IBRO Neuroscience Reports最新文献

{"title":"The role of SGK1 in neurologic diseases: A friend or foe?","authors":"Xiuze Chen ,&nbsp;Haixian Kang ,&nbsp;Yechen Xiao","doi":"10.1016/j.ibneur.2024.12.003","DOIUrl":"10.1016/j.ibneur.2024.12.003","url":null,"abstract":"<div><div>Serum and glucocorticoid-regulated kinase 1 (SGK1), a member of the AGC family of serine/threonine protein kinases, is one of the most conserved protein kinases in eukaryotic evolution. SGK1 is expressed to varying degrees in various types of cells throughout the body, and plays an important role in hypertension, ion channels, oxidative stress, neurological disorders, and cardiovascular regulation. In recent years, a number of scholars have devoted themselves to the study of the role and function of SGK1 in neurological diseases. Therefore, this article reviews the role of SGK1 in Alzheimer's disease, Parkinson's disease, epilepsy, stroke and other neurological diseases in recent years, and puts forward some insights on the role of SGK1 in neurological diseases and its relationship with disease activities.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"17 ","pages":"Pages 503-512"},"PeriodicalIF":2.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11683284/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142906907","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":"Anticonvulsant effects of pentoxifylline on seizures induced by pentylenetetrazole and maximal electroshock in male mice: The role of the nitrergic pathway","authors":"Mohammad Keshavarzi ,&nbsp;Moein Ghasemi ,&nbsp;Mohammad Amin Manavi ,&nbsp;Ahmad Reza Dehpour ,&nbsp;Hamed Shafaroodi","doi":"10.1016/j.ibneur.2024.11.013","DOIUrl":"10.1016/j.ibneur.2024.11.013","url":null,"abstract":"<div><h3>Introduction</h3><div>Epilepsy remains a challenge, with one-third of patients experiencing refractory seizures despite current anti-seizure medications. The nitrergic system, which involves nitric oxide (NO) and NO synthase (NOS) enzymes, plays a complex role in seizure pathophysiology. Pentoxifylline (PTPh), an FDA-approved phosphodiesterase inhibitor, has anticonvulsant effects; however, its relationship with the pathway is unclear. This study focused at how the nitrergic system could be involved in PTPh’s anticonvulsant effects.</div></div><div><h3>Methods</h3><div>Seizures were induced in male mice by intravenous pentylenetetrazole (PTZ) infusion (absence-like seizures), intraperitoneal PTZ injection, and maximal electroshock (generalized tonic-clonic seizures). PTPh was administered at various doses, alone or in combination with the NO precursor L-arginine, as well as non-selective (L-NAME) and selective NOS inhibitors (nNOS inhibitor 7-NI and iNOS inhibitor aminoguanidine). Seizure thresholds, latencies, incidence, and mortality were assessed. Moreover, in the next paradigm, using maximal electroshock model, we evaluate possible protective effects of PTPh against generalized tonic-clonic seizures and subsequent mortality.</div></div><div><h3>Results</h3><div>In the intravenous PTZ model, PTPh (≥150 mg/kg) increased the seizure threshold, potentiated by L-arginine but reduced by L-NAME and 7-nitroindazole. In the intraperitoneal PTZ model, 150 mg/kg PTPh decreased tonic seizure frequency, which was mitigated by aminoguanidine. However, PTPh failed to prolong clonic seizure latency. In the maximal electroshock test, 100 mg/kg PTPh protected against tonic seizure incidence (reduced by aminoguanidine). Although PTPh could not reduce mortality, its combination with L-NAME or 7-nitroindazole increased mortality compared with the vehicle-treated group.</div></div><div><h3>Conclusion</h3><div>PTPh exerted anticonvulsant effects against absence-like and generalized tonic-clonic seizures, likely through modulation of the nitrergic system involving neuronal, endothelial, and inducible NOS isoform. These findings provide novel insights into the complex interplay between NO signaling and the anticonvulsant actions of PTPh, highlighting the potential therapeutic implications of targeting the NO pathway in epilepsy management.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"17 ","pages":"Pages 485-492"},"PeriodicalIF":2.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11664280/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142881899","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":"Post-stroke effects of IC87201 on neurobehavioral function and brain injuries: A stereological study","authors":"Maryam Mohammadian ,&nbsp;Aminollah Bahaoddini ,&nbsp;Mohammad Reza Namavar","doi":"10.1016/j.ibneur.2024.11.012","DOIUrl":"10.1016/j.ibneur.2024.11.012","url":null,"abstract":"<div><h3>Objectives</h3><div>Stroke is the second leading cause of global death and is characterized by excitotoxic neuronal death caused by NMDA (N-Methyl-D-Aspartate) receptor overactivation. The present study was conducted to investigate the therapeutic potential of IC87201, a novel small molecule interfering with the NMDA receptor intracellular signaling pathway, in reducing the extent of ischemic stroke-induced brain damage.</div></div><div><h3>Materials and Methods</h3><div>Cerebral ischemia was induced by the middle cerebral artery occlusion (MCAO) method in 24 anesthetized adult male rats for one hour. The animals were randomized into sham, MCAO, MCAO+ DXM (Dextromethorphan hydrobromide monohydrate) as an NMDA antagonist, and MCAO+ IC87201 groups which in the last two groups, DXM (50 mg/kg) and IC87201 (10 mg/kg) were injected intraperitoneally after ischemia. The neurobehavioral scores were appraised for 7 days and after that, brain tissue was appropriately prepared to perform the stereological evaluations.</div></div><div><h3>Results</h3><div>The administration of IC87201 significantly recovered post-ischemia damages, including neurobehavioral function, reduction of volume of the total hemisphere, cortex, and striatum in rat brain, and the percentage of infarcted areas. Additionally, in the striatum region, IC87201 caused an increase in the total number of neuronal and non-neuronal cells as well as a decrease in the total number of dead cells. Some of these parameters were improved by DXM, but in general, IC87201 outperformed that.</div></div><div><h3>Conclusions</h3><div>IC87201 was successful in minimizing ischemia-induced damage, especially in the striatal region. In addition, IC87201, as a molecule that acts on the intracellular signaling cascade of the NMDA receptor, performed better than DXM, as an antagonist of this receptor.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"17 ","pages":"Pages 463-470"},"PeriodicalIF":2.0,"publicationDate":"2024-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142721416","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":"Causes and countermeasures for the increased infection and COVID-19 mortality rates in patients with schizophrenia","authors":"Zhen-Ying Li ,&nbsp;Yu-Qian Li ,&nbsp;Jing-Ru Zhou ,&nbsp;Jie Wang ,&nbsp;Kun-Ze Liu ,&nbsp;Peng Wang ,&nbsp;Chun-Mei Gong ,&nbsp;Han Wang ,&nbsp;Yu-Jing Zhang ,&nbsp;Yu Cao ,&nbsp;Yue Gu ,&nbsp;Han-Bo Zhang ,&nbsp;Hui Lu ,&nbsp;Li-Fang Lu ,&nbsp;Ren-Jun Feng","doi":"10.1016/j.ibneur.2024.11.009","DOIUrl":"10.1016/j.ibneur.2024.11.009","url":null,"abstract":"<div><div>Schizophrenia (SCZ) is a common psychiatric disorder that has a complex pathological mechanism. During the Coronavirus disease 2019 (COVID-19) epidemic, patients with SCZ had substantially higher rates of infection with SARS-CoV-2, the virus that causes COVID-19, as well as higher COVID-19 mortality relative to patients with other mental disorders. However, the reasons for these increased rates in patients with SCZ remain unknown. In this review, we hypothesize that certain molecular pathways exhibit abnormal function in both COVID-19 and SCZ, with a focus on those related to energy metabolism dysregulation, immune system disruption, and abnormalities of the central nervous system. We review that dysregulation of energy metabolism can result in disruptions to the immune system and abnormalities within the central nervous system (CNS). Furthermore, immune system disturbances may also contribute to CNS abnormalities in both SCZ and COVID-19. We also discuss macro-factors associated with the high infection and mortality rates of COVID-19 in patients with SCZ, including sociodemographic factors, reduced access to psychiatric healthcare, structural barriers to COVID-19 vaccination, and proposed approaches to mitigate these macro-factors.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"17 ","pages":"Pages 456-462"},"PeriodicalIF":2.0,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142700757","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":"Alterations in Neuroligin-2 and BDNF proteins associated with anxiety-like behavior in salicylate-induced tinnitus rats","authors":"Saeid Mahmoudian ,&nbsp;Ali Fathi Jouzdani ,&nbsp;Ahmadreza Nazeri ,&nbsp;Kasra Bagherian ,&nbsp;Mohadeseh Beiranvand ,&nbsp;Zeinab Akbarnejad","doi":"10.1016/j.ibneur.2024.11.007","DOIUrl":"10.1016/j.ibneur.2024.11.007","url":null,"abstract":"<div><div>Given the high prevalence of tinnitus and anxiety among patients, understanding the mechanisms that increase anxiety is crucial. Neuroligin 2 (NLGN2) is an anxiety-related protein that has received much attention in recent years. On the other hand, the Brain-Derived Neurotrophic Factor (BDNF) affects various neurotransmitter systems, neuropeptides, and intracellular signaling pathways. These are neurochemical systems that, if out of balance, could lead to anxiety behavior. This is the first study to investigate whether changes in protein expression in the amygdala nucleus are associated with high anxiety in tinnitus. After inducing and confirming tinnitus in rats using gap-prepulse inhibition of the acoustic startle (GPIAS) and Pre-pulse inhibition (PPI), the Elevated Plus Maze (EPM) and the Open Field Test (OFT) were used to assess anxiety levels in both groups. Subsequently, amygdala tissue samples were collected from both groups and analyzed for NLGN2 and BDNF protein expression. The GPIAS score decreased following sodium salicylate administration in the tinnitus group, while the PPI score did not change. Additionally, the tinnitus group exhibited higher anxiety levels than the control group in both behavioral tests. Moreover, NLGN2 protein expression was increased in the amygdala nucleus of sodium salicylate-induced tinnitus rats compared to controls, while BDNF protein expression was reduced. These findings suggest that increased NLGN2 and decreased BDNF protein levels in the amygdala nucleus contribute to tinnitus-related anxiety and identify these proteins as potential therapeutic targets for tinnitus.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"17 ","pages":"Pages 407-414"},"PeriodicalIF":2.0,"publicationDate":"2024-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142662840","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":"Understanding the influence of digital technology on human cognitive functions: A narrative review","authors":"Eugénia Correia de Barros","doi":"10.1016/j.ibneur.2024.11.006","DOIUrl":"10.1016/j.ibneur.2024.11.006","url":null,"abstract":"<div><div>In the era of rapid digitalization, the widespread integration of digital technology into various aspects of daily life has sparked significant interest in understanding its impact on cognitive mental processes. While the emerging data suggests that its influence may be positive or negative, the depth of evidence regarding neurobiological mechanisms remains limited. This review aims to synthesize previously published studies and develop a comprehensive framework that systematically categorizes digital technologies, the cognitive functions they impact, and developmental stages around the concept of neuroplasticity, while clearly illustrating their interconnections. Despite acknowledged limitations, through an exhaustive approach, this paper intends to offer a dynamic perspective on the effects of digital media on the human brain, before the onset of addiction.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"17 ","pages":"Pages 415-422"},"PeriodicalIF":2.0,"publicationDate":"2024-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142662841","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":"Neonatal maternal separation impairs cognitive function and synaptic plasticity in adult male CD-1 mice","authors":"Zhen-Yu Hu ,&nbsp;Ru-Meng Wei ,&nbsp;Fei-Hu ,&nbsp;Ke Yu ,&nbsp;Shi-Kun Fang ,&nbsp;Xue-Yan Li ,&nbsp;Yue-Ming Zhang ,&nbsp;Gui-Hai Chen","doi":"10.1016/j.ibneur.2024.11.001","DOIUrl":"10.1016/j.ibneur.2024.11.001","url":null,"abstract":"<div><div>Maternal separation (MS) increases the risk of occurrence of anxiety, depression, and learning and memory impairment in offspring. However, the underlying molecular biological mechanisms remain unclear. In the current study, offspring CD-1 mice were separated from their mothers from postnatal day 4 to postnatal day 21. At 3 months of age, the male offspring were selected for the evaluation of anxiety- and depression-like behaviors and learning and memory function. Western blotting and RT-PCR were used to examine the expression levels of brain-derived neurotrophic factor, tyrosine kinase receptor B, postsynaptic density-95, and synaptophysin. Long-term potentiation (LTP) and long-term depression (LTD) were recorded at Schaffer collateral/CA1 synapses. Furthermore, basal synaptic transmission was evaluated via the recording of the frequency and amplitude of miniature excitatory postsynaptic currents (mEPSCs). The results showed that adult offspring CD-1 mice displayed anxiety- and depressive-like behaviors as well as impaired spatial learning and memory abilities. Electrophysiological analysis indicated that MS impaired LTP, enhanced LTD, and reduced the frequency of mEPSCs in pyramidal neurons in the CA1 region. Our findings suggested that MS can lead to anxiety, depression, and cognitive deficits, and these effects are associated with alterations in the levels of synaptic plasticity-associated proteins, consequently, also synaptic plasticity.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"17 ","pages":"Pages 431-440"},"PeriodicalIF":2.0,"publicationDate":"2024-11-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142700755","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":"Valproic acid attenuates the severity of astrogliosis in the hippocampus of animal models of temporal lobe epilepsy","authors":"Hu Feng,&nbsp;Jiamin Luo,&nbsp;Zhiwei Li,&nbsp;Yuxiao Zhao,&nbsp;Yamei Liu,&nbsp;Hongyan Zhu","doi":"10.1016/j.ibneur.2024.11.003","DOIUrl":"10.1016/j.ibneur.2024.11.003","url":null,"abstract":"<div><div>Reactive astrogliosis is one of the most frequency neuropathological alterations in the hippocampus of animal models and patients with temporal lobe epilepsy (TLE). Valproic acid (VPA), a widely used antiepileptic drug (AED), acts by blocking ion channels and enhancing GABAergic activity. This study investigated the effects of VPA on hippocampal astrogliosis in a rat model of TLE. The results demonstrated that chronic administration of VPA at a dose of 200 mg/kg significantly reduced the severity of astrogliosis and ameliorated neuronal loss in the hippocampus at the early and middle stages post-status epilepticus (SE), while also improving cognitive impairments at the middle and late stages in KA-SE rats. Long-term administration of VPA at 400 mg/kg attenuated astrogliosis in the hippocampus at the middle stage post-SE, but lacked neuroprotective effects and exacerbated cognitive impairments at the late stage. These findings suggest that VPA at an appropriate dose could mitigate hippocampal astrogliosis, potentially offering a new antiepileptic mechanism for its long-term use.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"17 ","pages":"Pages 471-479"},"PeriodicalIF":2.0,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142721417","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":"Exploring the potential of probiotics in Alzheimer's disease and gut dysbiosis","authors":"Sowmiya S ,&nbsp;Dhivya L.S. ,&nbsp;Praveen Rajendran ,&nbsp;Harikrishnan N ,&nbsp;Ankul Singh S","doi":"10.1016/j.ibneur.2024.11.004","DOIUrl":"10.1016/j.ibneur.2024.11.004","url":null,"abstract":"<div><div>Alzheimer's disease is a fatal neurodegenerative disorder that causes memory loss and cognitive decline in older people. There is increasing evidence suggesting that gut microbiota alteration is a cause of Alzheimer’s disease pathogenesis. This review explores the link between gut dysbiosis and the development of Alzheimer's disease contributing to neuroinflammation, amyloid β accumulation, and cognitive decline. We examine the recent studies that illustrate the gut-brain axis (GBA) as a bidirectional communication between the gut and brain and how its alteration can influence neurological health. Furthermore, we discuss the potential of probiotic supplementation as a management approach to restore gut microbiota balance, and ultimately improve cognitive function in AD patients. Based on current research findings, this review aims to provide insights into the promising role of probiotics in Alzheimer's disease management and the need for further investigation into microbiota-targeted interventions.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"17 ","pages":"Pages 441-455"},"PeriodicalIF":2.0,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142700756","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":"Hyperphosphorylated tau targeting human serum albumin Fusion protein as therapeutics for Alzheimer’s diseases","authors":"Sookhee Bang,&nbsp;Jeong Kuen Song,&nbsp;Kwan Hee Lee","doi":"10.1016/j.ibneur.2024.11.005","DOIUrl":"10.1016/j.ibneur.2024.11.005","url":null,"abstract":"<div><h3>Introduction</h3><div>Neurofibrillary tangles (NFTs) are composed of hyperphosphorylated forms of microtubule-associated protein tau (Tau), which is responsible for neurodegeneration in Alzheimer’s disease (AD). The hippocampal region has been a major focus of AD research because the deposits of phosphorylated tau protein in these regions are correlated with early memory deficits. Despite extensive studies, therapeutic strategies to reduce tau hyperphosphorylation and NFTs deposition remain unclear. AL04, a recently developed recombinant fusion protein comprising Cystatin C, human serum albumin, and a novel blood brain barrier (BBB) penetrating peptide, is currently under investigation. Previous studies have demonstrated its effectiveness in reducing amyloid beta plaques in AD mouse model.</div></div><div><h3>Methods</h3><div>In this study, we investigated the effects of AL04 on lowering hyperphosphorylated tau and NFTs in JNPL3 mouse model harboring human tau-P301L mutation. 3-month-old female mice intraperitoneally received AL04 (5 mg/kg) or PBS treatment every other week for 24 weeks. We used confocal microscopy and western blot to visualize and analyze changes in hyperphosphorylated tau Ser202/Thr205 labeled with AT8 antibody in the brain.</div></div><div><h3>Results</h3><div>We found that the AL04 treatment decreases hyperphosphorylated tau at PP2A-sensitive epitope Ser202/Thr205 in the hippocampus of the brain. In the brain lysates of AL04 treated mice, we observed the reduction of I2PP2A, inhibitor of PP2A, and the induction of autophagy receptor proteins such as SQSTM-1/p62 and OPTN.</div></div><div><h3>Conclusion</h3><div>Our data suggests that AL04 can be used as an AD prophylactic/therapeutic agent as it lowers the hyperphosphorylated tau by downregulating I2PP2A. We also propose that AL04 can induce the degradation of hyperphosphorylated tau aggregates through the upregulation of the autophagy pathway.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"17 ","pages":"Pages 423-430"},"PeriodicalIF":2.0,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142662835","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}