Wearable biosensors have the potential to revolutionize health monitoring, yet reliable, time‐resolved hormone and cytokine tracking remains elusive. This study introduces a dual‐framework approach to enable circadian and immune profiling through perspired sweat sensing. First, sweat–saliva thresholds were calibrated for cortisol, melatonin, interleukin‐6 and tumor necrosis factor‐alpha, achieving significant classification performance (Area Under the Curve >0.80) for physiologically relevant salivary benchmarks. Second, circadian rhythmicity of each biomarker was modeled using circaCompare, revealing distinct oscillatory patterns stratified by age, gender, and stress. Young adults exhibited robust melatonin–cortisol phase separation and rhythmic immune signals. Older participants showed dampened amplitudes, phase shifts, and inflammatory dominance. Notably, stress exposure induced earlier cortisol peaks (Δ ≈ 6.7 h), suppressed melatonin rhythms, and heightened immune amplitude variability—hallmarks of circadian misalignment. These findings establish sweat as a valid, real‐time medium for capturing endocrine and immune cycles, with analytical tools capable of uncovering early physiological strain. This work lays a foundation for personalized chronobiological monitoring and stress‐risk screening in naturalistic settings.
{"title":"A wearable biosensing platform for continuous monitoring of inflammatory and metabolic biomarkers for real‐time health tracking and personalized care","authors":"Annapoorna Ramasubramanya, Preeti Singh, Akash Kumar, Kai‐Chun Lin, Shalini Prasad, Sriram Muthukumar","doi":"10.1002/btm2.70104","DOIUrl":"https://doi.org/10.1002/btm2.70104","url":null,"abstract":"Wearable biosensors have the potential to revolutionize health monitoring, yet reliable, time‐resolved hormone and cytokine tracking remains elusive. This study introduces a dual‐framework approach to enable circadian and immune profiling through perspired sweat sensing. First, sweat–saliva thresholds were calibrated for cortisol, melatonin, interleukin‐6 and tumor necrosis factor‐alpha, achieving significant classification performance (Area Under the Curve >0.80) for physiologically relevant salivary benchmarks. Second, circadian rhythmicity of each biomarker was modeled using circaCompare, revealing distinct oscillatory patterns stratified by age, gender, and stress. Young adults exhibited robust melatonin–cortisol phase separation and rhythmic immune signals. Older participants showed dampened amplitudes, phase shifts, and inflammatory dominance. Notably, stress exposure induced earlier cortisol peaks (Δ ≈ 6.7 h), suppressed melatonin rhythms, and heightened immune amplitude variability—hallmarks of circadian misalignment. These findings establish sweat as a valid, real‐time medium for capturing endocrine and immune cycles, with analytical tools capable of uncovering early physiological strain. This work lays a foundation for personalized chronobiological monitoring and stress‐risk screening in naturalistic settings.","PeriodicalId":9263,"journal":{"name":"Bioengineering & Translational Medicine","volume":"47 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145993215","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Osteoarthritis (OA) is a degenerative joint disease characterized by cartilage degradation, subchondral bone remodeling, and joint microenvironment imbalance. Emerging evidence identifies pathological osteoclast–chondrocyte crosstalk as a key OA driver, mediated through RANKL/RANK/OPG, NF‐κB, HIF‐2α, and VEGF signaling pathways that create a destructive bone–cartilage feedback loop. This review examines: (1) molecular mechanisms underlying this cellular communication, (2) therapeutic small‐molecule inhibitors targeting CatK, MMP‐13, NFATc1, and Runx2, and (3) innovative nanomedicine approaches including tissue‐specific nanoparticles, smart delivery systems, and combination therapies. We evaluate these strategies' preclinical validation in animal and organoid models while addressing translational challenges in biosafety, tissue targeting, and personalized delivery. By integrating intercellular signaling knowledge with advanced therapeutic technologies, we provide a framework for developing disease‐modifying OA treatments that bridges basic research with clinical precision medicine applications.
{"title":"Bridging the gap in OA therapeutics: Bioengineered strategies to target osteoclast–chondrocyte crosstalk","authors":"Enbo Zhang, Chi Ma, Xiaohe Fan, Bowen Gu, Bo Li","doi":"10.1002/btm2.70107","DOIUrl":"https://doi.org/10.1002/btm2.70107","url":null,"abstract":"Osteoarthritis (OA) is a degenerative joint disease characterized by cartilage degradation, subchondral bone remodeling, and joint microenvironment imbalance. Emerging evidence identifies pathological osteoclast–chondrocyte crosstalk as a key OA driver, mediated through RANKL/RANK/OPG, NF‐κB, HIF‐2α, and VEGF signaling pathways that create a destructive bone–cartilage feedback loop. This review examines: (1) molecular mechanisms underlying this cellular communication, (2) therapeutic small‐molecule inhibitors targeting CatK, MMP‐13, NFATc1, and Runx2, and (3) innovative nanomedicine approaches including tissue‐specific nanoparticles, smart delivery systems, and combination therapies. We evaluate these strategies' preclinical validation in animal and organoid models while addressing translational challenges in biosafety, tissue targeting, and personalized delivery. By integrating intercellular signaling knowledge with advanced therapeutic technologies, we provide a framework for developing disease‐modifying OA treatments that bridges basic research with clinical precision medicine applications.","PeriodicalId":9263,"journal":{"name":"Bioengineering & Translational Medicine","volume":"38 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145955091","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Joseph R. Vallin, Brandon J. Burbach, Qi Shao, Fang Zhou, Jacob S. Ankeny, Alessio Giubellino, Yoji Shimizu, Samira M. Azarin
Irreversible electroporation (IRE) is a focal ablative cancer therapy that destroys cells through membrane destabilization via pulsed electric fields. It also has the capacity to induce a systemic, anti‐tumor immune response, thus acting as an in situ vaccine. Although many studies characterize the immunogenicity of focal therapies by their released biochemical constituents, here we show that the biophysical context of the presentation of these immunogenic signals is vital to understanding downstream immune functions. Compared to thermal ablation or cryoablation, IRE generates similar numbers of exosome‐like particles (ELP, 50–200 nm) but significantly greater numbers of microparticles (MP, 200–1000 nm) and large debris particles (LDP, 2–6 μm) in both melanoma and pancreatic cancer cell lines. We show that LDPs contain antigen and tumor‐associated DNA, which dendritic cells (DCs) internalize in greater proportions from IRE‐treated cells compared to other treatments. For the submicron particles, we demonstrate both in vitro and in vivo that MPs induce greater T‐cell proliferation and differentiation compared to ELPs on a per‐particle basis. This novel biophysical analysis of the immunogenicity of IRE‐treated cancer cells opens a new avenue toward improving the systemic immune response to focal ablation‐based cancer immunotherapies via increasing cell fragmentation and particle generation.
{"title":"Cellular fragmentation underlies the immunogenicity of irreversible electroporation‐mediated tumor cell killing","authors":"Joseph R. Vallin, Brandon J. Burbach, Qi Shao, Fang Zhou, Jacob S. Ankeny, Alessio Giubellino, Yoji Shimizu, Samira M. Azarin","doi":"10.1002/btm2.70102","DOIUrl":"https://doi.org/10.1002/btm2.70102","url":null,"abstract":"Irreversible electroporation (IRE) is a focal ablative cancer therapy that destroys cells through membrane destabilization via pulsed electric fields. It also has the capacity to induce a systemic, anti‐tumor immune response, thus acting as an in situ vaccine. Although many studies characterize the immunogenicity of focal therapies by their released biochemical constituents, here we show that the biophysical context of the presentation of these immunogenic signals is vital to understanding downstream immune functions. Compared to thermal ablation or cryoablation, IRE generates similar numbers of exosome‐like particles (ELP, 50–200 nm) but significantly greater numbers of microparticles (MP, 200–1000 nm) and large debris particles (LDP, 2–6 μm) in both melanoma and pancreatic cancer cell lines. We show that LDPs contain antigen and tumor‐associated DNA, which dendritic cells (DCs) internalize in greater proportions from IRE‐treated cells compared to other treatments. For the submicron particles, we demonstrate both in vitro and in vivo that MPs induce greater T‐cell proliferation and differentiation compared to ELPs on a per‐particle basis. This novel biophysical analysis of the immunogenicity of IRE‐treated cancer cells opens a new avenue toward improving the systemic immune response to focal ablation‐based cancer immunotherapies via increasing cell fragmentation and particle generation.","PeriodicalId":9263,"journal":{"name":"Bioengineering & Translational Medicine","volume":"23 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145807471","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ronald H. Heisser, Angel Bu, Laura Schwendeman, Tamara Rossy, Pavankumar Umashankar, Vincent Butty, Ritu Raman
Exercise promotes human mobility by tuning the function of skeletal muscle, and recent studies highlight exercise's broader impacts on human health via muscle's paracrine and endocrine roles beyond force generation. In vitro models of tissue engineered skeletal muscle enable precise investigation of adaptation to exercise, with emerging approaches for optogenetic muscle stimulation providing a less invasive alternative to traditional techniques for electrical stimulation. In this study, we present a high‐throughput muscle culture and optical exercise protocol for scalable in vitro exercise studies. First, we characterize optical rheobase for 2D muscle monolayers, finding that optical intensities as low as 5 μW mm −2 can trigger functional contraction. We then leverage RNA sequencing to map changes in muscle gene expression in response to various optical exercise regimens, highlighting how changing stimulation parameters impact myogenic and broader physiological and pathological transcriptional responses. Our platform and results establish a practical foundation for high‐throughput in vitro exercise studies of skeletal muscle.
{"title":"Physiological and functional characterization for high‐throughput optogenetic skeletal muscle exercise assays","authors":"Ronald H. Heisser, Angel Bu, Laura Schwendeman, Tamara Rossy, Pavankumar Umashankar, Vincent Butty, Ritu Raman","doi":"10.1002/btm2.70101","DOIUrl":"https://doi.org/10.1002/btm2.70101","url":null,"abstract":"Exercise promotes human mobility by tuning the function of skeletal muscle, and recent studies highlight exercise's broader impacts on human health via muscle's paracrine and endocrine roles beyond force generation. In vitro models of tissue engineered skeletal muscle enable precise investigation of adaptation to exercise, with emerging approaches for optogenetic muscle stimulation providing a less invasive alternative to traditional techniques for electrical stimulation. In this study, we present a high‐throughput muscle culture and optical exercise protocol for scalable in vitro exercise studies. First, we characterize optical rheobase for 2D muscle monolayers, finding that optical intensities as low as 5 μW mm <jats:sup>−2</jats:sup> can trigger functional contraction. We then leverage RNA sequencing to map changes in muscle gene expression in response to various optical exercise regimens, highlighting how changing stimulation parameters impact myogenic and broader physiological and pathological transcriptional responses. Our platform and results establish a practical foundation for high‐throughput in vitro exercise studies of skeletal muscle.","PeriodicalId":9263,"journal":{"name":"Bioengineering & Translational Medicine","volume":"47 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145753036","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Devorah Cahn, Sanjay Pal, Alexa Stern, Nimit L. Patel, Timothy Gower, Senta M. Kapnick, Christopher M. Jewell, Gregg A. Duncan, Matthew T. Wolf
Barriers to nanoparticle drug delivery to the tumor microenvironment such as ECM deposition and clearance by the mononuclear phagocyte system have necessitated strategies for more effective tumor penetration. Adding polyethylene glycol (PEG) chains to the surface of nanoparticles (PEGylation) has been widely used to both enhance accumulation at the tumor site and increase blood circulation time. Recent work has also shown that immune cells (e.g., macrophages, dendritic cells, neutrophils) play an important role in the ability of NPs to effectively target and spread within a tumor. PEG chain characteristics such as size and branching affect how nanoparticles interact with tissues; however, it is unclear how PEGylation type affects NP uptake and cellular distribution in the tumor microenvironment. In this study, we evaluated the influence of both linear and branched PEGylation on nanoparticle biodistribution and uptake in tumor cells as well as tumor‐infiltrating immune cells. As compared to conventional surface coatings with linear PEG, we show that modifying PEG structure to a branched conformation increases nanoparticle accumulation in the spleen of tumor‐bearing mice, primarily due to significantly enhanced uptake by leukocytes. As compared to uncoated particles, we also found that nanoparticles densely coated with linear or branched PEG accumulated to a greater extent in tumors showing ≥8‐fold increases in uptake by tumor‐associated macrophages and dendritic cells. These studies provide insight into PEG architecture as a design parameter in nanomedicine that can facilitate the design of more effective cancer therapies.
{"title":"PEGylation strategies for enhanced nanoparticle delivery to tumor‐associated immune cells","authors":"Devorah Cahn, Sanjay Pal, Alexa Stern, Nimit L. Patel, Timothy Gower, Senta M. Kapnick, Christopher M. Jewell, Gregg A. Duncan, Matthew T. Wolf","doi":"10.1002/btm2.70098","DOIUrl":"https://doi.org/10.1002/btm2.70098","url":null,"abstract":"Barriers to nanoparticle drug delivery to the tumor microenvironment such as ECM deposition and clearance by the mononuclear phagocyte system have necessitated strategies for more effective tumor penetration. Adding polyethylene glycol (PEG) chains to the surface of nanoparticles (PEGylation) has been widely used to both enhance accumulation at the tumor site and increase blood circulation time. Recent work has also shown that immune cells (e.g., macrophages, dendritic cells, neutrophils) play an important role in the ability of NPs to effectively target and spread within a tumor. PEG chain characteristics such as size and branching affect how nanoparticles interact with tissues; however, it is unclear how PEGylation type affects NP uptake and cellular distribution in the tumor microenvironment. In this study, we evaluated the influence of both linear and branched PEGylation on nanoparticle biodistribution and uptake in tumor cells as well as tumor‐infiltrating immune cells. As compared to conventional surface coatings with linear PEG, we show that modifying PEG structure to a branched conformation increases nanoparticle accumulation in the spleen of tumor‐bearing mice, primarily due to significantly enhanced uptake by leukocytes. As compared to uncoated particles, we also found that nanoparticles densely coated with linear or branched PEG accumulated to a greater extent in tumors showing ≥8‐fold increases in uptake by tumor‐associated macrophages and dendritic cells. These studies provide insight into PEG architecture as a design parameter in nanomedicine that can facilitate the design of more effective cancer therapies.","PeriodicalId":9263,"journal":{"name":"Bioengineering & Translational Medicine","volume":"145 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145717266","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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