Human Gene最新文献

{"title":"Annexin A1 as a potential anti-inflammatory marker in diabetic foot ulcer: A cross-sectional study","authors":"Shwetha Shetty Kalladka ,&nbsp;Raushan Kumar Chaudhary ,&nbsp;Prakash Patil ,&nbsp;Praveenkumar Shetty ,&nbsp;Suchetha Kumari Nalilu ,&nbsp;Abhijith Shetty","doi":"10.1016/j.humgen.2025.201505","DOIUrl":"10.1016/j.humgen.2025.201505","url":null,"abstract":"<div><h3>Background</h3><div>Annexin A1 (AnxA1) is known to suppress inflammation by inhibiting the synthesis of pro-inflammatory molecules and promoting the release of immune-suppressive molecules. This suggests AnxA1 may be a vital marker for modulating inflammation and cell proliferation in Diabetic Foot Ulcer (DFU) patients. The current study aimed to investigate the expression and role of AnxA1 in relation to other key inflammatory molecules in DFU.</div></div><div><h3>Methods</h3><div>A cross-sectional study was conducted among 40 participants (20 DFU patients and 20 healthy subjects) to evaluate the expression of AnxA1, IL-10, IL-1β, IL-6, and TNF-α from both the blood and tissue samples.</div></div><div><h3>Results</h3><div>The mean relative expression of anti-inflammatory molecules such as AnxA1 (0.507, 0.442) and IL-10 (2.273, 0.602) were found to be downregulated in tissue and blood, respectively among DFU patients compared to healthy controls. Conversely, the pro-inflammatory molecules like IL-1β (2.393, 0.988), IL-6 (0.830, 0.748), and TNF-α (1.81, 1.099) were upregulated among DFU patients compared to healthy controls. The mean relative expression of AnxA1 and IL-1β was significantly higher in tissue and blood samples respectively of gangrenous DFU compared to non-gangrenous DFU (<em>P</em> &lt; 0.05). Furthermore, AnxA1 expression showed a significant negative correlation with HbA1c and triglyceride levels (in blood and tissue) as well as wound grade and cholesterol levels (in tissue).</div></div><div><h3>Conclusion</h3><div>The relative down-expression of AnxA1 in DFU patients and its negative correlation with HbA1c, total cholesterol, and triglycerides indicate that AnxA1 has the potential to decrease inflammatory harm in DFU. These findings highlight AnxA1 as a promising target for novel therapeutic strategies against diabetic foot ulceration.</div></div>","PeriodicalId":29686,"journal":{"name":"Human Gene","volume":"46 ","pages":"Article 201505"},"PeriodicalIF":0.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145465898","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":"Evaluation of the frequency of Dectin-1 rs3901533 A > C and rs7309123 G > C gene variants in patients with acute myeloid leukemia (AML): A case-control study","authors":"Davood Alinezhad Dezfuli ,&nbsp;Ehsan Sarbazjoda ,&nbsp;Nasrin Amirrajab ,&nbsp;Tina Vosoughi ,&nbsp;Alireza Momeni ,&nbsp;Mohammad Ali Jalali Far","doi":"10.1016/j.humgen.2025.201482","DOIUrl":"10.1016/j.humgen.2025.201482","url":null,"abstract":"<div><h3>Background</h3><div>Acute myeloid leukemia (AML) is a serious blood cancer mainly affecting adults, and its predisposing genetic factors remain unclear. While recent studies have linked dectin-1 polymorphisms to fungal infection risk in AML, their relationship with AML susceptibility has not been studied. This study evaluates the association between two dectin-1 single-nucleotide polymorphisms (SNPs) of rs3901533 A &gt; C and rs7309123 G &gt; C and AML risk.</div></div><div><h3>Methods &amp; materials</h3><div>A total of 103 participants (53 AML patients and 50 age- and sex-matched healthy controls) from the Iranian population were included in this study. Both of the polymorphisms were genotyped using the tetra-ARMS-PCR method.</div></div><div><h3>Results</h3><div>The genotype distributions of rs3901533 A &gt; C and rs7309123 G &gt; C polymorphisms did not differ significantly between AML patients and controls under additive, dominant, or recessive genetic models (<em>p-value</em> &gt; 0.05). Furthermore, allele frequencies for both SNPs showed no significant association with AML risk (<em>p-value</em> &gt; 0.05). None of the genotypes or alleles increased the risk of AML (<em>p-value</em> &gt; 0.05).</div></div><div><h3>Conclusions</h3><div>Neither the rs3901533 A &gt; C nor the rs7309123 G &gt; C polymorphisms are contributors to increased susceptibility to AML. However, further investigations are needed.</div></div>","PeriodicalId":29686,"journal":{"name":"Human Gene","volume":"46 ","pages":"Article 201482"},"PeriodicalIF":0.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145265696","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":"Corrigendum to ‘Dysregulated of the FAM138E and CLRN1-AS1 lncRNAs could be diagnosis biomarkers in colorectal cancer’ <Human Gene 39 (2024) 201249>","authors":"Zahra Karimi ,&nbsp;Nastaran Asghari Moghaddam ,&nbsp;Maryam Yousefi ,&nbsp;Mohammad Abdolvand ,&nbsp;Atefeh Zamani ,&nbsp;Nasrin Fatahi Dolatabadi ,&nbsp;Maryam Peymani","doi":"10.1016/j.humgen.2025.201496","DOIUrl":"10.1016/j.humgen.2025.201496","url":null,"abstract":"","PeriodicalId":29686,"journal":{"name":"Human Gene","volume":"46 ","pages":"Article 201496"},"PeriodicalIF":0.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145568668","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":"Transcriptomic meta-analysis of sarcoidosis peripheral blood using STARGEO identifies immune signatures and potential biomarkers","authors":"Maya Hammonds ,&nbsp;Sarah Voskamp ,&nbsp;Martha Londoni ,&nbsp;Peter Wearden ,&nbsp;Jennifer Nelson","doi":"10.1016/j.humgen.2025.201460","DOIUrl":"10.1016/j.humgen.2025.201460","url":null,"abstract":"<div><div>Over 90 % of sarcoidosis patients have pulmonary and mediastinal involvement, and late-stage disease may necessitate heart or lung transplantation. This study investigated the molecular mechanisms underlying sarcoidosis, a complex inflammatory disease, by analyzing differential gene expression patterns in peripheral blood samples. The Search Tag Analyze Resource for NCBI's Gene Expression Omnibus (STARGEO) platform was utilized to identify 218 sarcoidosis and 271 non-sarcoidosis peripheral blood samples. iPathwayGuide identified 639 genes with significant differential expression between sarcoidosis and control samples. The most upregulated genes were FCGR1CP, FCGR1B, PANDAR, DEFA1B, ANKRD22, and CARD17. Upstream regulators showing significant activation included IRF9, STAT2, IFNβ1, IFNG, and IRF7, which are largely involved in inflammatory responses. The top differentially expressed pathways were NOD-like receptor signaling, HSV-1 infection, Influenza A, COVID-19, and the intestinal immune network for IgA production. Differentially expressed genes and pathways play a large role in the immune system's response and regulation. These findings support the known involvement of specific immune responses in the pathogenesis of sarcoidosis. Notably, pathways upregulated in the immune response against several common viruses are also activated in sarcoidosis. The identified differentially expressed genes may serve as potential therapeutic targets, warranting further investigation.</div></div>","PeriodicalId":29686,"journal":{"name":"Human Gene","volume":"46 ","pages":"Article 201460"},"PeriodicalIF":0.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144887347","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":"The role of a novel m6A reader CSTF2 amplification and overexpression in head and neck cancer development","authors":"Paramasivam Arumugam ,&nbsp;Chandra Pandi ,&nbsp;Vijayashree Priyadharsini Jayaseelan","doi":"10.1016/j.humgen.2025.201473","DOIUrl":"10.1016/j.humgen.2025.201473","url":null,"abstract":"<div><h3>Objective</h3><div>This study examines the oncogenic role of cleavage stimulation factor subunit 2 (CSTF2), a newly identified N6-methyladenosine (m6A)-binding protein in the pathogenesis of head and neck squamous cell carcinoma (HNSCC). We also explored its amplification-driven overexpression, its prognostic significance, and its mechanistic contributions to tumor aggressiveness.</div></div><div><h3>Method</h3><div>A dataset of patients with HNSCC was used from the Cancer Genome Atlas (TCGA), which included information on clinical characteristics. Moreover, mRNA and protein expression data of CSTF2 were obtained from the Human Protein Atlas (HPA) database. Additionally, <em>CSTF2</em> mRNA levels were validated in an independent cohort of HNSCC patient tissues and cell lines using real-time PCR. The prognostic significance of <em>CSTF2</em> was evaluated using Kaplan-Meier survival plots. Additionally, protein-protein interaction networks of CSTF2 were established using the GeneMANIA database, and functional enrichment analysis was performed with Metascape.</div></div><div><h3>Result</h3><div>The study demonstrated that the <em>CSTF2</em> gene was significantly amplified, which correlated with elevated mRNA expression. Moreover, independent cohort analysis confirmed that <em>CSTF2</em> was overexpressed in HNSCC tissues and cell lines compared to non-tumorous tissues and normal cells. In addition, protein levels were markedly higher in HNSCC tissues, and elevated <em>CSTF2</em> mRNA expression was associated with poorer overall survival. Functional enrichment analysis showed that CSTF2 is involved in regulating oncogenic processes and the progression of HNSCC.</div></div><div><h3>Conclusion</h3><div>These data indicate that the <em>CSTF2</em> gene is amplified and overexpressed in HNSCC, indicating that this gene could be a significant prognostic marker and a potential therapeutic target for HNSCC.</div></div>","PeriodicalId":29686,"journal":{"name":"Human Gene","volume":"46 ","pages":"Article 201473"},"PeriodicalIF":0.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145044157","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":"miR-507 and miR-665 as central MicroRNA regulators in the ceRNA network of adrenocortical carcinoma: A systems biology approach","authors":"Javad Omidi","doi":"10.1016/j.humgen.2025.201498","DOIUrl":"10.1016/j.humgen.2025.201498","url":null,"abstract":"<div><div>MicroRNAs (miRNAs) are key regulators of post-transcriptional gene expression and have been increasingly implicated in the pathogenesis of rare malignancies such as adrenocortical carcinoma (ACC). Here, a systems biology approach was employed to construct and analyze context-specific competing endogenous RNA (ceRNA) networks using transcriptomic profiles from ACC tumors (TCGA) and normal adrenal tissues obtained from both GTEx 2025 and miRNATissueAtlas 2025 datasets, leveraging a novel integrative analytical framework specifically developed in this study. Comparative network topology revealed extensive regulatory rewiring in tumors, with miR-507 and miR-665 emerging as tumor-specific central miRNAs. While miR-507 was significantly upregulated and associated with favorable patient survival, miR-665 was downregulated and displayed radiation-sensitive expression dynamics. Target gene prediction and correlation analyses identified distinct sets of oncogenic and tumor-suppressive genes regulated by each miRNA. Functional enrichment and PPI network analysis indicated that miR-507 targets are strongly enriched in cell cycle, mitotic checkpoint, and chromosomal stability pathways, whereas miR-665 influences more context-dependent immune and signaling mechanisms. These findings support the prognostic and therapeutic potential of miR-507 in ACC and suggest a radiotherapy-modulated regulatory role for miR-665. This study demonstrates the power of multi-source transcriptomic integration for discovering functional miRNA hubs in rare endocrine cancers.</div></div>","PeriodicalId":29686,"journal":{"name":"Human Gene","volume":"46 ","pages":"Article 201498"},"PeriodicalIF":0.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145362204","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":"Curcumin-synthesized silver nanoparticles modulate inflammatory and thyroid-related gene expression in pubertal rats exposed to chlorpyrifos","authors":"Mohammad Hossein Gorji Dizabadi ,&nbsp;Maryam Rezaei ,&nbsp;Tahereh Farkhondeh ,&nbsp;Saeed Samargahndian ,&nbsp;Zahra Khademi ,&nbsp;Atena Mansouri","doi":"10.1016/j.humgen.2025.201503","DOIUrl":"10.1016/j.humgen.2025.201503","url":null,"abstract":"<div><h3>Introduction</h3><div>Green synthesis is a preferred method for producing silver nanoparticles (Ag-NPs). In addition to its advantages for industrial and biomedical applications, it also represents a promising research field. This study aimed to evaluate the effects of chlorpyrifos (CPF) on thyroid hormone levels and the expression of inflammatory factors while highlighting the therapeutic potential of curcumin-synthesized silver nanoparticles (CUR-Ag-NPs) in mitigating CPF-induced thyroid damage.</div></div><div><h3>Materials and methods</h3><div>Six groups of rats were studied: control, CPF (5 mg/kg), CUR-AgNPs 40 μg/kg, CUR-AgNPs 80 μg/kg, CPF+ CUR-AgNPs 40, μg/kg, and CPF+ CUR-AgNPs 80 μg/kg. Treatments were administered daily for 30 days. At the end of the study, the rats were anesthetized with ketamine (50 mg/kg), and xylazine, (10 mg/kg). Blood was collected for serum analysis of thyroid hormone levels and thyroid gland tissue was preserved in RNAlater to the evaluation of inflammation markers.</div></div><div><h3>Results</h3><div>CPF exposure increased the expression of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and nitric oxide synthase 2 (NOS2). Co-administration of CUR-AgNPs significantly reduced the expression of these genes. CPF also disrupted thyroid hormone secretion, while CUR-AgNPs treatment in CPF-exposed rats nearly restored thyroid function.</div></div><div><h3>Conclusion</h3><div>These findings suggest that CUR-AgNPs can attenuate CPF-induced thyroid toxicity, offering potential therapeutic value.</div></div>","PeriodicalId":29686,"journal":{"name":"Human Gene","volume":"46 ","pages":"Article 201503"},"PeriodicalIF":0.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145415608","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":"Integrated in silico and experimental analysis identifies MAGE-A3, TRIM28, and HLA-A as immunomodulatory targets in lung cancer","authors":"Gaurang Telang ,&nbsp;Smriti Mishra ,&nbsp;Anurag Sureshbabu ,&nbsp;Sagar Barage ,&nbsp;A.W. Santhosh Kumar ,&nbsp;Rajshri Singh","doi":"10.1016/j.humgen.2025.201492","DOIUrl":"10.1016/j.humgen.2025.201492","url":null,"abstract":"<div><div>MAGEA3, a cancer-testis antigen selectively expressed in tumors, has been widely explored as a target for cancer immunotherapy, yet its broader immunoregulatory function in the lung tumor microenvironment remains insufficiently characterized. In this study, we conducted an integrative in silico analysis using transcriptomic data from TCGA-LUSC to delineate the expression landscape, immune contexture, and molecular interactions of MAGEA3. Protein–protein interaction networks constructed via STRING and ranked through CytoHubba identified TRIM28 and HLA-A as key co-regulatory molecules, implicating MAGEA3 in transcriptional repression and antigen presentation. TIMER2.0 deconvolution revealed cell-type–specific associations, including differential relationships with CD8⁺ T cells, dendritic cells, and macrophages. Gene-wise survival modeling in TCGA-LUSC indicated MAGEA3 and MAGEA6 associate with reduced overall survival, whereas TRIM28 showed a borderline protective trend. Experimental validation via RT-qPCR in A549 cells confirmed detectable expression of MAGEA3, TRIM28, and HLA-A, reinforcing the computational predictions and highlighting potential cross-histological relevance. Collectively, these findings position MAGEA3 within immunomodulatory circuits of lung cancer and support its consideration in multimodal immunotherapeutic paradigms.</div></div>","PeriodicalId":29686,"journal":{"name":"Human Gene","volume":"46 ","pages":"Article 201492"},"PeriodicalIF":0.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145219618","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":"Systematic identification of molecular biomarkers and drug candidates targeting MAPK3 in multiple sclerosis","authors":"Bilal Khan,&nbsp;Ruqia Sartaj,&nbsp;Muhammad Rahiyab,&nbsp;Syed Shujait Ali,&nbsp;Zahid Hussain,&nbsp;Ishaq Khan,&nbsp;Arshad Iqbal","doi":"10.1016/j.humgen.2025.201436","DOIUrl":"10.1016/j.humgen.2025.201436","url":null,"abstract":"<div><div>Multiple sclerosis (MS) exists as a persistent autoimmune illness affecting the central nervous system because it produces demyelination and injures axons, besides causing CNS neuroinflammation. Research advances into MS pathophysiology have not solved the complexity of treating this condition. The research examined both vital MS-related molecular biomarkers as well as therapeutic possibilities through computational methods. GEO2R analyzed the gene expression dataset <span><span>GSE17393</span><svg><path></path></svg></span>, which reported that MS patients had differentially expressed genes than healthy controls. The biological processes involved in MS became clearer with the help of functional enrichment analyses, which contained both GO and KEGG pathway analysis. The STRING database enabled the construction of a PPI network, followed by hub gene identification through the CytoHubba application. The study revealed MAPK3 as the most influential hub gene essential for MS pathophysiological processes. Scientists used the Robetta server to forecast MAPK3's 3D structure, which they then optimized in Galaxy Refine before carrying out structural quality tests. Lab simulation using PyRx showed that potential medications such as Hypericin, Yibeissine, and Physalin F effectively bind with the MAPK3 protein. Among the compounds, Hypericin achieved the best binding affinity of −10.7 kcal/mol toward MAPK3, as Yibeissine and Physalin F reached −10.0 kcal/mol binding levels. MD simulations tested the stability of all MAPK3-ligand complex structures. The combination of ADME testing demonstrated that Yibeissine possessed ideal drug absorption features with strong blood-brain barrier penetration alongside good gastrointestinal absorption, yet Hypericin showed poor oral availability. The ProTox-II analysis revealed that the substance Hypericin presented major risks for mutation and cancer development, although Physalin F significantly damaged the human immune system. Current research indicates MAPK3 inhibition represents a promising treatment approach for MS, since Yibeissine stands out as the best drug candidate because it possesses an ideal ADME profile and low toxicity risks.</div></div>","PeriodicalId":29686,"journal":{"name":"Human Gene","volume":"45 ","pages":"Article 201436"},"PeriodicalIF":0.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144299018","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 case of Cockayne syndrome with two novel mutations in the ERCC6 gene: Expanding the phenotypic and genetic spectrum","authors":"Xinyao Wang,&nbsp;Lingzhao Min,&nbsp;Jia Wei,&nbsp;Xiaoqiang Wang","doi":"10.1016/j.humgen.2025.201420","DOIUrl":"10.1016/j.humgen.2025.201420","url":null,"abstract":"<div><div>A one-year-old East Asian boy presented with significant growth and developmental delays, including microcephaly, poor motor development, and feeding difficulties. He also exhibited poor visual and auditory tracking, along with occasional vomiting and skin vulnerability to sun exposure. Cranial CT revealed cortical dysplasia and a septum pellucidum cyst. Whole exome sequencing identified three heterozygous mutations in the ERCC6(Excision repair cross-complementation group 6) gene: two novel mutations (c.1557G &gt; A and c.1821 + 1del) inherited from the father and mother, respectively, and a third mutation (c.1820 A &gt; T) with uncertain pathogenicity, also inherited from the mother. The genetic findings led to a diagnosis of Cockayne syndrome, contributing to the expanding knowledge of the ERCC6 gene mutation spectrum and aiding in the clinical diagnosis and genetic counseling for the family. This case underscores the importance of accurate genetic diagnosis in managing prognosis and providing counseling for high-risk families.</div></div>","PeriodicalId":29686,"journal":{"name":"Human Gene","volume":"45 ","pages":"Article 201420"},"PeriodicalIF":0.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144203170","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}