Seungmin Shin, Yae-Jin Kim, Bernard J. C. Macatangay, Joshua C. Cyktor, Margaret G. Hines, Ze-Yu Sun, Kong Chen, John W. Mellors, Dimiter S. Dimitrov, Wei Li, Du-San Baek
NK and T cells are key effectors that eliminate cancer cells, but upregulation of the inhibitory receptor NKG2A on these cells attenuates antitumor immune responses. To counteract NKG2A inhibitory signaling, we identified two specific fully human monoclonal anti-NKG2A antibodies that block HLA-E ligand binding. These antibodies activated NK cells and enhanced antibody-dependent cellular cytotoxicity of tumor-targeting IgG1s both in vitro and in vivo. Bispecific engagers (BiNKs), generated by fusing NKG2A antibodies with tumor targeting binders, promoted immune synapse formation and directed cytotoxicity of NK and CD8+ T cells toward cancer cells. In a human PBMC-engrafted NSG mouse xenograft lung cancer model, an anti-HER2 × anti-NKG2A BiNK markedly inhibited tumor growth as a monotherapy or in combination with pertuzumab. Cell depletion studies revealed that the BiNK enhanced antitumor activity of both NK and T cells. NKG2A blockade with potent and specific, fully human antibodies and BiNKs show promise for further development as cancer immunotherapeutics.
{"title":"Discovery and preclinical evaluation of monoclonal antibodies and bispecific engagers targeting the NKG2A inhibitory receptor","authors":"Seungmin Shin, Yae-Jin Kim, Bernard J. C. Macatangay, Joshua C. Cyktor, Margaret G. Hines, Ze-Yu Sun, Kong Chen, John W. Mellors, Dimiter S. Dimitrov, Wei Li, Du-San Baek","doi":"10.1126/sciadv.adu0690","DOIUrl":"10.1126/sciadv.adu0690","url":null,"abstract":"<div >NK and T cells are key effectors that eliminate cancer cells, but upregulation of the inhibitory receptor NKG2A on these cells attenuates antitumor immune responses. To counteract NKG2A inhibitory signaling, we identified two specific fully human monoclonal anti-NKG2A antibodies that block HLA-E ligand binding. These antibodies activated NK cells and enhanced antibody-dependent cellular cytotoxicity of tumor-targeting IgG1s both in vitro and in vivo. Bispecific engagers (BiNKs), generated by fusing NKG2A antibodies with tumor targeting binders, promoted immune synapse formation and directed cytotoxicity of NK and CD8<sup>+</sup> T cells toward cancer cells. In a human PBMC-engrafted NSG mouse xenograft lung cancer model, an anti-HER2 × anti-NKG2A BiNK markedly inhibited tumor growth as a monotherapy or in combination with pertuzumab. Cell depletion studies revealed that the BiNK enhanced antitumor activity of both NK and T cells. NKG2A blockade with potent and specific, fully human antibodies and BiNKs show promise for further development as cancer immunotherapeutics.</div>","PeriodicalId":21609,"journal":{"name":"Science Advances","volume":"12 6","pages":""},"PeriodicalIF":12.5,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146111424","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}
Hybrid incompatibility can lead to lethality and sterility of F1 hybrids, promoting speciation. The cell biological basis underlying hybrid incompatibility remains largely unknown, especially in mammals. Here, we found that female hybrids between Mus musculus domesticus and Mus spicilegus mice are sterile due to the failure of homologous-chromosome separation in oocyte meiosis, producing aneuploid eggs. This nondisjunction phenotype was driven by the mislocalization of the cohesin protector, SGO2, along the chromosome arms instead of its typical centromeric enrichment, resulting in cohesin overprotection. The upstream kinase, BUB1, showed a higher activity in hybrid oocytes, explaining SGO2 mistargeting. Higher BUB1 activity was not observed in mitosis, consistent with viable hybrid mice. Cohesion defects were also evident in hybrid mice from another genus, Peromyscus, wherein cohesin protection is weakened. Defective cohesion in oocytes is a leading cause of reduced fertility. Our work provides evidence that a major cause of human infertility may play a positive role in mammalian speciation.
{"title":"Hybrid female sterility due to cohesin protection errors in mouse oocytes","authors":"Warif El Yakoubi, Bo Pan, Takashi Akera","doi":"10.1126/sciadv.adx9729","DOIUrl":"10.1126/sciadv.adx9729","url":null,"abstract":"<div >Hybrid incompatibility can lead to lethality and sterility of F1 hybrids, promoting speciation. The cell biological basis underlying hybrid incompatibility remains largely unknown, especially in mammals. Here, we found that female hybrids between <i>Mus musculus domesticus</i> and <i>Mus spicilegus</i> mice are sterile due to the failure of homologous-chromosome separation in oocyte meiosis, producing aneuploid eggs. This nondisjunction phenotype was driven by the mislocalization of the cohesin protector, SGO2, along the chromosome arms instead of its typical centromeric enrichment, resulting in cohesin overprotection. The upstream kinase, BUB1, showed a higher activity in hybrid oocytes, explaining SGO2 mistargeting. Higher BUB1 activity was not observed in mitosis, consistent with viable hybrid mice. Cohesion defects were also evident in hybrid mice from another genus, <i>Peromyscus</i>, wherein cohesin protection is weakened. Defective cohesion in oocytes is a leading cause of reduced fertility. Our work provides evidence that a major cause of human infertility may play a positive role in mammalian speciation.</div>","PeriodicalId":21609,"journal":{"name":"Science Advances","volume":"12 6","pages":""},"PeriodicalIF":12.5,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146111429","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}
Qiong Zhu, Jinning Zhang, Weichen Zhou, Shen-Ao Liang, Shengmiao Wang, Xinyu Cai, Fuyuan Li, Jin Li, Guojie Zhang, Huijuan Feng, Qiaomei Fu, Joshua M. Akey, Feng Zhang, Li Jin, Shuhua Xu, Hong-Xiang Zheng, Lu Chen
Archaic introgression introduced functionally relevant variants into modern humans, yet small-scale insertions remain understudied. Here, we leverage 2519 modern human genomes and four high-coverage archaic hominin genomes to systematically characterize nuclear mitochondrial DNA segments (NUMTs). We uncover 483 polymorphic NUMTs across globally diverse human populations and 10 in archaic genomes. By combining overlap with Neanderthal-derived and Denisovan-derived haplotypes, phylogenetic analyses, insertion time estimates, and haplotype colocalization, we identify five NUMTs introduced into modern humans via archaic hominin introgression. Functional analyses reveal that introgressed NUMTs can modulate gene expression, including allele-specific up-regulation of the immune-related gene RASGRP3, and reshape three-dimensional chromatin structure at loci such as SCD5 and HNRNPD. These findings highlight an underappreciated mechanism by which archaic mitochondrial fragments shape nuclear genome function and evolution. Our study reframes NUMTs not as passive genomic fossils but as dynamic elements influencing modern human diversity and adaptation.
{"title":"Introgressed mitochondrial fragments from archaic hominins alter nuclear genome function in modern humans","authors":"Qiong Zhu, Jinning Zhang, Weichen Zhou, Shen-Ao Liang, Shengmiao Wang, Xinyu Cai, Fuyuan Li, Jin Li, Guojie Zhang, Huijuan Feng, Qiaomei Fu, Joshua M. Akey, Feng Zhang, Li Jin, Shuhua Xu, Hong-Xiang Zheng, Lu Chen","doi":"10.1126/sciadv.aea0706","DOIUrl":"10.1126/sciadv.aea0706","url":null,"abstract":"<div >Archaic introgression introduced functionally relevant variants into modern humans, yet small-scale insertions remain understudied. Here, we leverage 2519 modern human genomes and four high-coverage archaic hominin genomes to systematically characterize nuclear mitochondrial DNA segments (NUMTs). We uncover 483 polymorphic NUMTs across globally diverse human populations and 10 in archaic genomes. By combining overlap with Neanderthal-derived and Denisovan-derived haplotypes, phylogenetic analyses, insertion time estimates, and haplotype colocalization, we identify five NUMTs introduced into modern humans via archaic hominin introgression. Functional analyses reveal that introgressed NUMTs can modulate gene expression, including allele-specific up-regulation of the immune-related gene <i>RASGRP3</i>, and reshape three-dimensional chromatin structure at loci such as <i>SCD5</i> and <i>HNRNPD</i>. These findings highlight an underappreciated mechanism by which archaic mitochondrial fragments shape nuclear genome function and evolution. Our study reframes NUMTs not as passive genomic fossils but as dynamic elements influencing modern human diversity and adaptation.</div>","PeriodicalId":21609,"journal":{"name":"Science Advances","volume":"12 6","pages":""},"PeriodicalIF":12.5,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146111415","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}
Min Zhang, Edgar Castro, Alexandra Shtein, Adjani A. Peralta, Mahdieh Danesh Yazdi, Xiao Wu, Joel D. Schwartz, Robert O. Wright, Yaguang Wei
The relationships between chronic exposure to wildfire smoke PM2.5 (particulate matter with aerodynamic diameter of ≤2.5 μm) and mortality remain poorly understood, with causal evidence being particularly scarce. In this ecological study, we used a doubly robust method, incorporating flexible generalized propensity score estimation that captured potential nonlinearity and interactions among confounders and relaxed the distribution form assumption for exposure, to estimate the effects of annual exposure to wildfire smoke PM2.5 on all-cause and cause-specific mortality in the contiguous United States from 2006 to 2020. We found that wildfire smoke PM2.5 was associated with increased mortality rate for all studied outcomes, except for deaths from transport accidents or falls, which served as negative outcome controls. Wildfire smoke PM2.5 was responsible for ~24,100 all-cause deaths per year in the contiguous United States. The exposure-response curve for all-cause mortality increased monotonically, with no evidence of a “safe” threshold. Among the six cause-specific outcomes, mortality from neurological disease showed the greatest increase per 0.1 μg/m3 increase in smoke PM2.5 exposure. Our study provided robust evidence for the chronic effect of wildfire smoke PM2.5 on mortality, underscoring the urgent need for targeted measures to mitigate the substantial and escalating burden of wildfires.
{"title":"Wildfire smoke PM2.5 and mortality rate in the contiguous United States: A causal modeling study","authors":"Min Zhang, Edgar Castro, Alexandra Shtein, Adjani A. Peralta, Mahdieh Danesh Yazdi, Xiao Wu, Joel D. Schwartz, Robert O. Wright, Yaguang Wei","doi":"10.1126/sciadv.adw5890","DOIUrl":"10.1126/sciadv.adw5890","url":null,"abstract":"<div >The relationships between chronic exposure to wildfire smoke PM<sub>2.5</sub> (particulate matter with aerodynamic diameter of ≤2.5 μm) and mortality remain poorly understood, with causal evidence being particularly scarce. In this ecological study, we used a doubly robust method, incorporating flexible generalized propensity score estimation that captured potential nonlinearity and interactions among confounders and relaxed the distribution form assumption for exposure, to estimate the effects of annual exposure to wildfire smoke PM<sub>2.5</sub> on all-cause and cause-specific mortality in the contiguous United States from 2006 to 2020. We found that wildfire smoke PM<sub>2.5</sub> was associated with increased mortality rate for all studied outcomes, except for deaths from transport accidents or falls, which served as negative outcome controls. Wildfire smoke PM<sub>2.5</sub> was responsible for ~24,100 all-cause deaths per year in the contiguous United States. The exposure-response curve for all-cause mortality increased monotonically, with no evidence of a “safe” threshold. Among the six cause-specific outcomes, mortality from neurological disease showed the greatest increase per 0.1 μg/m<sup>3</sup> increase in smoke PM<sub>2.5</sub> exposure. Our study provided robust evidence for the chronic effect of wildfire smoke PM<sub>2.5</sub> on mortality, underscoring the urgent need for targeted measures to mitigate the substantial and escalating burden of wildfires.</div>","PeriodicalId":21609,"journal":{"name":"Science Advances","volume":"12 6","pages":""},"PeriodicalIF":12.5,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146111414","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}
Patrick Eiring, Maximilian J. Steinhardt, Nele Bauer, Cornelia Vogt, Umair Munawar, Seungbin Han, Thomas Nerreter, Hermann Einsele, K. Martin Kortüm, Sören Doose, Markus Sauer
Super-resolution microscopy in combination with genetic labeling methods allows imaging of single proteins in cells. However, visualizing endogenous proteins on primary cells remains challenging due to the use of sterically demanding antibodies for labeling. Here, we demonstrate how immunolabeling conditions and antibody cross-linking influence the quantification and identification of membrane receptor stoichiometry on cells using single-molecule localization microscopy. We developed an optimized immunolabeling and analysis protocol and demonstrate the performance of the approach by resolving the molecular organization of endogenous CD45, CD69, and CD38 on Jurkat T cells. To demonstrate the usefulness of the method for immunotherapy applications, we investigated the interaction of primary multiple myeloma cells with the therapeutic monoclonal antibodies daratumumab and isatuximab and a polyclonal anti-CD38 antibody. Our approach might lay the foundation for improved personalized diagnostics and treatment with therapeutic antibodies.
{"title":"Single-molecule localization microscopy reveals the molecular organization of endogenous membrane receptors","authors":"Patrick Eiring, Maximilian J. Steinhardt, Nele Bauer, Cornelia Vogt, Umair Munawar, Seungbin Han, Thomas Nerreter, Hermann Einsele, K. Martin Kortüm, Sören Doose, Markus Sauer","doi":"10.1126/sciadv.aea2310","DOIUrl":"10.1126/sciadv.aea2310","url":null,"abstract":"<div >Super-resolution microscopy in combination with genetic labeling methods allows imaging of single proteins in cells. However, visualizing endogenous proteins on primary cells remains challenging due to the use of sterically demanding antibodies for labeling. Here, we demonstrate how immunolabeling conditions and antibody cross-linking influence the quantification and identification of membrane receptor stoichiometry on cells using single-molecule localization microscopy. We developed an optimized immunolabeling and analysis protocol and demonstrate the performance of the approach by resolving the molecular organization of endogenous CD45, CD69, and CD38 on Jurkat T cells. To demonstrate the usefulness of the method for immunotherapy applications, we investigated the interaction of primary multiple myeloma cells with the therapeutic monoclonal antibodies daratumumab and isatuximab and a polyclonal anti-CD38 antibody. Our approach might lay the foundation for improved personalized diagnostics and treatment with therapeutic antibodies.</div>","PeriodicalId":21609,"journal":{"name":"Science Advances","volume":"12 6","pages":""},"PeriodicalIF":12.5,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146111418","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}
Aquatic animals such as octopuses use soft suction cups to solve the persistent challenge of wet attachment on rough surfaces. Detachment has long been described as smooth drainage governed by a Reynolds-type pressure gradient. Combining spatiotemporal pressure mapping with confocal imaging of the fluid layer between a suction cup-substrate interface, we reveal a two-stage, nonequilibrium pathway for pressure equalization that challenges this conventional view. Suction-induced elastic deformation dynamically remodels the interfacial fluid, producing a self-coupled pressure channel system. Stage I is governed by an outward-moving invasion-percolation suction front with diffusion-like scaling. When internal suction falls below a critical value, the network opens globally, and stage II follows classical Poiseuille drainage. This mechanism defines a self-modifying percolation in which the flow remodels its own pathways, which advances our understanding of biological suction and viscous adhesion and suggests design principles for long-lived wet adhesives and hydrogel microfluidics.
{"title":"Self-modifying percolation governs detachment in soft suction wet adhesion","authors":"Abdallah Aly, M. Taher A. Saif","doi":"10.1126/sciadv.aeb4013","DOIUrl":"10.1126/sciadv.aeb4013","url":null,"abstract":"<div >Aquatic animals such as octopuses use soft suction cups to solve the persistent challenge of wet attachment on rough surfaces. Detachment has long been described as smooth drainage governed by a Reynolds-type pressure gradient. Combining spatiotemporal pressure mapping with confocal imaging of the fluid layer between a suction cup-substrate interface, we reveal a two-stage, nonequilibrium pathway for pressure equalization that challenges this conventional view. Suction-induced elastic deformation dynamically remodels the interfacial fluid, producing a self-coupled pressure channel system. Stage I is governed by an outward-moving invasion-percolation suction front with diffusion-like scaling. When internal suction falls below a critical value, the network opens globally, and stage II follows classical Poiseuille drainage. This mechanism defines a self-modifying percolation in which the flow remodels its own pathways, which advances our understanding of biological suction and viscous adhesion and suggests design principles for long-lived wet adhesives and hydrogel microfluidics.</div>","PeriodicalId":21609,"journal":{"name":"Science Advances","volume":"12 6","pages":""},"PeriodicalIF":12.5,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146111421","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}
Jinghui Liu, Elisa Nerli, Charlie Duclut, Amit S. Vishen, Naomi Berbee, Sylvia Kaufmann, Cesar Ponce, Aristides B. Arrenberg, Frank Jülicher, Rita Mateus
Organ injury triggers nonneuronal electric currents essential for regeneration. However, the mechanisms by which electrical signals are generated, sensed, and transmitted upon damage to promote organ growth remain unclear. Here, we uncover that organ repair relies on dynamic electrochemical coupling between membrane potential depolarization and intracellular signaling, essential to activate cell proliferation. By subsecond live imaging of locally injured zebrafish larval fins, we identify events across time and space: a millisecond, long-range, membrane depolarization gradient, followed by second-persistent intracellular calcium responses. In the subsequent hour, voltage sensing phosphatase senses the injury-driven membrane potential change and autonomously translates the electric signal intracellularly, promoting tissue-wide cell proliferation. Connecting these dynamics with an electrodiffusive model showed that ionic fluxes and electric potential become coupled in the fin’s interstitial space, enabling organ-wide signal spreading. Our work reveals the coupling between fast electrical signals and slower intracellular signaling, ensuring complete organ recovery.
{"title":"Injury-induced electrochemical coupling triggers organ growth","authors":"Jinghui Liu, Elisa Nerli, Charlie Duclut, Amit S. Vishen, Naomi Berbee, Sylvia Kaufmann, Cesar Ponce, Aristides B. Arrenberg, Frank Jülicher, Rita Mateus","doi":"10.1126/sciadv.aec0687","DOIUrl":"10.1126/sciadv.aec0687","url":null,"abstract":"<div >Organ injury triggers nonneuronal electric currents essential for regeneration. However, the mechanisms by which electrical signals are generated, sensed, and transmitted upon damage to promote organ growth remain unclear. Here, we uncover that organ repair relies on dynamic electrochemical coupling between membrane potential depolarization and intracellular signaling, essential to activate cell proliferation. By subsecond live imaging of locally injured zebrafish larval fins, we identify events across time and space: a millisecond, long-range, membrane depolarization gradient, followed by second-persistent intracellular calcium responses. In the subsequent hour, voltage sensing phosphatase senses the injury-driven membrane potential change and autonomously translates the electric signal intracellularly, promoting tissue-wide cell proliferation. Connecting these dynamics with an electrodiffusive model showed that ionic fluxes and electric potential become coupled in the fin’s interstitial space, enabling organ-wide signal spreading. Our work reveals the coupling between fast electrical signals and slower intracellular signaling, ensuring complete organ recovery.</div>","PeriodicalId":21609,"journal":{"name":"Science Advances","volume":"12 6","pages":""},"PeriodicalIF":12.5,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146111427","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}
Shijie Ruan, Wei Qin, Linyang Li, Tingting Li, Baochen Li, Xiao Liang, Lei Xi
Photoacoustic imaging has become a powerful tool for visualizing the brain morphology, function, and metabolism. However, severe optical scattering and high-frequency acoustic attenuation within the brain degrade the performance of photoacoustic brain imaging. To address such limitation, we propose a line scanning–based photoacoustic computed mesoscopic (PACMes) approach for noninvasive, high-resolution, and longitudinal visualization of cerebral vasculature inside the intact mouse brain. This technique uses converging near-infrared (NIR) lines scanned at multiple angles for tight optical excitation; a low-frequency, full-ring ultrasound transducer array for high-sensitivity detection; and a compound reconstruction algorithm integrating filtered back-projection and optical localization of photoacoustic signals to recover the image. We perform long-term (>5 months), noninvasive imaging of the entire cortex of mice through the intact scalp and skull with a field of view of 13 millimeters and a spatial resolution of 33 micrometers. The results demonstrate the potential of PACMes for investigating brain function and disease.
{"title":"Noninvasive photoacoustic computed mesoscopy for longitudinal brain imaging","authors":"Shijie Ruan, Wei Qin, Linyang Li, Tingting Li, Baochen Li, Xiao Liang, Lei Xi","doi":"10.1126/sciadv.aea1602","DOIUrl":"10.1126/sciadv.aea1602","url":null,"abstract":"<div >Photoacoustic imaging has become a powerful tool for visualizing the brain morphology, function, and metabolism. However, severe optical scattering and high-frequency acoustic attenuation within the brain degrade the performance of photoacoustic brain imaging. To address such limitation, we propose a line scanning–based photoacoustic computed mesoscopic (PACMes) approach for noninvasive, high-resolution, and longitudinal visualization of cerebral vasculature inside the intact mouse brain. This technique uses converging near-infrared (NIR) lines scanned at multiple angles for tight optical excitation; a low-frequency, full-ring ultrasound transducer array for high-sensitivity detection; and a compound reconstruction algorithm integrating filtered back-projection and optical localization of photoacoustic signals to recover the image. We perform long-term (>5 months), noninvasive imaging of the entire cortex of mice through the intact scalp and skull with a field of view of 13 millimeters and a spatial resolution of 33 micrometers. The results demonstrate the potential of PACMes for investigating brain function and disease.</div>","PeriodicalId":21609,"journal":{"name":"Science Advances","volume":"12 6","pages":""},"PeriodicalIF":12.5,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146111412","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}
The racial landscape of US neighborhoods shifted tremendously over the past decade, raising questions about how these changes are reflected in local schools. This study combines school zone shapefiles with census and Civil Rights Database data to explore whether neighborhood racial change in Black populations predicts changes in Black-white school suspension disparities from 2010 to 2018. We find that racial disparities in suspensions increased, particularly in neighborhoods experiencing substantial shifts in Black populations. These increases were especially pronounced in suburban and rural areas with shifting Black populations and all predominantly White neighborhoods. Although school discipline reforms aimed to reduce racial disparities, they only declined in certain types of neighborhoods, most notably in urban areas. Our findings advance insights into processes of school and neighborhood change, school discipline, and racial stratification, with broad policy implications.
{"title":"School discipline disparities increase when neighborhood Black population changes","authors":"Jennifer Candipan, Chantal A. Hailey","doi":"10.1126/sciadv.ady4239","DOIUrl":"10.1126/sciadv.ady4239","url":null,"abstract":"<div >The racial landscape of US neighborhoods shifted tremendously over the past decade, raising questions about how these changes are reflected in local schools. This study combines school zone shapefiles with census and Civil Rights Database data to explore whether neighborhood racial change in Black populations predicts changes in Black-white school suspension disparities from 2010 to 2018. We find that racial disparities in suspensions increased, particularly in neighborhoods experiencing substantial shifts in Black populations. These increases were especially pronounced in suburban and rural areas with shifting Black populations and all predominantly White neighborhoods. Although school discipline reforms aimed to reduce racial disparities, they only declined in certain types of neighborhoods, most notably in urban areas. Our findings advance insights into processes of school and neighborhood change, school discipline, and racial stratification, with broad policy implications.</div>","PeriodicalId":21609,"journal":{"name":"Science Advances","volume":"12 6","pages":""},"PeriodicalIF":12.5,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146111425","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}
Hu Hong, Qingshun Nian, Xun Guo, Qing Li, Chunyi Zhi
Aqueous batteries, with their inherent safety, operational simplicity, and cost-effectiveness, have emerged as promising candidates for grid-scale energy storage applications. However, the relatively low output voltage of aqueous systems continues to limit their achievable energy density. The aqueous electrolyte occupies a central role in addressing this limitation because it mediates ion transport and interfacial reactions at both the cathode and anode; accordingly, advances in electrolyte design are indispensable to meet future performance demands. In this review, we elucidate the core bottlenecks in aqueous electrolyte design, distill molecular-level design principles, and outline feasible pathways for future practical implementation. We aim to guide the development of next-generation aqueous electrolytes that harmonize outstanding electrochemical performance, thereby accelerating the transition from laboratory concepts to transformative energy solutions.
{"title":"Electrolyte design for aqueous batteries","authors":"Hu Hong, Qingshun Nian, Xun Guo, Qing Li, Chunyi Zhi","doi":"10.1126/sciadv.aeb4498","DOIUrl":"10.1126/sciadv.aeb4498","url":null,"abstract":"<div >Aqueous batteries, with their inherent safety, operational simplicity, and cost-effectiveness, have emerged as promising candidates for grid-scale energy storage applications. However, the relatively low output voltage of aqueous systems continues to limit their achievable energy density. The aqueous electrolyte occupies a central role in addressing this limitation because it mediates ion transport and interfacial reactions at both the cathode and anode; accordingly, advances in electrolyte design are indispensable to meet future performance demands. In this review, we elucidate the core bottlenecks in aqueous electrolyte design, distill molecular-level design principles, and outline feasible pathways for future practical implementation. We aim to guide the development of next-generation aqueous electrolytes that harmonize outstanding electrochemical performance, thereby accelerating the transition from laboratory concepts to transformative energy solutions.</div>","PeriodicalId":21609,"journal":{"name":"Science Advances","volume":"12 6","pages":""},"PeriodicalIF":12.5,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146111410","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}
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