Frontiers in Molecular Neuroscience最新文献

{"title":"Genetic and molecular mechanisms of hydrocephalus.","authors":"Xuehai Deng, Yiqian Chen, Qiyue Duan, Jianlin Ding, Zhong Wang, Junchi Wang, Xinlong Chen, Liangxue Zhou, Long Zhao","doi":"10.3389/fnmol.2024.1512455","DOIUrl":"10.3389/fnmol.2024.1512455","url":null,"abstract":"<p><p>Hydrocephalus is a neurological condition caused by aberrant circulation and/or obstructed cerebrospinal fluid (CSF) flow after cerebral ventricle abnormal dilatation. In the past 50 years, the diagnosis and treatment of hydrocephalus have remained understudied and underreported, and little progress has been made with respect to prevention or treatment. Further research on the pathogenesis of hydrocephalus is essential for developing new diagnostic, preventive, and therapeutic strategies. Various genetic and molecular abnormalities contribute to the mechanisms of hydrocephalus, including gene deletions or mutations, the activation of cellular inflammatory signaling pathways, alterations in water channel proteins, and disruptions in iron metabolism. Several studies have demonstrated that modulating the expression of key proteins, including TGF-β, VEGF, Wnt, AQP, NF-κB, and NKCC, can significantly influence the onset and progression of hydrocephalus. This review summarizes and discusses key mechanisms that may be involved in the pathogenesis of hydrocephalus at both the genetic and molecular levels. While obstructive hydrocephalus can often be addressed by removing the obstruction, most cases require treatment strategies that involve merely slowing disease progression by correcting CSF circulation patterns. There have been few new research breakthroughs in the prevention and treatment of hydrocephalus.</p>","PeriodicalId":12630,"journal":{"name":"Frontiers in Molecular Neuroscience","volume":"17 ","pages":"1512455"},"PeriodicalIF":3.5,"publicationDate":"2025-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11746911/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143004156","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":"Modeling of auditory neuropathy spectrum disorders associated with the <i>TEME43</i> variant reveals impaired gap junction function of iPSC-derived glia-like support cells.","authors":"Xiaoming Kang, Lu Ma, Jie Wen, Wei Gong, Xianlin Liu, Yihan Hu, Zhili Feng, Qiancheng Jing, Yuexiang Cai, Sijun Li, Xinzhang Cai, Kai Yuan, Yong Feng","doi":"10.3389/fnmol.2024.1457874","DOIUrl":"10.3389/fnmol.2024.1457874","url":null,"abstract":"<p><p>Auditory neuropathy spectrum disorder (ANSD) is an auditory dysfunction disorder characterized by impaired speech comprehension. Its etiology is complex and can be broadly categorized into genetic and non-genetic factors. <i>TMEM43</i> mutation is identified as a causative factor in ANSD. While some studies have been conducted using animal models, its pathogenic mechanisms in humans remain unclear. TMEM43 is predominantly expressed in cochlear glia-like support cells (GLSs) and plays a vital role in gap junction intercellular communication. In this work, we utilized induced pluripotent stem cells from an ANSD patient carrying the <i>TMEM43</i> gene mutation c.1114C>T (p.Arg372Ter) and directed their differentiation toward GLSs to investigate the effect of <i>TMEM43</i> mutation on the function of gap junctions in cochlear GLSs <i>in vitro</i>. Reduced expression of genes associated with GLSs characteristics and reduced gap junction intercellular communication in <i>TMEM43</i> mutant cell lines were observed compared to controls. Transcriptome analysis revealed that differentially expressed genes were significantly enriched in pathways related to cell proliferation, differentiation, extracellular space and adhesion. Furthermore, significant alterations were noted in the PI3K-Akt signaling pathway and the calcium signaling pathway, which could potentially influence gap junction function and contribute to hearing loss. In summary, our study based on patient-derived iPSCs sheds new light on the molecular mechanisms by which <i>TMEM43</i> mutations may lead to ANSD. These mutations could result in developmental defects in GLSs and a diminished capacity for gap junction function, which may be implicated in the auditory deficits observed in ANSD patients. Our study explored the pathological effects of the <i>TMEM43</i> mutation and its causal relationship with ANSD using a patient-derived iPSC-based GLSs model, providing a foundation for future mechanistic studies and potential drug screening efforts.</p>","PeriodicalId":12630,"journal":{"name":"Frontiers in Molecular Neuroscience","volume":"17 ","pages":"1457874"},"PeriodicalIF":3.5,"publicationDate":"2025-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11743952/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143004174","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":"Mapping the research landscape of microRNAs in pain: a comprehensive bibliometric analysis.","authors":"Huaiming Wang, Qin Li, Jiang Zou, Jinjun Shu, Aimin Zhang, Hongwei Zhang, Qi Zhao, Shunxin Liu, Chan Chen, Guo Chen","doi":"10.3389/fnmol.2024.1493822","DOIUrl":"https://doi.org/10.3389/fnmol.2024.1493822","url":null,"abstract":"<p><strong>Background and objectives: </strong>MicroRNAs (miRNAs) have demonstrated significant potential in pain medicine research, including mechanisms, diagnosis, and therapy. However, no relative bibliometric analysis has been performed to summarize the progress in this area quantitatively.</p><p><strong>Methods: </strong>Literature was retrieved from the Web of Science Core Collection online database. A total of 1,295 papers were retrieved between January 1, 2000 and September 21, 2023 and underwent visualization and analysis using R software [Library [bibliometrix] and biblioshiny packages], VOSviewer (version 1.6.18), CiteSpace software (version 6.2.R4), and the bibliometrics website (http://bibliometric.com).</p><p><strong>Results: </strong>Publications in this field have increased annually since 2000, demonstrating growing research interest. China emerged as the most productive country, followed by the United States and Germany. Keyword analysis identified \"expression,\" \"neuropathic pain,\" and \"microRNAs\" as the most relevant keywords. Extensive collaboration among countries and institutions was also observed.</p><p><strong>Conclusion: </strong>The bibliometric analysis revealed a rapid growth of publications related to miRNAs and pain in the past 2 decades. Keywords analysis indicates that \"expression,\" \"neuropathic pain,\" and \"microRNA\" are the most frequently used words in this research field. However, more robust and globally recognized basic studies and clinical trials from prestigious journals are required.</p>","PeriodicalId":12630,"journal":{"name":"Frontiers in Molecular Neuroscience","volume":"17 ","pages":"1493822"},"PeriodicalIF":3.5,"publicationDate":"2024-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11703907/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142947473","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 role of Aha1 in cancer and neurodegeneration.","authors":"Brian S J Blagg, Kevin C Catalfano","doi":"10.3389/fnmol.2024.1509280","DOIUrl":"https://doi.org/10.3389/fnmol.2024.1509280","url":null,"abstract":"<p><p>The 90 kDa Heat shock protein (Hsp90) is a family of ubiquitously expressed molecular chaperones responsible for the stabilization and maturation of >400 client proteins. Hsp90 exhibits dramatic conformational changes to accomplish this, which are regulated by partner proteins termed co-chaperones. One of these co-chaperones is called the activator or Hsp90 ATPase activity homolog 1 (Aha1) and is the most potent accelerator of Hsp90 ATPase activity. In conditions where Aha1 levels are dysregulated including cystic fibrosis, cancer and neurodegeneration, Hsp90 mediated client maturation is disrupted. Accumulating evidence has demonstrated that many disease states exhibit large hetero-protein complexes with Hsp90 as the center. Many of these include Aha1, where increased Aha1 levels drive disease states forward. One strategy to block these effects is to design small molecule disruptors of the Hsp90/Aha1 complex. Studies have demonstrated that current Hsp90/Aha1 small molecule disruptors are effective in both models for cancer and neurodegeration.</p>","PeriodicalId":12630,"journal":{"name":"Frontiers in Molecular Neuroscience","volume":"17 ","pages":"1509280"},"PeriodicalIF":3.5,"publicationDate":"2024-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11703849/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142947477","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":"Analysis of the pathogenicity and pathological characteristics of <i>NOTCH3</i> gene-sparing cysteine mutations <i>in vitro</i> and <i>in vivo</i> models.","authors":"Zhenping Gong, Wan Wang, Ying Zhao, Yadan Wang, Ruihua Sun, Haohan Zhang, Fengyu Wang, Yaru Lu, Jiewen Zhang","doi":"10.3389/fnmol.2024.1391040","DOIUrl":"https://doi.org/10.3389/fnmol.2024.1391040","url":null,"abstract":"<p><strong>Background: </strong>Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is one of the most common inherited cerebral small vessel diseases caused by the NOTCH3 gene mutation. This mutation leads to the accumulation of NOTCH3 extracellular domain protein (NOTCH3^ECD) into the cerebral arterioles, causing recurrent stroke, white matter lesions, and cognitive impairment. With the development of gene sequencing technology, cysteine-sparing mutations can also cause CADASIL disease, however, the pathogenicity and pathogenic mechanisms of cysteine-sparing mutations remain controversial.</p><p><strong>Objective: </strong>To analyze the pathogenicity and pathological features of cysteine-sparing mutations in both <i>in vitro</i> and <i>in vivo</i> mouse models.</p><p><strong>Methods: </strong>A cysteine-sparing mutant of NOTCH3^ECD R75Q was constructed by lentiviral transfection <i>in vitro</i>, and the <i>NOTCH3 R75Q</i> knock-in mouse model was constructed by CRISPR/Cas-mediated genome engineering <i>in vivo</i>. A cycloheximide pulse-chase experiment was used to analyze the degradation of NOTCH3 extracellular domain proteins, and the deposition characteristics of NOTCH3^ECD were quantitatively analyzed by immunohistochemical staining. The characteristics of the smooth muscle cells and granular osmiophilic materials were observed using electron microscopy.</p><p><strong>Results: </strong>We elucidated that the <i>NOTCH3 R75Q</i> mutation is pathogenic. NOTCH3^ECD R75Q was found to be resistant to protein degradation and more likely to cause abnormal aggregation of NOTCH3^ECD, resulting in reduced cell activity <i>in vitro</i>. The <i>NOTCH3 R75Q</i> mouse model showed pathological characteristics of CADASIL, with age-dependent NOTCH3^ECD, granular osmiophilic material, and degenerated smooth muscle cells detected in the brain.</p><p><strong>Conclusion: </strong>To our knowledge, this is the first study to analyze the pathogenicity of <i>NOTCH3 R75Q</i> cysteine-sparing mutations in both <i>in vitro</i> and <i>in vivo</i> models. We demonstrate that NOTCH3^ECD induced by <i>NOTCH3 R75Q</i> mutation has toxic effects on cells and reveal the deposition characteristics of NOTCH3^ECD in the brain. This provides a feasible model and lays the foundation for further studies on the pathogenesis and therapeutic strategies of <i>NOTCH3</i> cysteine-sparing mutations.</p>","PeriodicalId":12630,"journal":{"name":"Frontiers in Molecular Neuroscience","volume":"17 ","pages":"1391040"},"PeriodicalIF":3.5,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11695339/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142931358","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":"Activation of mechanoreceptor Piezo1 inhibits enteric neuronal growth and migration <i>in vitro</i>.","authors":"Chioma Moneme, Oluyinka O Olutoye, Michał F Sobstel, Yuwen Zhang, Xinyu Zhou, Jacob L Kaminer, Britney A Hsu, Chengli Shen, Arabinda Mandal, Hui Li, Ling Yu, Swathi Balaji, Sundeep G Keswani, Lily S Cheng","doi":"10.3389/fnmol.2024.1474025","DOIUrl":"10.3389/fnmol.2024.1474025","url":null,"abstract":"<p><strong>Introduction: </strong>Dysfunction of the enteric nervous system (ENS) is linked to a myriad of gastrointestinal (GI) disorders. Piezo1 is a mechanosensitive ion channel found throughout the GI tract, but its role in the ENS is largely unknown. We hypothesize that Piezo1 plays an important role in the growth and development of the ENS.</p><p><strong>Methods: </strong>Enteric neural crest-derived progenitor cells (ENPC) were isolated from adult mouse intestine and propagated in culture as neurospheres. ENPC-derived neurons were then subject to <i>in vitro</i> stretch in the presence or absence of Piezo1 antagonist (GsMTx4). Transcriptomes of stretched and unstretched ENPC-derived cells were compared using bulk RNA sequencing. Enteric neurons were also cultured under static conditions in the presence of Piezo1 agonist (Yoda1) or antagonist. Neuronal phenotype, migration, and recovery from injury were compared between groups.</p><p><strong>Results: </strong>Though stretch did not cause upregulation of Piezo1 expression in enteric neurons, both stretch and Piezo1 activation produced similar alterations in neuronal morphology. Compared to control, neurite length was significantly shorter when stretched and in the presence of Piezo1 activation. Piezo1 inhibition prevented a significant reduction in neurite length in stretched neurons. Piezo1 inhibition also led to significantly increased neuronal migration, whereas Piezo1 activation resulted in significantly decreased neuronal migration and slower neuronal recovery from injury.</p><p><strong>Conclusion: </strong>Mechanotransduction plays an important role in regulating normal GI function. Our results suggest that the Piezo1 mechanoreceptor may play an important role in the ENS as its activation leads to decreased neuronal growth and migration. Piezo1 could be an important target for diseases of ENS dysfunction and development.</p>","PeriodicalId":12630,"journal":{"name":"Frontiers in Molecular Neuroscience","volume":"17 ","pages":"1474025"},"PeriodicalIF":3.5,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11695422/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142931340","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: Endothelial-monocyte activating polypeptide II suppresses the <i>in vitro</i> glioblastoma-induced angiogenesis by inducing autophagy.","authors":"","doi":"10.3389/fnmol.2024.1543503","DOIUrl":"https://doi.org/10.3389/fnmol.2024.1543503","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.3389/fnmol.2017.00208.].</p>","PeriodicalId":12630,"journal":{"name":"Frontiers in Molecular Neuroscience","volume":"17 ","pages":"1543503"},"PeriodicalIF":3.5,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11689653/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142914616","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":"Sensory innervation in the prostate and a role for calcitonin gene-related peptide in prostatic epithelial proliferation.","authors":"Hanyu Xia, Travis J Jerde, Jill C Fehrenbacher","doi":"10.3389/fnmol.2024.1497735","DOIUrl":"10.3389/fnmol.2024.1497735","url":null,"abstract":"<p><strong>Introduction: </strong>The prostate is densely innervated like many visceral organs and glands. However, studies to date have focused on sympathetic and parasympathetic nerves and little attention has been given to the presence or function of sensory nerves in the prostate. Recent studies have highlighted a role for sensory nerves beyond perception of noxious stimuli, as anterograde release of neuropeptides from sensory nerves can affect vascular tone and local immune responses.</p><p><strong>Methods: </strong>To identify the degree of sensory innervation in the prostate, we utilized state-of-the-art tissue clearing and microscopy to visualize sensory innervation in the different lobes of the mouse prostate. To determine whether sensory nerves have a role in regulating proliferation within the prostate, we used an intersectional genetic and toxin approach to ablate peptidergic sensory nerves systemically.</p><p><strong>Results: </strong>We found that sensory neurons are abundant in the prostate both in nerve bundles along the vasculature and as independent nerve fibers wrapped around prostatic acini in a net-like fashion. In addition to the dense innervation of the prostate, we found that <i>Calca</i> haploinsufficiency, the genotype control for our intersectional ablation model, results in a diminished level of Ki67 staining in the stromal compartment of the dorsal lobe and a diminishing Ki67 trend in other lobes.</p><p><strong>Discussion: </strong>These findings suggest that sensory neurons might have developmental or homeostatic effects within the prostate. Further studies are warranted to assess the role of sensory neurons and the sensory neuropeptides on prostatic development and on proliferation in the presence of pro-inflammatory stimuli such as bacterial infection or tumor cells.</p>","PeriodicalId":12630,"journal":{"name":"Frontiers in Molecular Neuroscience","volume":"17 ","pages":"1497735"},"PeriodicalIF":3.5,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11688385/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142914617","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":"Insights into the molecular underlying mechanisms and therapeutic potential of endoplasmic reticulum stress in sensorineural hearing loss.","authors":"Guanzhen Li, Huiming Yang, Peiyuan Zhang, Yan Guo, Lili Yuan, Shujiao Xu, Yingxue Yuan, Huabao Xiong, Haiyan Yin","doi":"10.3389/fnmol.2024.1443401","DOIUrl":"10.3389/fnmol.2024.1443401","url":null,"abstract":"<p><p>Sensorineural hearing loss (SNHL) is characterized by a compromised cochlear perception of sound waves. Major risk factors for SNHL include genetic mutations, exposure to noise, ototoxic medications, and the aging process. Previous research has demonstrated that inflammation, oxidative stress, apoptosis, and autophagy, which are detrimental to inner ear cells, contribute to the pathogenesis of SNHL; however, the precise mechanisms remain inadequately understood. The endoplasmic reticulum (ER) plays a key role in various cellular processes, including protein synthesis, folding, lipid synthesis, cellular calcium and redox homeostasis, and its homeostatic balance is essential to maintain normal cellular function. Accumulation of unfolded or misfolded proteins in the ER leads to endoplasmic reticulum stress (ERS) and activates the unfolded protein response (UPR) signaling pathway. The adaptive UPR has the potential to reestablish protein homeostasis, whereas the maladaptive UPR, associated with inflammation, oxidative stress, apoptosis, and autophagy, can lead to cellular damage and death. Recent evidence increasingly supports the notion that ERS-mediated cellular damage responses play a crucial role in the initiation and progression of various SNHLs. This article reviews the research advancements on ERS in SNHL, with the aim of elucidating molecular biological mechanisms underlying ERS in SNHL and providing novel insights for the treatment.</p>","PeriodicalId":12630,"journal":{"name":"Frontiers in Molecular Neuroscience","volume":"17 ","pages":"1443401"},"PeriodicalIF":3.5,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11688397/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142914615","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":"Circulating miR-134 in mesial temporal lobe epilepsy: implications in hippocampal sclerosis development and drug resistance.","authors":"Bárbara Guerra Leal, Cláudia Carvalho, Cristina Santos, Raquel Samões, Ricardo Martins-Ferreira, Catarina Teixeira, Diana Rodrigues, Joel Freitas, Carolina Lemos, Rui Chorão, João Ramalheira, João Lopes, António Martins da Silva, Paulo Pinho E Costa, João Chaves","doi":"10.3389/fnmol.2024.1512860","DOIUrl":"10.3389/fnmol.2024.1512860","url":null,"abstract":"","PeriodicalId":12630,"journal":{"name":"Frontiers in Molecular Neuroscience","volume":"17 ","pages":"1512860"},"PeriodicalIF":3.5,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11688299/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142914614","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}