Metabolic brain disease最新文献

{"title":"The effect of N-acetylcysteine on apoptosis and NGF-Akt/Bad pathway in the hippocampus tissue of cerebral ischemia-reperfusion in male rats.","authors":"Hamed Saniei, Roya Naderi","doi":"10.1007/s11011-025-01641-7","DOIUrl":"10.1007/s11011-025-01641-7","url":null,"abstract":"<p><p>Apoptosis is the primary pathological feature of neuronal injury caused by cerebral ischemia-reperfusion (I/R). The detailed molecular mediators are still being debated. This study aims to examine the effects of cerebral ischemia-reperfusion on apoptosis and NGF-Akt/Bad axis in rat hippocampus alone and in combination with NAC (N-Acetylcysteine). Rats were subjected to common carotid artery occlusion (CCAO) for 20 min followed by 24 h reperfusion. NAC (150 mg/kg) was given intraperitoneally (ip) one hour before ischemia and five minutes before reperfusion. TUNEL staining of hippocampus neurons revealed that the number of apoptotic neurons was elevated 24 h after reperfusion. At the molecular levels, I/R injury resulted in an increased protein expression of cleaved caspase3/procaspase3 ratio and cytochrome c level with a concomitant down-regulation of NGF, p-AKT/AKT, p-Bad/Bad and p-Trk/Trk ratio. NAC treatment significantly reduced the apoptotic damage and also reversed NGF, p-AKT/AKT, p-Bad/Bad, and p-Trk/Trk ratio in hippocampus neurons in I/R rats. In conclusion, our data showed that NGF-Akt/Bad axis may play a regulatory role in hippocampus cell death, providing a new target for a novel therapeutic strategy during transit ischemic stroke. NAC has been shown to reverse molecular alterations, suggesting its potential as an effective agent against hippocampal apoptosis following acute I/R injury.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 5","pages":"217"},"PeriodicalIF":3.2,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144234544","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Brain morphological changes in type 2 diabetes patients with painful peripheral neuropathy.","authors":"Miao He, Jiaying Yang, Xueqing Liu, Jiamin Zhou, Xuewei Zhang, Jing Li, Xiali Shao, Wenhui Li, Yuzhou Guan, Weihong Zhang, Feng Feng","doi":"10.1007/s11011-025-01643-5","DOIUrl":"10.1007/s11011-025-01643-5","url":null,"abstract":"<p><p>We investigates changes in brain volume and cortical thickness in patients with type 2 diabetes mellitus (T2DM) and peripheral neuropathy (DPN), particularly those with neuropathic pain. 105 participants were divided into three groups: T2DM (n = 26), T2DM with DPN (n = 42), and healthy controls (HCs, n = 37). The DPN group was further divided into painless (n = 22) and painful (n = 20) subgroups. Participants underwent clinical neuropsychological testing, electromyography, and brain MRI scans. Voxel-based morphometry was used to analyze gray matter volume (GMV) and cortical thickness. Associations between morphological changes and clinical/neuropsychological indicators were assessed. Average cortical thickness of the three patient subgroups was significantly reduced compared to the HCs. GMV loss in the DPN_ pain group was confined to the cerebellum, right putamen/pallidum, and caudate, while GMV increased in the brainstem. Multiple regression analysis showed correlations between brain regions and factors such as cholesterol levels, neuropathic pain severity, and nerve amplitudes (P < 0.001). The volume of right lateral geniculate nucleus volume was linked to the DN4 score (r = 0.593, P = 0.015) and onset age (r = -0.541, P = 0.031). Specific brain regions and the cortices are more vulnerable to the effects of neuropathic pain and peripheral nerve damage.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 5","pages":"216"},"PeriodicalIF":3.2,"publicationDate":"2025-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144192019","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gut microbiota and serum metabolomics unveil the role of Phellinus ribis polysaccharides in improving Alzheimer's disease symptoms in senescence-accelerated mice.","authors":"Zhiyuan Zhang, Shuai Wang, Rong Rong, Guoying Zhang, Zheng Li, Yuanyuan Li, Rongxiang Wang, Yuhong Liu, Kejian Li","doi":"10.1007/s11011-025-01632-8","DOIUrl":"10.1007/s11011-025-01632-8","url":null,"abstract":"<p><p>Alzheimer's disease (AD), a complex neurodegenerative disorder with limited therapeutic options, urgently requires innovative strategies targeting its underlying mechanisms. Phellinus ribis polysaccharides (PRG), a bioactive compound with proven neuroprotective and microbiota-modulating effects, hold promise for addressing AD pathology through gut-brain axis regulation. This study aims to investigate the effects of PRG on the gut microbiota composition and serum metabolomic profile of a senescence-accelerated mouse model (SAMP8) and to reveal its potential mechanisms in alleviating symptoms of AD. The gut microbiota composition of SAMP8 mice treated with PRG was analyzed using 16S rRNA gene sequencing. Non-targeted metabolomics, based on ultra-performance liquid chromatography quadrupole/electrostatic field orbitrap high-resolution mass spectrometry, was employed to analyze changes in metabolites in the serum samples. Spearman correlation analysis was further used to explore the association between gut microbiota and serum metabolites. PRG significantly improved gut dysbiosis in SAMP8 mice by increasing the abundance of beneficial bacterial genera, reducing pathogenic bacteria levels, and restoring the dominance of advantageous bacterial phyla. Serum metabolomics analysis revealed that PRG intervention led to significant changes in AD-related metabolites, including phenylalanine and oxidative stress markers. Combined analysis indicated a correlation between changes in gut microbiota and serum metabolites. PRG can alleviate AD symptoms in senescence-accelerated mice by regulating gut microbiota and serum metabolites, providing scientific evidence for PRG as a potential therapeutic agent for AD. This study explores the role of gut microbiota and serum metabolites under PRG intervention in neurodegenerative diseases.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 5","pages":"215"},"PeriodicalIF":3.2,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144187382","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Quinoa extract restored behavioral damage and neurotoxicity induced by a Parkinson's disease-like model in Drosophila melanogaster.","authors":"Magna Sotelo Barrientos, Marcia Rósula Poetini, Eliana Jardim Fernandes, Luana Barreto Meichtry, Elize Aparecida Santos Musachio, Stífani Machado Araujo, Sirlei Patricia Souza, Kétnne Hanna Poleto Pinto, Murilo Ricardo Sigal Carriço, Rafael Roehrs, Marina Prigol, Gustavo Petri Guerra","doi":"10.1007/s11011-025-01640-8","DOIUrl":"10.1007/s11011-025-01640-8","url":null,"abstract":"","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 5","pages":"214"},"PeriodicalIF":3.2,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144187383","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unlocking the neuroprotective potential of peptide nucleic acids 5 (PNA5) in neurological diseases: molecular mechanisms to therapeutic approaches.","authors":"Pratyush Porel, Garry Hunjan, Navpreet Kaur, Vipul Sharma, Manpreet Kaur, Yukti Mittal, Ramandeep Kaur, Khadga Raj Aran","doi":"10.1007/s11011-025-01629-3","DOIUrl":"10.1007/s11011-025-01629-3","url":null,"abstract":"<p><p>Peptide nucleic acids (PNAs) are synthetic nucleic acid analogues offering distinct structural and functional advantages over conventional RNA and DNA, positioning them as powerful molecules in molecular biology. Recently, PNAs have gained significant attention for their potential in the prevention and management of neurological diseases, including Alzheimer's disease (AD), Parkinson's disease (PD), multiple sclerosis (MS), Huntington's disease (HD), amyotrophic lateral sclerosis (ALS), stroke, traumatic brain injury (TBI), spinal cord injury (SCI), depression, and anxiety. PNA5, a specific PNA variant, is highly expressed in neocortical association regions, particularly in primates, and plays a critical role in high-level cognitive functions such as reasoning, decision-making, and problem-solving. It can form stable, sequence-specific hybridizations with nucleic acids, resist nuclease degradation, and efficiently cross cellular membranes, making them ideal candidates for targeting disease-related genes in the brain. PNA5 has shown neuroprotective properties by improving cognitive function, reducing neuroinflammation, and preserving the integrity of the blood-brain barrier (BBB). Additionally, it supports critical processes such as neural migration, axon guidance, and synaptogenesis, which are vital for maintaining proper brain function. This review explores the mechanisms by which PNAs, particularly PNA5, exert therapeutic effects in neurological disorders. It highlights their role in gene modulation, protein regulation, and potential strategies for enhancing PNA delivery to the central nervous system (CNS) and its related disorders.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 5","pages":"213"},"PeriodicalIF":3.2,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144174252","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting Acyl-CoA synthetase long-chain family member 4: a potential approach for the treatment of cerebral ischemia/reperfusion injury.","authors":"Nikita Patil, Lokesh Kumar Bhatt","doi":"10.1007/s11011-025-01638-2","DOIUrl":"10.1007/s11011-025-01638-2","url":null,"abstract":"<p><p>Cerebral ischemia/reperfusion injury causes high rates of morbidity and death. Recent studies have shown that ferroptosis, a type of controlled cell death brought on by lipid peroxidation, worsens cerebral ischemia/reperfusion injury. Acyl-CoA synthetase long-chain family member 4 (ACSL4) has emerged as a crucial enzyme in lipid metabolism and ferroptosis in the context of ischemia/reperfusion injury, influencing neuronal cell death. Increased vulnerability to ferroptosis and worsening ischemia/reperfusion injury outcomes are linked to elevated ACSL4 levels. Comprehending the molecular processes underlying ACSL4-mediated ferroptosis may result in novel approaches to treating cerebral ischemia/reperfusion injury. The present review discusses ACSL4 as a potential target for treating cerebral ischemia/reperfusion injury, focusing on ACSL4-mediated ferroptosis and signal transduction.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 5","pages":"212"},"PeriodicalIF":3.2,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144142930","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MiR-134-5p/BDNF/TrkB/CREB signaling pathway involved in the depression-like behaviors in mice following exposure to benzo[a]pyrene.","authors":"Tingyi Zhao, Huan Li, Yunge Jia, Na Xia, Xin Li, Hongmei Zhang","doi":"10.1007/s11011-025-01637-3","DOIUrl":"10.1007/s11011-025-01637-3","url":null,"abstract":"<p><p>Benzo[a]pyrene (B[a]P) is known to cause depression-like symptoms in mice, however, the mechanisms are still unclear. The present study aimed to establish a mouse model of depression-like behavior induced by B[a]P and to elucidate the possible underlying mechanisms. Forty robust male ICR mice were randomly categorized into 4 groups and received intraperitoneal injections (i.p.) of peanut oil or B[a]P at doses of 0.5, 2, or 10 mg/kg, 30 times over a period of 60 days. Behavioral assessments were conducted to evaluate depression-like symptoms, identify neuronal structural alterations and cellular apoptosis, and measure the protein levels of brain-derived neurotrophic factor (BDNF), tropomyosin receptor kinase B (TrkB), phosphorylated TrkB (p-TrkB), cAMP-response element binding protein (CREB) and phosphorylated CREB (p-CREB) in the cerebral cortex. To further explore the regulatory role of miRNA, small RNA sequencing was performed in HT22 cells treated with B[a]P at concentrations of 0.2, 2, and 20 µM, which revealed the dysregulated miRNA expression profiles. The interaction between miR-134-5p and BDNF mRNA was examined, along with its inhibitory effects in both in vivo and in vitro contexts. Findings indicated that B[a]P exposure significantly induced depression-like behavior and neuronal damage in mice in a dose-dependent manner, in contrast to the controls, and was associated with a reduction in BDNF/TrkB/CREB signaling pathway proteins in the cerebral cortex. As compared to the respective controls, B[a]P exposure notably triggered an irregular miRNA expression profile (encompassing miR-10b-5p, miR-124-3p, miR-134-5p, and miR-155-5p) in both the cerebral cortex of mice and HT22 cells. Owing to its uniform alterations in expression profiles in vivo and in vitro, miR-134-5p was chosen as the target miRNA for follow-up mechanistic research employing a miR-134-5p inhibitor (at concentrations of 100 nM) in HT22 cells. Following a 48-hour in vitro treatment with B[a]P (20 µM), there was a notable reduction in proteins linked to the BDNF/TrkB/CREB signaling pathway, in contrast to DMSO controls. This decrease was markedly ameliorated in HT22 cells that had been transfected with the miR-134-5p inhibitor. The research uncovered the pivotal function of the BDNF/TrkB/CREB signaling pathway in B[a]P-induced depressive-like behavior in vivo, and showed a regulatory role of miR-134-5p in this pathway. These findings suggest a potential intervention target against the depression-like behaviors resulting from B[a]P exposure.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 5","pages":"210"},"PeriodicalIF":3.2,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144128176","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuroprotective potential of carvacrol: restoration of oxidative balance and mitigation of brain injury markers in isoproterenol-induced rats.","authors":"Betül Bağcı, Şeyma Aydın, Elif Dalkılınç, Selim Çomaklı, Sefa Küçükler, Selçuk Özdemir","doi":"10.1007/s11011-025-01634-6","DOIUrl":"10.1007/s11011-025-01634-6","url":null,"abstract":"<p><p>This research investigated the protective properties of Carvacrol (CVC) against Isoproterenol (ISO)-induced oxidative stress, neuroinflammation, and mitochondrial dysfunction in rats. The findings showed that CVC treatment did not significantly modify baseline oxidative stress levels in healthy rats but successfully alleviated ISO-induced oxidative damage by augmenting antioxidant enzyme activity and diminishing lipid peroxidation, as demonstrated by a reduction in MDA levels. These findings indicate that CVC can reinstate antioxidant capability and reduce oxidative damage. Concerning neuroinflammation, ISO therapy markedly increased the expression of pro-inflammatory markers, including TNF-α, IL-1β, c-Fos, BDNF, Nfl, and GFP, signifying a robust inflammatory and damage response. The injection of CVC following ISO exposure markedly decreased the expression of these markers, suggesting that CVC may exert a neuroprotective effect by regulating the inflammatory response and mitigating neuronal and glial damage. CVC demonstrated a notable protective effect on mitochondrial integrity, evidenced by the decreased mRNA expression of mitochondrial damage markers, including NSE, s100B, CALP1, and CALM1 in the CVC-treated groups, showing that CVC mitigates mitochondrial dysfunction. The analysis revealed no significant alterations in the expression levels of Aβ40, pTau181, and tTau across all groups, indicating that these biomarkers were not substantially influenced by CVC treatment under the study's conditions. However, β-amyloid accumulation varied significantly between groups, highlighting the need for further research to explore CVC's potential implications in amyloid-related diseases. These findings endorse CVC's neuroprotective efficacy and therapeutic potential in neurological disorders associated with oxidative stress, inflammation, and mitochondrial impairment.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 5","pages":"211"},"PeriodicalIF":3.2,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12102131/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144128178","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The emerging role of chitinase-3-like-1 protein in neurodegeneration.","authors":"Veerta Sharma, Thakur Gurjeet Singh","doi":"10.1007/s11011-025-01636-4","DOIUrl":"10.1007/s11011-025-01636-4","url":null,"abstract":"<p><p>Neurodegenerative diseases (NDDs) are characterised by the progressive degeneration of neurons in the brain, resulting in impairments in memory, cognition, and motor abilities. Common pathological features include altered energy metabolism, neuroinflammation, death of neurons, aberrant protein aggregation, and synaptic dysfunction. Chitinase-3-like-1 (CHI3-L1) is an evolutionarily conserved protein involved in variety of biological processes such as neuroinflammation, tissue remodelling and angiogenesis. Elevated levels of CHI3-L1 have been detected in the cerebrospinal fluid and plasma of patients with NDDs, suggesting its involvement in disease progression. As a critical regulator of neuroinflammation, CHI3-L1 modulates the activity of astrocyte and microglia, causing the production of pro-inflammatory cytokines that worsens disease progression. In addition to its involvement in disease pathophysiology, it has emerged as a potential biomarker for the diagnosis and monitoring of neurological diseases. However, significant knowledge gaps persist regarding its molecular mechanisms, interactions with inflammatory mediators, and influence on blood-brain barrier integrity. Therefore, this review highlights the emerging role of CHI3-L1 in neurodegeneration and describes future research approaches targeted at unlocking its therapeutic potential in treating NDDs.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 5","pages":"209"},"PeriodicalIF":3.2,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144111402","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rhoifolin as a potential anxiolytic drug for the effects of nicotine withdrawal: beneficial effects on behavior, neuroinflammation, and oxidative stress.","authors":"Alaa M Hammad, Suhair Sunoqrot, Thanaa Al-Zuhd, Mohammed Waleed, Ali I M Ibrahim, F Scott Hall, Alaa R Al-Tamimi, Eveen Al-Shalabi","doi":"10.1007/s11011-025-01627-5","DOIUrl":"10.1007/s11011-025-01627-5","url":null,"abstract":"<p><p>Cigarette smoke exposure induces oxidative stress and neuroinflammation, contributing to nicotine dependence and withdrawal-related anxiety. Rhoifolin (ROF), a naturally occurring flavonoid glycoside, possesses notable oxidative stress and inflammation reducing properties. This study investigated the potential ameliorative effects of ROF against cigarette smoke-induced neuroinflammation, oxidative damage, and withdrawal-induced anxiety-like behavior in rats. Rats were allocated into four treatment groups: a control group subjected only to ambient air; a nicotine (NIC) group exposed to cigarette smoke five days a week for seven weeks; a NIC/ROF group similarly exposed to smoke, but also treated with 20 mg/kg ROF daily for the last three weeks; and a ROF-only group treated with ROF while subjected to room air. Cigarette smoke exposure evoked anxiety during withdrawal periods, elevated levels of proinflammatory cytokines IL-1β and TNF-α, and a markedly reduced levels of key antioxidant enzymes superoxide dismutase, catalase, and glutathione peroxidase. ROF treatment significantly reversed these effects, reducing anxiety, lowering inflammatory markers, and restoring antioxidant enzyme activity to near-normal levels. Molecular modeling simulations showed a potential binding interaction for ROF at an allosteric pocket in each of the antioxidant enzyme structures, providing a potential mechanism by which ROF might act as an activator of these enzymes, thereby promoting antioxidant activity. Our findings suggest that ROF exhibits anxiolytic effects related to cigarette smoke exposure, likely mediated by its ameliorative role against inflammation and oxidative stress, supporting its potential role in improving behavioral outcomes of cigarette smoke withdrawal.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 5","pages":"208"},"PeriodicalIF":3.2,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144111341","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}