Molecular Therapy最新文献

Engineering a solution for allogeneic CAR-T rejection. 异体 CAR-T 排斥的工程解决方案。

IF 12.4 1区医学

Molecular Therapy Pub Date : 2024-09-11 DOI: 10.1016/j.ymthe.2024.08.025

Leila Amini,Lena Peter,Michael Schmueck-Henneresse

引用次数: 0

Targeting Rap1b signaling cascades with CDNF: Modulating Platelet Activation, Regulating Plasma Oxylipins and Mitigating Reperfusion Injury in stroke. 用 CDNF 靶向 Rap1b 信号级联：调节血小板活化、调节血浆氧脂和减轻中风的再灌注损伤。

IF 12.4 1区医学

Molecular Therapy Pub Date : 2024-09-09 DOI: 10.1016/j.ymthe.2024.09.005

Jui-Sheng Wu,Helike Lõhelaid,Chih-Chin Shih,Hock-Kean Liew,Vicki Wang,Wei-Fen Hu,Yuan-Hao Chen,Mart Saarma,Mikko Airavaara,Kuan-Yin Tseng

{"title":"Targeting Rap1b signaling cascades with CDNF: Modulating Platelet Activation, Regulating Plasma Oxylipins and Mitigating Reperfusion Injury in stroke.","authors":"Jui-Sheng Wu,Helike Lõhelaid,Chih-Chin Shih,Hock-Kean Liew,Vicki Wang,Wei-Fen Hu,Yuan-Hao Chen,Mart Saarma,Mikko Airavaara,Kuan-Yin Tseng","doi":"10.1016/j.ymthe.2024.09.005","DOIUrl":"https://doi.org/10.1016/j.ymthe.2024.09.005","url":null,"abstract":"Cerebral reperfusion injury in stroke, stemming from interconnected thrombotic and inflammatory signatures, often involves platelet activation, aggregation and its interaction with various immune cells, contributing to microvascular dysfunction. However, the regulatory mechanisms behind this platelet activation and the resulting inflammation are not well understood, complicating the development of effective stroke therapies. Utilizing animal models and platelets from hemorrhagic stroke patients, our research demonstrates that human cerebral dopamine neurotrophic factor (CDNF) acts as an endogenous antagonist, mitigating platelet aggregation and associated neuroinflammation. CDNF moderates mitochondrial membrane potential, reactive oxygen species production, and intracellular calcium in activated platelets by interfering with GTP binding to Rap1b, thereby reducing Rap1b activation and downregulating the Rap1b-MAPK-PLA2 signaling pathway, which decreases release of the pro-inflammatory mediator thromboxane A2. Additionally, CDNF reduces the inflammatory response in BV2 microglial cells co-cultured with activated platelets. Consistent with ex vivo findings, subcutaneous administration of CDNF in a rat model of ischemic stroke significantly reduces platelet activation, aggregation, lipid mediator production, infarct volume, and neurological deficits. In summary, our study highlights CDNF as a promising therapeutic target for mitigating platelet-induced inflammation and enhancing recovery in stroke. Harnessing the CDNF pathway may offer a novel therapeutic strategy for stroke intervention.","PeriodicalId":19020,"journal":{"name":"Molecular Therapy","volume":null,"pages":null},"PeriodicalIF":12.4,"publicationDate":"2024-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142170719","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 chimeric anti-inflammatory and anti-vascularization immunomodulator prevents high-risk corneal transplantation rejection via ex vivo gene therapy. 嵌合抗炎和抗血管免疫调节剂通过体外基因疗法预防高风险角膜移植排斥反应。

IF 12.1 1区医学

Molecular Therapy Pub Date : 2024-09-07 DOI: 10.1016/j.ymthe.2024.09.007

Brian C Gilger, Tomoko Hasegawa, R Bryan Sutton, Jacquelyn J Bower, Chengwen Li, Matthew L Hirsch

{"title":"A chimeric anti-inflammatory and anti-vascularization immunomodulator prevents high-risk corneal transplantation rejection via ex vivo gene therapy.","authors":"Brian C Gilger, Tomoko Hasegawa, R Bryan Sutton, Jacquelyn J Bower, Chengwen Li, Matthew L Hirsch","doi":"10.1016/j.ymthe.2024.09.007","DOIUrl":"https://doi.org/10.1016/j.ymthe.2024.09.007","url":null,"abstract":"Corneal blindness affects greater than 5 million individuals, with over 180,000 corneal transplantations (CTs) performed annually. Inhigh-risk CTs, almost all grafts are rejected within 10 years. Herein, adeno-associated virus (AAV) ex vivo gene therapy was investigated to establish immune tolerance in the corneal allograft to prevent high-risk CT rejection. Our previous work has demonstrated that HLA-G contributes to ocular immune privilege by inhibiting both immune cells and neovascularization; however, homodimerization is a rate-limiting step for optimal HLA-G function. Therefore, a chimeric protein termed single chain immunomodulator (sclM), was engineered to mimic the native activity of the secreted HLA-G dimer complex and eliminate the need for homodimerization. In a murine corneal burn model, AAV8-sclM significantly reduced corneal vascularization and fibrosis. Next, ex vivo AAV8-scIM gene delivery to corneal allografts was evaluated in a high-risk CT rejection rabbit model. All sclM treated corneas were well tolerated and transparent after 42 days while 83% of vehicle treated corneas were rejected. Histologically, AAV-scIM treated corneas were devoid of immune cell infiltration, vascularization, with minimal fibrosis at the host-graft interface. The data collectively demonstrate that sclM gene therapy prevents corneal neovascularization, reduces trauma-induced corneal fibrosis, and prevents allogeneic CT rejection in a high-risk large animal model.","PeriodicalId":19020,"journal":{"name":"Molecular Therapy","volume":null,"pages":null},"PeriodicalIF":12.1,"publicationDate":"2024-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142154617","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 CD25×TIGIT bispecific antibody induces anti-tumor activity through selective intratumoral Treg cell depletion. CD25×TIGIT 双特异性抗体通过选择性消耗瘤内 Treg 细胞诱导抗肿瘤活性。

IF 12.1 1区医学

Molecular Therapy Pub Date : 2024-09-07 DOI: 10.1016/j.ymthe.2024.09.010

Xin Wei, Linlin Zhao, Fang Yang, Yajing Yang, Huixiang Zhang, Kaixin Du, Xinxin Tian, Ruihua Fan, Guangxu Si, Kailun Wang, Yulu Li, Zhizhong Wei, Miaomiao He, Jianhua Sui

{"title":"A CD25×TIGIT bispecific antibody induces anti-tumor activity through selective intratumoral Treg cell depletion.","authors":"Xin Wei, Linlin Zhao, Fang Yang, Yajing Yang, Huixiang Zhang, Kaixin Du, Xinxin Tian, Ruihua Fan, Guangxu Si, Kailun Wang, Yulu Li, Zhizhong Wei, Miaomiao He, Jianhua Sui","doi":"10.1016/j.ymthe.2024.09.010","DOIUrl":"https://doi.org/10.1016/j.ymthe.2024.09.010","url":null,"abstract":"Intratumoral regulatory T cells (Tregs) express high levels of CD25 and TIGIT, which are also recognized as markers of effector T cell (Teff) activation. Targeting these molecules each alone with monoclonal antibodies (mAbs) poses a risk of concurrently depleting both Teffs and peripheral Tregs, thereby compromising the effectiveness and selectivity of intratumoral Treg depletion. Here, leveraging the increased abundance of CD25+ TIGIT+ double positive Tregs in the solid tumor microenvironment (but not in peripheral tissues), we explored the feasibility of using a CD25×TIGIT bispecific antibody (bsAb) to selectively deplete intratumoral Tregs. We initially constructed a bsAb co-targeting mouse CD25 and TIGIT, NSWm7210, and found that NSWm7210 conferred enhanced intratumoral Treg depletion, Teff activation, and tumor suppression as compared to the parental monotherapies in mouse models. We subsequently constructed a bsAb co-targeting human CD25 and TIGIT (NSWh7216), which preferentially eliminated CD25+ TIGIT+ double positive cells over single positive cells in vitro. NSWh7216 exhibited enhanced anti-tumor activity without toxicity of peripheral Tregs in CD25 humanized mice compared to the parental monotherapies. Our study illustrates the use of CD25×TIGIT bsAbs as effective agents against solid tumors based on selective depletion of intratumoral Tregs.","PeriodicalId":19020,"journal":{"name":"Molecular Therapy","volume":null,"pages":null},"PeriodicalIF":12.1,"publicationDate":"2024-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142154616","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

Case study of CD19-directed chimeric antigen receptor T-cell therapy in a subject with immune-mediate necrotizing myopathy treated in the RESET-Myositis™ phase I/II trial. 在 RESET-Myositis™ I/II 期试验中对一名免疫性中度坏死性肌病患者进行 CD19 引导嵌合抗原受体 T 细胞疗法的病例研究。

IF 12.1 1区医学

Molecular Therapy Pub Date : 2024-09-07 DOI: 10.1016/j.ymthe.2024.09.009

Jenell Volkov, Daniel Nunez, Tahseen Mozaffar, Jason Stadanlick, Mallorie Werner, Zachary Vorndran, Alexandra Ellis, Jazmean Williams, Justin Cicarelli, Quynh Lam, Thomas Furmanak, Chris Schmitt, Fatemeh Hadi-Nezhad, Daniel Thompson, Claire Miller, Courtney Little, David Chang, Samik Basu

{"title":"Case study of CD19-directed chimeric antigen receptor T-cell therapy in a subject with immune-mediate necrotizing myopathy treated in the RESET-Myositis™ phase I/II trial.","authors":"Jenell Volkov, Daniel Nunez, Tahseen Mozaffar, Jason Stadanlick, Mallorie Werner, Zachary Vorndran, Alexandra Ellis, Jazmean Williams, Justin Cicarelli, Quynh Lam, Thomas Furmanak, Chris Schmitt, Fatemeh Hadi-Nezhad, Daniel Thompson, Claire Miller, Courtney Little, David Chang, Samik Basu","doi":"10.1016/j.ymthe.2024.09.009","DOIUrl":"https://doi.org/10.1016/j.ymthe.2024.09.009","url":null,"abstract":"Under compassionate use, chimeric antigen receptor (CAR) T-cells have elicited durable remissions in patients with refractory idiopathic inflammatory myopathies (IIM)1. Here, we report on the safety, efficacy, and correlative data of the first subject with the immune-mediated necrotizing myopathy (IMNM) subtype of IIM who received a fully human, 4-1BBz anti-CD19-CAR T-cell therapy (CABA-201) in the RESET-Myositis™ phase I/II trial (NCT06154252). CABA-201 was well-tolerated following infusion. Notably, no evidence of cytokine release syndrome (CRS) or immune effector-cell associated neurotoxicity syndrome (ICANS) was observed. CK levels decreased, and muscular strength improved post-infusion. Peripheral B-cells were depleted rapidly following infusion, and the subject achieved peripheral B-cell aplasia by day 15 post-infusion. Peripheral B-cells returned at 2 months post-infusion and were almost entirely transitional. Autoantibodies to SRP-9, SRP-72, SRP-54, and Ro-52, decreased relative to baseline whereas antibodies associated with pathogens and vaccinations remained stable. The infusion product consisted of predominantly CD4+ effector memory T-cells & exhibited in vitro cytolytic activity. Post-infusion, CABA-201 expansion peaked at day 15 and was preceded by a serum IFN-γ peak on day 8 with peaks in serum IL-12p40 and IP-10 on day 15. These data detail the safety, efficacy, and pharmacodynamics of CABA-201 in the first IMNM subject.","PeriodicalId":19020,"journal":{"name":"Molecular Therapy","volume":null,"pages":null},"PeriodicalIF":12.1,"publicationDate":"2024-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142154630","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

CasRx-based Wnt activation promotes alveolar regeneration while ameliorating pulmonary fibrosis in a mouse model of lung injury. 基于 CasRx 的 Wnt 激活可促进肺泡再生，同时改善小鼠肺损伤模型中的肺纤维化。

IF 12.1 1区医学

Molecular Therapy Pub Date : 2024-09-07 DOI: 10.1016/j.ymthe.2024.09.008

Shengxi Shen, Ping Wang, Pei Wu, Pengyu Huang, Tian Chi, Wenqing Xu, Ying Xi

{"title":"CasRx-based Wnt activation promotes alveolar regeneration while ameliorating pulmonary fibrosis in a mouse model of lung injury.","authors":"Shengxi Shen, Ping Wang, Pei Wu, Pengyu Huang, Tian Chi, Wenqing Xu, Ying Xi","doi":"10.1016/j.ymthe.2024.09.008","DOIUrl":"https://doi.org/10.1016/j.ymthe.2024.09.008","url":null,"abstract":"Wnt/β-catenin signaling is an attractive target for regenerative medicine. A powerful driver of stem cell activity and hence tissue regeneration, Wnt signaling can promote fibroblast proliferation and activation, leading to fibrosis, while prolonged Wnt signaling is potentially carcinogenic. Thus, to harness its therapeutic potential, the activation of Wnt signaling must be transient, reversible and tissue-specific. In the lung, Wnt signaling is essential for alveolar stem cell activity and alveolar regeneration, which is impaired in lung fibrosis. Activation of Wnt/β-catenin signaling in lung epithelium may have anti-fibrotic effects. Here, we used intratracheal AAV6 injection to selectively deliver CasRx into lung epithelium, where it reversibly activates Wnt signaling by simultaneously degrading mRNAs encoding Axin1 and Axin2, negative regulators of Wnt/β-catenin signaling. Interestingly, CasRx mediated Wnt activation specifically in lung epithelium not only promotes alveolar type II cell (AT2) proliferation and alveolar regeneration, but also inhibits lung fibrosis resulted from bleomycin-induced injury, relevant in both preventive and therapeutic settings. Our study offers an attractive strategy for treating pulmonary fibrosis, with general implications for regenerative medicine.","PeriodicalId":19020,"journal":{"name":"Molecular Therapy","volume":null,"pages":null},"PeriodicalIF":12.1,"publicationDate":"2024-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142154631","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

Prevention of Prostate Cancer Metastasis by a CRISPR-delivering Nanoplatform for Interleukin-30 Genome Editing. 通过CRISPR递送纳米平台进行白细胞介素-30基因组编辑，预防前列腺癌转移。

IF 12.1 1区医学

Molecular Therapy Pub Date : 2024-09-06 DOI: 10.1016/j.ymthe.2024.09.011

Cristiano Fieni, Stefania Livia Ciummo, Carlo Sorrentino, Simona Marchetti, Simone Vespa, Paola Lanuti, Lavinia Vittoria Lotti, Emma Di Carlo

{"title":"Prevention of Prostate Cancer Metastasis by a CRISPR-delivering Nanoplatform for Interleukin-30 Genome Editing.","authors":"Cristiano Fieni, Stefania Livia Ciummo, Carlo Sorrentino, Simona Marchetti, Simone Vespa, Paola Lanuti, Lavinia Vittoria Lotti, Emma Di Carlo","doi":"10.1016/j.ymthe.2024.09.011","DOIUrl":"https://doi.org/10.1016/j.ymthe.2024.09.011","url":null,"abstract":"Prostate-cancer (PC) is a leading cause of cancer-related deaths in men worldwide. Interleukin-(IL)-30 is a PC-progression driver, and its suppression would be strategic for fighting metastatic disease. Biocompatible Lipid-Nanoparticles (NPs) were loaded with CRISPR/Cas9gRNA to delete human(h)IL30-gene and functionalized with anti-PSCA-Abs (Cas9hIL30-PSCA-NPs). Efficiency of the NPs in targeting IL30 and metastatic potential of PC cells was examined in vivo, in xenograft models of lung metastasis, and in vitro, by using 2-Organ-on-Chip (2-OC), containing 3D-spheroids of IL30+PC-Endothelial-Cell(EC) co-cultures in circuit with either Lung-mimicking-spheroids, or Bone-marrow(BM)-niche-mimicking-scaffolds. Cas9hIL30-PSCA-NPs demonstrated circulation stability, genome editing efficiency, without off-target effects and organ toxicity. Intravenous injection of three-doses/13-days, or five-doses/20-days, of NPs in mice bearing circulating PC cells and micro-emboli substantially hindered lung metastasization. Cas9hIL30-PSCA-NPs inhibited PC cell proliferation and expression of IL30 and metastasis-drivers, such as CXCR2, CXCR4, IGF1, L1CAM, METAP2, MMP2 and TNFSF10, whereas CDH1 was up-regulated. PC-Lung and PC-BM 2-OCs revealed that Cas9hIL30-PSCA-NPs suppressed PC cell release of CXCL2/GROβ, which in vivo was associated with intra-metastatic myeloid cell infiltrates, and of DKK1, OPG and IL6, which in vitro boosted endothelial-network formation and cancer cell migration. Development of a patient-tailored nanoplatform for selective CRISPR-mediated IL30 gene deletion is a clinically valuable tool against PC progression.","PeriodicalId":19020,"journal":{"name":"Molecular Therapy","volume":null,"pages":null},"PeriodicalIF":12.1,"publicationDate":"2024-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142146005","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

Autologous CD7 CAR T cells generated without T-cell pre-selection in pediatric patients with relapsed/refractory T-ALL: a phase I trial. 在复发/难治性 T-ALL 儿科患者中未进行 T 细胞预选而生成的自体 CD7 CAR T 细胞：I 期试验。

IF 12.1 1区医学

Molecular Therapy Pub Date : 2024-09-06 DOI: 10.1016/j.ymthe.2024.09.006

Liping Zhao, Chuo Li, Shiyu Zuo, Yajing Han, Biping Deng, Zhuojun Ling, Yanlei Zhang, Shuixiu Peng, Jinlong Xu, Jiajia Duan, Zelin Wang, Xinjian Yu, Qinlong Zheng, Xiuwen Xu, Ying Yuan, Zhenglong Tian, Kaiting Tang, Yibing Zhang, Qing Niu, Jiecheng Zhang, Alex H Chang, Yuechen Luo, Xiaoming Feng, Jing Pan

{"title":"Autologous CD7 CAR T cells generated without T-cell pre-selection in pediatric patients with relapsed/refractory T-ALL: a phase I trial.","authors":"Liping Zhao, Chuo Li, Shiyu Zuo, Yajing Han, Biping Deng, Zhuojun Ling, Yanlei Zhang, Shuixiu Peng, Jinlong Xu, Jiajia Duan, Zelin Wang, Xinjian Yu, Qinlong Zheng, Xiuwen Xu, Ying Yuan, Zhenglong Tian, Kaiting Tang, Yibing Zhang, Qing Niu, Jiecheng Zhang, Alex H Chang, Yuechen Luo, Xiaoming Feng, Jing Pan","doi":"10.1016/j.ymthe.2024.09.006","DOIUrl":"https://doi.org/10.1016/j.ymthe.2024.09.006","url":null,"abstract":"Chimeric antigen receptor (CAR) T-cell therapy showed preliminary activity in patients with refractory or relapsed T-cell acute lymphoblastic leukemia (r/r T-ALL). However, many obstacles remain, including manufacturing difficulties and risk of infections. This phase I study (NCT04840875) evaluated autologous CD7 CAR T cells manufactured without pre-selection of healthy T cells in r/r T-ALL. Thirty patients (29 children and one adult) with a median of two lines of prior therapy but without detectable peripheral leukemia were enrolled. Excluding three cases of manufacturing failures, a total of 27 (90%) patients received infusions after products were confirmed free of leukemia contamination, including 16 (59%) meeting planned target doses. Common adverse events within 30 days included grade 3-4 cytopenias (100%), grade 1-2 (70%) and 3-4 (7%; including one dose-limiting toxicity) cytokine release syndrome, grade 1 neurotoxicity (7%), grade 2 infection (4%), and grade 2 graft-versus-host disease (4%). Two patients developed grade 2 infections after day 30. At day 30, 96% responded and 85% achieved CR or CRi. 74% underwent transplantation. Twelve-month progression-free survival with and without censoring transplantation was 22% (95%CI 4-100) and 57% (41-81), respectively. These results support that autologous CD7 CAR T-cell therapy without T-cell pre-selection is feasible in patients with r/r T-ALL.","PeriodicalId":19020,"journal":{"name":"Molecular Therapy","volume":null,"pages":null},"PeriodicalIF":12.1,"publicationDate":"2024-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142145995","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

T cell-redirecting therapies in hematological malignancies: Current developments and novel strategies for improved targeting. 血液恶性肿瘤中的 T 细胞重定向疗法：血液恶性肿瘤中的 T 细胞重定向疗法：改善靶向性的当前发展和新策略》（Current Developments and Novel Strategies for Improved Targeting.

IF 12.1 1区医学

Molecular Therapy Pub Date : 2024-09-04 Epub Date: 2024-08-05 DOI: 10.1016/j.ymthe.2024.07.028

Georgina S F Anderson, Michael A Chapman

引用次数: 0

Decoding the healing dialogues for tissue repair. 解码组织修复的愈合对话。

IF 12.1 1区医学

Molecular Therapy Pub Date : 2024-09-04 Epub Date: 2024-08-22 DOI: 10.1016/j.ymthe.2024.08.008

Subhadip Ghatak

引用次数: 0