Journal of World Mitochondria Society最新文献_第3页

Thiosulfate protects against hepatic ischemia-reperfusion injury via improving the mitochondrial stress response 硫代硫酸盐通过改善线粒体应激反应来保护肝脏缺血再灌注损伤

Journal of World Mitochondria Society Pub Date : 2016-09-27 DOI: 10.18143/JWMS_V2I2_1994

Luisa Ungelenk, A. Medyukhina, A. Press, S. Nietzsche, C. Kan, M. Clemens, D. Uta, M. Bachtler, A. Pasch, A. Lupp, Rui Wang, M. Figge, S. Heinemann, U. Settmacher, R. Wetzker, S. Weis, M. Bauer

{"title":"Thiosulfate protects against hepatic ischemia-reperfusion injury via improving the mitochondrial stress response","authors":"Luisa Ungelenk, A. Medyukhina, A. Press, S. Nietzsche, C. Kan, M. Clemens, D. Uta, M. Bachtler, A. Pasch, A. Lupp, Rui Wang, M. Figge, S. Heinemann, U. Settmacher, R. Wetzker, S. Weis, M. Bauer","doi":"10.18143/JWMS_V2I2_1994","DOIUrl":"https://doi.org/10.18143/JWMS_V2I2_1994","url":null,"abstract":"Objective: Ischemia-reperfusion injury (IRI) complicates revascularization and organ transplantation [1]. Increased reactive oxygen species and subsequent mitochondrial dysfunction induce tissue dysfunction and injury after ischemia-reperfusion [2]. The gasotransmitter hydrogen sulfide (H2S) protects against IRI, but its therapeutic utility remains elusive [3]. We investigated whether sodium thiosulfate (STS) protective in IRI, mimicking the effects of H2S.Methodology: We analysed the effects of STS on mitochondrial respiration and function using an ex vivo isolated liver IRI model and assessed serology, histology, mitophagy markers and electron microscopic changes. We also performed in vivo intravital microscopy.Results: Mice deficient in the endogenous H2S-producing enzyme cystathionine gamma-lyase showed increased mitochondrial dysfunction during hepatic IRI. The fast-releasing H2S donor (NaHS) ameliorated dysfunction but with narrow therapeutic window. In contrast, STS produced similar protective effects but with greater than an order of magnitude broader therapeutic window, while additionally acting as an antioxidant. STS significantly reduced LDH release ex vivo correlating with decreased autophagy and preservation of mitochondrial ultra-structure. Finally, STS protected against tissue injury in vivo by reducing necrosis and decreasing circulating markers of tissue injury.Conclusion: STS, a well-tolerated drug to treat e.g. cyanide poisoning, is a potential drug to treat hepatic IRI.","PeriodicalId":266249,"journal":{"name":"Journal of World Mitochondria Society","volume":"97 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2016-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"133182941","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

Repair of DNA double-strand breaks in mitochondria: Implications in mitochondrial genome maintenance 线粒体DNA双链断裂的修复:线粒体基因组维持的意义

Journal of World Mitochondria Society Pub Date : 2016-09-27 DOI: 10.18143/JWMS_V2I2_1998

Sumedha Dahal, S. Tadi, R. Sebastian, S. Raghavan

{"title":"Repair of DNA double-strand breaks in mitochondria: Implications in mitochondrial genome maintenance","authors":"Sumedha Dahal, S. Tadi, R. Sebastian, S. Raghavan","doi":"10.18143/JWMS_V2I2_1998","DOIUrl":"https://doi.org/10.18143/JWMS_V2I2_1998","url":null,"abstract":"Mitochondrial DNA (mtDNA) is frequently exposed to oxidative damage compared to nuclear DNA. mtDNA deletions are associated with mitochondrial disorders. Deletions identified in humans are flanked by short direct repeats; however, mechanism of DNA rearrangements is yet to be elucidated. Besides maintenance of genomic stability in mitochondria is poorly understood. Here, we investigate the mechanisms of DSB repair in mitochondria. While classical-NHEJ was undetectable, microhomology mediated endjoining (MMEJ) efficiently repaired DSBs in mitochondria. Immunoblotting, immunoprecipitation and other assays suggest the involvement of CtIP, FEN1, MRE11 and PARP1 in mitochondrial MMEJ. Knockdown experiments demonstrated that DNA LIGASE III, but not LIGASE IV or LIGASE I, is primarily responsible for final sealing of DSBs during mitochondrial MMEJ. These observations highlight the central role of MMEJ and its functions in deletions and in many human mitochondrial disorders. Further, we show that HR mediated repair is more efficient in mitochondria of testes as compared to brain, kidney and spleen. Interestingly, sequence analyses revealed a predominant reciprocal exchange mechanism, while 35% consisted of gene conversion. Colocalization and immunoblotting studies revealed the role of MRN complex in HR mediated repair in mitochondria. These observations highlight the importance of HR in mitochondrial genome maintenance.","PeriodicalId":266249,"journal":{"name":"Journal of World Mitochondria Society","volume":"71 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2016-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"133907286","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

Modulation of the oxidative stress associated with respiratory chain dysfunction and mPTP opening 与呼吸链功能障碍和mPTP开放相关的氧化应激调节

Journal of World Mitochondria Society Pub Date : 2016-09-27 DOI: 10.18143/JWMS_V2I2_2001

Annie Borgne Sanchez, M. Porceddu, N. Buron, C. Pertuiset

{"title":"Modulation of the oxidative stress associated with respiratory chain dysfunction and mPTP opening","authors":"Annie Borgne Sanchez, M. Porceddu, N. Buron, C. Pertuiset","doi":"10.18143/JWMS_V2I2_2001","DOIUrl":"https://doi.org/10.18143/JWMS_V2I2_2001","url":null,"abstract":"The mitochondrion is deeply involved in ROS production through electron leak that occur in the respiratory chain. Measurement of mitochondrial ROS is useful to evaluate the consequences of MRC inhibition, electron leak, complex I dysfunction and stimulation of some oxidative pathways induced by chemicals or natural products. These parameters measured on isolated mitochondria allow identification of direct mitochondrial impairment with subsequent toxicity on skin, blood or organs. On the other hand, the mitochondrion is itself a target of ROS (vicious circle or cellular ROS) which may lead to irreversible damage of mtDNA or mitochondrial membrane lipids and proteins, resulting in mitochondrial dysfunction. For example, permeability transition pore (mPTP) susceptibility to oxidative stress is observed in various pathological cases (aging, neuronal injury, cardiac reperfusion injury...). Such damages can be reproduced on isolated mitochondria to identify mitochondrial protective molecules against oxidative stress induced-mPTP opening. In conclusion, simultaneous assessment of mitochondrial integrity, function and ROS production is a valuable toolbox to identify the risk of compound-induced liability in human, in particular regarding organ toxicity. Such approach can also be used to identify antioxidant properties of compounds in order to preserve mitochondrial integrity and cell life.","PeriodicalId":266249,"journal":{"name":"Journal of World Mitochondria Society","volume":"16 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2016-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"133855727","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

Mitochondrial genome variability of 205 Arabian endurance horses 205匹阿拉伯耐力马的线粒体基因组变异

Journal of World Mitochondria Society Pub Date : 2016-09-27 DOI: 10.18143/JWMS_V2I2_1999

Alexandre Heurteau, C. Hoede, A. Ricard, D. Esquerré, Caroline Morgenthaler, N. Mach, C. Robert, E. Barrey

{"title":"Mitochondrial genome variability of 205 Arabian endurance horses","authors":"Alexandre Heurteau, C. Hoede, A. Ricard, D. Esquerré, Caroline Morgenthaler, N. Mach, C. Robert, E. Barrey","doi":"10.18143/JWMS_V2I2_1999","DOIUrl":"https://doi.org/10.18143/JWMS_V2I2_1999","url":null,"abstract":"Objectives:The objectives of this study were to propose a new strategy to call genetic variants in mitochondrial genome, and determine whether some variants are associated to endurance performance.Methodology:DNA was isolated from peripheral blood and mtDNA was amplified by 5 overlapping amplicons and then sequenced by Illumina Miseq. We chose a reference genome (GenBank ID : JN398380.1) that we « circularized » to improve terminals' alignments. After quality filtering and alignment, GATK (v3.5) was used to detect SNPs, indels and heteroplasmy. Association between SNPs and performance in endurance was tested using mixed model with fixed SNP Effect and random additive genetic effect with relationship matrix.Results:We got 590 variable positions of which 72% were known through studies of mitochondrial variability in horses [1,2]. 80% of the protein coding variants are silent and the transition/transversion ratio is 22.5. We observed 1.5% of non-haploid genotype. We graphically described the variants and the observed heteroplasmy in terms of localization, diversity, potential effects along the mitochondrial genome. Our preliminary analysis do not allow to associate some of the variants to performance.Conclusions:Despite a very strong conservative selection, 590 variants were identified on mtDNA of endurance horses.","PeriodicalId":266249,"journal":{"name":"Journal of World Mitochondria Society","volume":"120 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2016-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"132732397","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

Mitochondrial protein TMEM70: key role in the biogenesis of ATP synthase verified in a mouse knockout model 线粒体蛋白TMEM70:在小鼠敲除模型中证实ATP合酶生物发生中的关键作用

Journal of World Mitochondria Society Pub Date : 2016-09-27 DOI: 10.18143/JWMS_v2i2_2004

J. Kovalčíková, M. Vrbacký, H. Nůsková, T. Mráček, I. Beck, R. Sedláček, J. Houštěk

{"title":"Mitochondrial protein TMEM70: key role in the biogenesis of ATP synthase verified in a mouse knockout model","authors":"J. Kovalčíková, M. Vrbacký, H. Nůsková, T. Mráček, I. Beck, R. Sedláček, J. Houštěk","doi":"10.18143/JWMS_v2i2_2004","DOIUrl":"https://doi.org/10.18143/JWMS_v2i2_2004","url":null,"abstract":"TMEM70 is a transmembrane protein localized in the inner mitochondrial membrane and involved in the biogenesis of the eukaryotic ATP synthase, but its molecular role in this process is still unknown. TMEM70 mutations cause isolated deficiency of ATP synthase often resulting in a fatal neonatal mitochondrial encephalocardiomyopathy in patients. Generation of Tmem70 knockout mice resulted in embryonically lethal Tmem70-/- embryos [1]. To obtain adult Tmem70-/- mice we generated the tamoxifen inducible knockout. The weight of mice dramatically decreased and they died by week 8 past Cre-mediated excision. Despite of the similar efficiency of Tmem70 deletion in liver and heart, blue native electrophoresis demonstrated more pronounced decrease of fully assembled F1Fo ATP synthase and accumulation of F1 subcomplex in liver than in heart. SDS electrophoresis showed more decreased level of F1-α subunit in liver, which has also impaired ATPase hydrolytic activity. Moreover the oxygen consumption induced by addition of cytochrome c indicated damaged liver mitochondria in the treated mice in comparison to controls. Most likely, this can be explained by slower turnover of ATP synthase in heart than in liver. In conclusion, induction of Tmem70 knockout in adult mice impairs primarily liver, contrasting with predominantly cardiologic presentation in human patients.","PeriodicalId":266249,"journal":{"name":"Journal of World Mitochondria Society","volume":"30 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2016-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"128583079","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

AFM Analyses of Mitochondria: Genome Structure and Dynamics in Living Cell 线粒体的AFM分析:活细胞的基因组结构和动力学

Journal of World Mitochondria Society Pub Date : 2016-09-27 DOI: 10.18143/JWMS_V2I2_1997

K. Takeyasu, R. Ohniwa, Katashi Deguchi, Jamie L. Gilmore

引用次数: 0

Radiation-induced metabolic disorders: potential role for the mitochondria in skeletal muscle 辐射引起的代谢紊乱:骨骼肌中线粒体的潜在作用

Journal of World Mitochondria Society Pub Date : 2016-09-27 DOI: 10.18143/JWMS_V2I2_2003

Nadia Maria Lopes Amorim, Sarah Bould, C. Lucas, A. Kee, D. Simar, E. Hardeman

{"title":"Radiation-induced metabolic disorders: potential role for the mitochondria in skeletal muscle","authors":"Nadia Maria Lopes Amorim, Sarah Bould, C. Lucas, A. Kee, D. Simar, E. Hardeman","doi":"10.18143/JWMS_V2I2_2003","DOIUrl":"https://doi.org/10.18143/JWMS_V2I2_2003","url":null,"abstract":"Over 2/3 of childhood cancer survivors treated with total body irradiation develop metabolic complications. Given that skeletal muscle plays a major role in insulin-stimulated glucose disposal, we aimed to investigate the role of skeletal muscle in impaired whole body metabolism following irradiation.Mice were exposed to a single dose of 5.95Gy and 5 weeks post-irradiation (baseline) were fed a high-fat diet (HFD) for 12 weeks. Energy expenditure, glucose homeostasis and insulin sensitivity were assessed throughout the HFD period and metabolic functions were measured at baseline and endpoint in skeletal muscles and muscle stem cells.Irradiated mice had increased respiratory exchange ratio on HFD despite similar food intake. Lipid metabolism and citrate synthase activity in muscle were impaired compared to the non-irradiated mice suggesting altered fat utilisation and compromised mitochondrial function. Irradiated mice showed altered fasting glucose and impaired ex-vivo insulin-stimulated glucose uptake in muscles after 12 weeks of HFD. Muscle stem cells isolated from irradiated mice showed both impaired lipid and glucose oxidation, suggesting long-term memory of the exposure to irradiation.We propose that irradiation may alter skeletal muscle mitochondrial metabolism resulting in impaired whole body metabolism and insulin resistance.","PeriodicalId":266249,"journal":{"name":"Journal of World Mitochondria Society","volume":"11 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2016-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"126407644","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

Journal of World Mitochondria Society Pub Date : 2016-09-26 DOI: 10.18143/JWMS_V2I2_1992

T. Daňhelovská, M. Tesařová, M. Rodinová, V. Stránecký, J. Sládková, A. Vondráčková, J. Křížová, J. Zamecnik, T. Honzík, H. Hansíková, J. Zeman

{"title":"DNM1L-related mitochondrial fission defect presenting as spastic paraparesis and optic atrophy","authors":"T. Daňhelovská, M. Tesařová, M. Rodinová, V. Stránecký, J. Sládková, A. Vondráčková, J. Křížová, J. Zamecnik, T. Honzík, H. Hansíková, J. Zeman","doi":"10.18143/JWMS_V2I2_1992","DOIUrl":"https://doi.org/10.18143/JWMS_V2I2_1992","url":null,"abstract":"DNM1L gene encodes the dynamin 1- like protein DNM1L (Drp1) which is crucial in the mitochondrial fusion process as well as fusion of peroxisomes. We describe a patient with novel heterozygous de novo DNM1L mutation c. 176C>T (p.Thr59Ile), which further expands the associated clinical spectrum. The patient exhibits axial hypotonia, spastic paraparesis, neo- and paleo-cerebellar syndrome and optic atrophy. Muscle biopsy revealed mild decrease in CI+III activity, increased SDH and decreased COX activity staining in 5% of muscle fibers. Protein analysis in cultured skin fibroblasts revealed altered amount of some OXPHOS subunits. Furthermore, regular occurrence of “mega-mitochondria” along elongated mitochondrial network was found in cultured myoblasts which confirms impaired mitochondrial dynamic. Novel mutation c. 176C>T (p.Thr59Ile) in DNM1L gene was identified by exome sequencing and affects highly conserved Thr59 in the GTPase domain of the protein. Trp59 has been previously shown to be indispensable for GTPase reaction (Wenger et al 2013). All previously described missense mutations in 3 patients with varied phenotype were localized in the middle domain important for the protein oligomerization. To conclude, our results further expand clinical phenotypes (including optic atrophy) associated with DNM1L mutations.","PeriodicalId":266249,"journal":{"name":"Journal of World Mitochondria Society","volume":"21 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2016-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"114804209","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

NO donor and ONOO- donor regulated expression of porphyrin transporter NO供体和ONOO供体调节卟啉转运蛋白的表达

Journal of World Mitochondria Society Pub Date : 2016-09-26 DOI: 10.18143/JWMS_V2I2_1985

Hiromi Kurokawa, H. Ito, H. Matsui

{"title":"NO donor and ONOO- donor regulated expression of porphyrin transporter","authors":"Hiromi Kurokawa, H. Ito, H. Matsui","doi":"10.18143/JWMS_V2I2_1985","DOIUrl":"https://doi.org/10.18143/JWMS_V2I2_1985","url":null,"abstract":"We reported that the nitric oxygen (NO) inactivation of a catalytic enzyme ferrochelatase increased by intracellular porphyrin accumulation: the ferrochelatase chelates iron into protoporphyrin to form protoheme. Since high NO concentration of cell is cancer specific phenomenon, the cellular porphyrin accumulation is a cancer specific event. Not only the porphyrin biosynthesis, but NO may also regulate porphyrin transports. Reactive nitrogen species such as NO or peroxynitrite (ONOO-) have physiological activity. ONOO- is generated by a fast reaction between NO and superoxide anion. Thus it is not well known that which compounds are important to accumulation of porphyrin. In this study, we investigated whether expression of porphyrin transporter is effected by NO donor (NOC18) or ONOO- donor (SIN1). Expression of heme carrier protein 1 (HCP-1), is known of porphyrin transporter, was determined by Western blot analysis and it was up-regulated by treatment with NOC18 or SIN1. In order to investigate cellular uptake manner of hematopophyrin derivatives (HpD) in association with NO donor or ONOO- donor, cellular uptake of HpD was examined by measuring fluorescent intensities of HpD after exposing it to cells. From these results, both NO donor and ONOO- donor regulated expression of porphyrin transporter and accumulation of porphyrin.","PeriodicalId":266249,"journal":{"name":"Journal of World Mitochondria Society","volume":"122 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2016-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"122907767","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

On the role of mitochondrial dysfunction in the molecular pathology of major depressive disorder 线粒体功能障碍在重度抑郁症分子病理中的作用

Journal of World Mitochondria Society Pub Date : 2016-09-26 DOI: 10.18143/JWMS_V2I2_1993

V. Milenkovic, Anna Weinfurtner, R. Rupprecht, C. Wetzel

{"title":"On the role of mitochondrial dysfunction in the molecular pathology of major depressive disorder","authors":"V. Milenkovic, Anna Weinfurtner, R. Rupprecht, C. Wetzel","doi":"10.18143/JWMS_V2I2_1993","DOIUrl":"https://doi.org/10.18143/JWMS_V2I2_1993","url":null,"abstract":"The molecular etiology of major depressive disorder (MDD) is still not exactly known. We believe today that a combination of genetic, neurobiological and psychosocial factors lead to cellular/molecular dysfunction and increase the vulnerability of neuronal and other somatic cells. Additional stress contribute to the etiology of MDD promoting the development of the disease. Neurobiological factors include monoaminergic, glutamatergic and GABAergic neurotransmitter systems as well as the involvement of the immune system and neurotrophic factors. The dysregulation of neurogenesis, apoptosis and neuronal plasticity as well as mitochondrial dysfunction are factors shown to play significant roles in the pathology of MDD. Based on the hypothesis that MDD could be caused by mitochondrial dysfunction, we set out to identify and characterize molecular pathomechanisms in cells derived from depressed patients. To establish a human cellular model of depression, we obtained skin fibroblast biopsies from depressed patients and gender and age matched healthy controls. Using the fluorescent cationic dyes JC-1 and TMRE, we found the mitochondrial membrane potential to be significantly depolarized in MDD fibroblasts. The depolarized mitochondrial membrane potential indicates a bioenergetic disbalance probably as consequence of mitochondrial dysfunction reflecting the hypometabolism associated with MDD. Deeper investigation of underlying molecular mechanisms will follow.","PeriodicalId":266249,"journal":{"name":"Journal of World Mitochondria Society","volume":"10 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2016-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"128697708","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