Interdisciplinary Medicine最新文献

{"title":"The regulation of stem cell fate and its application in neural regeneration","authors":"Yuexin He,&nbsp;Xingyu Chen,&nbsp;Minghong He,&nbsp;Zhe Li","doi":"10.1002/inmd.70137","DOIUrl":"https://doi.org/10.1002/inmd.70137","url":null,"abstract":"<p>Regulating the fate of stem cells (SCs) is a key technical problem in the field of regenerative medicine and tissue engineering, which involves the comprehensive effect of many factors. The commonly used types of SCs were summarized, and the research progress of regulating the fate of SCs through physical factors, biological factors and chemical factors were discussed. It also reviewed the applications and mechanism of SCs in repairing neurodegenerative diseases, optic nerve injury, auditory nerve injury, traumatic peripheral nerve injury, etc. Finally, the future regulatory strategies and development were prospects. The aim is to provide a new idea and method for the treatment of neural regeneration.</p>","PeriodicalId":100686,"journal":{"name":"Interdisciplinary Medicine","volume":"4 5","pages":""},"PeriodicalIF":13.6,"publicationDate":"2026-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/inmd.70137","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148994504","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting eIF5A combats breast cancer progression by ClpP-dependent mitochondrial oxidative stress","authors":"Jinmei Zhu,&nbsp;Baoyuan Tang,&nbsp;Bei Xie,&nbsp;Haohua Deng,&nbsp;Haitang Yang,&nbsp;Lei Ma,&nbsp;Ziqing Zhang,&nbsp;Yicheng Ma,&nbsp;Xingyuan Ma,&nbsp;Shuaiyang Wang,&nbsp;Jing Li,&nbsp;Lei Zhao,&nbsp;Wengui Shi,&nbsp;Linjing Li","doi":"10.1002/inmd.70140","DOIUrl":"https://doi.org/10.1002/inmd.70140","url":null,"abstract":"<p>Breast cancer (BC) poses a persistent global health challenge, necessitating new therapeutic targets. The oncogenic translation factor Eukaryotic translation initiation factor 5A (eIF5A), while implicated in other cancers, lacks a mechanistic definition in BC. In this study, we found that eIF5A was significantly overexpressed in BC and correlated with poor clinical outcomes. Knocking down of eIF5A could suppress BC cell proliferation and migration in vitro, induce apoptosis and cell cycle arrest, and inhibit tumor growth in vivo in the MMTV-PyMT model. Mechanistically, eIF5A depletion induced mitochondrial dysfunction, characterized by elevated reactive oxygen species (ROS), reduced mitochondrial membrane potential (ΔΨm), compromised ATP synthesis and enhanced oxidative damage. These defects, along with the impaired tumorigenicity, were rescued by overexpressing the mitochondrial protease ATP-dependent Clp protease proteolytic subunit (ClpP). We further demonstrated that eIF5A promoted tumor progression, at least in part, by binding to and enhancing the translation of <i>ClpP</i> mRNA, leading to upregulation of ClpP. Importantly, we identified the eIF5A-ClpP axis as a key regulator of mitochondrial redox homeostasis in BC, and its disruption effectively suppressed malignant phenotypes. These findings established the eIF5A-ClpP axis as a mechanistically grounded and therapeutically targetable vulnerability for BC intervention.</p>","PeriodicalId":100686,"journal":{"name":"Interdisciplinary Medicine","volume":"4 5","pages":""},"PeriodicalIF":13.6,"publicationDate":"2026-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/inmd.70140","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148994183","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting the intratumoral microbiota to overcome cancer immunotherapy resistance","authors":"Bufu Tang,&nbsp;Tong Jiang,&nbsp;Yaling Lin,&nbsp;Wei Zhang,&nbsp;Hongjie Fan,&nbsp;Minjie Yang,&nbsp;Bingzhe Li,&nbsp;Yaozu Liu,&nbsp;Changyu Li,&nbsp;Xuran Jin,&nbsp;Wen Zhang,&nbsp;Zhiping Yan,&nbsp;Qianqian Zhao,&nbsp;Xuefeng Kan,&nbsp;Xudong Qu","doi":"10.1002/inmd.70155","DOIUrl":"https://doi.org/10.1002/inmd.70155","url":null,"abstract":"<p>Cancer remains a significant global health threat. The tumor microenvironment (TME) is a sophisticated ecological niche that exerts a pivotal effect on treatment outcomes. Among the diverse components composing the TME, the intratumoral microbiota (IM) has become a research focus, which can regulate tumor initiation, progression, and therapeutic response. The link between cancer and microorganisms dates back 4000 years. Advanced sequencing technologies have revealed that the unique microbial communities within tumors serve a dual function: directly modulating tumor cell biology via metabolic processes and shaping TME immunity through interactions with immune and matrix components. Their metabolites act as mediators either inducing immunosuppression via immune metabolic reprogramming or triggering systemic immunity through pattern recognition receptors. Consequently, IM imbalances may contribute to immune evasion and therapeutic resistance. This article addresses immunotherapy resistance and treatment failure, systematically exploring the origins and detection methods of IM, elucidating its regulatory mechanisms within the TME, examining its impact on immunotherapy efficacy, assessing the utility of IM in diagnostic biomarker applications, and discussing the technical challenges and a roadmap for further inquiry, directed toward providing a comprehensive framework to advance precision immunotherapy in cancer treatment.</p>","PeriodicalId":100686,"journal":{"name":"Interdisciplinary Medicine","volume":"4 5","pages":""},"PeriodicalIF":13.6,"publicationDate":"2026-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/inmd.70155","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148994310","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Current strategies to enhance the target efficiency of advanced multifunctional ultrasound contrast agents in ischemic diseases","authors":"Yangyang Zhou,&nbsp;Jing Lin,&nbsp;Yu Chen,&nbsp;Jiaqi Zhao","doi":"10.1002/inmd.70160","DOIUrl":"https://doi.org/10.1002/inmd.70160","url":null,"abstract":"<p>Ischemic diseases, such as myocardial infarction, stroke, and peripheral ischemia, are leading causes of death and disability worldwide. The complex pathophysiological mechanisms underlying ischemia-reperfusion injury pose formidable obstacles to early diagnosis and precise therapeutic intervention. In recent years, the development of novel multifunctional ultrasound contrast agents (UCAs) has established an innovative platform for disease visualization at both microcirculatory and molecular levels, thereby advancing the integration of diagnostic and therapeutic approaches. The effectiveness of these advanced carriers critically depends on their capacity for selective accumulation within target lesions. This review systematically summarizes recent advances in multifunctional UCAs for the diagnosis and treatment of ischemic diseases, along with advanced strategies designed to enhance targeting efficiency. Although several of these approaches have not yet been widely implemented in the context of ischemic conditions, they nevertheless offer conceptual frameworks and inspiration for future research. This review aims to provide both a theoretical foundation and technical insights to support the development of novel UCAs-based targeted theranostic systems.</p>","PeriodicalId":100686,"journal":{"name":"Interdisciplinary Medicine","volume":"4 5","pages":""},"PeriodicalIF":13.6,"publicationDate":"2026-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/inmd.70160","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148994316","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitochondria-targeted nanomedicine for cancer therapy: Targeting strategies, therapeutic mechanisms, and translational challenges","authors":"Linfeng Xiao,&nbsp;Xiaowei Chang,&nbsp;Jun Zhang,&nbsp;Yinshan Hong,&nbsp;Wenhui Cao,&nbsp;Zhewu Zhao,&nbsp;Yu-E. Wang,&nbsp;Yanling Yang","doi":"10.1002/inmd.70166","DOIUrl":"https://doi.org/10.1002/inmd.70166","url":null,"abstract":"<p>Mitochondria are central regulators of cellular energy metabolism, redox homeostasis, and programmed cell death, making them highly attractive targets for cancer therapy. Rapid advances in nanotechnology have enabled the rational design of mitochondria-targeted nanomedicines for subcellularly precise drug delivery. At present, mitochondrial targeting is mainly achieved by surface modification with lipophilic cations or functional peptides. Nanoparticles (NPs) equipped with these moieties can preferentially accumulate in tumor-cell mitochondria and enhance antitumor efficacy through multiple mechanisms, including disruption of redox balance, interference with energy metabolism, damage to mitochondrial structure, and induction of immunogenic cell death. These systems may also reduce systemic toxicity and help overcome therapeutic resistance. However, a comprehensive framework for the rational design of mitochondria-targeted nanoparticles remains lacking. In this review, we summarize current design strategies for mitochondria-targeted nanoparticles, discuss their multidimensional antitumor mechanisms, and highlight recent advances in their applications in cancer therapy. We further examine the major challenges related to targeting efficiency, biosafety, and clinical translation. This review aims to provide a useful reference for the development of next-generation mitochondria-targeted nanotherapeutics with improved precision and efficacy.</p>","PeriodicalId":100686,"journal":{"name":"Interdisciplinary Medicine","volume":"4 5","pages":""},"PeriodicalIF":13.6,"publicationDate":"2026-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/inmd.70166","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148994516","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"3D printing of cell-free implants: A promising avenue for cartilage regeneration and joint preservation (5/2026)","authors":"Liangbin Zhou,&nbsp;Shangsi Chen,&nbsp;Boguang Yang,&nbsp;Yiting Lei,&nbsp;Hegeng Li,&nbsp;Haoyue Luo,&nbsp;Xiaoshuai Wang,&nbsp;Qiongjiao Zeng,&nbsp;Jiahui Lai,&nbsp;Fei Jin,&nbsp;Rocky S. Tuan,&nbsp;Zhong Alan Li","doi":"10.1002/inmd.70175","DOIUrl":"https://doi.org/10.1002/inmd.70175","url":null,"abstract":"<p>Articular cartilage injury and osteoarthritis affect hundreds of millions worldwide, yet current treatments, from microfracture to autologous chondrocyte implantation, remain plagued by their limited efficacy. In this perspective, Zhou and colleagues argue for a transformative paradigm shift: moving beyond cell-based therapies toward 3D-printed cell-free implants that harness the body's intrinsic regenerative capacity.</p><p>The authors present a compelling case for leveraging endogenous stem/progenitor cells (ESPCs) through meticulously engineered biomaterial scaffolds. Unlike conventional approaches requiring costly in vitro cell expansion, these acellular implants are designed to actively recruit, retain, and guide resident stem cells toward functional cartilage and bone regeneration. By integrating precise biophysical cues (topography, stiffness, porosity) with biochemical signals (chemoattractants, growth factors, immunomodulatory agents), 3D printing enables patient-specific customization and spatiotemporal control unattainable with traditional manufacturing.</p><p>The article critically examines the biological mechanisms underlying endogenous regeneration, contrasts cell-free versus cell-based strategies, and navigates the complex translational pathway from bench to bedside. While challenges remain, including long-term stability, optimal cue combinations, and efficacy in aged or osteoarthritic joints, the convergence of advanced biomaterials, biofabrication technologies, artificial intelligence, and organ-on-a-chip technologies promises to accelerate clinical adoption.</p><p>This timely perspective challenges the assumption that exogenous cells are indispensable for cartilage repair, proposing instead that well-designed cell-free devices could democratize access to regenerative care. For the growing aging population affected by degenerative joint diseases, 3D-printed acellular scaffolds represent a cost-effective, scalable, and ethically advantageous pathway toward functional joint preservation and restored quality of life.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":100686,"journal":{"name":"Interdisciplinary Medicine","volume":"4 5","pages":""},"PeriodicalIF":13.6,"publicationDate":"2026-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/inmd.70175","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148994645","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reversing brain aging: Targeting energy metabolism in endogenous neural stem cells","authors":"Chong Chen,&nbsp;Jiayi Wang,&nbsp;Jimin Yu,&nbsp;Yiran Zhou,&nbsp;Lihai Liu,&nbsp;Jing Liu,&nbsp;Liang Wang","doi":"10.1002/inmd.70159","DOIUrl":"https://doi.org/10.1002/inmd.70159","url":null,"abstract":"<p>Brain aging is a primary driver of human aging, and the decline of endogenous neural stem cells (eNSCs) is a central mechanism in this process. eNSCs, located in the subventricular zone and subgranular zone, are essential for neuronal regeneration and brain repair. Their aging process is closely associated with dysregulated energy metabolism, which is specifically manifested as homeostatic imbalances in key metabolic pathways, including the tricarboxylic acid cycle, glycolysis, oxidative phosphorylation, fatty acid oxidation, and amino acid metabolism. This metabolic dysregulation serves both as a hallmark and a catalyst of brain aging and related disorders. Targeting eNSC energy metabolism is a promising strategy for counteracting brain aging. Interventions such as targeting mitochondrial function of eNSCs, modulating key metabolic pathways and therapeutic targets in eNSCs, and targeted activation of eNSCs, can activate eNSCs and promote nerve regeneration. Shifting brain senescence from an irreversible process to a modifiable process represents a transformative paradigm in aging research. Elucidating the molecular mechanism that regulates the changes in the metabolic lineage of eNSCs during brain aging will not only accelerate the cure of neurological diseases but also open up a new perspective for the development of advanced brain functions.</p>","PeriodicalId":100686,"journal":{"name":"Interdisciplinary Medicine","volume":"4 5","pages":""},"PeriodicalIF":13.6,"publicationDate":"2026-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/inmd.70159","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148994042","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recent advances and clinical applications of 3D printing for female reproductive organ regeneration and gynecological disease","authors":"Chan Hum Park,&nbsp;In-Sun Hong","doi":"10.1002/inmd.70157","DOIUrl":"https://doi.org/10.1002/inmd.70157","url":null,"abstract":"<p>The integration of three-dimensional (3D) printing and bioprinting technologies has significantly reshaped the landscape of gynecological medicine, offering innovative strategies to address clinical challenges related to reproductive organ disorders and gynecological malignancies. This review systematically examines recent advancements and clinical applications of 3D printing in female reproductive health, with a focus on tissue engineering and personalized medical solutions for complex gynecological conditions. Specifically, it discusses cutting-edge developments in 3D bioprinting techniques tailored for regenerating uterine endometrium, ovarian, cervical, vaginal, and pelvic tissues, while highlighting the crucial role of advanced biomaterials, bioinks, and patient-specific scaffold fabrication. Furthermore, it critically evaluates personalized 3D printing approaches in gynecological oncology, including targeted drug delivery systems, precision brachytherapy applicators, and anatomical models designed to improve surgical outcomes and therapeutic efficacy in endometrial, cervical, and ovarian cancers. Despite significant technological advancements, persistent challenges remain, such as limitations in materials, control over drug release, vascularization strategies, and regulatory hurdles. The review concludes by outlining future research directions, focusing on the integration of advanced imaging, artificial intelligence-driven design, and multimodal therapeutic platforms. Ultimately, the incorporation of these sophisticated 3D printing solutions into routine clinical practice promises to set new benchmarks in precision gynecology, substantially enhancing patient-specific therapeutic outcomes and quality of life.</p>","PeriodicalId":100686,"journal":{"name":"Interdisciplinary Medicine","volume":"4 5","pages":""},"PeriodicalIF":13.6,"publicationDate":"2026-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/inmd.70157","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148994052","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"FAM107A loss facilitates TTK-OPTN-mediated mitophagy to drive docetaxel resistance in castration-resistant prostate cancer","authors":"Yishan Zhang,&nbsp;Fan Zou,&nbsp;Mingdong Wang,&nbsp;Chenyue Wu,&nbsp;Yingwei Xie,&nbsp;Yongjun Quan,&nbsp;Wei Yan,&nbsp;Yupeng Zheng,&nbsp;Lianhua Li,&nbsp;Yuexin Liu,&nbsp;Jian Yu,&nbsp;Hao Ping","doi":"10.1002/inmd.70141","DOIUrl":"https://doi.org/10.1002/inmd.70141","url":null,"abstract":"<p>Docetaxel remains a mainstay in the treatment of prostate cancer; however, docetaxel resistance continues to pose a major challenge and is associated with unfavorable patient outcomes. Efforts to overcome known resistance mechanisms have largely failed to improve survival, often increasing toxicity. In this study, we demonstrated that FAM107A expression is downregulated during the development of docetaxel resistance in prostate cancer, and its overexpression enhances cellular sensitivity to docetaxel both in vitro and in vivo. Transcriptomic analyses identified TTK as a downstream effector, which was further validated in vitro. TTK can activate mitophagy, facilitate the timely clearance of damaged mitochondria, reduce intracellular reactive oxygen species levels, and thereby promote docetaxel resistance. We further confirmed the role of the FAM107A-TTK-mitophagy axis in docetaxel resistance in castration-resistant prostate cancer (CRPC) patients at single-cell resolution. Integrated proteomic profiling and co-immunoprecipitation assays revealed that TTK interacts with OPTN, a key mediator of mitophagy. Finally, we showed that the TTK inhibitor CFI-402257 combined with docetaxel exhibited favorable efficacy and safety in vivo against CRPC. Collectively, our findings revealed for the first time the critical role of the FAM107A-TTK-OPTN mitophagy axis in docetaxel resistance and suggest that targeting this axis may represent a promising therapeutic strategy to overcome docetaxel resistance.</p>","PeriodicalId":100686,"journal":{"name":"Interdisciplinary Medicine","volume":"4 5","pages":""},"PeriodicalIF":13.6,"publicationDate":"2026-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/inmd.70141","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148994114","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"3D printing of cell-free implants: A promising avenue for cartilage regeneration and joint preservation","authors":"Liangbin Zhou,&nbsp;Shangsi Chen,&nbsp;Boguang Yang,&nbsp;Yiting Lei,&nbsp;Hegeng Li,&nbsp;Haoyue Luo,&nbsp;Xiaoshuai Wang,&nbsp;Qiongjiao Zeng,&nbsp;Jiahui Lai,&nbsp;Fei Jin,&nbsp;Rocky S. Tuan,&nbsp;Zhong Alan Li","doi":"10.1002/inmd.70161","DOIUrl":"https://doi.org/10.1002/inmd.70161","url":null,"abstract":"<p>Cartilage regeneration and joint preservation are confronted with tremendous challenges. Traditional cell-based treatments, while effective in some cases, still encounter many limitations, including immunogenicity, high costs, and logistical problems concerning cell sourcing, in vitro expansion, and storage. Recent progress in 3D printing technologies offers a promising alternative: 3D-printed cell-free implants. By exploiting biomaterial-driven activation and augmentation of the pro-regenerative roles of endogenous stem/progenitor cells (ESPCs), via spatiotemporally controlled biophysical and biochemical cues, these medical devices can offer a scalable patient-specific solution for cartilage or osteochondral regeneration. This perspective article argues that their success hinges on optimizing intricate scaffold design and fabrication to mimic native tissue hierarchy, elucidating ESPC recruitment and repair mechanisms, and addressing regulatory barriers to clinical translation. Fulfilling these criteria could democratize access to regenerative care while circumventing the ethical and practical pitfalls of exogenous cell- and in vitro-expanded autologous cell-based interventions.</p>","PeriodicalId":100686,"journal":{"name":"Interdisciplinary Medicine","volume":"4 5","pages":""},"PeriodicalIF":13.6,"publicationDate":"2026-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/inmd.70161","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148994317","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}