Biochemistry and Biophysics Reports最新文献

{"title":"The high-risk model associated with SYTL4 predicts poor prognosis and correlates with immune infiltration in AML","authors":"Ke Shi ,&nbsp;Dan Li ,&nbsp;Bo-Hui Peng ,&nbsp;Qiang Guo","doi":"10.1016/j.bbrep.2024.101859","DOIUrl":"10.1016/j.bbrep.2024.101859","url":null,"abstract":"<div><div>Acute myeloid leukemia (AML) currently lacks a definitive cure. Studies have highlighted the involvement of SYTL4 expression levels in neoplasms, yet its specific roles in AML remain unexplored in the literature. Utilizing the TCGA and XENA databases, this study investigated SYTL4 expression levels in AML and identified associations between SYTL4 overexpression and clinicopathological features, prognosis, and immune infiltration in AML patients through genomic analysis. ROC analysis demonstrated the diagnostic value of SYTL4 overexpression in AML. Kaplan-Meier survival, Cox regression, and Lasso analyses were employed to explore SYTL4-coexpressed long non-coding RNAs linked to AML patient prognosis, alongside the construction of nomograms and risk models. SYTL4 expression was significantly elevated in AML and correlated with FAB classification, cytogenetic risk, IDH1 R140 mutation, and NPM1 mutation in cancer patients. SYTL4 overexpression signaled a poor prognosis, serving as a risk indicator for assessing adverse outcomes in AML patients. SYTL4 expression levels also correlated with AML immune cell levels and markers. COX regression analysis revealed that LINC01700, CPNE8-AS1, HOXA10-AS, LINC00899, and SYTL4 influenced adverse AML prognosis. Patients in the high-risk group for these factors experienced significantly poor outcomes, which were closely associated with aDC, CD8 T cells, and TH17 cells. In summary, SYTL4 overexpression is linked to poor prognosis and immune infiltration in AML, with the constructed risk model intended as a prognostic evaluation tool for AML patients.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"41 ","pages":"Article 101859"},"PeriodicalIF":2.3,"publicationDate":"2024-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142743792","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"KLF14 inhibits tumor progression via FOSL1 in glioma","authors":"Xiaohua Wang ,&nbsp;Xinjuan Qu ,&nbsp;Xuelai Liu ,&nbsp;Kaiyue Wang ,&nbsp;Yongfang Yang ,&nbsp;Yujuan Zhang ,&nbsp;Zhenguo Wang ,&nbsp;Guangjian Fan ,&nbsp;Yuming Li ,&nbsp;Yuanyuan Zeng ,&nbsp;Hongwei Chen ,&nbsp;Ting Zhu","doi":"10.1016/j.bbrep.2024.101885","DOIUrl":"10.1016/j.bbrep.2024.101885","url":null,"abstract":"<div><h3>Background</h3><div>Glioma, the most frequent central nervous system malignancy, is often promoted by the overexpression of Fos-like antigen 1 (FOSL1). However, the regulation of FOSL1 remains unexplored. The present study aimed to investigate the regulatory mechanism of FOSL1 to identify potential therapeutic targets for glioblastoma.</div></div><div><h3>Methods</h3><div>This study's initial investigation utilized dual-luciferase reporter gene assays and quantitative polymerase chain reaction (qPCR) assays to establish that Kruppel-like factor 14 (KLF14) inhibits the transcription of FOSL1. Subsequent immunohistochemistry and western blotting (WB) assays on glioma tissues confirmed a negative association between FOSL1 and KLF14. This study generated KLF14 knockdown cells and double knockdown cells of KLF14 and FOSL1 and further assessed cell growth through various experimental methods. The impact of KLF14 on tumor cell migration via FOSL1 was determined using qPCR and WB assays. A xenograft tumor model was utilized to verify tumor growth suppression by KLF14.</div></div><div><h3>Results</h3><div>The present study demonstrated that KLF14 restrains FOSL1 transcription and is inversely correlated with FOSL1 in glioma tissues. KLF14 overexpression was found to counteract FOSL1's effect on cell migration and epithelial-to-mesenchymal transition in glioma cells, which coincided with decreased Snail2 and cluster of differentiation 44 (CD44) expressions. Further, KLF14 overexpression was shown to hinder tumor progression in vivo.</div></div><div><h3>Conclusion</h3><div>This study highlights that FOSL1 is negatively regulated by KLF14 in glioblastoma and suggests that KLF14 overexpression can mitigate tumor growth by inhibiting FOSL1, thus identifying KLF14 as a novel molecular target for treating glioblastoma. Further research into the interplay and regulatory dynamics between KLF14 and FOSL1 under varying stress conditions can enhance the precision of glioblastoma treatment.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"41 ","pages":"Article 101885"},"PeriodicalIF":2.3,"publicationDate":"2024-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142719775","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of calcium ions on the aggregation of highly phosphorylated tau","authors":"Toru Tanaka ,&nbsp;Sachiyo Ohashi ,&nbsp;Akihiko Takashima ,&nbsp;Shunsuke Kobayashi","doi":"10.1016/j.bbrep.2024.101887","DOIUrl":"10.1016/j.bbrep.2024.101887","url":null,"abstract":"<div><div>Tau is typically an axonal protein, but in neurons of brains affected by Alzheimer's disease (AD), aggregation of hyperphosphorylated tau in the somatodendritic compartment causes neuronal death. We have previously demonstrated that tau mRNA is transported within dendrites and undergoes immediate translation and hyperphosphorylation of AD epitopes in response to NMDA receptor stimulation. Although this explains the emergence of hyperphosphorylated tau in dendrites, the relationship between tau hyperphosphorylation and aggregation is not well understood. In this study, we found that recombinant highly phosphorylated tau purified from NG108-15 rodent neuroblastoma/glioma cells transfected with both tau and GSK3β expression vectors bound calcium ions and formed sarkosyl-insoluble aggregates. In addition, thioflavin T analysis revealed that this highly phosphorylated tau tended to aggregate on its own, further facilitated by calcium ions. When NG108-15 cells expressing the highly phosphorylated tau were treated with calcium ionophore, sarkosyl-insoluble tau was generated. Interestingly, these cells exhibited resistance to both calcium ionophore-induced cytotoxicity and glutamate-induced excitotoxicity. We further found that sarkosyl-insoluble phosphorylated tau was increased in cultured hippocampal neurons due to glutamate-induced hyperactivity. Our data suggest that hyperphosphorylated tau synthesized in response to NMDA receptor stimulation contributes to regulation of neuronal activity by binding calcium ions, but that this calcium binding may cause tau to adopt an aggregated form.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"40 ","pages":"Article 101887"},"PeriodicalIF":2.3,"publicationDate":"2024-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142699884","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cyclosporine and fedratinib combination therapy via modulating Th17/Treg balance in Rat model of membranous glomerulonephritis","authors":"Ali Ghassabi ,&nbsp;Maryam Hosseini ,&nbsp;Hemayat Abdoli Goungormaz ,&nbsp;Mohammad Sadegh Soltani-Zangbar ,&nbsp;Mahsa Beomidehagh ,&nbsp;Davoud Rostamzadeh ,&nbsp;Mohammadbagher Pirouzpanah ,&nbsp;Arshad Ghaffari-Nasab ,&nbsp;Arash Khaki ,&nbsp;Leili Aghebati-Maleki ,&nbsp;Elham Badihi ,&nbsp;Farshid Afandideh ,&nbsp;Reihane Shahabirad ,&nbsp;Ali Akbar Shekarchi ,&nbsp;Javad Ahmadian Heris ,&nbsp;Leila Roshangar ,&nbsp;Jalal Etemadi ,&nbsp;Mehdi Yousefi","doi":"10.1016/j.bbrep.2024.101874","DOIUrl":"10.1016/j.bbrep.2024.101874","url":null,"abstract":"<div><div>A progressive kidney disease associated with inflammation and the immune system is called membrane glomerulonephritis (MGN). The present study investigatedthe combination of cyclosporine and fedratinib on Th17/regulatory T cells (Tregs) in rat models of MGN. Rats were given several doses of anti-Fx1A to induce MGN, and the resultant five groups of rats were fedratinib-cyclosporin receiving PHN rats, fedratinib, cyclosporin, and healthy rats. Following that, the blood's biochemistry was ascertained, and splenocytes were separated to use flow cytometry to look into the proportion of Th17 and Treg cells in the blood. A real-time PCR test was used to assess the corresponding Tregs and Th17 cell transcription factors andtheir related cytokine gene expressions. Finally, serum analysis was employed to indicate serum cytokines signatures of Th17 cells and Tregs through ELISA. The combination of cyclosporine-fedratinib induced noticeably diminished levels of serum total protein, albumin, and urea in rats versus the PHN group. Th17 cell frequency and its related transcription factors and cytokines genes showed increased expression in the PHN model compared to the control group and PHN groups with different treatments.</div><div>In contrast, Tregs frequency and its related transcription factors and cytokines genes showed decreased expression in the PHN model compared to the control group and PHN groups with different treatments. Serum cytokine assay confirmed gene expression results. The combination of cyclosporine and fedratinib was capable of reducing Th17 cells in favor of Tregs enhancement in PHN rats, suggesting a novel combination therapy in the treatment of MGN.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"40 ","pages":"Article 101874"},"PeriodicalIF":2.3,"publicationDate":"2024-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142699921","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of gastric cancer biomarkers through in-silico analysis of microarray based datasets","authors":"Arbaz Akhtar ,&nbsp;Yasir Hameed ,&nbsp;Samina Ejaz ,&nbsp;Iqra Abdullah","doi":"10.1016/j.bbrep.2024.101880","DOIUrl":"10.1016/j.bbrep.2024.101880","url":null,"abstract":"<div><div>Gastric cancer is among the most prevalent cancers worldwide including in Pakistan. Late diagnosis of gastric cancer leads to reduced survival. The present study aimed to investigate biomarkers for early diagnosis and prognosis of gastric cancer. For this purpose, the ten microarray-based gene expression datasets (GSE54129, GSE79973, GSE161533, GSE103236, GSE33651, GSE19826, GSE118916, GSE112369, GSE13911, and GSE81948) were retrieved from GEO database and analyzed by GEO2R to identify differentially expressed genes. Datasets were arranged in subsets of different dataset combinations to identify common DEGs. The gene ontology and functional pathway enrichment analysis of common DEGs was performed by DAVID tool. Pan-cancer analysis was conducted by UALCAN database. Survival analysis of common DEGs was done by Kaplan-Meier plotter. A total of 71 common DEGs were identified in different combinations of datasets. Among them, only 5 DEGs namely ATP4B, ATP4A, CCKBR, KCNJ15, and KCNJ16 were detected to be common in all the datasets. The GO and pathway analysis represented that the identified DEGs are involved in gastric acid secretion and collecting duct acid secretion pathways. Further expression validation of these five genes using three additional datasets (GSE31811, GSE26899, and GSE26272) confirmed their differential expression in gastric cancer samples. The pan-cancer analysis also revealed aberrant expression of DEGs in various cancers. The survival analysis showed the association of these 5 DEGs with poor survival of gastric cancer patients. To conclude, this study revealed a panel of 5 genes, which can be employed as diagnostic and prognostic biomarkers of gastric cancer patients.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"40 ","pages":"Article 101880"},"PeriodicalIF":2.3,"publicationDate":"2024-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142699922","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Delphinidin induces a fast-to-slow muscle fiber type shift through the AMPK signaling pathway in C2C12 myotubes","authors":"Motoki Murata ,&nbsp;Rina Takahashi ,&nbsp;Yuki Marugame ,&nbsp;Yoshinori Fujimura ,&nbsp;Hirofumi Tachibana","doi":"10.1016/j.bbrep.2024.101884","DOIUrl":"10.1016/j.bbrep.2024.101884","url":null,"abstract":"<div><div>Delphinidin, a plant anthocyanidin, suppresses disuse muscle atrophy in mice. However, its effect on muscle fiber type shift is unclear. To examine whether delphinidin affects skeletal muscle fiber type, differentiated C2C12 cells were treated with delphinidin. Results revealed that delphinidin upregulated the mRNA expression of myosin heavy chain type I (MyHCI), troponin C1, troponin I1, and MyHCIIx and increased slow MyHC protein level in C2C12 myotubes. Delphinidin also enhanced succinic dehydrogenase (SDH) activities and suppressed lactate dehydrogenase (LDH) activity. Adenosine monophosphate–activated protein kinase (AMPK) inhibition attenuated delphinidin-induced MyHCI upregulation and MyHCIIb downregulation. We investigated the effect of delphinidin on the upstream factors involved in AMPK activation. Delphinidin increased liver kinase B1 (LKB1) phosphorylation and nuclear respiratory factor 1 (NRF1) and calcium/calmodulin-dependent protein kinase 2 (CaMKK2) protein levels. In conclusion, delphinidin induced muscle fiber type conversion from fast-twitch to slow-twitch muscles through the AMPK signaling pathway.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"40 ","pages":"Article 101884"},"PeriodicalIF":2.3,"publicationDate":"2024-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142699883","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comparative effects of metformin and varying intensities of exercise on miR-133a expression in diabetic rats: Insights from machine learning analysis","authors":"Elahe Alivaisi ,&nbsp;Sabrieh Amini ,&nbsp;Karimeh Haghani ,&nbsp;Hori Ghaneialvar ,&nbsp;Fatemeh Keshavarzi","doi":"10.1016/j.bbrep.2024.101882","DOIUrl":"10.1016/j.bbrep.2024.101882","url":null,"abstract":"<div><div>This study investigated the effects of metformin, high-intensity interval training (HIIT), and moderate-intensity continuous training (MCT) on miR-133a expression in a diabetic rat model. miR-133a, a microRNA associated with skeletal muscle insulin resistance, served as a key indicator of treatment efficacy. Diabetic rats exhibited elevated miR-133a levels compared to healthy controls. Both HIIT and MCT, alone and in combination with metformin, significantly reduced miR-133a expression. Importantly, the combination of HIIT and metformin demonstrated the most potent effect, reducing miR-133a levels more than other treatments. We used the CatBoost algorithm to develop a predictive model for miR-133a expression based on metabolic parameters. The model accurately predicted miR-133a levels using body weight, blood glucose, insulin levels, and cholesterol metrics. The findings suggest a potential clinical strategy combining metformin and exercise, with miR-133a potentially serving as a biomarker for personalized diabetes management.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"40 ","pages":"Article 101882"},"PeriodicalIF":2.3,"publicationDate":"2024-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142699962","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vav family exchange factors: Potential regulator in atherosclerosis","authors":"Yu Zhang ,&nbsp;Yongwei Ren ,&nbsp;Tao Zhou ,&nbsp;Zhengtao Qian ,&nbsp;Zhengyang Bao","doi":"10.1016/j.bbrep.2024.101878","DOIUrl":"10.1016/j.bbrep.2024.101878","url":null,"abstract":"<div><div>The Vav family of guanosine nucleotide exchange factors (GEFs) regulates the phosphorylation of tyrosinase, influencing various physiological and pathological processes by modulating the binding of Rho GTPases to GDP/GTP. Recent research has highlighted the critical role of Vav family activation in tumorigenesis, neurological disorders, immune-related dysfunctions, and other diseases. This review offers a comprehensive overview of the structure and function of Vav proteins and their significant impact on the pathophysiology of atherosclerosis. In addition, we pay attention to the development of diagnostic and therapeutic targets centered around Vav proteins.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"40 ","pages":"Article 101878"},"PeriodicalIF":2.3,"publicationDate":"2024-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142699923","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Decoding differentially expressed genes to identify potential immunity associated biomarkers in Tuberculosis: An integrative bioinformatics approach","authors":"Ankur Datta,&nbsp;Divyanshi Gupta,&nbsp;Diya Waryani,&nbsp;George Priya Doss C","doi":"10.1016/j.bbrep.2024.101870","DOIUrl":"10.1016/j.bbrep.2024.101870","url":null,"abstract":"<div><div>Tuberculosis (TB) poses a significant threat to the Indian population, with India accounting for 20 % of the global TB cases. The current study aims to identify molecular biomarkers for better diagnostics by comparing the transcriptome signatures of healthy individuals against TB-affected individuals. Next-generation sequencing (NGS) tools were used to identify critical differentially expressed genes (DEGs). 302 DEGs were identified based on a logFC threshold of |3| and adjusted p-value &lt; 0.05. STRING database was used to plot the interactions amongst the 302 DEGs. The DEGs were functionally annotated, highlighting numerous physiological functions affected due to the dysregulation of the identified hub genes. <em>TLR4</em>, <em>FCGR1A</em>, <em>ITGAM</em>, <em>LTF,</em> and <em>CXCR2</em> were the hub genes identified and observed to dysregulate crucial physiological functions. <em>TLR4</em> has been implicated in the progression of TB in various populations, and the findings of this study will enable researchers to improve the current landscape of diagnostics for TB.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"40 ","pages":"Article 101870"},"PeriodicalIF":2.3,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142699961","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of a novel mutation in PATL2 gene associated with the germinal vesicle arrest of oocytes","authors":"Aili Yu ,&nbsp;Zhiqing Huang ,&nbsp;Hang Shi ,&nbsp;Yanying Lin ,&nbsp;Xuefen Cai ,&nbsp;Zhanghong Ke ,&nbsp;Beihong Zheng ,&nbsp;Yan Sun","doi":"10.1016/j.bbrep.2024.101886","DOIUrl":"10.1016/j.bbrep.2024.101886","url":null,"abstract":"<div><div>The aim of this study was to investigate the genetic factors of a patient with germinal vesicle arrest in oocytes. Clinical data and blood samples were collected from the patient and some were amplified for high-throughput gene and Sanger sequencing. Several molecular and cellular experiments were performed to determine the association between the gene mutation and germinal vesicle arrest. Two mutation sites (c.1282G &gt; T and c.1247C &gt; A) were found in the <em>PATL2</em> gene. The c.1282G &gt; T mutation is associated with oocyte maturation abnormalities according to previous research, whereas c.1247C &gt; A is a novel mutation of unknown clinical significance. In cell transfection experiments, qRT-PCR, immunofluorescence, and Western blotting revealed that the mRNA and protein levels of the <em>PATL2</em> gene with the c.1247C &gt; A mutation were reduced. Sanger sequencing suggested that the patient inherited the <em>PATL2</em> mutations from her parents via a compound heterozygous mode of inheritance. Collectively, this study describes the <em>PATL2</em>-gene c.1247C &gt; A mutation associated with germinal vesicle arrest in oocytes, providing a useful target for genetic and background tests for patients presenting with oocyte maturation abnormalities and/or germinal vesicle arrest following multiple unsuccessful attempts with assisted reproductive technology.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"40 ","pages":"Article 101886"},"PeriodicalIF":2.3,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142699925","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}