Tissue Barriers最新文献

{"title":"DENV-NS1 drives novel microRNAs to disrupt cerebral endothelial barrier functions.","authors":"Apoorva, Sunit Kumar Singh","doi":"10.1080/21688370.2026.2749828","DOIUrl":"https://doi.org/10.1080/21688370.2026.2749828","url":null,"abstract":"<p><p>Dengue virus non-structural protein 1 (DENV-NS1) plays a key role in the vascular leakage associated with severe dengue; however, the molecular mechanisms by which NS1 induces endothelial dysfunction remain poorly understood. This study aimed to identify a new aspect of the pathogenic strategy: the post-transcriptional reprogramming of host endothelial cells via microRNAs (miRNAs) in NS1-induced DENV pathogenesis. Small RNA sequencing and subsequent bioinformatic analysis identified novel miRNA-gene regulatory networks responsive to DENV-NS1 in human brain microvascular endothelial cells. Multiple dysregulated novel miRNAs were identified as potential regulators of critical antiviral components (STAT1, SOCS1-6, OAS1), suggesting suppressed interferon signaling. Downregulation of identified novel miRNAs targeting IL-6, IL-10, IL-1α, IL-17A, CXCR4, and CXCR5 indicates increased pro-inflammatory cytokine production and chemokine-driven immune cell recruitment, thereby worsening endothelial inflammation and vascular leakage. The simultaneous targeting of cytoskeletal regulators (RAC1, ROCK1/2) and tight junction proteins (CLDN1, CLDN2, CLDN16, CLDN22) suggests a two-phase disruption of endothelial stability, characterized by cytoskeletal remodeling and compromised tight junction integrity as a bystander effect of DENV-NS1. The downregulation of several miRNAs targeting XIAP, MDM2/4, and SMAD family genes established the involvement of novel miRNAs in apoptosis regulation and TGF-β/SMAD-mediated endothelial cell signaling. Our findings suggest that DENV-NS1 alters endothelial miRNA networks, leading to reduced antiviral immunity, increased inflammation, and compromised vascular integrity. This study identifies novel miRNA-mediated regulatory nodes that could function as therapeutic targets to prevent or mitigate dengue-associated vascular leakage.</p>","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2749828"},"PeriodicalIF":3.1,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149228743","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Emerging roles of migrasomes in blood-tissue barrier integrity and intercellular signaling.","authors":"Amal Ahmed El-Sheikh, Rashid A Aldahhan","doi":"10.1080/21688370.2026.2738431","DOIUrl":"https://doi.org/10.1080/21688370.2026.2738431","url":null,"abstract":"<p><p>Migrasomes are a newly recognized class of migration-dependent organelles that arise along retraction fibers of migrating cells and are released into the extracellular milieu. Structurally and biogenetically distinct from extracellular vesicles, migrasomes function as signaling hubs that mediate localized transfer of bioactive cargo and coordinate intercellular communication. Accumulating evidence indicates that migrasomes participate in diverse biological processes, including developmental patterning, immune regulation, and tumor progression. Blood-tissue barriers (including the blood-brain, glomerular, thymic, retinal, and placental barriers) are specialized interfaces that regulate molecular and cellular exchange between the circulation and tissues. These barriers rely on tightly coordinated interactions among barrier-forming endothelial cells, junctional complexes, basement membranes, and supporting stromal components to preserve tissue homeostasis. Despite emerging studies on migrasome biology, a comprehensive mechanistic understanding of migrasome-barrier interactions across the full spectrum of blood-tissue barrier systems remains lacking. This review addresses that gap by proposing an integrative conceptual framework for migrasome signaling within barrier microenvironments, examining how migrasome-mediated signaling influences cellular crosstalk and functional regulation within these interfaces in both health and disease. We also discuss technological advances, current limitations, and key knowledge gaps, highlighting the need for barrier-focused mechanistic studies to determine whether migrasomes act as active regulators of barrier integrity and signaling or represent secondary byproducts of cellular migration within barrier microenvironments.</p>","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2738431"},"PeriodicalIF":3.1,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149128582","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of mononuclear cells, stem cells, and exosomes in hypothyroid testicular dysfunction in rats via modulation of ZO-1, SIRT/FOXO. Focusing on blood testes barrier.","authors":"Yasmine Osama Mohamed Mokhtar, Nada Amgad Mohamed Abdel Majeed, Manar Fouli Gaber Ibrahim, Randa Ahmed Ibrahim, Nashwa Fathy Gamal El-Tahawy","doi":"10.1080/21688370.2026.2738428","DOIUrl":"https://doi.org/10.1080/21688370.2026.2738428","url":null,"abstract":"<p><p>Bone marrow mesenchymal stem cells (BMSCs) are stromal cells that can self-renew. Exosomes (EXOs) perform many biological functions particularly in cell-cell communication. Peripheral blood mononuclear cells (PBMNCs) have the ability to differentiate into numerous mature functional cell types in specific microenvironments. This study aimed to compare the possible ameliorating effect of BMSCs, EXOs, and PBMNCs on hypothyroidism-induced testicular damage in adult male rats. Forty‑eight adult male albino rats were divided randomly into five groups: control, hypothyroidism (HT), BMSCs-treated, EXOs-treated, and PBMNCs-treated groups. Testes and thyroids were dissected and prepared for biochemical, histological, and immunohistochemical studies. After induction of HT, the results showed an apparent decrease in testes weight and abnormal semen analysis. Additionally, a significant decrease in antioxidant markers, thickness of the germinal epithelium, PAS staining, and testes BCL2 anti-apoptotic marker. It showed histological changes. Additionally, a significant decrease in SIRT-1 and ZO-1immune stained cells. A significant increase in testes BAX apoptotic marker, FOXO-1 immuno-expression, and deficient blood testes barrier with abnormal spermatogenic cells in electron microscopy were also detected. Improvement in all mentioned parameters in treated groups was noticed. Our study suggested that PBMNCs holds promise for alleviating hypothyroidism in rats on biochemical, histological, and immunohistochemical basis.</p>","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2738428"},"PeriodicalIF":3.1,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149082095","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Barrier function of the Vero E6 cell monolayer.","authors":"Júlia Tárnoki-Zách, Elöd Méhes, Bernadett Pályi, Szilvia Bősze, András Czirók","doi":"10.1080/21688370.2026.2736960","DOIUrl":"https://doi.org/10.1080/21688370.2026.2736960","url":null,"abstract":"<p><p>Vero E6 cells are a standard model in virology research because of their broad susceptibility to viral infection. However, their ability to form functional barrier layers has received less attention. Here, we show that Vero E6 cells cultured on transwell inserts develop continuous monolayers with moderate transepithelial electrical resistance (TEER), reaching approximately 30 Ω·cm² in serum-containing medium and 45 Ω·cm² in virus production medium. The permeability coefficient (P_app) for 4 kDa FITC-dextran, a common measure for paracellular transport, is 3.7 × <math><mrow><msup><mn>10</mn><mrow><mo>-</mo><mn>6</mn></mrow></msup></mrow></math> cm/s, comparable to established endothelial models such as HUVEC or corneal endothelium. Immunofluorescence confirms the presence of tight junction (ZO-1) and adherens junction (β-catenin) proteins. Chelation of calcium with EGTA causes a dose-dependent, reversible decrease in TEER and a marked increase in permeability, confirming the calcium sensitivity of the barrier. These findings suggest that Vero E6 cells serve as a valuable epithelial barrier model, facilitating studies on viral entry, immune evasion, and drug delivery.</p>","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2736960"},"PeriodicalIF":3.1,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149075980","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A simulation of recreational and addictive methamphetamine use on the integrity of the blood-brain barrier endothelium using an <i>in vitro</i> BBB model.","authors":"Kelly Fick, David Fisher, Khayelihle Brian Makhathini, Chontrelle Willemse","doi":"10.1080/21688370.2026.2728887","DOIUrl":"https://doi.org/10.1080/21688370.2026.2728887","url":null,"abstract":"<p><p>Methamphetamine (Meth) is a widely abused psychostimulant implicated in severe neuropathologies, such as hemorrhagic stroke, which arises from disruptions to the blood-brain barrier (BBB). The selectively permeable BBB, composed primarily of brain microvascular endothelial cells (BMVECs) forms the cerebral capillaries and serves as the brain's protective interface against circulating toxins and pathogens. Despite its recognized susceptibility to Meth, the direct effects of Meth exposure on BMVECs remain insufficiently understood. To model the two types of Meth users, recreational and addictive, bEnd.5 cells were exposed to Meth for 24 hours only or daily. Changes in cellular division, mitochondrial activity, cellular morphology, and barrier integrity were assessed using the trypan blue exclusion assay, XTT, Hematoxylin and Eosin (H&E) stain, and transendothelial electrical resistance (TEER), respectively. Acute Meth exposure suppressed cellular division and reduced Mitochondrial activity (MA) in a 24-hour oscillatory manner, while chronic Meth exposure induced a sustained suppression of cellular division. Morphological analyses revealed nuclear abnormalities consistent with mitotic disruption. Both exposure conditions reduced endothelial monolayer integrity over the 96-hours; however, chronic exposure caused exacerbated decreases in barrier integrity. Notably, even acute Meth exposure was sufficient to initiate long-term BBB endothelium dysfunction. These findings demonstrate a continuum of BBB vulnerability arising from both recreational and addictive Meth use, underscoring the critical need for early intervention to avert progressive cerebrovascular, hemorrhagic, and neurological damage.</p>","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2728887"},"PeriodicalIF":3.1,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148991543","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Estrogen-dependent regulation of lipolysis-stimulated lipoprotein receptor via G-protein-coupled estrogen receptor 1 in breast cancer malignancy.","authors":"Misaki Takada, Akira Takasawa, Taishi Akimoto, Kumi Takasawa, Taro Murakami, Akinori Tada, Yusuke Ono, Naoya Nakahashi, Makoto Emori, Daisuke Kyuno, Kazufumi Magara, Hiroaki Shima, Masanori Goto, Masaki Murata, Shintaro Sugita, Tsuyoshi Saito, Makoto Osanai","doi":"10.1080/21688370.2026.2731724","DOIUrl":"https://doi.org/10.1080/21688370.2026.2731724","url":null,"abstract":"<p><p>The lipolysis-stimulated lipoprotein receptor (LSR) is a tight junction protein implicated in tumor progression, yet its regulatory mechanisms in breast cancer (BC) remain unclear. We found that high LSR expression correlates with poor overall survival in BC patients. RNA interference-mediated LSR knockdown significantly reduced cell proliferation, migration, and invasion, indicating its contribution to malignant phenotypes. Our investigation into its regulation revealed that estrogen increases LSR expression in both ERα-positive and ERα-negative BC cells. This upregulation is mediated predominantly by the membrane-type G protein-coupled estrogen receptor GPER1 and requires activation of the ERK and PI3K-Akt pathways. Immunohistochemical analysis of surgical specimens confirmed that LSR and GPER1 are overexpressed in ductal carcinoma in situ and invasive ductal carcinoma compared with normal epithelium, with their expression levels showing a significant positive correlation. These findings identify an E2-GPER1-LSR signaling axis that promotes BC malignancy independently of nuclear ER status. Thus, LSR represents a promising prognostic biomarker and therapeutic target, and targeting the GPER1-mediated pathway may provide new insights into tumor progression and endocrine therapy response.</p>","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2731724"},"PeriodicalIF":3.1,"publicationDate":"2026-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148971587","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NEK2 is involved in the mediation of the effects of LPS in endothelial cells.","authors":"Md Matiur Rahman Sarker, Saikat Fakir, Madan Sigdel, Nektarios Barabutis","doi":"10.1080/21688370.2026.2732890","DOIUrl":"https://doi.org/10.1080/21688370.2026.2732890","url":null,"abstract":"<p><p>Endothelial impairment has been associated with cell and tissue dysfunction. In this study, we investigated the effects of never in mitosis gene A-related kinase 2 (NEK2) silencing in lipopolysaccharides (LPS) - induced injury in bovine pulmonary artery endothelial cells (BPAEC) and human lung microvascular endothelial cells (HULEC-5a). Our observations suggest that NEK2 silencing alleviates LPS-induced cofilin, myosin light chain 2 (MLC2), mitogen activated protein kinases (MAPKs), Janus kinase 2 (JAK2), signal transducer and activator of transcriptions (STATs) activation; and suppressed paracellular hyperpermeability, and reactive oxygen species (ROS) generation. Based on those findings, it is suggested that NEK2 is involved in the mediation of LPS-induced endothelial responses.</p>","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2732890"},"PeriodicalIF":3.1,"publicationDate":"2026-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148963671","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cathepsin D as a central regulator of extracellular matrix remodeling in wound healing and chronic tissue pathologies.","authors":"Shobith Rangappa, Thammanna Gowda Ss, Parimala Hanumesh, Prashantha K, Manjula Rv","doi":"10.1080/21688370.2026.2730865","DOIUrl":"https://doi.org/10.1080/21688370.2026.2730865","url":null,"abstract":"<p><p>Wound healing is a dynamic and multifactorial process involving coordinated interactions among extracellular matrix (ECM) components, growth factors, proteolytic enzymes, and immune and stromal cells. An essential yet often underappreciated aspect of this process is restoration of the epithelial permeability barrier, which prevents fluid loss and microbial invasion following injury. Disruption of this coordination contributes to chronic, non-healing wounds such as diabetic ulcers and venous leg ulcers, which remain major clinical challenges. Recent advances identify cathepsins, particularly cathepsin D, as key proteases that extend beyond lysosomal degradation to regulate critical events in tissue repair. Cathepsin D modulates keratinocyte proliferation, fibroblast invasion, angiogenesis, and ECM remodeling, and supports re-epithelialization through processing of structural proteins such as transglutaminase 1. Emerging evidence indicates that cathepsin D indirectly influences junctional remodeling, including tight and adherens junction dynamics, thereby facilitating permeability barrier reformation during wound closure. Its activity is regulated by oxidative stress, advanced glycation end products, inflammatory mediators, and iron metabolism - factors highly relevant to chronic wound microenvironments. Beyond proteolysis, cathepsin D shapes fibroblast and macrophage phenotypes and processes vascular endothelial growth factor (VEGF), integrating metabolic and signaling pathways essential for tissue regeneration. Collectively, these findings position cathepsin D as a mechanistic regulator and promising therapeutic target in wound biology. This review synthesizes mechanistic insights linking cathepsin D-mediated proteolysis to epithelial junction reorganization and permeability barrier recovery, and highlights emerging therapeutic strategies for improving chronic wound healing.</p>","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2730865"},"PeriodicalIF":3.1,"publicationDate":"2026-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148921146","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Solute transport through the glomerular filtration barrier: the podocyte slit diaphragms' role in maintaining glomerular basement membrane integrity and podocyte-to-endothelial crosstalk.","authors":"Azin Azadi, Chang-Joon Lee, David W Smith, Bruce S Gardiner","doi":"10.1080/21688370.2026.2721728","DOIUrl":"https://doi.org/10.1080/21688370.2026.2721728","url":null,"abstract":"<p><p>The glomerular filtration barrier (GFB) is a size- and charge-selective filter regulating the passage of blood-borne solutes into the urinary space. However, solutes within the GFB may also originate from podocyte secretion, including extracellular matrix (ECM) components and signaling molecules. We developed a two-dimensional computational solute transport model incorporating two cross-sectional GFB geometries: one based on averaged rodent data and one reconstructed from a healthy adult human glomerular image. Four cases were examined, defined by the solute's source and its ability to pass the podocyte slit diaphragm. To account for a wide range of solute types, solute mobility, described by the effective diffusion coefficient (<i>D</i>_<i>eff</i>), was varied over six orders of magnitude. For blood-borne solutes unable to pass the slit diaphragm, a steep concentration gradient forms, with the highest concentration adjacent to the podocytes. This gradient becomes steeper as <i>D</i>_<i>eff</i> decreases, corresponding to larger or less mobile solutes. This finding has implications for barrier clogging and for mechanisms that may increase <i>D</i>_<i>eff</i>, including the role of ECM fixed charge density or ECM turnover. For podocyte-synthesized solutes to move against filtrate flow, without being rapidly lost to the urinary space, the model suggests solutes must possess properties preventing passage through the slit diaphragm. This result provides context for the relatively large signaling molecule complexes and ECM components. Together, these findings suggest that the structural organization of the GFB, particularly the slit diaphragm, enables solute distribution and directional transport, and therefore provides insight into GFB maintenance and pathology.</p>","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2721728"},"PeriodicalIF":3.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148866881","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Decoding the multidimensional landscape of skin aging: molecular pathways and next-generation diagnostics & therapeutics.","authors":"Megha Sharma, Sonam Chawla","doi":"10.1080/21688370.2026.2721715","DOIUrl":"https://doi.org/10.1080/21688370.2026.2721715","url":null,"abstract":"<p><p>Skin aging is a multifactorial, dynamically regulated biological process modulated by the synergistic interplay of intrinsic genetic programming and extrinsic environmental stressors. Chronological skin aging is dominated by molecular signatures such as telomere attrition, mitochondrial dysfunction, epigenetic drift, and fibroblast senescence. Extrinsic factors such as UV-induced photooxidation, pollution, lifestyle toxins accelerate ROS surge, DNA photolesions, and extracellular matrix fragmentation. Extrinsic and intrinsic pathways converge to cause epidermal thinning, collagen degradation, barrier dysfunction, pigmentation heterogeneity and inflammaging-driven microenvironmental collapse. In this review, we decode the structural, cellular, molecular, and biomechanical axes of skin aging, highlighting ROS-driven MAPK (Mitogen-activated protein kinase)/NF-κB (Nuclear factor kappa-B) activation, PI3K/Akt-mTOR (Phosphoinositide 3-kinase/Mechanistic target of rapamycin) dysregulation, TGF-β/Smad (Transforming growth factor-β/SMAD signaling) impairment, Wnt/β-catenin (Wnt signaling pathway/β-catenin) decline, mechanotransduction failure, and sirtuin-mediated mitochondrial compromise as central mediators. We also discuss skin dysbiosis‑driven lipid barrier disruption, and senescence‑associated secretory phenotype‑driven inflammaging as underlying factors for systemic inflammatory disorder-like phenotype in aged skin. Cutting-edge diagnostic advances - Cutometer®-based elasticity mapping, corneometry, AI-assisted histopathology etc are discussed for aiding rapid and objective precision in quantifying biological age. Mechanism of action and application of emerging and innovative dermato-therapeutics - probiotic/postbiotic-based microbiome modulation, nanoformulation-driven targeted delivery, epigenetic reprogramming, senolytics, and mitochondrial revitalization are discussed in terms of their current limitations (specificity, stability), highlighting future scope for action. In summary, skin aging is a multidimensional process, orchestrated at a molecular level, and clinically actionable-one that will enable the next leap in personalized anti-aging innovation and precision dermatology frameworks.</p>","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2721715"},"PeriodicalIF":3.1,"publicationDate":"2026-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148813884","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}