Neural Plasticity最新文献

{"title":"Progression in Time of Dentate Gyrus Granule Cell Layer Widening due to Excitotoxicity Occurs along In Vivo LTP Reinstatement and Contextual Fear Memory Recovery","authors":"Karina Hernández Mercado, Araceli Martínez Moreno, Luis Francisco Rodríguez Durán, M. Escobar, A. Zepeda","doi":"10.21203/rs.3.rs-1344273/v1","DOIUrl":"https://doi.org/10.21203/rs.3.rs-1344273/v1","url":null,"abstract":"The dentate gyrus (DG) is the gateway of sensory information arriving from the perforant pathway (PP) to the hippocampus. The adequate integration of incoming information into the DG is paramount in the execution of hippocampal-dependent cognitive functions. An abnormal DG granule cell layer (GCL) widening due to granule cell dispersion has been reported under hyperexcitation conditions in animal models as well as in patients with mesial temporal lobe epilepsy, but also in patients with no apparent relation to epilepsy. Strikingly, it is unclear whether the presence and severity of GCL widening along time affect synaptic processing arising from the PP and alter the performance in hippocampal-mediated behaviors. To evaluate the above, we injected excitotoxic kainic acid (KA) unilaterally into the DG of mice and analyzed the evolution of GCL widening at 10 and 30 days post injection (dpi), while analyzing if KA-induced GCL widening affected in vivo long-term potentiation (LTP) in the PP-DG pathway, as well as the performance in learning and memory through contextual fear conditioning. Our results show that at 10 dpi, when a subtle GCL widening was observed, LTP induction, as well as contextual fear memory, were impaired. However, at 30 dpi when a pronounced increase in GCL widening was found, LTP induction and contextual fear memory were already reestablished. These results highlight the plastic potential of the DG to recover some of its functions despite a major structural alteration such as abnormal GCL widening.","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":"32 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2022-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85590231","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Preferential Involvement of BRCA1/BARD1, Not Tip60/Fe65, in DNA Double-Strand Break Repair in Presenilin-1 P117L Alzheimer Models","authors":"Marcella M. Authiat, Emmanuelle Gruz-Gibelli, Julien Colas, E. Bianchi, Marta Garcia-Arauzo, P. Marin, F. Herrmann, A. Savioz","doi":"10.1155/2022/3172861","DOIUrl":"https://doi.org/10.1155/2022/3172861","url":null,"abstract":"Recently, we showed that DNA double-strand breaks (DSBs) are increased by the Aβ42-amyloid peptide and decreased by all-trans retinoic acid (RA) in SH-SY5Y cells and C57BL/6J mice. The present work was aimed at investigating DSBs in cells and murine models of Alzheimer's disease carrying the preseniline-1 (PS1) P117L mutation. We observed that DSBs could hardly decrease following RA treatment in the mutated cells compared to the wild-type cells. The activation of the amyloidogenic pathway is proposed in the former case as Aβ42- and RA-dependent DSBs changes were reproduced by an α-secretase and a γ-secretase inhibitions, respectively. Unexpectedly, the PS1 P117L cells showed lower DSB levels than the controls. As the DSB repair proteins Tip60 and Fe65 were less expressed in the mutated cell nuclei, they do not appear to contribute to this difference. On the contrary, full-length BRCA1 and BARD1 proteins were significantly increased in the chromatin compartment of the mutated cells, suggesting that they decrease DSBs in the pathological situation. These Western blot data were corroborated by in situ proximity ligation assays: the numbers of BRCA1-BARD1, not of Fe65-Tip60 heterodimers, were increased only in the mutated cell nuclei. RA also enhanced the expression of BARD1 and of the 90 kDa BRCA1 isoform. The increased BRCA1 expression in the mutated cells can be related to the enhanced difficulty to inhibit this pathway by BRCA1 siRNA in these cells. Overall, our study suggests that at earlier stages of the disease, similarly to PS1 P117L cells, a compensatory mechanism exists that decreases DSB levels via an activation of the BRCA1/BARD1 pathway. This supports the importance of this pathway in neuroprotection against Alzheimer's disease.","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":"40 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2022-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85382143","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Deficient Autophagy in Microglia Aggravates Repeated Social Defeat Stress-Induced Social Avoidance","authors":"Mai Sakai, Zhiqian Yu, Ryo Hirayama, Masaomi Nakasato, Yoshie Kikuchi, Chiaki Ono, H. Komatsu, M. Nakanishi, Hatsumi Yoshii, D. Stellwagen, T. Furuyashiki, M. Komatsu, Hiroaki Tomita","doi":"10.1155/2022/7503553","DOIUrl":"https://doi.org/10.1155/2022/7503553","url":null,"abstract":"Major depressive disorder (MDD) is associated with repeated exposure to environmental stress. Autophagy is activated under various stress conditions that are associated with several diseases in the brain. This study was aimed at elucidating the autophagy signaling changes in the prefrontal cortex (PFC) under repeated social defeat (RSD) to investigate the involvement of microglial autophagy in RSD-induced behavioral changes. We found that RSD stress, an animal model of MDD, significantly induced initial autophagic signals followed by increased transcription of autophagy-related genes (Atg6, Atg7, and Atg12) in the PFC. Similarly, significantly increased transcripts of ATGs (Atg6, Atg7, Atg12, and Atg5) were confirmed in the postmortem PFC of patients with MDD. The protein levels of the prefrontal cortical LC3B were significantly increased, whereas p62 was significantly decreased in the resilient but not in susceptible mice and patients with MDD. This indicates that enhanced autophagic flux may alleviate stress-induced depression. Furthermore, we identified that FKBP5, an early-stage autophagy regulator, was significantly increased in the PFC of resilient mice at the transcript and protein levels. In addition, the resilient mice exhibited enhanced autophagic flux in the prefrontal cortical microglia, and the autophagic deficiency in microglia aggravated RSD-induced social avoidance, indicating that microglial autophagy involves stress-induced behavioral changes.","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":"87 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2022-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73053966","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular Factors Mediating Neural Cell Plasticity Changes in Dementia Brain Diseases.","authors":"Wojciech Kozubski,&nbsp;Kevin Ong,&nbsp;Wioletta Waleszczyk,&nbsp;Matthew Zabel,&nbsp;Jolanta Dorszewska","doi":"10.1155/2021/8834645","DOIUrl":"https://doi.org/10.1155/2021/8834645","url":null,"abstract":"<p><p>Neural plasticity-the ability to alter a neuronal response to environmental stimuli-is an important factor in learning and memory. Short-term synaptic plasticity and long-term synaptic plasticity, including long-term potentiation and long-term depression, are the most-characterized models of learning and memory at the molecular and cellular level. These processes are often disrupted by neurodegeneration-induced dementias. Alzheimer's disease (AD) accounts for 50% of cases of dementia. Vascular dementia (VaD), Parkinson's disease dementia (PDD), dementia with Lewy bodies (DLB), and frontotemporal dementia (FTD) constitute much of the remaining cases. While vascular lesions are the principal cause of VaD, neurodegenerative processes have been established as etiological agents of many dementia diseases. Chief among such processes is the deposition of pathological protein aggregates <i>in vivo</i> including <i>β</i>-amyloid deposition in AD, the formation of neurofibrillary tangles in AD and FTD, and the accumulation of Lewy bodies composed of <i>α</i>-synuclein aggregates in DLB and PDD. The main symptoms of dementia are cognitive decline and memory and learning impairment. Nonetheless, accurate diagnoses of neurodegenerative diseases can be difficult due to overlapping clinical symptoms and the diverse locations of cortical lesions. Still, new neuroimaging and molecular biomarkers have improved clinicians' diagnostic capabilities in the context of dementia and may lead to the development of more effective treatments. Both genetic and environmental factors may lead to the aggregation of pathological proteins and altered levels of cytokines, such that can trigger the formation of proinflammatory immunological phenotypes. This cascade of pathological changes provides fertile ground for the development of neural plasticity disorders and dementias. Available pharmacotherapy and disease-modifying therapies currently in clinical trials may modulate synaptic plasticity to mitigate the effects neuropathological changes have on cognitive function, memory, and learning. In this article, we review the neural plasticity changes seen in common neurodegenerative diseases from pathophysiological and clinical points of view and highlight potential molecular targets of disease-modifying therapies.</p>","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":"2021 ","pages":"8834645"},"PeriodicalIF":3.1,"publicationDate":"2021-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8021472/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25589955","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sexism-Related Stigma Affects Pain Perception.","authors":"Ming Zhang,&nbsp;Yuqi Zhang,&nbsp;Zhihui Li,&nbsp;Li Hu,&nbsp;Yazhuo Kong","doi":"10.1155/2021/6612456","DOIUrl":"https://doi.org/10.1155/2021/6612456","url":null,"abstract":"<p><p>People with stigmatized characteristics tend to be devalued by others in a given society. The negative experiences related to stigma cause individuals to struggle as they would if they were in physical pain and bring various negative outcomes in the way that physical pain does. However, it is unclear whether stigma related to one's identity would affect their perception of physical pain. To address this issue, using sexism-related paradigms, we found that females had reduced pain threshold/tolerance in the Cold Pressor Test (Experiment 1) and an increased rating for nociceptive laser stimuli with fixed intensity (Experiment 2). Additionally, we observed that there was a larger laser-evoked N1, an early laser-evoked P2, and a larger magnitude of low-frequency component in laser-evoked potentials (LEPs) in the stigma condition than in the control condition (Experiment 3). Our study provides behavioral and electrophysiological evidence that sexism-related stigma affects the pain perception of females.</p>","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":"2021 ","pages":"6612456"},"PeriodicalIF":3.1,"publicationDate":"2021-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8019650/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25589953","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dynamical Mechanisms for Gene Regulation Mediated by Two Noncoding RNAs in Long-Term Memory Formation.","authors":"Lijie Hao,&nbsp;Zhuoqin Yang","doi":"10.1155/2021/6668389","DOIUrl":"https://doi.org/10.1155/2021/6668389","url":null,"abstract":"<p><p>Noncoding RNAs such as miRNAs and piRNAs have long-lasting effects on the regulation of gene expression involved in long-term synaptic changes. To characterize gene regulation mediated by small noncoding RNAs associated with long-term memory in <i>Aplysia</i>, we consider two noncoding RNAs stimulated by 5-HT into a gene regulatory network motif model, including miR-124 that binds to and inhibits the mRNA of CREB1 and piR-F that facilitates serotonin-dependent DNA methylation to lead to repression of CREB2. Codimension-1 and -2 bifurcation analyses of 5-HT regulating both miR-124 and piR-F and a negative feedback strength for oscillation reveal rich dynamical properties of bistability and oscillations robust to variations in all other parameters. More importantly, we verify three stimulus protocols of 5-HT in experiments by our model and find that application of five pulses of 5-HT leads to a transient decrease of miR-124 but increase of piR-F concentrations, which matters sustained high level of CREB1 concentration associated with long-term memory. Furthermore, we perform bifurcation analyses for the concentrations of miR-124 and piR-F as two parameters to explore dynamical mechanisms underlying the epigenetic regulation in long-term memory formation. This study provides insights into revealing regulatory roles of epigenetic changes in gene expression involving noncoding RNAs associated with synaptic plasticity.</p>","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":"2021 ","pages":"6668389"},"PeriodicalIF":3.1,"publicationDate":"2021-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8016590/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25572930","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A New Neurorehabilitative Postsurgery Intervention for Facial Palsy Based on Smile Observation and Hand-Mouth Motor Synergies.","authors":"Elisa De Stefani,&nbsp;Anna Barbot,&nbsp;Chiara Bertolini,&nbsp;Mauro Belluardo,&nbsp;Gioacchino Garofalo,&nbsp;Nicola Bruno,&nbsp;Bernardo Bianchi,&nbsp;Andrea Ferri,&nbsp;Pier Francesco Ferrari","doi":"10.1155/2021/8890541","DOIUrl":"https://doi.org/10.1155/2021/8890541","url":null,"abstract":"<p><strong>Objective: </strong>To perform a preliminary test of a new rehabilitation treatment (FIT-SAT), based on mirror mechanisms, for gracile muscles after smile surgery.</p><p><strong>Method: </strong>A pre- and postsurgery longitudinal design was adopted to study the efficacy of FIT-SAT. Four patients with bilateral facial nerve paralysis (Moebius syndrome) were included. They underwent two surgeries with free muscle transfers, one year apart from each other. The side of the face first operated on was rehabilitated with the traditional treatment, while the second side was rehabilitated with FIT-SAT. The FIT-SAT treatment includes video clips of an actor performing a unilateral or a bilateral smile to be imitated (FIT condition). In addition to this, while smiling, the participants close their hand in order to exploit the overlapped cortical motor representation of the hand and the mouth, which may facilitate the synergistic activity of the two effectors during the early phases of recruitment of the transplanted muscles (SAT). The treatment was also aimed at avoiding undesired movements such as teeth grinding. <i>Discussion</i>. Results support FIT-SAT as a viable alternative for smile rehabilitation after free muscle transfer. We propose that the treatment potentiates the effect of smile observation by activating the same neural structures responsible for the execution of the smile and therefore by facilitating its production. Closing of the hand induces cortical recruitment of hand motor neurons, recruiting the transplanted muscles, and reducing the risk of associating other unwanted movements such as teeth clenching to the smile movements.</p>","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":"2021 ","pages":"8890541"},"PeriodicalIF":3.1,"publicationDate":"2021-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8016575/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25572902","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Research on Differential Brain Networks before and after WM Training under Different Frequency Band Oscillations.","authors":"Yin Tian,&nbsp;Huishu Zhou,&nbsp;Huiling Zhang,&nbsp;Tianhao Li","doi":"10.1155/2021/6628021","DOIUrl":"https://doi.org/10.1155/2021/6628021","url":null,"abstract":"<p><p>Previous studies have shown that different frequency band oscillations are associated with cognitive processing such as working memory (WM). Electroencephalogram (EEG) coherence and graph theory can be used to measure functional connections between different brain regions and information interaction between different clusters of neurons. At the same time, it was found that better cognitive performance of individuals indicated stronger small-world characteristics of resting-state WM networks. However, little is known about the neural synchronization of the retention stage during ongoing WM tasks (i.e., online WM) by training on the whole-brain network level. Therefore, combining EEG coherence and graph theory analysis, the present study examined the topological changes of WM networks before and after training based on the whole brain and constructed differential networks with different frequency band oscillations (i.e., theta, alpha, and beta). The results showed that after WM training, the subjects' WM networks had higher clustering coefficients and shorter optimal path lengths than before training during the retention period. Moreover, the increased synchronization of the frontal theta oscillations seemed to reflect the improved executive ability of WM and the more mature resource deployment; the enhanced alpha oscillatory synchronization in the frontoparietal and fronto-occipital regions may reflect the enhanced ability to suppress irrelevant information during the delay and pay attention to memory guidance; the enhanced beta oscillatory synchronization in the temporoparietal and frontoparietal regions may indicate active memory maintenance and preparation for memory-guided attention. The findings may add new evidence to understand the neural mechanisms of WM on the changes of network topological attributes in the task-related mode.</p>","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":"2021 ","pages":"6628021"},"PeriodicalIF":3.1,"publicationDate":"2021-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8007374/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25566041","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitochondrial Dysfunction and Sirtuins: Important Targets in Hearing Loss","authors":"Lingjun Zhang, Zhengde Du, S. Gong","doi":"10.1155/2021/5520794","DOIUrl":"https://doi.org/10.1155/2021/5520794","url":null,"abstract":"Mitochondrial dysfunction has been suggested to be a risk factor for sensorineural hearing loss (SNHL) induced by aging, noise, ototoxic drugs, and gene. Reactive oxygen species (ROS) are mainly derived from mitochondria, and oxidative stress induced by ROS contributes to cochlear damage as well as mitochondrial DNA mutations, which may enhance the sensitivity and severity of hearing loss and disrupt ion homeostasis (e.g., Ca2+ homeostasis). The formation and accumulation of ROS further undermine mitochondrial components and ultimately lead to apoptosis and necrosis. SIRT3–5, located in mitochondria, belong to the family of sirtuins, which are highly conserved deacetylases dependent on nicotinamide adenine dinucleotide (NAD+). These deacetylases regulate diverse cellular biochemical activities. Recent studies have revealed that mitochondrial sirtuins, especially SIRT3, modulate ROS levels in hearing loss pathologies. Although the precise functions of SIRT4 and SIRT5 in the cochlea remain unclear, the molecular mechanisms in other tissues indicate a potential protective effect against hearing loss. In this review, we summarize the current knowledge regarding the role of mitochondrial dysfunction in hearing loss, discuss possible functional links between mitochondrial sirtuins and SNHL, and propose a perspective that SIRT3–5 have a positive effect on SNHL.","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":"1 1","pages":"1-10"},"PeriodicalIF":3.1,"publicationDate":"2021-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75304664","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Interaction of Indirect and Hyperdirect Pathways on Synchrony and Tremor-Related Oscillation in the Basal Ganglia.","authors":"Xia Shi,&nbsp;Danwen Du,&nbsp;Yuan Wang","doi":"10.1155/2021/6640105","DOIUrl":"https://doi.org/10.1155/2021/6640105","url":null,"abstract":"<p><p>Low-frequency oscillatory activity (3-9 Hz) and increased synchrony in the basal ganglia (BG) are recognized to be crucial for Parkinsonian tremor. However, the dynamical mechanism underlying the tremor-related oscillations still remains unknown. In this paper, the roles of the indirect and hyperdirect pathways on synchronization and tremor-related oscillations are considered based on a modified Hodgkin-Huxley model. Firstly, the effects of indirect and hyperdirect pathways are analysed individually, which show that increased striatal activity to the globus pallidus external (GPe) or strong cortical gamma input to the subthalamic nucleus (STN) is sufficient to promote synchrony and tremor-related oscillations in the BG network. Then, the mutual effects of both pathways are analysed by adjusting the related currents simultaneously. Our results suggest that synchrony and tremor-related oscillations would be strengthened if the current of these two paths are in relative imbalance. And the network tends to be less synchronized and less tremulous when the frequency of cortical input is in the theta band. These findings may provide novel treatments in the cortex and striatum to alleviate symptoms of tremor in Parkinson's disease.</p>","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":"2021 ","pages":"6640105"},"PeriodicalIF":3.1,"publicationDate":"2021-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7984917/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25535814","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}