Frontiers in Cellular Neuroscience最新文献

{"title":"Editorial: Mechanisms of neurodegeneration in amyotrophic lateral sclerosis and related disorders.","authors":"Danyllo Oliveira, Agnes Lumi Nishimura","doi":"10.3389/fncel.2024.1531449","DOIUrl":"https://doi.org/10.3389/fncel.2024.1531449","url":null,"abstract":"","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"18 ","pages":"1531449"},"PeriodicalIF":4.2,"publicationDate":"2024-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11655186/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142863858","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aging promotes an increase in mitochondrial fragmentation in astrocytes.","authors":"Ana Paula Bergamo Araujo, Gabriele Vargas, Lívia de Sá Hayashide, Isadora Matias, Cherley Borba Vieira Andrade, Jorge José de Carvalho, Flávia Carvalho Alcantara Gomes, Luan Pereira Diniz","doi":"10.3389/fncel.2024.1496163","DOIUrl":"https://doi.org/10.3389/fncel.2024.1496163","url":null,"abstract":"<p><strong>Introduction: </strong>Brain aging involves a complex interplay of cellular and molecular changes, including metabolic alterations and the accumulation of senescent cells. These changes frequently manifest as dysregulation in glucose metabolism and mitochondrial function, leading to reduced energy production, increased oxidative stress, and mitochondrial dysfunction-key contributors to age-related neurodegenerative diseases.</p><p><strong>Methods: </strong>We conducted experiments on two models: young (3-4 months) and aged (over 18 months) mice, as well as cultures of senescent and control mouse astrocytes. Mitochondrial content and biogenesis were analyzed in astrocytes and neurons from aged and young animals. Cultured senescent astrocytes were examined for mitochondrial membrane potential and fragmentation. Quantitative PCR (qPCR) and immunocytochemistry were used to measure fusion- and fission-related protein levels. Additionally, transmission electron microscopy provided morphological data on mitochondria.</p><p><strong>Results: </strong>Astrocytes and neurons from aged animals showed a significant reduction in mitochondrial content and a decrease in mitochondrial biogenesis. Senescent astrocytes in culture exhibited lower mitochondrial membrane potential and increased mitochondrial fragmentation. qPCR and immunocytochemistry analyses revealed a 68% increase in fusion-related proteins (mitofusin 1 and 2) and a 10-fold rise in DRP1, a key regulator of mitochondrial fission. Transmission electron microscopy showed reduced perimeter, area, and length-to-diameter ratio of mitochondria in astrocytes from aged mice, supported by elevated DRP1 phosphorylation in astrocytes of the cerebral cortex.</p><p><strong>Discussion: </strong>Our findings provide novel evidence of increased mitochondrial fragmentation in astrocytes from aged animals. This study sheds light on mechanisms of astrocytic metabolic dysfunction and mitochondrial dysregulation in brain aging, highlighting mitochondrial fragmentation as a potential target for therapeutic interventions in age-related neurodegenerative diseases.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"18 ","pages":"1496163"},"PeriodicalIF":4.2,"publicationDate":"2024-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11655212/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142863857","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuronal activity inhibits mitochondrial transport only in synaptically connected segments of the axon.","authors":"Tom Venneman, Pieter Vanden Berghe","doi":"10.3389/fncel.2024.1509283","DOIUrl":"https://doi.org/10.3389/fncel.2024.1509283","url":null,"abstract":"<p><p>Due to their large scale and uniquely branched architecture, neurons critically rely on active transport of mitochondria in order to match energy production and calcium buffering to local demand. Consequently, defective mitochondrial trafficking is implicated in various neurological and neurodegenerative diseases. A key signal regulating mitochondrial transport is intracellular calcium. Elevated Ca²⁺ levels have been demonstrated to inhibit mitochondrial transport in many cell types, including neurons. However, it is currently unclear to what extent calcium-signaling regulates axonal mitochondrial transport during realistic neuronal activity patterns. We created a robust pipeline to quantify with high spatial resolution, absolute Ca²⁺ concentrations. This allows us to monitor Ca²⁺ dynamics with pixel precision in the axon and other neuronal compartments. We found that axonal calcium levels scale with firing frequency in the range of 0.1-1 μM, whereas KCl-induced depolarization generated levels almost a magnitude higher. As expected, prolonged KCl-induced depolarization did inhibit axonal mitochondrial transport in primary hippocampal neurons. However, physiologically relevant neuronal activity patterns only inhibited mitochondrial transport in axonal segments which made connections to a target neuron. In \"non-connecting\" axonal segments, we were unable to trigger this inhibitory mechanism using realistic firing patterns. Thus, we confirm that neuronal activity can indeed regulate axonal mitochondrial transport, and reveal a spatial pattern to this regulation which went previously undetected. Together, these findings indicate a potent, but localized role for activity-related calcium fluctuations in the regulation of axonal mitochondrial transport.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"18 ","pages":"1509283"},"PeriodicalIF":4.2,"publicationDate":"2024-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11652138/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142853684","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MorphoGlia, an interactive method to identify and map microglia morphologies, demonstrates differences in hippocampal subregions of an Alzheimer's disease mouse model.","authors":"Juan Pablo Maya-Arteaga, Humberto Martínez-Orozco, Sofía Diaz-Cintra","doi":"10.3389/fncel.2024.1505048","DOIUrl":"https://doi.org/10.3389/fncel.2024.1505048","url":null,"abstract":"<p><p>Microglia are dynamic central nervous system cells crucial for maintaining homeostasis and responding to neuroinflammation, as evidenced by their varied morphologies. Existing morphology analysis often fails to detect subtle variations within the full spectrum of microglial morphologies due to their reliance on predefined categories. Here, we present MorphoGlia, an interactive, user-friendly pipeline that objectively characterizes microglial morphologies. MorphoGlia employs a machine learning ensemble to select relevant morphological features of microglia cells, perform dimensionality reduction, cluster these features, and subsequently map the clustered cells back onto the tissue, providing a spatial context for the identified microglial morphologies. We applied this pipeline to compare the responses between saline solution (SS) and scopolamine (SCOP) groups in a SCOP-induced mouse model of Alzheimer's disease, with a specific focus on the hippocampal subregions CA1 and Hilus. Next, we assessed microglial morphologies across four groups: SS-CA1, SCOP-CA1, SS-Hilus, and SCOP-Hilus. The results demonstrated that MorphoGlia effectively differentiated between SS and SCOP-treated groups, identifying distinct clusters of microglial morphologies commonly associated with pro-inflammatory states in the SCOP groups. Additionally, MorphoGlia enabled spatial mapping of these clusters, identifying the most affected hippocampal layers. This study highlights MorphoGlia's capability to provide unbiased analysis and clustering of microglial morphological states, making it a valuable tool for exploring microglial heterogeneity and its implications for central nervous system pathologies.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"18 ","pages":"1505048"},"PeriodicalIF":4.2,"publicationDate":"2024-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11653188/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142853682","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Traversing the epigenetic landscape: DNA methylation from retina to brain in development and disease.","authors":"Chunxiu Xu, Xuefei Fu, Huan Qin, Kai Yao","doi":"10.3389/fncel.2024.1499719","DOIUrl":"10.3389/fncel.2024.1499719","url":null,"abstract":"<p><p>DNA methylation plays a crucial role in development, aging, degeneration of various tissues and dedifferentiated cells. This review explores the multifaceted impact of DNA methylation on the retina and brain during development and pathological processes. First, we investigate the role of DNA methylation in retinal development, and then focus on retinal diseases, detailing the changes in DNA methylation patterns in diseases such as diabetic retinopathy (DR), age-related macular degeneration (AMD), and glaucoma. Since the retina is considered an extension of the brain, its unique structure allows it to exhibit similar immune response mechanisms to the brain. We further extend our exploration from the retina to the brain, examining the role of DNA methylation in brain development and its associated diseases, such as Alzheimer's disease (AD) and Huntington's disease (HD) to better understand the mechanistic links between retinal and brain diseases, and explore the possibility of communication between the visual system and the central nervous system (CNS) from an epigenetic perspective. Additionally, we discuss neurodevelopmental brain diseases, including schizophrenia (SZ), autism spectrum disorder (ASD), and intellectual disability (ID), focus on how DNA methylation affects neuronal development, synaptic plasticity, and cognitive function, providing insights into the molecular mechanisms underlying neurodevelopmental disorders.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"18 ","pages":"1499719"},"PeriodicalIF":4.2,"publicationDate":"2024-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11637887/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142827867","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The underlying molecular mechanisms of Fyn in neonatal hypoxic-ischaemic encephalopathy.","authors":"Jiao Zhou, Xiang Lu, Haichuan Wang","doi":"10.3389/fncel.2024.1476856","DOIUrl":"10.3389/fncel.2024.1476856","url":null,"abstract":"<p><p>Fyn is a cytoplasmic tyrosine kinase (TK) that is a nonreceptor and a member of the Src family of kinases (SFKs). It is involved in several transduction pathways in the central nervous system (CNS), such as oligodendrocyte development, myelination, axon guidance, and synaptic transmission. Owing to its wide range of activities in the molecular signaling pathways that underpin both neuropathologic and neurodevelopmental events, Fyn has remained of great interest for more than a century. Accumulating preclinical data have highlighted the potential role of Fyn in the pathophysiology of neonatal hypoxic-ischaemic encephalopathy (HIE). By mediating important signaling pathways, Fyn may control glutamate excitotoxicity, promote neuroinflammation and facilitate the death of neurons caused by oxidative stress. In this review, we address new evidence regarding the role of Fyn in the pathogenesis of this condition, with the aim of providing a reference for the development of new strategies to improve the prognosis of neonatal HIE. In addition, we also offer insights into additional Fyn-related molecular mechanisms involved in HIE pathology.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"18 ","pages":"1476856"},"PeriodicalIF":4.2,"publicationDate":"2024-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11631624/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142812468","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The BE (2)-M17 neuroblastoma cell line: revealing its potential as a cellular model for Parkinson's disease.","authors":"Angel Carvajal-Oliveros, Camila Román-Martínez, Enrique Reynaud, Eduardo Martínez-Martínez","doi":"10.3389/fncel.2024.1485414","DOIUrl":"10.3389/fncel.2024.1485414","url":null,"abstract":"<p><p>Parkinson's disease is a pathology with a wide range of <i>in vivo</i> and <i>in vitro</i> models available. Among these, the SH-SY5Y neuroblastoma cell line is one of the most employed. This model expresses catecholaminergic markers and can differentiate and acquire various neuronal phenotypes. However, challenges persist, primarily concerning the variability of growth media, expression of dopaminergic markers, and a wide variety of differentiation protocols have been reported in the literature without direct comparison between them. This lack of standardized differentiation conditions impacts result reproducibility and it makes it very difficult to compare the results obtained from different research groups. An alternative cellular model is the neuroblastoma BE (2)-M17 which exhibits a high basal expression of numerous dopaminergic markers such as tyrosine hydroxylase (TH), vesicular monoamine transporter 2 (VMAT2), and dopamine transporter (DAT). The BE (2)-M17 cells show neuronal properties, grows rapidly in conventional media, and can easily be differentiated to increase their dopaminergic phenotype. In this review, we will thoroughly explore the properties of the BE (2)-M17 cell line and discuss its potential as an excellent model for studying Parkinson's disease.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"18 ","pages":"1485414"},"PeriodicalIF":4.2,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11628309/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142806683","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Interlaminar and varicose-projection astrocytes: toward a new understanding of the primate brain.","authors":"Caterina Ciani, Carmen Falcone","doi":"10.3389/fncel.2024.1477753","DOIUrl":"10.3389/fncel.2024.1477753","url":null,"abstract":"<p><p>In the last years, science started to move toward a more <i>glio-neurocentric</i> view, in which astrocytes are hypothesized to be directly involved in cognitive functions. Indeed, astrocytes show a variety of shapes with species-specific characteristics, suggesting a specialization of roles during evolution. Interlaminar (ILA) and varicose-projection (VP-As) astrocytes show an anatomical organization that is different compared to the classical horizontal net typically formed by protoplasmic and fibrous astrocytes. ILAs show a modular architecture with the soma in the first cortical layer and processes toward the deep layers with species-specific length. VP-As reside in the deep layers of the cortex, are characterized by varicosities on the longest processes, and are individual-specific. These characteristics suggest roles that are more complex than what was theorized until now. Here, we recapitulate what we know so far from literature from the first time ILAs were described to the most recent discoveries, spanning from morphology description, hypothesis on the development to their features in diseases. For a complete glance on this topic, we included a final paragraph on which techniques and models were used to study ILAs and VP-As, and what new avenues may be opened thanks to more novel methods.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"18 ","pages":"1477753"},"PeriodicalIF":4.2,"publicationDate":"2024-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11626530/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142800091","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regulation of cochlear hair cell function by intracellular calcium stores.","authors":"Ghanshyam P Sinha, Gregory I Frolenkov","doi":"10.3389/fncel.2024.1484998","DOIUrl":"10.3389/fncel.2024.1484998","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Introduction: &lt;/strong&gt;Mammalian hearing depends on the dual mechanosensory and motor functions of cochlear hair cells. Both these functions may be regulated by Ca&lt;sup&gt;2+&lt;/sup&gt; release from intracellular stores. However, it is still unclear how exactly intracellular Ca&lt;sup&gt;2+&lt;/sup&gt; release may affect either hair cell mechano-electrical transduction (MET) or prestin-dependent electromotility in outer hair cells (OHCs).&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;Here, we used photo-activatable (caged) compounds to generate fast increases of either Ca&lt;sup&gt;2+&lt;/sup&gt; or inositol-3-phosphate (IP&lt;sub&gt;3&lt;/sub&gt;) in the cytosol of young postnatal rodent auditory hair cells, thereby stimulating either Ca&lt;sup&gt;2+&lt;/sup&gt;- or IP&lt;sub&gt;3&lt;/sub&gt;- induced releases of Ca&lt;sup&gt;2+&lt;/sup&gt; from intracellular stores. Fast Ca&lt;sup&gt;2+&lt;/sup&gt; imaging was used to monitor propagation of Ca&lt;sup&gt;2+&lt;/sup&gt; signals along the length of a hair cell. To access potential physiological role(s) of intracellular Ca&lt;sup&gt;2+&lt;/sup&gt; releases, we used whole cell patch clamp to record: i) OHC voltage-dependent capacitance, a known electrical correlate of prestin-based electromotility, and ii) MET currents evoked by stereocilia bundle deflections with fluid-jet. In the latter experiments, changes of mechanical stiffness of the hair bundles were also quantified from video recordings of stereocilia movements.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Ca&lt;sup&gt;2+&lt;/sup&gt; uncaging at the OHC apex initiated Ca&lt;sup&gt;2+&lt;/sup&gt; wave propagating to the base of the cell with subsequent Ca&lt;sup&gt;2+&lt;/sup&gt; build-up there. Ca&lt;sup&gt;2+&lt;/sup&gt; uncaging at the OHC base generated long-lasting and apparently self-sustained Ca&lt;sup&gt;2+&lt;/sup&gt; responses, further confirming Ca&lt;sup&gt;2+&lt;/sup&gt;-induced Ca&lt;sup&gt;2+&lt;/sup&gt; release in the OHC basal region. Photoactivated IP&lt;sub&gt;3&lt;/sub&gt; initiated a slow increase of cytosolic Ca&lt;sup&gt;2+&lt;/sup&gt; ([Ca&lt;sup&gt;2+&lt;/sup&gt;] &lt;sub&gt;&lt;i&gt;i&lt;/i&gt;&lt;/sub&gt; ) throughout the whole OHC, confirming the presence of slow-activated IP&lt;sub&gt;3&lt;/sub&gt;-gated Ca&lt;sup&gt;2+&lt;/sup&gt; stores in OHCs. Interestingly, Ca&lt;sup&gt;2+&lt;/sup&gt; uncaging produced no effects on OHC voltage-dependent capacitance. In an OHC, the rise of [Ca&lt;sup&gt;2+&lt;/sup&gt;] &lt;sub&gt;&lt;i&gt;i&lt;/i&gt;&lt;/sub&gt; is known to decrease axial stiffness of the cell and may modulate the stiffness of mechanosensory stereocilia bundles. To separate these two phenomena, we explored the potential effects of intracellular Ca&lt;sup&gt;2+&lt;/sup&gt; release on mechanical properties of stereocilia bundles in cochlear inner hair cells (IHCs). Ca&lt;sup&gt;2+&lt;/sup&gt; uncaging at the apex of an IHC caused a long-lasting increase in mechanical stiffness of stereocilia bundle without any changes in the amplitude or deflection sensitivity of the MET current.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Discussion: &lt;/strong&gt;We concluded that the most likely physiological role of IP&lt;sub&gt;3&lt;/sub&gt;-gated Ca&lt;sup&gt;2+&lt;/sup&gt; release at the apex of the cell is the regulation of hair bundle stiffness. In contrast, Ca&lt;sup&gt;2+&lt;/sup&gt;-induced Ca&lt;sup&gt;2+&lt;/sup&gt; release at the base of OHCs seems to regulate","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"18 ","pages":"1484998"},"PeriodicalIF":4.2,"publicationDate":"2024-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11625566/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142800023","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction: Effect of histone deacetylase inhibitors trichostatin A and valproic acid on hair cell regeneration in zebrafish lateral line neuromasts.","authors":"","doi":"10.3389/fncel.2024.1530876","DOIUrl":"https://doi.org/10.3389/fncel.2024.1530876","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.3389/fncel.2014.00382.].</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"18 ","pages":"1530876"},"PeriodicalIF":4.2,"publicationDate":"2024-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11626386/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142800024","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}