Cells最新文献

{"title":"Potential Physiological Convergence Between GLP-1 Receptor Signaling and Hepatocyte TAZ in Metabolic Liver Disease: From Metabolic Homeostasis to Fibrotic Remodeling.","authors":"Mohammed F Gholam","doi":"10.3390/cells15191813","DOIUrl":"10.3390/cells15191813","url":null,"abstract":"<p><p>Metabolic dysfunction-associated steatotic liver disease (MASLD) progresses when nutrient excess, insulin resistance, adipose dysfunction, and hepatocellular stress overwhelm hepatic adaptation. Glucagon-like peptide-1 receptor agonists (GLP-1RAs) improve weight, glycemic control, and steatohepatitis, and semaglutide has demonstrated histological improvement in metabolic dysfunction-associated steatohepatitis (MASH). In parallel, the transcriptional coactivator with PDZ-binding motif (TAZ; WWTR1) has emerged as a nutrient-, cholesterol-, and mechanics-responsive regulator linking stressed hepatocytes to inflammation and fibrogenesis through Hippo-YAP/TAZ signaling and Indian hedgehog. This narrative review integrates incretin physiology with cell-specific TAZ biology across the gut-brain-axis, adipose tissue, pancreatic islets, liver sinusoidal endothelial cells, hepatocytes, immune cells, and hepatic stellate cells. Recent evidence that semaglutide can signal through intrahepatic sinusoidal endothelial GLP-1 receptors provides a weight-loss-independent route to reduced hepatic inflammation and fibrosis; however, it does not establish that TAZ is a downstream mediator. The evidence therefore supports a multilevel convergence model in which GLP-1RAs lower metabolic and inflammatory inputs that favor TAZ activation, while direct GLP-1RA-to-TAZ signaling remains a testable hypothesis. Receptor-validated, cell-specific, weight-controlled, and longitudinal human studies are needed to distinguish mediation from parallel response and to determine whether TAZ-pathway biomarkers can guide mechanism-based therapy.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"15 19","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13664139/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149191112","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Kaempferol Restores Cilia Length Through Axonemal Microtubule Stabilization.","authors":"Xuyao Dai, Yi Zhao, Ruodan Xu, Ning Li","doi":"10.3390/cells15191806","DOIUrl":"10.3390/cells15191806","url":null,"abstract":"<p><p>Ciliary shortening disrupts cilium-dependent signaling and tissue homeostasis and contributes to diverse ciliopathies and acquired disorders. However, the underlying mechanisms and pharmacological strategies for restoring ciliary length remain poorly understood. Here, we identify Kaempferol (Kae) as a previously unrecognized small-molecule regulator of ciliary length. Transcriptomic profiling showed that Kae-responsive genes were enriched in cytoskeleton- and microtubule-related processes, including microtubule organization and motor protein activity, suggesting that cytoskeletal regulation may contribute to its effects on ciliary length. Further investigation demonstrated that Kae promoted ciliary elongation under basal conditions and restored ciliary length across mechanistically distinct defect models, including SARS-CoV-2 non-structural protein 13 (NSP13) expression, Ciliobrevin D-mediated dynein inhibition, and centrosomal protein 290 (CEP290) deficiency. Mechanistically, Kae enhanced microtubule stability, as indicated by increased acetylated α-tubulin (ACTUB) expression, greater resistance to nocodazole-induced depolymerization, and enhanced microtubule recovery. Consistent with these cellular effects, Kae promoted microtubule recovery and preserved ciliary ultrastructure in the NSP13-induced airway injury model in vivo. These findings establish Kae as a pharmacological modulator of ciliary length and highlight axonemal microtubule stabilization as a potential strategy for restoring dysfunctional cilia.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"15 19","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13664028/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149191527","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dissecting Adult Peripheral Cellular Immunity to <i>Bordetella pertussis</i>: Innate-Associated IFN-γ Responses, Transient T-Cell Recall, and HLA-A*02-Associated CD8+ Reactivity.","authors":"Alexandra Maleeva, Varvara Shokina, Zlata Naydenysheva, Anna Lyapina, Eleonora Sadykova","doi":"10.3390/cells15191807","DOIUrl":"10.3390/cells15191807","url":null,"abstract":"<p><p><i>Bordetella pertussis</i> elicits both innate and adaptive cellular responses, yet their relative contributions to peripheral interferon-γ (IFN-γ) measurements and the temporal dynamics of circulating T-cell reactivity in adults remain incompletely defined. <i>B. pertussis</i>-reactive cellular immunity was investigated in 42 adult donors, including 26 healthy donors and 16 donors with a history of pertussis, using standard and modified IFN-γ enzyme-linked immunospot (ELISpot) assays with a chemically inactivated whole-cell <i>B. pertussis</i> preparation, bacterial innate-biased stimuli, and a peptide-based T-cell recall control, together with human leukocyte antigen A*02 (HLA-A*02) genotyping. Short-term stimulation of unfractionated peripheral blood mononuclear cells (PBMCs) generated readily detectable IFN-γ spot formation that was not clearly stratified by childhood vaccination background or previous pertussis history. In a subset of seven donors, lipopolysaccharide and <i>B. pertussis</i>-derived lipooligosaccharide generated strong total PBMC signals but little detectable pattern-defined T-cell-associated spot formation, whereas the whole-cell pertussis preparation retained a detectable T-cell-associated component under modified assay conditions. Among seven donors available for longitudinal follow-up after pertussis, pattern-defined T-cell-associated IFN-γ spot frequencies in peripheral blood were highest at the recovery sampling point, were significantly reduced at one month, decreased further by three months, remained markedly reduced at six months, and approached background levels at 12 months after recovery. Directly measured CD8+ IFN-γ responses were preferentially detected in HLA-A*02-positive donors. These findings indicate that cellular composition and sampling time affect the interpretation of peripheral IFN-γ responses to <i>B. pertussis</i> and show an association between HLA-A*02 status and detectable CD8+ reactivity.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"15 19","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13664011/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149191615","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of Metabolic Pathways and Products on Early Mammalian Embryonic Development.","authors":"Hu Tao, Zaidong Hua, Jingwei Wei, Xiangxing Zhu, Qi Xiong","doi":"10.3390/cells15191808","DOIUrl":"10.3390/cells15191808","url":null,"abstract":"<p><strong>Background: </strong>The study of early mammalian embryonic development is the basis for the cultivation of embryonic stem cells (ESCs), assisted reproductive technology (ART), and understanding and preventing early embryonic developmental defects. Metabolism is the most fundamental physiological activity of embryonic development. Studies have shown that specific metabolic pathways and metabolites play key roles in embryonic development. These roles involve the regulation of signal transduction in addition to the provision of energy to the organism.</p><p><strong>Aim of review: </strong>This review examines the factors affecting the critical moments of embryonic development, such as oocyte maturation, zygotic gene activation, cell compaction, and two genealogical differentiations. It also presents the characteristics of embryonic metabolism at this time. This review aims to provide new insights and approaches for improving early mammalian embryonic development by clarifying the relationship between embryonic metabolism and its developmental processes. Furthermore, the review emphasizes embryonic metabolism as a potential indicator for assessing the level of embryonic development in vitro, providing a new basis for assessment in assisted reproductive technologies. Key Scientific Concepts of Review: This review is focused on three main key concepts. First, we demonstrate known regulatory mechanisms of embryonic development to enhance the potential of early embryonic development. Second, we elucidate the potential role of metabolic processes and their products in early embryonic development. Third, we provide new foundations and perspectives for the study of the early embryo from the perspective of cellular metabolism.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"15 19","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13664230/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149191626","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PARP1 Deficiency Attenuates Cisplatin Nephrotoxicity and Renal COX-2/PGE2 Response.","authors":"Theophilus Bhatti, Jia-Bin Yu, Ji-Yeong Bae, Jinu Kim","doi":"10.3390/cells15191810","DOIUrl":"10.3390/cells15191810","url":null,"abstract":"<p><p>Cisplatin is a widely used chemotherapeutic agent whose clinical utility is limited by nephrotoxicity, characterized by tubular injury and renal inflammation. Poly(ADP-ribose) polymerase 1 (PARP1) contributes to cisplatin-induced kidney injury and inflammatory signaling, but the downstream inflammatory pathways involved remain incompletely defined. Here, we investigated whether PARP1 modulates the renal cyclooxygenase-2 (COX-2)/prostaglandin E2 (PGE2) response during cisplatin-induced acute kidney injury (AKI). Female wild-type and <i>Parp1</i>-knockout (KO) mice on a C57BL/6 background received a single intraperitoneal injection of cisplatin (20 mg/kg) and were evaluated at days 1 and 4, while male mice were evaluated at day 4 for renal function. Renal function, tubular injury, inflammatory gene expression, NF-κB activation, <i>Ptgs2</i> mRNA and COX-2 protein expression, and kidney PGE2 levels were assessed. Cisplatin markedly increased plasma creatinine and blood urea nitrogen levels and induced tubular injury in both the renal cortex and outer stripe of the outer medulla, whereas these changes were significantly attenuated in <i>Parp1</i> KO mice at day 4. At day 4, cisplatin-induced renal expression of <i>Il1b</i>, <i>Il6</i>, <i>Ccl5</i>, <i>Cxcl1</i>, and <i>Cxcl2</i> was also substantially reduced by <i>Parp1</i> deficiency. Cisplatin increased renal NF-κB p65 activation, as assessed by the p-p65/t-p65 ratio, in wild-type mice, whereas this response was significantly attenuated in <i>Parp1</i> KO mice. Consistently, cisplatin increased renal <i>Ptgs2</i> mRNA expression, COX-2 protein abundance, and PGE2 levels in wild-type mice, whereas all three responses were significantly attenuated in <i>Parp1</i> KO mice. In particular, the cisplatin-induced increase in renal PGE2 was nearly abolished in the absence of PARP1. These findings demonstrate that PARP1 deficiency attenuates cisplatin-induced renal dysfunction, tubular injury, and inflammatory responses and identify suppression of NF-κB activation and the COX-2/PGE2 response as features of this protective phenotype. The results support a potential PARP1-NF-κB-COX-2/PGE2 signaling axis in cisplatin nephrotoxicity.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"15 19","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13664194/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149191728","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antigen-Presentation Competence in Gynecologic Cancers: Mechanisms, Evidence and Translational Priorities.","authors":"Zihao Xu, Yifan Liu, Jun Xu, Mengxin Xiong","doi":"10.3390/cells15191809","DOIUrl":"10.3390/cells15191809","url":null,"abstract":"<p><p>Immune-checkpoint biomarkers in gynecologic cancers primarily estimate antigenic potential or characterize an inhibited immune response. However, they do not establish whether malignant cells are visible to antigen-specific lymphocytes. We define antigen-presentation competence as the capacity of the tumor-immune ecosystem to generate antigenic peptides, display them through functional human leukocyte antigen molecules, prime cognate T cells through professional antigen-presenting cells, and permit recognition of malignant cells by effector lymphocytes. Recurrent defects have been reported at each step in cervical, endometrial, and ovarian cancers, but the evidence is not equally mature across these diseases. Cervical studies emphasize human papillomavirus-associated immune selection and antigen-processing machinery abnormalities; endometrial cancer provides relatively direct treatment-linked evidence for major histocompatibility complex class I and interferon-pathway defects; and ovarian cancer offers direct immunopeptidomic and multiregion evidence that antigen availability, presentation, and immune recognition can diverge. Taken together, the literature makes antigen-presentation competence a testable functional framework. It does not yet justify a biomarker or clinical score. Prospective work will need spatial and longitudinal measurements of tumor presentation, dendritic-cell priming, and T-cell recognition. A key test is whether these measurements improve prediction beyond mismatch repair, polymerase epsilon, programmed death-ligand 1, and tumor mutational burden.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"15 19","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13664500/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149191487","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Novel Therapeutic Targets and Approaches, Genetic Markers and Signaling Pathways in Neoplasms-An Overview.","authors":"Daria Chudakova","doi":"10.3390/cells15191805","DOIUrl":"10.3390/cells15191805","url":null,"abstract":"<p><p>Cancer remains one of the major global health problems [...].</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"15 19","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13664521/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149191617","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypoxia-ROS-HSP Triad Axis in Cancer: Mechanisms, Crosstalk, and Therapeutic Implications.","authors":"Manish Kumar Singh, Hyeong Rok Yun, Jyotsna Ranbhise, Sunhee Han, Seung Geun Yeo, Fu-Shi Quan, Bonglee Kim, Sung Soo Kim, Insug Kang","doi":"10.3390/cells15191802","DOIUrl":"10.3390/cells15191802","url":null,"abstract":"<p><p>Cancer remains one of the leading causes of mortality worldwide, accounting for approximately 20% of all deaths and posing a major threat to global health. Mechanistically, tumorigenesis is driven by complex molecular and cellular mechanisms that enable malignant cells to evade current therapeutic interventions, thereby limiting treatment efficacy and contributing to disease progression. Despite extensive efforts to identify and target key molecular regulators and signaling pathways involved in cancer development, effective and durable treatments remain limited for many cancers, underscoring the need for novel treatment strategies. Consequently, diverse therapeutic strategies are being developed to overcome barriers to treatment response, improve clinical outcomes, and extend patient survival. Among emerging therapeutic targets, HSPs have attracted considerable attention because of their critical roles in maintaining proteostasis, promoting tumor cell survival, and facilitating resistance to therapy. In addition to stress adaptation, oxidative stress and hypoxia are key components of the tumor microenvironment that promote malignant progression through extensive crosstalk with oncogenic signaling pathways. Growing evidence indicates that these pathways are highly interconnected and collectively contribute to cancer metastasis and poor clinical outcomes. In this review, we explore the mechanistic interplay among HSPs, reactive oxygen species (ROS), and hypoxia across various cancers, highlight their potential as integrated therapeutic targets, and explore future strategies to develop more effective anticancer interventions.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"15 19","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13664626/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149191492","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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 Role of the Immunoglobulin Superfamily of Cell Adhesion Molecules in Intellectual Disability.","authors":"Nishat Zaman, Karina Bui, Vladimir Sytnyk","doi":"10.3390/cells15191801","DOIUrl":"10.3390/cells15191801","url":null,"abstract":"<p><p>Immunoglobulin superfamily (IgSF) cell adhesion molecules (CAMs) are cell surface glycoproteins that play critical roles during multiple stages of synapse formation, including axon and dendrite growth and guidance, target recognition, axo-dendritic contact formation and its maturation into a functional synapse. Intellectual disability is a condition characterized by significant limitations in intellectual functioning and adaptive behaviors. Growing evidence indicates that deficits in synapse formation underlie the pathogenesis of intellectual disability. In this review, we discuss studies showing that levels and functions of IgSF CAMs are affected in various syndromes and disorders associated with intellectual disability, including Fragile X syndrome, Rett syndrome, Down syndrome, autism spectrum disorder, L1 syndrome and fetal alcohol spectrum disorders. We highlight functional studies in cellular and animal models showing that changes in levels and functions of IgSF CAMs impair synapse formation and induce learning and behavioral abnormalities resembling those found in people with intellectual disability. Together, these studies indicate that IgSF CAMs need to be considered as important therapeutic targets for treating intellectual disability and their functions need to be assessed when new treatments of this condition are developed.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"15 19","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13664354/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149191589","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Saccharopine and α-Aminoadipic Acid as Potential Biomarkers for Mitochondrial Stress in Neurons.","authors":"Anna-Katharina Ückert, Anja Land, Regina Pape, Mahshid Alimohammadi, Ivano Amelio, Marcel Leist","doi":"10.3390/cells15191804","DOIUrl":"10.3390/cells15191804","url":null,"abstract":"<p><p>Redox stress and subsequent metabolic reprogramming are well-known consequences of neuronal exposure to mitochondrial toxicants. Here, we investigated, using human neuronal cultures, how such changes are quantitatively reflected in the patterns of cellular and extracellular amino acids. We asked whether these alterations may yield a mechanistically anchored biomarker for the type of neurotoxicity resulting from the impairment of the respiratory chain. Using a targeted metabolomics approach, we quantified intra- and extracellular amino acid pools and their temporal dynamics. Data were obtained from differentiated LUHMES neurons exposed to the complex I inhibitors berberine, 1-methyl-4-phenylpyridinium (MPP⁺), and tebufenpyrad, as well as to the non-mitochondrial toxicants MG-132 (proteasome inhibitor), RSL3 (glutathione peroxidase 4 inhibitor), and aerugine (fungal oxidative toxicant). The reductive stress, caused by mitochondrial inhibitors, was reflected in a characteristic and specific re-routing of amino acid metabolism, including increased Asn/Asp and Gln/Glu ratios and an upregulation of the electron acceptor Pro in neurons. Most conspicuous were the pronounced and reproducible increases in the lysine catabolites saccharopine (sacc) and α-aminoadipic acid (α-AAA). These two potential biomarkers of neuronal mitotoxicity were not altered by other types of toxicants. Moreover, the extent of concentration changes in sacc and α-AAA roughly correlated with the damaging effects of mitotoxicants, when assay conditions were (exposure period and exposure concentration). Our data provide an exemplary reference map of absolute amino acid concentrations in human cells and their culture medium. Moreover, sacch and α-AAA emerge as candidate biomarkers for neuroactive mitotoxicants and potentially for pathologies associated with impaired neuronal mitochondrial function.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"15 19","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13664059/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149191537","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}