Journal of receptor and signal transduction research最新文献_第3页

Structure-based identification of triazole-based PARP1 inhibitors: insights from docking and molecular dynamics simulations. 基于结构的三唑类PARP1抑制剂鉴定：来自对接和分子动力学模拟的见解

IF 2.3

Journal of receptor and signal transduction research Pub Date : 2025-12-12 DOI: 10.1080/10799893.2025.2598534

Hardha Balachandran, Gowramma Byran, Veera Venkata Satyanarayana Reddy Karri, Senthil Kumar Murugesan, Kalirajan Rajagopal

{"title":"Structure-based identification of triazole-based PARP1 inhibitors: insights from docking and molecular dynamics simulations.","authors":"Hardha Balachandran, Gowramma Byran, Veera Venkata Satyanarayana Reddy Karri, Senthil Kumar Murugesan, Kalirajan Rajagopal","doi":"10.1080/10799893.2025.2598534","DOIUrl":"https://doi.org/10.1080/10799893.2025.2598534","url":null,"abstract":"Background: Poly (ADP-ribose) polymerase 1 (PARP1) is a critical enzyme involved in DNA repair mechanisms, making it a promising target for anticancer drug development. Triazole derivatives have shown potential as PARP1 inhibitors, but systematic evaluation of a large library remains limited.Objective: To perform comprehensive in silico screening and molecular dynamics simulations of 180 triazole derivatives to identify potent PARP1 inhibitors and evaluate their binding stability and interaction profiles.Methods: A library of 180 triazole derivatives was subjected to molecular docking against the active site of PARP1 using [Schrodinger suite 2024-4]. Top-ranking compounds based on binding affinity were selected for further molecular dynamics (MD) simulations using to assess the stability of the ligand-protein complexes over a 100 ns simulation period. Binding free energies were calculated using MM-GBSA approaches. Key protein-ligand interactions were analyzed to elucidate binding mechanisms.Results: Docking results identified 10 triazole derivatives with superior binding affinities -9.4 to -5.5 kcal/mol compared to reference inhibitors. MD simulations confirmed stable binding conformations with root mean square deviation (RMSD) fluctuations within acceptable limits. Interaction analysis highlighted crucial hydrogen bonds and hydrophobic contacts with catalytic residues of PARP1.Conclusion: The integrated in silico screening and molecular dynamics simulation approach successfully identified promising triazole derivatives as potential PARP1 inhibitors. These findings provide valuable insights for the rational design and optimization of novel anticancer agents targeting PARP1.","PeriodicalId":520688,"journal":{"name":"Journal of receptor and signal transduction research","volume":" ","pages":"1-13"},"PeriodicalIF":2.3,"publicationDate":"2025-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145746544","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}

引用次数: 0

ZC3H13-induced KLRB1 upregulation relieves the injury of myocardial infarction through N [6]-methyladenosine methylation. zc3h13诱导的KLRB1上调通过N[6]-甲基腺苷甲基化减轻心肌梗死损伤。

IF 2.3

Journal of receptor and signal transduction research Pub Date : 2025-12-01 Epub Date: 2025-11-01 DOI: 10.1080/10799893.2025.2582097

Juan Zhou, Shun Zhang

{"title":"ZC3H13-induced KLRB1 upregulation relieves the injury of myocardial infarction through N [6]-methyladenosine methylation.","authors":"Juan Zhou, Shun Zhang","doi":"10.1080/10799893.2025.2582097","DOIUrl":"10.1080/10799893.2025.2582097","url":null,"abstract":"Myocardial infarction (MI) is caused by blocked blood flow that leads to tissue damage and impaired cardiac function. This study explored the function and mechanism of Killer Cell Lectin-Like Receptor B1 (KLRB1) in MI, and examined how n6-methyladenosine (m6A) modification regulates its function. The expressions of KLRB1 in MI cell model was evaluated using qRT-PCR and western blotting. The effect of KLRB1 on MI injury was assessed in both cell and animal models. In cell model, cell viability, apoptosis, and inflammation were evaluated using CCK-8, flow cytometry, and enzyme-linked immunosorbent assay (ELISA). In animal model, cardiac function, infract area, structure, apoptosis, injury marker, and inflammation were examined through echocardiography, 2,3,5-Triphenyltetrazolium chloride (TTC) staining, hematoxylin and eosin (H&E) staining, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), and ELISA. The relationship between KLRB1 and ZC3H13 was explored using qRT-PCR, western blotting, and methylated RNA immunoprecipitation (MeRIP) assay. KLRB1 showed substantial downregulation in MI. KLRB1 was downregulated in MI, and its overexpression enhanced cell viability, reduced apoptosis and inflammation, and improved infarct size and tissue structure in vivo. ZC3H13 was downregulated in MI. ZC3H13 was downregulated in the MI, and its overexpression increased KLRB1 mRNA and protein levels via regulating KLRB1 m6A modification. In conclusion, these findings suggest that KLRB1 alleviates the MI injury, and ZC3H13 induces the upregulation of KLRB1 through m6A modification. These results may provide insight into the ZC3H13/KLRB1 axis as a potential therapeutic avenue for reducing myocardial injury and improving cardiac outcomes after MI.","PeriodicalId":520688,"journal":{"name":"Journal of receptor and signal transduction research","volume":" ","pages":"281-290"},"PeriodicalIF":2.3,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145426922","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}

引用次数: 0

Identification of novel lead molecules against the EGFR kinase domain using structure-based virtual screening, molecular docking, and molecular dynamics simulations. 利用基于结构的虚拟筛选、分子对接和分子动力学模拟鉴定抗EGFR激酶结构域的新型先导分子。

IF 2.3

Journal of receptor and signal transduction research Pub Date : 2025-12-01 Epub Date: 2025-11-23 DOI: 10.1080/10799893.2025.2590462

Mythreyi Jannu, Umakanth Naik Vankadoth, Umamaheswari Amineni, Rajeswari Jinka

{"title":"Identification of novel lead molecules against the EGFR kinase domain using structure-based virtual screening, molecular docking, and molecular dynamics simulations.","authors":"Mythreyi Jannu, Umakanth Naik Vankadoth, Umamaheswari Amineni, Rajeswari Jinka","doi":"10.1080/10799893.2025.2590462","DOIUrl":"10.1080/10799893.2025.2590462","url":null,"abstract":"Epidermal growth factor receptor (EGFR) is a transmembrane protein belonging to the receptor tyrosine kinase (RTK) superfamily, reported as a promising anticancer target in treating diverse malignancies. Previous studies on microarray gene expression and methylation status in cell and animal models revealed the differential expression of EGFR at the early stages of cellular transformation. Additionally, an unpublished study of methylation analysis of EGFR gene promoters conducted in human cancer-related samples showed a several-fold increase in EGFR gene expression, suggesting epigenetic upregulation in tumors. Considering these findings, in the present study, we selected inactive (DFGout) (D: aspartic acid, F: phenylalanine, G: glycine) and active (DFGin) confirmations of EGFR to identify novel lead molecules against aberrant EGFR activity in cancer. Extra precision (XP) docking, molecular mechanics/generalized born surface area (MM/GBSA), molecular dynamics (MD) simulations, and ADME/T were performed, and the results showed that the lead 1 molecule of each target exhibited a better binding affinity and favorable stability than the existing ligands.","PeriodicalId":520688,"journal":{"name":"Journal of receptor and signal transduction research","volume":" ","pages":"291-304"},"PeriodicalIF":2.3,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145592758","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}

引用次数: 0

Targeting ubiquitin-specific peptidase 22 (USP22) as a nexus for drug repurposing in anticancer therapeutic development. 靶向泛素特异性肽酶22 （USP22）在抗癌治疗发展中的作用。

IF 2.3

Journal of receptor and signal transduction research Pub Date : 2025-10-01 Epub Date: 2025-08-23 DOI: 10.1080/10799893.2025.2548246

Saad Ali Alshehri, Abdulrhman Alsayari, Mohammad Abohassan, Mohammad Ali Abdullah Almoyad, Shadma Wahab

{"title":"Targeting ubiquitin-specific peptidase 22 (USP22) as a nexus for drug repurposing in anticancer therapeutic development.","authors":"Saad Ali Alshehri, Abdulrhman Alsayari, Mohammad Abohassan, Mohammad Ali Abdullah Almoyad, Shadma Wahab","doi":"10.1080/10799893.2025.2548246","DOIUrl":"10.1080/10799893.2025.2548246","url":null,"abstract":"Ubiquitin-specific peptidase 22 (USP22) has emerged as a promising target in cancer research because of its pivotal role in tumor progression, metastasis, and therapy resistance. USP22 is frequently overexpressed in multiple malignancies and facilitates essential cellular processes, including DNA repair, cell cycle regulation, and cancer stem cell (CSC) maintenance. The strength of these attributes makes it an attractive candidate for therapeutic intervention. Despite the advances in conventional cancer treatment, recurrent and resistant USP22-overexpressing tumors demand novel treatment strategies. Drug repurposing is a cost-effective and efficient approach to overcome this challenge by taking advantage of FDA-approved drugs, wherein the safety profiles of used drugs are known for different therapeutic uses. To identify potential repurposed USP22 inhibitors, this study used an integrated computational workflow consisting of molecular docking and molecular dynamics (MD) simulations. The virtual screening of FDA-approved compounds from DrugBank revealed that Ergotamine showed high binding affinities and specific interactions with the USP22 binding pocket. Pharmacokinetic evaluations demonstrate that Ergotamine has an appropriate drug profile and biological activities in anticancer interventions. The stability and conformational dynamics of the USP22-Ergotamine complex were investigated by all-atom MD simulations for 300 ns. The robustness of these interactions was verified in these simulations and MM/PBSA, and insights into the molecular mechanisms that underlie their ability to inhibit USP22 were provided. Our findings reveal a potentially promising role for Ergotamine as a repurposed USP22 inhibitor that would be worthwhile to validate experimentally for therapeutic development against cancer.","PeriodicalId":520688,"journal":{"name":"Journal of receptor and signal transduction research","volume":" ","pages":"269-280"},"PeriodicalIF":2.3,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144985935","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}

引用次数: 0

N-methyl-d-aspartate receptor is involved in the progression of anxiety disorders with thyroid tumors. n -甲基-d-天冬氨酸受体参与甲状腺肿瘤伴焦虑障碍的进展。

IF 2.3

Journal of receptor and signal transduction research Pub Date : 2025-10-01 Epub Date: 2025-07-31 DOI: 10.1080/10799893.2025.2540309

Meilan Su, Yuan Chang, Xiaoting Wu, Qinglin Wang, Song Wang

{"title":"N-methyl-d-aspartate receptor is involved in the progression of anxiety disorders with thyroid tumors.","authors":"Meilan Su, Yuan Chang, Xiaoting Wu, Qinglin Wang, Song Wang","doi":"10.1080/10799893.2025.2540309","DOIUrl":"10.1080/10799893.2025.2540309","url":null,"abstract":"Background: Anxiety disorders (ADs) and thyroid tumors (TTs) are prevalent and frequently co-occur. Previous studies suggest that the N-methyl-d-aspartate receptor (NMDAR) may play a role in their co-occurrence, but the understanding of their relationship is not comprehensive. The aim of this study was to investigate the role of NMDAR in the progression of animal models of AD with TT.Methods: We developed an animal model of AD with TT in Balb/c mice using chronic unpredictable mild stress (CUMS) combined with subcutaneous IHH4 cell xenotransplantation. Mice were treated with d-serine and MK-801 to assess behavioral changes and tumor growth. The expression of NMDAR subunits in the thyroid and transplanted TT tissues was also analyzed.Results: The combination of CUMS and IHH4 cell xenotransplantation helped successfully create an AD with TT model, which exhibited stable anxiety-like behavior, a high tumor formation rate, and ease of implementation. d-Serine alleviated anxiety behaviors but increased NR2A subunit activity in both thyroid and TT tissues, disrupted the normal structure of the thyroid, and accelerated TT growth. In contrast, MK-801 had the opposite effect.Conclusions: NMDAR, particularly the NR2A subunit, plays a crucial role in TT progression associated with AD. In the clinical drug selection for the patients with ADs with concomitant TT, special attention should be paid to the two-sidedness of drugs. The CUMS and IHH4 xenotransplantation model is an effective tool for studying AD with TT.","PeriodicalId":520688,"journal":{"name":"Journal of receptor and signal transduction research","volume":" ","pages":"259-268"},"PeriodicalIF":2.3,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144755574","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}

引用次数: 0

Orphan G-protein coupled receptor 75 (GPR75), a unique and controversial potential therapeutic target. 孤儿g蛋白偶联受体75 (GPR75)，一个独特的和有争议的潜在治疗靶点。

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Journal of receptor and signal transduction research Pub Date : 2025-10-01 Epub Date: 2025-08-04 DOI: 10.1080/10799893.2025.2541777

Teodora Stratulat, Alexandru Babes, Sorin Tunaru

引用次数: 0

The role of G protein-coupled receptor 4 in inflammatory diseases and its potential clinical significance. G蛋白偶联受体4在炎症性疾病中的作用及其潜在的临床意义

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Journal of receptor and signal transduction research Pub Date : 2025-08-01 Epub Date: 2025-07-06 DOI: 10.1080/10799893.2025.2529174

Qilimuge Bai, Gegentuya Bao, Yali Yan, Saqirina Hereid, Xiaohong Bai, Liang Bao

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Paradoxical action of zolpidem: interplay between dysregulation of the synergetic actions of γ-aminobutyric acid type A receptors and neuronal cotransporters (KCC2/NKCC1). 唑吡坦的矛盾作用：γ-氨基丁酸A型受体和神经元共转运蛋白（KCC2/NKCC1）协同作用失调之间的相互作用。

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Journal of receptor and signal transduction research Pub Date : 2025-08-01 Epub Date: 2025-07-21 DOI: 10.1080/10799893.2025.2530105

Ahmad Tarmizi Che Has, Fatin H Mohamad, Muhammad Zulfadhli Othman, Khairul Bariyyah Abd Halim

{"title":"Paradoxical action of zolpidem: interplay between dysregulation of the synergetic actions of γ-aminobutyric acid type A receptors and neuronal cotransporters (KCC2/NKCC1).","authors":"Ahmad Tarmizi Che Has, Fatin H Mohamad, Muhammad Zulfadhli Othman, Khairul Bariyyah Abd Halim","doi":"10.1080/10799893.2025.2530105","DOIUrl":"10.1080/10799893.2025.2530105","url":null,"abstract":"Zolpidem, or commercially known as Ambien or Stilnox, is a sedative-hypnotic agent, which is usually prescribed to manage sleeping difficulties in individuals with insomnia. The site of its sedative-hypnotic action is the γ-aminobutyric acid type A receptor, which it shares with benzodiazepines. However, this substance has been consistently associated to awaken patients with brain injuries such as trauma, stroke, disorders of consciousness and has also been expanded to the recovery of brain function in the event of hypoxic damage, cerebrovascular ischemic injury, infection of the central nervous system, toxins and poisoning, degenerative diseases, tumors, and congenital disorders. Aside from that, the effect has been observed in a wide spectrum of neurological diseases, from movement disorders such as Parkinson's disease and dystonia to neurological deficits and anaphylactic hypoxia. The wide spectrum of injuries and disorders reported poses a challenge in investigating the exact mechanisms of action underlying the awakening effect. Therefore, the main question is how it is possible for a substance originally intended as a sedative-hypnotic agent to induce an awakening effect? In this review, we discuss the synergetic roles of GABAA receptors, which are the target receptor for zolpidem, along with neuronal cation-Cl- co-transporters KCC2/NKCC1 in regulating the inhibitory nature of the GABAergic transmission in brain injury, which might explain the awakening effect of zolpidem in brain injuries.","PeriodicalId":520688,"journal":{"name":"Journal of receptor and signal transduction research","volume":" ","pages":"220-229"},"PeriodicalIF":2.3,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144677199","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}

引用次数: 0

A novel anticancer candidate, coumarin-3-carboxamide derivative inhibits cell proliferation and migration in MDA-MB-231 cell line. 香豆素-3-羧酰胺衍生物是一种新的抗癌候选物质，可抑制MDA-MB-231细胞株的细胞增殖和迁移。

IF 2.3

Journal of receptor and signal transduction research Pub Date : 2025-08-01 Epub Date: 2025-06-02 DOI: 10.1080/10799893.2025.2513696

Sevide Sencan, Hulya Celik Onar

{"title":"A novel anticancer candidate, coumarin-3-carboxamide derivative inhibits cell proliferation and migration in MDA-MB-231 cell line.","authors":"Sevide Sencan, Hulya Celik Onar","doi":"10.1080/10799893.2025.2513696","DOIUrl":"10.1080/10799893.2025.2513696","url":null,"abstract":"Breast cancer is one of the leading cancer types in terms of morbidity and mortality worldwide. Although developing technology, early diagnosis and treatment opportunities provide positive contributions to the treatment of breast cancer, research on new drugs that are less toxic to healthy cells, safer and more effective for cancer cells, increasing the quality of life of the patient is still ongoing. Coumarin and its derivatives have been shown great interest to develop safer and more effective anticancer drugs. Therefore, we investigated the anticancer activity of novel coumarin-3-carboxamide derivative 3i in MDA-MB-231 cells. We found that coumarin-3-carboxamide derivative 3i inhibited cell proliferation, colony formation and migration. However, coumarin-3-carboxamide derivative 3i did not induce apoptosis and autophagy. Consequently, our findings suggest for the first time that novel coumarin-3-carboxamide 3i has anticancer activity and may be an important drug candidate for the treatment of triple-negative breast cancer. Further investigations are required to elucidate its impact on breast cancer.","PeriodicalId":520688,"journal":{"name":"Journal of receptor and signal transduction research","volume":" ","pages":"230-236"},"PeriodicalIF":2.3,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144201330","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}

引用次数: 0

Preeclamptic plasma disrupts endothelial function and promotes inflammation in endothelial cells: beneficial effects of glibenclamide and MCC950 in this scenario. 子痫前期血浆破坏内皮功能并促进内皮细胞炎症：格列本脲和MCC950在这种情况下的有益作用

IF 2.3

Journal of receptor and signal transduction research Pub Date : 2025-08-01 Epub Date: 2025-07-21 DOI: 10.1080/10799893.2025.2535579

Karoliny Nune Santos, Juliana Q Bizzotto, Thainá O Bueno-Pereira, Mariana Romao-Veiga, Vanessa R Ribeiro-Vasques, Larissa Ragozo Cardoso Oliveira, Valéria C Sandrim, Priscila R Nunes

{"title":"Preeclamptic plasma disrupts endothelial function and promotes inflammation in endothelial cells: beneficial effects of glibenclamide and MCC950 in this scenario.","authors":"Karoliny Nune Santos, Juliana Q Bizzotto, Thainá O Bueno-Pereira, Mariana Romao-Veiga, Vanessa R Ribeiro-Vasques, Larissa Ragozo Cardoso Oliveira, Valéria C Sandrim, Priscila R Nunes","doi":"10.1080/10799893.2025.2535579","DOIUrl":"10.1080/10799893.2025.2535579","url":null,"abstract":"Preeclampsia (PE) is characterized by systemic endothelial dysfunction and remains a significant clinical challenge. Activation of NLRP3 inflammasome, reactive oxygen species (ROS) production, and pyroptosis and autophagy are important mechanisms in this condition. To evaluate the NLRP3 inhibitors effects: glibenclamide (GB) and MCC950, on markers of inflammation, endothelial dysfunction, cell death, and oxidative stress in an in vitro model of PE. Plasma from pregnant women with PE and normotensive pregnant women (NT) was used to investigate its impact on NLRP3 inflammasome activation (NLRP3, TLR4, MyD88, and caspase-1) in endothelial cells (ECs), analyzed by Western Blotting; effects of pharmacological inhibition on the function of ECs was assessed by the evaluation of permeability (VE-cadherin) and markers of endothelial dysfunction by flow cytometry (Flt-1, VEGFR2, E-selectin, VCAM-1, and ICAM-1), as well as cytotoxicity measured by lactate dehydrogenase (LDH), oxidative stress (ROS, nitric oxide - NO and antioxidant capacity), autophagy, and pyroptosis (interleukin IL-1β and high-mobility group box one - HMGB1). Both GB and MCC950 reduced NLRP3 inflammasome activation and its related effects in ECs exposed to PE plasma, including lowered IL-1β, caspase-1, modulated adhesion molecules expression, as well as decreased ROS and cytotoxicity. GB increased NO and restored VE-cadherin expression, while MCC950 enhanced antioxidant capacity. GB also induced autophagy, unlike MCC950. The NLRP3 inhibitors showed the potential to mitigate endothelial dysfunction, oxidative stress, and inflammation, suggesting both compounds hold potential therapeutic value for PE through distinct mechanisms.","PeriodicalId":520688,"journal":{"name":"Journal of receptor and signal transduction research","volume":" ","pages":"237-249"},"PeriodicalIF":2.3,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144677200","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}

引用次数: 0