Pub Date : 2026-09-30Epub Date: 2026-07-06DOI: 10.1016/j.scib.2026.07.007
Zhangcheng Li, Can Wang, Zhi Liang, Zerui Liu, Zhangao Wang, Renzi Gong, Kangrui Ji, Shengyin Wang, Jiawen Tian, Chong Hou
Fiber-based light-emitting devices hold promise for next-generation wearable electronics and human-machine interfaces. However, optoelectronic stability under extreme deformation remains challenging due to mechanical incompatibility at heterogeneous solid-solid interfaces and the difficulty of reconciling conflicting functionalities within fiber electrodes. Here, a liquid-electrode ultra-stretchable monolithic illuminating (LUMI) fiber is presented to address these interfacial limitations. Fabricated via scalable thermal drawing, the LUMI fiber consists of a central liquid metal core and symmetric ionic liquid channels embedded in a unified thermoplastic elastomer matrix. This architecture forms adaptive liquid-solid interfaces, ensuring robust electrical contact and maintaining uniform radial electric fields during dynamic deformation. As a result, the LUMI fiber exhibits excellent omnidirectional luminescence uniformity, sustaining up to 500% tensile strain while preserving stable luminance over 15,000 stretching cycles. Its versatility is further demonstrated by seamless integration into complex textile patterns and adaptability to dynamic, irregular surfaces. Overall, this work provides a comprehensive strategy for developing durable, scalable, and high-performance interactive fibers, advancing the frontiers of stretchable displays and electronic skins.
{"title":"A liquid-electrode ultra-stretchable monolithic illuminating fiber","authors":"Zhangcheng Li, Can Wang, Zhi Liang, Zerui Liu, Zhangao Wang, Renzi Gong, Kangrui Ji, Shengyin Wang, Jiawen Tian, Chong Hou","doi":"10.1016/j.scib.2026.07.007","DOIUrl":"10.1016/j.scib.2026.07.007","url":null,"abstract":"<div><div>Fiber-based light-emitting devices hold promise for next-generation wearable electronics and human-machine interfaces. However, optoelectronic stability under extreme deformation remains challenging due to mechanical incompatibility at heterogeneous solid-solid interfaces and the difficulty of reconciling conflicting functionalities within fiber electrodes. Here, a liquid-electrode ultra-stretchable monolithic illuminating (LUMI) fiber is presented to address these interfacial limitations. Fabricated via scalable thermal drawing, the LUMI fiber consists of a central liquid metal core and symmetric ionic liquid channels embedded in a unified thermoplastic elastomer matrix. This architecture forms adaptive liquid-solid interfaces, ensuring robust electrical contact and maintaining uniform radial electric fields during dynamic deformation. As a result, the LUMI fiber exhibits excellent omnidirectional luminescence uniformity, sustaining up to 500% tensile strain while preserving stable luminance over 15,000 stretching cycles. Its versatility is further demonstrated by seamless integration into complex textile patterns and adaptability to dynamic, irregular surfaces. Overall, this work provides a comprehensive strategy for developing durable, scalable, and high-performance interactive fibers, advancing the frontiers of stretchable displays and electronic skins.</div></div>","PeriodicalId":421,"journal":{"name":"Science Bulletin","volume":"71 18","pages":"Pages 4714-4722"},"PeriodicalIF":20.7,"publicationDate":"2026-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148534798","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}
Pulmonary fibrosis (PF) is a progressive and fatal lung disorder driven by abnormal fibroblast activation and excessive extracellular matrix (ECM) deposition, leading to structural and functional decline. Existing therapies can slow progression but fail to interrupt fibrotic remodeling. Here, we engineered HUCMSC-Lipo, an inhalable biomimetic formulation fusing human umbilical cord mesenchymal stem cell (HUCMSC) membranes with artificial phospholipids, with formulation parameters systematically optimized using a Bayesian optimization (BO) framework to ensure structural stability and nebulization compatibility. HUCMSC-Lipo maintained membrane functionality and structural integrity for effective nebulized delivery. We successfully established a non-human primate (NHP) PF model and innovatively developed a multidimensional evaluation framework. Utilizing a range of methods, including but not limited to positron emission tomography/computed tomography (PET/CT) molecular imaging with radiolabeled fibroblast activation protein (FAP) inhibitors, we confirmed that HUCMSC-Lipo suppressed fibrotic progression and restored pulmonary function by targeting the regulation of fibroblast activation. Mechanistically, THY-1 enrichment in HUCMSC-Lipo bound integrin receptors to block the FAK/PI3K signaling cascade and restore fibroblast mechanosensitivity, fundamentally turning off the pathological activation “switch” in fibroblasts. Our work presents an inhalable biomimetic formulation that combines therapeutic efficacy with synthetic accessibility, offering a mechanism-targeted approach to PF treatment with strong clinical translatability.
{"title":"Inhalable HUCMSC-Lipo biomimetic formulation inhibits fibroblast activation in mouse and non-human primate pulmonary fibrosis models","authors":"Fangyu Zhao, Yige Sun, Haoran Wang, Dayong Hou, Rui Zhang, Wenjing Xia, Yongchen Zhang, Luyao Li, Xueqi Zhao, Kaiqi Wang, Wenwen Pan, Jiannan Wang, Kai Wang, Lili Yang, Wei Chen, Xin Li, Chunyang Nong, Huiying Lu, Yi Zhang, Zhaoyang Zhang, Xilin Sun","doi":"10.1016/j.scib.2026.08.013","DOIUrl":"10.1016/j.scib.2026.08.013","url":null,"abstract":"<div><div>Pulmonary fibrosis (PF) is a progressive and fatal lung disorder driven by abnormal fibroblast activation and excessive extracellular matrix (ECM) deposition, leading to structural and functional decline. Existing therapies can slow progression but fail to interrupt fibrotic remodeling. Here, we engineered HUCMSC-Lipo, an inhalable biomimetic formulation fusing human umbilical cord mesenchymal stem cell (HUCMSC) membranes with artificial phospholipids, with formulation parameters systematically optimized using a Bayesian optimization (BO) framework to ensure structural stability and nebulization compatibility. HUCMSC-Lipo maintained membrane functionality and structural integrity for effective nebulized delivery. We successfully established a non-human primate (NHP) PF model and innovatively developed a multidimensional evaluation framework. Utilizing a range of methods, including but not limited to positron emission tomography/computed tomography (PET/CT) molecular imaging with radiolabeled fibroblast activation protein (FAP) inhibitors, we confirmed that HUCMSC-Lipo suppressed fibrotic progression and restored pulmonary function by targeting the regulation of fibroblast activation. Mechanistically, THY-1 enrichment in HUCMSC-Lipo bound integrin receptors to block the FAK/PI3K signaling cascade and restore fibroblast mechanosensitivity, fundamentally turning off the pathological activation “switch” in fibroblasts. Our work presents an inhalable biomimetic formulation that combines therapeutic efficacy with synthetic accessibility, offering a mechanism-targeted approach to PF treatment with strong clinical translatability.</div></div>","PeriodicalId":421,"journal":{"name":"Science Bulletin","volume":"71 18","pages":"Pages 4694-4713"},"PeriodicalIF":20.7,"publicationDate":"2026-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148838864","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-09-30Epub Date: 2026-08-25DOI: 10.1016/j.scib.2026.08.057
Xin Li, Nan Zang, Qianru Zhao, Yuxiang Sun, Udhaya Kumar Siva Kumar, Mengyu Hua, Wenjun Zhou, Yanyan Qi, Hu Chen, Longqing Xia, Jun Qin, Lei Sun, Chaitra Rai, Chao Cheng, Zhandong Liu, Li Chen, Yong Xu, Zhaoyong Hu, Hongjie Li, Xinguo Hou, Zheng Sun
Normal estrogen exposure, as observed in eumenorrheic women of reproductive age, is important for neurocognition, as demonstrated by postmenopausal hormone replacement. However, the cognitive effects of sustained high-level estrogen in the context of oral contraceptives or pregnancy are unclear. Here, we show that high estrogen induces temporary memory dysfunction in mice without affecting mood-related behaviors or exploratory motivation, which is associated with altered gene expression in the lateral hypothalamus (LH). Depletion of neuronal estrogen receptor α/β (ERα/β) in the LH rescues estrogen- or pregnancy-induced cognitive dysfunction. Single-nucleus RNA-seq revealed that ERα, the predominant ER in the LH, is enriched in Gamma-Aminobutyric Acid-releasing (GABAergic) neurons and that high-level estrogen downregulates GABA-A receptor signaling within LHGABA neurons, concurrent with increased spontaneous firing activity of LHGABA neurons during high estrogen exposure or pregnancy. LHGABA neurons project to the hippocampal Cornu Ammonis 3 (CA3). Chemogenetic suppression of CA3-projecting LHGABA neurons protects against high estrogen-induced cognitive dysfunction, while activation of CA3-projecting LHGABA neurons causes cognitive dysfunction. Lastly, we observed task-specific memory impairment in women during late pregnancy, which was associated with elevated circulating estrogen levels even after correcting for other covariates. These findings delineate a molecular and neural mechanism underlying the cognitive effects of high-level estrogen, with implications for understanding the brain fog associated with pregnancy or oral contraceptives.
{"title":"High-level estrogen impairs memory via estrogen receptor signaling in a hypothalamic–hippocampal neural circuit","authors":"Xin Li, Nan Zang, Qianru Zhao, Yuxiang Sun, Udhaya Kumar Siva Kumar, Mengyu Hua, Wenjun Zhou, Yanyan Qi, Hu Chen, Longqing Xia, Jun Qin, Lei Sun, Chaitra Rai, Chao Cheng, Zhandong Liu, Li Chen, Yong Xu, Zhaoyong Hu, Hongjie Li, Xinguo Hou, Zheng Sun","doi":"10.1016/j.scib.2026.08.057","DOIUrl":"10.1016/j.scib.2026.08.057","url":null,"abstract":"<div><div>Normal estrogen exposure, as observed in eumenorrheic women of reproductive age, is important for neurocognition, as demonstrated by postmenopausal hormone replacement. However, the cognitive effects of sustained high-level estrogen in the context of oral contraceptives or pregnancy are unclear. Here, we show that high estrogen induces temporary memory dysfunction in mice without affecting mood-related behaviors or exploratory motivation, which is associated with altered gene expression in the lateral hypothalamus (LH). Depletion of neuronal estrogen receptor α/β (ERα/β) in the LH rescues estrogen- or pregnancy-induced cognitive dysfunction. Single-nucleus RNA-seq revealed that ERα, the predominant ER in the LH, is enriched in Gamma-Aminobutyric Acid-releasing (GABAergic) neurons and that high-level estrogen downregulates GABA-A receptor signaling within LH<sup>GABA</sup> neurons, concurrent with increased spontaneous firing activity of LH<sup>GABA</sup> neurons during high estrogen exposure or pregnancy. LH<sup>GABA</sup> neurons project to the hippocampal Cornu Ammonis 3 (CA3). Chemogenetic suppression of CA3-projecting LH<sup>GABA</sup> neurons protects against high estrogen-induced cognitive dysfunction, while activation of CA3-projecting LH<sup>GABA</sup> neurons causes cognitive dysfunction. Lastly, we observed task-specific memory impairment in women during late pregnancy, which was associated with elevated circulating estrogen levels even after correcting for other covariates. These findings delineate a molecular and neural mechanism underlying the cognitive effects of high-level estrogen, with implications for understanding the brain fog associated with pregnancy or oral contraceptives.</div></div>","PeriodicalId":421,"journal":{"name":"Science Bulletin","volume":"71 18","pages":"Pages 4762-4779"},"PeriodicalIF":20.7,"publicationDate":"2026-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148878913","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-09-30Epub Date: 2026-08-02DOI: 10.1016/j.scib.2026.08.006
Xiaoxuan Xu, Wenzhe Yi, Xiangshi Sun, Zhiwen Zhao, Jialin Duan, Ting Wu, Xiaoting Shan, Jie Li, Dangge Wang, Yaping Li
The efficacy of conventional in vivo CAR therapy is compromised by the biophysical barrier of tumor infiltration. Here, this work develops a lipoplex-based, tumor-penetrating and hypoxia-responsive in vivo CAR strategy that enables in situ CAR-T/NK engineering within solid tumors, thereby enhancing immunotherapy against triple-negative breast cancer.
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常规体内CAR治疗的疗效受到肿瘤浸润的生物物理屏障的影响。在这里，本研究开发了一种基于脂质体、肿瘤穿透性和缺氧反应性的体内CAR- t策略，使实体瘤内的CAR- t /NK原位工程成为可能，从而增强了针对三阴性乳腺癌的免疫治疗。下载：下载高分辨率图片（277KB）下载：下载全尺寸图片
{"title":"In situ generation of NKG2D CAR T/NK cells via a tumor-targeted lipoplex for enhancing cancer immunotherapy","authors":"Xiaoxuan Xu, Wenzhe Yi, Xiangshi Sun, Zhiwen Zhao, Jialin Duan, Ting Wu, Xiaoting Shan, Jie Li, Dangge Wang, Yaping Li","doi":"10.1016/j.scib.2026.08.006","DOIUrl":"10.1016/j.scib.2026.08.006","url":null,"abstract":"<div>The efficacy of conventional <em>in vivo</em> CAR therapy is compromised by the biophysical barrier of tumor infiltration. Here, this work develops a lipoplex-based, tumor-penetrating and hypoxia-responsive <em>in vivo</em> CAR strategy that enables <em>in situ</em> CAR-T/NK engineering within solid tumors, thereby enhancing immunotherapy against triple-negative breast cancer.</div><div><span><figure><span><img><ol><li><span><span>Download: <span>Download high-res image (277KB)</span></span></span></li><li><span><span>Download: <span>Download full-size image</span></span></span></li></ol></span></figure></span></div>","PeriodicalId":421,"journal":{"name":"Science Bulletin","volume":"71 18","pages":"Pages 4606-4610"},"PeriodicalIF":20.7,"publicationDate":"2026-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148719531","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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