Frontiers in Cellular Neuroscience最新文献

{"title":"Schwann cell-derived exosomes ameliorate peripheral neuropathy induced by ablation of dicer in Schwann cells","authors":"Lei Wang, XueRong Lu, Alexandra Szalad, Xian Shuang Liu, Yi Zhang, Xinli Wang, William Anthony Golembieski, Brianna Powell, Mikkala Mccann, Mei Lu, Michael Chopp, Zheng Gang Zhang","doi":"10.3389/fncel.2024.1462228","DOIUrl":"https://doi.org/10.3389/fncel.2024.1462228","url":null,"abstract":"BackgroundMicroRNAs (miRNAs) in Schwann cells (SCs) mediate peripheral nerve function. Ablating Dicer, a key gene in miRNA biogenesis, in SCs causes peripheral neuropathy. Exosomes from healthy SCs (SC-Exo) ameliorate diabetic peripheral neuropathy in part via miRNAs. Thus, using transgenic mice with conditional and inducible ablation of Dicer in proteolipid protein (PLP) expressing SCs (PLP-cKO), we examined whether SC-Exo could reduce peripheral neuropathy in PLP-cKO mice.MethodsPLP-cKO mice at the age of 16 weeks (8 week post-Tamoxifen) were randomly treated with SC-Exo or saline weekly for 8 weeks. Age-and sex-matched wild-type (WT) littermates were used as controls. Peripheral neurological functions, sciatic nerve integrity, and myelination were analyzed. Quantitative RT-PCR and Western blot analyses were performed to examine miRNA and protein expression in sciatic nerve tissues, respectively.ResultsCompared to the WT mice, PLP-cKO mice exhibited a significant decrease in motor and sensory conduction velocities, thermal sensitivity, and motor coordination. PLP-cKO mice exhibited substantial demyelination and axonal damage of the sciatic nerve. Treatment of PLP-cKO mice with SC-Exo significantly ameliorated the peripheral neuropathy and sciatic nerve damage. PLP-cKO mice showed a substantial reduction in a set of Dicer-related miRNAs known to regulate myelination, axonal integrity, and inflammation such as miR-138, −146a and − 338 in the sciatic nerve. In addition, PLP-cKO mice exhibited significant reduction of myelin forming proteins, early growth response 2 (EGR2) and sex determining region Y-box10 (Sox10), but significantly increased myelination inhibitors, Notch1, c-Jun, and Sox2 and the axonal growth inhibitor phosphatase and tens in homolog (PTEN). However, SC-Exo treatment reversed the PLP-cKO altered miRNAs and proteins.ConclusionThis study demonstrates that exogenous SC-Exo ameliorate peripheral neuropathy induced by Dicer ablation in PLP expressing SCs. The therapeutic benefit may be mediated by the SC-Exo altered miRNAs and their targeted genes.","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"128 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142191400","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Stimulating myelin restoration with BDNF: a promising therapeutic approach for Alzheimer's disease","authors":"Ioanna Zota, Konstantina Chanoumidou, Achille Gravanis, Ioannis Charalampopoulos","doi":"10.3389/fncel.2024.1422130","DOIUrl":"https://doi.org/10.3389/fncel.2024.1422130","url":null,"abstract":"Alzheimer's Disease (AD) is a chronic neurodegenerative disorder constituting the most common form of dementia (60%−70% of cases). Although AD presents majorly a neurodegenerative pathology, recent clinical evidence highlights myelin impairment as a key factor in disease pathogenesis. The lack of preventive or restorative treatment is emphasizing the need to develop novel therapeutic approaches targeting to the causes of the disease. Recent studies in animals and patients have highlighted the loss of myelination of the neuronal axons as an extremely aggravating factor in AD, in addition to the formation of amyloid plaques and neurofibrillary tangles that are to date the main pathological hallmarks of the disease. Myelin breakdown represents an early stage event in AD. However, it is still unclear whether myelin loss is attributed only to exogenous factors like inflammatory processes of the tissue or to impaired oligodendrogenesis as well. Neurotrophic factors are well established protective molecules under many pathological conditions of the neural tissue, contributing also to proper myelination. Due to their inability to be used as drugs, many research efforts are focused on substituting neurotrophic activity with small molecules. Our research team has recently developed novel micromolecular synthetic neurotrophin mimetics (MNTs), selectively acting on neurotrophin receptors, and thus offering a unique opportunity for innovative therapies against neurodegenerative diseases. These small sized, lipophilic molecules address the underlying biological effect of these diseases (neuroprotective action), but also they exert significant neurogenic actions inducing neuronal replacement of the disease areas. One of the significant neurotrophin molecules in the Central Nervous System is Brain-Derived-Neurotrophin-Factor (BDNF). BDNF is a neurotrophin that not only supports neuroprotection and adult neurogenesis, but also mediates pro-myelinating effects in the CNS. BDNF binds with high-affinity on the TrkB neurotrophin receptor and enhances myelination by increasing the density of oligodendrocyte progenitor cells (OPCs) and playing an important role in CNS myelination. Conclusively, in the present review, we discuss the myelin pathophysiology in Alzheimer's Diseases, as well as the role of neurotrophins, and specifically BDNF, in myelin maintenance and restoration, revealing its valuable therapeutic potential against AD.","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"12 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142191401","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial: The roles of peripheral immune cells and their circulatory effector molecules in neuropsychiatric disorders.","authors":"Bernhard T Baune,Eve-Marie Tremblay,Karl Bechter,Li Tian","doi":"10.3389/fncel.2024.1471683","DOIUrl":"https://doi.org/10.3389/fncel.2024.1471683","url":null,"abstract":"","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"2 1","pages":"1471683"},"PeriodicalIF":5.3,"publicationDate":"2024-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142260211","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A comprehensive review of electrophysiological techniques in amyotrophic lateral sclerosis research","authors":"Keyuan Ren, Qinglong Wang, Douglas Jiang, Ethan Liu, Julie Alsmaan, Rui Jiang, Seward B. Rutkove, Feng Tian","doi":"10.3389/fncel.2024.1435619","DOIUrl":"https://doi.org/10.3389/fncel.2024.1435619","url":null,"abstract":"Amyotrophic lateral sclerosis (ALS), a devastating neurodegenerative disease, is characterized by progressive motor neuron degeneration, leading to widespread weakness and respiratory failure. While a variety of mechanisms have been proposed as causes of this disease, a full understanding remains elusive. Electrophysiological alterations, including increased motor axon excitability, likely play an important role in disease progression. There remains a critical need for non-animal disease models that can integrate electrophysiological tools to better understand underlying mechanisms, track disease progression, and evaluate potential therapeutic interventions. This review explores the integration of electrophysiological technologies with ALS disease models. It covers cellular and clinical electrophysiological tools and their applications in ALS research. Additionally, we examine conventional animal models and highlight advancements in humanized models and 3D organoid technologies. By bridging the gap between these models, we aim to enhance our understanding of ALS pathogenesis and facilitate the development of new therapeutic strategies.","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"5 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142191402","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The evolution of mesenchymal stem cell-derived neural progenitor therapy for Multiple Sclerosis: from concept to clinic","authors":"Majid Ghareghani, Ayanna Arneaud, Serge Rivest","doi":"10.3389/fncel.2024.1428652","DOIUrl":"https://doi.org/10.3389/fncel.2024.1428652","url":null,"abstract":"This review delves into the generation and therapeutic applications of mesenchymal stem cell-derived neural progenitors (MSC-NPs) in Multiple Sclerosis (MS), a chronic autoimmune disease characterized by demyelination, neuroinflammation, and progressive neurological dysfunction. Most current treatment paradigms primarily aimed at regulating the immune response show little success against the neurodegenerative aspect of MS. This calls for new therapies that would play a role in neurodegeneration and functional recovery of the central nervous system (CNS). While utilizing MSC was found to be a promising approach in MS therapy, the initiation of MSC-NPs therapy is an innovation that introduces a new perspective, a dual-action plan, that targets both the immune and neurodegenerative mechanisms of MS. The first preclinical studies using animal models of the disease showed that MSC-NPs could migrate to damaged sites, support remyelination, and possess immunomodulatory properties, thus, providing a solid basis for their human application. Based on pilot feasibility studies and phase I clinical trials, this review covers the transition from preclinical to clinical phases, where intrathecally administered autologous MSC-NPs has shown great hope in treating patients with progressive MS by providing safety, tolerability, and preliminary efficacy. This review, after addressing the role of MSCs in MS and its animal model of experimental autoimmune encephalomyelitis (EAE), highlights the significance of the MSC-NP therapy by organizing its advancement processes from experimental models to clinical translation in MS treatment. It points out the continuing obstacles, which require more studies to improve therapeutic protocols, uncovers the mechanisms of action, and establishes long-term efficacy and safety in larger controlled trials.","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"22 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142191403","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Astrocyte Ca2+ in the dorsal striatum suppresses neuronal activity to oppose cue-induced reinstatement of cocaine seeking","authors":"Navid S. Tavakoli, Samantha G. Malone, Tanner L. Anderson, Ryson E. Neeley, Artin Asadipooya, Michael T. Bardo, Pavel I. Ortinski","doi":"10.3389/fncel.2024.1347491","DOIUrl":"https://doi.org/10.3389/fncel.2024.1347491","url":null,"abstract":"Recent literature supports a prominent role for astrocytes in regulation of drug-seeking behaviors. The dorsal striatum, specifically, is known to play a role in reward processing with neuronal activity that can be influenced by astrocyte Ca<jats:sup>2+</jats:sup>. However, the manner in which Ca<jats:sup>2+</jats:sup> in dorsal striatum astrocytes impacts neuronal signaling after exposure to self-administered cocaine remains unclear. We addressed this question following over-expression of the Ca<jats:sup>2+</jats:sup> extrusion pump, hPMCA2w/b, in dorsal striatum astrocytes and the Ca<jats:sup>2+</jats:sup> indicator, GCaMP6f, in dorsal striatum neurons of rats that were trained to self-administer cocaine. Following extinction of cocaine-seeking behavior, the rats over-expressing hMPCA2w/b showed a significant increase in cue-induced reinstatement of cocaine seeking. Suppression of astrocyte Ca<jats:sup>2+</jats:sup> increased the amplitude of neuronal Ca<jats:sup>2+</jats:sup> transients in brain slices, but only after cocaine self-administration. This was accompanied by decreased duration of neuronal Ca<jats:sup>2+</jats:sup> events in the cocaine group and no changes in Ca<jats:sup>2+</jats:sup> event frequency. Acute administration of cocaine to brain slices decreased amplitude of neuronal Ca<jats:sup>2+</jats:sup> in both the control and cocaine self-administration groups regardless of hPMCA2w/b expression. These results indicated that astrocyte Ca<jats:sup>2+</jats:sup> control over neuronal Ca<jats:sup>2+</jats:sup> transients was enhanced by cocaine self-administration experience, although sensitivity to acutely applied cocaine remained comparable across all groups. To explore this further, we found that neither the hMPCA2w/b expression nor the cocaine self-administration experience altered regulation of neuronal Ca<jats:sup>2+</jats:sup> events by NPS-2143, a Ca<jats:sup>2+</jats:sup> sensing receptor (CaSR) antagonist, suggesting that plasticity of neuronal signaling after hPMCA2w/b over-expression was unlikely to result from elevated extracellular Ca<jats:sup>2+</jats:sup>. We conclude that astrocyte Ca<jats:sup>2+</jats:sup> in the dorsal striatum impacts neurons via cell-intrinsic mechanisms (e.g., gliotransmission, metabolic coupling, etc.) and impacts long-term neuronal plasticity after cocaine self-administration differently from neuronal response to acute cocaine. Overall, astrocyte Ca<jats:sup>2+</jats:sup> influences neuronal output in the dorsal striatum to promote resistance to cue-induced reinstatement of cocaine seeking.","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"395 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142191404","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Old innovations and shifted paradigms in cellular neuroscience.","authors":"Riccardo Fesce","doi":"10.3389/fncel.2024.1460219","DOIUrl":"10.3389/fncel.2024.1460219","url":null,"abstract":"<p><p>Once upon a time the statistics of quantal release were fashionable: \"<i>n</i>\" available vesicles (fusion sites), each with probability \"<i>p</i>\" of releasing a quantum. The story was not so simple, a nice paradigm to be abandoned. Biophysicists, experimenting with \"black films,\" explained the astonishing rapidity of spike-induced release: calcium can trigger the fusion of lipidic vesicles with a lipid bilayer, by masking the negative charges of the membranes. The idea passed away, buried by the discovery of NSF, SNAPs, SNARE proteins and synaptotagmin, Munc, RIM, complexin. Electrophysiology used to be a field for few adepts. Then came patch clamp, and multielectrode arrays and everybody became electrophysiologists. Now, optogenetics have blossomed, and the whole field has changed again. Nice surprise for me, when Alvarez de Toledo demonstrated that release of transmitters could occur through the transient opening of a pore between the vesicle and the plasma-membrane, no collapse of the vesicle in the membrane needed: my mentor Bruno Ceccarelli had cherished this idea (\"kiss and run\") and tried to prove it for 20 years. The most impressive developments have probably regarded IT, computers and all their applications; machine learning, AI, and the truly spectacular innovations in brain imaging, especially functional ones, have transformed cognitive neurosciences into a new extraordinarily prolific field, and certainly let us imagine that we may finally understand what is going on in our brains. Cellular neuroscience, on the other hand, though the large public has been much less aware of the incredible amount of information the scientific community has acquired on the cellular aspects of neuronal function, may indeed help us to eventually understand the mechanistic detail of how the brain work. But this is no more in the past, this is the future.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"18 ","pages":"1460219"},"PeriodicalIF":4.2,"publicationDate":"2024-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11371623/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142135072","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":"Regulatory T cells administration reduces anxiety-like behavior in mice submitted to chronic restraint stress.","authors":"Yamila Cepeda, Roberto Elizondo-Vega, Camila Garrido, Catalina Tobar, Matías Araneda, Patricia Oliveros, Patricio Ordenes, Claudio Carril, Pía M Vidal, Patricia Luz-Crawford, María A García-Robles, Karina Oyarce","doi":"10.3389/fncel.2024.1406832","DOIUrl":"10.3389/fncel.2024.1406832","url":null,"abstract":"<p><strong>Background: </strong>Major depression disorder (MDD) and anxiety are common mental disorders that significantly affect the quality of life of those who suffer from them, altering the person's normal functioning. From the biological perspective, the most classical hypothesis explaining their occurrence relies on neurotransmission and hippocampal excitability alterations. However, around 30% of MDD patients do not respond to medication targeting these processes. Over the last decade, the involvement of inflammatory responses in depression and anxiety pathogenesis has been strongly acknowledged, opening the possibility of tackling these disorders from an immunological point of view. In this context, regulatory T cells (Treg cells), which naturally maintain immune homeostasis by suppressing inflammation could be promising candidates for their therapeutic use in mental disorders.</p><p><strong>Methods: </strong>To test this hypothesis, C57BL/6 adult male mice were submitted to classical stress protocols to induce depressive and anxiety-like behavior; chronic restriction stress (CRS), and chronic unpredictable stress (CUS). Some of the stressed mice received a single adoptive transfer of Treg cells during stress protocols. Mouse behavior was analyzed through the open field (OFT) and forced swim test (FST). Blood and spleen samples were collected for T cell analysis using cell cytometry, while brains were collected to study changes in microglia by immunohistochemistry.</p><p><strong>Results: </strong>Mice submitted to CRS and CUS develop anxiety and depressive-like behavior, and only CRS mice exhibit lower frequencies of circulating Treg cells. Adoptive transfer of Treg cells decreased anxiety-like behavior in the OFT only in CRS model, but not depressive behavior in FST in neither of the two models. In CRS mice, Treg cells administration lowered the number of microglia in the hippocampus, which increased due this stress paradigm, and restored its arborization. However, in CUS mice, Treg cells administration increased microglia number with no significant effect on their arborization.</p><p><strong>Conclusion: </strong>Our results for effector CD4⁺ T cells in the spleen and microglia number and morphology in the hippocampus add new evidence in favor of the participation of inflammatory responses in the development of depressive and anxiety-like behavior and suggest that the modulation of key immune cells such as Treg cells, could have beneficial effects on these disorders.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"18 ","pages":"1406832"},"PeriodicalIF":4.2,"publicationDate":"2024-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11349540/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142106011","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":"Editorial: Cellular and molecular mechanisms in social and repetitive behaviours: a focus on cortico-striatal circuitry.","authors":"Ilaria Morella, Riccardo Brambilla, Yann Herault","doi":"10.3389/fncel.2024.1470882","DOIUrl":"10.3389/fncel.2024.1470882","url":null,"abstract":"","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"18 ","pages":"1470882"},"PeriodicalIF":4.2,"publicationDate":"2024-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11338908/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142035621","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":"Exploring the biological basis of acupuncture treatment for traumatic brain injury: a review of evidence from animal models","authors":"Minmin Wu, Wenjing Song, Lili Teng, Jinting Li, Jiayu Liu, Hanwen Ma, Ge Zhang, Jiongliang Zhang, Qiuxin Chen","doi":"10.3389/fncel.2024.1405782","DOIUrl":"https://doi.org/10.3389/fncel.2024.1405782","url":null,"abstract":"Traumatic brain injury (TBI) occurs when external physical forces impact the brain, potentially causing long-term issues such as post-traumatic stress disorders and cognitive and physical dysfunctions. The diverse nature of TBI pathology and treatment has led to a rapid acceleration in research on its biological mechanisms over the past decade. This surge presents challenges in assessing, managing, and predicting outcomes for TBI cases. Despite the development and testing of various therapeutic strategies aimed at mitigating neurological decline after TBI, a definitive cure for these conditions remains elusive. Recently, a growing focus has been on preclinical research investigating acupuncture as a potential treatment method for TBI sequelae. Acupuncture, being a cost-effective non-pharmacological therapy, has demonstrated promise in improving functional outcomes after brain injury. However, the precise mechanisms underlying the anticipated improvements induced by acupuncture remain poorly understood. In this study, we examined current evidence from animal studies regarding acupuncture’s efficacy in improving functional outcomes post-TBI. We also proposed potential biological mechanisms, such as glial cells (microglia astrocytes), autophagy, and apoptosis. This information will deepen our understanding of the underlying mechanisms through which acupuncture exerts its most beneficial effects post-TBI, assisting in forming new clinical strategies to maximize benefits for these patients.","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"75 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141931193","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}