Christian M. Mendiondo, Andrew R. King, Felipe Morales, David Leyton-Cifuentes, Theodore J. Pabst, Eric M. Brey, Christopher R. Rathbone
{"title":"Fibro-Adipogenic Progenitors From Skeletal Muscle Enhance Microvascular Angiogenesis in a 3D Model","authors":"Christian M. Mendiondo, Andrew R. King, Felipe Morales, David Leyton-Cifuentes, Theodore J. Pabst, Eric M. Brey, Christopher R. Rathbone","doi":"10.1002/adbi.70162","DOIUrl":"https://doi.org/10.1002/adbi.70162","url":null,"abstract":"<p>Skeletal muscle tissue is highly vascularized, and angiogenesis plays a key role in both muscle homeostasis and regeneration. Despite their importance in regulating various processes within skeletal muscle, little is known about the role of muscle-resident fibro-adipogenic progenitors (FAPs) in promoting microvascular angiogenesis. In order to better understand the effects of FAPs on angiogenesis, FAPs were co-cultured with adipose-derived microvascular fragments (MVFs) in three-dimensional fibrin hydrogels. We further tested if pre-culturing FAPs in brown adipogenic induction media (BAM) influences their ability to promote MVF angiogenesis. MVFs co-cultured with control FAPs or BAM FAPs for 5 days exhibit robust microvascular network formation with significantly increased vessel percentage area and average vessel length compared to MVFs alone. FAPs cultured in BAM prior to co-culture with MVFs alter vascular network development compared to MVFs co-cultured with control FAPs by significantly increasing average vessel length. Collectively, these results indicate that FAPs are key regulators of microvascular angiogenesis and that BAM FAPs have an improved capacity to promote increases in average vessel length. The current findings support the transplantation of FAPs and MVFs and modulation of FAP pro-angiogenic properties as potential therapeutic approaches for enhancing skeletal muscle angiogenesis in the context of injury and disease.</p>","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":"10 10","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/adbi.70162","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149177539","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Zeyu Cui, Wei Wu, Yanchen Lai, Te Liu, Fangfang Dou, Lian Yang, Gang Zou
{"title":"Amniotic Epithelial Stem Cells-Derived Exosomes Attenuate the Lesion of Alveolar Epithelial Cells Induced by SARS-CoV-2 Spike Protein via SENP3- Triggered FGF9 deSUMOylation","authors":"Zeyu Cui, Wei Wu, Yanchen Lai, Te Liu, Fangfang Dou, Lian Yang, Gang Zou","doi":"10.1002/adbi.70163","DOIUrl":"https://doi.org/10.1002/adbi.70163","url":null,"abstract":"<div>\u0000 \u0000 <p>The spike (S) protein plays a pivotal role in the invasion of host cells by SARS-CoV-2 (COVID-19). However, the underlying mechanism of spike protein interaction with host cells remains elusive. Here, it was found that human amniotic epithelial stem cells (HuAECs)-derived exosomes were able to mitigate the cell cycle arrest and lesions of human type II alveolar epithelial primary cells (hAEPC-II) in vitro induced by SARS-CoV-2 S protein. Mechanistically, HuAECs transfered <i>SENP</i> mRNA to hAEPC-II by releasing exosomes, induced FGF9 protein deSUMOylation and stimulated its expression in hAEPC-II. Silencing endogenous <i>SENP3</i> mRNA in HuAECs using siRNA weakens the protective effect of HuAECs-derived exosomes on hAEPC-II. Meanwhile, HuAEC-derived exosomes significantly improved lung tissue damage, inflammatory and fibrosis symptoms of humanized hACE2<sup>KI/KI</sup> transgenic mice treated to S protein in vivo. In conclusion, this study reveals a novel mechanism by which HuAECs transfered <i>SENP</i> mRNA to hAEPC-II by releasing exosomes and attenuate the lesion of hAEPC-II induced by SARS-CoV-2 spike protein.</p>\u0000 </div>","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":"10 10","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149177540","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Miriam Greve, Peter Schertl, Frank Schaarschmidt, Constantin von Kaisenberg, Cornelius Miller, Susanna Spindler, Sophia Rudorf, Cornelia Lee-Thedieck
{"title":"Hematopoietic Stem and Progenitor Cells Establish Dynamic Podosome-Like Structures to Interact with Fibronectin","authors":"Miriam Greve, Peter Schertl, Frank Schaarschmidt, Constantin von Kaisenberg, Cornelius Miller, Susanna Spindler, Sophia Rudorf, Cornelia Lee-Thedieck","doi":"10.1002/adbi.70159","DOIUrl":"10.1002/adbi.70159","url":null,"abstract":"<p>To keep their stem cell properties, hematopoietic stem and progenitor cells (HSPCs) need to interact with their stem cell niche in the bone marrow. Yet, the way in which HSPCs anchor to this specific microenvironment composed of niche cells and extracellular matrix (ECM) is not well understood. Here, the adhesion structures established by HSPCs upon contact with the ECM component fibronectin are investigated with regard to their appearance, maturity state, and composition. HSPCs adhere in a dynamic manner and display varying morphologies, with most cells displaying a round shape and the establishment of many podosome-like structures (PLS). The PLS consist of F-actin puncta, co-localized with phosphorylated PYK2, vinculin, and paxillin. These proteins assemble towards the periphery of the structure, and this pattern is more pronounced in cells with a round shape and higher PLS numbers. We also find strong indications that cells with a round shape or displaying higher levels of PLS are less differentiated and less likely to be of myeloid lineage. The study highlights the dynamic adhesion behavior of HSPCs and points to PLS as structures of interest in the interaction between these cells and their niche. Podosome-like structures are found in the majority of hematopoietic stem and progenitor cells. These structures are more maturely established in round cells, and cells establishing the structures in higher quantities are more naïve.</p>","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":"10 9","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13617278/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149069043","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"IGF2BP1-Mediated m6A Modification Enhances the Stability of circ_0088302 to Promote Gastric Cancer Progression","authors":"Jianjie Li, Xiaoxue Xi, Yang Wang, Hua Li","doi":"10.1002/adbi.70160","DOIUrl":"10.1002/adbi.70160","url":null,"abstract":"<div>\u0000 \u0000 <p><b>Background</b>: Circular RNAs (circRNAs) are recognized as critical regulators of gastric cancer (GC) progression. Nevertheless, the biological function of circ_0088302 in gastric cancer and its epitranscriptomic regulatory mechanism remain unclear. <b>Methods</b>: The expression of circ_0088302 was analyzed based on plasma circRNA data from GSE93541 and RT-qPCR, and its subcellular localization was determined by RNA-FISH. Cellular malignant phenotypes were evaluated using CCK-8 assay, colony-formation assay, wound-healing assay, Transwell assay, and flow cytometry. MeRIP-qPCR, RIP, dual-luciferase reporter assay, and actinomycin D assay were performed to assess m<sup>6</sup>A modification, IGF2BP1 binding, candidate m<sup>6</sup>A sites, and RNA stability. AVJ16 was used to inhibit IGF2BP1 function. <b>Results</b>: circ_0088302 was highly expressed in plasma samples from GC patients and GC cells. Knockdown of circ_0088302 repressed cell viability, colony formation, and migration, and promoted cell apoptosis. circ_0088302 exhibited m<sup>6</sup>A enrichment and bound to IGF2BP1, and the predicted 292 site was involved in IGF2BP1-dependent regulation. IGF2BP1 knockdown reduced circ_0088302 levels and accelerated its degradation. AVJ16 suppressed the viability of GC cells and abrogated the malignant phenotypes induced by circ_0088302 overexpression. <b>Conclusion</b>: IGF2BP1 may facilitate the malignant phenotypes of GC cells by maintaining the RNA stability of m<sup>6</sup>A-modified circ_0088302, suggesting that the IGF2BP1/circ_0088302 axis may represent a potential therapeutic target for GC.</p>\u0000 </div>","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":"10 9","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149069059","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Xiaoyao San Alleviates Depression-Associated Dry Eye via the LncRNA-Nespas/TAK1 Axis by Suppressing Central and Peripheral Inflammation","authors":"Jun Peng, Junyao Li, Ying Ni, Tiantian Gao, Huilin Liu, Yajing Wang, Hongping Long, Jian Shi, Hanqing Wang, Mingxia Xie","doi":"10.1002/adbi.70158","DOIUrl":"10.1002/adbi.70158","url":null,"abstract":"<div>\u0000 \u0000 <p>Depression commonly manifests alongside dry eye disease (DED), and effective targeted treatments for this comorbid disorder are currently limited. Xiaoyao San (XYP), a traditional Chinese herbal formulation, is widely applied for the management of mood disturbances. This study explored the therapeutic effects and underlying molecular mechanism of XYP against depression-associated DED. A mouse model of comorbid depression and DED was generated by exposing animals to chronic unpredictable mild stress in a low-humidity environment. XYP notably ameliorated depressive-like phenotypes, restored tear secretion, and relieved corneal injury (<i>p</i> < 0.05 or <i>p</i> < 0.01). Molecular analyses revealed that XYP suppressed TAK1 expression and p38/NF-κB phosphorylation, and strengthened the interaction between lncRNA-Nespas and TAK1 in vivo. These regulatory effects were recapitulated in LPS/ATP-challenged BV2 microglia and hyperosmotic stress-exposed human corneal epithelial cells. Of note, genetic silencing of lncRNA-Nespas significantly reversed the anti-inflammatory actions of XYP. Collectively, XYP alleviates depression-associated DED by targeting the lncRNA-Nespas/TAK1 signaling axis, which suppresses inflammation in both the central nervous system and ocular tissues.</p>\u0000 </div>","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":"10 9","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149029460","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Gaurav Srivastava, Aakash Patel, Alice Rodriguez-Fuguet, Akanksh Jambagi, Himanshi Jangir, Ahmad Nawaz, Afeef Mahmud, Camden Dwelle, Xiufang Guo, James Hickman
{"title":"Development of a Multi-Organ Microphysiological (MPS) Model to Study Age-Related Comorbidities","authors":"Gaurav Srivastava, Aakash Patel, Alice Rodriguez-Fuguet, Akanksh Jambagi, Himanshi Jangir, Ahmad Nawaz, Afeef Mahmud, Camden Dwelle, Xiufang Guo, James Hickman","doi":"10.1002/adbi.70147","DOIUrl":"10.1002/adbi.70147","url":null,"abstract":"<p>Comorbidities, the concurrent presence of two or more medical conditions, present significant challenges for diagnosis and treatment. Skeletal muscle sarcopenia and hypertrophic cardiomyopathy (HCM) are two distinct yet interrelated conditions, often co-existing in elderly individuals and exacerbating disease progression. Mechanistic understanding of sarcopenia-HCM comorbidity is limited, largely based on clinical correlation analyses and a few available mouse models. To facilitate pathophysiological research and accelerate therapeutic development, a more efficient human-relevant in vitro model is needed. This study presents a human-based sarcopenia-HCM comorbidity model in a multi-organ microphysiological system (MPS) that incorporates primary human hepatocytes, human induced pluripotent stem cells (hiPSC)-derived skeletal muscle and cardiomyocytes. The phenotypes for sarcopenia and HCM were first induced and characterized in single-organ systems, then assembled and analyzed in a multi-organ MPS, maintained in circulated serum-free medium. The functional phenotypes of skeletal muscle, cardiomyocytes, and hepatocytes, as well as inter-organ interactions in this organ-chip system align with clinical reports. This MPS comorbidity platform will enable pathophysiological investigation of sarcopenia, HCM, their comorbidity, and testing of therapeutic efficacy, toxicity, and pharmacokinetics. This study highlights how multi-organ MPS can revolutionize preclinical research as a human-relevant, cost-effective, and ethical alternative for studying comorbidities.</p>","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":"10 9","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/adbi.70147","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148987575","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The Impact of S-220–Loaded Silk Hydrogels on In Vitro Neurite Outgrowth in 2 and 3 Dimensions","authors":"Hongming Ma, F. Philipp Seib, Wenlong Huang","doi":"10.1002/adbi.70157","DOIUrl":"10.1002/adbi.70157","url":null,"abstract":"<p>Silk hydrogels have attracted increasing interest as biocompatible substrates for neural cell culture and regenerative research. Recent research has shown that activation of exchange protein directly activated by cAMP 2 (Epac2) promotes neurite outgrowth in several neuronal models. Here, we investigated the effects of <i>Bombyx mori</i> silk hydrogel, alone or in combination with S-220, a non-hydrolysable cAMP analogue that selectively activates Epac2, on neurite outgrowth. Epac2 activation significantly and dose-dependently enhanced both the total and longest neurite length. Neurons cultured on silk hydrogel alone exhibited neurite outgrowth comparable to control neurons, indicating good biocompatibility of the hydrogel. Addition of S-220 to the culture medium with silk hydrogel modestly improved neurite morphology; however, incorporation of S-220 directly into the hydrogel did not enhance neurite outgrowth but instead reduced neurite length. A subsequently established three-dimensional cortical neuron culture model using silk hydrogel supported neurite extension and increased branching complexity beyond that observed with two-dimensional cultures, despite a shorter overall neurite length. Collectively, these findings support silk hydrogel as a permissive biomaterial substrate for in vitro cortical neuron culture. The system provides a useful platform for investigating neurite outgrowth, neuron-biomaterial interactions and the delivery of bioactive compounds in two- and three-dimensional neural cultures.</p>","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":"10 9","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13552258/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148904992","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Targeting MAPK Pathways in Skin, Thyroid, and Pancreatic Cancer: A Perspective on Synthetic Inhibitors and Natural Modulators","authors":"Divya Wasnik, K. Venkateswara Swamy, Renu Vyas","doi":"10.1002/adbi.70156","DOIUrl":"10.1002/adbi.70156","url":null,"abstract":"<div>\u0000 \u0000 <p>Cancer frequently arises from the impaired functioning of the Mitogen-activated protein kinase (MAPK) signaling system, driven by mutation or overexpression of key signaling components. RAF, MEK, ERK, and KRAS inhibitors have significantly improved clinical outcomes, but efficacy is still restricted due to pathway reactivation, adaptive resistance, and signaling cross-talk. These limitations have led to the search for novel therapeutic approaches and molecular targets in the MAPK network. Melanoma, thyroid carcinoma, and pancreatic adenocarcinoma were selected because MAPK pathway alterations contribute to their pathogenesis and influence treatment response. This review examines the biological importance of MAPK signaling in these cancers and discusses MAPK-targeted therapies, mechanisms of resistance, and combination treatment options. It also addresses the expanding evidence on natural compounds that modulate MAPK- related signaling networks and reviews recent transcriptomic findings that have enhanced the identification of clinically relevant molecular targets. Additionally, MAP4K4 has been linked to tumor progression and metastasis, and poor clinical outcomes, indicating its potential as a therapeutic target for future clinical studies. The findings presented in this review suggest that combining transcriptomic evidence with molecular and pharmacological analyses could aid target prioritization and accelerate the development of targeted strategies for MAPK-driven malignancies.</p>\u0000 </div>","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":"10 9","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148904927","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"How Epitranscriptomic Machinery Senses Environmental Cues","authors":"Shayan Jalali, Ehsan Pashay Ahi","doi":"10.1002/adbi.70154","DOIUrl":"https://doi.org/10.1002/adbi.70154","url":null,"abstract":"<p>Environmental fluctuations remodel RNA modification landscapes, yet the routes that connect cue detection to writer–eraser–reader control remain dispersed across disciplines. Here, we consolidate upstream mechanisms capable of driving epitranscriptomic change and organize them by response speed. At the fastest proximal level, catalytic output can be modulated through shifts in substrate and cofactor availability, redox and ionic state, temperature, and direct chemical or metal interference with enzyme active sites, although transcriptome-wide RNA readouts may appear later. Over minutes to hours, cue-responsive signaling can reach the machinery through post-translational modification, partner switching, subcellular trafficking, and stress-induced condensates that may gate access to modified transcripts. Across hours to days, regulator abundance and specificity are reshaped by transcriptional programs, translational control, and protein quality-control pathways, enabling adaptation and, in some contexts, persistence. We propose a kinetics-to-sensors approach for interpreting time-resolved epitranscriptomic datasets and prioritizing perturbations that discriminate among candidate upstream inputs. We also outline conceptual gaps and experimental practices needed to establish causal cue-to-mark chains.</p>","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":"10 9","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/adbi.70154","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148859909","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Single-Cell Glycomics of the Pancreatic Tumor Microenvironment: Technologies, Glyco-Immune Checkpoints, and Tumor–Immune Communication","authors":"Dinh Xuan Tuan Anh, Hiroaki Tateno","doi":"10.1002/adbi.70152","DOIUrl":"10.1002/adbi.70152","url":null,"abstract":"<p>In this Review, we summarize recent conceptual and technological advances in single-cell glycomics, with a particular focus on emerging strategies that enable glycan-resolved analysis of tumor–immune interactions. We highlight single-cell glycan and RNA sequencing (scGR-seq), a methodology that converts glycan information into amplifiable nucleic acid signals, enabling simultaneous profiling of transcriptomes and glycomes at the single-cell level. In parallel, we introduce GlycoChat, a computational framework designed to systematically infer and visualize glycan–lectin interaction networks within the TME. Integrative application of these approaches to pancreatic ductal adenocarcinoma (PDAC) reveals extensive glycan remodeling during epithelial–mesenchymal transition (EMT) and demonstrates that basal-like PDAC cells selectively reinforce interactions with lectin receptors expressed on innate immune cells, particularly tumor-associated macrophages. These EMT-driven glycan–lectin circuits are proposed to transmit immunosuppressive signals within the TME and show a strong association with clinical outcomes. Collectively, these advances highlight glycans as active mediators, rather than solely passive tumor markers of immune regulation, and provide a conceptual framework for understanding and potentially exploiting glycan-mediated immune regulation in cancer.</p>","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":"10 8","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13505752/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148817164","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}