NeuroSci最新文献

{"title":"Unraveling Attention-Deficit/Hyperactivity Disorder Etiology: Current Challenges and Future Directions in Treatment.","authors":"Abhishek Poddar, Sreelatha Gaddam, Shivakumar Sonnaila, Venkata Suryanarayana Murthy Bavaraju, Shilpi Agrawal","doi":"10.3390/neurosci6020041","DOIUrl":"10.3390/neurosci6020041","url":null,"abstract":"<p><p>Attention-Deficit/Hyperactivity Disorder (ADHD) is a complex neurodevelopmental disorder with a multifactorial etiology involving genetic, epigenetic, and environmental factors. This review focuses on the current understanding of these contributing elements, examining how they interact to influence ADHD development. Genetic predispositions, environmental exposures, and epigenetic modifications collectively shape the risk and manifestation of the disorder. Despite advancements in research, significant challenges remain in identifying precise mechanisms and translating them into effective treatments. The variability of symptoms across individuals, influenced by factors such as age, gender, and cultural background, further complicates diagnosis and treatment. Addressing these challenges requires a deeper investigation into the underlying causes of ADHD and the development of tailored interventions. This review aims to highlight both the progress made in understanding ADHD etiology and the current gaps in treatment approaches, calling for more targeted research and personalized therapeutic strategies.</p>","PeriodicalId":74294,"journal":{"name":"NeuroSci","volume":"6 2","pages":""},"PeriodicalIF":1.6,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12101162/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144129769","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Echoes of Dormancy: Anomic Aphasia Unveils Neurocysticercosis Reactivation in a Patient on Semaglutide.","authors":"Marcos Osorio Borjas, Robert J Hernandez, Angelo Lopez-Lacayo, Dalina Laffita Perez, Yanie Oliva, Julio Mercado, Hussain Hussain","doi":"10.3390/neurosci6020040","DOIUrl":"10.3390/neurosci6020040","url":null,"abstract":"<p><p>Neurocysticercosis (NCC), a parasitic infection caused by <i>Taenia solium</i> larvae, remains a leading cause of acquired epilepsy worldwide, particularly in regions with inadequate sanitation and healthcare access. We present a case of NCC reactivation in a 64-year-old female who developed anomic aphasia-a rare manifestation of NCC-decades after her initial diagnosis. The patient's clinical course was complicated by a potential trigger of semaglutide, which potentially attenuated the protective inflammatory response maintained by astrocytes and microglia, leading to the reactivation of dormant cysts. Brain imaging confirmed localized cystic changes, and treatment with antiparasitic agents and corticosteroids led to marked clinical improvement. This case highlights the complexity of NCC reactivation, highlighting the interplay of metabolic, immune, and parasitic factors. It emphasizes the need for vigilance in managing patients with dormant infections and investigating potential risks associated with novel therapeutic agents like GLP-1 receptor agonists. Further research is essential to unravel the mechanisms linking metabolic modulation to parasitic reactivation, offering insights into prevention and treatment strategies.</p>","PeriodicalId":74294,"journal":{"name":"NeuroSci","volume":"6 2","pages":""},"PeriodicalIF":1.6,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12101238/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144129676","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of Outgrowth Potential of Rat Pheochromocytoma Cells Supplied with Highly Purified Rapidly Expanding Clones and Potential Application to Trigeminal Nerve Regeneration.","authors":"Mrunalini Ramanathan, Md Mahbobur Rahman, Ankhtsetseg Shijirbold, Md Rashel Mahmod, Hiromi Miyauchi, Yumi Matsuzaki, Takahiro Kanno, Yuki Fujita","doi":"10.3390/neurosci6020039","DOIUrl":"10.3390/neurosci6020039","url":null,"abstract":"<p><strong>Background: </strong>Mesenchymal stem/stromal cells (MSCs) are non-hematopoietic, plastic-adherent, and self-renewing cells capable of in vitro trilineage differentiation into fat, bone, and cartilage tissue. Suggestively, MSCs have additional plasticity, as demonstrated by their ability to differentiate in vitro into myocytes, neuron-like cells, and hepatocytes. MSCs are ideal for therapeutic application owing to their numerous advantages; they exhibit limited growth and differentiation abilities, leading to heterogeneous cell populations with inconsistent functions. However, highly purified MSCs, namely, rapidly expanding clones (RECs) that are isolated by single-cell sorting, display uniform functionality. RECs have the potential to offer many benefits, such as transplantable cells for treating several disorders of bone, heart, peripheral nerves, brain, and other organs. This study aimed to assess the effects of RECs on the pheochromocytoma (PC12) cell line, a well-known neuronal cell model.</p><p><strong>Methods: </strong>PC12 cells were cultured under the following conditions: co-culture with RECs, treatment with REC-derived conditioned medium (CM), or co-culture with RECs using Transwell inserts for 7 days. The cells were stained with anti-βIII-tubulin antibody; the lengths of neurites were measured by image analysis.</p><p><strong>Results: </strong>Regarding the co-culture with RECs, PC12's outgrowth was significantly increased. The RECs expressed nerve growth factor (NGF), a neurotrophic factor that could act on PC12 cells to trigger cellular differentiation.</p><p><strong>Conclusions: </strong>Our findings suggest that RECs via direct culture, intercellular communication in Transwell culture, and RECs CM promoted PC12 cell survival and outgrowth via NGF signaling.</p>","PeriodicalId":74294,"journal":{"name":"NeuroSci","volume":"6 2","pages":""},"PeriodicalIF":1.6,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12101362/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144129637","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Deciphering the Structural and Functional Effects of the R1150W Non-Synonymous Variant in SCN9A Linked to Altered Pain Perception.","authors":"Faisal A Al-Allaf, Zainularifeen Abduljaleel, Mohammad Athar","doi":"10.3390/neurosci6020038","DOIUrl":"10.3390/neurosci6020038","url":null,"abstract":"<p><p>The SCN9A gene, a critical regulator of pain perception, encodes the voltage-gated sodium channel Nav1.7, a key mediator of pain signal transmission. This study conducts a multimodal assessment of SCN9A, integrating genetic variation, structural architecture, and molecular dynamics to elucidate its role in pain regulation. Using advanced computational methods, I-TASSER simulations generated structural decoys of the SCN9A homology domain, producing an ensemble of conformational states. SPICKER clustering identified five representative models with a C-score of -3.19 and TM-score of 0.36 ± 0.12, reflecting moderate structural similarity to experimental templates while highlighting deviations that may underpin functional divergence. Validation via ProSA-web supported model reliability, yielding a Z-score of -1.63, consistent with native-like structures. Central to the analysis was the R1150W non-synonymous variant, a potential pathogenic variant. Structural modeling revealed localized stability in the mutant conformation but disrupted hydrogen bonding and altered charge distribution. Its pathogenicity was underscored by a high MetaRNN score (0.7978498) and proximity to evolutionarily conserved regions, suggesting functional importance. Notably, the variant lies within the Sodium-Ion-Transport-Associated Domain, where perturbations could impair ion conductance and channel gating-mechanisms critical for neuronal excitability. These findings illuminate how SCN9A variants disrupt pain signaling, linking genetic anomalies to molecular dysfunction. While computational insights advance mechanistic understanding, experimental validation is essential to confirm the variant's impact on Nav1.7 dynamics and cellular physiology. By refining SCN9A's molecular blueprint and highlighting its therapeutic potential as a target for precision analgesics, this work provides a roadmap for mitigating pain-related disorders through channel-specific modulation. Integrating structural bioinformatics with functional genomics, this study deciphers SCN9A's role in pain biology, laying the groundwork for novel strategies to manage pathological pain.</p>","PeriodicalId":74294,"journal":{"name":"NeuroSci","volume":"6 2","pages":""},"PeriodicalIF":1.6,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12101298/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144129674","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pre-Clinical Models of Penetrating Brain Injury: Study Protocol for a Scoping Review.","authors":"Cindy K Wong, Jennifer E Dinalo, Patrick D Lyden, Gene Sung, Roy A Poblete","doi":"10.3390/neurosci6020037","DOIUrl":"10.3390/neurosci6020037","url":null,"abstract":"<p><p>Penetrating brain injuries (PBI) constitute a significant subset of traumatic brain injuries, characterized by high morbidity and mortality due to their unique pathophysiological mechanisms. Despite its clinical prevalence in civilian and military settings, progress in translational research remains limited due to a lack of well-characterized pre-clinical models that accurately replicate human PBI. Existing models often fail to adequately simulate critical aspects such as ballistic dynamics, tissue cavitation, and secondary injury cascades, limiting their translational relevance and hindering therapeutic advancements. This scoping review aims to systematically evaluate existing pre-clinical models, including animal, computational, ballistic, and hybrid simulations, to assess their methodological rigor, translational applicability and reported outcome measures. Using PRISMA-ScR guidelines, we will conduct a comprehensive literature search across multiple databases, extracting data on model characteristics, injury induction techniques, histopathological findings, biomolecular markers, and functional assessments. Additionally, bibliometric analyses will provide insights into research trends and gaps in PBI modeling, particularly concerning replicating real-world injury mechanisms and long-term functional outcomes. Through this evaluation, we aim to identify optimal experimental frameworks for studying PBI pathophysiology and recovery mechanisms while informing future model development for therapeutic advancements. The findings from this review will serve as a foundation for advancing pre-clinical PBI research, guiding future model development and therapeutic innovations, and ultimately enhancing treatment strategies and patient outcomes.</p>","PeriodicalId":74294,"journal":{"name":"NeuroSci","volume":"6 2","pages":""},"PeriodicalIF":1.6,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12101342/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144129642","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Neuroanatomical Correlates of Dyspnea: An Activation Likelihood Estimation Meta-Analysis.","authors":"Christoph Müller, Jens Kerl, Dominic Dellweg","doi":"10.3390/neurosci6020036","DOIUrl":"https://doi.org/10.3390/neurosci6020036","url":null,"abstract":"<p><p>The sensation of dyspnea is related to various cardiopulmonary and neuromuscular diseases and is characterized by its sensory and affective qualities. Although there is a vast number of studies investigating its pathophysiology, less is known about the neuroanatomy of dyspnea perception. An activation likelihood estimation (ALE) meta-analysis of 13 studies investigating different breathing challenges using either PET or fMRI was performed to demonstrate the neuroanatomical correlates of dyspnea perception. The ALE meta-analysis was performed using the GingerAle software 3.0.2 and was displayed with the Mango software 4.1. Synthesizing the results of all included studies, clusters involving the insula and cingulated cortex in both hemispheres were observed. Subgroup analysis for the restrained breathing condition revealed activation involving the right and left cingulate cortex and left anterior cingulate cortex. For the loaded breathing condition, statistically significant activation was found for the postcentral gyrus, the superior temporal gyrus, and the right thalamus. The combined ALE map for both conditions showed activity patterns in the right cingulate cortex, the right insula, and the right thalamus. This ALE meta-analysis demonstrates that two separate neuronal pathways related to either the affective or intensity domain are involved in the central processing of dyspnea perception.</p>","PeriodicalId":74294,"journal":{"name":"NeuroSci","volume":"6 2","pages":""},"PeriodicalIF":1.6,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12015910/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144051783","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Systematic Review and Meta-Analysis on the Safety of Antiplatelet Discontinuation Following Stent-Assisted Coil Embolization for Cerebral Aneurysms.","authors":"Mohammed Maan Al-Salihi, Maryam Sabah Al-Jebur, Ahmed Abd Elazim, Ram Saha, Ahmed Saleh, Farhan Siddiq, Ali Ayyad","doi":"10.3390/neurosci6020034","DOIUrl":"https://doi.org/10.3390/neurosci6020034","url":null,"abstract":"<p><strong>Background: </strong>Stent-assisted coil embolization (SACE) is a common endovascular technique for managing intracranial aneurysms. The permanent presence of a stent inside the cerebral artery necessitates the postoperative use of antiplatelets. However, a consensus about how long to continue on it remains debated. This systematic review aims to discuss and quantify the risk of ischemic complications after antiplatelet discontinuation following SACE.</p><p><strong>Methods: </strong>PubMed, Cochrane Library, Scopus, and Web of Science (WOS) were systematically searched for studies assessing the outcomes after antiplatelet discontinuation following SACE for cerebral aneurysms. The primary outcome was the odds of ischemic complications after antiplatelet discontinuation. Using a random-effects model, the pooled event rate, along with a 95% confidence interval (CI), was calculated. The Comprehensive Meta-Analysis software (CMA) software was used for the analysis. The Newcastle-Ottawa Scale (NOS) was used for the quality assessment.</p><p><strong>Results: </strong>A total of five observational cohort studies were included in this systematic review. The studies recruited cases from 2009 and 2020, predominantly in Korea and Japan. Data from 18,425 cases obtained from four studies were analyzed. The duration of antiplatelet therapy varied widely across the included studies. Additionally, most studies reported a median follow-up of 24 months or more after antiplatelet discontinuation. We extracted and analyzed the odds of thromboembolic complications occurring within 6 to 24 months after the discontinuation of antiplatelets. The pooled rate of thromboembolism after antiplatelet discontinuation in this meta-analysis was 0.01 (95% CI: 0.006 to 0.018).</p><p><strong>Conclusion: </strong>This review demonstrates that the risk of thromboembolic complications after discontinuing antiplatelet therapy post-SACE is low. However, no strong consensus exists on the ideal duration for maintaining dual- or single-antiplatelet therapy. Further prospective studies with longer follow-ups are warranted to clarify the optimal durations needed to balance thromboembolic risk with hemorrhagic complications.</p>","PeriodicalId":74294,"journal":{"name":"NeuroSci","volume":"6 2","pages":""},"PeriodicalIF":1.6,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12015894/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144013963","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SPEED: A Graphical User Interface Software for Processing Eye Tracking Data.","authors":"Daniele Lozzi, Ilaria Di Pompeo, Martina Marcaccio, Matias Ademaj, Simone Migliore, Giuseppe Curcio","doi":"10.3390/neurosci6020035","DOIUrl":"https://doi.org/10.3390/neurosci6020035","url":null,"abstract":"<p><p>Eye tracking is a tool that is widely used in scientific research, enabling the acquisition of precise and detailed data on an individual's eye movements during interaction with visual stimuli, thus offering a rich source of information on visual perception and associated cognitive processes. In this work, a new software called SPEED (labScoc Processing and Extraction of Eye tracking Data) is presented to process data acquired by Pupil Lab Neon (Pupil Labs, Berlin, Germany). The software is written in Python which helps researchers with the feature extraction step without any coding skills. This work also presents a pilot study in which five healthy subjects were included in research investigating oculomotor correlates during MDMT (Moral Decision-Making Task) and testing possible autonomic predictors of participants' performance. A statistically significant difference was observed in reaction times and in the number of blinks made during the choice between the conditions of the personal and impersonal dilemma.</p>","PeriodicalId":74294,"journal":{"name":"NeuroSci","volume":"6 2","pages":""},"PeriodicalIF":1.6,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12015838/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144055072","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Stratification of Patients with Burning Mouth Syndrome in the Croatian Population: A Single-Center Cross-Sectional Study.","authors":"Ana Glavina, Ana Trlaja, Dinko Martinović, Antonija Tadin, Liborija Lugović-Mihić","doi":"10.3390/neurosci6020033","DOIUrl":"https://doi.org/10.3390/neurosci6020033","url":null,"abstract":"<p><p>The objective of the study was to determine the relationship between burning, xerostomia, dysgeusia and other subjective symptoms in patients with burning mouth syndrome (BMS). This cross-sectional study was conducted at the Dental Polyclinic Split, Split, Croatia. A total of 71 patients with BMS, i.e., 60 women and 11 men, were included in the study. The patients were divided into four subgroups: burning (B), burning and xerostomia (BX), burning and dysgeusia (BD), burning, xerostomia and dysgeusia (BXD). The following data were collected from all patients: sociodemographic status, comorbidities, medications, characteristics of the burning, presence of other subjective symptoms, topography of the burning. The majority of patients with BMS were women (86.0%) with an average age of about 65 years. Gastrointestinal diseases were the most common comorbidity (48.35%), and the most commonly used medications were proton pump inhibitors (PPIs) (29.8%). In the largest number of patients (N = 34), the burning symptom worsened in the evening hours (<i>p</i> = 0.059). The majority of BMS patients suffered from burning symptoms that occurred continuously (N = 54, 75.13%) and from an improvement (reduction/cessation) of symptoms during meals (N = 54, 76.65%). Of the other subjective symptoms, changes in the morphology of the tongue (10.6%) and a feeling of swelling (9.1%) were the most common. The tongue was the most common localization (67.35%). The multivariable logistic regression analysis showed a statistically significant effect of female gender (<i>p</i> = 0.049) as a potential positive predictor in subgroup B. The sociodemographic and medical data collected cannot explain the different occurrence of symptoms in the four subgroups of patients with BMS.</p>","PeriodicalId":74294,"journal":{"name":"NeuroSci","volume":"6 2","pages":""},"PeriodicalIF":1.6,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12015932/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144052739","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Decoupling Alpha Desynchronization from Neural Resource Use: Evidence from Cognitive Load Modulation.","authors":"Manuel Vázquez-Marrufo, Rocío Caballero-Díaz, Esteban Sarrias-Arrabal, Rubén Martín-Clemente","doi":"10.3390/neurosci6020032","DOIUrl":"https://doi.org/10.3390/neurosci6020032","url":null,"abstract":"<p><p>In prior studies, desynchronization of the induced alpha band (non-phase-locked but time-locked) has been observed across various cognitive tasks. Proposed hypotheses for the cognitive role of this alpha decrement include neural activation, an inhibition/timing mechanism, or a reduction in \"neural noise\". This study aimed to examine the effect of cognitive load on induced alpha activity using two versions of a go/no-go visual task: a single-target (ST) version with one target and one distractor, and a double-target (DT) version with two targets and two distractors. EEG was recorded from 58 electrodes, and Temporal Spectral Evolution (TSE) was used for time-frequency analysis. Behavioral results revealed faster reaction times in the ST task compared to the DT task. The P3 component displayed delayed latency and reduced amplitude under increased cognitive load, consistent with prior findings. However, the latencies and amplitudes of evoked and induced alpha responses were unaffected by cognitive load. This suggests that increased alpha desynchronization in subjects with cognitive impairment should not be interpreted as enhanced neural resource recruitment due to task difficulty. Instead, it may reflect other mechanisms unrelated to cognitive load differences in task performance.</p>","PeriodicalId":74294,"journal":{"name":"NeuroSci","volume":"6 2","pages":""},"PeriodicalIF":1.6,"publicationDate":"2025-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12015836/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144013987","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}