Pub Date : 2024-03-04DOI: 10.1038/s41551-024-01178-7
Qiang Feng, Zachary Bennett, Anthony Grichuk, Raymundo Pantoja, Tongyi Huang, Brandon Faubert, Gang Huang, Mingyi Chen, Ralph J. DeBerardinis, Baran D. Sumer, Jinming Gao
Extracellular pH impacts many molecular, cellular and physiological processes, and hence is tightly regulated. Yet, in tumours, dysregulated cancer cell metabolism and poor vascular perfusion cause the tumour microenvironment to become acidic. Here by leveraging fluorescent pH nanoprobes with a transistor-like activation profile at a pH of 5.3, we show that, in cancer cells, hydronium ions are excreted into a small extracellular region. Such severely polarized acidity (pH <5.3) is primarily caused by the directional co-export of protons and lactate, as we show for a diverse panel of cancer cell types via the genetic knockout or inhibition of monocarboxylate transporters, and also via nanoprobe activation in multiple tumour models in mice. We also observed that such spot acidification in ex vivo stained snap-frozen human squamous cell carcinoma tissue correlated with the expression of monocarboxylate transporters and with the exclusion of cytotoxic T cells. Severely spatially polarized tumour acidity could be leveraged for cancer diagnosis and therapy. Hydronium ions bordering cancer cells are highly concentrated into a small extracellular region, and in tumour tissue such severely polarized acidity correlates with the expression of monocarboxylate transporters and with the exclusion of cytotoxic T cells.
{"title":"Severely polarized extracellular acidity around tumour cells","authors":"Qiang Feng, Zachary Bennett, Anthony Grichuk, Raymundo Pantoja, Tongyi Huang, Brandon Faubert, Gang Huang, Mingyi Chen, Ralph J. DeBerardinis, Baran D. Sumer, Jinming Gao","doi":"10.1038/s41551-024-01178-7","DOIUrl":"10.1038/s41551-024-01178-7","url":null,"abstract":"Extracellular pH impacts many molecular, cellular and physiological processes, and hence is tightly regulated. Yet, in tumours, dysregulated cancer cell metabolism and poor vascular perfusion cause the tumour microenvironment to become acidic. Here by leveraging fluorescent pH nanoprobes with a transistor-like activation profile at a pH of 5.3, we show that, in cancer cells, hydronium ions are excreted into a small extracellular region. Such severely polarized acidity (pH <5.3) is primarily caused by the directional co-export of protons and lactate, as we show for a diverse panel of cancer cell types via the genetic knockout or inhibition of monocarboxylate transporters, and also via nanoprobe activation in multiple tumour models in mice. We also observed that such spot acidification in ex vivo stained snap-frozen human squamous cell carcinoma tissue correlated with the expression of monocarboxylate transporters and with the exclusion of cytotoxic T cells. Severely spatially polarized tumour acidity could be leveraged for cancer diagnosis and therapy. Hydronium ions bordering cancer cells are highly concentrated into a small extracellular region, and in tumour tissue such severely polarized acidity correlates with the expression of monocarboxylate transporters and with the exclusion of cytotoxic T cells.","PeriodicalId":19063,"journal":{"name":"Nature Biomedical Engineering","volume":null,"pages":null},"PeriodicalIF":26.8,"publicationDate":"2024-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140026590","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}
Pub Date : 2024-02-29DOI: 10.1038/s41551-024-01180-z
Ninad Kumbhojkar, Supriya Prakash, Tatsuya Fukuta, Kwasi Adu-Berchie, Neha Kapate, Rocky An, Solomina Darko, Vineeth Chandran Suja, Kyung Soo Park, Alexander P. Gottlieb, Michael Griffith Bibbey, Malini Mukherji, Lily Li-Wen Wang, David J. Mooney, Samir Mitragotri
Tumour-associated neutrophils can exert antitumour effects but can also assume a pro-tumoural phenotype in the immunosuppressive tumour microenvironment. Here we show that neutrophils can be polarized towards the antitumour phenotype by discoidal polymer micrometric ‘patches’ that adhere to the neutrophils’ surfaces without being internalized. Intravenously administered micropatch-loaded neutrophils accumulated in the spleen and in tumour-draining lymph nodes, and activated splenic natural killer cells and T cells, increasing the accumulation of dendritic cells and natural killer cells. In mice bearing subcutaneous B16F10 tumours or orthotopic 4T1 tumours, intravenous injection of the micropatch-loaded neutrophils led to robust systemic immune responses, a reduction in tumour burden and improvements in survival rates. Micropatch-activated neutrophils combined with the checkpoint inhibitor anti-cytotoxic T-lymphocyte-associated protein 4 resulted in strong inhibition of the growth of B16F10 tumours, and in complete tumour regression in one-third of the treated mice. Micropatch-loaded neutrophils could provide a potent, scalable and drug-free approach for neutrophil-based cancer immunotherapy. The intravenous injection of neutrophils bearing discoidal polymer microscale ‘patches’ on their surfaces reduces tumour burden in mice owing to the patch-induced polarization of the neutrophils towards an antitumour phenotype.
{"title":"Neutrophils bearing adhesive polymer micropatches as a drug-free cancer immunotherapy","authors":"Ninad Kumbhojkar, Supriya Prakash, Tatsuya Fukuta, Kwasi Adu-Berchie, Neha Kapate, Rocky An, Solomina Darko, Vineeth Chandran Suja, Kyung Soo Park, Alexander P. Gottlieb, Michael Griffith Bibbey, Malini Mukherji, Lily Li-Wen Wang, David J. Mooney, Samir Mitragotri","doi":"10.1038/s41551-024-01180-z","DOIUrl":"10.1038/s41551-024-01180-z","url":null,"abstract":"Tumour-associated neutrophils can exert antitumour effects but can also assume a pro-tumoural phenotype in the immunosuppressive tumour microenvironment. Here we show that neutrophils can be polarized towards the antitumour phenotype by discoidal polymer micrometric ‘patches’ that adhere to the neutrophils’ surfaces without being internalized. Intravenously administered micropatch-loaded neutrophils accumulated in the spleen and in tumour-draining lymph nodes, and activated splenic natural killer cells and T cells, increasing the accumulation of dendritic cells and natural killer cells. In mice bearing subcutaneous B16F10 tumours or orthotopic 4T1 tumours, intravenous injection of the micropatch-loaded neutrophils led to robust systemic immune responses, a reduction in tumour burden and improvements in survival rates. Micropatch-activated neutrophils combined with the checkpoint inhibitor anti-cytotoxic T-lymphocyte-associated protein 4 resulted in strong inhibition of the growth of B16F10 tumours, and in complete tumour regression in one-third of the treated mice. Micropatch-loaded neutrophils could provide a potent, scalable and drug-free approach for neutrophil-based cancer immunotherapy. The intravenous injection of neutrophils bearing discoidal polymer microscale ‘patches’ on their surfaces reduces tumour burden in mice owing to the patch-induced polarization of the neutrophils towards an antitumour phenotype.","PeriodicalId":19063,"journal":{"name":"Nature Biomedical Engineering","volume":null,"pages":null},"PeriodicalIF":28.1,"publicationDate":"2024-02-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139996854","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}
Pub Date : 2024-02-21DOI: 10.1038/s41551-024-01182-x
Appealing against an editor’s negative decision is likely to be more fruitful when considering the basis of the editorial assessment and offering ways forward.
对编辑的否定性决定提出上诉，如果能考虑到编辑评估的依据并提出前进的方向，可能会更有成效。
{"title":"How to appeal well","authors":"","doi":"10.1038/s41551-024-01182-x","DOIUrl":"10.1038/s41551-024-01182-x","url":null,"abstract":"Appealing against an editor’s negative decision is likely to be more fruitful when considering the basis of the editorial assessment and offering ways forward.","PeriodicalId":19063,"journal":{"name":"Nature Biomedical Engineering","volume":null,"pages":null},"PeriodicalIF":28.1,"publicationDate":"2024-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41551-024-01182-x.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139915868","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-02-20DOI: 10.1038/s41551-023-01147-6
Ningqiang Gong, Xuexiang Han, Lulu Xue, Margaret M. Billingsley, Xisha Huang, Rakan El-Mayta, Jingya Qin, Neil C. Sheppard, Carl H. June, Michael J. Mitchell
The broader clinical use of bispecific T cell engagers for inducing anti-tumour toxicity is hindered by their on-target off-tumour toxicity and the associated neurotoxicity and cytokine-release syndrome. Here we show that the off-tumour toxicity of a supramolecular bispecific T cell engager binding to the T cell co-receptor CD3 and to the human epidermal growth factor receptor 2 on breast tumour cells can be halted by disengaging the T cells from the tumour cells via the infusion of the small-molecule drug amantadine, which disassembles the supramolecular aggregate. In mice bearing human epidermal growth factor receptor 2-expressing tumours and with a human immune system, high intravenous doses of such a ‘switchable T cell nanoengager’ elicited strong tumour-specific adaptive immune responses that prevented tumour relapse, while the infusion of amantadine restricted off-tumour toxicity, cytokine-release syndrome and neurotoxicity. Supramolecular chemistry may be further leveraged to control the anti-tumour activity and off-tumour toxicity of bispecific antibodies. The off-tumour toxicity of a supramolecular bispecific T cell engager can be halted by disengaging T cells from the tumour cells via the disassembly of the supramolecular aggregate through the infusion of the small-molecule drug amantadine.
双特异性T细胞诱导剂诱导抗肿瘤毒性的更广泛临床应用受到其靶向瘤外毒性及相关神经毒性和细胞因子释放综合征的阻碍。在这里，我们展示了一种与乳腺肿瘤细胞上的 T 细胞共受体 CD3 和人表皮生长因子受体 2 结合的超分子双特异性 T 细胞吸引子的瘤外毒性，通过输注能分解超分子聚合体的小分子药物金刚烷胺，使 T 细胞与肿瘤细胞分离，从而阻止其瘤外毒性。在携带人类表皮生长因子受体 2 表达肿瘤并具有人类免疫系统的小鼠身上，大剂量静脉注射这种 "可切换 T 细胞纳米啮合剂 "可引起强烈的肿瘤特异性适应性免疫反应，从而防止肿瘤复发，同时金刚烷胺的输注限制了瘤外毒性、细胞因子释放综合征和神经毒性。可以进一步利用超分子化学来控制双特异性抗体的抗肿瘤活性和瘤外毒性。
{"title":"Small-molecule-mediated control of the anti-tumour activity and off-tumour toxicity of a supramolecular bispecific T cell engager","authors":"Ningqiang Gong, Xuexiang Han, Lulu Xue, Margaret M. Billingsley, Xisha Huang, Rakan El-Mayta, Jingya Qin, Neil C. Sheppard, Carl H. June, Michael J. Mitchell","doi":"10.1038/s41551-023-01147-6","DOIUrl":"10.1038/s41551-023-01147-6","url":null,"abstract":"The broader clinical use of bispecific T cell engagers for inducing anti-tumour toxicity is hindered by their on-target off-tumour toxicity and the associated neurotoxicity and cytokine-release syndrome. Here we show that the off-tumour toxicity of a supramolecular bispecific T cell engager binding to the T cell co-receptor CD3 and to the human epidermal growth factor receptor 2 on breast tumour cells can be halted by disengaging the T cells from the tumour cells via the infusion of the small-molecule drug amantadine, which disassembles the supramolecular aggregate. In mice bearing human epidermal growth factor receptor 2-expressing tumours and with a human immune system, high intravenous doses of such a ‘switchable T cell nanoengager’ elicited strong tumour-specific adaptive immune responses that prevented tumour relapse, while the infusion of amantadine restricted off-tumour toxicity, cytokine-release syndrome and neurotoxicity. Supramolecular chemistry may be further leveraged to control the anti-tumour activity and off-tumour toxicity of bispecific antibodies. The off-tumour toxicity of a supramolecular bispecific T cell engager can be halted by disengaging T cells from the tumour cells via the disassembly of the supramolecular aggregate through the infusion of the small-molecule drug amantadine.","PeriodicalId":19063,"journal":{"name":"Nature Biomedical Engineering","volume":null,"pages":null},"PeriodicalIF":28.1,"publicationDate":"2024-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139913076","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}
Pub Date : 2024-02-20DOI: 10.1038/s41551-023-01128-9
Yunhua Shi, Daniel Reker, James D. Byrne, Ameya R. Kirtane, Kaitlyn Hess, Zhuyi Wang, Natsuda Navamajiti, Cameron C. Young, Zachary Fralish, Zilu Zhang, Aaron Lopes, Vance Soares, Jacob Wainer, Thomas von Erlach, Lei Miao, Robert Langer, Giovanni Traverso
In vitro systems that accurately model in vivo conditions in the gastrointestinal tract may aid the development of oral drugs with greater bioavailability. Here we show that the interaction profiles between drugs and intestinal drug transporters can be obtained by modulating transporter expression in intact porcine tissue explants via the ultrasound-mediated delivery of small interfering RNAs and that the interaction profiles can be classified via a random forest model trained on the drug–transporter relationships. For 24 drugs with well-characterized drug–transporter interactions, the model achieved 100% concordance. For 28 clinical drugs and 22 investigational drugs, the model identified 58 unknown drug–transporter interactions, 7 of which (out of 8 tested) corresponded to drug-pharmacokinetic measurements in mice. We also validated the model’s predictions for interactions between doxycycline and four drugs (warfarin, tacrolimus, digoxin and levetiracetam) through an ex vivo perfusion assay and the analysis of pharmacologic data from patients. Screening drugs for their interactions with the intestinal transportome via tissue explants and machine learning may help to expedite drug development and the evaluation of drug safety. A machine-learning model trained on interactions between oral drugs and intestinal drug transporters obtained by modulating their expression in intact porcine tissue can be used to predict drug–transporter and drug–drug interactions.
{"title":"Screening oral drugs for their interactions with the intestinal transportome via porcine tissue explants and machine learning","authors":"Yunhua Shi, Daniel Reker, James D. Byrne, Ameya R. Kirtane, Kaitlyn Hess, Zhuyi Wang, Natsuda Navamajiti, Cameron C. Young, Zachary Fralish, Zilu Zhang, Aaron Lopes, Vance Soares, Jacob Wainer, Thomas von Erlach, Lei Miao, Robert Langer, Giovanni Traverso","doi":"10.1038/s41551-023-01128-9","DOIUrl":"10.1038/s41551-023-01128-9","url":null,"abstract":"In vitro systems that accurately model in vivo conditions in the gastrointestinal tract may aid the development of oral drugs with greater bioavailability. Here we show that the interaction profiles between drugs and intestinal drug transporters can be obtained by modulating transporter expression in intact porcine tissue explants via the ultrasound-mediated delivery of small interfering RNAs and that the interaction profiles can be classified via a random forest model trained on the drug–transporter relationships. For 24 drugs with well-characterized drug–transporter interactions, the model achieved 100% concordance. For 28 clinical drugs and 22 investigational drugs, the model identified 58 unknown drug–transporter interactions, 7 of which (out of 8 tested) corresponded to drug-pharmacokinetic measurements in mice. We also validated the model’s predictions for interactions between doxycycline and four drugs (warfarin, tacrolimus, digoxin and levetiracetam) through an ex vivo perfusion assay and the analysis of pharmacologic data from patients. Screening drugs for their interactions with the intestinal transportome via tissue explants and machine learning may help to expedite drug development and the evaluation of drug safety. A machine-learning model trained on interactions between oral drugs and intestinal drug transporters obtained by modulating their expression in intact porcine tissue can be used to predict drug–transporter and drug–drug interactions.","PeriodicalId":19063,"journal":{"name":"Nature Biomedical Engineering","volume":null,"pages":null},"PeriodicalIF":28.1,"publicationDate":"2024-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139913075","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}
Pub Date : 2024-02-19DOI: 10.1038/s41551-023-01150-x
Wenchao Gu, Sijin Luozhong, Simian Cai, Ketaki Londhe, Nadine Elkasri, Robert Hawkins, Zhefan Yuan, Kai Su-Greene, Yujie Yin, Margaret Cruz, Yu-Wei Chang, Patrick McMullen, Chunyan Wu, Changwoo Seo, Akash Guru, Wenting Gao, Tara Sarmiento, Chris Schaffer, Nozomi Nishimura, Richard Cerione, Qiuming Yu, Melissa Warden, Robert Langer, Shaoyi Jiang
The blood–brain barrier (BBB) restricts the systemic delivery of messenger RNAs (mRNAs) into diseased neurons. Although leucocyte-derived extracellular vesicles (EVs) can cross the BBB at inflammatory sites, it is difficult to efficiently load long mRNAs into the EVs and to enhance their neuronal uptake. Here we show that the packaging of mRNA into leucocyte-derived EVs and the endocytosis of the EVs by neurons can be enhanced by engineering leucocytes to produce EVs that incorporate retrovirus-like mRNA-packaging capsids. We transfected immortalized and primary bone-marrow-derived leucocytes with DNA or RNA encoding the capsid-forming activity-regulated cytoskeleton-associated (Arc) protein as well as capsid-stabilizing Arc 5’-untranslated-region RNA elements. These engineered EVs inherit endothelial adhesion molecules from donor leukocytes, recruit endogenous enveloping proteins to their surface, cross the BBB, and enter the neurons in neuro-inflammatory sites. Produced from self-derived donor leukocytes, the EVs are immunologically inert, and enhanced the neuronal uptake of the packaged mRNA in a mouse model of low-grade chronic neuro-inflammation. The delivery of mRNAs into neurons at inflammatory sites in vivo can be enhanced by engineering leucocytes to produce extracellular vesicles incorporating mRNA-packaging retrovirus-like capsids.
血脑屏障（BBB）限制了将信使核糖核酸（mRNA）全身性地输送到患病神经元。虽然白细胞衍生的细胞外囊泡 (EV) 可以在炎症部位穿过 BBB，但很难将长 mRNA 有效地装载到 EV 中并提高神经元对它们的吸收。在这里，我们发现可以通过改造白细胞，使其产生包含类似逆转录病毒的mRNA包装囊的EVs，从而增强mRNA包装到白细胞衍生的EVs中以及神经元对EVs的内吞。我们用编码囊体形成活性调控细胞骨架相关蛋白（Arc）以及囊体稳定Arc 5'-非翻译区RNA元件的DNA或RNA转染了永生化和原发性骨髓衍生白细胞。这些工程化的 EV 继承了供体白细胞的内皮粘附分子，在其表面招募内源性包膜蛋白，穿过 BBB，进入神经炎症部位的神经元。在低度慢性神经炎症的小鼠模型中，由自身衍生的供体白细胞产生的EVs具有免疫惰性，能增强神经元对包装mRNA的吸收。
{"title":"Extracellular vesicles incorporating retrovirus-like capsids for the enhanced packaging and systemic delivery of mRNA into neurons","authors":"Wenchao Gu, Sijin Luozhong, Simian Cai, Ketaki Londhe, Nadine Elkasri, Robert Hawkins, Zhefan Yuan, Kai Su-Greene, Yujie Yin, Margaret Cruz, Yu-Wei Chang, Patrick McMullen, Chunyan Wu, Changwoo Seo, Akash Guru, Wenting Gao, Tara Sarmiento, Chris Schaffer, Nozomi Nishimura, Richard Cerione, Qiuming Yu, Melissa Warden, Robert Langer, Shaoyi Jiang","doi":"10.1038/s41551-023-01150-x","DOIUrl":"10.1038/s41551-023-01150-x","url":null,"abstract":"The blood–brain barrier (BBB) restricts the systemic delivery of messenger RNAs (mRNAs) into diseased neurons. Although leucocyte-derived extracellular vesicles (EVs) can cross the BBB at inflammatory sites, it is difficult to efficiently load long mRNAs into the EVs and to enhance their neuronal uptake. Here we show that the packaging of mRNA into leucocyte-derived EVs and the endocytosis of the EVs by neurons can be enhanced by engineering leucocytes to produce EVs that incorporate retrovirus-like mRNA-packaging capsids. We transfected immortalized and primary bone-marrow-derived leucocytes with DNA or RNA encoding the capsid-forming activity-regulated cytoskeleton-associated (Arc) protein as well as capsid-stabilizing Arc 5’-untranslated-region RNA elements. These engineered EVs inherit endothelial adhesion molecules from donor leukocytes, recruit endogenous enveloping proteins to their surface, cross the BBB, and enter the neurons in neuro-inflammatory sites. Produced from self-derived donor leukocytes, the EVs are immunologically inert, and enhanced the neuronal uptake of the packaged mRNA in a mouse model of low-grade chronic neuro-inflammation. The delivery of mRNAs into neurons at inflammatory sites in vivo can be enhanced by engineering leucocytes to produce extracellular vesicles incorporating mRNA-packaging retrovirus-like capsids.","PeriodicalId":19063,"journal":{"name":"Nature Biomedical Engineering","volume":null,"pages":null},"PeriodicalIF":28.1,"publicationDate":"2024-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139906155","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}
Pub Date : 2024-02-12DOI: 10.1038/s41551-024-01181-y
Sjoukje J C van der Stegen, Pieter L Lindenbergh, Roseanna M Petrovic, Hongyao Xie, Mame P Diop, Vera Alexeeva, Yuzhe Shi, Jorge Mansilla-Soto, Mohamad Hamieh, Justin Eyquem, Annalisa Cabriolu, Xiuyan Wang, Ramzey Abujarour, Tom Lee, Raedun Clarke, Bahram Valamehr, Maria Themeli, Isabelle Riviere, Michel Sadelain
{"title":"Author Correction: Generation of T-cell-receptor-negative CD8αβ-positive CAR T cells from T-cell-derived induced pluripotent stem cells.","authors":"Sjoukje J C van der Stegen, Pieter L Lindenbergh, Roseanna M Petrovic, Hongyao Xie, Mame P Diop, Vera Alexeeva, Yuzhe Shi, Jorge Mansilla-Soto, Mohamad Hamieh, Justin Eyquem, Annalisa Cabriolu, Xiuyan Wang, Ramzey Abujarour, Tom Lee, Raedun Clarke, Bahram Valamehr, Maria Themeli, Isabelle Riviere, Michel Sadelain","doi":"10.1038/s41551-024-01181-y","DOIUrl":"https://doi.org/10.1038/s41551-024-01181-y","url":null,"abstract":"","PeriodicalId":19063,"journal":{"name":"Nature Biomedical Engineering","volume":null,"pages":null},"PeriodicalIF":28.1,"publicationDate":"2024-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139723462","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}
Pub Date : 2024-01-24DOI: 10.1038/s41551-024-01177-8
Charles W. F. Chan, Bei Wang, Lang Nan, Xiner Huang, Tianjiao Mao, Hoi Yee Chu, Cuiting Luo, Hin Chu, Gigi C. G. Choi, Ho Cheung Shum, Alan S. L. Wong
{"title":"Author Correction: High-throughput screening of genetic and cellular drivers of syncytium formation induced by the spike protein of SARS-CoV-2","authors":"Charles W. F. Chan, Bei Wang, Lang Nan, Xiner Huang, Tianjiao Mao, Hoi Yee Chu, Cuiting Luo, Hin Chu, Gigi C. G. Choi, Ho Cheung Shum, Alan S. L. Wong","doi":"10.1038/s41551-024-01177-8","DOIUrl":"10.1038/s41551-024-01177-8","url":null,"abstract":"","PeriodicalId":19063,"journal":{"name":"Nature Biomedical Engineering","volume":null,"pages":null},"PeriodicalIF":28.1,"publicationDate":"2024-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41551-024-01177-8.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139546802","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-22DOI: 10.1038/s41551-024-01176-9
A handy go-between may soon assist authors and editors.
一个方便的中间人可能很快就会为作者和编辑提供帮助。
{"title":"Hail the AI journal editor","authors":"","doi":"10.1038/s41551-024-01176-9","DOIUrl":"10.1038/s41551-024-01176-9","url":null,"abstract":"A handy go-between may soon assist authors and editors.","PeriodicalId":19063,"journal":{"name":"Nature Biomedical Engineering","volume":null,"pages":null},"PeriodicalIF":28.1,"publicationDate":"2024-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41551-024-01176-9.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139521611","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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