Nature最新文献

{"title":"China’s AI research is booming: what it’s like to be on the front line","authors":"Elizabeth Gibney","doi":"10.1038/d41586-026-03223-8","DOIUrl":"10.1038/d41586-026-03223-8","url":null,"abstract":"China trains more AI talent than any other country. Nature spoke to analysts and scientists about how AI research there compares to the United States.","PeriodicalId":18787,"journal":{"name":"Nature","volume":"658 8136","pages":"598-600"},"PeriodicalIF":56.1,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149177725","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A guide to the Nature Index.","authors":"","doi":"10.1038/d41586-026-03206-9","DOIUrl":"https://doi.org/10.1038/d41586-026-03206-9","url":null,"abstract":"","PeriodicalId":18787,"journal":{"name":"Nature","volume":" ","pages":""},"PeriodicalIF":56.1,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149183002","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Computational design of metalloproteases.","authors":"Anqi Chen, Kejia Wu, Hojae Choi, Preetham Venkatesh, Samuel J Pellock, Nikita Hanikel, Hojeong Shin, Declan Evans, Kieran Didi, Lars L Schaaf, Cristina Díaz-Perlas, Brian Coventry, Donghyo Kim, Seth M Woodbury, Pengfei Ji, Shingo Honda, Asim K Bera, Hannah Nguyen, Alex Kang, Yanqing Wang, Xinting Li, Stacey Gerben, Lemuel Chang, Xiao Yan, Benjamí Oller-Salvia, Anthony A Hyman, Donald Hilvert, David Baker","doi":"10.1038/s41586-026-11167-2","DOIUrl":"https://doi.org/10.1038/s41586-026-11167-2","url":null,"abstract":"<p><p>De novo design of enzymes that cleave amide bonds represents a major challenge^1,2. Here we use RFdiffusion methods^3,4 to de novo design proteins with water-activating zinc-based active sites adjacent to a peptide substrate binding pocket. Of 135 designs tested, 36% catalyse cleavage of their cognate peptide substrates at the targeted scissile bond. The best design accelerates peptide-bond hydrolysis by more than 10⁸-fold relative to the uncatalysed reaction; four substitutions increase this acceleration to more than 10¹⁰-fold by improving active-site preorganization⁵. We use this approach to design metalloproteases that selectively cleave the human disease-associated proteins TDP-43, amyloid-β and serum amyloid A, with rate enhancements of up to 10⁹-fold. We further design caged cytokines and receptor antagonists that are selectively activated by the designed proteases, enabling bioorthogonal control of cell state. Thus, de novo design can yield highly active, programmable proteases with applications in therapeutics, biotechnology and bioremediation.</p>","PeriodicalId":18787,"journal":{"name":"Nature","volume":" ","pages":""},"PeriodicalIF":56.1,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149183222","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Educational intervention can rewire village social networks.","authors":"Marios Papamichalis, Laura Forastiere, Edoardo M Airoldi, Nicholas A Christakis","doi":"10.1038/s41586-026-11154-7","DOIUrl":"https://doi.org/10.1038/s41586-026-11154-7","url":null,"abstract":"<p><p>Social networks shape behaviour, affect information dissemination and undergird collective action. And they can be exploited in the design of interventions in these domains^1-7. Although social networks obey fundamental principles, such as the degree distribution^8,9, they can nevertheless evolve as ties form and break. Here, through a randomized controlled trial involving a total of 8,331 people in 110 remote Honduran villages, we evaluate the secondary effects of a 22-month public-health intervention¹ on pre-existing social-network structure. We used a design in which a varying fraction of village households received the intervention, and villages in which no one received the intervention were used as the primary reference group. In 'low-dosage' villages (in which 5-30% of households received the intervention), people who received the intervention tended to sever ties with untreated individuals to whom they previously went for health advice. Conversely, in high-dosage villages (50-100%), treated individuals increased their ties. These average changes are explained mainly by tie dynamics; that is, treated-treated pairs persist and form new links, whereas treated-untreated ties dissolve. A mediation analysis indicates that absorption of health information increases the likelihood of tie formation and persistence. The rewiring patterns generally lasted for three years after the intervention ceased. Moreover, although the intervention delivered health information, it reshaped friendship and financial ties, not just health-advice connections. In aggregate, the introduction of a new information regime acted as a kind of social institution, rewiring individuals' connections even though the overall degree distribution of village-wide networks remained relatively stable.</p>","PeriodicalId":18787,"journal":{"name":"Nature","volume":" ","pages":""},"PeriodicalIF":56.1,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149183261","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Catalytic transfer of carbon atoms enables spirofusion of C-C σ-bonds.","authors":"Hayato Fujimoto, Masayuki Mizutani, Kazuya Imachi, Teruki Nishioka, Reona Ikeda, Mamoru Tobisu","doi":"10.1038/s41586-026-11242-8","DOIUrl":"https://doi.org/10.1038/s41586-026-11242-8","url":null,"abstract":"<p><p>Spirocyclic frameworks, polycyclic structures in which two rings share a single carbon atom, constitute key structural motifs across diverse areas, including optoelectronic and hole-transporting materials^1-3, ligand design for coordination complexes^4-6, and numerous natural products⁷. In a spiro skeleton, the two molecular units adopt an orthogonal arrangement, generating a rigid three-dimensional (3D) architecture. Introducing a single carbon atom to join two components to form the spiro centre therefore represents a direct strategy for constructing such frameworks. Previous carbon-atom-transfer approaches have largely relied on π-bond reactivity, whereas controlled insertion of a carbon atom into C-C σ-bonds remains challenging^8-11. Here we report a rhodium-catalysed spiro-carbon-atom insertion reaction that converts biphenylene substrates into spirocyclic structures through sequential C-C bond activation. Using N-isocyanoiminophosphorane (PINC)^12-14 as an atomic carbon equivalent, the reaction forms four new C-C bonds at a spiro centre. The transformation enables both homo- and cross-spirofusion of biphenylenes and can be extended to reactions combining σ- and π-bond activation. These results establish a catalytic strategy for constructing structurally complex spirocyclic frameworks through C-C σ-bond activation, with a single carbon atom serving as a central linchpin.</p>","PeriodicalId":18787,"journal":{"name":"Nature","volume":" ","pages":""},"PeriodicalIF":56.1,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149183302","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"This is why butterflies are so hard to catch.","authors":"Nick Petrić Howe","doi":"10.1038/d41586-026-03301-x","DOIUrl":"https://doi.org/10.1038/d41586-026-03301-x","url":null,"abstract":"","PeriodicalId":18787,"journal":{"name":"Nature","volume":" ","pages":""},"PeriodicalIF":56.1,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149183387","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"China’s extraordinary rise in science and how it will change the world","authors":"Xiaoying You","doi":"10.1038/d41586-026-03222-9","DOIUrl":"10.1038/d41586-026-03222-9","url":null,"abstract":"The nation is on a trajectory to lead the world in science, a development that will reshape technological advancement, innovation and the balance of global power.","PeriodicalId":18787,"journal":{"name":"Nature","volume":"658 8136","pages":"594-597"},"PeriodicalIF":56.1,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149177729","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Alveolar stem cells go beyond making gas-exchange cells to repair damaged airways.","authors":"","doi":"10.1038/d41586-026-03085-0","DOIUrl":"https://doi.org/10.1038/d41586-026-03085-0","url":null,"abstract":"","PeriodicalId":18787,"journal":{"name":"Nature","volume":" ","pages":""},"PeriodicalIF":56.1,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149183003","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Capillary-selective vasodilation through myosin inhibition halts ischaemic cascades.","authors":"Máté Pénzes, Máté Winternitz, Ádám I Horváth, Svetlana Mastitskaya, Usman Awan, Tamás Szimler, Camille Glaser, Carlos Kikuti, Marie Juillé, Leila Heidsieck, Anna Á Rauscher, Tímea Bálint, Dávid Nagy, Tamás Radovits, Alex Ali Sayour, C Michael Gibson, Anne Houdusse, Máté Gyimesi, András Málnási-Csizmadia","doi":"10.1038/s41586-026-11171-6","DOIUrl":"https://doi.org/10.1038/s41586-026-11171-6","url":null,"abstract":"<p><p>In acute myocardial infarction and acute kidney injury, capillary no-reflow denotes that capillary blood flow is still blocked despite successful arterial reperfusion. This is associated with substantially increased mortality and reinfarction risk; nevertheless, no targeted therapy exists so far^1,2. Because capillary no-reflow is driven by smooth muscle myosin-mediated hypercontraction of capillary pericytes, we developed R(+)2501, a myosin-specific and capillary-selective vasodilator. In reperfused animal models of acute myocardial infarction and acute kidney injury, direct in vivo imaging showed that R(+)2501 rapidly restored capillary flow, an effect sustained even after rapid drug clearance. Ex vivo experiments confirmed reversal of pericyte constriction directly. Restoration of capillary blood flow, together with clearance of trapped neutrophils, linked resolution of capillary no-reflow to attenuation of an early driver of reperfusion injury. R(+)2501 enhanced capillary perfusion while preserving coronary autoregulation and systemic haemodynamics, and markedly improved survival during acute reperfusion. We further found that acute myocardial infarction induced renal capillary no-reflow, which was reversed by R(+)2501, suggesting that capillary no-reflow contributes to the pathophysiology of cardiorenal syndrome type I. These findings establish pericyte-targeted smooth muscle myosin inhibition as a therapeutic strategy to restore microvascular perfusion and halt the ischaemic cascade across organs, while defining a specific physiological role for capillaries and pericytes in circulatory regulation.</p>","PeriodicalId":18787,"journal":{"name":"Nature","volume":" ","pages":""},"PeriodicalIF":56.1,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149183255","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Divergent genomic evolution in astrocytomas and oligodendrogliomas.","authors":"Tamrin Chowdhury, C Mircea S Tesileanu, Emre Kocakavuk, Kevin C Johnson, Joo Ho Lee, Zeynep Erson-Omay, Chaewon Heo, Kenneth Aldape, Samirkumar B Amin, Kevin J Anderson, David M Ashley, Floris P Barthel, Jill S Barnholtz-Sloan, Daniel J Brat, Andrew R Brodbelt, Ana Valeria Castro, Elizabeth B Claus, Jennifer M Connelly, Joseph F Costello, Indrani Datta, Carol Elliott, Gaetano Finocchiaro, Pim J French, Hui K Gan, Luciano Garofano, Padmaja L Ghospurkar, Anna Golebiewska, Pranav S Gundla, Beth Hermes, Chibo Hong, Youri Hoogstrate, Craig Horbinski, Jason T Huse, Antonio Iavarone, Cihat Karadag, Mustafa Khasraw, Mathilde C M Kouwenhoven, Peter S LaViolette, Kay Li, Allison Lowman, Katy McCortney, Hyo-Eun Moon, Nader Sanai, MacLean P Nasrallah, H K Ng, D Ryan Ormond, Bethany Kwan, Marta Padovan, Sun Ha Paek, Laila M Poisson, Sushant Puri, Erica Shen, Shwetal Mehta, Andrew E Sloan, Wies R Vallentgoed, Erwin G Van Meir, Rachael Vaubel, Taylor E Wade, Annemiek M E Walenkamp, Colin Watts, Tobias Weiss, Michael Weller, Pieter Wesseling, Kerryn Westcott, Bart A Westerman, Gordon Y Ye, W K Alfred Yung, Frederick S Varn, Roel G W Verhaak","doi":"10.1038/s41586-026-11150-x","DOIUrl":"https://doi.org/10.1038/s41586-026-11150-x","url":null,"abstract":"<p><p>Astrocytomas and oligodendrogliomas are isocitrate dehydrogenase (IDH)-mutant gliomas that most commonly arise in adults under the age of 50 and exhibit variable responses to treatment^1-3. To understand the genetic drivers of disease progression, here we used whole-genome and whole-exome sequencing to characterize longitudinally collected tumour specimens from 183 patients with IDH-mutant glioma. Samples were collected through the Glioma Longitudinal Analysis (GLASS) Consortium⁴. Most primary surgery samples were classified as grade 2 on the basis of histology (73% for astrocytomas and 93% for oligodendrogliomas). We validated known genomic markers of tumour progression, including hypermutation and homozygous deletion of CDKN2A or CDKN2B (hereafter, CDKN2A/B)⁵, and discovered genetic alterations that distinguish between the evolutionary trajectories of astrocytomas and those of oligodendrogliomas. Mutations in phosphatidylinositol 3-kinase (PI3K) and NOTCH1 were newly acquired in recurrent oligodendrogliomas, regardless of treatment, and were associated with an increased tumour mutational burden. In recurrent astrocytomas, however, again irrespective of treatment, acquired focal oncogene amplifications and CDKN2A/B homozygous deletions were associated with an increase in chromosomal imbalances, which converged with markers of chromosomal instability such as chromothripsis and whole-genome doubling. In both types of IDH-mutant glioma, we observed a convergence of acquired alterations, genome-wide changes and worse patient outcomes, suggesting that treatment-refractory clones were being selected. Treatment with temozolomide was associated with the mutational signatures SBS11 and SBS119 in both tumour types, whereas the radiotherapy-associated ID8 signature increased in astrocytomas specifically. We show that the genomes of oligodendrogliomas and astrocytomas adapt to the selective pressures of tumour progression and treatment in distinct ways, suggesting that oligodendrogliomas and astrocytomas differ in their responses to treatment-induced DNA damage.</p>","PeriodicalId":18787,"journal":{"name":"Nature","volume":" ","pages":""},"PeriodicalIF":56.1,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149183294","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}