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Extreme precipitation reshapes nutrient flows and balance in North America’s largest river basin 极端降水重塑了北美最大河流流域的养分流动和平衡
IF 13.6 1区 综合性期刊 Q1 MULTIDISCIPLINARY SCIENCES Pub Date : 2026-03-20 DOI: 10.1126/sciadv.aea3260
Zihao Bian, Shufen Pan, Ge Sun, Steven G. McNulty, Xingchen Tony Wang, Changchun Huang, Hanqin Tian
Extreme precipitation events, intensified by climate change, are increasingly disrupting nutrient dynamics in large river systems worldwide. Beyond altering the magnitude of individual nutrient fluxes, extreme precipitation may fundamentally reshape nutrient composition and stoichiometric balances, with critical implications for aquatic ecosystem health. Here, we apply an integrated data-model framework to assess how these events have altered nitrogen (N) and phosphorus (P) fluxes across the Mississippi River Basin from 1980 to 2018. We find that extreme rainfall disproportionately increases P export relative to N, driven primarily by enhanced soil erosion and mobilization of particulate-bound nutrients. Concurrent temporal and spatial changes in extreme precipitation regimes have induced declining N:P ratios in headwater streams and cumulative nutrient loads, shifting export stoichiometry toward the Redfield ratio. Therefore, extreme precipitation can increase nutrient fluxes that fuel harmful algal blooms, yet at the same time reduce N:P ratios that may favor less toxic communities. This trade-off calls for watershed management strategies that go beyond managing nutrient quantity alone.
气候变化加剧的极端降水事件正日益破坏全球大型河流系统的营养动态。除了改变单个养分通量的大小外,极端降水可能从根本上重塑营养成分和化学计量平衡,对水生生态系统健康具有重要影响。在这里,我们应用一个综合数据模型框架来评估这些事件如何改变1980年至2018年密西西比河流域的氮(N)和磷(P)通量。我们发现,极端降雨不成比例地增加了相对于氮的磷输出,这主要是由土壤侵蚀加剧和颗粒结合养分的动员所驱动的。极端降水条件的时空同步变化导致了源流氮磷比和累积养分负荷的下降,使出口化学计量向Redfield比转移。因此,极端降水可以增加营养通量,助长有害藻华,但同时降低氮磷比,可能有利于毒性较小的群落。这种权衡需要流域管理战略,而不仅仅是管理营养量。
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引用次数: 0
Erratum for the Research Article "AND-1 is a critical regulator of R-loop dynamics and a target to overcome endocrine resistance" by Z. Li et al. Z. Li等人的研究文章“and -1是R-loop动力学的关键调节因子和克服内分泌抵抗的靶标”的校误。
IF 13.6 1区 综合性期刊 Q1 MULTIDISCIPLINARY SCIENCES Pub Date : 2026-03-20 DOI: 10.1126/sciadv.aeg8118
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引用次数: 0
Ultrasensitive soft vibration sensors based on atomically thin metal dichalcogenide ribbon networks 基于原子级薄金属二硫化物带网络的超灵敏软振动传感器
IF 13.6 1区 综合性期刊 Q1 MULTIDISCIPLINARY SCIENCES Pub Date : 2026-03-20 DOI: 10.1126/sciadv.aeb6733
Chengyi Xu, Xufan Li, Lukas Felix Michalek, Jaeho Park, Eunyoung Kim, Zhiyu Zhang, Raymond R. Unocic, Eric Tianjiao Zhao, Wei-Chun Hsu, Baiyu Shi, Shuang Wu, Yang Yang, Avetik R. Harutyunyan, Zhenan Bao
The rapid progress of artificial intelligence (AI) and the internet of things (IoT) has driven growing demand for high-performance, skin-compatible vibration sensors capable of capturing subtle physiological and environmental signals. Low-dimensional materials offer unique advantages in sensitivity and flexibility, yet challenges remain in achieving high strain responsiveness, mechanical robustness, and large-area uniformity. Here, we report an ultrasensitive, low-profile, and stretchable vibration sensor based on large-area single-layer molybdenum disulfide (MoS 2 ) ribbon networks (SLRNs) grown via a vapor-liquid-solid mechanism. Embedding SLRNs within a thermoplastic elastomer [styrene-ethylene-butylene-styrene (SEBS)] yields record-high sensitivity among MoS 2 -based sensors, with gauge factors up to 5300 at <1.6% strain. This response arises from nanocrack-mediated electron transport induced by the thermal expansion mismatch between MoS 2 and SEBS. The ~6-micrometer-thick sensors detect vibrations and acoustic signals over a wide frequency range (>500 hertz), enabling deconvolution of complex stimuli. This work establishes a path toward ultrathin, ultrasensitive wearable sensors for health care and robotic applications.
人工智能(AI)和物联网(IoT)的快速发展推动了对高性能、皮肤兼容的振动传感器的需求不断增长,这些传感器能够捕捉细微的生理和环境信号。低维材料在灵敏度和灵活性方面具有独特的优势,但在实现高应变响应性,机械稳健性和大面积均匀性方面仍然存在挑战。在这里,我们报告了一种基于大面积单层二硫化钼(MoS 2)带状网络(SLRNs)的超灵敏、低外形和可拉伸振动传感器,该网络通过气-液-固机制生长。将SLRNs嵌入热塑性弹性体[苯乙烯-乙烯-丁烯-苯乙烯(SEBS)]中,在基于MoS 2的传感器中产生了创纪录的高灵敏度,在<;1.6%应变下,测量因子高达5300。这种响应是由MoS 2和SEBS之间的热膨胀失配引起的纳米裂纹介导的电子传递引起的。约6微米厚的传感器可以在宽频率范围内(>;500赫兹)检测振动和声学信号,从而实现复杂刺激的反卷积。这项工作为医疗保健和机器人应用的超薄、超灵敏的可穿戴传感器开辟了一条道路。
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引用次数: 0
Dengue infection elicits skin tissue-resident and circulating CD8 + T cells associated with protection from hospitalization 登革热感染引起皮肤组织驻留和循环CD8 + T细胞与住院保护相关
IF 13.6 1区 综合性期刊 Q1 MULTIDISCIPLINARY SCIENCES Pub Date : 2026-03-20 DOI: 10.1126/sciadv.aea7987
Noor Zayanah Hamis, Justin SG Ooi, Ka-Wai Cheung, Valerie Chew, Michaela Gregorova, Eugenia Ziying Ong, Kuan Rong Chan, Tun-Linn Thein, Yee-Sin Leo, David Chien Boon Lye, Eng Eong Ooi, Laura Rivino
Dengue is spreading globally, and there is urgent need to define immune correlates of protection for this disease. Dengue infection first occurs in the skin following the bite of an infected mosquito; however, knowledge of host immune responses within this site remains sparse. We investigated the phenotypic, functional, and transcriptional profiles of skin and blood T cells in 73 patients with dengue and 10 healthy volunteers. We show that the skin T cell compartment undergoes marked reshaping and is strongly enriched with proliferating CD4 + and CD8 + T cells compared with the blood of patients. Activated skin CD8 + T cells expressed a core transcriptional signature of tissue-resident memory T (T RM ) cells, supporting their differentiation to the T RM cell lineage during infection. The magnitude of skin and blood CD8 + T cell responses were associated with protection from hospitalization in this cohort. These data support a protective role of skin-resident and circulating CD8 + T cells in dengue and warrant evaluation of vaccination strategies inducing skin T RM cells to enhance protective immunity.
登革热正在全球蔓延,迫切需要确定保护该疾病的免疫相关因素。登革热感染首先发生在被感染蚊子叮咬后的皮肤上;然而,对这个部位的宿主免疫反应的了解仍然很少。我们研究了73名登革热患者和10名健康志愿者的皮肤和血液T细胞的表型、功能和转录谱。我们发现,与患者的血液相比,皮肤T细胞区室经历了明显的重塑,并且富含增殖的CD4 +和CD8 + T细胞。激活的皮肤CD8 + T细胞表达了组织驻留记忆T (trm)细胞的核心转录特征,支持它们在感染期间向T RM细胞谱系分化。在该队列中,皮肤和血液CD8 + T细胞反应的大小与住院保护有关。这些数据支持皮肤驻留和循环CD8 + T细胞在登革热中的保护作用,并为评估诱导皮肤T - RM细胞增强保护性免疫的疫苗接种策略提供了依据。
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引用次数: 0
TLR9-activating cholesterol azetidine derivative–assisted therapeutic vaccines for cancer immunotherapy tlr9激活胆固醇偶氮啶衍生物辅助癌症免疫治疗疫苗
IF 13.6 1区 综合性期刊 Q1 MULTIDISCIPLINARY SCIENCES Pub Date : 2026-03-20 DOI: 10.1126/sciadv.aeb2465
Junbin Chen, Miao Su, Boya Yu, Mingda Yang, Huiye Wang, Xianzhu Yang, Jun Wang
Therapeutic cancer vaccines show great promise for de novo induction of antigen-specific T cell responses against tumors. However, weak coordination between innate immune activation and antigen delivery remains a major obstacle to vaccine efficacy. Here, we present a cholesterol azetidine derivative–assisted polymeric carrier, Aze-Chol NP, which stimulates innate immunity and primes tumor-specific CD8 + T cell responses. Mechanistically, Aze-Chol NP induces maturation and activation of dendritic cells (DCs) through the Toll-like receptor 9 (TLR9) pathway while simultaneously delivering protein or peptide antigens to DCs in lymph nodes. The Aze-Chol NP–based nanovaccines markedly inhibited tumor growth and prolonged survival in melanoma and human papillomavirus tumor models. Moreover, combining the nanovaccine with an anti–PD-L1 antibody produced a strong synergistic effect and long-term immune memory, achieving 80% survival beyond 100 days and complete rejection of tumor cell rechallenge. Overall, our study demonstrates that this TLR9-activating carrier provides an effective and straightforward strategy for developing potent cancer vaccines.
治疗性癌症疫苗在从头诱导针对肿瘤的抗原特异性T细胞反应方面显示出巨大的希望。然而,先天免疫激活和抗原递送之间的协调不力仍然是影响疫苗效力的主要障碍。在这里,我们提出了一种胆固醇氮杂啶衍生物辅助聚合物载体,Aze-Chol NP,它可以刺激先天免疫并启动肿瘤特异性CD8 + T细胞反应。在机制上,Aze-Chol NP通过toll样受体9 (TLR9)途径诱导树突状细胞(DCs)的成熟和激活,同时将蛋白质或肽抗原传递到淋巴结的DCs。基于Aze-Chol np的纳米疫苗在黑色素瘤和人乳头瘤病毒肿瘤模型中显著抑制肿瘤生长并延长生存期。此外,纳米疫苗与抗pd - l1抗体结合可产生强大的协同效应和长期免疫记忆,100天以上存活率达到80%,完全排斥肿瘤细胞再攻击。总的来说,我们的研究表明,这种tlr9激活载体为开发强效癌症疫苗提供了一种有效而直接的策略。
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引用次数: 0
Lysosomal down-regulation of the mu opioid receptor is opposed by the Retromer complex 阿片受体的溶酶体下调受到反转录复合体的反对
IF 13.6 1区 综合性期刊 Q1 MULTIDISCIPLINARY SCIENCES Pub Date : 2026-03-20 DOI: 10.1126/sciadv.adx8715
Aleksandra Dagunts, Hayden Adoff, Brandon Novy, Lamya Ben Ameur, Monica De Maria, Arpiar Saunders, Braden T. Lobingier
A critical homeostatic mechanism for regulating G protein–coupled receptor (GPCR) activity is agonist-induced GPCR endocytosis and trafficking to the lysosome for proteolytic down-regulation. The mu opioid receptor (MOR) is a notable example of this type of cellular regulation, where prolonged exposure to high-efficacy opioid drugs causes MOR to traffic to the lysosome. Here, we used functional genomics to identify cellular proteins that control MOR lysosomal down-regulation. We found that the central regulator of MOR postendocytic trafficking is the Retromer complex, which rescues MOR from opioid-induced down-regulation by promoting MOR recycling from endosomes to the plasma membrane. Critically, MOR accesses the Retromer recycling pathway through its noncanonical bileucine recycling motif, and this mechanism controls how MOR is regulated following chronic exposure to opioid drugs. Additionally, we show that this bileucine pathway for Retromer-based recycling is present in other classes of membrane proteins including the glucose transporter GLUT4.
调节G蛋白偶联受体(GPCR)活性的一个关键稳态机制是激动剂诱导的GPCR内吞并转运到溶酶体以下调蛋白水解。mu阿片受体(MOR)是这种类型的细胞调节的一个显著例子,其中长时间暴露于高效阿片药物导致MOR运输到溶酶体。在这里,我们使用功能基因组学来鉴定控制MOR溶酶体下调的细胞蛋白。我们发现MOR内吞后转运的中心调节因子是Retromer复合体,它通过促进MOR从核内体到质膜的再循环,将MOR从阿片类药物诱导的下调中拯救出来。重要的是,MOR通过其非规范的胆红素循环基序进入Retromer循环途径,该机制控制了慢性阿片类药物暴露后MOR的调节方式。此外,我们发现这种以反转录物为基础的再循环的胆红素途径存在于其他类型的膜蛋白中,包括葡萄糖转运蛋白GLUT4。
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引用次数: 0
Transcription activation mechanism of a noncanonical DNA damage response pathway by the WYL-activator, DriD wyl激活子DriD对非典型DNA损伤反应通路的转录激活机制
IF 13.6 1区 综合性期刊 Q1 MULTIDISCIPLINARY SCIENCES Pub Date : 2026-03-20 DOI: 10.1126/sciadv.aec6337
Rajiv R. Singh, Amani Chinni, Emily Cannistraci, Raul Salinas, Sunny Yadav, Kevin Gozzi, Maria A. Schumacher
DNA damage repair mechanisms are vital for cell survival. In the bacterium, Caulobacter crescentus , DriD is the master regulator of a unique, noncanonical DNA damage pathway. DriD binding to ssDNA, produced upon DNA damage, stimulates its ability to activate transcription from several promoters involved in DNA damage responses. However, the mechanism by which DriD interfaces with the RNAP holoenzyme to activate transcription from its multiple promoters has been unclear. Here, we describe cryo-EM structures of DriD-ssDNA bound to RNAP-holoenzyme and three DriD-regulated promoters. Each subunit of homodimeric DriD contains an DNA binding N -terminal winged helix-turn-helix (wHTH) connected to WYL domains by a linker 3-helix bundle (3HB) module. The structures reveal a mechanism of assembly on promoters whereby DriD’s 3HBs bind the RNAP α-CTD and β domains, anchoring the RNAP-holoenzyme to regulated promoters. The 3HBs form autoinhibitory contacts with DNABDs in apo DriD and therefore acts as an ssDNA-driven trigger domain, switching between DNABD-bound apo and RNAP-bound forms upon ssDNA-mediated activation. Thus, the structures reveal a unique transcription activation mechanism, likely conserved among the large family of homodimeric WYL activators.
DNA损伤修复机制对细胞存活至关重要。在一种叫做新月形Caulobacter crescent的细菌中,DriD是一种独特的非典型DNA损伤途径的主要调节因子。DNA损伤后产生的DriD与ssDNA结合,刺激其激活DNA损伤应答中涉及的几个启动子的转录能力。然而,DriD与RNAP全酶结合以激活其多个启动子转录的机制尚不清楚。在这里,我们描述了与rnap -全酶结合的DriD-ssDNA和三个drid调控启动子的低温电镜结构。同二聚体DriD的每个亚基包含一个DNA结合N端带翼螺旋-旋螺旋(wHTH),通过连接子3-螺旋束(3HB)模块连接到WYL结构域。这些结构揭示了启动子上的组装机制,即DriD的3HBs结合RNAP α-CTD和β结构域,将RNAP全酶固定在受调节的启动子上。在载脂蛋白DriD中,3HBs与dabd形成自抑制接触,因此充当ssdna驱动的触发域,在ssdna介导的激活时,在dabd结合的载脂蛋白和rnap结合的形式之间切换。因此,这些结构揭示了一种独特的转录激活机制,可能在同质二聚体WYL激活因子大家族中保守。
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引用次数: 0
In 2 O 3 -CNT catalysts enable >500-hour stable CO 2 -to-methanol hydrogenation via vacancy stabilization 在2 O 3 -碳纳米管催化剂中,通过空位稳定实现bbb50 - 500小时稳定的CO 2到甲醇加氢
IF 13.6 1区 综合性期刊 Q1 MULTIDISCIPLINARY SCIENCES Pub Date : 2026-03-20 DOI: 10.1126/sciadv.aea7041
Lei Zhang, Yuxiang Yang, Hao Yan, Xinlei Ji, Hua An, Jianyu Rao, Yixuan Zhou, Chang-jun Liu, Xi Chen, Ning Yan
Indium oxide (In 2 O 3 ) is a promising catalyst for carbon dioxide (CO 2 ) hydrogenation to methanol but suffers from rapid deactivation due to localized over-reduction of surface In 3+ species into inactive metallic In 0 near hydrogen (H 2 ) activation sites. Here, we exploit a proton-electron dual-transfer mechanism through a physically integrated In 2 O 3 -carbon nanotube (In 2 O 3 -CNT) system, achieving simultaneous enhancement of catalytic performance and durability. The optimal In 2 O 3 -CNT system gives the highest methanol production rate of 1250.6 grams kilograms In2O3 −1 hour −1 at 320°C. Particularly, the hybrid system maintains catalytic stability for >500 hours, representing the highest durability among reported In 2 O 3 catalysts. Mechanistic studies and multiple characterization techniques reveal that the conductive CNT network regulates surface redox dynamics by facilitating electron transfer and redistribution. This process promotes the formation of oxygen vacancies for CO 2 activation while preventing localized electron accumulation and In 0 segregation. The CNT-mediated redox modulation stabilizes a dynamic InO x surface phase by balancing H 2 -induced reduction and CO 2 -driven oxidation, thereby sustaining catalytic activity over extended operation.
氧化铟(in2o3)是一种很有前途的催化二氧化碳(CO 2)加氢制甲醇的催化剂,但由于在氢(H 2)活化位点附近,表面的in3 +物种局部过度还原为无活性的金属in0,因此它的失活速度很快。在这里,我们利用质子-电子双转移机制,通过物理集成的In 2o3 -碳纳米管(In 2o3 -CNT)系统,实现了催化性能和耐久性的同时增强。在320℃下,最佳的In2O3 -CNT体系的甲醇产率最高,为1250.6 g kg In2O3−1小时−1。值得一提的是,该混合动力系统可保持500小时的催化稳定性,是目前所报道的In 2o3催化剂中耐久性最高的。机理研究和多种表征技术表明,导电碳纳米管网络通过促进电子转移和再分配来调节表面氧化还原动力学。这一过程促进了CO 2活化的氧空位的形成,同时防止了局部电子积累和In 0偏析。碳纳米管介导的氧化还原调制通过平衡h2诱导的还原和CO 2驱动的氧化来稳定动态的InO x表面相,从而在长时间的操作中保持催化活性。
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引用次数: 0
Erratum for the Research Article, "Cooperative role of distinctive TP53 and PTEN combined loss in the peripheral T cell lymphoma-GATA3 molecular subgroup" by W.G. Lone et al. W.G. Lone等人的研究文章“TP53和PTEN联合缺失在外周T细胞淋巴瘤- gata3分子亚群中的协同作用”的勘误。
IF 13.6 1区 综合性期刊 Q1 MULTIDISCIPLINARY SCIENCES Pub Date : 2026-03-20 DOI: 10.1126/sciadv.aeg5995
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引用次数: 0
Magnetic coupling transforms random snapping into ordered sequences in soft metamaterials 磁耦合将软超材料中的随机断裂转换为有序序列
IF 13.6 1区 综合性期刊 Q1 MULTIDISCIPLINARY SCIENCES Pub Date : 2026-03-20 DOI: 10.1126/sciadv.aec3182
Haoze Sun, Gabriel Alkuino, Yinding Chi, Yevhen Zabila, Haitao Qing, Denys Makarov, Teng Zhang, Jie Yin
Mechanical metamaterials achieve multistep, programmable responses through sequential deformation driven by snapping instabilities, yet these sequences are typically governed by unavoidable imperfections, resulting in random and uncontrollable behavior. Here, we harness intra- and interlayer magnetic interactions coupled with elasticity to reprogram the ordering of sequential buckling instabilities in kirigami-inspired soft magnetic metamaterials. In single-layer systems, intralayer coupling among magnetized units produces random snapping sequences but generates strongly nonlinear-spiked force-displacement responses with pronounced hysteresis, in contrast to the simultaneous buckling of unmagnetized sheets. In multilayer assemblies, interlayer magnetic interactions trigger chain reaction–like propagation, transforming randomness into robust, directional snapping across structures. This mechanism establishes a paradigm for deterministic, multistep mechanical responses without continuously applied fields and opens avenues for adaptive materials in energy dissipation, waveguiding, reconfigurable soft robotics, and biomedical devices.
机械超材料通过由断裂不稳定性驱动的顺序变形实现多步骤、可编程的响应,然而这些序列通常由不可避免的缺陷控制,导致随机和不可控的行为。在这里,我们利用层内和层间的磁相互作用加上弹性来重新编程基里伽米启发的软磁超材料的顺序屈曲不稳定性。在单层系统中,磁化单元之间的层内耦合产生随机的断裂序列,但与未磁化片的同时屈曲相比,产生强烈的非线性尖刺力-位移响应,并具有明显的滞后。在多层组件中,层间磁相互作用触发链式反应式传播,将随机性转化为跨结构的鲁棒性、方向性断裂。该机制为确定性、多步骤机械响应建立了一个范例,无需连续应用领域,并为自适应材料在能量耗散、波导、可重构软机器人和生物医学设备方面开辟了道路。
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引用次数: 0
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