{"title":"The mechanisms in glucose metabolism of aging hippocampus","authors":"Rui He, Fuxing Zhao, Zhiyu Yang, Tingting Wang, Yaohui Zhang, Jinglan Quan, Gaohong Zhu","doi":"10.1002/ibra.12201","DOIUrl":"https://doi.org/10.1002/ibra.12201","url":null,"abstract":"<p>With the intensification of the aging society, the incidence of various neurodegenerative diseases is on the rise. The hippocampus is susceptible to age-related neuronal decline and is the earliest and crucial region affected in the transition from healthy aging to neurodegenerative diseases. Before the diagnosis of neurodegenerative diseases, there is already a decline in brain energy metabolism, with the disruption of energy metabolism serving as the primary mechanism leading to neuronal damage. This triggers complex signaling mechanisms both inside and outside the brain during the aging process. Glucose serves as the primary energy source for brain tissues, and a decrease in glucose metabolism is an early indicator of age-related functional changes in the brain. Therefore, understanding the pathophysiological basis of glucose metabolism in the aging hippocampus, as well as the underlying mechanisms, is crucial in comprehending cognitive aging. Such understanding is integral for early intervention and the mitigation of memory and learning impairments caused by energy metabolism. In this review, we have delved into the characteristics of energy metabolism, focusing specifically on glucose metabolism, as well as exploring the molecular foundations and associated mechanisms present within hippocampal neuronal cells under both normal and aging conditions. Notably, our investigation has highlighted the vital roles played by ALG5 and STT3A, key molecules involved in N-glycosylation, in influencing GLUT expression and the rate of membrane transport, regulating glucose metabolism, and thereby influencing cellular glucose uptake. The exploration of this study direction holds considerable promise for future endeavors.</p>","PeriodicalId":94030,"journal":{"name":"Ibrain","volume":"11 4","pages":"457-475"},"PeriodicalIF":0.0,"publicationDate":"2025-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ibra.12201","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145739902","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}
IbrainPub Date : 2025-06-13DOI: 10.1002/ibra.12200
Nicole van Heerden, Lané Prigge, Gerda Venter
{"title":"Histological investigation of the interthalamic adhesion and periventricular region: Evidence for midline neural connectivity","authors":"Nicole van Heerden, Lané Prigge, Gerda Venter","doi":"10.1002/ibra.12200","DOIUrl":"https://doi.org/10.1002/ibra.12200","url":null,"abstract":"<p>The interthalamic adhesion (IA), which may not be present in all humans, is a midline structure that connects the two thalami within the brain's third ventricle. A review of the known literature regarding the IA shows few histological studies and controversy regarding the organization of neurons within this region. This study conducted an anatomical investigation of the human IA in adult South African samples. Samples were obtained from 20 human adult embalmed cadavers: 11 from brains with a visible IA and 9 from brains without this feature. All the samples were harvested using sagittal sections of the area. Three additional samples were sectioned horizontally, yielding 33 tissue blocks. Before observation, these samples were appropriately processed for light microscopy and stained with haematoxylin and eosin, as well as cresyl violet. The results showed that no specific structural arrangements of the neurons were identifiable. The appearance appeared random, except for a distinguishable range in the frequency and dispersion of specific cells upon basic observation. Microglia were the most abundant cell type, and blood vessels were also observed. This study reports a novel inspection of the general histology of the thalamus, specifically of the IA and the periventricular (PVR) region, in midsagittal sections and three horizontal sections. This study confirmed the presence of pyramidal neurons within the IA, forming a bridge between the PVR region of the thalami, thus providing evidence to suggest that the IA could serve as a potential bridge for neural connections crossing over the brain's midline.</p>","PeriodicalId":94030,"journal":{"name":"Ibrain","volume":"11 3","pages":"375-384"},"PeriodicalIF":0.0,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ibra.12200","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145146253","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}
IbrainPub Date : 2025-05-12DOI: 10.1002/ibra.12199
Leto-Aikaterini Tziveleka, Mariafrancesca Cascione, Paolo Pellegrino, Annalisa Bianco, Stefano Leporatti, Valeria De Matteis
{"title":"Immunomodulatory natural polysaccharide-based nanoparticles for the treatment of neurodegenerative diseases","authors":"Leto-Aikaterini Tziveleka, Mariafrancesca Cascione, Paolo Pellegrino, Annalisa Bianco, Stefano Leporatti, Valeria De Matteis","doi":"10.1002/ibra.12199","DOIUrl":"https://doi.org/10.1002/ibra.12199","url":null,"abstract":"<p>Polysaccharide-based nanoparticles offer significant potential for the treatment of neurodegenerative diseases and the modulation of inflammatory responses in the central nervous system. These biopolymers, when derived from natural sources, possess inherent immunomodulatory properties, which can be leveraged to regulate immune activity, positioning them as promising candidates for both prophylactic and therapeutic strategies. Furthermore, when integrated with other materials, polysaccharides form nanocomposites with enhanced structural, physicochemical, and biological properties, making them highly versatile platforms for drug delivery in the central nervous system. This review provides a comprehensive analysis of polysaccharide-based nanoparticles, focusing on their application in the treatment of three major neurodegenerative diseases: Alzheimer's disease, Parkinson's disease, and multiple sclerosis. Emphasis is placed on optimizing these nanomaterials for targeted drug delivery and immune modulation, underscoring their potential to improve therapeutic outcomes in neurodegenerative disorders. The review also examines the structural, chemical, and biological characteristics of key polysaccharides, and explores their innovative roles in combating neuroinflammation and neurodegeneration.</p>","PeriodicalId":94030,"journal":{"name":"Ibrain","volume":"11 3","pages":"277-296"},"PeriodicalIF":0.0,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ibra.12199","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145146250","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":"Nanotechnology in brain cancer treatment: The role of gold nanoparticles as therapeutic enhancers","authors":"Simona Tarantino, Annalisa Bianco, Valeria De Matteis, Edoardo Scarpa, Rosaria Rinaldi","doi":"10.1002/ibra.12198","DOIUrl":"https://doi.org/10.1002/ibra.12198","url":null,"abstract":"<p>Brain cancer, with glioblastoma (GBM) being one of the most aggressive and treatment-resistant cancers, represents a leading cause of mortality and morbidity worldwide. Its complex nature and the presence of the blood-brain barrier (BBB) significantly hinder the effectiveness of conventional therapies, posing major challenges for treatment development. In this context, nanotechnology—particularly nanomedicine—has emerged as a promising strategy to overcome these barriers and enhance standard treatments like chemotherapy and radiotherapy (RT). This review focuses on three of the most challenging brain neoplasms—GBM, brain metastases, and pediatric brain tumors—and explores the growing role of nanoparticle-based therapies, with special emphasis on gold nanoparticles (AuNPs). Owing to their unique physicochemical properties, such as surface functionalization, biocompatibility, and the ability to cross the BBB, AuNPs have shown great potential in selectively delivering drugs, enhancing RT as radiosensitizers, and reducing systemic toxicity. Despite their therapeutic advantages, concerns remain regarding the long-term safety of AuNPs. Their small size and ability to cross biological barriers may lead to unintended biodistribution, immune responses, and cytotoxic effects. Reported risks include inflammatory reactions, apoptosis, and developmental toxicity, highlighting the need for comprehensive safety assessments. AuNPs offer a promising avenue for improving therapeutic efficacy and patient survival in brain cancers. However, their clinical application requires further in-depth preclinical and clinical evaluation to ensure both effectiveness and safety</p>","PeriodicalId":94030,"journal":{"name":"Ibrain","volume":"11 2","pages":"119-145"},"PeriodicalIF":0.0,"publicationDate":"2025-05-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ibra.12198","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144315350","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":"Navigating the treatment landscape of Alzheimer's disease: Current strategies and future directions","authors":"Tapas Kumar Mohapatra, Reena Rani Nayak, Ankit Ganeshpurkar, Prashant Tiwari, Dileep Kumar","doi":"10.1002/ibra.12197","DOIUrl":"https://doi.org/10.1002/ibra.12197","url":null,"abstract":"<p>Alzheimer's disease (AD), a neurodegenerative disease leading to dementia, lacks a single definitive diagnosis. While current medications only manage symptoms, the ideal treatment would restore cognition. Traditional therapies targeting beta-amyloid haven't yielded significant results, while new approaches target tau protein tangles, protein degradation pathways, inflammation, and neurotrophic factor depletion. Autophagy, a cellular degradation and recycling process, has emerged as a crucial hallmark and contributor to the pathogenesis of AD. Notably, autophagy induction has emerged as a promising therapeutic approach, with inducers like celastrol and caudatin promoting the degradation of toxic protein aggregates. Additionally, innovative drug formulations, such as nanoparticles, are being explored for targeted drug delivery. Research is increasingly focusing on neuroinflammation and developing multi-targeted drugs to address various aspects of AD, potentially leading to preventive strategies in the early stages. This review summarizes the current state and emerging trends in AD drug development.</p>","PeriodicalId":94030,"journal":{"name":"Ibrain","volume":"11 2","pages":"162-184"},"PeriodicalIF":0.0,"publicationDate":"2025-05-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ibra.12197","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144314939","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}
IbrainPub Date : 2025-04-22DOI: 10.1002/ibra.12196
Lucia Iafrate, Gianluca Cidonio
{"title":"The rise of 3D bioprinting advancements in modeling neurodegenerative diseases","authors":"Lucia Iafrate, Gianluca Cidonio","doi":"10.1002/ibra.12196","DOIUrl":"https://doi.org/10.1002/ibra.12196","url":null,"abstract":"<p>Neurodegenerative diseases (NDs) are disorders that drastically alter the physiological functioning of neurons in the brain. These processes are often accompanied by abnormal protein aggregates that alter the physical and chemical properties of brain tissue and peripheral nerves. The causes of NDs are complex, involving genetic factors, neuroinflammation, oxidative stress, environmental influences, and lifestyle, while symptoms and progression vary significantly based on the mechanisms of cell death. Currently, no definitive treatment exists for NDs, as the underlying degenerative processes remain poorly understood. Existing therapies focus on symptom alleviation but are insufficient to halt or prevent disease progression. This highlights the urgent need for strategies that mimic the pathophysiology of NDs, facilitating deeper insights and the development of effective treatments. Conventional in vitro and in vivo models attempt to replicate NDs but often fail to capture the physiological complexity of nervous tissue and its interactions. In this context, 3D microfluidic bioprinting emerges as a transformative technology. By enabling precise deposition of cells and biomaterials, it allows the creation of in vitro models with a high degree of structural and functional complexity. These advancements provide a valuable platform for faithfully modeling NDs, bridging critical gaps in our understanding, and paving the way toward innovative therapeutic approaches.</p>","PeriodicalId":94030,"journal":{"name":"Ibrain","volume":"11 2","pages":"259-267"},"PeriodicalIF":0.0,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ibra.12196","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144315388","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}
IbrainPub Date : 2025-04-10DOI: 10.1002/ibra.12195
Sana Mohammadi, Sadegh Ghaderi, Masoud Hoseini Pourasl, Farzad Fatehi
{"title":"Prefrontal cortex iron content in neurodegeneration and healthy subjects: A systematic review","authors":"Sana Mohammadi, Sadegh Ghaderi, Masoud Hoseini Pourasl, Farzad Fatehi","doi":"10.1002/ibra.12195","DOIUrl":"https://doi.org/10.1002/ibra.12195","url":null,"abstract":"<p>Iron accumulation in the prefrontal cortex (PFC) has been implicated in neurodegeneration and cognitive decline. Magnetic resonance imaging (MRI) enables noninvasive quantification of brain iron content and deposition. This review aimed to summarize the evidence on the MRI-based assessment of PFC iron accumulation in healthy individuals and patients with neurodegeneration. A systematic preliminary literature review was conducted using the PubMed, Scopus, Web of Science, and Embase databases. MRI techniques for capturing susceptibility changes reflecting iron, such as susceptibility-weighted imaging (SWI), quantitative susceptibility mapping (QSM), and R2* mapping, were included. Data were extracted, and narrative synthesis was performed. Twelve studies that measured PFC iron levels using MRI in diseases with neurodegeneration (five studies) and healthy subjects (seven studies) were included. In general, studies involving diseases with neurodegeneration have found that increased PFC iron content correlates with cognitive impairment. Aging studies on healthy subjects have reported that age-related accumulation of PFC iron, particularly in the dorsolateral, medial, and anterior subregions, increases with age, and is associated with reduced dopamine signaling and poorer cognition. MRI techniques, such as QSM, can quantify prefrontal iron accumulation in diseases with neurodegeneration and aging. As imaging biomarkers, increased prefrontal iron levels may contribute to neurodegeneration and cognitive decline. Longitudinal studies combining advanced QSM and other advanced neuroimaging techniques with cognitive assessments may further elucidate the effects of iron dysregulation on PFC function. Thus, our findings highlight the importance of MRI as a sensitive tool for assessing PFC iron content and its potential role in understanding the pathogenesis of neurodegeneration and the effects of aging on the brain.</p>","PeriodicalId":94030,"journal":{"name":"Ibrain","volume":"11 2","pages":"215-227"},"PeriodicalIF":0.0,"publicationDate":"2025-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ibra.12195","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144314983","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}
IbrainPub Date : 2025-03-22DOI: 10.1002/ibra.12194
Mani Abdul Karim
{"title":"Mapping the landscape of brain stimulation research: A global scientometric review on cognitive impairment","authors":"Mani Abdul Karim","doi":"10.1002/ibra.12194","DOIUrl":"https://doi.org/10.1002/ibra.12194","url":null,"abstract":"<p>Several noninvasive brain stimulation techniques have gained significant attention in neurocognitive science and clinical research due to their potential efficacy in addressing neurological, psychiatric, and cognitive impairments. This study explores global trends and research hotspots in brain stimulation research for cognitive impairment and related disorders. Using a data set from 1989 to 2024 sourced from the Web of Science Core Collection, 4156 records were analyzed through bibliometric methods, including publication trends, country or region, and institutional analysis, and document co-citation analysis (DCA). Results revealed a steady increase in research, with a significant increase in publications during the period from 2019 to 2023. The USA led in citation counts (1117), centrality (0.37), while China topped the burst value (72.31). The University of London led in citation counts (235), whereas Capital Medical University topped the sigma value (1.77). Transcranial magnetic stimulation (TMS) and repetitive TMS (rTMS) dominated the top positions in DCA analysis. Emerging trends were identified through burst keywords, including “transcranial Doppler,” “subthalamic nucleus stimulation,” “cerebral blood flow,” “vascular dementia,” and “cardiopulmonary bypass.” These emerging research hotspots underscore the growing focus on vascular aspects of cognitive impairment and advanced brain stimulation methods. Additionally, newer noninvasive techniques like fast gamma magnetic stimulation, paired-associative stimulation with TMS (PAS-TMS), and theta-burst stimulation are identified as promising avenues for future research, offering significant potential for therapeutic advancements. This study provides a comprehensive overview of the global landscape, trends, and future directions in brain stimulation research for cognitive impairment.</p>","PeriodicalId":94030,"journal":{"name":"Ibrain","volume":"11 2","pages":"185-204"},"PeriodicalIF":0.0,"publicationDate":"2025-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ibra.12194","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144315391","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":"Cordycepin mediates neuroprotection against apoptosis via ERK/CREB signaling activation in Aβ1–42-induced neuronal cell models","authors":"Wenshu Zhou, Cheng Wang, Yige Tan, Philip Lazarovici, Xiaoyan Wen, Shaoping Li, Wenhua Zheng","doi":"10.1002/ibra.12192","DOIUrl":"https://doi.org/10.1002/ibra.12192","url":null,"abstract":"<p>The aggregation of β-amyloid (Aβ) peptides has been associated with the onset of Alzheimer's disease (AD) by causing neurotoxicity due to oxidative stress and apoptosis. Cordycepin is a natural derivative of the nucleoside adenosine that displays potent antioxidant, antitumor, anti-inflammatory, and neuroprotective properties. However, the mechanism of the neuroprotective effect of cordycepin toward Aβ-induced neurotoxicity, as well as underlying mechanisms, is still unclear. In this study, we found that cordycepin conferred neuroprotection to catecholaminergic PC12 neuronal cell cultures exposed to Aβ<sub>1–42</sub>-insult by reducing the production of reactive oxygen species, restoring the mitochondrial membrane potential, and inhibiting apoptosis. Cordycepin stimulated the phosphorylation of extracellular signal-regulated kinase (ERK) and cyclic AMP-responsive element-binding protein (CREB) in a time- and concentration-dependent manner. Inhibition of the ERK pathway reduced the neuroprotective effect of cordycepin. Similar results were obtained with hippocampal HT22 neuronal cell cultures. Cumulatively, these findings suggest that cordycepin-induced neuroprotection toward Aβ<sub>1–42</sub> neurotoxic insult may involve activation of the ERK/CREB pathway. This study expands our knowledge of the neuroprotective function of cordycepin and suggests that it holds promise as a natural lead compound for drug development in AD.</p>","PeriodicalId":94030,"journal":{"name":"Ibrain","volume":"11 1","pages":"84-97"},"PeriodicalIF":0.0,"publicationDate":"2025-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ibra.12192","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143633012","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}
IbrainPub Date : 2025-01-22DOI: 10.1002/ibra.12193
Meng-Dan Su, Tian-Hong Wang, Hao-Wen Zhang, Ke-Yu Cao, Fei Liu
{"title":"Association between Parkinson's disease and risk of colorectal cancer: A systematic review and meta-analysis","authors":"Meng-Dan Su, Tian-Hong Wang, Hao-Wen Zhang, Ke-Yu Cao, Fei Liu","doi":"10.1002/ibra.12193","DOIUrl":"https://doi.org/10.1002/ibra.12193","url":null,"abstract":"<p>This study aims to investigate the relationship between Parkinson's disease (PD) and colorectal cancer (CRC) risk by a systematic review and meta-analysis. Using Embase, Pubmed, and Cochrane Library databases, 21 articles reporting clinical data of 1,635,873 PD patients and 10,388,842 healthy individuals were finally included. Based on the results of pooled analysis, we found that PD patients exhibited a decreased risk of CRC (relative risk (RR) = 0.74; 95% confidence interval (CI), 0.68–0.80). In contrast to case-control (RR = 0.80; 95% CI, 0.64–1) and cohort studies (RR = 0.72; 95% CI, 0.66–0.79), the combined risk of PD patients with CRC in Asian nations (RR = 0.67; 95% CI, 0.58–0.78) was lower than that in Western countries (RR = 0.76; 95% CI, 0.70–0.82). In comparison to rectal cancer (RR = 0.82; 95% CI, 0.69–0.97), PD patients exhibited a lower combined risk of colon cancer (RR = 0.76; 95% CI, 0.67–0.86). Furthermore, the combined CRC risks for patients in studies published before 2010 and after 2010 were 0.76 (RR = 0.76; 95% CI, 0.66–0.88) and 0.74 (RR = 0.74; 95% CI, 0.68–0.80), respectively. These findings indicate that patients with PD had a reduced risk of CRC. Future studies are merited in exploring pathological molecular linkages or underlying mechanisms of inverse association between CRC and PD.</p>","PeriodicalId":94030,"journal":{"name":"Ibrain","volume":"11 2","pages":"205-214"},"PeriodicalIF":0.0,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ibra.12193","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144315389","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}