Molecular Biology Reports最新文献

{"title":"Trilobatin attenuates allergic airway inflammation via multi-target suppression of NLRP3 inflammasome activation and caspase-3 signaling.","authors":"Songbai Fang, Weidong Liu, Suidong Ouyang, Jianyuan Chen","doi":"10.1007/s11033-026-13021-0","DOIUrl":"https://doi.org/10.1007/s11033-026-13021-0","url":null,"abstract":"<p><strong>Background: </strong>Asthma is a heterogeneous chronic airway disease characterized by persistent inflammation, airway hyperresponsiveness, and airway remodeling, largely driven by type 2 immune responses. Trilobatin (TLB), a flavonoid derived from Lithocarpus polystachyus (Sweet Tea), exhibits anti-inflammatory and antioxidant properties. However, its therapeutic effects and underlying molecular mechanisms in asthma remain insufficiently elucidated. This study aimed to investigate the potential targets and mechanisms underlying the anti-asthmatic effects of TLB.</p><p><strong>Methods and results: </strong>An integrated approach combining network pharmacology, molecular docking, and experimental validation was employed to investigate the mechanisms of TLB. Candidate TLB targets were identified and intersected with asthma-associated genes to construct a protein-protein interaction network, followed by functional enrichment analyses. Molecular docking highlighted caspase-3 (CASP3) and matrix metalloproteinase-9 (MMP9) as potential key targets with favorable binding affinities. These findings were further investigated in a house dust mite-induced murine model of asthma. TLB treatment alleviated airway inflammation and reduced proinflammatory cytokine production. Mechanistic analyses further indicated that TLB inhibited NLRP3 inflammasome activation and CASP3-associated apoptotic signaling in lung tissue.</p><p><strong>Conclusion: </strong>TLB alleviates allergic airway inflammation in experimental asthma, potentially through the coordinated regulation of NLRP3 inflammasome activation and CASP3-associated apoptotic signaling. These findings provide mechanistic insights into the anti-asthmatic effects of TLB and support its further investigation as a potential therapeutic candidate for asthma.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149270799","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Prospect of exosomal circular RNAs in breast Cancer: presents and future.","authors":"Elham Zokaei, Farzaneh Darbeheshti, Nima Rezaei","doi":"10.1007/s11033-026-13019-8","DOIUrl":"https://doi.org/10.1007/s11033-026-13019-8","url":null,"abstract":"","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149270732","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Urinary circRNA hsa_circ_0001334: a potential non-invasive early indicator of subsequent renal allograft rejection.","authors":"Samar Bizhani, Afsoon Afshari, Ramin Yaghobi, Jamshid Roozbeh","doi":"10.1007/s11033-026-13047-4","DOIUrl":"https://doi.org/10.1007/s11033-026-13047-4","url":null,"abstract":"<p><strong>Background: </strong>Kidney allograft rejection is a major cause of graft loss. The need for non‑invasive biomarkers to complement invasive biopsy is urgent. Circular RNAs (circRNAs) are stable regulatory molecules that function as microRNA (miRNA) sponges within competitive endogenous RNA (ceRNA) networks, making them promising candidates for non-invasive biomarker development. This study aimed to investigate whether early postoperative expression of specific ceRNA axes, particularly hsa_circ_0001334/hsa-miR‑665/CNR2, is associated with subsequent kidney transplant rejection.</p><p><strong>Methods and results: </strong>We enrolled 52 subjects; 15 recipients with biopsy‑proven rejection, 17 clinically stable recipients, and 20 healthy controls. Using SYBR Green‑based quantitative real‑time PCR, we measured expression of hsa_circ_0001334, hsa_circ_0071475, their host genes (MCM2, TNM3), related miRNAs (hsa-miR‑665, hsa-miR‑1208, hsa-miR‑1183), and target mRNAs (CNR2, ADORA2B) in paired urine and blood samples. Non‑parametric tests, Spearman correlation, and receiver‑operating‑characteristic (ROC) curve analysis were employed. Urinary hsa_circ_0001334 was markedly upregulated in the subsequent rejection group (p < 0.0001), whereas its linear host gene MCM2 remained unchanged. hsa_circ_0071475 showed only a modest elevation compared to healthy controls and no change in blood. An expression pattern consistent with a putative ceRNA relationship was observed, with lower urinary hsa-miR-665 expression and higher CNR2 expression in recipients who subsequently developed biopsy-proven rejection. ROC analysis demonstrated excellent preliminary predictive discrimination for urinary hsa_circ_0001334, with an area under the curve (AUC) of 1.00 (p = 0.0006).</p><p><strong>Conclusion: </strong>Our findings suggest a potential involvement of the hsa_circ_0001334/hsa-miR-665/CNR2 axis in immune-mediated injury during kidney allograft rejection. Urinary hsa_circ_0001334 may serve as a potential non-invasive biomarker for early risk stratification of subsequent rejection, though further validation in larger independent cohorts and functional studies are required to confirm its clinical utility.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149270819","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Genetic and epigenetic landscape of non-familial sudden cardiac death.","authors":"Natalia Baulina, Natalia Matveeva, Maxim Kozin, Olga Favorova, Ivan Kiselev","doi":"10.1007/s11033-026-12977-3","DOIUrl":"https://doi.org/10.1007/s11033-026-12977-3","url":null,"abstract":"","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149270686","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A novel PGAP1 splice-site variant expanding the clinical and molecular spectrum of GPI-anchor disorders.","authors":"Seyyed-Saleh Hashemi, Reza Moazzami, Ali Miri","doi":"10.1007/s11033-026-13043-8","DOIUrl":"10.1007/s11033-026-13043-8","url":null,"abstract":"<p><strong>Background/objective: </strong>Genetic defects affecting the biosynthesis and remodeling of glycosylphosphatidylinositol (GPI) anchors constitute a recently recognized group of autosomal recessive neurodevelopmental disorders with highly variable clinical presentations. Among the genes involved in this pathway, PGAP1 encodes an endoplasmic reticulum-associated inositol deacylase that plays a critical role in the initial step of GPI-anchor remodeling. Pathogenic variants in PGAP1 have been reported in only a limited number of families worldwide and are associated with clinical features such as global developmental delay, intellectual disability, seizures, microcephaly, and variable systemic manifestations.</p><p><strong>Methods: </strong>Here, we describe a patient harboring a novel homozygous splice-site variant (NM_024989.4.1173 + 1G > A) with neurodevelopmental impairment. The potential effect on splicing was assessed using in silico tools (SpliceAI, HSF, and varSEAK), while the potential structural consequences were evaluated using AlphaFold and PyMOL. Segregation analysis was performed to assess the inheritance pattern and provide additional evidence for variant classification. A comprehensive review of previously reported cases was also conducted to broaden the known phenotypic spectrum.</p><p><strong>Results: </strong>The novel variant, which was absent from all public databases, was classified as likely pathogenic according to ACMG guidelines. Computational analyses consistently predicted significant disruption of splicing, while structural modeling suggested conformational alterations associated with the predicted in-frame deletion.</p><p><strong>Conclusion: </strong>Our findings expand the phenotypic heterogeneity of PGAP1-related disorders and provide further insight into the molecular basis of GPI-anchor remodeling defects. The findings also highlight the utility of genomic analysis for establishing a molecular diagnosis in patients with unexplained neurodevelopmental abnormalities.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149270832","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular Mechanisms of Immunomodulation by Neural Stem Cells in Spinal Cord Injury: From Macrophage Polarization to Therapeutic Plasticity.","authors":"Arman A Gholami, Hamideh Babaloo, Karim Rahmatov, Assad Ward, Aziz Kubaev, Ilkhom Otajonov, Akmal Xaitov, Fatemeh Mortazavi Moghadam","doi":"10.1007/s11033-026-13070-5","DOIUrl":"https://doi.org/10.1007/s11033-026-13070-5","url":null,"abstract":"<p><p>Spinal cord injury (SCI) triggers a chronic neuroinflammatory cascade driven by persistent M1 macrophage polarization, creating a hostile microenvironment that inhibits axonal regeneration and perpetuates secondary tissue damage. Neural stem cells (NSCs) offer a promising therapeutic strategy through immunomodulation, reshaping the inflammatory landscape rather than merely replacing lost neurons. This review synthesizes evidence on the molecular mechanisms by which NSCs reprogram the immune response. NSCs suppress TLR4/NF-κB signaling to shift macrophages from a neurotoxic M1 phenotype toward a pro-regenerative M2 phenotype, engage in reciprocal dialogue with T cells and microglia to create a neurogenic niche, secrete neurotrophic factors that upregulate KCC2 and restore GABAergic inhibition, and modulate purinergic signaling to attenuate neuropathic pain. However, the evidence base remains incomplete. Most studies provide correlative rather than causal evidence, and the M1/M2 framework does not fully capture macrophage heterogeneity after SCI, particularly in the chronic phase where foam cells, pro-fibrotic phenotypes, and disease-associated subpopulations emerge. The subacute window is generally associated with superior outcomes, but optimal timing varies with injury severity, model, cell source, transplantation route, and cell dose. Clinical translation remains at an early stage; phase I trials have established feasibility and short-term safety, but most lacked control groups and adequate sample sizes. Adverse effects, including allodynia, tumorigenicity, and immune-related complications, underscore that neural cell transplantation is not inherently safe. Future progress requires adequately powered trials with objective endpoints, biomarker development, refined immunomodulation strategies, and careful monitoring for adverse effects.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149270687","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of INHA polymorphism with fertility in Kreishi ewes.","authors":"Siraj A Hashem, Mervan Bayraktar, Tahreer M Al-Thuwaini","doi":"10.1007/s11033-026-13058-1","DOIUrl":"https://doi.org/10.1007/s11033-026-13058-1","url":null,"abstract":"<p><strong>Background: </strong>Litter size is an important reproductive trait in sheep, and INHA is a candidate gene involved in reproductive regulation. However, the association of specific INHA variants with litter size in Kreishi sheep remains insufficiently characterized. This study examined INHA polymorphisms in 100 Kreishi ewes aged 3-4 years.</p><p><strong>Methods and results: </strong>The animals were classified according to litter size into single-bearing (n = 46) and twin-bearing (n = 54) groups. PCR amplification and bidirectional Sanger sequencing were used to identify the variant. The association between genotype and litter size was evaluated using the chi-square test and binary logistic regression. The potential functional and structural effects of the resulting substitution were assessed using SIFT, PolyPhen-2, DynaMut2, and PyMOL. The c.425 C > T substitution resulted in the missense change p.Ser142Phe and was detected in three genotypes: CC, CT, and TT. Genotype distribution differed significantly between single- and twin-bearing ewes (χ² = 30.87, P < 0.0001). Relative to the TT genotype, CT was associated with increased odds of twin birth (odds ratio [OR] = 6.77, 95% confidence interval [CI]: 1.59-28.72), while CC showed a higher estimated association with twin birth (OR = 16.51, 95% CI: 5.56-49.08).</p><p><strong>Conclusions: </strong>The INHA c.425 C > T (p.Ser142Phe) variant was significantly associated with litter size in the studied Kreishi ewes. SIFT, PolyPhen-2, and DynaMut2 predicted deleterious, potentially damaging, and destabilizing effects, respectively, while PyMOL indicated a conserved overall protein fold with localized structural changes around residue 142. Validation in larger, independent populations is needed before using it as a molecular marker for reproductive selection.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149270806","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Androgen receptor signaling in hepatocellular carcinoma: mechanisms of male predominance and therapeutic opportunities.","authors":"Yang Zhou, Yiyu Qin","doi":"10.1007/s11033-026-12976-4","DOIUrl":"https://doi.org/10.1007/s11033-026-12976-4","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is two to four times more common in men than in women. The sex distribution of viral hepatitis, alcohol use and adiposity explains only part of this difference, which points to sex-specific host biology as a further driver. The androgen receptor (AR), a ligand-activated transcription factor expressed in hepatocytes and in most HCC, is a strong candidate: both epidemiologic and experimental data implicate it in the male excess. This review draws that evidence together. Prospective cohorts link higher circulating testosterone and sex hormone-binding globulin to liver cancer risk, although raising SHBG experimentally suppresses rather than promotes hepatocarcinogenesis, a discordance that bears on how those associations should be read, and experimental studies group the underlying biology into several modules: constitutively active AR and its splice variants, kinase-driven phosphorylation of the receptor, downstream effectors of proliferation, invasion and angiogenesis, non-coding RNA circuits, androgen-metabolizing enzymes and the systemic endocrine axis, and the effect of androgen on the tumor immune microenvironment. The weight of each module differs across hepatitis B virus (HBV)-related, hepatitis C virus (HCV)-related, metabolic dysfunction-associated and anabolic steroid-induced disease. Therapeutic work remains largely preclinical and has centered on AR antagonists combined with tyrosine kinase inhibitors or immune checkpoint blockade, on degraders aimed at AR splice variants, on proteolysis-targeting chimeras and nucleic-acid approaches that eliminate ligand-independent receptor states, and on enzyme inhibitors. Two problems still limit translation: AR appears oncogenic in most settings but tumor-suppressive in some, and androgen suppresses antitumor immunity in certain contexts while enhancing it in others. Clarifying when each holds is what will determine whether AR-directed therapy, already established in prostate cancer, can be extended to liver cancer.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149270842","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dipicolinic acid has an anti-inflammatory effect and inhibits the expression of NF-κB, miR-101a, miR-140 and miR-195 in diclofenac-induced myocardial injury in rats.","authors":"E D Kryl'skii, T N Popova, A N Verevkin, O A Scherbakova, V P Sergin","doi":"10.1007/s11033-026-13014-z","DOIUrl":"https://doi.org/10.1007/s11033-026-13014-z","url":null,"abstract":"<p><strong>Background: </strong>Nonsteroidal anti-inflammatory drugs, including diclofenac, are commonly used to alleviate inflammation and pain associated with various medical conditions. Prolonged use of these medications may lead to complications related to the cardiovascular system. One of the primary mechanisms of myocardial damage associated with diclofenac is oxidative stress, which is closely linked with the activation of inflammation. The current study aims to evaluate the efficacy of dipicolinic acid (DPA) as a potential treatment for diclofenac-induced cardiac injury. Additionally, the study will investigate the effects of DPA on the expression levels of transcription factor NF-κB and microRNAs (miRNAs), specifically miR-101a, miR-140, and miR-195, which play a role in regulating inflammation.</p><p><strong>Methods and results: </strong>The results of the study demonstrated that the implementation of DPA led to a substantial reduction in the levels of cardiomyocytes cytolytic markers in the blood serum of the animals, compared to the values observed in the group with myocardial injury. These alterations were associated with decreased concentrations of free radical-induced oxidation products of lipid, protein, and DNA, including diene conjugates, carbonylated proteins, and 8-hydroxy-2-deoxyguanosine. The improvement in the oxidative status of rats was accompanied by a reduction in the levels of pro-inflammatory cytokine mRNA and myeloperoxidase activity. The DPA treatment also reduced the expression of the p65 subunit of the NF-κB factor and miR-101a, miR-140, and miR-195, which were found to be involved in pro-inflammatory signaling.</p><p><strong>Conclusions: </strong>Therefore, the administration of DPA in diclofenac-induced myocardial injury is associated with an improvement in oxidative status and the inhibition of the inflammatory response, which may involve the modulation of the NF-κB, miR-101, miR-140, and miR-195 expression.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149270709","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"miR-21a-5p targets DDX58 to suppress TLR2/NF-κB signaling and protect the blood-brain barrier after injury.","authors":"Jing Yang, Ning Tang, Ruanxian Dai, Hao Fu, Shiyi Li, Qiang Meng","doi":"10.1007/s11033-026-13010-3","DOIUrl":"10.1007/s11033-026-13010-3","url":null,"abstract":"<p><strong>Background: </strong>Damage to the blood-brain barrier (BBB) plays a pivotal role in the pathogenesis of various neurological disorders. miR-21a-5p has been implicated in the modulation of BBB injury. Understanding the molecular targets of miR-21a-5p is crucial for developing targeted interventions in BBB repair.</p><p><strong>Methods: </strong>The target gene of miR-21a-5p was identified through bioinformatics analysis and validated using a dual luciferase reporter assay. The expression of target gene was further confirmed in both in vivo and in vitro models of BBB injury. BBB injury cell models were employed to assess the effects of target gene overexpression and silencing on brain microvascular endothelial cell (BMEC) activity, as well as on the TLR2/NF-κB signaling pathway and associated BBB proteins. miR-21a-5p overexpression and silencing were utilized to assess the impact of target gene on BBB integrity.</p><p><strong>Results: </strong>DDX58 was identified as a direct target of miR-21a-5p and is shown to modulate BBB injury. DDX58 expression was found to be upregulated in models of BBB damage. Exosomes containing miR-21a-5p mitigated BBB damage, which was associated with downregulated DDX58 expression in vivo and in vitro. Overexpression of DDX58 in BMECs resulted in reduced cellular viability, increased expression of TLR2 and phosphorylated p65 (p-p65), as well as elevated levels of matrix metalloproteinases (MMP-2/9), which are associated with BBB disruption. This was accompanied by a reduction in tight junction proteins, including claudin-5, occludin, and ZO-1. Conversely, silencing DDX58 expression exhibited the opposite effects. Both miR-21a-5p treatment and DDX58 interference alleviated BBB injury. Co-overexpression of DDX58 during miR-21a-5p treatment reversed the protective effects of miR-21a-5p, exacerbating BBB injury.</p><p><strong>Conclusion: </strong>miR-21a-5p targets and downregulates DDX58, which is associated with reduced expression of TLR2/NF-κB-related markers, decreased MMP-2/9 levels, and protection of tight junction integrity.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13696569/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149270745","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}