Nature Biomedical Engineering最新文献

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A pig with functional human immunity 具有人类功能性免疫力的猪
IF 28.1 1区 医学
Nature Biomedical Engineering Pub Date : 2025-06-11 DOI: 10.1038/s41551-025-01426-4
Christopher K. Tuggle, Crystal L. Loving, Beau R. Webber
{"title":"A pig with functional human immunity","authors":"Christopher K. Tuggle, Crystal L. Loving, Beau R. Webber","doi":"10.1038/s41551-025-01426-4","DOIUrl":"https://doi.org/10.1038/s41551-025-01426-4","url":null,"abstract":"Genetically modified immunodeficient pigs support the development of functional human B and T cells and represent a preclinical model for investigating human haematopoiesis and a bioreactor for large-scale production of human immune cells for diverse therapies.","PeriodicalId":19063,"journal":{"name":"Nature Biomedical Engineering","volume":"43 1","pages":""},"PeriodicalIF":28.1,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144260479","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Hitchhiking albumin to STING tumours 搭便车白蛋白到STING肿瘤
IF 28.1 1区 医学
Nature Biomedical Engineering Pub Date : 2025-06-11 DOI: 10.1038/s41551-025-01401-z
Shuyue Ye, Jinming Gao
{"title":"Hitchhiking albumin to STING tumours","authors":"Shuyue Ye, Jinming Gao","doi":"10.1038/s41551-025-01401-z","DOIUrl":"https://doi.org/10.1038/s41551-025-01401-z","url":null,"abstract":"A small-molecule STING agonist is conjugated to a nanobody that binds to serum albumins to increase tumour accumulation and augment antitumour immunity.","PeriodicalId":19063,"journal":{"name":"Nature Biomedical Engineering","volume":"585 1","pages":""},"PeriodicalIF":28.1,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144260478","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Potentiating cancer immunotherapies with modular albumin-hitchhiking nanobody–STING agonist conjugates 模块化白蛋白搭便车纳米体- sting激动剂缀合物增强癌症免疫治疗
IF 28.1 1区 医学
Nature Biomedical Engineering Pub Date : 2025-06-11 DOI: 10.1038/s41551-025-01400-0
Blaise R. Kimmel, Karan Arora, Neil C. Chada, Vijaya Bharti, Alexander J. Kwiatkowski, Jonah E. Finkelstein, Ann Hanna, Emily N. Arner, Taylor L. Sheehy, Lucinda E. Pastora, Jinming Yang, Hayden M. Pagendarm, Payton T. Stone, Ebony Hargrove-Wiley, Brandie C. Taylor, Lauren A. Hubert, Barbara M. Fingleton, Katherine N. Gibson-Corley, Jody C. May, John A. McLean, Jeffrey C. Rathmell, Ann Richmond, W. Kimryn Rathmell, Justin M. Balko, John T. Wilson
{"title":"Potentiating cancer immunotherapies with modular albumin-hitchhiking nanobody–STING agonist conjugates","authors":"Blaise R. Kimmel, Karan Arora, Neil C. Chada, Vijaya Bharti, Alexander J. Kwiatkowski, Jonah E. Finkelstein, Ann Hanna, Emily N. Arner, Taylor L. Sheehy, Lucinda E. Pastora, Jinming Yang, Hayden M. Pagendarm, Payton T. Stone, Ebony Hargrove-Wiley, Brandie C. Taylor, Lauren A. Hubert, Barbara M. Fingleton, Katherine N. Gibson-Corley, Jody C. May, John A. McLean, Jeffrey C. Rathmell, Ann Richmond, W. Kimryn Rathmell, Justin M. Balko, John T. Wilson","doi":"10.1038/s41551-025-01400-0","DOIUrl":"https://doi.org/10.1038/s41551-025-01400-0","url":null,"abstract":"<p>The enhancement of antitumour immunity via agonists of the stimulator of interferon genes (STING) pathway is limited by pharmacological barriers. Here we show that the covalent conjugation of a STING agonist to anti-albumin nanobodies via site-selective bioconjugation chemistries prolongs the circulation of the agonist in the blood and increases its accumulation in tumour tissue, stimulating innate immune programmes that increased the infiltration of activated natural killer cells and T cells, which potently inhibited the growth of mouse tumours. The technology is modular, as demonstrated by the recombinant integration of a second nanobody domain targeting programmed death-ligand 1 (PD-L1), which further increased the accumulation of the agonist in tumours while blocking immunosuppressive PD-1/PD-L1 interactions. The bivalent nanobody–STING agonist conjugate stimulated robust antigen-specific T-cell responses and long-lasting immunological memory and conferred enhanced therapeutic efficacy. It was also effective as a neoadjuvant treatment to adoptive T-cell therapy. As a modular approach, hitchhiking STING agonists on serum albumin may serve as a broadly applicable strategy for augmenting the potency of systemically administered cancer immunotherapies.</p>","PeriodicalId":19063,"journal":{"name":"Nature Biomedical Engineering","volume":"8 1","pages":""},"PeriodicalIF":28.1,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144260480","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Neuroimaging endophenotypes reveal underlying mechanisms and genetic factors contributing to progression and development of four brain disorders 神经影像学内表型揭示了促进四种脑部疾病进展和发展的潜在机制和遗传因素
IF 28.1 1区 医学
Nature Biomedical Engineering Pub Date : 2025-06-06 DOI: 10.1038/s41551-025-01412-w
Junhao Wen, Ioanna Skampardoni, Ye Ella Tian, Zhijian Yang, Yuhan Cui, Guray Erus, Gyujoon Hwang, Erdem Varol, Aleix Boquet-Pujadas, Ganesh B. Chand, Ilya M. Nasrallah, Theodore D. Satterthwaite, Haochang Shou, Li Shen, Arthur W. Toga, Andrew Zalesky, Christos Davatzikos
{"title":"Neuroimaging endophenotypes reveal underlying mechanisms and genetic factors contributing to progression and development of four brain disorders","authors":"Junhao Wen, Ioanna Skampardoni, Ye Ella Tian, Zhijian Yang, Yuhan Cui, Guray Erus, Gyujoon Hwang, Erdem Varol, Aleix Boquet-Pujadas, Ganesh B. Chand, Ilya M. Nasrallah, Theodore D. Satterthwaite, Haochang Shou, Li Shen, Arthur W. Toga, Andrew Zalesky, Christos Davatzikos","doi":"10.1038/s41551-025-01412-w","DOIUrl":"https://doi.org/10.1038/s41551-025-01412-w","url":null,"abstract":"<p>Recent work leveraging artificial intelligence has offered promise to dissect disease heterogeneity by identifying complex intermediate brain phenotypes, called dimensional neuroimaging endophenotypes (DNEs). We advance the argument that these DNEs capture the degree of expression of respective neuroanatomical patterns measured, offering a dimensional neuroanatomical representation for studying disease heterogeneity and similarities of neurologic and neuropsychiatric diseases. We investigate the presence of nine DNEs derived from independent yet harmonized studies on Alzheimer’s disease, autism spectrum disorder, late-life depression and schizophrenia in the UK Biobank study. Phenome-wide associations align with genome-wide associations, revealing 31 genomic loci (<i>P</i> &lt; 5 × 10<sup>−8</sup>/9) associated with the nine DNEs. The nine DNEs, along with their polygenic risk scores, significantly enhanced the predictive accuracy for 14 systemic disease categories, particularly for conditions related to mental health and the central nervous system, as well as mortality outcomes. These findings underscore the potential of the nine DNEs to capture the expression of disease-related brain phenotypes in individuals of the general population and to relate such measures with genetics, lifestyle factors and chronic diseases.</p>","PeriodicalId":19063,"journal":{"name":"Nature Biomedical Engineering","volume":"26 1","pages":""},"PeriodicalIF":28.1,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144228581","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
A deep learning system for detecting silent brain infarction and predicting stroke risk 用于检测无症状性脑梗死和预测中风风险的深度学习系统
IF 28.1 1区 医学
Nature Biomedical Engineering Pub Date : 2025-06-06 DOI: 10.1038/s41551-025-01413-9
Nan Jiang, Hongwei Ji, Zhouyu Guan, Yuesong Pan, Chenxin Deng, Yuchen Guo, Dan Liu, Tingli Chen, Shiyu Wang, Yilan Wu, Dawei Yang, An Ran Ran, Haslina Hamzah, Miao Li Chee, Changchang Yin, Benjamin Sommer Thinggaard, Frederik N. Pedersen, Qingsheng Peng, Ten Cheer Quek, Jocelyn Hui Lin Goh, Sarkaaj Singh, Anis Syazwani Abd Raof, Jian Wen Samuel Lee-Boey, Yuwei Lu, Shan Huang, Jia Shu, Shujie Yu, Yixiao Jin, Tingyao Li, Yiming Qin, Jing Wang, Xiaolong Yang, Tingting Hu, Zheyuan Wang, Yaoning Zhao, Seungmin Lee, Xiaoer Wei, Haotian Zheng, Yuehua Li, Jie Shen, Yan Zhou, Shiqun Lin, Chan Wu, Rongping Dai, Lei Ruan, Ruth E. Hogg, David Wright, Ya Xing Wang, Yingfeng Zheng, Gavin Siew Wei Tan, Charumathi Sabanayagam, Yuqian Bao, Cuntai Zhang, Ping Zhang, Weiwen Zou, Minyi Guo, Xiaokang Yang, Gareth J. McKay, Jakob Grauslund, Lee-Ling Lim, Zixiao Li, Carol Y. Cheung, Yih Chung Tham, Ching-Yu Cheng, Yongjun Wang, Qionghai Dai, Weiping Jia, Huating Li, Bin Sheng, Tien Yin Wong
{"title":"A deep learning system for detecting silent brain infarction and predicting stroke risk","authors":"Nan Jiang, Hongwei Ji, Zhouyu Guan, Yuesong Pan, Chenxin Deng, Yuchen Guo, Dan Liu, Tingli Chen, Shiyu Wang, Yilan Wu, Dawei Yang, An Ran Ran, Haslina Hamzah, Miao Li Chee, Changchang Yin, Benjamin Sommer Thinggaard, Frederik N. Pedersen, Qingsheng Peng, Ten Cheer Quek, Jocelyn Hui Lin Goh, Sarkaaj Singh, Anis Syazwani Abd Raof, Jian Wen Samuel Lee-Boey, Yuwei Lu, Shan Huang, Jia Shu, Shujie Yu, Yixiao Jin, Tingyao Li, Yiming Qin, Jing Wang, Xiaolong Yang, Tingting Hu, Zheyuan Wang, Yaoning Zhao, Seungmin Lee, Xiaoer Wei, Haotian Zheng, Yuehua Li, Jie Shen, Yan Zhou, Shiqun Lin, Chan Wu, Rongping Dai, Lei Ruan, Ruth E. Hogg, David Wright, Ya Xing Wang, Yingfeng Zheng, Gavin Siew Wei Tan, Charumathi Sabanayagam, Yuqian Bao, Cuntai Zhang, Ping Zhang, Weiwen Zou, Minyi Guo, Xiaokang Yang, Gareth J. McKay, Jakob Grauslund, Lee-Ling Lim, Zixiao Li, Carol Y. Cheung, Yih Chung Tham, Ching-Yu Cheng, Yongjun Wang, Qionghai Dai, Weiping Jia, Huating Li, Bin Sheng, Tien Yin Wong","doi":"10.1038/s41551-025-01413-9","DOIUrl":"https://doi.org/10.1038/s41551-025-01413-9","url":null,"abstract":"<p>Current brain imaging to detect silent brain infarctions (SBIs) is not feasible for the general population. Here, to overcome this challenge, we developed a retinal image-based deep learning system, DeepRETStroke, to detect SBI and refine stroke risk. We use 895,640 retinal photographs to pretrain the DeepRETStroke system, which encodes a domain-specific foundation model for representing eye–brain connections. Then, we validated the downstream clinical tasks of DeepRETStroke using 213,762 retinal photographs from diverse datasets across China, Singapore, Malaysia, the USA, the UK and Denmark to detect SBI and predict stroke events. DeepRETStroke performed well in internal validation datasets, with areas under the curve of 0.901 for predicting incident stroke and 0.769 for predicting recurrent stroke. External validations demonstrated consistent performances across diverse datasets. Finally, in a prospective study comprising 218 participants with stroke, we assessed the performance of DeepRETStroke compared with clinical traits in guiding strategies for stroke recurrence prevention. Altogether, the retinal image-based deep learning system, DeepRETStroke, is superior to clinical traits in predicting stroke events, especially by incorporating the detection of SBI, without the need for brain imaging.</p>","PeriodicalId":19063,"journal":{"name":"Nature Biomedical Engineering","volume":"17 1","pages":""},"PeriodicalIF":28.1,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144228479","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Mechanically knocking out titin reveals protein tension loss as a trigger of muscle disease 机械地敲除titin揭示了蛋白质张力损失是肌肉疾病的触发因素
IF 28.1 1区 医学
Nature Biomedical Engineering Pub Date : 2025-06-05 DOI: 10.1038/s41551-025-01403-x
Roberto Silva-Rojas, Natalia Vicente, Manuel Gavilán-Herrera, Verónica Labrador-Cantarero, Jon Sicilia, Olga Giménez-Sáez, Andra C. Dumitru, Mateo I. Sánchez, Mara Gato-Vilaseca, Diana Velázquez-Carreras, Juan Antonio López, Jesús Vázquez, Elías Herrero-Galán, Miguel A. López-Unzu, Maria Rosaria Pricolo, Jorge Alegre-Cebollada
{"title":"Mechanically knocking out titin reveals protein tension loss as a trigger of muscle disease","authors":"Roberto Silva-Rojas, Natalia Vicente, Manuel Gavilán-Herrera, Verónica Labrador-Cantarero, Jon Sicilia, Olga Giménez-Sáez, Andra C. Dumitru, Mateo I. Sánchez, Mara Gato-Vilaseca, Diana Velázquez-Carreras, Juan Antonio López, Jesús Vázquez, Elías Herrero-Galán, Miguel A. López-Unzu, Maria Rosaria Pricolo, Jorge Alegre-Cebollada","doi":"10.1038/s41551-025-01403-x","DOIUrl":"https://doi.org/10.1038/s41551-025-01403-x","url":null,"abstract":"<p>Titin, the elastic protein scaffold of muscle sarcomeres, has multifunctional roles in mechanosignalling and is implicated in muscle disease. However, the consequences of disrupting titin’s mechanical function in vivo remain incompletely understood. Here, by leveraging site-directed polypeptide severing as a ‘mechanical knock-out’ method for abolishing force transmission across titin, we show that the loss of titin tension in homozygous mechanically knocked-out muscles reduces force generation and induces severe atrophy and widespread transcriptional dysregulation. Although mechanically knocked-out myofibres persist, they shrink and undergo progressive sarcomere depletion, which correlates with the rapid upregulation of muscle-specific RING finger protein 1 (MuRF1) and with altered levels of other titin-associated atrophy regulators. The affected fibres also exhibit mitochondrial aggregation and myonuclei internalization, preceded by desmin mislocalization. Heterozygous mechanically knocked-out muscles show milder phenotypes that closely resemble titin-related human myopathy. Our findings suggest that slack titin molecules drive muscle disease, potentially through mechanisms shared with other mechanical proteins.</p>","PeriodicalId":19063,"journal":{"name":"Nature Biomedical Engineering","volume":"4 1","pages":""},"PeriodicalIF":28.1,"publicationDate":"2025-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144218891","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Microfluidics combined with electron microscopy for rapid and high-throughput mapping of antibody–viral glycoprotein complexes 微流体结合电子显微镜快速和高通量定位抗体-病毒糖蛋白复合物
IF 28.1 1区 医学
Nature Biomedical Engineering Pub Date : 2025-06-03 DOI: 10.1038/s41551-025-01411-x
Leigh M. Sewall, Rebeca de Paiva Froes Rocha, Grace Gibson, Michelle Louie, Zhenfei Xie, Sandhya Bangaru, Andy S. Tran, Gabriel Ozorowski, Subhasis Mohanty, Nathan Beutler, Thomas F. Rogers, Dennis R. Burton, Albert C. Shaw, Facundo D. Batista, Blanca Chocarro Ruiz, Alba Torrents de la Peña, Andrew B. Ward
{"title":"Microfluidics combined with electron microscopy for rapid and high-throughput mapping of antibody–viral glycoprotein complexes","authors":"Leigh M. Sewall, Rebeca de Paiva Froes Rocha, Grace Gibson, Michelle Louie, Zhenfei Xie, Sandhya Bangaru, Andy S. Tran, Gabriel Ozorowski, Subhasis Mohanty, Nathan Beutler, Thomas F. Rogers, Dennis R. Burton, Albert C. Shaw, Facundo D. Batista, Blanca Chocarro Ruiz, Alba Torrents de la Peña, Andrew B. Ward","doi":"10.1038/s41551-025-01411-x","DOIUrl":"https://doi.org/10.1038/s41551-025-01411-x","url":null,"abstract":"<p>Understanding the mechanistic interplay between antibodies and invading pathogens is essential for vaccine development. Current methods are labour and time intensive and limited by sample preparation bottlenecks. Here we present microfluidic electron microscopy-based polyclonal epitope mapping (mEM), which combines microfluidics with single-particle electron microscopy for the structural characterization of immune complexes using small volumes of sera (&lt;4 µl). First, we used mEM to map polyclonal antibodies present in sera from infected and vaccinated individuals against five viral glycoproteins using negative-stain electron microscopy. The mEM detected a greater number of epitopes compared with conventional polyclonal epitope structural mapping methods. Second, we used mEM and cryo-electron microscopy to characterize two coronavirus spikes and one HA glycoprotein with and without polyclonal antibodies. Finally, we mapped individual antibody responses over time in mice vaccinated with human immunodeficiency virus envelope N332-GT5. mEM enables the rapid, high-throughput mapping of antibodies targeting a broad range of glycoproteins, facilitating a better understanding of infection and guiding structure-based vaccine design.</p>","PeriodicalId":19063,"journal":{"name":"Nature Biomedical Engineering","volume":"30 1","pages":""},"PeriodicalIF":28.1,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144201583","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Mechanical forces drive degenerative spine disease through ROCK signalling 机械力通过ROCK信号驱动退行性脊柱疾病
IF 28.1 1区 医学
Nature Biomedical Engineering Pub Date : 2025-06-03 DOI: 10.1038/s41551-025-01398-5
{"title":"Mechanical forces drive degenerative spine disease through ROCK signalling","authors":"","doi":"10.1038/s41551-025-01398-5","DOIUrl":"https://doi.org/10.1038/s41551-025-01398-5","url":null,"abstract":"Repetitive mechanical forces on the spine cause spinal ligament hypertrophy through an unknown molecular mechanism. We observed in ligaments obtained from patients undergoing surgical spine decompression that force-driven Rho-associated kinase (ROCK) signalling causes accumulation of myofibroblasts from fibroblasts and show that ROCK signalling inhibitors block this force-dependent molecular mechanism contributing to spinal ligament fibrosis.","PeriodicalId":19063,"journal":{"name":"Nature Biomedical Engineering","volume":"81 1","pages":""},"PeriodicalIF":28.1,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144201582","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
NAD+ biosynthesis and mitochondrial repair in acute kidney injury via ultrasound-responsive thylakoid-integrating liposomes 超声响应类囊体整合脂质体对急性肾损伤NAD+生物合成和线粒体修复的影响
IF 28.1 1区 医学
Nature Biomedical Engineering Pub Date : 2025-06-03 DOI: 10.1038/s41551-025-01402-y
Yao Lei, Yuzhu Wu, Wan-Ru Zhuang, Helin Zhao, Weidong Nie, Guanghao Wu, Dai-Wen Pang, Hai-Yan Xie
{"title":"NAD+ biosynthesis and mitochondrial repair in acute kidney injury via ultrasound-responsive thylakoid-integrating liposomes","authors":"Yao Lei, Yuzhu Wu, Wan-Ru Zhuang, Helin Zhao, Weidong Nie, Guanghao Wu, Dai-Wen Pang, Hai-Yan Xie","doi":"10.1038/s41551-025-01402-y","DOIUrl":"https://doi.org/10.1038/s41551-025-01402-y","url":null,"abstract":"<p>Acute kidney injury (AKI) impairs the energy metabolism and antioxidant capacity of renal proximal tubular cells. Here we show that ultrasound-responsive liposomes integrating thylakoid fragments and encapsulating <span>l</span>-ascorbic acid can restore the energy supply and antioxidant capacity of the tubular cells as well as renal function in animal models of AKI. After intravenous injection, the liposomes preferentially accumulated in the injured kidneys and were internalized by proximal tubular cells. Quinolinate phosphoribosyltransferase expressed in thylakoid catalysed the biosynthesis of nicotinamide adenine dinucleotide (NAD<sup>+</sup>), prompting the recovery of damaged mitochondria. Local ultrasound stimulation activated electron transfer from ascorbic acid, which led to the cytoplasmic formation of NADH and to the restoration of adenosine triphosphate through the malate-aspartate shuttle. Concurrently, the enhanced pentose phosphate pathway facilitated NADPH biosynthesis and reduced the levels of reactive oxygen species. In mice and piglets with AKI, low doses of the liposomes prevented kidney damage.</p>","PeriodicalId":19063,"journal":{"name":"Nature Biomedical Engineering","volume":"168 1","pages":""},"PeriodicalIF":28.1,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144201584","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
A brain–computer interface working definition 脑机接口工作定义
IF 28.1 1区 医学
Nature Biomedical Engineering Pub Date : 2025-06-02 DOI: 10.1038/s41551-025-01414-8
Marc W. Slutzky, Mariska J. Vansteensel, Christian Herff, Robert A. Gaunt
{"title":"A brain–computer interface working definition","authors":"Marc W. Slutzky, Mariska J. Vansteensel, Christian Herff, Robert A. Gaunt","doi":"10.1038/s41551-025-01414-8","DOIUrl":"https://doi.org/10.1038/s41551-025-01414-8","url":null,"abstract":"&lt;p&gt;We read with interest the Comment that suggests a taxonomy for brain–computer interfaces (BCIs) based on application&lt;sup&gt;1&lt;/sup&gt;, and we agree that a nomenclature of different types of BCI may be useful for discussing this broad and expanding field comprised of stakeholders with different backgrounds and expertise, including groups new to BCI, such as media, investors and students. Nevertheless, we feel compelled to respond regarding the working definition of BCIs proposed in the article. The definition endorsed by the authors was that a BCI includes “any technology that records brain activity and processes it on an electronic device, or any technology that stimulates brain activity based on computations performed on an electronic device”. Although this may be accurate on a strictly semantic basis — that is, recording and stimulating technically meet the definition of an interface as both involve interactions between two systems — it diverges both from the historical definition of BCIs&lt;sup&gt;2&lt;/sup&gt; and from the results obtained in a consensus survey recently performed by the BCI Society. The survey was sent to a broad range of stakeholders in the field, including scientists, engineers, physicians, therapists, regulators and industry members. Based on the results of this survey and continued discussion, 57% of 137 respondents, all recent or current members of the BCI Society, agreed upon a working definition, reflecting the potential need to revisit this important topic in the future. This working definition was carefully created by an ad hoc committee of the BCI Society, as follows: “A brain-computer interface is a system that measures brain activity and converts it in (nearly) real-time into functionally useful outputs to replace, restore, enhance, supplement, and/or improve the natural outputs of the brain, thereby changing the ongoing interactions between the brain and its external or internal environments. It may additionally modify brain activity using targeted delivery of stimuli to create functionally useful inputs to the brain”.&lt;/p&gt;&lt;p&gt;We believe that this definition captures more clearly the essential features of a BCI and helps to distinguish it from other technologies that interface with or record from the brain, such as clinical electroencephalography and magnetoencephalography used for diagnostic purposes, functional magnetic resonance imaging or nuclear medicine scans, that are all consistent with the recently proposed definition&lt;sup&gt;1&lt;/sup&gt;. These technologies all record brain activity and perform computations on electronic devices, yet no one would consider them BCIs. Other devices such as open-loop deep brain stimulators could also be included under the proposed BCI definition&lt;sup&gt;1&lt;/sup&gt;, as they stimulate the brain based on computations performed on an electronic device. Yet, the responses to the BCI Society survey indicate an overall preference for a definition that includes measuring and responding to brain activity, not sim","PeriodicalId":19063,"journal":{"name":"Nature Biomedical Engineering","volume":"37 1","pages":""},"PeriodicalIF":28.1,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144193034","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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