectional crosstalk between ZEB1 and sex steroid signalling. Endometriosis is a hormone-dependent disease, and its defining therapeutic problem is progesterone resistance: lesions fail to respond to the progestational drugs used to suppress them. The review marshals evidence that oestrogen, specifically 17β-estradiol, induces ZEB1 expression, and that ZEB1 in turn suppresses progesterone receptor pathways. This creates a self-reinforcing circuit in which the oestrogen-ZEB1 axis dismantles the molecular machinery that progesterone therapy depends upon. Experimental work has demonstrated that high ZEB1 expression accompanies 17β-estradiol-induced EMT in endometriotic cells, and parallel findings from other hormone-driven diseases reinforce the mechanism: in breast cancer, ZEB1 induces oestrogen receptor-α promoter hypermethylation and confers antiestrogen resistance, and ZEB-family members have been shown to regulate endocrine therapy sensitivity through both canonical and non-canonical routes. In endometriosis, EMT itself has been shown to contribute to the downregulation of progesterone receptor expression in lesions, and the near-uniform loss of progesterone receptor isoform B in ectopic tissue is a long-standing observation that the ZEB1 framework now helps to explain mechanistically.

The review also devotes substantial attention to the non-coding RNA dimension of ZEB1 regulation, describing a multilayered feedback architecture that locks the mesenchymal state in place. The miR-200 family of microRNAs normally targets the 3′ untranslated regions of ZEB1 and ZEB2 transcripts, holding EMT in check. In ectopic lesions, this double-negative feedback loop is subverted: ZEB1 represses miR-200 transcription, and the resulting loss of miR-200 pressure allows ZEB1 protein to accumulate. Long non-coding RNAs add another tier. The lncRNA AFAP1-AS1, for example, promotes EMT in endometriosis in a ZEB1-correlated manner, and the metastasis-associated transcript MALAT1 has been implicated in the same circuitry, with miR-200c suppressing endometriotic progression in vitro and in vivo by targeting it. Circular RNAs complete the picture. The circRNA circZFPM2 has been shown to promote EMT by sponging miR-205-5p and thereby releasing ZEB1 from repression, while hsa_circ_0063526 acts through the miR-141-5p/EMT axis and circATRNL1 acts upstream by upregulating the EMT cofactor YAP1. Together these competing endogenous RNA networks—a concept also validated in metastatic cancer by J Clin Invest work—build a ceRNA web that perpetuates ZEB1 expression long after the initial pro-EMT stimulus has passed.

The authors then connect ZEB1 to the two great downstream consequences of endometriotic lesions: chronic inflammation and fibrosis. Through interactions with the TGF-β pathway—upstream signals such as TGF-β1 activate SMAD2/3, which cooperate with ZEB1 to drive the mesenchymal programme—ZEB1-linked cells reshape the lesion microenvironment. Fibroblast-to-myofibroblast transdifferentiation, marked by α-smooth muscle actin expression, generates the dense extracellular matrix characteristic of endometriotic implants, and analogous MRTF-A–ZEB1–IRF9 axes have been documented in renal fibrosis. Inflammation completes the loop: pro-inflammatory cytokines such as TNF-α, IL-6 and IL-10, and peritoneal fluid cytokine profiles that differ across endometriosis subphenotypes, feed back into EMT signalling through MAPK, ERK, PI3K/AKT and NF-κB pathways, while immune evasion mechanisms—including indoleamine 2,3-dioxygenase-mediated suppression of natural killer cell cytotoxicity—shield ectopic tissue from immune clearance. ZEB1’s own roles in immune cell biology and in macrophage efferocytosis and mitochondrial dynamics add further dimensions to this immunological interplay.

A distinctive strength of the review is its engagement with modern genomics and the heterogeneity it has revealed. Single-cell transcriptomic analyses of endometriosis, published in Nature Genetics and the Journal of Pathology, have identified distinct hormonal, immunologic and inflammatory signatures among the cell populations constituting lesions, and spatial transcriptomics is beginning to map how intermediate fibroblast and myeloid cell distributions shape lesion architecture. ZEB1 expression, the authors note, is not uniform: it varies by lesion subtype, anatomical site and microenvironmental context, which helps explain why superficial peritoneal, ovarian endometrioma and deep infiltrating disease behave so differently and respond so unevenly to therapy. This heterogeneity argues strongly against a one-size-fits-all anti-ZEB1 strategy and supports the emerging precision-medicine framing of the oestrogen-ZEB1-TGF-β axis as the central therapeutic target.

The review is refreshingly candid about the translational paradox at the heart of any ZEB1-directed therapy. Far from being a purely pathological molecule, ZEB1 has indispensable physiological functions in the female reproductive tract. In vitro studies show that ZEB1 modulates endometrial receptivity through EMT in endometrial epithelial cells, and work in mice demonstrates that it promotes EMT of endometrial epithelium and plays a critical role in embryo implantation. ZEB1 is also detected in granulosa cells of women undergoing IVF, regulates wound angiogenesis and closure, participates in corneal homeostasis, and contributes to endometrial repair during menstruation through epithelial migration and mesenchymal–epithelial transition. Blanking ZEB1 systemically, therefore, risks impairing fertility, tissue regeneration and wound healing—the very outcomes clinicians are trying to protect. Any therapeutic strategy would need to be lesion-specific, temporally controlled and carefully titrated, perhaps by targeting upstream oestrogen-driven induction, the TGF-β/ALK5 arm, the non-coding RNA sponges, or post-translational stabilisation mechanisms such as ZEB1 acetylation, phosphorylation and ubiquitin-proteasome turnover via regulators like USP51 and SIAH1/2.

The authors also stress the need for better experimental models to establish causal rather than merely correlative relevance. shRNA- and siRNA-based knockdown of ZEB1 in endometriotic cells, three-dimensional patient-derived endometriosis models for drug evaluation, and multi-omics approaches that integrate transcriptomic, epigenomic and proteomic data—including recent ubiquitination-focused studies of endometriosis fibrosis—are all highlighted as tools that could convert the ZEB1 hypothesis into testable interventions. Biomarker development is another avenue: ZEB-family levels in plasma and peritoneal fluid, in combination with existing miRNA signatures, could one day support non-invasive diagnosis, a long-standing unmet need given that current detection still relies on laparoscopy.

Ultimately, the review’s central claim is that the oestrogen–ZEB1–TGF-β axis functions as a signalling hub through which the hormonal, inflammatory and epigenetic drivers of endometriosis converge and perpetuate one another. By identifying ZEB1 as the point of integration, the authors provide a mechanistic scaffold that could explain progesterone resistance, fibrotic progression and recurrence within a single framework, and they chart a cautious but concrete path toward mechanism-based, lesion-specific precision therapies. For a disease that has historically been managed with blunt hormonal and surgical instruments, the prospect of intervening at the level of a single, druggable transcriptional circuit represents one of the more compelling conceptual advances in endometriosis research in recent years.

Hospitality businesses are warning of a jobs bloodbath as Andy Burnham launches a huge 'tourist tax' raid, with England's mayors and local councils given new powers to impose uncapped levies on overnight stays.

The post Fears of ‘Jobs Bloodbath’ as Burnham Launches Huge ‘Tourist Tax’ Raid appeared first on The Daily Sceptic.

Anunciados oficialmente hoje, os iPhones 18 Pro e 18 Pro Max tiveram os detalhes sobre as capacidades das baterias revelados pela Apple nas etiquetas de eficiência energética nas páginas de seus produtos na União Europeia.

O iPhone 18 Pro Max apresentou um aumento na capacidade da bateria muito mais expressivo do que o iPhone 18 Pro, em comparação com a geração anterior. Eis as capacidades dos modelos que ainda possuem bandeja para cartão SIM, segundo a Apple:

Modelo	iPhone 17 Pro	iPhone 18 Pro	Diferença em mAh
Pro (SIM físico)	3.988mAh	4.056mAh	+68 (+1,7%)
Pro Max (SIM físico)	4.823mAh	5.391mAh	+568 (+11,8%)

Os números, como podemos ver, batem com as especificações que vazaram em um órgão chinês no começo de julho passado.

Ainda de acordo com a Apple, o iPhone 18 Pro com bandeja para chip físico possui uma autonomia de até 34 horas para reprodução de vídeo, enquanto o iPhone 18 Pro Max pode chegar a até 43 horas. No uso típico, o primeiro atinge até 23 horas, enquanto o segundo pode durar até 29 horas.

As capacidades de bateria dos iPhones 18 Pro exclusivamente com eSIM ainda não foram confirmadas — mas, também conforme a Apple, essa versão do iPhone 18 Pro possui uma autonomia de até 36 horas para reprodução de vídeo e de até 45 horas no iPhone 18 Pro Max. No uso típico, eles possuem autonomias de até 24 horas e 30 horas, respectivamente.

Nos baseando nos números vazados pelo órgão chinês, muito provavelmente as capacidades dos modelos somente com eSIM serão estas:

Modelo	iPhone 17 Pro	iPhone 18 Pro	Diferença em mAh
Pro (eSIM)	4.252mAh	4.288mAh	+36 (+0,8%)
Pro Max (eSIM)	5.088mAh	5.567mAh	+479 (+9,4%)

Vale notar que a disponibilidade dos modelos somente com eSIM não sofreu alterações, de modo que eles estão disponíveis nas seguintes regiões: Arábia Saudita, Bahrein, Canadá, Catar, Emirados Árabes Unidos, Estados Unidos, Guam, Ilhas Virgens Americanas, Japão, Kuwait, México e Omã. Em todos os outros países (incluindo Brasil e Portugal, é claro), os aparelhos contam com a bandeja para cartão Nano-SIM físico.

via MacRumors

In one of the most comprehensive investigations of its kind, researchers have taken a major step toward untangling the biology underlying suicide risk, moving the field beyond long-standing debates about whether suicidal behavior is simply a consequence of psychiatric illness. By integrating large-scale genetic data with cutting-edge approaches that map how genes act in specific brain cells and circuits, an international team has identified shared genetic liability that cuts across psychiatric diagnoses while also pinpointing druggable biological pathways that could one day inform prevention strategies. The study, published in Translational Psychiatry, offers a sweeping synthesis of how inherited risk factors may translate into molecular vulnerabilities, and it does so with a level of resolution that previous candidate-gene approaches could never achieve.

Suicide remains one of the leading causes of death worldwide, claiming more than 700,000 lives each year according to global health estimates. Despite decades of research, clinical prediction remains stubbornly imprecise, and biological models of suicidal behavior have historically been hampered by small sample sizes, inconsistent findings, and a tendency to conflate suicide risk with the psychiatric disorders with which it so often co-occurs. Major depression, bipolar disorder, schizophrenia, and substance use disorders all carry elevated suicide risk, yet most people with these conditions never attempt suicide, while some individuals who die by suicide have no diagnosed psychiatric illness at all. This paradox has long suggested to researchers that suicidal behavior may possess partially distinct biological underpinnings, and the new study set out to test that hypothesis with unprecedented statistical power.

At the heart of the work lies genome-wide association study methodology, or GWAS, which scans hundreds of thousands to millions of genetic variants spread across the entire genome in very large groups of people, comparing individuals who have experienced suicidal thoughts or behaviors with those who have not. Each variant is tested for statistical association with the outcome, and the results can be combined into polygenic risk scores, numerical summaries of a person’s inherited liability based on the cumulative small effects of thousands of variants. Because no single common variant exerts a large effect, the field depends on aggregating data across massive biobanks and cohorts, a strategy that has only become feasible in the past decade as datasets containing hundreds of thousands of individuals became available.

The research team took particular care to address a central confound: psychiatric disorders themselves are highly heritable, and any genetic signal linked to suicide could simply reflect inherited liability to depression or schizophrenia rather than to suicide specifically. To disentangle this, the investigators applied sophisticated statistical techniques, including genetic correlation analysis and conditional modeling, which allow researchers to ask how much genetic overlap remains between suicidal behavior and psychiatric conditions after accounting for their shared heritability. Their findings revealed a complex architecture. Substantial genetic correlations confirmed that suicide risk shares a meaningful fraction of its inherited basis with major psychiatric disorders, supporting the idea of a common pool of genetic liability. Yet the analyses also uncovered signals that persisted beyond what could be explained by those disorders, pointing to biological mechanisms that may be more specific to the emergence of suicidal thoughts and actions.

A key conceptual innovation of the study is its framing of “shared genetic liability” as a bridge between diagnoses. Rather than treating suicide as an epiphenomenon of any single disorder, the researchers modeled it as a transdiagnostic phenomenon, one whose risk emerges partly from inherited vulnerabilities that cut across diagnostic categories. This perspective aligns with a growing movement in biological psychiatry that emphasizes symptom dimensions and mechanisms over traditional diagnostic boundaries. From this vantage point, the genetic variants that raise risk for depression, PTSD, and schizophrenia may do so partly because they converge on shared molecular pathways, and those same pathways may govern an individual’s threshold for suicidal crises regardless of which diagnosis they carry.

Identifying genetic variants, however, is only the first step. A GWAS signal typically points to a genomic region rather than a specific causal gene or mechanism, since many associated variants fall in non-coding stretches of DNA that regulate gene activity from a distance. To translate statistical associations into biological insight, the team deployed a battery of functional genomics approaches. Transcriptome-wide association studies, known as TWAS, integrate gene expression data to identify genes whose genetically predicted expression levels are linked to suicide risk. Tissue and cell-type enrichment analyses then ask whether the implicated genes are unusually active in particular organs or cell populations. The results converged strikingly on brain tissue, and more specifically on neuronal populations, providing support for the idea that inherited suicide risk is mediated largely through gene regulation within the central nervous system.

The study’s most clinically provocative findings concern druggable biology. Using databases that catalog the protein targets of approved and investigational medications, the researchers examined whether genes implicated in suicide risk were over-represented among known drug targets. The analysis identified several classes of candidate targets, including components of neurotransmitter signaling systems, ion channels, and intracellular signaling cascades that are already the focus of pharmacological development for other conditions. This “druggable genome” approach, which has gained traction in genetics research across many diseases, offers a pragmatic shortcut for translational science: rather than waiting decades for entirely new therapeutic classes to be invented, researchers can prioritize existing or in-development compounds whose molecular targets intersect with genetically implicated pathways.

Among the pathways receiving attention in the analysis were those involving glutamatergic and GABAergic neurotransmission, the primary excitatory and inhibitory systems of the brain, which have repeatedly surfaced in studies of mood disorders and stress response. The endocannabinoid system and inflammatory signaling pathways also appeared in the convergent analyses, consistent with a broader literature linking immune dysregulation and allostatic load to suicidal ideation. Importantly, the authors emphasize that these findings identify hypotheses rather than ready-made treatments. Genetic association with a drug target does not guarantee that modulating that target will reduce suicide risk, and any therapeutic application would require extensive preclinical validation and carefully designed clinical trials. Nevertheless, the work provides a principled, data-driven map for where to look, replacing decades of largely failed candidate-gene speculation with a genome-wide evidence base.

The methodological rigor underpinning the study deserves emphasis, because the genetics of suicidal behavior has a troubled history. Early candidate-gene studies, which typically examined a handful of variants in genes related to serotonin signaling, produced findings that largely failed to replicate and in some cases were later shown to reflect statistical artifacts, small samples, and publication bias. The field has since undergone a reckoning, and modern efforts adhere to far stricter standards: preregistered analyses, very large and ancestrally diverse cohorts, replication in independent samples, and conservative multiple-testing corrections that demand genome-wide significance thresholds on the order of five times ten to the negative eighth power. The new study reflects these lessons, applying sensitivity analyses to guard against confounding from psychiatric comorbidity and examining whether findings generalize across ancestral groups, an issue of considerable importance given that most genetic discovery to date has been conducted in populations of European ancestry.

The implications for clinical practice, while still distant, are worth considering. Polygenic risk scores for suicide-related outcomes currently explain only a small fraction of individual differences in risk, far too little to be used as stand-alone screening tools, and their predictive performance is degraded in populations not represented in the discovery data. Researchers in the field are careful to stress that genetic risk is not destiny: suicidal behavior arises from an intricate interplay of inherited vulnerability, mental illness, trauma, substance use, social isolation, access to lethal means, and the availability of support. What genetics offers is not a crystal ball but a window into mechanism, and mechanistic knowledge is the raw material from which better biomarkers, risk stratification tools, and ultimately targeted interventions are built. In the near term, the druggable pathway findings are most valuable as a guide for laboratory science, directing neurobiologists toward molecular systems whose manipulation might alter suicide-relevant phenotypes in animal models and cellular assays.

Looking forward, the study signals where the field must go next. Sample sizes for suicide-specific genetic analyses remain smaller than those for major psychiatric disorders, and expanding representation across ancestries is essential if the benefits of this research are to be shared equitably. Integrating genetic data with longitudinal measures of life stress, neural imaging, and digital phenotyping may eventually allow researchers to model how inherited liability interacts with environmental triggers across the lifespan. Functional experiments in induced pluripotent stem cell-derived neurons and brain organoids could test whether the implicated genes genuinely alter stress-response circuitry or resilience. And randomized trials in patients carrying high genetic liability, though ethically and logistically complex, represent the logical endpoint of the druggable-target approach.

What the study ultimately delivers is a reframe. Suicide risk, in this analysis, is not an amorphous clinical outcome but a measurable, partly heritable trait whose genetic architecture is now being resolved with the same tools that have transformed our understanding of heart disease, diabetes, and schizophrenia. By demonstrating that shared genetic liability links suicide risk across diagnostic boundaries and by mapping that liability onto specific, pharmacologically tractable biology, the researchers have converted a long-standing clinical puzzle into a concrete research agenda. The path from genetic correlation to effective prevention is long, and no genetic finding will soon replace the human work of crisis intervention, connection, and care. But for a problem that has defied biological explanation for generations, the identification of shared, druggable mechanisms represents a genuine and hard-won advance, one that may shape suicide research for years to come.

Late last week, word started leaking that the National Institutes of Health (NIH) had reached an agreement with the Department of Defense that would see part of the NIH's budget used to fund research at the Department of Defense. So, on the Friday just prior to a US holiday weekend, the Department of Defense released a copy of the agreement and confirmed that it had been signed roughly a month earlier. The move is striking for a number of reasons, ranging from the existing budget disparities between the two parties involved to the fact that the money would be used for projects that the current NIH leadership has explicitly rejected.

The agreement itself sets up a system where the NIH would transfer money to the Department of Defense to fund staff and projects that would "support the advanced development of medical countermeasures against pandemic influenza, chemical, biological, radiological, and nuclear (CBRN) threats, and emerging infectious diseases." The money would come out of the budget for the NIH's National Institute of Allergy and Infectious Diseases, or NIAID, to which Congress has allocated $6.6 billion in 2026. The agreement is set to run for a decade.

Left unspecified is just how much of the NIAID budget will be spent on Defense projects. Reporting by Nature suggests that the Department of Defense was looking for up to a third of its total budget but was being told to settle for about 10 percent. There's obviously an enormous disparity between the budgets of these two agencies, given that the 2026 Defense budget is roughly $1 trillion. That budget is under considerable strain, however, due to the open-ended nature of the conflict with Iran. The deal has also been announced at a time when the NIH has been struggling to issue sufficient grants to use the money that Congress allocated to it.

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© Artem Onoprienko

Late last week, word started leaking that the National Institutes of Health (NIH) had reached an agreement with the Department of Defense that would see part of the NIH's budget used to fund research at the Department of Defense. So, on the Friday just prior to a US holiday weekend, the Department of Defense released a copy of the agreement and confirmed that it had been signed roughly a month earlier. The move is striking for a number of reasons, ranging from the existing budget disparities between the two parties involved to the fact that the money would be used for projects that the current NIH leadership has explicitly rejected.

The agreement itself sets up a system where the NIH would transfer money to the Department of Defense to fund staff and projects that would "support the advanced development of medical countermeasures against pandemic influenza, chemical, biological, radiological, and nuclear (CBRN) threats, and emerging infectious diseases." The money would come out of the budget for the NIH's National Institute of Allergy and Infectious Diseases, or NIAID, to which Congress has allocated $6.6 billion in 2026. The agreement is set to run for a decade.

Left unspecified is just how much of the NIAID budget will be spent on Defense projects. Reporting by Nature suggests that the Department of Defense was looking for up to a third of its total budget but was being told to settle for about 10 percent. There's obviously an enormous disparity between the budgets of these two agencies, given that the 2026 Defense budget is roughly $1 trillion. That budget is under considerable strain, however, due to the open-ended nature of the conflict with Iran. The deal has also been announced at a time when the NIH has been struggling to issue sufficient grants to use the money that Congress allocated to it.

Read full article

Comments

© Artem Onoprienko

The reagents of the feedstock are never produced by processes as on the early Earth. Production requires substantial energy and controlled industrial procedures

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A bacterial molecule called gladiolin can disarm invasive Candida albicans and strengthen the effects of a major antifungal drug. Candida albicans usually lives harmlessly in the human body, but under the wrong conditions it can transform into an invasive form capable of damaging tissue and causing life-threatening infection. Researchers from Monash University and the University [...]

Avec l’intelligence artificielle qui s’invite désormais dans les devoirs des collégiens et lycéens, de nombreuses familles font face à un dilemme : faut-il en limiter l’usage ou, au contraire, permettre à son enfant de suivre le mouvement ? Une étude révèle à quel point les pratiques des autres...

Machine vision is becoming a practical part of Apple’s U.S. factory training strategy, giving smaller manufacturers access to techniques that help production systems inspect what they make. The recent opening of the Houston manufacturing training center extends that effort into a working electronics production campus, while courses developed with Michigan State University introduce businesses to image analysis, machine learning, and automated quality checks.

For a manufacturer, the attraction can be straightforward: finding a missing component before a product leaves the line, identifying a surface defect before more material is added, or recognizing an assembly error while it can still be corrected cheaply.

These are manageable problems with measurable costs. They also offer an accessible starting point for businesses interested in AI but unsure where it belongs inside their operations.

Machine Vision Enters the Manufacturing Curriculum

The Apple Manufacturing Academy’s current course catalog includes Machine Learning with Vision, a course introducing machine learning and deep learning through practical activities using Apple devices. It sits alongside instruction in automation, quality fundamentals, manufacturing data, maintenance, and process improvement.

That placement gives the subject useful context. A camera can produce an image, but a factory needs a decision: accept the part, flag it for review, check its position, or investigate a process that may be drifting out of tolerance.

Machine vision connects image capture to those operational decisions. Some applications use established rules to measure dimensions or identify patterns. Others use machine learning to recognize acceptable variations and defects that are difficult to describe through fixed rules.

The academy’s public description confirms introductory activities with Apple devices. It does not identify a particular iPhone, Mac configuration, software framework, or industrial camera package that every participant must use.

For smaller businesses, the educational value is learning how to define an inspection problem before purchasing equipment. A company that understands what it needs to detect can have a much more productive conversation with an automation supplier.

Houston Brings Training Closer to Production

Apple opened its 20,000-square-foot Advanced Manufacturing Center on August 13. According to the Houston opening announcement, the free program offers small and medium-sized businesses instruction in advanced manufacturing, interactive labs, and experience with representative production equipment.

The first cohort worked with machine learning for quality control and advanced automation. Participants also explored production challenges, used a holographic table, and assembled and laser etched a product.

The location adds context: the center occupies the same Houston facility that builds advanced AI servers and is scheduled to begin Mac mini manufacturing this year. Its teaching program includes final assembly principles and design considerations for printed circuit board assembly.

Houston is the company’s second U.S. manufacturing learning site, following the Detroit academy established with Michigan State University in August 2025. By the Houston opening, Apple said the academy had helped nearly 1,000 workers, students, and entrepreneurs.

That figure measures people reached through the program. It should not be interpreted as 1,000 factories already operating AI inspection systems.

A Useful Inspection Starts With a Specific Problem

Imagine a small business assembling control panels. Each panel needs the same set of connectors, positioned correctly before the enclosure closes. A machine vision station could check for a missing connector while the assembly remains accessible.

The value comes from catching that error at the right moment. Discovering it after packaging creates extra handling and rework. Discovering it after delivery may involve a return, a service visit, and an unhappy customer.

A useful pilot would therefore begin with that single inspection point. The business could compare the existing process with the assisted one, recording missed defects, unnecessary rechecks, inspection time, and the cost of correcting mistakes.

The camera is only part of the exercise. Workers must agree on what constitutes a defect, collect representative examples, and decide what happens when the result is uncertain.

Those decisions draw heavily on experience already present on the factory floor. An operator may know that an unusual mark is harmless, while a barely visible change in alignment predicts a later assembly problem. Turning that knowledge into consistent inspection criteria is valuable work in its own right.

These are examples of how manufacturers could apply the training, rather than projects Apple has announced for individual participants.

Teaching Machine Vision to Handle Ordinary Variation

A demonstration can look impressive when every part arrives clean, centered, and evenly lit. Production introduces variation: different surface finishes, reflections, changing positions, and batches that look slightly different while remaining within specification.

The inspection system must distinguish those acceptable differences from actual failures. Otherwise, it can reject good products or allow defective ones to continue.

Industrial vision supplier Cognex’s deployment guidance recommends validating systems across product models, defect types, and manufacturing lines. It also describes an approach in which automated inspection handles preliminary checks while experienced inspectors review borderline cases.

For a business learning machine vision, that offers a realistic way to introduce the technology. Employees can compare its decisions with their own, investigate disagreements, and determine whether the results justify extending its role.

An inspection system also needs an owner after installation. Someone must understand when a product change requires new examples, when equipment needs attention, and when performance has slipped. Training that responsibility into the workforce helps prevent an initially successful project from becoming an unreliable fixture.

Smaller Manufacturers Are Already Applying the Training

The academy’s reach extends beyond companies producing consumer electronics. In its May update on participating manufacturers, Apple highlighted Block Imaging, a Michigan business that services and refurbishes medical imaging equipment.

The company hosted visitors during the academy’s Spring Forum and described applying techniques learned from Apple engineers and Michigan State experts to its operations. Apple reported that the academy had supported more than 150 American businesses at that point.

The announcement did not identify a particular machine vision deployment at Block Imaging or publish a percentage improvement attributable to visual inspection. It does provide an example of the training reaching businesses whose work differs substantially from building an iPhone.

That wider participation could benefit Apple indirectly. More capable domestic manufacturers can support equipment maintenance, tooling, components, and specialized production services. Participation itself does not establish a supplier relationship, but the skills can be used across customers and industries.

Access Without a Large Training Budget

The academy’s participation information says eligible small and medium-sized U.S. manufacturers can take courses free of charge. Online learning includes on-demand materials and interactive modules, while in-person sessions add workshops and more personalized instruction.

Digital badges are available for different topics, and completed course materials remain accessible for review. That gives a business room to train an employee around existing production commitments and return to the material when an actual project begins.

Free instruction does not remove the eventual cost of cameras, lighting, integration, maintenance, or employee time. It can help a manufacturer understand those costs before committing to a system.

The first proposal brought back to the factory might be modest: inspect one recurring defect at one station and record the results for several weeks. A supervisor can then weigh the time saved against the extra reviews, maintenance, and mistakes. That is the kind of evidence a business owner can use when deciding whether to install a second station.

The post Machine Vision Joins Apple’s U.S. Factory Training Push appeared first on AppleMagazine.

After health officials in Pennsylvania found that two young children died from measles, the Centers for Disease Control and Prevention is refusing to count their deaths as being caused by the deadly virus.

“This week’s measles outbreaks update will not include the two measles-associated deaths reported by the Pennsylvania Department of Health on Aug. 25,” the CDC posted on its website, in a high unusual announcement.

It’s a precedent shattering action. The New York Times called it an “extraordinary move for the CDC,” breaking with the agency’s long-standing procedure of accepting data shared by states.

The challenge by the CDC comes amid a political showdown between health secretary Robert F. Kennedy Jr, who oversees the CDC, and Pennsylvania’s Democratic governor Josh Shapiro.

At a news conference last week, Shapiro announced the deaths of the two children from measles and condemned Kennedy for spreading vaccine misinformation, saying that “there’s real life consequences for spreading misinformation.”

RFK Jr responded on social media by accusing Shapiro of taking “giddy delight” in their deaths and even suggested he may even “fabricated” them. The CDC’s own announcement that it would not be counting the deaths as measles related came just days after the public spat.

According to the latest reporting, one of the deceased was a newborn with a ruptured spleen, and the other was a child of unknown age. Both were unvaccinated and tested positive for measles, the Pennsylvania Health Department said, per the NYT. They came from Lancaster County, the center of a measles outbreak where 242 people have been infected with the disease so far, the most in the state.

Conflicting information over the children’s deaths gave rise to the heated controversy.

Though the state’s health department said both deaths were due to measles, Lancaster County coroner Stephen Diamantoni, a Republican, said that his office’s pathologist determined that the newborn — which was born infected with virus which it inherited from its mother — died of a ruptured spleen, not measles.

But some top medical experts have pushed back against Diamontoni. Measles can enlarge a baby’s spleen and make them prone to rupturing during birth,  wrote Paul Offit, a renowned vaccine and pediatric infectious disease expert at Children’s Hospital of Philadelphia, in a widely reported essay on Substack. Once the spleen ruptures, it’s difficult to determine if it was enlarged after the fact.

Offit called on Diamontoni to provide more details surrounding the newborn’s death — and that, if it wasn’t measles, to offer an alternative explanation for the baby’s ruptured spleen. Since ruptured spleens in newborns is exceedingly rare and can be caused only by a handful of disorders or infections, he said, if one of those conditions wasn’t found in the child, then the “only obvious cause left would be measles.”

None of this explains why the CDC also refused to count the other child’s death, few details on whom have been released ot the public.

The Department of Health and Human Services, which oversees the CDC, defended its decision in a statement.

“The two measles-associated deaths announced by Pennsylvania have not been confirmed based on the information currently available to CDC,” it said, per the NYT.  “The information currently posted reflects the best available information and our commitment to transparency and telling the American people the truth — a foundational principle of the Trump administration.”

More on viruses: Authorities Alarmed When Person With Measles Spends Entire Day Frolicking Around Universal Studios

The post The CDC Is Now Denying That Specific Children Died From Measles, in a Scandal Potentially Beyond Anything in Its History appeared first on Futurism.

Victorian buyers previewed distant mansions through lenses and creativity

The University at Buffalo is celebrating the deployment of eight new 40-foot electric transit buses, which are now quietly transporting students, staff, and campus visitors per day. The buses are the first in UB’s Stampede fleet to ditch diesel, kicking off a four-year effort to electrify the university’s campus transportation system.

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Under a new partnership, the Defense Department would play a larger role in biodefense and pandemic preparedness. Democrats warned it could allow a Pentagon cash grab.

It is surprising to me that the authors of these studies did not consider it more of a priority to understand the mechanics of robustness.

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