Pub Date : 2026-02-01Epub Date: 2025-04-16DOI: 10.1016/j.eng.2025.04.006
Wei Wang
{"title":"Can DNA Be Glycosylated?","authors":"Wei Wang","doi":"10.1016/j.eng.2025.04.006","DOIUrl":"10.1016/j.eng.2025.04.006","url":null,"abstract":"","PeriodicalId":11783,"journal":{"name":"Engineering","volume":"57 ","pages":"Pages 6-9"},"PeriodicalIF":11.6,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147386702","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-01Epub Date: 2025-12-18DOI: 10.1016/j.eng.2025.12.007
Demin Zhou , Dezhong Ji , Jiandong Jiang
{"title":"From Flu to Therapy: Development of Influenza Viruses as Platforms for Combating Infections and Cancer","authors":"Demin Zhou , Dezhong Ji , Jiandong Jiang","doi":"10.1016/j.eng.2025.12.007","DOIUrl":"10.1016/j.eng.2025.12.007","url":null,"abstract":"","PeriodicalId":11783,"journal":{"name":"Engineering","volume":"57 ","pages":"Pages 16-17"},"PeriodicalIF":11.6,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145785553","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-01Epub Date: 2025-07-01DOI: 10.1016/j.eng.2025.04.027
Renkuan Zhai , Zhangqi Pan , Yuanshi Kou , Chuang Yang , Yang Ruan , Chenli Xu , Linjie He , Jianfeng Zang
Magnetic resonance imaging (MRI) systems, outfitted with internal gradient coils capable of manipulating magnetic gradients in three-dimensional (3D) space, offer an intriguing platform for the navigation of medical magnetic robots. These robots offer considerable promise for applications in minimally invasive therapy, targeted drug delivery, and theranostic interventions. However, an MRI-driven robot presents a challenging contradiction between real-time control and image resolution, resulting in suboptimal tracking accuracy—attributed to the inefficiency of conventional signal acquisition and the presence of metal artifacts. In this paper, we report a multi-frequency excitation sequence with dual-echo (MFDE) that reduces the repetition time (TR) to 30 ms, allowing the precise tracking of magnetic particles (relative error < 1%) without artifacts. The duty cycle of the driving gradient is as high as 77%, and perturbations from the imaging gradients are eliminated. Expanding on these foundations, we adapted our technique to 3D operations. We established an integrated platform for imaging and motion control by creating a three-view window and developing a control joystick to be used in conjunction with the platform. Demonstrations of navigation in a maze, in a phantom vessel, and in vivo animal trials validate its feasibility and effectiveness, providing a significant advancement in the field of MRI-guided magnetic robot control.
{"title":"Multi-Frequency Dual-Echo Magnetic Resonance Imaging for Real-Time and Artifact-Free Magnetic Robot Navigation","authors":"Renkuan Zhai , Zhangqi Pan , Yuanshi Kou , Chuang Yang , Yang Ruan , Chenli Xu , Linjie He , Jianfeng Zang","doi":"10.1016/j.eng.2025.04.027","DOIUrl":"10.1016/j.eng.2025.04.027","url":null,"abstract":"<div><div>Magnetic resonance imaging (MRI) systems, outfitted with internal gradient coils capable of manipulating magnetic gradients in three-dimensional (3D) space, offer an intriguing platform for the navigation of medical magnetic robots. These robots offer considerable promise for applications in minimally invasive therapy, targeted drug delivery, and theranostic interventions. However, an MRI-driven robot presents a challenging contradiction between real-time control and image resolution, resulting in suboptimal tracking accuracy—attributed to the inefficiency of conventional signal acquisition and the presence of metal artifacts. In this paper, we report a multi-frequency excitation sequence with dual-echo (MFDE) that reduces the repetition time (TR) to 30 ms, allowing the precise tracking of magnetic particles (relative error < 1%) without artifacts. The duty cycle of the driving gradient is as high as 77%, and perturbations from the imaging gradients are eliminated. Expanding on these foundations, we adapted our technique to 3D operations. We established an integrated platform for imaging and motion control by creating a three-view window and developing a control joystick to be used in conjunction with the platform. Demonstrations of navigation in a maze, in a phantom vessel, and <em>in vivo</em> animal trials validate its feasibility and effectiveness, providing a significant advancement in the field of MRI-guided magnetic robot control.</div></div>","PeriodicalId":11783,"journal":{"name":"Engineering","volume":"57 ","pages":"Pages 189-199"},"PeriodicalIF":11.6,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144534026","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-01Epub Date: 2025-07-26DOI: 10.1016/j.eng.2025.07.023
Hongwei Sun , Ning Xing , Jiayu Zou , Yuqi Rong , Yang Shi , Han Ding , Hai-Tao Zhang
This study establishes a high-speed nano-positioning stage composed of a symmetrically driven structure with multiple parallel-bonded thin piezoelectric ceramic layers capable of performing micro- or nano-scale manipulations. Accordingly, a neural-network-based switching output regulation controller (NN-SORC) was developed to compensate for the associated hysteresis nonlinearity. To address the challenges of slow floating-point computation speeds and low compilation efficiency, a closed-loop control system with a field-programmable gate array–central processing unit (FPGA–CPU) dual-layer data-processing framework was developed. A feedback linearization method was designed to linearize the hysteresis nonlinearity of the framework, resulting in a switching-tracking error system. With the assistance of Lyapunov theory and an average dwell time technique, sufficient conditions were derived to ensure the asymptotic stability of the NN-SORC governing closed-loop system using the switching reference signals often encountered in realistic micro-/nano-scale detection and manufacturing processes. Finally, extensive comparative experiments were conducted to verify the effectiveness and superiority of the proposed NN-SORC scheme.
{"title":"Neural Network-Based Switching Output Regulation Control for High-Speed Nano-Positioning Stages","authors":"Hongwei Sun , Ning Xing , Jiayu Zou , Yuqi Rong , Yang Shi , Han Ding , Hai-Tao Zhang","doi":"10.1016/j.eng.2025.07.023","DOIUrl":"10.1016/j.eng.2025.07.023","url":null,"abstract":"<div><div>This study establishes a high-speed nano-positioning stage composed of a symmetrically driven structure with multiple parallel-bonded thin piezoelectric ceramic layers capable of performing micro- or nano-scale manipulations. Accordingly, a neural-network-based switching output regulation controller (NN-SORC) was developed to compensate for the associated hysteresis nonlinearity. To address the challenges of slow floating-point computation speeds and low compilation efficiency, a closed-loop control system with a field-programmable gate array–central processing unit (FPGA–CPU) dual-layer data-processing framework was developed. A feedback linearization method was designed to linearize the hysteresis nonlinearity of the framework, resulting in a switching-tracking error system. With the assistance of Lyapunov theory and an average dwell time technique, sufficient conditions were derived to ensure the asymptotic stability of the NN-SORC governing closed-loop system using the switching reference signals often encountered in realistic micro-/nano-scale detection and manufacturing processes. Finally, extensive comparative experiments were conducted to verify the effectiveness and superiority of the proposed NN-SORC scheme.</div></div>","PeriodicalId":11783,"journal":{"name":"Engineering","volume":"57 ","pages":"Pages 227-235"},"PeriodicalIF":11.6,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144712212","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-01Epub Date: 2025-10-30DOI: 10.1016/j.eng.2025.10.018
Peter E.D. Love , Jane Matthews , Weili Fang
Action errors—unintentional deviations from goals, rules, or standards—are an inevitable part of work in construction. Understanding how individuals and organizations can embrace and “learn through errors” (i.e., how to handle them effectively) is crucial for contributing to project success. However, within construction, a prevailing belief persists that errors can and should be eliminated, fostering a zero-tolerance mindset. Organizations that adopt this mindset risk stifling their capacity to learn, innovate, and improve profitability. While errors can indeed have negative consequences, they also play a vital role in enabling learning and innovation. Given the limited empirical research on action errors in construction, this paper aims to stimulate inquiry into this promising area of study. It briefly outlines different forms of error orientation and proposes directions for future research relevant to construction organizations. The contributions of this paper are twofold, as it: ① advocates for construction organizations to broaden their understanding of errors to enhance their learning capability and ② identifies ways in which organizations can improve their capacity to learn and innovate through error management.
{"title":"Moving Beyond a Zero Tolerance Mindset: Embracing Action Errors in Construction","authors":"Peter E.D. Love , Jane Matthews , Weili Fang","doi":"10.1016/j.eng.2025.10.018","DOIUrl":"10.1016/j.eng.2025.10.018","url":null,"abstract":"<div><div>Action errors—unintentional deviations from goals, rules, or standards—are an inevitable part of work in construction. Understanding how individuals and organizations can embrace and “learn through errors” (i.e., how to handle them effectively) is crucial for contributing to project success. However, within construction, a prevailing belief persists that errors can and should be eliminated, fostering a zero-tolerance mindset. Organizations that adopt this mindset risk stifling their capacity to learn, innovate, and improve profitability. While errors can indeed have negative consequences, they also play a vital role in enabling learning and innovation. Given the limited empirical research on action errors in construction, this paper aims to stimulate inquiry into this promising area of study. It briefly outlines different forms of error orientation and proposes directions for future research relevant to construction organizations. The contributions of this paper are twofold, as it: ① advocates for construction organizations to broaden their understanding of errors to enhance their learning capability and ② identifies ways in which organizations can improve their capacity to learn and innovate through error management.</div></div>","PeriodicalId":11783,"journal":{"name":"Engineering","volume":"57 ","pages":"Pages 159-164"},"PeriodicalIF":11.6,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145383370","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Immunoglobulin G (IgG) N-glycans are associated with aging. In this study, we introduce a novel strategy for discovering aging-associated IgG glycans and establish a prediction model on the basis of their absolute concentration alterations. We employed glycomic quantification technology to identify alterations in the amount of IgG glycan in natural aging and antiaging (caloric restriction (CR)) models and discovered aging-related glycans. The glycomic analysis revealed key features: downregulation of the bisected glycan GP3 (F(6)A2B) and upregulation of the digalactosylated glycan GP8 (F(6)A2G2). These glycan changes showed significant fold changes from an early stage. Using external standards of these two glycans, we subsequently measured their absolute concentrations, allowing for us to establish a predictive model, abGlycoAge, for biological aging. The abGlycoAge index suggested a younger state under CR, with an average age reduction of 3.9–14.0 weeks. Additionally, RNA sequencing of splenic B cells revealed that Derl3, Smarcb1, Ankrd55, Tbkbp1, and Slc38a10 may contribute to alterations in GP3 and GP8 during the aging process. In a preliminary therapeutic study, we tested IgG modified with young signature N-glycans (IgG-Ny). High-dose IgG-Ny showed promising results, alleviating aging-related physiological declines, including reductions in inflammatory markers and improvements in organ senescence, particularly in the brain, kidney, and lungs. This research provides new insights into glycan changes during aging and lays the groundwork for potential antiaging therapies. GP3 and GP8 may serve as biomarkers for aging, offering new perspectives on aging mechanisms and therapeutic approaches.
{"title":"Absolute Quantification of Aging-Associated Glycans in IgG for Biological Age Prediction: Insights from Glycomics and Transcriptomics","authors":"Huijuan Zhao , Jiteng Fan , Jing Han, Wenjun Qin, Jichen Sha, Weilong Zhang, Yong Gu, Xiaonan Ma, Jianxin Gu, Shifang Ren","doi":"10.1016/j.eng.2025.07.042","DOIUrl":"10.1016/j.eng.2025.07.042","url":null,"abstract":"<div><div>Immunoglobulin G (IgG) <em>N</em>-glycans are associated with aging. In this study, we introduce a novel strategy for discovering aging-associated IgG glycans and establish a prediction model on the basis of their absolute concentration alterations. We employed glycomic quantification technology to identify alterations in the amount of IgG glycan in natural aging and antiaging (caloric restriction (CR)) models and discovered aging-related glycans. The glycomic analysis revealed key features: downregulation of the bisected glycan GP3 (F(6)A2B) and upregulation of the digalactosylated glycan GP8 (F(6)A2G2). These glycan changes showed significant fold changes from an early stage. Using external standards of these two glycans, we subsequently measured their absolute concentrations, allowing for us to establish a predictive model, abGlycoAge, for biological aging. The abGlycoAge index suggested a younger state under CR, with an average age reduction of 3.9–14.0 weeks. Additionally, RNA sequencing of splenic B cells revealed that <em>Derl3</em>, <em>Smarcb1</em>, <em>Ankrd55</em>, <em>Tbkbp1</em>, and <em>Slc38a10</em> may contribute to alterations in GP3 and GP8 during the aging process. In a preliminary therapeutic study, we tested IgG modified with young signature <em>N</em>-glycans (IgG-Ny). High-dose IgG-Ny showed promising results, alleviating aging-related physiological declines, including reductions in inflammatory markers and improvements in organ senescence, particularly in the brain, kidney, and lungs. This research provides new insights into glycan changes during aging and lays the groundwork for potential antiaging therapies. GP3 and GP8 may serve as biomarkers for aging, offering new perspectives on aging mechanisms and therapeutic approaches.</div></div>","PeriodicalId":11783,"journal":{"name":"Engineering","volume":"57 ","pages":"Pages 113-125"},"PeriodicalIF":11.6,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144906014","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-01Epub Date: 2025-03-07DOI: 10.1016/j.eng.2025.02.016
Kangkang Yang , Xueying Li , Minchao Lai , Weiwei Zhao , Wanli Song , Shaobin Chen , Wenzhe Li
Recent studies indicate the involvement of glycosylation in the pathogenesis of Alzheimer’s disease (AD). α2,6-Sialylation, catalyzed by α2,6-sialyltransferase-I (ST6Gal-I), corresponds to the development of the infant brain and nervous system, however the mechanism of aberrant α2,6-sialylation affects multiple physiological and pathological conditions remains unclear. The present study, in vitro and in vivo, showed that expression of ST6Gal-I and α2,6-sialylation levels were up-regulated in cerebrospinal fluid and sera of AD patients. In addition, levels of α2,6-sialylation were also increased in brain and sera of AD model mice. Furthermore, deletion of ST6Gal-I reduced β-site amyloid precursor protein cleaving enzyme 1 (BACE1) levels and alleviated the impairment of learning and memory induced by scopolamine in rats. BACE1, a hyper-sialylated protein, plays a critical role in amyloid-β42 (Aβ42) production. ST6Gal-I knockdown in Neuro-2a neuroblastoma cells (ST6Gal-I-KD-N2a) reduced the expression of BACE1 via promoting its ubiquitination. Deletion of ST6Gal-I suppressed amyloid precursor protein (APP) cleaved by BACE1, followed by a decrease in Aβ42 production, while alleviated Aβ42-induced apoptosis. This study first reveals a significant role of α2,6-sialylation in development and progression of AD, suggesting that ST6Gal-I is a novel glycan therapeutic target for AD diagnosis and treatment.
{"title":"Ablation of ST6Gal-I Downregulates BACE1 Expression and Suppresses Production of Aβ42 Plaques in Alzheimer’s Disease","authors":"Kangkang Yang , Xueying Li , Minchao Lai , Weiwei Zhao , Wanli Song , Shaobin Chen , Wenzhe Li","doi":"10.1016/j.eng.2025.02.016","DOIUrl":"10.1016/j.eng.2025.02.016","url":null,"abstract":"<div><div>Recent studies indicate the involvement of glycosylation in the pathogenesis of Alzheimer’s disease (AD). α2,6-Sialylation, catalyzed by α2,6-sialyltransferase-I (ST6Gal-I), corresponds to the development of the infant brain and nervous system, however the mechanism of aberrant α2,6-sialylation affects multiple physiological and pathological conditions remains unclear. The present study, <em>in vitro</em> and <em>in vivo</em>, showed that expression of ST6Gal-I and α2,6-sialylation levels were up-regulated in cerebrospinal fluid and sera of AD patients. In addition, levels of α2,6-sialylation were also increased in brain and sera of AD model mice. Furthermore, deletion of <em>ST6Gal-I</em> reduced β-site amyloid precursor protein cleaving enzyme 1 (BACE1) levels and alleviated the impairment of learning and memory induced by scopolamine in rats. BACE1, a hyper-sialylated protein, plays a critical role in amyloid-β<sub>42</sub> (Aβ<sub>42</sub>) production. <em>ST6Gal-I</em> knockdown in Neuro-2a neuroblastoma cells (<em>ST6Gal-I</em>-KD-N2a) reduced the expression of BACE1 via promoting its ubiquitination. Deletion of <em>ST6Gal-I</em> suppressed amyloid precursor protein (APP) cleaved by BACE1, followed by a decrease in Aβ<sub>42</sub> production, while alleviated Aβ<sub>42</sub>-induced apoptosis. This study first reveals a significant role of α2,6-sialylation in development and progression of AD, suggesting that ST6Gal-I is a novel glycan therapeutic target for AD diagnosis and treatment.</div></div>","PeriodicalId":11783,"journal":{"name":"Engineering","volume":"57 ","pages":"Pages 58-71"},"PeriodicalIF":11.6,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147386555","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}