Durante años intentamos matar al mosquito del dengue antes de que pique. Científicos argentinos exploran otra idea inversamente radical: una vacuna que haga que nuestra sangre lo ataque después de habernos picado


HP Z Runtime simplifica servir LLMs no Linux com vLLM, API OpenAI e gestão prática para GPUs.
O post HP Z Runtime chega ao Linux com foco em LLMs e vLLM apareceu primeiro em Blog do Edivaldo - Informações e Notícias sobre Linux.
Fernando Alexandre afirma que a nova Lei da Ciência e Inovação, aprovada em Conselho de Ministros, vai permitir mitigar a fragmentação do sistema científico nacional. Segundo o ministro da Educação, Ciência e Inovação, o diploma tem um "quadro conceptual diferente", permitindo a qualquer entidade "candidatar-se ao selo da entidade de investigação".
The post Governo aprova revisão da Lei da Ciência para reorganizar o sistema nacional de investigação e inovação appeared first on Tek Notícias.


For more than four decades, pathologists have glimpsed something unsettling under the microscope in the earliest stages of certain cancers: cells with nuclei far larger than they should be, swollen and distorted, lurking in tissue that otherwise appears on the verge of catastrophe. These so-called giant-nucleus cells, or karyomegalic cells, were first spotted in the 1980s in animal experiments involving iron-induced oxidative stress, yet their biological identity and their role in the genesis of cancer remained stubbornly obscure. Now, a team of researchers in Japan has provided the most detailed portrait of these cells to date, and their findings suggest that the enormous nuclei may be far more than a curiosity—they could be the founding population of early cancer, visible before any tumor exists, and potentially useful as a predictor of patient outcomes.
The study, led by Shinya Toyokuni, professor emeritus at Nagoya University Graduate School of Medicine, together with assistant professor Yingyi Kong and colleagues, was published in Redox Biology. The work addresses a deceptively simple question: when iron overload kills most cells in a tissue through oxidative damage, who survives, and what do the survivors become? Iron is an essential micronutrient, but in excess it is a potent carcinogen. Its chemistry is both the reason we need it and the reason it can harm us. Iron catalyzes the formation of hydroxyl radicals from hydrogen peroxide through the Fenton reaction, and these radicals shred DNA, oxidize lipids, and damage proteins. When the damage is severe enough, a form of programmed cell death called ferroptosis is triggered—an iron-dependent demise characterized by lipid peroxidation cascades that rupture the cell membrane. Ferroptosis has become one of the hottest topics in cancer biology precisely because it links iron metabolism, oxidative stress, and cell fate in a single mechanism.
Toyokuni’s team reasoned that if ferroptosis sweeps through iron-damaged tissue, the cells that escape it must be exceptional in some way, and those exceptions might be the seed of malignancy. To find out, they turned to a well-established animal model in which ferric nitrilotriacetate, a carcinogenic iron compound, is injected into rats, delivering a bolus of iron to the kidneys. The compound accumulates in the proximal tubules, where it catalyzes oxidative damage and, over months, produces renal cell carcinoma. In the experiments, the researchers collected kidney tissue before the injection and again one and three weeks afterward. Crucially, they also included a second experimental group: rats carrying a single mutated copy of the BRCA1 gene, the same gene that, when mutated in humans, dramatically raises the risk of breast and ovarian cancers and is associated with renal carcinoma in certain contexts.
The methodological heart of the study lies in its marriage of two technologies. The first is spatial transcriptomics, a technique that maps gene activity across individual cells within a tissue section while preserving the tissue’s original architecture—so researchers can see not only which genes are active but where in the tissue those transcriptional programs are operating. The second is computational nuclear morphometry, which quantifies the size, shape, and density of cell nuclei in the same samples. By overlaying the two datasets, the team could link the physical appearance of each cell—above all, the size of its nucleus—to its underlying transcriptional state. This integration is important because morphological atypia has long been the currency of diagnostic pathology, but connecting that atypia to molecular signatures at single-cell resolution is a recent capability.
What emerged within a week of iron administration was striking. Giant-nucleus cells appeared in the damaged kidneys, and these cells were not simply wounded cells awaiting death. They showed elevated expression of potent oncogenes, including Myc and Met, and they had acquired resistance to ferroptosis—the very cell death pathway that was eliminating their neighbors. In other words, the extreme oxidative environment had functioned as a brutal selective pressure, and the cells best adapted to survive it had activated a program that resembles, in miniature, the hallmark machinery of cancer. The enrichment of Myc, a transcription factor that drives cell growth and proliferation, and Met, a receptor tyrosine kinase involved in invasive growth, paints a picture of cells that are not merely enduring damage but reorganizing themselves around it.
The BRCA1 connection proved equally consequential. BRCA1 is best known as a guardian of the genome, a scaffold for the homologous recombination machinery that repairs double-strand DNA breaks. In the BRCA1-mutant rats, giant-nucleus cells emerged with distinctly different biological profiles from those in wild-type animals. The interpretation the researchers offer is that BRCA1 deficiency cripples DNA repair, so more of the damaged cells that would otherwise die or be repaired instead survive in their injured, genome-compromised state—becoming precancerous giant-nucleus cells. Electron microscopy and cellular respiration measurements reinforced this idea at the subcellular level: cells from BRCA1-mutant rats showed mitochondrial remodeling, with impaired iron handling and compromised respiratory function. Mitochondria, long appreciated as power plants, are also central regulators of ferroptosis and iron metabolism, and their disarray in the mutant animals may be both a consequence of BRCA1 loss and a driver of the abnormal iron biology that feeds karyomegaly.
Using their combined gene-expression and nuclear-shape data, the researchers went further and classified the giant-nucleus cells into six distinct types. One type possessed extremely large nuclei and gene signatures of stress-induced growth arrest—cells that appear to have locked themselves into a senescent-like state, consistent with profiles reported in earlier studies. Another type, found more frequently in BRCA1-mutant kidneys, showed heightened activity of cancer-related genes alongside elongated nuclei, a combination the authors interpret as a potential precancerous state. The taxonomy matters because it reframes giant-nucleus cells from a single enigmatic category into a spectrum, some members of which may be harmless or even protective while others carry genuine malignant potential.
One of the most provocative findings concerns the cells surrounding the giants. Even morphologically normal cells near giant-nucleus cells exhibited gene expression changes that appear to promote survival, suggesting that the karyomegalic cells remodel their local microenvironment in ways that extend beyond their own borders. In BRCA1-mutant kidneys, the team also documented a substantial increase in stromal cells—non-cancerous supportive cells including immune and connective tissue elements—around the damaged regions. The local tissue environment, the tumor niche in the language of modern oncology, was being reshaped long before any tumor could be called a tumor. This raises the possibility that a single conspicuous cell, easily identified by its nucleus under a conventional microscope, could serve as a sentinel for a whole neighborhood of incipient malignancy.
The leap from rat kidneys to human medicine came through two complementary analyses. First, the researchers mined TCGA-KIRC, a large public database of kidney cancer patients, asking whether tumors carrying gene-expression patterns resembling the cancer-prone giant-nucleus cells were associated with different clinical trajectories. They were: patients whose tumors shared the gene patterns of the cancer-prone giant-nucleus cells had shorter survival times, while those with patterns resembling the healthier giant-nucleus cell types had better outcomes. Not all giant-nucleus cells, in other words, are created equal, and the transcriptional fingerprints defined in the rat model appear to carry prognostic weight in human disease. Second, in a small pilot study, the team examined breast tissue from seven individuals with inherited BRCA1 mutations and fifteen without, observing abnormal nuclear features similar to those in the animal model in the mutation carriers. While the sample size is modest, the parallel hints that karyomegaly may be a cross-tissue marker of BRCA1-linked precancerous change.
The broader implications run in two directions. Clinically, the promise is that giant-nucleus cells, being easy to spot under the microscope, could function as early indicators of cancer—visible warnings in tissue that would otherwise be classified as merely damaged or inflamed. The TCGA survival data suggest that their gene-expression signatures might even stratify patients by risk once a tumor has formed. Scientifically, the study offers a concrete mechanism connecting an environmental exposome factor—iron-catalyzed oxidative stress—to a defined, transcriptionally characterized precancerous population, with ferroptosis resistance as the pivot. It also implies testable therapeutic hypotheses: if blocking mitochondrial remodeling or reversing ferroptosis resistance could prevent the persistence of the precancerous cells, early intervention might stop cancer before it starts. Toyokuni and his colleagues are careful to note that long-term studies will be needed to determine how giant-nucleus cells actually progress into tumor cells, whether such interventions can work, and whether nuclear shape combined with gene patterns can be validated as a diagnostic in larger patient cohorts. But the central message is already legible: some of the earliest chapters of cancer may be written in cells that have grown too large to be ignored.
Article Title: Iron-catalyzed oxidative stress reveals an exposome-related ferroptosis-resistant karyomegalic niche in BRCA1-linked renal carcinogenesis.
Article References: Kong, Y., Shiraki, Y., Furuhashi, K., Maruyama, S., Imaoka, T., Enomoto, A., & Toyokuni, S. (2026). Iron-catalyzed oxidative stress reveals an exposome-related ferroptosis-resistant karyomegalic niche in BRCA1-linked renal carcinogenesis. Redox Biology, 95, Article 104293. https://doi.org/10.1016/j.redox.2026.104293
Image Credits: AI Generated
DOI: 10.1016/j.redox.2026.104293
Keywords: giant-nucleus cells, karyomegaly, ferroptosis, BRCA1, iron-catalyzed oxidative stress, spatial transcriptomics, renal carcinogenesis, mitochondrial remodeling, nuclear morphometry, precancerous cells, TCGA-KIRC, Nagoya University

Dopo un agosto particolarmente ricco, Nvidia sembra aver rallentato leggermente il ritmo per la sua piattaforma di streaming di videogiochi GeForce NOW, che il mese oltre a nuovi giochi aveva ricevuto un’applicazione nativa per Linux, il supporto a Firefox e la sincronizzazione con GOG. Ma l'appuntamento del giovedì sera con i nuovi titoli della settimana non poteva mancare, ecco cosa è uscito:
Non è nuovo, ma da segnalare anche che Valheim è arrivato alla versione 1.0 stabile ed è quindi uscito dall'accesso anticipato.
Boots on the ground, this #GFNThursday. 👢@WARDOGS, Valheim and other games have been added to the GeForce NOW Library.
See which games 👉 https://t.co/SwIwlP56Ga pic.twitter.com/ZuifO0kbSsPiccolo prezzo per un ottimo smartphone? Honor 400 Lite, compralo al miglior prezzo da Amazon Marketplace a 130 euro.CLICCA QUI PER CONTINUARE A LEGGERE


Un equipo de la EHU descubre una estructura en forma de decágono en las nubes de Saturno. La investigación liderada por el catedrático Agustín Sánchez-Lavega se ha apoyado en las imágenes obtenidas por el telescopio Hubble y una amplia red de astrónomos aficionados y permitirá avanzar en el conocimiento de los fenómenos atmosféricos en los planetas gaseosos.
Cuando las naves espaciales Voyager 1 y Voyager 2 sobrevolaron en los años 1980 y 1981 el planeta Saturno, entre sus muchos descubrimientos, destacó la presencia en sus nubes superiores de una formación con geometría hexagonal rodeando al polo norte del planeta. Dicha estructura, conocida como el hexágono de Saturno, ha sobrevivido hasta nuestros días, a lo largo de más de un año de ese planeta (que equivale a unos 30 años terrestres). Nunca se había observado nada semejante en ningún planeta del Sistema Solar y su naturaleza sigue siendo un desafío para los meteorólogos planetarios.

Curiosamente, a pesar de la simetría en la distribución de los vientos y en la dinámica atmosférica en Saturno, durante todos los años transcurridos desde entonces, no se había observado una estructura semejante en el hemisferio sur, lo que desconcertaba a la comunidad investigadora. Pero en el año 2023, a medida que el hemisferio sur del planeta se iba haciendo más visible, las imágenes tomadas con el Telescopio Espacial Hubble (HST) mostraban no un hexágono sino una estructura decagonal (un polígono de diez lados) alrededor de la región polar sur del planeta. Las imágenes obtenidas posteriormente con el HST en los años 2024 y 2025, así como las obtenidas con telescopios en Tierra, confirmaron su existencia. Las imágenes muestran que algunos vértices del decágono están menos contrastados que otros, lo que sugiere que se trata de un fenómeno en desarrollo, quizás por ahora menos estable que el hexágono.
«Estamos realmente sorprendidos por este descubrimiento, totalmente inesperado, y que abre las puertas a una investigación detallada en los próximos años de esta peculiar estructura atmosférica y a su comparación con el hexágono», declara Agustín Sánchez-Lavega, profesor emérito de la EHU en la Escuela de Ingeniería de Bilbao, quien lidera el estudio que se publica en la revista de alto impacto Science Advances.

Para poder seguir la evolución del decágono con regularidad, la investigación se ha apoyado en las imágenes obtenidas por una amplia red de astrónomos aficionados que con sus telescopios han sido capaces, a lo largo del año 2025, de observar los vértices del decágono, lo que ha permitido estudiar con precisión su movimiento. Al igual que el hexágono, el decágono se encuentra inmerso en una corriente en chorro cuya velocidad máxima es de unos 400 kilómetros por hora, si bien el propio decágono se mueve como un todo, lentamente con respecto a la rotación del planeta, a unos 10 kilómetros por hora. Simultáneamente, sus vértices avanzan realizando un movimiento oscilante, con un período de unos 32 días, algo no observado en el hexágono.
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En paralelo, gracias a observaciones en el infrarrojo realizadas con el telescopio VLT del Observatorio Europeo Austral (ESO), realizadas por un equipo angloamericano, se ha podido estudiar la estructura térmica en la región del decágono y obtener medidas de los vientos que muestran cambios en su velocidad con la altura. Simultáneamente, las imágenes del HST obtenidas en diferentes rangos espectrales muestran una estratificación vertical en las nubes y nieblas superiores que conforman el decágono.
La naturaleza del fenómeno desafía los modelos atmosféricos. «No sabemos si tanto el hexágono como el decágono son estructuras enraizadas en profundidad en la atmósfera del planeta, bajo las capas de nubes superiores, o bien se trata de formaciones meteorológicas superficiales, que afectan solo a dichas nubes», explica Sánchez-Lavega. Para explorar estas ideas, en colaboración con investigadores de la Universidad Politécnica de Cataluña (UPC), se han llevado a cabo simulaciones numéricas sobre un modelo simplificado de atmósfera que muestran, preliminarmente, que una onda con geometría decagonal puede generarse de diferentes formas y sobrevivir un tiempo sobre la corriente en chorro sobre la que se asienta.
La investigación abre muchas preguntas básicas sobre los fenómenos atmosféricos en los planetas gaseosos. ¿Por qué solo Saturno forma este tipo de ondas poligonales? ¿Guarda el fenómeno alguna relación con la disposición poligonal de cinco y ocho lados de los ciclones que rodean a los polos de Júpiter? Nuevas observaciones del fenómeno a lo largo de los próximos años, en los que la visibilidad del hemisferio sur del planeta se irá incrementando, ayudarán a su caracterización y a la realización de modelos avanzados que permitan resolver este curioso rompecabezas atmosférico.
Referencia:
Agustín Sánchez-Lavega, Amy A. Simon, Michael H. Wong, Leigh N. Fletcher, Arrate Antuñano, Ricardo Hueso, Peio Iñurrigarro, Aida Flix-Bellmunt, Arnau Miró, Enrique García-Melendo, Trevor Barry, Jean-Paul Oger, Glenn S. Orton, Itziar Garate-Lopez (2026) A decagon wave around Saturn’s south pole Science Advances doi: 10.1126/sciadv.aee4251
Edición realizada por César Tomé López a partir de materiales suministrados por UPV/EHU Komunikazioa
El artículo El decágono en las nubes de Saturno se ha escrito en Cuaderno de Cultura Científica.




Anche i blindati del futuro avranno un problema che fino a pochi anni fa sembrava secondario, quello dell'alimentazione. Ora che la tecnologia si fa sempre più avanzata, produrre abbastanza elettricità è un aspetto fondamentale. Pensiamo ad esempio a come riuscire a sostenere radar, sensori, computer, comunicazioni protette, contromisure elettroniche e sistemi anti-drone, sia sempre più esoso. Detto in parole semplici, serve sempre più energia.
Un tempo l’M2 Bradley americano andava alla grande, ma ora non basta più puntare soltanto su corazza e potenza di fuoco. E così, scopriamo che il primo prototipo Lynx XM30 è arrivato nelle mani dell’US Army e ora è pronto a entrare nella fase di test governativi. Ne seguiranno altri sette in realtà, tutti destinati ad addestramento sul campo e simulazioni operative, e sarà proprio grazie al programma XM30, che si arriverà infine alla sostituzione del Bradley.
A quel che ne sappiamo, il risultato finale sarà un veicolo all'avanguardia e capace anche di cooperare con sistemi robotici e semi-autonomi. La caratteristica più interessante è la propulsione ibrido-elettrica.
