Exploration of medicine最新文献

{"title":"Impact exerted by scaffolds and biomaterials in periodontal bone and tissue regeneration engineering: new challenges and perspectives for disease treatment","authors":"S. Santonocito, S. Ferlito, Alessandro Polizzi, V. Ronsivalle, G. Reitano, A. Lo Giudice, G. Isola","doi":"10.37349/emed.2023.00135","DOIUrl":"https://doi.org/10.37349/emed.2023.00135","url":null,"abstract":"The periodontium is an appropriate target for regeneration, as it cannot restore its function following disease. Significantly, the periodontium's limited regenerative capacity could be enhanced through the development of novel biomaterials and therapeutic approaches. Notably, the regenerative potential of the periodontium depends not only on its tissue-specific architecture and function but also on its ability to reconstruct distinct tissues and tissue interfaces, implying that the development of tissue engineering techniques can offer new perspectives for the organized reconstruction of soft and hard periodontal tissues. With their biocompatible structure and one-of-a-kind stimulus-responsive property, hydrogels have been utilized as an excellent drug delivery system for the treatment of several oral diseases. Furthermore, bioceramics and three-dimensional (3D) printed scaffolds are also appropriate scaffolding materials for the regeneration of periodontal tissue, bone, and cartilage. This work aims to examine and update material-based, biologically active cues and the deployment of breakthrough bio-fabrication technologies to regenerate the numerous tissues that comprise the periodontium for clinical and scientific applications.","PeriodicalId":72999,"journal":{"name":"Exploration of medicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45075045","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":"Oxidative stress and inflammation: the root causes of aging","authors":"Sobhon Prasert, Savedvanich Gavin, Weerakiet Sawaek","doi":"10.37349/emed.2023.00129","DOIUrl":"https://doi.org/10.37349/emed.2023.00129","url":null,"abstract":"Oxygen free radicals [reactive oxygen species (ROS)] and nitrogen free radicals [reactive nitrogen species (RNS)] are generated by mitochondria during adenosine triphosphate synthesis, and catalytic activities of cytochrome P450, nicotinamide adenine dinucleotide phosphate oxidases (NOXs), cyclooxygenases, and nitric oxide synthases during drug catabolism, phagocytosis, and acute inflammation. Under normal circumstances, low levels of ROS and RNS provide redox signalings that control many essential physiological processes. As age progresses ROS and RNS increase excessively due to dysfunctional mitochondria, dysregulated NOX, and other free-radical generating sources, leading to oxidative stress, which causes oxidation and denaturation of key cellular components including DNA, proteins, and lipids, which become abnormal, constituting damage-associated molecular pattern (DAMP), recognized as ‘non-self’ by immune cells, leading to inflammation which is mediated by nuclear factor kappa B-inflammasome, p38-c-Jun N-terminal kinase and Janus kinase-signal transducer and activator of transcription pathways. DAMPs are continuously released from damaged and senescent cells, causing an otherwise normally transient inflammation turning into systemic chronic inflammation, the root cause of aging and age-associated diseases (AADs). Cells restore redox balance by activating the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway that induces the synthesis and release of antioxidation molecules and enzymes including haem oxygenase-1, which also inhibits the three inflammatory pathways. Furthermore, upregulation of autophagy (AP) can get rid of abnormal molecules, prevent the generation of DAMPs, and attenuate inflammation. Both AP and Nrf2 signalings decrease with age. The upregulations of Nrf2, AP, and downregulation of inflammation are controlled by sensors of energy and stress levels, i.e., adenosine monophosphate-activated protein kinase, silent information regulator 1, and Sestrins, as well as the extracellular matrix, while mammalian targets for rapamycin complex 1, a nutrient sensor, act in the opposite direction. If the balance of these sensor systems becomes dysregulated, aging process accelerates, and the risk of AADs increases.","PeriodicalId":72999,"journal":{"name":"Exploration of medicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41839652","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":"Assessing cardiac contractility in hypertension with heart failure with preserved ejection fraction: the value of left ventricular strain","authors":"S. Rabkin","doi":"10.37349/emed.2023.00128","DOIUrl":"https://doi.org/10.37349/emed.2023.00128","url":null,"abstract":"Aim: Hypertension (HTN) is a major cause of heart failure but the precise pathways by which HTN leads to heart failure are not resolved. Newer echocardiographic techniques permit assessment of myocardial contraction in different orientations defining left ventricular (LV) shortening as percentage longitudinal, circumferential and radial strain.\u0000Methods: A systematic search was conducted of Medline and Embase. The search was conducted from the inception of each database on June 30, 2022. Search terms “left ventricular strain” or speckle tracking AND heart failure with preserved ejection fraction or diastolic dysfunction AND HTN.\u0000Results: Six studies were identified and subject to detailed review. LV ejection fraction (LVEF) was not significantly different in patients with heart failure with preserved ejection fraction (HFpEF) and HTN compared to individuals with or without HTN. Global longitudinal strain (GLS) and global circumferential strain (GCS) were significantly (P < 0.0001) different (lower) in patients with HFpEF and HTN compared to patients with HTN without HFpEF and control individuals without HTN or other conditions. In contrast, global radial strain (GRS) was not significantly (P < 0.054) different in patients with HFpEF and HTN compared to individuals without HTN or other conditions. GRS was significantly (P < 0.01) different in individuals with HFpEF and HTN compared to individuals with HTN.\u0000Conclusions: Assessment of LV strain is an important advance in the assessment of LV function in patients with HTN and HFpEF as it identifies patients with reduced LV strain while there was no difference in LVEF. GLS and GCS provide the best separation between patients with HFpEF and HTN compared to individuals with HTN without HFpEF. This study advances the possibility of redefining the classification of heart function and heart failure for patients with HTN by either classifying patients mainly by LV strain or sub-classifying patients with HTN and HFpEF by LV strain.","PeriodicalId":72999,"journal":{"name":"Exploration of medicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45014638","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":"An overview of current strategies and future prospects in drug repurposing in tuberculosis","authors":"Dilpreet Singh, Amrinder Singh, P. Chawla","doi":"10.37349/emed.2023.00125","DOIUrl":"https://doi.org/10.37349/emed.2023.00125","url":null,"abstract":"A large number of the population faces mortality as an effect of tuberculosis (TB). The line of treatment in the management of TB faces a jolt with ever-increasing multi-drug resistance (DR) cases. Further, the drugs engaged in the treatment of TB are associated with different toxicities, such as renal and hepatic toxicity. Different combinations are sought for effective anti-tuberculosis (anti-TB) effects with a decrease in toxicity. In this regard, drug repurposing has been very promising in improving the efficacy of drugs by enhancement of bioavailability and widening the safety margin. The success in drug repurposing lies in specified binding and inhibition of a particular target in the drug molecule. Different drugs have been repurposed for various ailments like cancer, Alzheimer’s disease, acquired immunodeficiency syndrome (AIDS), hair loss, etc. Repurposing in anti-TB drugs holds great potential too. The use of whole-cell screening assays and the availability of large chemical compounds for testing against Mycobacterium tuberculosis poses a challenge in this development. The target-based discovery of sites has emerged in the form of phenotypic screening as ethionamide R (EthR) and malate synthase inhibitors are similar to pharmaceuticals. In this review, the authors have thoroughly described the drug repurposing techniques on the basis of pharmacogenomics and drug metabolism, pathogen-targeted therapy, host-directed therapy, and bioinformatics approaches for the identification of drugs. Further, the significance of repurposing of drugs elaborated on large databases has been revealed. The role of genomics and network-based methods in drug repurposing has been also discussed in this article.","PeriodicalId":72999,"journal":{"name":"Exploration of medicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41540424","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":"m6 RNA methylation: an emerging common target in the immune response to cancer and severe acute respiratory syndrome-coronavirus-2 infection","authors":"Hiromichi Sato, T. Hara, Chihiro Otsuka, Yasuko Arao, Yoshiko Tsuji, Yumiko Hamano, Mirei Ogita, E. di Luccio, Takaaki Hirotsu, A. Vecchione, Hideshi Ishii","doi":"10.37349/emed.2023.00127","DOIUrl":"https://doi.org/10.37349/emed.2023.00127","url":null,"abstract":"m6A RNA methylation, a predominant type of RNA modification, is involved in regulating mRNA splicing, stability, and translation as well as the interaction between nucleoproteins and noncoding RNAs. Recent studies have revealed that m6A RNA methylation plays a critical role in the self-to-non-self-recognition of immune cells against endogenous mutations in cancer and exogenous organism-related infections. As an epigenetic mechanism, m6A RNA modification induces immune cell signal transduction, which is altered in the tumor microenvironment, as detected in liquid biopsy. Furthermore, m6A RNA methylation-related inflammation is involved in the cellular response to viral infections, including the emerging severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) infection. Given the importance of the immune response in maintaining homeostasis in higher eukaryotes, m6A RNA methylation could be useful not only for the early detection of cancer but also for SARS-CoV-2 screening during a global pandemic.","PeriodicalId":72999,"journal":{"name":"Exploration of medicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42548362","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":"N-type calcium channel blockers: a new approach towards the treatment of chronic neuropathic pain","authors":"Shikha Choudhary, Raminderjit Kaur, Aafrin Waziri, A. Garg, R. Kadian, M. Alam","doi":"10.37349/emed.2023.00126","DOIUrl":"https://doi.org/10.37349/emed.2023.00126","url":null,"abstract":"Neuropathic pain (NP) remains maltreated for a wide number of patients by the currently available treatments and little research has been done in finding new drugs for treating NP. Ziconotide (PrialtTM) had been developed as the new drug, which belongs to the class of ω-conotoxin MVIIA. It inhibits N-type calcium channels. Ziconotide is under the last phase of the clinical trial, a new non-narcotic drug for the management of NP. Synthetically it has shown the similarities with ω-conotoxin MVIIA, a constituent of poison found in fish hunting snails (Conus magus). Ziconotide acts by selectively blocking neural N-type voltage-sensitized Ca2+ channels (NVSCCs). Certain herbal drugs also have been studied but no clinical result is there and the study is only limited to preclinical data. This review emphasizes the N-type calcium channel inhibitors, and their mechanisms for blocking calcium channels with their remedial prospects for treating chronic NP.","PeriodicalId":72999,"journal":{"name":"Exploration of medicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42125798","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":"Oxidative stress, inflammation, dysfunctional redox homeostasis and autophagy cause age-associated diseases","authors":"P. Sobhon, Gavin Savedvanich, S. Weerakiet","doi":"10.37349/emed.2023.00124","DOIUrl":"https://doi.org/10.37349/emed.2023.00124","url":null,"abstract":"Aging and age-associated diseases (AADs) are growing risk factors in societies worldwide. During aging, there is an accumulation of excessive oxygen free radicals [reactive oxygen species (ROS)] and nitrogen free radicals [reactive nitrogen species (RNS)] due to dysfunctional mitochondria, dysregulated catalytic activities of cytochrome P450 (CYP), nicotinamide adenine dinucleotide (NAD) phosphate [NADP(H)] oxidase (NOX), cyclooxygenases, and nitric oxide synthases (NOS) over the threshold of physiological levels, creating oxidative stress (OS). Excessive ROS and RNS oxidize, break, denature, and sometimes cause aggregations of key cellular components including DNA, proteins, and lipids. Normally, these denatured molecules and their aggregates are eliminated by autophagy (AP) and ubiquitin-proteosome system (UPS). However, these two proteostatic mechanisms are impaired as age progresses. As a result, these abnormal molecules turn into damage-associated molecular patterns (DAMPs), recognized as non-self by immune cells, leading to systemic chronic inflammation (SCI), which together with OS are the major causes of aging and AADs. Therefore, instead of trying to prevent and cure AADs individually, the logical approach should be the restoration of redox homeostasis by the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway which can prevent the damaging effect of OS and the upregulation of AP and UPS to eliminate DAMPs, and together they attenuate SCI to lessen the effect of inflammation. The central regulators, adenosine monophosphate-activated protein kinase (AMPK), sirtuin 1 (SIRT1), and Sestrins, synergistically control the restoration of the redox homeostasis by activating Nrf2, the upregulation of AP-UPS, and the inhibition of SCI. The activation of these central regulators can be achieved by exercise, caloric restriction (CR), and intakes of certain CR mimetic natural compounds. Consequently, the activations of these regulators may lead to the prevention and/or attenuation of the AADs.","PeriodicalId":72999,"journal":{"name":"Exploration of medicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45339039","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 docking analysis of peptide-based antiviral agents against SARS-CoV-2 main protease: an approach towards drug repurposing","authors":"A. Chaurasiya, Abhimannu Shome, P. Chawla","doi":"10.37349/emed.2023.00123","DOIUrl":"https://doi.org/10.37349/emed.2023.00123","url":null,"abstract":"Aim:\u0000\u0000Utilizing the therapeutic potentials of previously approved medications against a new target or pharmacological response is known as drug repurposing. The health and scientific communities are under continual pressure to discover new compounds with antiviral potential due to the rising reports of viral resistance and the occurrence and re-emergence of viral outbreaks. The use of antiviral peptides has emerged as an intriguing option in this search. Here, this article includes the current United States Food and Drug Administration (FDA)-approved antiviral peptides that might be enforced for the treatment of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and carried out docking study of the viral protease inhibitors.\u0000Methods:\u0000\u0000In silico techniques like molecular docking was carried out using Autodock Vina software.\u0000Results:\u0000\u0000The molecular docking studies of peptide-based antiviral agents against SARS-CoV-2 [Protein Data Bank (PDB) ID: 7P35] using docking software AutoDockTools 1.5.6. Among all the docked ligands, compound velpatasvir showed interaction with residues ILE213, GLN256, LEU141, GLN189, GLU166, HIS41, CYS145, and ASN142, and displayed the highest docking score of –8.2 kcal/mol. This medication could be a novel treatment lead or candidate for treating SARS-CoV-2.\u0000Conclusions:\u0000\u0000To conclude, a docking study of peptide based antiviral compounds for their binding mode in the catalytic domain of SARS-CoV-2 receptor is reported. On molecular docking, the compounds have showed remarkable binding affinity with the amino acids of receptor chain A. The compounds occupied the same binding cavity as the reference compound maintaining the interactions with conserved amino acid residues essential for significant inhibitory potential, especially for compound velpatasvir with binding score of –8.2 kcal/mol.","PeriodicalId":72999,"journal":{"name":"Exploration of medicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48024197","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":"Disparities and trends in suicidal ideations for inflammatory bowel disease hospitalizations: a decade-long national database analysis","authors":"Hassam Ali, Pratik Patel, R. Dhillon, Shiza Sarfraz, S. Poola, L. Smith-Martinez, Karina Fatakhova, R. Rajapakse","doi":"10.37349/emed.2023.00122","DOIUrl":"https://doi.org/10.37349/emed.2023.00122","url":null,"abstract":"Aim: Patients with inflammatory bowel disease (IBD) are more likely to develop anxiety or depression. The study aimed to describe the trends and disparities of suicidal ideation (SI) in hospitalized IBD patients.\u0000Methods: A retrospective study was conducted using the National Inpatient Sample (NIS) database, to analyze SI among the IBD hospitalizations from 2009 to 2019. Bivariate analysis was conducted using a chi-square test for categorical variables and an independent t-test for continuous variables. For prevalence, the trend over time was evaluated using the score test.\u0000Results: There were 1,724 IBD hospitalizations with SI for the study period. There was a male (53.8%) and white race (74.2%) predominance. The mean age was 41.47 ± 0.25 years. The hospital stay decreased for IBD hospitalizations with SI from 7.97 days in 2009 to 7.57 days in 2019 (P < 0.001). The mean hospital charge increased from $44,664 in 2009 to $66,639 in 2019 (P < 0.001). The prevalence of SIs increased from 0.17% in 2009 to 0.29% in 2019 (P < 0.001). The mean age of these hospitalizations increased from 38 years in 2009 to 42.3 years in 2019 (P = 0.02). The prevalence of generalized anxiety disorder (GAD) increased from < 1% in 2009 to 12.19% in 2019 (P < 0.001). The prevalence of depression increased from 18.04% in 2009 to 51.21% in 2019 (P < 0.001). Inpatient mortality increased from 0% in 2009 to 2.43% in 2019 (P = 0.024). Among IBD hospitalizations, the male gender had a higher association with SIs than females (odds ratio 1.32 [95% confidence intervals (CI) 1.06–1.66], P = 0.014).\u0000Conclusions: There is a rise of SI among the IBD population. Specialized protocols should be in place in clinical settings and communities to identify and assess high-risk patients.","PeriodicalId":72999,"journal":{"name":"Exploration of medicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45659771","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":"An association study of the PNPLA3 I148M polymorphism (rs738409) with serum lipids in patients with dyslipidemia","authors":"D. Ioannidou, E. Makri, S. Polyzos, Charikleia Ntenti, D. Agapakis, G. Germanidis, A. Goulas","doi":"10.37349/emed.2023.00121","DOIUrl":"https://doi.org/10.37349/emed.2023.00121","url":null,"abstract":"Aim: One single nucleotide polymorphism (SNP) rs738409 in the patatin-like phospholipase domain-containing protein 3 (PNPLA3) gene has been considered a major genetic risk factor of nonalcoholic fatty liver disease (NAFLD). Data have indicated that NAFLD is related to insulin resistance and dyslipidemia, but whether rs738409 is associated with circulating lipid and lipoproteins is not fully elucidated. The main aim of this study was to assess the association of rs738409 with lipid and lipoprotein levels in patients with dyslipidemia.\u0000Methods: This was a post-hoc analysis of a study in patients with dyslipidemia recruited on an outpatient basis. Morning blood samples were collected after a 12-h fast. Genomic DNA was extracted from whole-blood samples.\u0000Results: One hundred seventy-five patients with dyslipidemia were included (97 women). Lipid levels [total cholesterol (TC), triglycerides (TGs), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C)] or glycosylated hemoglobin (HbA1c) were not associated with the SNP, even after adjustment for gender, body mass index (BMI) and type 2 diabetes mellitus (T2DM), using either the additive (CC vs. CG vs. GG) or the dominant (CC vs. GG + CG) inheritance model. When data were stratified for obesity, significant associations between the variant and TC (P = 0.014) or LDL-C levels (P = 0.046) in the non-obese were observed. Pairwise comparison revealed significant changes only in TC between CC and CG genotypes (P = 0.012).\u0000Conclusions: No association was shown between rs738409 SNP and lipid/lipoprotein levels in patients with dyslipidemia. In subgroup analysis, TC was higher in non-obese, but not in obese, patients with CC, compared to CG carriers.","PeriodicalId":72999,"journal":{"name":"Exploration of medicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43670024","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}