Journal of cellular signaling最新文献

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Novel Therapeutic Strategies for Exosome-Related Diseases 外泌体相关疾病的新治疗策略
Journal of cellular signaling Pub Date : 2022-06-02 DOI: 10.33696/signaling.3.072
H. Ageta, K. Tsuchida
{"title":"Novel Therapeutic Strategies for Exosome-Related Diseases","authors":"H. Ageta, K. Tsuchida","doi":"10.33696/signaling.3.072","DOIUrl":"https://doi.org/10.33696/signaling.3.072","url":null,"abstract":"The multivesicular body (MVB), also called late endosome, is a subset of specialized endosomal compartments rich in intraluminal vesicles (ILVs). Multiple ILVs accumulate within MVBs [1,2]. ILVs are formed by invagination of the limiting membrane of early endosomes and budding into the lumen of the organelle. ILVs sequester specific proteins, lipids and cytosolic components. Although exosome release is known to be mediated by MVB, its regulation is not fully understood. Once MVBs fuse with lysosomes, the cargo of the ILVs is degraded. On the other hand, when MVBs fuse with the plasma membrane, the contents of ILVs are secreted outside the cell via exosomes. Most synthesized proteins are modified by post-translational modifiers, which regulate the amount, localization, stability, and activity of proteins. Post-translational modifications (PTM) are involved in the regulation of cellular functions [3]. The formation of MVB is known to be regulated by the endosomal sorting complexes required for transport (ESCRT) systems [1], as well as tetraspanins and UBLs. ESCRT systems are also dependent on ubiquitination [4]. Recently, ubiquitin and UBLs were reported to be involved in the regulation of ILV and MVB. Proteins modified by ubiquitin, SUMO, or UBL3 were incorporated into MVB.","PeriodicalId":73645,"journal":{"name":"Journal of cellular signaling","volume":"54 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77538641","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
TRPM8 Channels and SOCE: Modulatory Crosstalk between Na+ and Ca2+ Signaling TRPM8通道和SOCE: Na+和Ca2+信号之间的调制串扰
Journal of cellular signaling Pub Date : 2022-02-24 DOI: 10.33696/signaling.3.063
G. H. Bomfim
{"title":"TRPM8 Channels and SOCE: Modulatory Crosstalk between Na+ and Ca2+ Signaling","authors":"G. H. Bomfim","doi":"10.33696/signaling.3.063","DOIUrl":"https://doi.org/10.33696/signaling.3.063","url":null,"abstract":"The electrochemical driving forces across the plasma membrane mediated by ion channels, pumps, and exchangers are essential for cellular homeostasis, regulating a wide range of biological processes [1,2]. Although both excitable (e.g., neurons) and non-excitable (e.g., lymphocytes) cells manage their cellular functions through plasmalemmal ion flux, excitable cells change the membrane potential mediated by depolarization and voltage-gated ion channels, while nonexcitable cells control this process by the different downstream processes and ligand-gated ion channels [2,3]. Sodium (Na+) is the principal extracellular cation, being carried to the intracellular space mainly through inward Na+ currents (INa) [2]. Pioneering studies documented that inhibition of INa, but not the calcium (Ca2+) absence, abolished the action potential, indicating that Na+ influx is essential for cell excitability, action Abstract","PeriodicalId":73645,"journal":{"name":"Journal of cellular signaling","volume":"73 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83349024","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: 1
AID and APOBEC3 Involvements in Non-Conventional IgD Class Switch Recombination in Mice AID和APOBEC3参与小鼠非常规IgD类开关重组
Journal of cellular signaling Pub Date : 2022-02-24 DOI: 10.33696/signaling.3.066
Mélissa Ferrad, N. Ghazzaui, Hussein Issaoui, J. Cook-Moreau, Y. Denizot
{"title":"AID and APOBEC3 Involvements in Non-Conventional IgD Class Switch Recombination in Mice","authors":"Mélissa Ferrad, N. Ghazzaui, Hussein Issaoui, J. Cook-Moreau, Y. Denizot","doi":"10.33696/signaling.3.066","DOIUrl":"https://doi.org/10.33696/signaling.3.066","url":null,"abstract":"Melissa Ferrad1,#, Nour Ghazzaui1,#, Hussein Issaoui2, Jeanne Cook-Moreau1, Yves Denizot1* 1Equipe Labellisée LIGUE 2018, UMR CNRS 7276, INSERM U1262, Université de Limoges, CBRS, rue Pr. Descottes, 87025 Limoges, France 2Present address : Nour Ghazzaui Vaccine Research Institute, INSERM U955, Hôpital Henri Mondor, 94010 Créteil, France; Hussein Issaoui Université Côte d'Azur, INSERM U1065, Centre Méditerranéen de Médecine Moléculaire (C3 M), 06204, Nice, France #These authors contributed equally to this work *Correspondence should be addressed to Yves Denizot, yves.denizot@unilim.fr","PeriodicalId":73645,"journal":{"name":"Journal of cellular signaling","volume":"64 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91267873","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
Differentiation and Subtype Specification of Enteric Neurons: Current Knowledge of Transcription Factors, Signaling Molecules and Signaling Pathways Involved 肠神经元的分化和亚型规范:转录因子、信号分子和信号通路的最新知识
Journal of cellular signaling Pub Date : 2022-02-24 DOI: 10.33696/signaling.3.064
Nastasia Popowycz, L. Uyttebroek, G. Hubens, L. Nassauw
{"title":"Differentiation and Subtype Specification of Enteric Neurons: Current Knowledge of Transcription Factors, Signaling Molecules and Signaling Pathways Involved","authors":"Nastasia Popowycz, L. Uyttebroek, G. Hubens, L. Nassauw","doi":"10.33696/signaling.3.064","DOIUrl":"https://doi.org/10.33696/signaling.3.064","url":null,"abstract":"The enteric nervous system (ENS) forms the largest component of the autonomic nervous system (ANS). In humans, it contains between 200 and 600 million neurons which are part of intrinsic neuronal circuits managing to generate reflex gastrointestinal (GI) contractile activity without intervention of the central nervous system (CNS) [1,2]. The ENS is located along the length of the GI tract and oversees controlling the main functions such as secretion, motility, and blood flow. In addition, it is also responsible for the communication with the immune system and microbiome [3–5]. The ENS contains a network of neurons and glial cells which are dispersed over two major ganglionated and interconnected plexuses, the myenteric (Auerbach) plexus, and the submucosal (Meissner) plexus. In larger mammals, the submucosal plexus is further subdivided into smaller plexuses [4,6-10]. The neurons of the myenteric plexus are primarily involved in GI motility regulation, while the neurons of the submucosal plexus are involved in the regulation of secretion and vascular tone [3,6,11,12]. The ENS is a highly complex nervous system of which the functioning is dependent on many different neuronal subtypes. To keep an overview of the neuronal subtypes, they are categorized in different classes according to certain characteristics. Among these features are their morphology, electrical properties, chemical coding, and Abstract","PeriodicalId":73645,"journal":{"name":"Journal of cellular signaling","volume":"26 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90830738","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
Expression and Localization of Phosphoinositide-Specific Phospholipases C in Cultured, Differentiating and Stimulated Human Osteoblasts 磷酸肌肽特异性磷脂酶C在培养、分化和刺激的人成骨细胞中的表达和定位
Journal of cellular signaling Pub Date : 2022-02-24 DOI: 10.33696/signaling.3.067
Sara Daisy Casoni, Alessia Romanelli, M. Checchi, Serena Truocchio, M. Ferretti, C. Palumbo, V. L. Vasco
{"title":"Expression and Localization of Phosphoinositide-Specific Phospholipases C in Cultured, Differentiating and Stimulated Human Osteoblasts","authors":"Sara Daisy Casoni, Alessia Romanelli, M. Checchi, Serena Truocchio, M. Ferretti, C. Palumbo, V. L. Vasco","doi":"10.33696/signaling.3.067","DOIUrl":"https://doi.org/10.33696/signaling.3.067","url":null,"abstract":"Sara Daisy Casoni1#, Alessia Romanelli1#, Marta Checchi1, Serena Truocchio1,2, Marzia Ferretti1, Carla Palumbo1, Vincenza Rita Lo Vasco1* 1Human Morphology Section, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, Largo del Pozzo, 41121 Modena, Italy 2Biomedical and Neuromotor Sciences DIBINEM, University of Bologna, Italy #These authors contributed equally to this work *Correspondence should be addressed to Vincenza Rita Lo Vasco, MD, PhD, ritalovasco@hotmail.it","PeriodicalId":73645,"journal":{"name":"Journal of cellular signaling","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89284951","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
Interferon Gamma, MHC Class I Regulation and Immunotherapy 干扰素γ, MHC I类调节和免疫治疗
Journal of cellular signaling Pub Date : 2022-02-24 DOI: 10.33696/signaling.3.065
Maria Gómez-Herranz, Magdalena Pilch, T. Hupp, S. Kote
{"title":"Interferon Gamma, MHC Class I Regulation and Immunotherapy","authors":"Maria Gómez-Herranz, Magdalena Pilch, T. Hupp, S. Kote","doi":"10.33696/signaling.3.065","DOIUrl":"https://doi.org/10.33696/signaling.3.065","url":null,"abstract":"The activation of endogenous IFNγ signaling pathway or the administration of recombinant IFNγ increases the expression of MHC-I. MHC-I molecules are core elements for antigen recognition in tumor cells. A better understanding of the regulation of their expression would contribute to counteracting tumor immune escape and enduring permanent tumor rejection. Efficient and functional expression of HLAs dramatically impacts the number of tumor-associated antigens presented to CTL for cell recognition. Many patients diagnosed with various types of cancer have inhibited the IFNγ signaling pathway. This review explores how anomalies associated with IFNγ signaling in tumor cells affect HLA-I expression, current immunotherapies association, and outcome. Globally, MHC-I lesions could be divided into reversible and permanent. Irreversible lesions cannot be recapitulated; hence, the patient will not respond to immunotherapies requiring MHC-I activity. However, gaining precise and systematic molecular knowledge improves tumor stratification, which could help predict which tumors will recover expression of MHC-I. Complementary IFNγ effectors can function as a compensatory mechanism that restores the expression of HLA-I proteins in tumors with deleterious IFNγ pathways. For those non-responsive patients with inactive IFNγ pathways, designing personalized approaches to recover HLA-I expression can make the tumor sensitive to immunotherapy, leading to a better outcome.","PeriodicalId":73645,"journal":{"name":"Journal of cellular signaling","volume":"33 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80410332","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
The Outcome of Tumor Ablation Therapies is Determined by Stress Signaling Networks 肿瘤消融治疗的结果是由应激信号网络决定的
Journal of cellular signaling Pub Date : 2022-02-24 DOI: 10.33696/signaling.3.062
M. Korbelik
{"title":"The Outcome of Tumor Ablation Therapies is Determined by Stress Signaling Networks","authors":"M. Korbelik","doi":"10.33696/signaling.3.062","DOIUrl":"https://doi.org/10.33696/signaling.3.062","url":null,"abstract":"Increasingly prominent roles in interventional oncology are held by various tumor ablation therapies performed by direct applications of local acute trauma-inducing insult to the targeted lesion aiming for its rapid in situ destruction. These therapies include treatments based on various forms of thermal energy delivery (photothermal, cryoablation, microwave ablation, radiofrequency ablation), non-thermal illumination (photodynamic therapy), electric field exposure, or high hydrostatic pressure [1-3]. Common injury inflicted in cells of tumors treated by ablation therapies is the impairment of proteostasis due to accumulation of misfolded/damaged proteins. This is sensed by afflicted cells as a trauma typically associated with thermal or oxidative stress that threatens the integrity and homeostasis at the affected site [4]. These types of stress provoke evolutionary well conserved canonic protection mechanisms based on cellular stress signaling network that serves to re-balance biochemical activities within the cell. They work by conversing the incoming signal (appearance of stressor molecule) towards downstream effector molecules involved in transcriptome reprogramming aimed at activation or inhibition of targeted biochemical tasks [4,5]. The aim of this commentary is to emphasize that the activity of the engaged intracellular signaling pathways determines the fate of involved tumor cells and ultimately the outcome of the applied therapies.","PeriodicalId":73645,"journal":{"name":"Journal of cellular signaling","volume":"15 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91297051","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: 1
c-JUN n-Terminal Kinase (JNK) Signaling in Autosomal Dominant Polycystic Kidney Disease 常染色体显性多囊肾病中c-JUN n-末端激酶(JNK)信号传导
Journal of cellular signaling Pub Date : 2022-02-17 DOI: 10.33696/Signaling.3.068
Abigail O. Smith, J. Jonassen, Kenley M. Preval, R. Davis, G. Pazour
{"title":"c-JUN n-Terminal Kinase (JNK) Signaling in Autosomal Dominant Polycystic Kidney Disease","authors":"Abigail O. Smith, J. Jonassen, Kenley M. Preval, R. Davis, G. Pazour","doi":"10.33696/Signaling.3.068","DOIUrl":"https://doi.org/10.33696/Signaling.3.068","url":null,"abstract":"Polycystic kidney disease is an inherited degenerative disease in which the uriniferous tubules are replaced by expanding fluid-filled cysts that ultimately destroy organ function. Autosomal dominant polycystic kidney disease (ADPKD) is the most common form, afflicting approximately 1 in 1,000 people and is caused by mutations in the transmembrane proteins polycystin-1 (Pkd1) and polycystin-2 (Pkd2). The mechanisms by which polycystin mutations induce cyst formation are not well understood, however pro-proliferative signaling must be involved for tubule epithelial cell number to increase over time. We recently found that the stress-activated mitogen-activated protein kinase (MAPK) pathway c-Jun N-terminal kinase (JNK) pathway is activated in cystic disease and genetically removing JNK reduces cyst growth driven by a loss of Pkd2. This review covers the current state of knowledge of signaling in ADPKD with an emphasis on the JNK pathway.","PeriodicalId":73645,"journal":{"name":"Journal of cellular signaling","volume":"12 1","pages":"62 - 78"},"PeriodicalIF":0.0,"publicationDate":"2022-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80255919","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: 1
Oxidative DNA Damage: A Role in Altering Neuronal Function. 氧化性DNA损伤:在改变神经元功能中的作用。
Journal of cellular signaling Pub Date : 2022-01-01 DOI: 10.33696/signaling.3.079
Adib Behrouzi, Mark R Kelley, Jill C Fehrenbacher
{"title":"Oxidative DNA Damage: A Role in Altering Neuronal Function.","authors":"Adib Behrouzi,&nbsp;Mark R Kelley,&nbsp;Jill C Fehrenbacher","doi":"10.33696/signaling.3.079","DOIUrl":"https://doi.org/10.33696/signaling.3.079","url":null,"abstract":"<p><p>A role for oxidative stress in the etiology of myriad neuropathologies is well accepted. However, the specific effects of oxidative DNA damage in the onset or promotion of neuronal dysfunction have been less studied. In our recent publication by Behrouzi <i>et al</i>. (Oxidative DNA Damage and Cisplatin Neurotoxicity Is Exacerbated by Inhibition of OGG1 Glycosylase Activity and APE1 Endonuclease Activity in Sensory Neurons), inhibition of enzymes that play a role in repairing oxidative DNA damage exacerbated neurotoxic effects of the chemotherapeutic agent, cisplatin. In this Commentary, we aim to expand on the contribution of oxidative DNA damage to other neuropathologies within the peripheral and central nervous systems, including irritable bowel disease, aging and Alzheimer's disease, amyotrophic lateral sclerosis, and other neurodegenerative diseases. Consistently, clinical neuropathology and disease progression correlates with increases in oxidative DNA damage within clinical biopsies. Progress in animal models of these diseases has elucidated a causative role for oxidative DNA damage in disease progression, as dampening the DNA repair response exacerbates disease, whereas promoting DNA repair mitigates disease. Overall, this Commentary highlights the importance of expanding our studies on oxidative DNA damage in the nervous system, as enhancing oxidative DNA repair might prove to be a potential therapeutic target for the mitigation of neurodegeneration.</p>","PeriodicalId":73645,"journal":{"name":"Journal of cellular signaling","volume":"3 3","pages":"160-166"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9534318/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33510517","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 3
Redox Homeostasis in Well-differentiated Primary Human Nasal Epithelial Cells. 分化良好的原代人鼻上皮细胞的氧化还原稳态。
Journal of cellular signaling Pub Date : 2022-01-01 DOI: 10.33696/signaling.3.083
Ayaho Yamamoto, Peter D Sly, Anna Henningham, Nelufa Begum, Abrey J Yeo, Emmanuelle Fantino
{"title":"Redox Homeostasis in Well-differentiated Primary Human Nasal Epithelial Cells.","authors":"Ayaho Yamamoto,&nbsp;Peter D Sly,&nbsp;Anna Henningham,&nbsp;Nelufa Begum,&nbsp;Abrey J Yeo,&nbsp;Emmanuelle Fantino","doi":"10.33696/signaling.3.083","DOIUrl":"https://doi.org/10.33696/signaling.3.083","url":null,"abstract":"<p><p>Oxidative stress (OS) in the airway epithelium is associated with inflammation, cell damage, and mitochondrial dysfunction that may initiate or worsen respiratory disease. Redox regulation maintains the equilibrium of pro-oxidant/antioxidant reactions but can be disturbed by environmental exposures. The mechanism(s) underlying the induction and impact of OS on airway epithelium and how these influences on respiratory disease is poorly understood. The aim of this study was to develop a stress response model in primary human nasal epithelial cells (NECs) grown at the air-liquid interface (ALI) into a well-differentiated epithelium and to use this model to investigate the mechanisms underlying OS. Hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>) was used to induce acute OS and the responses were measured with trans epithelial electrical resistance (TEER), membrane permeability, cell death (LDH release), mitochondrial reactive oxygen species (mtROS) generation, redox status (GSH/GSSG ratio), cellular ATP, and signaling pathways (SIRT1, FOXO3, p53, p21, PINK1, PARKIN, NRF2). Following 25 mM (sensitive) or 50mM (resistant) H<sub>2</sub>O<sub>2</sub> exposure, cell integrity decreased (<i>p</i><0.05), GSH/GSSG ratio reduced (<i>p</i><0.05), and ATP production declined by 83% (<i>p</i><0.05) in the sensitive and 55% (<i>p</i><0.05) in the resistant group; mtROS production increased 3.4-fold (<i>p</i><0.001). Significant inter-individual differences between healthy humans with regards to susceptibility to OS, and differential activation of various pathways (FOXO3, PARKIN) were observed. These intra-individual differences in susceptibility to OS may be attributed to resistant individuals having more mitochondria or greater mitochondrial function.</p>","PeriodicalId":73645,"journal":{"name":"Journal of cellular signaling","volume":"3 4","pages":"193-206"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9912202/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10704085","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
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