Burns & Trauma最新文献

{"title":"Adipose-derived stem cell peptide 5 alleviates hypertrophic scarring through targeting pyruvate carboxylase or p50 to coordinate PI3K/AKT/mTOR-autophagy and NF-κB/IL-6 signaling","authors":"Ling Chen, Enyuan Zhang, Siqi Zeng, Qiyue Yan, Jingyun Li, Qian Li, Jun Li, Zezhang Zhu","doi":"10.1093/burnst/tkag040","DOIUrl":"https://doi.org/10.1093/burnst/tkag040","url":null,"abstract":"Background Hypertrophic scars are a major clinical challenge with limited treatments. In this study, the therapeutic potential of adipose-derived stem cell peptide 5 (ADSCP5), a novel peptide from adipose-derived stem cell-conditioned medium, was investigated. Methods We used in vitro hypertrophic scar fibroblast, macrophage–fibroblast coculture and human umbilical vein endothelial cell (HUVEC) assays, RNA sequencing, pathway analysis, peptide pull-down, molecular docking, cellular thermal shift assays, surface plasmon resonance, immunofluorescence colocalization analysis, western blotting, rescue experiments, reactive oxygen species (ROS), autophagy tests, and mitochondrial membrane potential assays and untargeted metabolomics. The efficacy of ADSCP5 was validated in rabbit and porcine scar models. Results In hypertrophic scar fibroblasts, ADSCP5 significantly downregulated the expression of collagen genes (COL1A1, COL1A2, and COL3A1) and actin alpha 2, smooth muscle (ACTA2) without affecting cell proliferation, apoptosis, or migration. Transcriptomic, enrichment and western blot analyses confirmed that ADSCP5 reduced the protein levels of phosphorylated p65 (p-p65, NF-κB subunit), p-PI3K, p-AKT, and p-mTOR. Moreover, ADSCP5 decreased IL-6 transcription. Mechanistically, ADSCP5 bound directly to pyruvate carboxylase (PC) or the NF-κB subunit p50. This interaction resulted in the downregulation of PC or the upregulation of p50, ultimately inhibiting collagen expression, a finding confirmed by rescue assays. Furthermore, ADSCP5 induced reactive oxygen species (ROS) generation and autophagy, altered global metabolism, and modulated macrophage–fibroblast crosstalk to suppress fibrosis. It also exhibited antiangiogenic effects in HUVECs. In both the rabbit and porcine scar models, ADSCP5 treatment effectively attenuated collagen deposition and scar hyperplasia, increased the number of macrophages (increased CD68), reduced angiogenesis (decreased VEGFA and CD34), and promoted autophagy (reduced p62). Conclusion Overall, the results of this study demonstrate that ADSCP5 alleviates hypertrophic scarring by directly binding to PC and p50, suppressing the PI3K/AKT/mTOR and NF-κB pathways, reducing IL-6 and collagen production, promoting ROS and autophagy, and modulating metabolic, macrophage and angiogenic responses. These findings position ADSCP5 as a promising therapeutic agent for hypertrophic scar prevention and treatment.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"11 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148286868","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}

{"title":"4-phenylbutyric acid alleviated sepsis-induced myocardial dysfunction by inhibition of MAM formation to improve mitochondrial dynamic balance in myocardial cells","authors":"Yue Wu, Yijin Fang, Yuanqun Zhou, Qinghui Li, Liyong Zou, Xiaodan Wang, Li Wang, Ying Zheng, Liangming Liu, Yu Zhu","doi":"10.1093/burnst/tkag039","DOIUrl":"https://doi.org/10.1093/burnst/tkag039","url":null,"abstract":"Background Sepsis-related myocardial dysfunction significantly increases the mortality risk of sepsis. However, its underlying mechanism remains incompletely understood, and effective therapeutic strategies are still lacking. Transcriptomic profiling from septic patients showed endoplasmic reticulum stress (ERS) were the main pathways participating in the occurrence of sepsis myocardial dysfunction. Therefore, this study aimed to explore the protective effect of 4-phenylbutyric acid (4-PBA) on sepsis-induced myocardial injury and specify its molecular regulatory mechanism, to provide experimental basis for clinical intervention of septic myocardial dysfunction. Methods In vivo and in vitro models of sepsis were used, and 4-PBA (5 mg/kg) was administered for intervention. Mitochondria-associated ER-membrane (MAM) formation, mitochondrial dynamics, mitochondrial function, glycolytic metabolism, and protein lactylation were systematically examined. Molecular docking and site-directed mutation were applied to verify the direct binding and catalytic sites of 4-PBA. Results 4-PBA significantly alleviated sepsis-induced myocardial dysfunction. The mechanism was closely related to 4-PBA inhibiting MAM formation and improving the mitochondrial dynamic balance and mitochondrial function. 4-PBA inhibited MAM formation mainly via decreasing the lactate production and lactylation of Arpc1b-K308 by inhibiting the glycolysis limiting enzyme HK2, and 4-PBA inhibited HK2 activity by binding K621 and K624 catalytic sites. Conclusions The results indicate that 4-PBA protects cardiac function following sepsis by recovering mitochondrial dynamics balance. This finding provides a novel therapeutic strategy and potential target for sepsis induced myocardial dysfunction.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"17 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148286869","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}

{"title":"Hypoxia and metabolic adaptation drive self-organization in organoid morphogenesis and tissue regeneration.","authors":"Hans I-Chen Harn","doi":"10.1093/burnst/tkag038","DOIUrl":"https://doi.org/10.1093/burnst/tkag038","url":null,"abstract":"","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"11 1","pages":"tkag038"},"PeriodicalIF":5.3,"publicationDate":"2026-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148441067","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}

{"title":"Tissue regeneration strategies based on mesenchymal stem cell-derived extracellular vesicles: from bench to bedside.","authors":"Shi-Han Mu, Rang Li, Peng-Fei Wang, Ying-Shuang Shi, Yu-Wei Zhou, Yan Jin, Fang Jin, Bing-Dong Sui","doi":"10.1093/burnst/tkag030","DOIUrl":"10.1093/burnst/tkag030","url":null,"abstract":"<p><p>Regenerative medicine is undergoing a paradigm shift from live-cell therapies to cell-free strategies. Within this evolving field, mesenchymal stem cell-derived extracellular vesicles (MSC-EVs) have emerged as a leading platform. These nanoscale vesicles deliver bioactive cargo that mediates critical therapeutic functions, including immunomodulation, angiogenesis, and anti-fibrosis. Furthermore, they offer improved safety, greater potential for standardization, and enhanced scalability compared to traditional live-cell therapies. However, clinical translation remains constrained by several challenges, such as inherent vesicle heterogeneity, limited targeting specificity, and bottlenecks in large-scale manufacturing. This review systematically examines the biogenesis of MSC-EVs, focusing specifically on exosomes, microvesicles, and apoptotic vesicles. We evaluate their functional performance across diverse regeneration contexts, encompassing orofacial, barrier, musculoskeletal, and visceral tissue regeneration. We further highlight innovative engineering strategies designed to enhance therapeutic efficacy, such as surface modification, cargo loading, and biomaterial-integrated delivery systems. In addition, we introduce an emerging approach utilizing engineered MSC aggregate-derived EVs inspired by organ morphogenesis. Finally, this article details the strategic framework required for clinical translation. The framework encompasses scalable production, rigorous quality control, comprehensive non-clinical studies, evolving regulatory pathways, and the current clinical trial landscape. Collectively, this work provides an integrated roadmap for advancing MSC-EVs as a next-generation precision platform for cell-free therapeutics.</p>","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"14 ","pages":"tkag030"},"PeriodicalIF":11.0,"publicationDate":"2026-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13430040/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148668571","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}

{"title":"UPRmt as a Central Stress-Integration Hub: Mechanisms and Implications in Disease Contexts","authors":"Yanmin Xin, Yiting He, Xingguo Liu","doi":"10.1093/burnst/tkag037","DOIUrl":"https://doi.org/10.1093/burnst/tkag037","url":null,"abstract":"The mitochondrial unfolded protein response (UPRmt) is a conserved mitochondrial stress response that is activated by mitochondrial dysfunction to maintain proteostasis. Although UPRmt has been extensively studied in aging and cancer, its role in trauma and critical illness remains poorly understood. Here, we propose a unifying conceptual framework in which UPRmt functions as a central stress-integration hub that senses and coordinates adaptive responses following acute injury. We systematically review the mechanisms of UPRmt activation triggered by diverse insults and highlight how UPRmt integrates mitochondrial-nuclear communication, and crosstalk with other stress-responses such as the integrated stress response (ISR) and mitophagy. Beyond cell-autonomous regulation, UPRmt also coordinates systemic adaptation through mitokine-mediated interorgan signaling. Importantly, we emphasize the context-dependent role of UPRmt in trauma and critical illness. Moderate activation promotes mitochondrial recovery, limits reactive oxygen species (ROS) accumulation, and supports immune cell function, thereby enhancing tissue resilience and repair. In contrast, sustained or dysregulated UPRmt contributes to mitochondrial failure, sterile inflammation, and the progression to systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndrome (MODS). Furthermore, we discuss emerging evidence linking UPRmt to immune regulation and inflammatory responses, and propose that targeting key regulatory nodes within this stress-integration network may offer novel therapeutic strategies for a broad spectrum of human diseases. Crucially, we synthesize how UPRmt mechanisms contribute to post-traumatic mitochondrial damage, sterile inflammation, SIRS, and MODS. We propose that targeting key regulatory nodes within this stress-integration network may offer novel therapeutic strategies for trauma, burns, and critical illness.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"55 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148286879","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}

{"title":"Preclinical Evaluation of a Bioartificial Kidney Loaded with Functional Renal Tubular Cells in a Bama Miniature Pig Model of Acute Renal Failure","authors":"Yunming Xiao, Chuyue Zhang, Tianyi Yang, Yiyu Huang, Xu Wang, Xiaoxiao Liu, Mengfei Li, Shaoyuan Cui, Guangrui Geng, Xiang Li, Qinggang Li, Xiangmei Chen","doi":"10.1093/burnst/tkag036","DOIUrl":"https://doi.org/10.1093/burnst/tkag036","url":null,"abstract":"Background Severe acute kidney injury (AKI) is associated with high mortality. Current blood purification technologies fail to replace the biological functions of renal tubular epithelial cells (RTECs), such as active transport, acid–base homeostasis, and endocrine regulation. The integration of viable RTECs into an extracorporeal circuit to construct a bioartificial kidney represents a potential strategy for renal functional support. However, its translation is constrained by the rapid loss of seed cell phenotypes, immune and coagulation activation triggered by conventional materials, and a lack of in vivo validation in large animal models. Methods We engineered a renal tubule assist device (RAD) that integrates viable cells with a functionalized interface. First, we established an immortalized human proximal tubule cell line (iRTEC) and achieved scalable expansion using a microcarrier system. Second, we fabricated a cell-supporting interface (CA/PLL-PNF) with antioxidant properties and enhanced hemocompatibility via the layer-by-layer self-assembly of poly-L-lysine and chlorogenic acid onto polyacrylonitrile nanofibrous membranes. Finally, we assembled these components into a flat-plate bioreactor and evaluated its extracorporeal performance in a Bama miniature pig model after bilateral nephrectomy. Results iRTECs were stably expanded on microcarriers while maintaining a proximal tubule phenotype, and these cells outperformed existing cell lines in terms of amino acid hydrolysis and transmembrane transport, acid–base regulation, water transport, and endocrine responsiveness. With respect to the supporting interface, CA/PLL-PNF effectively scavenged diverse free radicals and mitigated cellular oxidative stress. Proteomic analysis confirmed that this modification remodeled the plasma protein corona, which significantly reduced the adsorption of complement and coagulation factors. In the bilaterally nephrectomized pig model, the RAD safely maintained extracorporeal circulation for 4 hours—the duration of routine clinical dialysis—and preserved internal homeostasis. The antioxidant interface significantly attenuated circulating lipid peroxidation during treatment. Compared with hemofiltration alone, the RAD significantly enhanced the clearance of middle-molecule toxins (β2-microglobulin) and reduced proinflammatory cytokine levels at the outlet, demonstrating its capacity for the active modulation of local inflammation. Conclusions This study established a renal support platform that integrates viable cells and functional materials. The device exhibited multidimensional biological efficacy in toxin clearance and internal homeostasis regulation and achieved stable extracorporeal circulation in a preclinical large animal model, which provides experimental evidence for advanced organ support strategies in the setting of severe AKI.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"42 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148286400","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}

{"title":"Bio-enhanced silk fibroin-based scaffolds for chronic diabetic foot ulcers.","authors":"Victoria Cubina Lopez, Jewelia Durant, Katherine R Hixon","doi":"10.1093/burnst/tkag035","DOIUrl":"10.1093/burnst/tkag035","url":null,"abstract":"<p><p>Diabetic foot ulcers (DFUs) represent a growing clinical challenge, driven by an aging global population and the increasing prevalence of diabetes. Affecting millions worldwide, DFUs remain one of the most serious complications of diabetes, frequently progressing to infection, amputation, and elevated mortality. Standard treatments typically include pressure offloading, circulation improvement, infection control, and topical wound care; however, many chronic DFUs fail to respond to these interventions due to persistent inflammation, impaired vascularization, and microbial burden. These challenges have accelerated interest in regenerative medicine approaches, including stem cells, growth factors, and skin substitutes. Among these, skin substitutes have shown particular promise; among Food and Drug Administration-approved options, products such as the collagen-Manuka honey-hydroxyapatite patch from SweetBio (Apis®) have demonstrated improved outcomes in patients with chronic ulcers. Silk fibroin (SF), a natural biopolymer with established clinical use, has emerged as a promising platform for chronic wound management due to its biocompatibility, tunable degradation, and capacity for controlled bio-additive delivery. SF scaffolds can be fabricated through various methods tailored to wound-healing applications: electrospun fibrous mats with high surface-area-to-volume ratio, freeze-dried porous constructs with interconnected architecture, and hydrogels designed for controlled drug delivery. In this review, we critically examine how SF scaffolds enhanced with bio-additives modulate cellular responses, redirect dysregulated healing pathways, accelerate wound closure, and promote tissue regeneration in diabetic wounds. We synthesize recent advances in preclinical and clinical studies, identify key translational barriers, and outline future directions for advancing SF-based dressings toward clinical adoption. Collectively, this review positions bio-enhanced SF scaffolds as next-generation, disease-informed candidates for improving outcomes in chronic DFU care.</p>","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"14 ","pages":"tkag035"},"PeriodicalIF":11.0,"publicationDate":"2026-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13429051/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148663479","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}

{"title":"Altered Sensorimotor Neuroplasticity in Subacute Patients with Non-Severe Burn Injury","authors":"Grant Rowe, Mark Fear, Dale W Edgar, Aleksandra Miljevic, Tyler Osborne, Natalie Morellini, Merrilee Needham, Ann-Maree Vallence, Fiona Wood","doi":"10.1093/burnst/tkag034","DOIUrl":"https://doi.org/10.1093/burnst/tkag034","url":null,"abstract":"Background Burn injuries affect the central nervous system, and evidence suggests they induce changes in cortical excitability related to motor dysfunction. The current study investigated markers of neuroplasticity in the motor cortex and motor performance in the subacute period following burn injury. Methods Thirty-four patients with a non-severe burn injury (total body surface area: 1.0 ± 2.0%; 16 females; age: 46.0 ± 14.0 years) participated in a longitudinal study with assessments ranging from ~1 to ~17 weeks post-injury. Transcranial magnetic stimulation (TMS) was used to evaluate motor cortex excitability and short- and long-intracortical inhibition (SICI; LICI) before and after application of paired associative stimulation (PAS) to induce neuroplasticity. Motor performance was assessed using the Purdue Pegboard. Results Patients showed improvements in bilateral motor performance from ~3 to ~6 weeks post-injury. PAS did not induce any change in net motor cortex excitability or SICI but increased LICI, which was greatest ~6 weeks post-injury. Adjusted modelling showed that greater PAS-induced increase in LICI was associated with better bilateral motor performance, suggesting an association between PAS-induced neuroplasticity of long-acting inhibitory circuits in the primary motor cortex and motor function following burn injury. Discussion These findings highlight a potential role for neuroplasticity of inhibitory circuits in the motor cortex in recovery of motor function following burn injury. Conclusion The data provide a neurophysiological basis to test whether targeting inhibitory networks in the subacute period after burn injury can enhance or expedite functional recovery.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"7 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148286401","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}

{"title":"Application of electrospun piezoelectric nanofibers in wound healing.","authors":"Jing Wang, Jianhua Feng, Chengzhi Zhang, Xiankui Gao, Changjun Jia, Tianming Zhao, Seeram Ramakrishna, Hongye Guan","doi":"10.1093/burnst/tkag032","DOIUrl":"10.1093/burnst/tkag032","url":null,"abstract":"<p><p>Wound healing is essential for maintaining organismal homeostasis and barrier function, posing significant challenges particularly in the management of hard-to-heal wounds such as diabetic ulcers. This review systematically summarizes the functional properties of piezoelectric electrospun biomaterials and their biological mechanisms in promoting wound healing via electrical stimulation (ES). Piezoelectric nanofiber wound dressings fabricated by electrospinning technology offer dual advantages: on one hand, their unique fibrous architecture enables adaptation to irregular wound contours, facilitates rapid hemostasis, and provides an effective barrier against microbial invasion; on the other hand, their inherent piezoelectric effect converts micromechanical deformations into localized electrical signals in real time, thereby modulating cellular behaviors and accelerating tissue repair. This review highlights recent studies elucidating the mechanisms by which ES promotes wound healing, and the functional characteristics of piezoelectric fibrous dressings. It aims to establish a theoretical foundation for the rational design and performance optimization of next-generation intelligent piezoelectric wound dressings, thereby advancing their clinical translation and industrial development.</p>","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"14 ","pages":"tkag032"},"PeriodicalIF":11.0,"publicationDate":"2026-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13592679/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149015769","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}

{"title":"Skin organoids as a new biological standard.","authors":"Imaan Ahmed, Abbas Shafiee","doi":"10.1093/burnst/tkag033","DOIUrl":"10.1093/burnst/tkag033","url":null,"abstract":"","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"14 ","pages":"tkag033"},"PeriodicalIF":11.0,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13251885/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148223456","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}