Current Cardiology Reviews最新文献

{"title":"Exploring the Involvement of New Members of the Interleukin Family in Cardiovascular Disease.","authors":"Abdullah Al Noman, Sanzida Alam Flora, Monty Datta, Fahmida Afrose, Nushaiba Binte Hasan, Tahamina Akhter, Nayeema Jameel Anuva, Rashmi Pathak, Himanshu Sharma","doi":"10.2174/011573403X330079241213071055","DOIUrl":"https://doi.org/10.2174/011573403X330079241213071055","url":null,"abstract":"<p><p>Cardiovascular diseases remain a significant reason for illness and death globally. Although certain interleukins have been extensively researched about cardiovascular disease (CVD), new findings have identified unique members of the interleukin family that could potentially play a role in cardiovascular well-being and ailments. This review discusses the current understanding of the role of these recently identified interleukins, such as IL-27, IL-31, IL-32, IL-33, and the IL-28 group (IL-28A, IL-28B, IL-29), in the development of cardiovascular diseases. Every interleukin has various impacts achieved through particular receptors and signaling pathways that affect inflammatory processes, differentiation of immune cells, and the functioning of blood vessels. IL-27 controls the development of inflammatory Th17 cells and might decrease inflammation in atherosclerosis. IL-31 plays a role in the interaction between the immune system and nerves, as well as in itching. IL-32 enhances the generation of inflammatory proteins and has been linked to coronary artery disease. IL-33 has beneficial effects on the cardiovascular system, whereas its imitation receptor sST2 could potentially be used as a biomarker. Additional studies are needed to investigate the antiviral and immune-system regulating effects of the IL-28 group in cardiovascular diseases. In general, explaining the ways in which new interleukins contribute to the progression of cardiovascular diseases can help discover fresh targets for therapy and new approaches toward enhancing the prevention and treatment of heart disorders. Additional research on the way these cytokines engage with established disease pathways is necessary.</p>","PeriodicalId":10832,"journal":{"name":"Current Cardiology Reviews","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143022593","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":"Dyspnea and Heart Failure: The Role of the Diaphragm.","authors":"Pablo Marino Corrêa Nascimento, Mario Luiz Ribeiro, Bernardo Nascimento Lourenço, Humberto Villacorta, Antonio José Lagoeiro Jorge, Nazareth de Novaes Rocha, Wolney de Andrade Martins","doi":"10.2174/011573403X330739241216185852","DOIUrl":"https://doi.org/10.2174/011573403X330739241216185852","url":null,"abstract":"<p><strong>Background: </strong>Dyspnea and exertional intolerance are the most common clinical manifestations of Heart Failure (HF). One of the possible mechanisms of both symptoms in HF patients is weakness of the inspiratory muscles.</p><p><strong>Aim: </strong>Because the diaphragm is the main inspiratory muscle, this review aimed to investigate the contribution of diaphragmatic function to the genesis of dyspnea or exercise intolerance in HF patients.</p><p><strong>Methods: </strong>Original articles, clinical trials, and cohort or case-control studies published between January 2003 and March 2023 were included. The population, variables, and outcome strategy were the basis of this review, including studies that assessed HF patients, diaphragmatic function, and dyspnea or exercise tolerance. The PubMed/MEDLINE, Embase, and BVS/LILACS databases were searched.</p><p><strong>Results: </strong>A total of 353 articles were identified from electronic databases. After removing duplicate articles and screening based on titles, abstracts, and full texts, nine articles were included in the qualitative synthesis of this review. These studies were quite heterogeneous in their methodologies; however, most, except two, demonstrated an association among diaphragmatic dysfunction, dyspnea, and exertional intolerance in HF patients.</p><p><strong>Conclusion: </strong>Although few studies have assessed the contribution of diaphragmatic function to dyspnea and exertional intolerance in HF individuals, the vast majority of articles included in this review found such an association, especially when diaphragmatic function was assessed using ultrasound.</p>","PeriodicalId":10832,"journal":{"name":"Current Cardiology Reviews","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143022581","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 New Mechanism of Supraventricular Tachycardia: Gene Mutation.","authors":"Jie Gao, Rong Luo, Xiaoping Li","doi":"10.2174/011573403X320610250108113731","DOIUrl":"https://doi.org/10.2174/011573403X320610250108113731","url":null,"abstract":"<p><strong>Background: </strong>Supraventricular tachycardia (SVT) is very common in daily clinical practice, especially in the emergency department, with rapid onset and urgent management. The review highlights the recent genetic predispositions and mechanisms in SVT.</p><p><strong>Methods: </strong>Through analysis of epidemiology, familial clustering, and gene mutations of the relevant literature，the review elucidates the genetic properties and potential pathophysiology of SVT.</p><p><strong>Results: </strong>There are many pathophysiological mechanisms related to atrioventricular node reentrant tachycardia (AVNRT) and atrioventricular reentrant tachycardia (AVRT). Currently, there is relatively little research on inappropriate sinus tachycardia (IST), atrial tachycardia (AT), and congenital junctional ectopic tachycardia (CJET). It seems that every type of SVT has gene mutations in ion channels, with three types of SVT having gene mutations in signaling pathways, and others including gene mutations in beta-adrenergic-receptor autoantibodies, autonomic nervous system, and AV node structure.</p><p><strong>Conclusion: </strong>SVT has certain genetic characteristics and is often associated with other heart diseases. From the analysis of mutated genes in SVT, it appears to be a type of cardiac ion channel disease. Unlike common ion channel diseases, it is more insidious and more susceptible to external factors. The confirmation of the genetic basis of SVT provides direction for future hazard stratification assessment and gene targeted therapy drug research.</p>","PeriodicalId":10832,"journal":{"name":"Current Cardiology Reviews","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143001569","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":"Unlocking Platelet Mechanisms through Multi-Omics Integration: A Brief Review.","authors":"Muhammad Mazhar Fareed, Maryam Qasmi, Zarmina Khan, Haider Ali, Stavros Stavrakis, Carola Y Förster, Sergey Shityakov","doi":"10.2174/011573403X334382241210064101","DOIUrl":"https://doi.org/10.2174/011573403X334382241210064101","url":null,"abstract":"<p><p>Platelets, tiny cell fragments measuring 2-4 μm in diameter without a nucleus, play a crucial role in blood clotting and maintaining vascular integrity. Abnormalities in platelets, whether genetic or acquired, are linked to bleeding disorders, increased risk of blood clots, and cardiovascular diseases. Advanced proteomic techniques offer profound insights into the roles of platelets in hemostasis and their involvement in processes such as inflammation, metastasis, and thrombosis. This knowledge is vital for drug development and identifying diagnostic markers for platelet activation. Platelet activation is an exceptionally rapid process characterized by various posttranslational modifications, including protein breakdown and phosphorylation. By utilizing multiomics technologies and biochemical methods, researchers can thoroughly investigate and define these posttranslational pathways. The absence of a nucleus in platelets significantly simplifies mass spectrometry-based proteomics and metabolomics, as there are fewer proteins to analyze, streamlining the identification process. Additionally, integrating multiomics approaches enables a comprehensive examination of the platelet proteome, lipidome, and metabolome, providing a holistic understanding of platelet biology. This multifaceted analysis is critical for elucidating the complex mechanisms underpinning platelet function and dysfunction. Ultimately, these insights are crucial for advancing therapeutic strategies and improving diagnostic tools for platelet-related disorders and cardiovascular diseases. The integration of multi-omics technologies is paving the way for a deeper understanding of platelet mechanisms, with significant implications for biomedical research and clinical applications.</p>","PeriodicalId":10832,"journal":{"name":"Current Cardiology Reviews","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142983041","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":"Molecular and Functional Significance of Growth Differentiation Factor-15: A Review on Cardiovascular-Kidney-Metabolic Biomarker.","authors":"Krishna Tiwari, Aswini Saravanan, Abhishek Anil, Vikas Kumar Tiwari, Muhammad Aaqib Shamim, Surjit Singh, Pradeep Dwivedi, Surender Deora, Shoban Babu Varthya","doi":"10.2174/011573403X332671241121063641","DOIUrl":"https://doi.org/10.2174/011573403X332671241121063641","url":null,"abstract":"<p><p>Cardiovascular-kidney-metabolic (CKM) syndrome is the association between obesity, diabetes, CKD (chronic kidney disease), and cardiovascular disease. GDF-15 mainly acts through the GFRAL (Glial cell line-derived neurotrophic factor Family Receptor Alpha-Like) receptor. GDF-15 and GDFRAL complex act mainly through RET co-receptors, further activating Ras and phosphatidylinositol-3-kinase (PI3K)/Akt pathways through downstream signaling. GDF-15 decreases cardiac dysfunction and hypertrophy by inducing HIF-α (hypoxia-inducible factor-1α). It causes increased fractional shortening and a significant decrease in ventricular dilation through the induction of the SMAD 2/3. GDF-15 prevents hyperglycemia-induced apoptosis in diabetes mellitus. GDF-15 causes anorexia by influencing the central systems regulating metabolism and appetite. Therefore, targeting GDF-15 can be useful for the treatment of anorexia caused by cancer as well as the prevention of resulting weight loss. GDF-15 has an important role in predicting mortality in acute kidney injury. Its high levels are related to eGFR decline and also have a prognostic role in CKD patients. Growth differentiation factor-15 (GDF-15) is a vital biomarker for diagnosis, treatment, and prognosis of CKM syndrome. Elevated GDF-15 levels can be utilised as a biomarker to determine the suitable metformin dosage. In light chain amyloidosis, a raised level of GDF-15 predicts early death in heart failure and renal disease patients. In vivo, studies using GDF-15 analogs and antibodies against GFRAL to affect metabolic parameters and ventricular dilatation have shown potential for GDF-15-based therapeutic interventions. This review aims to study the role of GDF-15 in CKM syndrome and establish it as a CKM biomarker.</p>","PeriodicalId":10832,"journal":{"name":"Current Cardiology Reviews","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142946064","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":"Successful Use of Proprotein Convertase Subtilisin/Kexin Type 9 Inhibitors in Hypertriglyceridemia-induced Acute Pancreatitis: A Case Report.","authors":"Rundi Qi, Hailei Liu, Xin Li, Minglong Chen","doi":"10.2174/011573403X343784241115055037","DOIUrl":"https://doi.org/10.2174/011573403X343784241115055037","url":null,"abstract":"<p><strong>Background: </strong>Managing hypertriglyceridemia-induced acute pancreatitis (HTG-AP) can be challenging, particularly due to the need for rapid triglyceride reduction to below 500mg/dL (5.645mmol/L).</p><p><strong>Case report: </strong>This is a case describing a 39-year-old female patient who presented to the Emergency Department with acute abdominal pain resulting from severe HTG-AP. However, under conventional therapy with oral lipid-lowering drugs, the triglyceride levels remained uncontrolled. Oral moderate-intensity statins could not only reduce low-density lipoprotein cholesterol (LDLc) by 25%-50%. However, increasing the dose could not further reduce blood lipids while increasing the risk of liver damage. After the administration of proprotein convertase subtilisin/ kexin type 9 inhibitor (PCSK9i), the triglyceride levels were well controlled with no additional side effects, and the symptoms of the patients were completely relieved.</p><p><strong>Conclusions: </strong>In cases of unsatisfactory lipid control under conventional therapy, PCSK9i may offer a viable option for managing HTG-AP.</p>","PeriodicalId":10832,"journal":{"name":"Current Cardiology Reviews","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142946067","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 Intersection of Heart Failure and Iron Deficiency Anemia: Diagnostic and Therapeutic Approaches.","authors":"Maleesha Bw Thammitage, Naji Moussa, Ali Rezvani, Damandeep Kaur Dhillon, Miryam Lisseth Obando Gamarra, Kanwaraj Singh, Abdul Hawwa, Alejandra Felix Vincente, Sehajpreet Kaur, Kiranmayee Seshasai Nemalapuri, Devika Poonwassie, Manju Rai","doi":"10.2174/011573403X331380241111091452","DOIUrl":"10.2174/011573403X331380241111091452","url":null,"abstract":"<p><p>Iron deficiency anemia (IDA) is highly prevalent among individuals with heart failure (HF), impacting 40-70% of patients and serving as a significant prognostic indicator. Linked with oxidative metabolism and myocardial cell damage, IDA exacerbates HF symptoms, including reduced exercise capacity, diminished quality of life, and heightened cardiovascular morbidity. This review explores the diagnosis, treatment, clinical outcomes, prognostic indicators, and forthcoming challenges associated with IDA in HF patients. Crucially, addressing IDA in HF is critical for enhancing prognosis, including clinical outcomes, quality of life, hospitalizations, and survival rates. While oral iron therapy shows efficacy in reducing mortality and hospitalizations, it falls short in improving exercise capacity and quality of life, often deterring patients due to side effects. In contrast, intravenous (IV) iron therapy is highly effective in enhancing hematological parameters, functional capacity, and reducing HF hospitalizations. Optimizing IV iron dosing based on individual patient characteristics is essential for balancing treatment efficacy and adverse effects. Emphasizing individualized approaches, with IV iron emerging as a superior option, underscores the necessity for ongoing research to refine dosing strategies and explore novel therapies. Compliance remains paramount for positive outcomes with IDA treatment, with oral supplementation being cost-effective and easily accessible. However, parenteral supplementation proves beneficial for patients intolerant to oral therapy. Addressing IDA through tailored interventions, including oral or parenteral supplementation, is pivotal in averting complications and improving outcomes in HF patients. This paper consolidates insights into the diagnosis, treatment, impact, pathophysiology, clinical outcomes, research gaps, and future directions concerning IDA in HF patients, drawing on extensive literature to offer a comprehensive understanding of this critical issue.</p>","PeriodicalId":10832,"journal":{"name":"Current Cardiology Reviews","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142946069","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":"Identifying Biomarkers for Atherosclerosis via Gene Expression and Biological Networking.","authors":"Sangeeta Chhotaray, Soumya Jal","doi":"10.2174/011573403X340118241113025519","DOIUrl":"https://doi.org/10.2174/011573403X340118241113025519","url":null,"abstract":"<p><strong>Background: </strong>Atherosclerosis is a chronic disease caused by the accumulation of lipids, inflammatory cells, and fibrous elements in arterial walls, leading to plaque formation and cardiovascular conditions like coronary artery disease, stroke, and peripheral arterial disease. Factors like hyperlipidemia, hypertension, smoking, and diabetes contribute to its development. Diagnosis relies on imaging and biomarkers, while management includes lifestyle modifications, pharmacotherapy, and surgical interventions. Computational biology is transforming biological knowledge into clinical practice by identifying biomarkers that can predict clinical outcomes. This involves omics data, predictive modeling, and data integration. Statistical analysis-based methods are also being developed to develop and integrate methods for screening, diagnosing, and prognosing atherosclerosis.</p><p><strong>Methodology: </strong>The present work aimed to uncover critical genes and pathways to enhance the understanding of the mechanism of atherosclerosis. GSE23746 was analyzed to find differentially expressed genes (DEGs) using 19 control samples and 76 atherosclerotic samples.</p><p><strong>Result: </strong>A total of 76 DEGs were identified. Analysed DEGs using Gene Ontology (GO) and Kyoto Encyclopaedia of Genes and Genomes (KEGG) to generate enrichment datasets. A Protein- Protein Interaction (PPI) network of DEGs was created utilizing the Search Tool for the Retrieval of Interacting Genes (STRING).</p><p><strong>Conclusion: </strong>Ten hub genes, namely EGR1, PTGS2, TNF, NFKBIA, CXCL8, TNFAIP3, CCL3, IL1B, PTPRC, and CD83, were found to be significantly linked to atherosclerosis. Furthermore, the metabolic pathway analysis through KEGG and STRING provides potential targets for therapeutic interventions through HUB genes to diagnose the illness at an early stage, which aids in the reduction of cardiovascular risk. From risk factor profiling to the discovery of novel biomarkers, several components such as phospholipids, ANGPTL3, LCAT, and the proteinencoded OCT-1 gene, play a vital role in crucial processes. These compounds are potential therapeutic targets for early diagnosis of atherosclerotic lesions and future novel biomarkers.</p>","PeriodicalId":10832,"journal":{"name":"Current Cardiology Reviews","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142946061","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":"Unlocking the Potential: Phytoestrogens and Cardiovascular Health.","authors":"Arvind Gulati, Himanshi Banker, Alina Amin Muhammad, Fnu Anamika, Rohit Jain","doi":"10.2174/011573403X333952241203050033","DOIUrl":"https://doi.org/10.2174/011573403X333952241203050033","url":null,"abstract":"<p><p>Phytoestrogens are plant-derived compounds resembling human estrogen and have recently gained attention due to their potential role in improving cardiovascular health. These compounds exert their effects through various mechanisms, including interactions with estrogen receptors, growth factor receptors, inflammatory mediators, thrombogenic reactions, and apoptotic pathways. This results in cardioprotective effects like modulating endothelial function, decreasing vessel tone, reducing inflammation, altering lipid profiles, and influencing arrhythmogenesis. Recent studies indicate the intricate and multidimensional association between phytoestrogens and cardiovascular disease. Despite the overwhelming evidence that phytoestrogen intake lowers the risk of myocardial infarction (MI), prevents atherosclerosis, improves cardiac function, prevents hypertension, and reduces the risk of arrhythmias, there have been studies that show contradictory outcomes. For this reason, the therapeutic use of phytoestrogens for the treatment of cardiovascular diseases, which appears to be extremely promising, should be handled cautiously, considering the individual variances, dosage, and the specific components of phytoestrogens. This review consolidates findings on the effects of phytoestrogens on the heart and blood vessels, explores the mechanisms behind these interactions, and seeks to determine the best methods for using phytoestrogens as a supplement in managing and preventing cardiovascular disease. By understanding these aspects, we can better evaluate the potential of phytoestrogens in cardiovascular health and develop guidelines for their safe and effective use.</p>","PeriodicalId":10832,"journal":{"name":"Current Cardiology Reviews","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142930847","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":"Serum Cortisol and Cardiovascular Disease Risk-A Potential Biomarker.","authors":"Wei Jet Oo, Chooi Ling Lim, Mun Hon Goh, Rhun Yian Koh","doi":"10.2174/011573403X328499241106064553","DOIUrl":"https://doi.org/10.2174/011573403X328499241106064553","url":null,"abstract":"<p><p>Cardiovascular Disease [CVD], the leading cause of death globally, poses a significant burden on the healthcare sector. Its association with stress and Cushing's Syndrome has driven cortisol, the 'stress hormone,' to be a potential candidate in determining CVD risk. Cortisol synthesis and release through the hypothalamic-pituitary-adrenal [HPA] axis are regulated by several hormones and receptors involved in the pathological cascade towards CVD. Evidence suggests that metabolic syndrome plays a major role in cortisol-mediated CVD risk. On the other hand, non-metabolic features are also implicated when the association between cortisol and CVD risk remains significant upon normalisation of metabolic parameters. Correspondingly, the treatment for hypercortisolism is often found effective in lowering CVD risk. Despite available evidence, several factors continue to hinder the clinical use of cortisol as a risk biomarker for CVD. This review provides an insight into the role of serum cortisol in CVD progression and risk, with emphasis on the mechanistic features and parameters.</p>","PeriodicalId":10832,"journal":{"name":"Current Cardiology Reviews","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142926501","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}