Molecular and Cellular Biochemistry最新文献

{"title":"Macrophage polarization-related gene SOAT1 is involved in inflammatory response and functional recovery after spinal cord injury.","authors":"Peng Peng, Huitao Wang, Zhen Pang, Hui Zhang, Sihan Hu, Xingyi Ma, Fangjing Yang, Yanqun Qiu, Fei Wang, Wendong Xu","doi":"10.1007/s11010-025-05246-7","DOIUrl":"10.1007/s11010-025-05246-7","url":null,"abstract":"<p><p>Macrophages polarization play crucial roles in regulating inflammation and functional recovery after spinal cord injury (SCI). This study aimed to investigate the key macrophage polarization-related genes (MPRGs) for the treatment of SCI. Our research involved identifying differentially expressed genes (DEGs), using immune infiltration analysis, weighted gene co-expression network analysis (WGCNA) and machine learning to screening out key MPRGs in the GSE5296. The discriminative potential of MPRGs were validated using expression analysis and receiver operating characteristic (ROC) curves in the GSE45376, while the distribution of hub MPRGs in different cell subtypes were visualized in the single-cell dataset GSE189070. The relationship between the MPRGs and immune infiltration was investigated through correlation analysis. Finally, we detected the effect of blocking sterol O-acyltransferase 1 (SOAT1) on macrophage polarization and functional recovery of SCI. A total of 52 MPRGs were identified. Elevated immune infiltration levels and activation of macrophage-associated biological pathways were noted after SCI. Machine learning determined SOAT1, LGALS3, HAVCR2, IRF8 and PTPRC as the hub MPRGs. External validation confirmed their expression, robust predictive value and distribution patterns. Immune infiltration analysis highlighted the strong correlation between SOAT1 and macrophages. Further, inhibiting of SOAT1 could enhance M2 macrophage polarization, improve inflammatory environment and promote functional recovery of SCI. Our study enhances the understanding of macrophage polarization-related genes in the inflammatory responses of SCI. Targeting SOAT1 emerges as a promising therapeutic strategy for SCI repair.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"4197-4212"},"PeriodicalIF":3.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143573138","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of pathogenic variants in the ABCG2 gene in patients with severe familial hyperuricemia and gout.","authors":"Yu Toyoda, Katerina Pavelcova, Jana Masinova, Lenka Hasikova, Jakub Zavada, Petra Hanova, Martin Klein, Jiri Vavra, Tappei Takada, Blanka Stiburkova","doi":"10.1007/s11010-025-05252-9","DOIUrl":"10.1007/s11010-025-05252-9","url":null,"abstract":"<p><p>We report the identification of two pathogenic variants in the ABCG2 gene, encoding a urate exporter, in two probands (male and female) with severe familial gouty phenotypes and hyperuricemia. Clinico-genetic analyses identified p.I63YfsTer54 (rs565722112) and p.G74D (rs199976573) as potentially causal mutations; functional analyses demonstrated that these two variants are deficient in plasma membrane localization and functionally null. Our data show that dysfunctional variants in the ABCG2 gene are strong risk factors for hyperuricemia and gout in both males and females.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"4259-4264"},"PeriodicalIF":3.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143625426","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring exhaled volatile organic compounds as potential biomarkers in anti-MDA5 antibody-positive interstitial lung disease.","authors":"Yuxuan Wang, Xuewen Wang, Luqin Yang, Ke Wang, Fengqin Zhang, Huihui Yue, Junqi Wang, Minhua Peng, Pengnan Fan, Xiangcheng Qiu, Han Zhang, Wei Lin, Yuhang Lin, Sitong Chen, Qian Geng, Chaotan Sima, Deming Liu, Ping Lu, Huilan Zhang","doi":"10.1007/s11010-025-05249-4","DOIUrl":"10.1007/s11010-025-05249-4","url":null,"abstract":"<p><p>Interstitial lung diseases (ILDs) are a group of pulmonary disorders characterized by fibrosis, inflammation, and lung tissue deterioration. Anti-melanoma differentiation-associated gene 5-positive dermatomyositis-associated interstitial lung disease (MDA5-ILD), a subtype, is associated with high mortality due to rapid progression and severe lung damage. Volatile organic compounds (VOCs) in exhaled breath, reflecting metabolic changes, have been identified as potential non-invasive biomarkers for various diseases, including respiratory conditions. However, their role in MDA5-ILD has not been extensively studied. This retrospective cohort study included 45 exhaled breath samples from 19 ILD patients, with 31 samples from 9 patients with MDA5-ILD and 10 samples from 7 patients with non-MDA5-ILD. VOCs were collected using thermal desorption tubes and analyzed via gas chromatography-mass spectrometry (GC-MS). Clinical data, including the APACHE II score, were integrated with VOC profiles. Two logistic regression models were developed: Model 1 based on 11 clinical indicators, and Model 2 integrating 11 clinical indicators with 5 VOC features. Model performance was evaluated using receiver operating characteristic (ROC) curve analysis, sensitivity, specificity, and accuracy metrics. Five VOCs-N-(2-Aziridinyl)ethanamine, Cyclohexanone, Nonanal, Dodecamethylcyclohexasiloxane, and 4-Methyltetradecane-were identified as significant biomarkers distinguishing MDA5-ILD from non-MDA5-ILD. Model 2, which integrated VOC data, outperformed Model 1, achieving an area under the curve (AUC) of 0.93 compared to 0.70. Model 2 also demonstrated enhanced accuracy (84.6% vs. 76.9%), specificity (66.7% vs. 33.3%), precision (90.0% vs. 81.8%), and F1-score (90.0% vs. 85.7%). Additionally, 1,3-Pentadiene and 3-Methylundecane were identified as potential markers of disease severity, with 1,3-Pentadiene negatively correlating and 3-Methylundecane positively correlating with both APACHE II scores and creatinine levels. VOCs in exhaled breath significantly enhance the diagnostic sensitivity and accuracy for detecting MDA5-ILD. In addition, VOCs show promise as disease severity markers, potentially aiding in the assessment of disease severity and progression. While the integration of VOCs holds great potential for improving diagnostic performance, further validation through larger, multicenter studies is necessary.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"4311-4323"},"PeriodicalIF":3.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143657658","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clonal hematopoiesis of indeterminate potential: contribution to disease and promising interventions.","authors":"Chongjie Li, Chunxiang Zhang, Xiuying Li","doi":"10.1007/s11010-025-05261-8","DOIUrl":"10.1007/s11010-025-05261-8","url":null,"abstract":"<p><p>In clonal hematopoiesis of indeterminate potential (CHIP), subpopulations of blood cells carrying somatic mutations expand as the individual ages, and this expansion may elevate risk of blood cancers as well as cardiovascular disease. Individuals at higher risk of CHIP and therefore of CHIP-associated disease can be identified through mutational profiling, and the apparently central role of inflammation in CHIP-associated disease has emerged as a potential therapeutic target. While CHIP is often associated with negative health outcomes, emerging evidence suggests that some CHIP-related mutations may also exert beneficial effects, indicating a more complex role in human health. This review examines current understanding of the epidemiology and clinical significance of CHIP and the role of inflammation in driving its association with disease risk. It explores the mechanisms linking CHIP to inflammation and risk of cardiovascular and other diseases, as well as the potential of personalizing therapies against those diseases for individuals with CHIP.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"4091-4106"},"PeriodicalIF":3.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143720589","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Histone H2A: a promising diagnostic marker in heart failure with reduced versus preserved ejection fraction.","authors":"Desislava K Tsoneva, Diana Buzova, Salvatore Daniele Bianco, Antoniya Kisheva, Mesut Rushid, Tanya Ivanova, Yoto Yotov, Jan Cerveny, Tommaso Mazza, Manlio Vinciguerra","doi":"10.1007/s11010-025-05254-7","DOIUrl":"10.1007/s11010-025-05254-7","url":null,"abstract":"<p><p>The diagnosis of heart failure with preserved left ventricle ejection fraction (HFpEF) remains a challenge, with score-based algorithms showing varying diagnostic performance and biomarkers sometimes inconclusive. This study aimed to examine whether circulating histones and histone complexes, which recently emerged as robust biomarkers of inflammation and stroke, show distinct profiles in plasma from healthy individuals, HF with reduced EF (HFrEF), and HFpEF patients. We evaluated the plasma histone profile of 30 sex/age-matched healthy individuals, 22 HFpEF and 25 HFrEF prior any therapeutic intervention. ImageStreamX-based detection approach was used to measure the levels of circulating particles positive for core histones H2A, H2B, H3, H4, histone variants macroH2A1.1 and macroH2A1.2. While we found increased levels of most of the histones and histone complexes in both HFpEF and HFrEF patients, H2A was significantly elevated only in HFpEF, compared to healthy individuals (p-value = 0.002) and to HFrEF (p-value = 0.00008). In line with these findings, H2A showed positive correlation with EF (r = 0.493). We identified a plasma histone profile able to detect HF and differentiate between HFpEF and HFrEF using a high throughput and imaging flow cytometry-adapted liquid biopsy.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"4343-4354"},"PeriodicalIF":3.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143692714","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Insulin resistance and cancer: molecular links and clinical perspectives.","authors":"Alfredo Caturano, Enes Erul, Roberto Nilo, Davide Nilo, Vincenzo Russo, Luca Rinaldi, Carlo Acierno, Maria Gemelli, Riccardo Ricotta, Ferdinando Carlo Sasso, Antonio Giordano, Caterina Conte, Yüksel Ürün","doi":"10.1007/s11010-025-05245-8","DOIUrl":"10.1007/s11010-025-05245-8","url":null,"abstract":"<p><p>The association between insulin resistance (IR), type 2 diabetes mellitus (T2DM), and cancer is increasingly recognized and poses an escalating global health challenge, as the incidence of these conditions continues to rise. Studies indicate that individuals with T2DM have a 10-20% increased risk of developing various solid tumors, including colorectal, breast, pancreatic, and liver cancers. The relative risk (RR) varies depending on cancer type, with pancreatic and liver cancers showing a particularly strong association (RR 2.0-2.5), while colorectal and breast cancers demonstrate a moderate increase (RR 1.2-1.5). Understanding these epidemiological trends is crucial for developing integrated management strategies. Given the global rise in T2DM and cancer cases, exploring the complex relationship between these conditions is critical. IR contributes to hyperglycemia, chronic inflammation, and altered lipid metabolism. Together, these factors create a pro-tumorigenic environment conducive to cancer development and progression. In individuals with IR, hyperinsulinemia triggers the insulin-insulin-like growth factor (IGF1R) signaling pathway, activating cancer-associated pathways such as mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3-kinase (PIK3CA), which promote cell proliferation and survival, thereby supporting tumor growth. Both IR and T2DM are linked to increased morbidity and mortality in patients with cancer. By providing an in-depth analysis of the molecular links between insulin resistance and cancer, this review offers valuable insights into the role of metabolic dysfunction in tumor progression. Addressing insulin resistance as a co-morbidity may open new avenues for risk assessment, early intervention, and the development of integrated treatment strategies to improve patient outcomes.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"3995-4014"},"PeriodicalIF":3.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143634292","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GDF15 attenuates Parkinson's disease progression via suppressing the activation of cGAS-STING pathway.","authors":"Jianli Wang, Ting Geng, Xiaomei Yao, Yiming Liu","doi":"10.1007/s11010-025-05265-4","DOIUrl":"10.1007/s11010-025-05265-4","url":null,"abstract":"<p><p>Growth differentiation Factor 15 (GDF15) plays an important role in the innate immune response. However, whether GDF15 could regulate Parkinson's disease (PD) remains unknown. In this study, we explored the function and underlying molecular mechanisms of GDF15 in PD. The protein and mRNA expressions were examined applying immunofluorescence staining, Western blot and qRT-PCR. Ferrous iron content was also assessed using an iron assay kit. The effect of GDF15 knockdown on mitochondrial membrane potential, ROS level, intracellular Fe²⁺ level and mitochondrial permeability transition pore opening in PD cell model was evaluated utilizing JC-1 staining, DCFH-DA fluorescent probe, ferro orange staining and calcein AM + Co²⁺ quencher staining. GDF15 was upregulated in the substantia nigra and striatum of PD mice and MPP⁺-caused SH-SY5Y cells. GDF15 knockdown aggravated parkinsonian symptoms in PD mice. Moreover, GDF15 knockdown aggravated dopamine neuronal damage, and promoted ferroptosis and inflammation in PD in vivo and in vitro. Besides, GDF15 knockdown could activate cGAS-STING pathway in vivo and in vitro PD model. We also found that the treatment of RU.521 could reverse the effect of GDF15 knockdown on dopamine neuronal damage, inflammation and ferroptosis in MPP⁺-induced SH-SY5Y cells. Similarly, the treatment of SR-717 could reverse the effect of GDF15 overexpression on dopamine neuronal damage, inflammation and ferroptosis in MPP⁺-induced SH-SY5Y cells. The results of this study demonstrated that GDF15 could attenuate dopamine neuronal damage, and inhibit ferroptosis and inflammation in PD via suppressing cGAS-STING pathway activation.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"4449-4466"},"PeriodicalIF":3.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143772449","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Myocardial infarction serum preconditioning bone marrow mesenchymal stem cell-derived exosomes enhance anti-fibrosis in rat myocardial infarction hearts.","authors":"Yang Gan, Changyi Wang, Ruili Liao, Pei Zhang, Yongmei Nie, Fengxu Yu, Juyi Wan, Bin Liao, Liang Mao, Hui Liu, Yong Fu","doi":"10.1007/s11010-025-05273-4","DOIUrl":"10.1007/s11010-025-05273-4","url":null,"abstract":"<p><p>Mesenchymal stem cells (MSCs) have been shown to attenuate myocardial fibrosis after myocardial infarction by secreting various bioactive molecules that positively affect the failing heart. We hypothesized that serum factors play an active role in the activation of bone marrow MSCs after myocardial infarction and explored the effect of differential exocytosis on cardiac repair after infarct serum preconditioning by examining whether exosomes derived from MSCs have a positive effect on cardiac fibrosis. Bone marrow MSCs were pretreated by collecting rat myocardial infarction serum, followed by the collection of myocardial infarction serum exosomes (MIS-EXO). In vivo, intramyocardial injection of exosomes was performed 30 min after permanent ligation of the anterior descending branches of Sprague Dawley rats, and echocardiography was performed at different time intervals to evaluate cardiac function. Hearts were sampled 4 weeks later, and the degree of myocardial fibrosis and inflammatory response were evaluated using hematoxylin and eosin and Masson's trichrome staining. Treatment with common culture-derived exosomes (CON-EXO) improved cardiac function and myocardial fibrosis after myocardial infarction in rats compared with the myocardial infarction group. In vitro, the antifibrotic effects of different exosomes on tumor growth factor-β-induced fibroblast fibrosis model were assessed by protein blotting, qPCR, and immunofluorescence. Compared with CON-EXO, MIS-EXO exerted superior therapeutic effects in terms of anti-inflammation, improvement of left ventricular function, and reduction of fibrosis. Infarct serum pretreatment with bone marrow mesenchymal stem cell-derived exosomes enhances the anti-cardiac fibrosis effect in rats after myocardial infarction.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"4417-4429"},"PeriodicalIF":3.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143764370","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Human-induced pluripotent stem cell-derived exosomes promote skin wound healing through activating FGF2-mediated p38 pathway.","authors":"Rongrong Zhang, Huilan Wu, Yongmiao Peng, Ke Sheng, Feifei Chen, Guanghui Zhu, Xiaoling Guo","doi":"10.1007/s11010-025-05244-9","DOIUrl":"10.1007/s11010-025-05244-9","url":null,"abstract":"<p><p>The acute and large area skin healing has been an intractable problem for both clinician and patient. Exosomes derived from human-induced pluripotent stem cells (hiPSC-Exos) have been a novel promising cell-free treatment on skin damage repair. In this study, in vivo skin trauma model of full-layer skin damage on mouse back and in vitro skin-like trauma model of human keratinocytes (HaCaT) scratches were established to investigate the effects of hiPSC-Exos on the acute wound healing, and its potential regulation mechanism would be tried to explore. Our in vivo results showed that hiPSC-Exos labeled with PKH26 could be well taken up by cells in the wound area, and could effectively accelerate acute skin wound healing by inhibiting the mRNA expressions of inflammation factors and chemokines such as Il-1β, Ccl2, Cxcl5, Ccl7 as well as promoting PCNA positive cell ratio. The in vitro data showed that hiPCS-Exos could markedly increase the numbers of EdU positive keratinocytes and expedite keratinocyte migration, which could be reversed by fibroblast growth factor receptor 3 (FGFR3) antagonist AZD4547 and p38 inhibitor SB203580. In addition, fibroblast growth factor 2 (FGF-2) was existent in hiPSC-Exos, and hiPSC-Exos could upregulate the p-p38/p38 level, which could be significantly reversed by AZD4547, but not affect the p-ERK/ERK and p-JNK/JNK levels in wound model tissues and cells. In conclusion, hiPSC-Exos may have the potential to promote wound healing by inhibiting cell inflammation as well as promoting cell proliferation and migration based on inherent FGF-2 targeting to FGFR3 to activate p38 pathway, which may serve as a promising candidate for skin healing.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"4227-4242"},"PeriodicalIF":3.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143597399","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An open letter to the NIH cardiovascular study section reviewers.","authors":"Ali J Marian","doi":"10.1007/s11010-025-05230-1","DOIUrl":"10.1007/s11010-025-05230-1","url":null,"abstract":"<p><p>The reviewers who serve at the National Institute of Health (NIH) study sections are in the unique position of identifying the most scientifically meritorious grant applications for consideration for funding. Consequently, the reviewers guide the direction of scientific discoveries in the US, which ultimately translate to patient care. Recently many investigators have expressed concerns about the quality of the reviews that they received from the National Heart, Lung, and Blood Institute (NHLBI) study section reviewers. I discuss some of these concerns, identify some of the deficiencies, and make suggestions to the reviewers on how to improve their review of the grant applications.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"3929-3933"},"PeriodicalIF":3.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143531638","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}