The rise of intelligent systems exacerbates scenario-specific limitations in conventional rigid electronics, revealing critical compatibility gaps across emerging application fields such as wearable devices, bioelectronics, soft robotics, human–machine interfaces, etc. Adaptive conductive systems serve as critical enablers for next-generation deformable electronics through engineering deformable conductors, innovating reconfigurable circuit topologies, and implementing intelligent systems, ensuring robust electrical connectivity and dynamic compliance in variable operating environments. This review presents the research advances of adaptive conductive systems from the perspective of material innovation, circuit interconnection design, system integration, and applications. Deformable conductors consist of substrates and conductive materials with their independent intrinsic properties and synergistic effects, structural designs and fabrication methods of conductive circuits with specialized stretchable configurations, as well as intelligent systems constructed via signal processing, machine learning, and coherent integration, are systematically summarized and reviewed. Finally, current challenges and future research perspectives of adaptive conductive systems are outlined, offering deep insights into research directions and strategies.
{"title":"Adaptive Conductive Systems: Enabling Deformable Electronics Through Engineered Materials, Circuits, and Intelligent Systems","authors":"Yufei Lu, Siyu Liang, Jingyi Niu, Jie Chen, Shuo Zhang, Hongjian Zhang, Dongsheng Jia, Wei Huang","doi":"10.1002/advs.77522","DOIUrl":"10.1002/advs.77522","url":null,"abstract":"<p>The rise of intelligent systems exacerbates scenario-specific limitations in conventional rigid electronics, revealing critical compatibility gaps across emerging application fields such as wearable devices, bioelectronics, soft robotics, human–machine interfaces, etc. Adaptive conductive systems serve as critical enablers for next-generation deformable electronics through engineering deformable conductors, innovating reconfigurable circuit topologies, and implementing intelligent systems, ensuring robust electrical connectivity and dynamic compliance in variable operating environments. This review presents the research advances of adaptive conductive systems from the perspective of material innovation, circuit interconnection design, system integration, and applications. Deformable conductors consist of substrates and conductive materials with their independent intrinsic properties and synergistic effects, structural designs and fabrication methods of conductive circuits with specialized stretchable configurations, as well as intelligent systems constructed via signal processing, machine learning, and coherent integration, are systematically summarized and reviewed. Finally, current challenges and future research perspectives of adaptive conductive systems are outlined, offering deep insights into research directions and strategies.</p>","PeriodicalId":117,"journal":{"name":"Advanced Science","volume":"13 58","pages":""},"PeriodicalIF":14.1,"publicationDate":"2026-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13591345/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149011678","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-10-19Epub Date: 2026-09-29DOI: 10.1002/advs.77498
<p>M. Eason, A. Sen, S. Cho, et al. “ Delivery of Pleckstrin-Homology Domains Suppresses PI3K/Akt Signaling and Breast Cancer Metastasis.” Advanced Science 13, no. 30 (2026): e18339, https://doi.org/10.1002/advs.202518339.</p><p>After the publication of the above article, the authors identified the following inadvertent errors, which were introduced during the manual copy-and-paste process used to compile the raw data master Excel files.</p><p><span>Figure 1B</span> The normalized densitometric values for total PI3K p85 relative to the housekeeping protein GAPDH were inadvertently duplicated and used for total Akt in replicates 2 and 3 in the <i>“Rep 2 & Rep 3”</i> worksheet of the “<i>Densitometry Raw Values & Analysis.xlsx”</i> file located in the <i>“Panel 1B”</i> folder deposited in FigShare. These errors have been corrected in the Excel file, with the revised values highlighted in yellow, and in the corresponding “<i>Prism Statistical Analysis.pzfx”</i> file. The corrected Excel and Prism files have been labeled as “Revised”.</p><p>This correction does not affect the statistical outcomes or the conclusions of Figure 1B. Specifically, pAkt T308 remains unchanged and highly significant (****<i>p</i> < 0.0001), pAkt S473 increases in significance from **<i>p</i> < 0.01 to ***<i>p</i> < 0.001, and the total AKT remains unaltered. The pAkt T308, pAkt S473, and total Akt graphs for Figure 1B have been recreated and are shown in comparison to the original ones.</p><p></p><p><span>Figure 2D-F:</span> The measurements in rows 21–24 of the <i>“Myr-oPH-Myc(3)”</i> columns in the “<i>Rep. 2&3, Sp, Vel, Persistence</i>” worksheet of the <i>“Raw Data & Analysis.xlsx</i>” file located in the <i>“Panel 2B-F”</i> folder deposited in FigShare were inadvertently duplicated from rows 17–20. This error has been corrected in the Excel file, with the corresponding cells left empty and highlighted in yellow, and in the associated <i>“Prism Statistical Analysis.pzfx”</i> file. The corrected Excel and Prism files have been labeled as “Revised”.</p><p>This correction does not affect the statistical outcomes for Figure 2D-F, which remain unchanged, or the conclusions of Figure 2. The graphs for Figure 2D-F have been recreated and are shown in comparison to the original ones.</p><p></p><p><span>Figure 8F-G</span> The measurements in rows 10–12 of the <i>“Kalirin”</i> columns in the <i>“Raw Data”</i> worksheet of the <i>“Speed & Velocity Rep 2 Raw Data & Analysis.xlsx”</i> file located in both <i>“Panel 8F”</i> (speed) and <i>“Panel 8G”</i> (velocity) folders deposited in FigShare were inadvertently duplicated from rows 7–9. For ease of access by the readership, the Excel file was deposited in both folders, as the speed and velocity values are calculated from cell tracking data consisting of the x- and y-coordinates and corresponding time points. This error has been corrected in the Excel file, with the corresponding cells left empty and
M. Eason, A. Sen, S. Cho,等。“pleckstrin同源结构域的传递抑制PI3K/Akt信号传导和乳腺癌转移。”高级科学13,第2期。30 (2026): e18339, https://doi.org/10.1002/advs.202518339.After在上述文章发表后,作者发现了以下无意的错误,这些错误是在手工复制和粘贴过程中引入的,用于编译原始数据主Excel文件。图1B总PI3K p85相对于管家蛋白GAPDH的归一化密度值被无意中重复,并用于重复2和3的总Akt,在“密度测定原始值&分析。xlsx”文件的“Rep 2 & Rep 3”工作表中,该文件位于FigShare的“Panel 1B”文件夹中。这些错误已经在Excel文件和相应的“Prism Statistical Analysis”中进行了更正,修改后的值以黄色突出显示。pzfx”文件。修改后的Excel和Prism文件已标注为“已修改”。这一修正并不影响统计结果或图1B的结论。具体而言,pAkt T308保持不变且高度显著(****p < 0.0001), pAkt S473从**p <; 0.01增加到**p <; 0.001, AKT总量保持不变。图1B中的pAkt T308、pAkt S473和总Akt图已被重新创建,并与原始图进行了对比。图2D-F:存放在FigShare中的“Panel 2B-F”文件夹中的“Raw Data & Analysis.xlsx”文件的“Rep. 2&3, Sp, Vel, Persistence”工作表中“myr - ph - myc(3)”列的21-24行测量数据无意中从17-20行复制。此错误已在Excel文件和相关的“Prism Statistical Analysis”中更正,相应的单元格为空并以黄色突出显示。pzfx”文件。修改后的Excel和Prism文件已标注为“已修改”。这种修正不影响图2D-F的统计结果,它保持不变,也不影响图2的结论。图2D-F的图形已经重新创建,并与原始图形进行了比较。图8F- g存放在FigShare中的“Panel 8F”(速度)和“Panel 8G”(速度)文件夹中的“Speed & Velocity Rep 2 Raw Data & Analysis.xlsx”文件的“原始数据”工作表中“Kalirin”列的10-12行测量值无意中从7-9行复制。为了便于读者访问,Excel文件存放在两个文件夹中,因为速度和速度值是根据单元格跟踪数据计算的,包括x坐标和y坐标以及相应的时间点。此错误已在Excel文件中更正,相应的单元格为空并以黄色突出显示。修改后的Excel文件已标注为“已修改”。图8F、G的图形是使用随机选择的数据点生成的。在此随机化过程中,不选择重复的测量值,详见同一Excel文件的“随机化后的数据(19)”工作表。因此,小组F和G不需要修改。总之,这些无意的错误不会影响相关小组和数据的结果,也不会改变整个研究的结论。作者真诚地为这个疏忽道歉。
{"title":"Correction to: “Delivery of Pleckstrin-Homology Domains Suppresses PI3K/Akt Signaling and Breast Cancer Metastasis”","authors":"","doi":"10.1002/advs.77498","DOIUrl":"10.1002/advs.77498","url":null,"abstract":"<p>M. Eason, A. Sen, S. Cho, et al. “ Delivery of Pleckstrin-Homology Domains Suppresses PI3K/Akt Signaling and Breast Cancer Metastasis.” Advanced Science 13, no. 30 (2026): e18339, https://doi.org/10.1002/advs.202518339.</p><p>After the publication of the above article, the authors identified the following inadvertent errors, which were introduced during the manual copy-and-paste process used to compile the raw data master Excel files.</p><p><span>Figure 1B</span> The normalized densitometric values for total PI3K p85 relative to the housekeeping protein GAPDH were inadvertently duplicated and used for total Akt in replicates 2 and 3 in the <i>“Rep 2 & Rep 3”</i> worksheet of the “<i>Densitometry Raw Values & Analysis.xlsx”</i> file located in the <i>“Panel 1B”</i> folder deposited in FigShare. These errors have been corrected in the Excel file, with the revised values highlighted in yellow, and in the corresponding “<i>Prism Statistical Analysis.pzfx”</i> file. The corrected Excel and Prism files have been labeled as “Revised”.</p><p>This correction does not affect the statistical outcomes or the conclusions of Figure 1B. Specifically, pAkt T308 remains unchanged and highly significant (****<i>p</i> < 0.0001), pAkt S473 increases in significance from **<i>p</i> < 0.01 to ***<i>p</i> < 0.001, and the total AKT remains unaltered. The pAkt T308, pAkt S473, and total Akt graphs for Figure 1B have been recreated and are shown in comparison to the original ones.</p><p></p><p><span>Figure 2D-F:</span> The measurements in rows 21–24 of the <i>“Myr-oPH-Myc(3)”</i> columns in the “<i>Rep. 2&3, Sp, Vel, Persistence</i>” worksheet of the <i>“Raw Data & Analysis.xlsx</i>” file located in the <i>“Panel 2B-F”</i> folder deposited in FigShare were inadvertently duplicated from rows 17–20. This error has been corrected in the Excel file, with the corresponding cells left empty and highlighted in yellow, and in the associated <i>“Prism Statistical Analysis.pzfx”</i> file. The corrected Excel and Prism files have been labeled as “Revised”.</p><p>This correction does not affect the statistical outcomes for Figure 2D-F, which remain unchanged, or the conclusions of Figure 2. The graphs for Figure 2D-F have been recreated and are shown in comparison to the original ones.</p><p></p><p><span>Figure 8F-G</span> The measurements in rows 10–12 of the <i>“Kalirin”</i> columns in the <i>“Raw Data”</i> worksheet of the <i>“Speed & Velocity Rep 2 Raw Data & Analysis.xlsx”</i> file located in both <i>“Panel 8F”</i> (speed) and <i>“Panel 8G”</i> (velocity) folders deposited in FigShare were inadvertently duplicated from rows 7–9. For ease of access by the readership, the Excel file was deposited in both folders, as the speed and velocity values are calculated from cell tracking data consisting of the x- and y-coordinates and corresponding time points. This error has been corrected in the Excel file, with the corresponding cells left empty and ","PeriodicalId":117,"journal":{"name":"Advanced Science","volume":"13 58","pages":""},"PeriodicalIF":14.1,"publicationDate":"2026-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13622750/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149079064","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Po-Hsiang Chen, Jia-Hua Wang, Ching Chen, Shih-Hsuan Fu, Rajan Deepan Chakravarthy, Hsin-Chieh Lin
Engineering multifunctional biointerfaces requires quantitative understanding of how buried nanoscale coating architectures govern biological function, yet such relationships remain inaccessible because non-destructive characterization of soft, curved interfaces is lacking. Here, we establish an integrated engineering-characterization-function platform that quantitatively resolves buried nanocoatings and directly correlates their architecture with interfacial performance. Using silicone hydrogel contact lenses as a representative biomedical substrate, robust semi-interpenetrating polymer network (semi-IPN) nanocoatings are fabricated and characterized by gas cluster ion beam X-ray photoelectron spectroscopy (GCIB-XPS), time-of-flight secondary ion mass spectrometry (ToF-SIMS), and a newly developed atomic force microscopy (AFM) modulus-based algorithm. This multimodal framework non-destructively maps vertical chemical gradients, nanometer-scale layer thicknesses, and interfacial mechanical distributions with sub-100 nm precision, enabling quantitative visualization of conformal buried nanocoatings. The resulting structure-function relationships guide the rational engineering of poly(2-hydroxyethyl methacrylate) (poly(HEMA)) interfaces with homogeneous surface coverage (∼89%), enhanced wettability, markedly reduced protein adsorption and cellular fouling, while fully preserving oxygen permeability, optical transparency, UV protection, and mechanical integrity. The platform further enables incorporation of functional monomers for light-triggered therapeutic release without compromising device performance. Beyond contact lenses, this work provides a generalizable strategy for quantitatively engineering and predicting multifunctional nanocoatings across diverse biomedical interfaces.
{"title":"Nanoscale Buried Interface Control in Silicone Hydrogels Enables a Biointerface Engineering Platform.","authors":"Po-Hsiang Chen, Jia-Hua Wang, Ching Chen, Shih-Hsuan Fu, Rajan Deepan Chakravarthy, Hsin-Chieh Lin","doi":"10.1002/advs.78148","DOIUrl":"https://doi.org/10.1002/advs.78148","url":null,"abstract":"<p><p>Engineering multifunctional biointerfaces requires quantitative understanding of how buried nanoscale coating architectures govern biological function, yet such relationships remain inaccessible because non-destructive characterization of soft, curved interfaces is lacking. Here, we establish an integrated engineering-characterization-function platform that quantitatively resolves buried nanocoatings and directly correlates their architecture with interfacial performance. Using silicone hydrogel contact lenses as a representative biomedical substrate, robust semi-interpenetrating polymer network (semi-IPN) nanocoatings are fabricated and characterized by gas cluster ion beam X-ray photoelectron spectroscopy (GCIB-XPS), time-of-flight secondary ion mass spectrometry (ToF-SIMS), and a newly developed atomic force microscopy (AFM) modulus-based algorithm. This multimodal framework non-destructively maps vertical chemical gradients, nanometer-scale layer thicknesses, and interfacial mechanical distributions with sub-100 nm precision, enabling quantitative visualization of conformal buried nanocoatings. The resulting structure-function relationships guide the rational engineering of poly(2-hydroxyethyl methacrylate) (poly(HEMA)) interfaces with homogeneous surface coverage (∼89%), enhanced wettability, markedly reduced protein adsorption and cellular fouling, while fully preserving oxygen permeability, optical transparency, UV protection, and mechanical integrity. The platform further enables incorporation of functional monomers for light-triggered therapeutic release without compromising device performance. Beyond contact lenses, this work provides a generalizable strategy for quantitatively engineering and predicting multifunctional nanocoatings across diverse biomedical interfaces.</p>","PeriodicalId":117,"journal":{"name":"Advanced Science","volume":" ","pages":"e78148"},"PeriodicalIF":14.1,"publicationDate":"2026-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149222869","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-10-19Epub Date: 2026-08-31DOI: 10.1002/advs.77424
Guoqing Xiang, Zhicheng Zhou, Xue Jiang, Zhenguang Du, Yangyang Zhan, Xinli Liu
Metabolic reprogramming and immune evasion are two key mechanisms that facilitate tumor progression. Tumor cells achieve their energy requirements for rapid proliferation through metabolic reprogramming, such as glucose metabolism, lipid metabolism, and amino acid metabolism. Tumor cell metabolic reprogramming can influence immune cell function in the tumor microenvironment through various mechanisms, ultimately facilitating tumor immune escape. Targeting tumor cell metabolism and combining metabolic regulation with immunotherapy can enhance anti-tumor immune cells, inhibit the function of immunosuppressive cells, improve anti-tumor therapy, and overcome immune escape. This review elucidates the regulatory mechanisms by which glucose, lipids, amino acid metabolism, nucleotide metabolism, oxidative phosphorylation, lactate, and hypoxia modulate the proliferation, differentiation, and function of anti-tumor immune cells and immunosuppressive cells. Regulatory strategies to restore the anti-tumor function of immune cells in response to metabolic changes were discussed. These strategies are expected to improve the effect of immunotherapy and are used in combination with other treatments to provide new ideas for cancer management.
{"title":"The Cancer Cell Metabolic Reprogramming Remodels the Tumor Microenvironment: Molecular Mechanisms and Therapeutic Strategies","authors":"Guoqing Xiang, Zhicheng Zhou, Xue Jiang, Zhenguang Du, Yangyang Zhan, Xinli Liu","doi":"10.1002/advs.77424","DOIUrl":"10.1002/advs.77424","url":null,"abstract":"<p>Metabolic reprogramming and immune evasion are two key mechanisms that facilitate tumor progression. Tumor cells achieve their energy requirements for rapid proliferation through metabolic reprogramming, such as glucose metabolism, lipid metabolism, and amino acid metabolism. Tumor cell metabolic reprogramming can influence immune cell function in the tumor microenvironment through various mechanisms, ultimately facilitating tumor immune escape. Targeting tumor cell metabolism and combining metabolic regulation with immunotherapy can enhance anti-tumor immune cells, inhibit the function of immunosuppressive cells, improve anti-tumor therapy, and overcome immune escape. This review elucidates the regulatory mechanisms by which glucose, lipids, amino acid metabolism, nucleotide metabolism, oxidative phosphorylation, lactate, and hypoxia modulate the proliferation, differentiation, and function of anti-tumor immune cells and immunosuppressive cells. Regulatory strategies to restore the anti-tumor function of immune cells in response to metabolic changes were discussed. These strategies are expected to improve the effect of immunotherapy and are used in combination with other treatments to provide new ideas for cancer management.</p>","PeriodicalId":117,"journal":{"name":"Advanced Science","volume":"13 58","pages":""},"PeriodicalIF":14.1,"publicationDate":"2026-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13528182/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148862692","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-10-19Epub Date: 2026-09-08DOI: 10.1002/advs.77675
Ke Liu, Xiyan Wang, Xiaozhen Liu, Chaoqi He, Da Qian, Xuli Meng, Liquan Zhu
Lysosome-targeting chimeras (LYTACs) have emerged as a strategy for eliminating secreted, extracellular, and plasma-membrane proteins by redirecting them to the endolysosomal system. By coupling target recognition to receptor-mediated uptake, LYTACs exploit endogenous trafficking pathways to access disease-associated proteins beyond the reach of conventional intracellular degradation mechanisms. Related target-intrinsic and cross-linking-driven strategies can likewise promote lysosomal target delivery without recruiting a separate clearance receptor. However, target internalization alone does not establish productive degradation. Following entry, target-containing complexes encounter a competitive endosomal network in which they may recycle, undergo retrograde transport or transcytosis, remain in non-degradative compartments, or proceed to lysosomes. Here, we present a routing-centered framework for understanding and designing extracellular and membrane-protein degradation. We discuss how target biology, receptor choice, tissue distribution, ligand competition, signaling liability, molecular architecture, and intracellular sorting shape degrader performance. We also outline evidence standards for distinguishing bona fide lysosome-dependent target loss from surface depletion, redistribution, epitope masking, shedding, secretion blockade, transcriptional effects, and nonspecific toxicity. Together, these principles define the transition from receptor hijacking to programmable endolysosomal routing.
{"title":"Targeted Lysosomal Degradation of Extracellular and Membrane Proteins: From Receptor Hijacking to Programmable Endolysosomal Routing","authors":"Ke Liu, Xiyan Wang, Xiaozhen Liu, Chaoqi He, Da Qian, Xuli Meng, Liquan Zhu","doi":"10.1002/advs.77675","DOIUrl":"10.1002/advs.77675","url":null,"abstract":"<p>Lysosome-targeting chimeras (LYTACs) have emerged as a strategy for eliminating secreted, extracellular, and plasma-membrane proteins by redirecting them to the endolysosomal system. By coupling target recognition to receptor-mediated uptake, LYTACs exploit endogenous trafficking pathways to access disease-associated proteins beyond the reach of conventional intracellular degradation mechanisms. Related target-intrinsic and cross-linking-driven strategies can likewise promote lysosomal target delivery without recruiting a separate clearance receptor. However, target internalization alone does not establish productive degradation. Following entry, target-containing complexes encounter a competitive endosomal network in which they may recycle, undergo retrograde transport or transcytosis, remain in non-degradative compartments, or proceed to lysosomes. Here, we present a routing-centered framework for understanding and designing extracellular and membrane-protein degradation. We discuss how target biology, receptor choice, tissue distribution, ligand competition, signaling liability, molecular architecture, and intracellular sorting shape degrader performance. We also outline evidence standards for distinguishing bona fide lysosome-dependent target loss from surface depletion, redistribution, epitope masking, shedding, secretion blockade, transcriptional effects, and nonspecific toxicity. Together, these principles define the transition from receptor hijacking to programmable endolysosomal routing.</p>","PeriodicalId":117,"journal":{"name":"Advanced Science","volume":"13 58","pages":""},"PeriodicalIF":14.1,"publicationDate":"2026-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13554502/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148910107","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-10-19Epub Date: 2026-09-27DOI: 10.1002/advs.77853
Amirbahador Zeynali, Mangirdas Malinauskas, Giuseppe Chirico
Multiphoton absorption enables three-dimensional fabrication of photoresists ranging from ceramics to hydrogels and has recently been extended to the writing of microstructures within the dermis, muscle, and brain of living animals. However, an intrinsic difficulty prevents its widespread application in vivo. Absorption, cure kinetics, heat accumulation, and matrix stiffness each vary steeply across neighboring micro-environments and across intervals spanning a single pulse to several minutes. Therefore, any pre-selected exposure drifts out of the safe and effective window as fabrication proceeds. Rigorous feedback control should ideally act simultaneously at three scales: between pulses to bound heating (microseconds), within each voxel to confirm cure and stiffness (milliseconds), and across the finished volume to verify geometry (seconds). Phase-resolved optical coherence tomography and luminescent thermometry already satisfy these demands, with photoacoustic, Brillouin, and diamond-defect techniques reaching further into depth, contrast, and sensitivity. We analyze critically how this technology supports predictive controllers at the three scales that learn tissue behavior on the fly, turning these readings into adaptive feedforward with supervisory feedback. We synthesize this toolkit into a single perspective toward adaptive intravital light interventions.
{"title":"Closing the Loop: High-Precision 3D Photofabrication in Living Tissues","authors":"Amirbahador Zeynali, Mangirdas Malinauskas, Giuseppe Chirico","doi":"10.1002/advs.77853","DOIUrl":"10.1002/advs.77853","url":null,"abstract":"<p>Multiphoton absorption enables three-dimensional fabrication of photoresists ranging from ceramics to hydrogels and has recently been extended to the writing of microstructures within the dermis, muscle, and brain of living animals. However, an intrinsic difficulty prevents its widespread application in vivo. Absorption, cure kinetics, heat accumulation, and matrix stiffness each vary steeply across neighboring micro-environments and across intervals spanning a single pulse to several minutes. Therefore, any pre-selected exposure drifts out of the safe and effective window as fabrication proceeds. Rigorous feedback control should ideally act simultaneously at three scales: between pulses to bound heating (microseconds), within each voxel to confirm cure and stiffness (milliseconds), and across the finished volume to verify geometry (seconds). Phase-resolved optical coherence tomography and luminescent thermometry already satisfy these demands, with photoacoustic, Brillouin, and diamond-defect techniques reaching further into depth, contrast, and sensitivity. We analyze critically how this technology supports predictive controllers at the three scales that learn tissue behavior on the fly, turning these readings into adaptive feedforward with supervisory feedback. We synthesize this toolkit into a single perspective toward adaptive intravital light interventions.</p>","PeriodicalId":117,"journal":{"name":"Advanced Science","volume":"13 58","pages":""},"PeriodicalIF":14.1,"publicationDate":"2026-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13616337/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149068654","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Inspired by ancient Chinese bamboo slips, this cover presents a reconfigurable conformal metasurface assembled from rigid planar subarrays resembling bamboo slips, enabling arbitrary developable curved surfaces and flexible manipulation of electromagnetic waves. More details can be found in the Research Article by Qifan Li, Long Li, and co-workers (DOI: 10.1002/advs.77188).