Neural PlasticityPub Date : 2015-01-01Epub Date: 2015-08-24DOI: 10.1155/2015/847136
Jena B Hales, Amber C Ocampo, Nicola J Broadbent, Robert E Clark
{"title":"Hippocampal Infusion of Zeta Inhibitory Peptide Impairs Recent, but Not Remote, Recognition Memory in Rats.","authors":"Jena B Hales, Amber C Ocampo, Nicola J Broadbent, Robert E Clark","doi":"10.1155/2015/847136","DOIUrl":"https://doi.org/10.1155/2015/847136","url":null,"abstract":"<p><p>Spatial memory in rodents can be erased following the infusion of zeta inhibitory peptide (ZIP) into the dorsal hippocampus via indwelling guide cannulas. It is believed that ZIP impairs spatial memory by reversing established late-phase long-term potentiation (LTP). However, it is unclear whether other forms of hippocampus-dependent memory, such as recognition memory, are also supported by hippocampal LTP. In the current study, we tested recognition memory in rats following hippocampal ZIP infusion. In order to combat the limited targeting of infusions via cannula, we implemented a stereotaxic approach for infusing ZIP throughout the dorsal, intermediate, and ventral hippocampus. Rats infused with ZIP 3-7 days after training on the novel object recognition task exhibited impaired object recognition memory compared to control rats (those infused with aCSF). In contrast, rats infused with ZIP 1 month after training performed similar to control rats. The ability to form new memories after ZIP infusions remained intact. We suggest that enhanced recognition memory for recent events is supported by hippocampal LTP, which can be reversed by hippocampal ZIP infusion. </p>","PeriodicalId":51299,"journal":{"name":"Neural Plasticity","volume":"2015 ","pages":"847136"},"PeriodicalIF":3.1,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2015/847136","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34182606","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}
Neural PlasticityPub Date : 2015-01-01Epub Date: 2015-05-06DOI: 10.1155/2015/481574
Luca Prosperini, Maria Cristina Piattella, Costanza Giannì, Patrizia Pantano
{"title":"Functional and Structural Brain Plasticity Enhanced by Motor and Cognitive Rehabilitation in Multiple Sclerosis.","authors":"Luca Prosperini, Maria Cristina Piattella, Costanza Giannì, Patrizia Pantano","doi":"10.1155/2015/481574","DOIUrl":"10.1155/2015/481574","url":null,"abstract":"<p><p>Rehabilitation is recognized to be important in ameliorating motor and cognitive functions, reducing disease burden, and improving quality of life in patients with multiple sclerosis (MS). In this systematic review, we summarize the existing evidences that motor and cognitive rehabilitation may enhance functional and structural brain plasticity in patients with MS, as assessed by means of the most advanced neuroimaging techniques, including diffusion tensor imaging and task-related and resting-state functional magnetic resonance imaging (MRI). In most cases, the rehabilitation program was based on computer-assisted/video game exercises performed in either an outpatient or home setting. Despite their heterogeneity, all the included studies describe changes in white matter microarchitecture, in task-related activation, and/or in functional connectivity following both task-oriented and selective training. When explored, relevant correlation between improved function and MRI-detected brain changes was often found, supporting the hypothesis that training-induced brain plasticity is specifically linked to the trained domain. Small sample sizes, lack of randomization and/or an active control group, as well as missed relationship between MRI-detected changes and clinical performance, are the major drawbacks of the selected studies. Knowledge gaps in this field of research are also discussed to provide a framework for future investigations. </p>","PeriodicalId":51299,"journal":{"name":"Neural Plasticity","volume":"2015 ","pages":"481574"},"PeriodicalIF":3.1,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4438192/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34197199","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}
Neural PlasticityPub Date : 2015-01-01Epub Date: 2015-05-14DOI: 10.1155/2015/671705
Achille Pasqualotto, Begüm Kobanbay, Michael J Proulx
{"title":"Neural Stimulation Has a Long-Term Effect on Foreign Vocabulary Acquisition.","authors":"Achille Pasqualotto, Begüm Kobanbay, Michael J Proulx","doi":"10.1155/2015/671705","DOIUrl":"https://doi.org/10.1155/2015/671705","url":null,"abstract":"<p><p>Acquisition of a foreign language is a challenging task that is becoming increasingly more important in the world nowadays. There is evidence suggesting that the frontal and temporal cortices are involved in language processing and comprehension, but it is still unknown whether foreign language acquisition recruits additional cortical areas in a causal manner. For the first time, we used transcranial random noise stimulation on the frontal and parietal brain areas, in order to compare its effect on the acquisition of unknown foreign words and a sham, or placebo, condition was also included. This type of noninvasive neural stimulation enhances cortical activity by boosting the spontaneous activity of neurons. Foreign vocabulary acquisition was tested both immediately and seven days after the stimulation. We found that stimulation on the posterior parietal, but not the dorsolateral prefrontal cortex or sham stimulation, significantly improved the memory performance in the long term. These results suggest that the posterior parietal cortex is directly involved in acquisition of foreign vocabulary, thus extending the \"linguistic network\" to this area. </p>","PeriodicalId":51299,"journal":{"name":"Neural Plasticity","volume":"2015 ","pages":"671705"},"PeriodicalIF":3.1,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2015/671705","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34205685","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":"CREB Regulates Experience-Dependent Spine Formation and Enlargement in Mouse Barrel Cortex.","authors":"Annabella Pignataro, Antonella Borreca, Martine Ammassari-Teule, Silvia Middei","doi":"10.1155/2015/651469","DOIUrl":"https://doi.org/10.1155/2015/651469","url":null,"abstract":"<p><p>Experience modifies synaptic connectivity through processes that involve dendritic spine rearrangements in neuronal circuits. Although cAMP response element binding protein (CREB) has a key function in spines changes, its role in activity-dependent rearrangements in brain regions of rodents interacting with the surrounding environment has received little attention so far. Here we studied the effects of vibrissae trimming, a widely used model of sensory deprivation-induced cortical plasticity, on processes associated with dendritic spine rearrangements in the barrel cortex of a transgenic mouse model of CREB downregulation (mCREB mice). We found that sensory deprivation through prolonged whisker trimming leads to an increased number of thin spines in the layer V of related barrel cortex (Contra) in wild type but not mCREB mice. In the barrel field controlling spared whiskers (Ipsi), the same trimming protocol results in a CREB-dependent enlargement of dendritic spines. Last, we demonstrated that CREB regulates structural rearrangements of synapses that associate with dynamic changes of dendritic spines. Our findings suggest that CREB plays a key role in dendritic spine dynamics and synaptic circuits rearrangements that account for new brain connectivity in response to changes in the environment. </p>","PeriodicalId":51299,"journal":{"name":"Neural Plasticity","volume":"2015 ","pages":"651469"},"PeriodicalIF":3.1,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2015/651469","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34202834","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}
Neural PlasticityPub Date : 2015-01-01Epub Date: 2015-05-27DOI: 10.1155/2015/591563
Bartłomiej Pochwat, Gabriel Nowak, Bernadeta Szewczyk
{"title":"Relationship between Zinc (Zn (2+) ) and Glutamate Receptors in the Processes Underlying Neurodegeneration.","authors":"Bartłomiej Pochwat, Gabriel Nowak, Bernadeta Szewczyk","doi":"10.1155/2015/591563","DOIUrl":"https://doi.org/10.1155/2015/591563","url":null,"abstract":"<p><p>The results from numerous studies have shown that an imbalance between particular neurotransmitters may lead to brain circuit dysfunction and development of many pathological states. The significance of glutamate pathways for the functioning of the nervous system is equivocal. On the one hand, glutamate transmission is necessary for neuroplasticity, synaptogenesis, or cell survival, but on the other hand an excessive and long-lasting increased level of glutamate in the synapse may lead to cell death. Under clinical conditions, hyperactivity of the glutamate system is associated with ischemia, epilepsy, and neurodegenerative diseases such as Alzheimer's, Huntington's, and many others. The achievement of glutamate activity in the physiological range requires efficient control by endogenous regulatory factors. Due to the fact that the free pool of ion Zn(2+) is a cotransmitter in some glutamate neurons; the role of this element in the pathophysiology of a neurodegenerative diseases has been intensively studied. There is a lot of evidence for Zn(2+) dyshomeostasis and glutamate system abnormalities in ischemic and neurodegenerative disorders. However, the precise interaction between Zn(2+) regulative function and the glutamate system is still not fully understood. This review describes the relationship between Zn(2+) and glutamate dependent signaling pathways under selected pathological central nervous system (CNS) conditions. </p>","PeriodicalId":51299,"journal":{"name":"Neural Plasticity","volume":"2015 ","pages":"591563"},"PeriodicalIF":3.1,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2015/591563","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33952338","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}
Neural PlasticityPub Date : 2015-01-01Epub Date: 2015-06-11DOI: 10.1155/2015/512156
David Parker
{"title":"Synaptic Variability Introduces State-Dependent Modulation of Excitatory Spinal Cord Synapses.","authors":"David Parker","doi":"10.1155/2015/512156","DOIUrl":"https://doi.org/10.1155/2015/512156","url":null,"abstract":"<p><p>The relevance of neuronal and synaptic variability remains unclear. Cellular and synaptic plasticity and neuromodulation are also variable. This could reflect state-dependent effects caused by the variable initial cellular or synaptic properties or direct variability in plasticity-inducing mechanisms. This study has examined state-dependent influences on synaptic plasticity at connections between excitatory interneurons (EIN) and motor neurons in the lamprey spinal cord. State-dependent effects were examined by correlating initial synaptic properties with the substance P-mediated plasticity of low frequency-evoked EPSPs and the reduction of the EPSP depression over spike trains (metaplasticity). The low frequency EPSP potentiation reflected an interaction between the potentiation of NMDA responses and the release probability. The release probability introduced a variable state-dependent subtractive influence on the postsynaptic NMDA-dependent potentiation. The metaplasticity was also state-dependent: it was greater at connections with smaller available vesicle pools and high initial release probabilities. This was supported by the significant reduction in the number of connections showing metaplasticity when the release probability was reduced by high Mg(2+) Ringer. Initial synaptic properties thus introduce state-dependent influences that affect the potential for plasticity. Understanding these conditions will be as important as understanding the subsequent changes. </p>","PeriodicalId":51299,"journal":{"name":"Neural Plasticity","volume":"2015 ","pages":"512156"},"PeriodicalIF":3.1,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2015/512156","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34283008","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}
Neural PlasticityPub Date : 2015-01-01Epub Date: 2015-06-14DOI: 10.1155/2015/576978
Rodrigo Machado-Vieira, Benicio N Frey, Ana C Andreazza, João Quevedo
{"title":"Translational Research in Bipolar Disorders.","authors":"Rodrigo Machado-Vieira, Benicio N Frey, Ana C Andreazza, João Quevedo","doi":"10.1155/2015/576978","DOIUrl":"https://doi.org/10.1155/2015/576978","url":null,"abstract":"Translational research is at the vanguard of contemporary psychiatry. Its bidirectional continuum (from bench to bedside and vice versa) has become a primary target in the search of personalized treatments in psychiatry. Although the term “translational” has various definitions, its common ground has focused on a better understanding of the pathophysiology of psychiatric disorders as well as on the identification of new diagnostic tests and development of new, improved treatments. In psychiatry, these aims seem more challenging than in other medical areas due to the complexity of brain mechanisms and behaviors. \u0000 \u0000Several other areas in medicine (e.g., oncology and endocrinology) have successfully decreased the gap between initial drug discovery steps and the subsequent approval of successful therapies for human diseases using translational approaches. In mental health, the use of tools and technologies that are able to positively impact health parameters in psychiatric conditions has been put forward as the ultimate objective of translational neuroscience research, which may tailor clinical practice [1]. Even though several advances have been obtained, this is a key but complex step to pursue, since psychiatric disorders have potential heterogeneous symptomatology, cognitive functioning, and comorbidities as well as having a wide range of genetic and environmental risk factors [2]. Furthermore, recent genome-wide association studies have identified potential candidate genes, but lack of replication by subsequent larger studies and low power have been major limitations in this field. \u0000 \u0000One example that fits well in this paradigm is bipolar disorder (BD). This is a major mental illness with high prevalence (especially when considering its spectrum), which still has low recovery rates and high rates of treatment-resistant cases, with consequent high morbidity and mortality rates. Despite this major public health issue, existing pharmacological treatments for BD are mostly modifications of older versions and have not been demonstrated to be superior to agents from the same class in terms of efficacy and effectiveness. Except for lithium, all first- and second-line treatments for BD phases and maintenance were first developed and approved for other disorders (e.g., anticonvulsants and atypical antipsychotics). It is noteworthy that the use of lithium has been progressively declining despite the strong evidence base in favor of its use [3, 4]. \u0000 \u0000Another degree of complexity is based on its pathophysiology. This involves dysfunctions at multiple levels and systems with a convergent impact at subcellular downstream cascades that directly regulate cellular resilience and neural plasticity. Some of these molecular targets include central and peripheral stress pathways, inflammation, intracellular signaling cascades, and organelles (mitochondria and endoplasmic reticulum) dysfunction [5]. In this context, some of these newly identified potential treatmen","PeriodicalId":51299,"journal":{"name":"Neural Plasticity","volume":"2015 ","pages":"576978"},"PeriodicalIF":3.1,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2015/576978","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34292618","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}
Neural PlasticityPub Date : 2015-01-01Epub Date: 2015-10-05DOI: 10.1155/2015/830871
Elise Wogensen, Hana Malá, Jesper Mogensen
{"title":"The Effects of Exercise on Cognitive Recovery after Acquired Brain Injury in Animal Models: A Systematic Review.","authors":"Elise Wogensen, Hana Malá, Jesper Mogensen","doi":"10.1155/2015/830871","DOIUrl":"https://doi.org/10.1155/2015/830871","url":null,"abstract":"<p><p>The objective of the present paper is to review the current status of exercise as a tool to promote cognitive rehabilitation after acquired brain injury (ABI) in animal model-based research. Searches were conducted on the PubMed, Scopus, and psycINFO databases in February 2014. Search strings used were: exercise (and) animal model (or) rodent (or) rat (and) traumatic brain injury (or) cerebral ischemia (or) brain irradiation. Studies were selected if they were (1) in English, (2) used adult animals subjected to acquired brain injury, (3) used exercise as an intervention tool after inflicted injury, (4) used exercise paradigms demanding movement of all extremities, (5) had exercise intervention effects that could be distinguished from other potential intervention effects, and (6) contained at least one measure of cognitive and/or emotional function. Out of 2308 hits, 22 publications fulfilled the criteria. The studies were examined relative to cognitive effects associated with three themes: exercise type (forced or voluntary), timing of exercise (early or late), and dose-related factors (intensity, duration, etc.). The studies indicate that exercise in many cases can promote cognitive recovery after brain injury. However, the optimal parameters to ensure cognitive rehabilitation efficacy still elude us, due to considerable methodological variations between studies. </p>","PeriodicalId":51299,"journal":{"name":"Neural Plasticity","volume":"2015 ","pages":"830871"},"PeriodicalIF":3.1,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2015/830871","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34294802","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}
Neural PlasticityPub Date : 2015-01-01Epub Date: 2015-05-18DOI: 10.1155/2015/676473
Katarzyna Popiolek-Barczyk, Natalia Kolosowska, Anna Piotrowska, Wioletta Makuch, Ewelina Rojewska, Agnieszka M Jurga, Dominika Pilat, Joanna Mika
{"title":"Parthenolide Relieves Pain and Promotes M2 Microglia/Macrophage Polarization in Rat Model of Neuropathy.","authors":"Katarzyna Popiolek-Barczyk, Natalia Kolosowska, Anna Piotrowska, Wioletta Makuch, Ewelina Rojewska, Agnieszka M Jurga, Dominika Pilat, Joanna Mika","doi":"10.1155/2015/676473","DOIUrl":"https://doi.org/10.1155/2015/676473","url":null,"abstract":"<p><p>Neuropathic pain treatment remains a challenge because pathomechanism is not fully understood. It is believed that glial activation and increased spinal nociceptive factors are crucial for neuropathy. We investigated the effect of parthenolide (PTL) on the chronic constriction injury to the sciatic nerve (CCI)-induced neuropathy in rat. We analyzed spinal changes in glial markers and M1 and M2 polarization factors, as well as intracellular signaling pathways. PTL (5 µg; i.t.) was preemptively and then daily administered for 7 days after CCI. PTL attenuated the allodynia and hyperalgesia and increased the protein level of IBA1 (a microglial/macrophage marker) but did not change GFAP (an astrocyte marker) on day 7 after CCI. PTL reduced the protein level of M1 (IL-1β, IL-18, and iNOS) and enhanced M2 (IL-10, TIMP1) factors. In addition, it downregulated the phosphorylated form of NF-κB, p38MAPK, and ERK1/2 protein level and upregulated STAT3. In primary microglial cell culture we have shown that IL-1β, IL-18, iNOS, IL-6, IL-10, and TIMP1 are of microglial origin. Summing up, PTL directly or indirectly attenuates neuropathy symptoms and promotes M2 microglia/macrophages polarization. We suggest that neuropathic pain therapies should be shifted from blanketed microglia/macrophage suppression toward maintenance of the balance between neuroprotective and neurotoxic microglia/macrophage phenotypes. </p>","PeriodicalId":51299,"journal":{"name":"Neural Plasticity","volume":"2015 ","pages":"676473"},"PeriodicalIF":3.1,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2015/676473","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33938854","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}
Neural PlasticityPub Date : 2015-01-01Epub Date: 2015-08-04DOI: 10.1155/2015/938023
Ragunathan Padmashri, Anand Suresh, Michael D Boska, Anna Dunaevsky
{"title":"Motor-Skill Learning Is Dependent on Astrocytic Activity.","authors":"Ragunathan Padmashri, Anand Suresh, Michael D Boska, Anna Dunaevsky","doi":"10.1155/2015/938023","DOIUrl":"https://doi.org/10.1155/2015/938023","url":null,"abstract":"<p><p>Motor-skill learning induces changes in synaptic structure and function in the primary motor cortex through the involvement of a long-term potentiation- (LTP-) like mechanism. Although there is evidence that calcium-dependent release of gliotransmitters by astrocytes plays an important role in synaptic transmission and plasticity, the role of astrocytes in motor-skill learning is not known. To test the hypothesis that astrocytic activity is necessary for motor-skill learning, we perturbed astrocytic function using pharmacological and genetic approaches. We find that perturbation of astrocytes either by selectively attenuating IP3R2 mediated astrocyte Ca(2+) signaling or using an astrocyte specific metabolic inhibitor fluorocitrate (FC) results in impaired motor-skill learning of a forelimb reaching-task in mice. Moreover, the learning impairment caused by blocking astrocytic activity using FC was rescued by administration of the gliotransmitter D-serine. The learning impairments are likely caused by impaired LTP as FC blocked LTP in slices and prevented motor-skill training-induced increases in synaptic AMPA-type glutamate receptor in vivo. These results support the conclusion that normal astrocytic Ca(2+) signaling during a reaching task is necessary for motor-skill learning. </p>","PeriodicalId":51299,"journal":{"name":"Neural Plasticity","volume":"2015 ","pages":"938023"},"PeriodicalIF":3.1,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2015/938023","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33982767","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}