Frontiers in bioscience (Landmark edition)最新文献

{"title":"Ratio of AT and GC Pairs in the Zones of Open States Genesis in DNA Molecules.","authors":"Anna Dorohova, Oksana Lyasota, Alexander Svidlov, Anastasia Anashkina, Elena Tekutskaya, Stepan Dzhimak, Mikhail Drobotenko","doi":"10.31083/j.fbl2911381","DOIUrl":"https://doi.org/10.31083/j.fbl2911381","url":null,"abstract":"<p><strong>Background: </strong>There is an assumption about the presence of a specific nucleotides sequence in DNA molecule, which contributes to the genesis of open states (OS). In addition, it would be logical to assume that OS zones should form in DNA regions with a large proportion of Adenine-Thymine (AT) pairs, since they contain fewer hydrogen bonds than Guanine- Cytosine (GC) base pairs. However, studies have shown that in areas rich in AT pairs, the probability of open states will not always be higher.</p><p><strong>Methods: </strong>In this work, for two genes containing different numbers of regions with a large AT pairs proportion, we calculated the ratio of AT and GC pairs in the OS zones. For calculations, we used a coarse-grained angular mechanical DNA model.</p><p><strong>Results: </strong>It has been established that small OS zones can appear on any part of the DNA molecule. They mainly consist of AT pairs, but as the size of OS zones increases, the content of AT pairs in them decreases.</p><p><strong>Conclusions: </strong>The occurrence of long-length OS zones is \"tied\" to regions of the DNA molecule with a large proportion of AT pairs; if there are several such areas, then, depending on the magnitude of the torque, OS zones can arise in different areas of the gene. Thus, the genesis probability of large OS zones in a DNA segment depends not only on the \"strength\" of the nucleotide sequence of this area, but also on the factors determining the dynamics of DNA.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 11","pages":"381"},"PeriodicalIF":3.3,"publicationDate":"2024-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142755992","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":"Regulatory T-cells: The Face-off of the Immune Balance.","authors":"Mahmoud Singer, Ahmed M Elsayed, Mohamed I Husseiny","doi":"10.31083/j.fbl2911377","DOIUrl":"https://doi.org/10.31083/j.fbl2911377","url":null,"abstract":"<p><p>Regulatory T-cells (Tregs) play a crucial role in maintaining immune homeostasis, ensuring a balanced immune response. Tregs primarily operate in an antigen-specific fashion, facilitated by their distinct distribution within discrete niches. Tregs have been studied extensively, from their point of origin in the thymus origin to their fate in the periphery or organs. Signals received from antigen-presenting cells (APCs) stimulate Tregs to dampen inflammation. Almost all tumors are characterized by a pathological abundance of immune suppression in their microenvironment. Conversely, the lack thereof proves detrimental to immunological disorders. Achieving a balanced expression of Tregs in relation to other immune compartments is important in establishing an effective and adaptable immune tolerance towards cancer cells and autoantigens. In the context of cancer, it is essential to decrease the frequency of Tregs to overcome tumor suppression. A lower survival rate is associated with the presence of excessive exhausted effector immune cells and an increased frequency of regulatory cells. However, when it comes to treating graft rejection and autoimmune diseases, the focus lies on immune tolerance and the transfer of Tregs. Here, we explore the complex mechanisms that Tregs use in human disease to balance effector immune cells.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 11","pages":"377"},"PeriodicalIF":3.3,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142756001","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":"Formation of the Native Topology of a Protein is due to the \"Conserved but Non-Functional\" Residues: A Case of Apomyoglobin Folding.","authors":"Valentina E Bychkova, Dmitry A Dolgikh, Vitalii A Balobanov, Alexei V Finkelstein","doi":"10.31083/j.fbl2911379","DOIUrl":"https://doi.org/10.31083/j.fbl2911379","url":null,"abstract":"<p><p>This paper is dedicated to the memory of Oleg B. Ptitsyn (1929-1999) and presents an answer to his question: \"What is the role of conserved non-functional residues in protein folding?\". This answer follows from the experimental works of three labs. The role of non-functional but conserved residues of apomyoglobin (apoMb) in the formation of the native protein fold in the molten globule state has been experimentally revealed. This research proves that the non-functional but conserved residues of apoMb are necessary for the formation and maintenance of the correct topological arrangement of the main elements in the apoMb secondary structure already in the early folding intermediate.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 11","pages":"379"},"PeriodicalIF":3.3,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142755928","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":"Chromomeres, Topologically Associating Domains and Structural Organization of Chromatin Bodies in Somatic Nuclei (Macronuclei) of Ciliates.","authors":"Vladimir Popenko, Pavel Spirin, Vladimir Prassolov, Olga Leonova","doi":"10.31083/j.fbl2911378","DOIUrl":"https://doi.org/10.31083/j.fbl2911378","url":null,"abstract":"<p><strong>Background: </strong>In the twentieth century, the textbook idea of packaging genomic material in the cell nucleus and metaphase chromosomes was the presence of a hierarchy of structural levels of chromatin organization: nucleosomes - nucleosomal fibrils -30 nm fibrils - chromomeres - chromonemata - mitotic chromosomes. Chromomeres were observed in partially decondensed chromosomes and interphase chromatin as ~100 nm globular structures. They were thought to consist of loops of chromatin fibres attached at their bases to a central protein core. However, Hi-C and other related methods led to a new concept of chromatin organization in the nuclei of higher eukaryotes, according to which nucleosomal fibrils themselves determine the spatial configuration of chromatin in the form of topologically associating domains (TADs), which are formed by a loop extrusion process and are regions whose DNA sequences preferentially contact each other. Somatic macronuclei of ciliates are transcriptionally active, highly polyploid nuclei. A feature of macronuclei is that their genome is represented by a large number of \"gene-sized\" (~1-25 kb) or of \"subchromosomal\" (~50-1700 kb) size minichromosomes. The inactive macronuclear chromatin of \"subchromosomal\" ciliates usually looks like bodies 100-200 nm in size. The aim of this work was to find out which of the models (chromomeres or TADs) is more consistent with the confocal and electron microscopic data on structural organization of chromatin bodies.</p><p><strong>Methods: </strong>Macronuclear chromatin of four \"subchromosomal\" ciliate species (<i>Bursaria truncatella</i>, <i>Paramecium multimicronucleatum</i>, <i>Didinium nasutum</i>, <i>Climacostomum virens</i>) was examined using electron microscopy and confocal microscopy during regular growth, starvation and encystment.</p><p><strong>Results: </strong>Chromatin bodies ~70-200 nm in size observed in the interphase macronuclei consisted of tightly packed nucleosomes. Some of them were interconnected by one or more chromatin fibrils. Under hypotonic conditions <i>in vitro</i>, chromatin bodies decompacted, forming rosette-shaped structures of chromatin fibrils around an electron-dense centre. When the activity of the macronucleus decreased during starvation or encystment, chromatin bodies assembled into chromonema-like fibrils 100-300 nm thick. This data allows us to consider chromatin bodies as analogues of chromomeres. On the other hand, most likely, the formation of DNA loops in chromatin bodies occurs by the loop extrusion as in TADs.</p><p><strong>Conclusions: </strong>The data obtained is well explained by the model, according to which the chromatin bodies of ciliate macronuclei combine features inherent in both chromomeres and TADs; that is, they can be considered as chromomeres with loops packed in the same way as the loops in TADs.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 11","pages":"378"},"PeriodicalIF":3.3,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142755794","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":"Diverse Cytokines Secreted by Adipocyte in Linking Cardio-Metabolic Disorder and SLE.","authors":"Min Lai, Kai Lin, Xiaofang Chen, Ye Cheng","doi":"10.31083/j.fbl2911373","DOIUrl":"https://doi.org/10.31083/j.fbl2911373","url":null,"abstract":"<p><p>Systemic lupus erythematosus (SLE) is a multi-factorial autoimmune-mediated disease with hyper-stimulation of immune cells especially the T lymphocytes. By this method, it might facilitate the systematic damages in multiple tissues and organs. Otherwise, SLE is also correlated with diverse cardio-metabolic comorbidities, including dyslipidemia, insulin resistance, and hypertension. It is worth-noting that the risk of cardio-metabolic disorders is significantly higher compared with the healthy patients which was reported as approximately one-third of SLE patients were proved as obesity. Notably, current focus is shifting to implementing cardio-metabolic protective strategies as well as elucidating underlying mechanisms of lupus-mediated obese status. On the other hand, adipocyte, as the most abundant endocrine cell in fat tissue, are dysfunctional in obese individuals with aberrant secretion of adipokines. It is proposing that the adipokine might link the pathology of cardio-metabolic disorders and SLE, whereas the related mechanism is complicated. In the current review, the functions of adipokine and the potential mechanisms by which the adipokine link cardio-metabolic disorders and SLE was well listed. Furthermore, the recommendations, which identify the adipokine as the potential therapeutic targets for the treatment of cardio-metabolic disorders and SLE, were also summarized.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 11","pages":"373"},"PeriodicalIF":3.3,"publicationDate":"2024-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142755898","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":"LncRNA-TUG1: Implications in the Myocardial and Endothelial Cell Oxidative Stress Injury Caused by Hemorrhagic Shock and Fluid Resuscitation.","authors":"Wei Li, Huaiyu Chen, Xueli Zhu, Mingrui Lin","doi":"10.31083/j.fbl2911376","DOIUrl":"https://doi.org/10.31083/j.fbl2911376","url":null,"abstract":"<p><strong>Background: </strong>LncRNA taurine-upregulated gene 1 (<i>TUG1</i>) can regulate vascular endothelial cell injury, a critical mechanism in treating hemorrhagic shock and fluid resuscitation (HS/R). Therefore, this study explored the influence of <i>TUG1</i> in HS/R.</p><p><strong>Methods: </strong>An <i>in vivo</i> rat model of ischemia-reperfusion (I/R) injury post-HS/R and an <i>in vitro</i> model of oxidative stress injury in rat cardiomyocyte cell line (H9C2) were constructed. <i>In vivo</i>, we silenced <i>TUG1</i> and quantified its expression along with inflammatory factors through quantitative reverse transcription polymerase chain reaction (qRT-PCR), mean arterial pressure (MAP) detection and blood gas analysis. Myocardial functional impairment was assessed via Triphenyl-2H-Tetrazolium Chloride (TTC), Hematoxylin and eosin, and Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling (TUNEL) stainings. Oxidative stress level in rat serum was measured. <i>In vitro</i>, we examined the changes of cell viability, apoptosis, oxidative stress levels, inflammatory factor secretion and nuclear factor-κB (NF-κB)/p65 expression by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), flow cytometry, Enzyme-linked immunosorbent assay (ELISA) and Western blot.</p><p><strong>Results: </strong><i>TUG1</i> level was elevated in rats of I/R model caused by HS/R. <i>TUG1</i> silencing ameliorated the decline in MAP, acid-base imbalance and myocardial tissue damage, and suppressed oxidative stress and inflammatory factor levels in model rat. <i>TUG1</i> silencing enhanced viability, impeded apoptosis, and reduced oxidative stress, inflammatory factor contents and NF-κB/p65 expression in H₂O₂ treated H9C2 cells.</p><p><strong>Conclusion: </strong><i>TUG1</i> participates in regulating oxidative stress damage and inflammation induced by HS/R.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 11","pages":"376"},"PeriodicalIF":3.3,"publicationDate":"2024-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142755971","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":"Oncolytic Vesicular Stomatitis Virus: Optimisation Strategies for Anti-Cancer Therapies.","authors":"Margarita Zinovieva, Anastasia Ryapolova, Alexander Karabelsky, Ekaterina Minskaia","doi":"10.31083/j.fbl2911374","DOIUrl":"https://doi.org/10.31083/j.fbl2911374","url":null,"abstract":"<p><p>Oncolytic viruses (OVs) represent a targeted anti-cancer therapy approach due to their ability not only to selectively infect and destroy malignant cells but also to induce an immune response. Vesicular stomatitis virus (VSV) offers a promising platform due to its low prevalence and pathogenicity in humans, lack of pre-existing immunity, easily manipulated genome, rapid growth to high titers in a broad range of cell lines, and inability to integrate into the host genome. However, despite its many advantages, many unresolved problems remain: problematic production based on the reverse genetics system, oncological selectivity, and the overall effectiveness of VSV monotherapy. This review will discuss various attempts at viral genome modifications aimed at improving the oncolytic properties of VSV. These strategies include inhibition of viral genes, modification of genes responsible for targeting cancer cells over healthy ones, insertion of foreign genes for boosting immune response, and changing the order of viral and inserted foreign genes. In addition, possible ways to improve VSV-based anti-tumor therapy and achieve higher efficiency will be considered by evaluating the effectiveness of various delivery methods as well as discussing treatment options by combining VSV with other groups of anticancer drugs.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 11","pages":"374"},"PeriodicalIF":3.3,"publicationDate":"2024-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142755984","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":"Circulating Extracellular Vesicles: An Effective Biomarker for Cancer Progression.","authors":"Madhura Chatterjee, Saurabh Gupta, Sayoni Nag, Ishita Rehman, Deepak Parashar, Arindam Maitra, Kaushik Das","doi":"10.31083/j.fbl2911375","DOIUrl":"https://doi.org/10.31083/j.fbl2911375","url":null,"abstract":"<p><p>Extracellular vesicles (EVs), the ubiquitous part of human biology, represent a small heterogenous, membrane-enclosed body that contains a diverse payload including genetic materials in the form of DNA, RNAs, small non-coding RNAs, etc. mostly mirroring their source of origin. Since, a vast majority of research has been conducted on how nucleic acids, proteins, lipids, and metabolites, associated with EVs can be effectively utilized to identify disease progression and therapeutic responses in cancer patients, EVs are increasingly being touted as valuable and reliable identifiers of cancer biomarkers in liquid biopsies. However, the lack of comprehensive clinical validation and effective standardization protocols severely limits its applications beyond the laboratories. The present review focuses on understanding the role of circulating EVs in different cancers and how they could potentially be treated as cancer biomarkers, typically due to the presence of bioactive molecules such as small non-coding RNAs, RNAs, DNA, proteins, etc., and their utilization for fine-tuning therapies. Here, we provide a brief general biology of EVs including their classification and subsequently discuss the source of circulatory EVs, the role of their associated payload as biomarkers, and how different cancers affect the level of circulatory EVs population.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 11","pages":"375"},"PeriodicalIF":3.3,"publicationDate":"2024-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142755815","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":"NUF2 Promotes Breast Cancer Metastasis via Activating Wnt/β-Catenin Pathways.","authors":"Nijiati AiErken, Xidi Wang, Jiamei Wang, Weisen Ma, Lingfei Cui, Mingxia Zhang, Weifeng Ma, Dongwei Liu","doi":"10.31083/j.fbl2911371","DOIUrl":"https://doi.org/10.31083/j.fbl2911371","url":null,"abstract":"<p><strong>Background: </strong>Breast cancer is the most common malignancy and the leading cause of cancer death among women. NDC80 kinetochore complex component (NUF2) is demonstrated to implicate the progression of human cancer. But the role of NUF2 in breast cancer progression is unclear. Here, we aimed to study the role and regulatory mechanisms of NUF2 in breast cancer metastasis.</p><p><strong>Methods: </strong>Immunohistochemistry was used to determine UNF2 expression in clinical samples. Transwell assas were used to determine the role of NUF2 in breast cancer migration and invasion. Animal model <i>in vivo</i> was used to determine the rold of NUF2 in breast cancer metastasis.</p><p><strong>Results: </strong>NUF2 was upregulated significantly in breast cancer tissues and cells. Worse prognosis was noted in patients with high NUF2 levels compared with that in patients with low NUF2 levels. NUF2 overexpression markedly enhanced, while NUF2 knockdown inhibited, breast cancer cell invasion and migration. Mechanistically, NUF2 was observed to upregulate Wnt/β-catenin signaling pathway activity. The promoting effect of NUF2 on cell migration and invasion were blocked by inhibition of the Wnt/β-catenin pathway.</p><p><strong>Conclusions: </strong>We revealed that NUF2 promotes breast cancer progression via activating Wnt/β-catenin signaling, suggesting that NUF2 might be a new potential target for breast cancer treatment.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 11","pages":"371"},"PeriodicalIF":3.3,"publicationDate":"2024-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142755975","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":"Joint Analysis of CCAAT/Enhancer-Binding Protein Beta and Interleukin 1 Beta in the Treatment and Prognosis of Diffuse Large B-Cell Lymphoma.","authors":"Hongmin Wang, Shuo Zhang, Mengmeng Wang, Chaozhong Wang, Jihong Xu, Ming Jiang, Xue Han, Xiaotong Yang, Liping Zhang, Baotong Chen, Aichun Liu","doi":"10.31083/j.fbl2911372","DOIUrl":"https://doi.org/10.31083/j.fbl2911372","url":null,"abstract":"<p><strong>Objective: </strong>The purpose of this study is to investigate the correlation between elevated levels of CCAAT/enhancer-binding protein beta (<i>CEBPB</i>) gene expression and unfavorable outcomes in diffuse large B-cell lymphoma (DLBCL). The goal is to elucidate potential therapeutic targets associated with this relationship.</p><p><strong>Methods: </strong>Differential expression and survival analyses were conducted using data from the Gene Expression Omnibus (GEO) database. The functions of <i>CEBPB</i> in DLBCL cells were investigated through cell culture, RNA extraction, quantitative real-time polymerase chain reaction (qRT-PCR), and Western blot. In addition, a weighted gene co-expression network analysis (WGCNA) was performed to pinpoint gene modules associated with <i>CEBPB</i>. Furthermore, experimental validation was carried out to explore the interaction between <i>CEBPB</i> and interleukin 1 beta (<i>IL1B</i>).</p><p><strong>Results: </strong>High levels of <i>CEBPB</i> expression are prominently observed in DLBCL, with its overabundance significantly linked to the diagnosis of DLBCL. Survival analysis reveals that patients exhibiting elevated <i>CEBPB</i> expression tend to experience a poorer prognosis. Further validation confirmed <i>CEBPB</i>'s role in promoting DLBCL cell proliferation and cell cycle progression. WGCNA identified <i>CEBPB</i>-related gene modules, with <i>IL1B</i> identified as a potential regulatory gene of <i>CEBPB</i>. The presence of high levels of <i>IL1B</i> has been correlated with an unfavorable prognosis in individuals diagnosed with DLBCL. Experiments demonstrate that <i>IL1B</i> promotes DLBCL cell proliferation through <i>CEBPB</i>.</p><p><strong>Conclusions: </strong>This study reveals the significant roles of <i>CEBPB</i> and <i>IL1B</i> in DLBCL, providing new theoretical foundations and potential molecular targets for the treatment and prognosis of DLBCL.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 11","pages":"372"},"PeriodicalIF":3.3,"publicationDate":"2024-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142755966","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}