Biochemistry and Biophysics Reports最新文献

{"title":"The gold complex auranofin sensitizes platinum resistant epithelial ovarian cancer cells to cisplatin","authors":"Farah H. Abdalbari ,&nbsp;Benjamin N. Forgie ,&nbsp;Edith Zorychta ,&nbsp;Alicia A. Goyeneche ,&nbsp;Abu Shadat M. Noman ,&nbsp;Carlos M. Telleria","doi":"10.1016/j.bbrep.2025.101996","DOIUrl":"10.1016/j.bbrep.2025.101996","url":null,"abstract":"<div><div>Although numerous drugs have been tested to treat ovarian cancer (OC), survival rates remain low as there has been no major improvement from platinum (Pt)–based therapy and there is a high rate of Pt resistance in these tumors. Following several rounds of chemotherapy, OC cells develop Pt-resistance by increasing DNA repair and antioxidant defense mechanisms. This study aimed to design a treatment to combat recurrent stages of OC by repurposing the anti-rheumatic gold complex auranofin (AF). We demonstrate that AF enhances the efficacy of cisplatin (CDDP) in Pt-resistant epithelial OC (EOC) cells. The drug combination enhanced mitochondrial-dependent apoptosis, PARP cleavage, DNA damage, and ROS overproduction. These results suggest the potential to combine AF with CDDP as a strategy to improve CDDP sensitivity in recurrent EOCs.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"42 ","pages":"Article 101996"},"PeriodicalIF":2.3,"publicationDate":"2025-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143735186","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":"Regulation of the expression of ferrochelatase in a murine model of diabetes mellitus type I","authors":"Leda María Oliveri ,&nbsp;Ana Maria Buzaleh ,&nbsp;Esther Noemí Gerez","doi":"10.1016/j.bbrep.2025.101989","DOIUrl":"10.1016/j.bbrep.2025.101989","url":null,"abstract":"<div><h3>Background</h3><div>Diabetes produces changes on cellular hemeprotein metabolism. The last enzyme of heme biosynthetic pathway is ferrochelatase (FECH), an enzyme that catalyzes the insertion of ferrous ion into protoporphyrin IX to produce heme. The aim of this work was to investigate whether FECH expression can be other key point in the regulation of heme biosynthesis in diabetic animals.</div></div><div><h3>Methods</h3><div>Mice were rendered diabetic with streptozotocin (STZ, 170 mg/kg body weight i.p. for 15 days). Liver FECH protein and mRNA levels were evaluated by Western blot and Northern blot respectively. Vanadate was used as a hypoglycemic agent. The levels of the transcription factor Sp1 bound to the FECH promoter were assessed by chromatin immunoprecipitation (ChIP).</div></div><div><h3>Results</h3><div>Hyperglycemia caused an increase in FECH mRNA levels but no changes in FECH protein expression. ChIP analysis revealed that the increase in FECH mRNA levels was due to enhanced Sp1 binding to the FECH promoter in diabetic animals, which was reduced by vanadate administration.</div></div><div><h3>Conclusions</h3><div>In diabetic animals, enhanced binding of Sp1 to the FECH promoter may be responsible for the increase in FECH mRNA levels. However, this increase was not reflected in the amount of FECH protein, which would confirm that FECH could be another control point in heme synthesis.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"42 ","pages":"Article 101989"},"PeriodicalIF":2.3,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143726160","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":"Decision tree-based machine learning algorithm for prediction of acute radiation esophagitis","authors":"Mostafa Alizade-Harakiyan ,&nbsp;Amin Khodaei ,&nbsp;Ali Yousefi ,&nbsp;Hamed Zamani ,&nbsp;Asghar Mesbahi","doi":"10.1016/j.bbrep.2025.101991","DOIUrl":"10.1016/j.bbrep.2025.101991","url":null,"abstract":"<div><h3>Background</h3><div>Radiation-induced esophagitis remains a significant challenge in thoracic and neck cancer treatment, impacting patient quality of life and potentially limiting therapeutic efficacy. This study aimed to develop and validate a decision tree-based model for predicting acute esophagitis grades in patients undergoing chemoradiotherapy.</div></div><div><h3>Methods</h3><div>Data from 100 patients receiving thoracic and neck radiotherapy were analyzed. The dataset comprised 33 features, including demographic, clinical, and dosimetric parameters. A decision tree classifier was implemented for both binary (Grade ≥2 vs. &lt;2) and multi-class (Grades 1, 2, and 3) classification. Model performance was evaluated using standard metrics including accuracy, precision, recall, and F1-score.</div></div><div><h3>Results</h3><div>The binary classification model achieved 97 % accuracy in distinguishing acute esophagitis. The multi-class model demonstrated 98 % accuracy in predicting specific grades. Key predictive features included V40 (volume receiving 40 Gy), V60, and average esophageal dose. The model generated interpretable decision rules, with V60 ≥ 2.3 strongly indicating Grade 3 esophagitis.</div></div><div><h3>Conclusions</h3><div>The decision tree model demonstrates high accuracy in predicting radiation-induced esophagitis grades while maintaining clinical interpretability. This approach offers potential for treatment optimization and personalized risk assessment in radiotherapy planning. The model's transparency and reliability make it a promising tool for clinical decision support in radiation oncology.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"42 ","pages":"Article 101991"},"PeriodicalIF":2.3,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143714879","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":"Drug design for cyclin-dependent kinase 9 (CDK9) inhibitors in silico","authors":"Kaori Asamitsu ,&nbsp;Takatsugu Hirokawa ,&nbsp;Takashi Okamoto","doi":"10.1016/j.bbrep.2025.101988","DOIUrl":"10.1016/j.bbrep.2025.101988","url":null,"abstract":"<div><div>Despite the potential of cyclin-dependent kinase 9 (CDK9) as a novel target for various malignancies and HIV replication in infected cells, no effective inhibitors have been developed. In the preceding study, we deciphered a hidden cavity in CDK9 upon molecular dynamics (MD) simulation of the CDK9/CyclinT1/Tat trimolecular complex. This cavity is located near the CDK9 ATP pocket (continuous cavity I, CCI) and extends to the cyclin T1 (CycT1) contact surface (CCII and CCIII). In this study, we searched for compounds similar to previously identified CDK9 inhibitors using cheminformatics to identify compounds that are better suited to this hidden cavity. We identified compounds that effectively targeted CCII and CCIII of CDK9. We confirmed their inhibitory effects on the CDK9/CycT1 complex <em>in vitro</em>. As these inhibitory compounds target only a portion (CCII and CCIII cavities) of CDK9, we examined their combinatorial effects with the known CDK inhibitor <strong>BS-181</strong>. As expected, this combination exerted an additive inhibitory effect on CDK9 expression. These findings confirm the presence of a CDK9 hidden cavity that was revealed transiently by MD simulations, thus providing promising evidence for the development of CDK9 inhibitors.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"42 ","pages":"Article 101988"},"PeriodicalIF":2.3,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143714880","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":"Integrating cuproptosis and immunosenescence: A novel therapeutic strategy in cancer treatment","authors":"Ali Ahmadizad Firouzjaei ,&nbsp;Seyed Hamid Aghaee-Bakhtiari","doi":"10.1016/j.bbrep.2025.101983","DOIUrl":"10.1016/j.bbrep.2025.101983","url":null,"abstract":"<div><div>Recent advancements in our understanding of cell death mechanisms have progressed beyond traditional apoptosis to encompass various forms of regulated cell death, notably cuproptosis. This copper-dependent cell death occurs when copper interacts with lipoylated enzymes in the tricarboxylic acid cycle, leading to protein aggregation and subsequent cell death. Alongside this, immunosenescence the gradual decline in immune function due to aging has emerged as a significant factor in cancer progression and response to treatment. Innovative strategies that integrate cuproptosis and immunosenescence are showing considerable promise in cancer therapy. By leveraging the altered copper metabolism in cancer cells, cuproptosis can selectively induce cell death, effectively targeting and eliminating tumors. Simultaneously, addressing immunosenescence can rejuvenate the aging immune system, enhancing its capacity to identify and destroy cancer cells. This dual approach creates a synergistic effect, optimizing therapeutic efficacy by directly attacking tumor cells while revitalizing the immune response. Such integration bolsters the defense against cancer progression and recurrence and holds great potential for advancing cancer treatment modalities and improving patient outcomes. This paper delves into the interactions between cuproptosis and immunosenescence, emphasizing their implications for developing innovative cancer therapies.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"42 ","pages":"Article 101983"},"PeriodicalIF":2.3,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143705599","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":"Ultrasound irradiation activates purine metabolism and mitochondrial respiration via the MAPK signaling pathway in myotubes","authors":"Xiaoqi Ma ,&nbsp;Noriaki Maeshige ,&nbsp;Atomu Yamaguchi ,&nbsp;Yunfei Fu ,&nbsp;Jihao Xing ,&nbsp;Qingcheng Guo ,&nbsp;Hao Lin ,&nbsp;Fuwen Lu ,&nbsp;Hiroyo Kondo ,&nbsp;Hidemi Fujino","doi":"10.1016/j.bbrep.2025.101984","DOIUrl":"10.1016/j.bbrep.2025.101984","url":null,"abstract":"<div><h3>Background</h3><div>Pulsed ultrasound (US) is widely used both as a diagnostic imaging tool and a therapeutic approach. However, many of the mechanisms underlying the therapeutic effects of non-thermal US remain unclear, especially in skeletal muscles, which play a crucial role in the body's metabolism. The aim of this study was to investigate the effects of US on myotubes.</div></div><div><h3>Methods</h3><div>In this study, C2C12 myoblasts were utilized. After differentiating into myotubes, the cells were exposed to US irradiation at an intensity of 3.0 W/cm², with a 20 % duty cycle, an acoustic frequency of 1 MHz, and a pulse repetition frequency of 100 Hz for 5 min. The cells were then collected and analyzed for genomic and metabolomic alterations, as well as mitochondrial function.</div></div><div><h3>Results</h3><div>Cell viability remained unaffected after US irradiation. The mitogen-activated protein kinase (MAPK) signaling pathway was the most activated, while the expression of various RNAs was significantly altered. Purine metabolism was highly activated, with an increase in the abundance of metabolites associated with this pathway. Furthermore, mitochondrial respiration in the myotubes increased following US irradiation.</div></div><div><h3>Conclusion</h3><div>This study investigated the impact of US irradiation on myotubes using genomic analysis, metabolomic analysis, and mitochondrial function. US irradiation activated the MAPK signaling pathway, which in turn enhanced purine metabolism and improved mitochondrial respiration.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"42 ","pages":"Article 101984"},"PeriodicalIF":2.3,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143697786","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":"Autophagy: The convergence point of aging and cancer","authors":"Anchala Pandey,&nbsp;Ankit Goswami ,&nbsp;B. Jithin ,&nbsp;Sanjeev Shukla","doi":"10.1016/j.bbrep.2025.101986","DOIUrl":"10.1016/j.bbrep.2025.101986","url":null,"abstract":"<div><div>Autophagy, a dynamic intracellular degradation system, is critical for cellular renovation and maintaining equilibrium. By eliminating damaged components and recycling essential molecules, autophagy safeguards cellular integrity and function. The versatility of the autophagy process across various biological functions enable cells to adapt and maintain homeostasis under unfavourable conditions. Disruptions in autophagy can shift a cell from a healthy state to a disease state or, conversely, support a return to health. This review delves into the multifaceted role of autophagy during aging and age-related diseases such as cancer, highlighting its significance as a unifying target with promising therapeutic implications. Cancer development is a dynamic process characterized by the acquisition of diverse survival capabilities for proliferating at different stages. This progression unfolds over time, with cancer cells exploiting autophagy to overcome encountered stress conditions during tumor development. Notably, there are several common pathways that utilize the autophagy process during aging and cancer development. This highlights the importance of autophagy as a crucial therapeutic target, holding the potential to not only impede the growth of tumor but also enhance the patient's longevity. This review aims to simplify the intricate relationship between cancer and aging, with a particular focus on the role of autophagy.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"42 ","pages":"Article 101986"},"PeriodicalIF":2.3,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143697785","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":"Single-cell RNA sequencing reveals the heterogeneity and regulatory modules of cell-specific RNA-binding proteins in patients with systemic lupus erythematosus","authors":"Sheng-Yan Lin ,&nbsp;Yikai Yu ,&nbsp;Daan Nie ,&nbsp;Lili Yang ,&nbsp;Yuxue Chen ,&nbsp;Yu Chen ,&nbsp;Cheng Wen ,&nbsp;Zhipeng Zeng","doi":"10.1016/j.bbrep.2025.101977","DOIUrl":"10.1016/j.bbrep.2025.101977","url":null,"abstract":"<div><h3>Background</h3><div>Systemic lupus erythematosus (SLE) is an autoimmune disorder characterized by immune dysregulation, heterogeneous clinical phenotypes, and a complex interplay of pathogenic mechanisms. RNA-binding proteins (RBPs), which orchestrate post-transcriptional gene regulation through dynamic interactions with target transcripts, are increasingly implicated in autoimmune pathogenesis. However, the cell-type-specific heterogeneity of RBPs expression and their regulatory networks in SLE remain poorly characterized.</div></div><div><h3>Methods</h3><div>To delineate RBPs dynamics in SLE skin microenvironment, we conducted a comprehensive single-cell transcriptomic analysis of publicly accessible single cell RNA sequencing (scRNA-seq) datasets from lesional skin biopsies of SLE patients and healthy controls (HC). Cell-type-specific RBPs expression patterns were systematically profiled across epidermal keratinocytes, dermal endothelial cells, and T cells. Complementary bulk RNA-Seq analyses employing Splicing Site Usage Variation Analysis (SUVA) were performed to identify immune gene-associated regulatory alternative splicing (RAS) events. Integrative co-expression networks linking RBPs, RAS events, and immune pathways were subsequently constructed.</div></div><div><h3>Results</h3><div>Single-cell resolution revealed marked heterogeneity in RBPs expression across keratinocyte, endothelial cell, and T cell in SLE compared to HC. Notably, disease-specific RBPs were enriched in pathways governing interferon response, cytokine signaling, and leukocyte activation. Cross-analysis with bulk transcriptomic data highlighted JUN and HLA-A as hub regulators exhibiting elevated expression in SLE T cells. Network modeling further uncovered coordinated interactions between JUN, HLA-A, and RAS events in immune genes, implicating their synergistic roles in modulating T cell effector functions.</div></div><div><h3>Conclusion</h3><div>Our multi-omics integration identifies JUN and HLA-A as central coordinators of alternative splicing programs in SLE T cells. These molecular hubs, embedded within immune regulatory networks, may drive pathogenic rewiring of T cell responses in SLE.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"42 ","pages":"Article 101977"},"PeriodicalIF":2.3,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143679098","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":"Evolutionary relationships and genetic diversity in the BlaTEM gene among selected gram-negative bacteria","authors":"Jackson Henry Katonge,&nbsp;Zainabu Khamis Ally","doi":"10.1016/j.bbrep.2025.101985","DOIUrl":"10.1016/j.bbrep.2025.101985","url":null,"abstract":"<div><div>This study investigates the genetic diversity and evolutionary relationships of the <em>blaTEM</em> gene, a major determinant of beta-lactam antibiotic resistance. We analyzed nucleotide sequences of 32 β-lactamase-producing strains from <em>Klebsiella pneumoniae</em>, <em>Escherichia coli</em>, <em>Pseudomonas aeruginosa</em>, <em>Proteus mirabilis</em>, and <em>Acinetobacter baumannii</em> obtained from public databases. Sequence analysis revealed 32 distinct sequences with 298 segregating sites and 303 mutations, indicating substantial genetic variability. A high level of haplotype diversity was observed, with 24 distinct haplotypes, reflecting evolutionary pressures and horizontal gene transfer. Phylogenetic analysis showed clear clades, suggesting the evolutionary relationships among <em>blaTEM</em> variants and interspecies gene transfer. The resistance profiles correlated with the genetic findings, particularly mutations. This analysis draws attention to the ongoing adaptive evolution of antibiotic resistance mechanisms, as well as the need for continued monitoring and novel therapeutic strategies. Further research with larger sample sizes and functional validation is needed to fully understand the implications of these variants in antibiotic resistance.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"42 ","pages":"Article 101985"},"PeriodicalIF":2.3,"publicationDate":"2025-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143679091","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":"The aggregation tendencies of the signal peptide regions of prone and not prone to aggregate proteins","authors":"Natalie G. Horgan,&nbsp;Anabela Djurovic-Topalovic,&nbsp;Taiwo A. Ademoye,&nbsp;Jessica S. Fortin","doi":"10.1016/j.bbrep.2025.101980","DOIUrl":"10.1016/j.bbrep.2025.101980","url":null,"abstract":"<div><div>Signal peptides are a sequence of peptides located at the N-terminus of proteins and determine the protein secretion pathway and their destinations. The N-region is positively charged and influences the orientation of translocation. When linked to the protein, signal peptides provide protection against misfolding events and the formation of amyloid fibrils, which are related to neurodegenerative and inflammatory diseases. An earlier study from our research group demonstrated the tendency/predisposition of misfolding and seeding events of the synthetic signal peptide of serum amyloid A1 (SAA1), which originates from humans and other animal species. The current study explores the propensity for misfolding of fourteen different synthetic signal peptides of both prone-to-aggregate and non-prone-to-aggregate proteins by an <em>in silico</em> program, Congo red (CR) binding assays, and transmission electron microscopy (TEM). Among the six signal peptides derived from aggregation-prone proteins, all of them were confirmed to misfold by electron microscopy and CR binding assays. More precisely, the signal peptides from the human and feline islet amyloid polypeptide (IAPP), SAA1, parathyroid hormone (PTH), transthyretin (TTR), and cathepsin K (CTSK) generated amyloid-like fibrils. Signal peptides from the non-prone-to-aggregate protein category were capable of misfolding, such as human collagen type X alpha 1 (COL10A1), granulin (GRN), luteinizing hormone beta polypeptide (LHB), serpin peptidase inhibitor A7 (SERPINA7), serpin peptidase inhibitor E (SERPINE1), serine protease 1 (PRSS1), and UDP glucuronosyltransferase family 1 member A1 signal peptides (UGT1A1). TTR signal peptide seeds accelerated the misfolding of TTR_1-25 fragment peptide —which was assessed by thioflavin T assays— and increased the formation of oligomers as validated by the photo-induced cross-linking of unmodified proteins assays. Overall, all the prone-to-aggregate signal peptides and seven out of the eight non-prone-to-aggregate signal peptides were confirmed to misfold as shown by TEM images. Studying the tendency of signal peptides to aggregate may provide key indicators into the mechanisms underlying protein misfolding.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"42 ","pages":"Article 101980"},"PeriodicalIF":2.3,"publicationDate":"2025-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143679081","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}