Neurochemistry international最新文献

{"title":"Optimizing cognitive and behavioural recovery after stroke: clinical integration of dietary supplements with a focus on ω-3 fatty acids.","authors":"Anand Krishnan, Prasanjit Saha, Manu Aravind, Sen Chandra Sreetama, Usha Rajamma, Rajesh Anantha Shenoi, Arnab Datta, Goutam Chandra","doi":"10.1016/j.neuint.2026.106287","DOIUrl":"https://doi.org/10.1016/j.neuint.2026.106287","url":null,"abstract":"<p><p>Stroke remains a leading cause of long-term disability worldwide, with many survivors experiencing persistent cognitive and behavioural impairments despite advancements in acute management. Post-stroke neurorecovery is often incomplete, contributing to dementia, depression, and reduced quality of life, particularly in low- and middle-income settings where access to advanced rehabilitation and therapeutics is limited. This highlights an urgent need for accessible, adjunctive strategies that can enhance functional recovery. Emerging preclinical evidence indicates that dietary supplements can modulate key biological processes underlying neurorecovery, including neuroplasticity, neuroinflammation, oxidative stress, mitochondrial function, and synaptic remodeling. In this narrative review, we examine the role of major classes of nutraceuticals such as omega-3 fatty acids, vitamins, minerals, polyphenols, and amino acids in supporting cognitive and behavioural recovery after stroke with particular emphasis on omega-3 fatty acids, given their central role in neuronal membrane integrity, lipid-mediated signaling, and resolution of inflammation. We integrate mechanistic insights with preclinical and clinical data explicitly highlighting that theoretical models and basic research demonstrate significant promise, while current clinical evidence remains heterogeneous and frequently inconclusive. We discuss how dietary supplementation might be strategically incorporated alongside conventional rehabilitation paradigms including physiotherapycognitive training, and pharmacotherapy. We further highlight emerging concepts such as the gut-brain axis, precision nutrition, and biomarker-guided interventions, which are shaping the future of personalized neurorehabilitation. Ultimately, while dietary supplements offer a promising, cost-effective and accessible adjunctive approach. their current clinical utility is constrained by mixed translational efficacy. Overcoming these limitations will require rigorous patient selection, optimized timing, and shift towards evidence-based personalized, multimodal strategies. This will be essential to fully harness their therapeutic potential in improving cognitive and behavioural outcomes in stroke recovery.</p>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":" ","pages":"106287"},"PeriodicalIF":5.5,"publicationDate":"2026-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149369710","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":"Pathway-selective G_i1, but not G_q, protein activation distinguishes hallucinogenic from non-hallucinogenic serotonin 5-HT_2A receptor agonists in the human cortex.","authors":"Patricia Miranda-Azpiazu, Rebeca Diez-Alarcia, Itziar Muneta-Arrate, Aintzane García-Bea, Rafael Maldonado, Benito Morentin, Javier González-Maeso, J Javier Meana","doi":"10.1016/j.neuint.2026.106285","DOIUrl":"https://doi.org/10.1016/j.neuint.2026.106285","url":null,"abstract":"<p><p>The serotonin 5-HT_2A receptor (5-HT_2AR) signaling involves canonical G_q/11 proteins and alternative pathways, such as recruitment of other G proteins. It has been proposed that the 5-HT_2AR-mediated activation of inhibitory G_i/o proteins accounts for the hallucinogenic properties of psychedelics. Here, the differential signaling patterns between hallucinogenic and non-hallucinogenic 5-HT_2AR agonists were evaluated in post-mortem human prefrontal cortex using [³⁵S]GTPγS binding assays coupled with antibody immunoprecipitation against different Gα protein subtypes. The hallucinogenic drugs (±)DOI, TCB-2, and LSD activated both G_q/11 and G_i1 proteins through 5-HT_2ARs. In contrast, the non-hallucinogenic (±)DOI analogous Ariadne and the LSD analogous agonists 2-Br-LSD and lisuride, at similar concentrations, were inactive in 5-HT_2AR-mediated activation of G_i1 proteins whereas activated G_q/11 proteins. G_i2, G_o, G_q/11, G_s, and G_z proteins were also triggered by the agonists but through receptor targets other than 5-HT_2ARs. The findings were confirmed using 5-HT_2AR knock-out mouse brain tissue. The alkylating agent NEM attenuated agonist-mediated G_i1 protein activation with null effect on transduction through G_q/11 proteins, supporting the involvement of inhibitory G proteins in the activity of hallucinogenic 5-HT_2AR drugs. In conclusion, G_i1 protein recruitment in human brain may be associated with the psychedelic properties of 5-HT_2AR agonists. The results suggest the existence of differential signaling consistent with functional selectivity in the 5-HT_2AR coupling to G proteins in the human brain, although a larger panel of drugs should be tested. These findings may help explain the differential behavioral responses elicited by psychedelic and non-psychedelic 5-HT_2AR agonists.</p>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":" ","pages":"106285"},"PeriodicalIF":5.5,"publicationDate":"2026-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149356974","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":"Inhibition of Ptbp1 in microglia alleviates neuroinflammation by the Cbx5-Ifitm3 axis.","authors":"Hongyi Yu, Meng Fu, Yushan Li, Wenqing Jia, Lan Yu, Xinyu Qi, Chao Wang, Xueling Ma","doi":"10.1016/j.neuint.2026.106286","DOIUrl":"https://doi.org/10.1016/j.neuint.2026.106286","url":null,"abstract":"<p><p>Polypyrimidine tract-binding protein 1 (Ptbp1) is a member of the heterogeneous nuclear ribonucleoproteins that govern numerous aspects of the messenger RNA life cycle, including splicing, stability, and translation. This study investigated its role in cerebral ischemia-reperfusion injury (CIRI) with a focus on microglia. A model of transient middle cerebral artery occlusion in mice and an oxygen-glucose deprivation/reperfusion (OGD/R) model in mouse BV2 cells were used. Ptbp1 was significantly upregulated in microglia following CIRI. Inhibition of Ptbp1 attenuated the inflammatory response in BV2 cells and reduced damage to co-cultured neurons under OGD/R conditions; it also reduced tissue inflammation, mitigated brain tissue damage, and improved neurological function on days 1, 3 and 7 after reperfusion in vivo. Mechanistically, Ptbp1 destabilized chromobox protein homolog 5 (Cbx5), thereby attenuating Cbx5/Suv39h1-mediated H3K9me3 enrichment and transcriptional repression at the interferon-induced transmembrane protein 3 (Ifitm3) promoter, promoting Ifitm3 expression and enhancing Tlr4/p65 signaling. The regulation of Cbx5 mRNA stability by Ptbp1 and the inhibitory effect of Cbx5 on Ifitm3 were also confirmed in IMG cells. The present findings suggest that Ptbp1 reduces the stability of Cbx5 mRNA, thereby attenuating Cbx5/Suv39h1-mediated transcriptional repression of Ifitm3, enhancing Tlr4/p65 signaling and the inflammatory response, and exacerbating neuronal damage and CIRI.</p>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":" ","pages":"106286"},"PeriodicalIF":5.5,"publicationDate":"2026-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149340228","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":"Region-specific regulation of astrocytic hepcidin-FPN1 axis dictates divergent iron handling in PC12 cells under MPP⁺ neurotoxicity.","authors":"Jing Ding, Wei Zhu, Jie Yang, Liluo Nie","doi":"10.1016/j.neuint.2026.106283","DOIUrl":"https://doi.org/10.1016/j.neuint.2026.106283","url":null,"abstract":"<p><p>Clinical studies show iron deposition in Parkinson's disease brains is regionally selective, mainly in the substantia nigra. Iron dysregulation is a key pathological mechanism. Astrocytes maintain brain iron homeostasis, but whether they exhibit regional heterogeneity via the hepcidin-FPN1 axis remains unclear. We examined iron-related protein/mRNA expression and iron content in astrocytes from forebrain (FB), midbrain (MB), and hindbrain (HB) co-cultured with PC12 cells under MPP⁺. RESULTS: (1) In monoculture, all regions showed downregulation of FPN1 protein and mRNA expression and increased hepcidin mRNA expression; DMT1 protein expression was upregulated in HB, and TfR1 mRNA expression was increased in HB and FB. (2) After co-culture, all regions showed FPN1 downregulation and TfR1/hepcidin/IRRP2 upregulation, most pronounced in MB. Regionally, FB further downregulated DMT1, while MB and HB maintained high DMT1. Iron content: MB and FB showed decreased intra- and extracellular iron; HB showed increased intracellular but decreased extracellular iron. All regions activated the hepcidin-FPN1 axis with different intensities. Our findings suggest that \"heterogeneous branch selection within a shared stress framework\" may govern regional sensitivity to MPP⁺-induced iron toxicity, channeling iron fate toward catalytic pools, sequestration, or extracellular leakage.</p>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":" ","pages":"106283"},"PeriodicalIF":5.5,"publicationDate":"2026-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149316863","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":"Editorial: Carbon monoxide/Heme oxygenase-1 in brain function & neurological diseases.","authors":"Helena L A Vieira, Roberta Foresti","doi":"10.1016/j.neuint.2026.106282","DOIUrl":"10.1016/j.neuint.2026.106282","url":null,"abstract":"","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":" ","pages":"106282"},"PeriodicalIF":5.5,"publicationDate":"2026-10-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149260350","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":"Expression of Concern: \"In vivo protection of synaptosomes by ferulic acid ethyl ester (FAEE) from oxidative stress mediated by 2,2-azobis(2-amidino-propane)dihydrochloride (AAPH) or Fe²⁺/H₂O₂: Insight into mechanisms of neuroprotection and relevance to oxidative stress-related neurodegenerative disorders\" [Neurochem. Int. 48, (2006), 318-327].","authors":"","doi":"10.1016/j.neuint.2026.106281","DOIUrl":"10.1016/j.neuint.2026.106281","url":null,"abstract":"","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":" ","pages":"106281"},"PeriodicalIF":5.5,"publicationDate":"2026-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149242435","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":"Disrupting PQBP1-eEF2 protein-protein interaction: From synaptic translation to immunity and cancer.","authors":"Emadeldin M Kamel, Sally Mostafa Khadrawy, Mohamed A M Ali, Noha A Ahmed, Nour Y S Yassin, Saleh Alkhedhairi, Faris F Aba Alkhayl, Al Mokhtar Lamsabhi","doi":"10.1016/j.neuint.2026.106154","DOIUrl":"10.1016/j.neuint.2026.106154","url":null,"abstract":"<p><p>Polyglutamine-binding protein 1 (PQBP1) has emerged as a multifaceted regulator of gene expression, acting not only in the nucleus to influence transcription and splicing but also in the cytoplasm to control protein synthesis. A recent discovery identified a direct interaction between PQBP1 and the translation elongation factor eEF2, unveiling a new checkpoint in the elongation phase of protein synthesis. PQBP1 binds preferentially to the non-phosphorylated form of eEF2 and protects it from phosphorylation at Thr56 by its kinase eEF2K. Through this mechanism, PQBP1 promotes continuous elongation under conditions where unchecked eEF2K activity would otherwise stall ribosomes. The PQBP1-eEF2 complex plays critical roles in maintaining global proteome homeostasis and enabling activity-dependent protein synthesis in neurons. Disruption of this protein-protein interaction (PPI), whether by genetic mutations in PQBP1 or by sequestration of PQBP1 in cellular aggregates, has been linked to pathological states ranging from intellectual disability and impaired synaptic plasticity to altered innate immune responses and possibly tumorigenesis. In this review, we summarize the current understanding of the PQBP1-eEF2 interaction, its structural basis and regulation, the physiological processes it governs, and the consequences of its disruption in disease. We also discuss therapeutic considerations - when stabilizing this interaction might be beneficial (e.g. to restore synaptic function in neurodegeneration) versus when inhibiting it could be advantageous (e.g. to dampen excessive translation in cancer). Finally, we highlight experimental strategies and open questions for future research on this newly recognized nexus of translation control.</p>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"196 ","pages":"106154"},"PeriodicalIF":5.5,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147643582","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":"Retinoic acid signaling regulates astrocyte reactivity by modulating MAPK/NF-κB pathways and mitochondrial integrity","authors":"Seo Hyun Yoo ,&nbsp;Dongyun Kim ,&nbsp;Gyu-Bum Yeon ,&nbsp;Jaeyeon Choi ,&nbsp;Jaewook Lee ,&nbsp;Dong-Wook Kim ,&nbsp;Hyunggee Kim ,&nbsp;Dae-Sung Kim","doi":"10.1016/j.neuint.2026.106134","DOIUrl":"10.1016/j.neuint.2026.106134","url":null,"abstract":"<div><div>Astrocytes respond to inflammatory stimuli by adopting a reactive state characterized by morphological, molecular, and functional changes that affect tissue repair and disease progression. A key feature of this transformation is the metabolic shift that supports inflammatory signaling and cytokine production. Retinoic acid (RA) modulates immune responses in the peripheral system; however, its role in astrocyte reactivity remains poorly understood. In this study, we investigated alterations in RA metabolism using an <em>in vitro</em> model of reactive astrocytes derived from human pluripotent stem cells. Reactivity was induced by treatment with tumor necrosis factor-α (TNF-α), interleukin-1α (IL-1α), and complement component 1q (C1q), collectively referred to as TIC, and characterized using comprehensive morphological, molecular and functional analyses. We found that the induced reactive astrocytes exhibited a marked downregulation of key biosynthetic enzymes in RA metabolism, leading to a net decrease in intracellular RA levels. Exogenous RA supplementation attenuated TIC-induced expression of pro- and anti-inflammatory mediators, including IL-6, IL-8, nitric oxide, IL-10, and TGFβ. Mechanistically, RA suppressed these inflammatory responses by inhibiting NF-κB activation, likely through upstream attenuation of ERK and p38 MAPK pathways via upregulation of MAPK phosphatase 1 (MKP-1). In neuron and TIC-treated astrocyte co-cultures, RA treatment reduced the density of cleaved caspase 3-positive apoptotic-like neurons, an effect accompanied by decreased nitric oxide levels. These observations coincided with the restoration of mitochondrial integrity and mitophagy. Taken together, these findings identify RA metabolism as a key regulatory node in astrocyte reactivity and suggest a potential therapeutic role for RA in neuroinflammatory conditions.</div></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"194 ","pages":"Article 106134"},"PeriodicalIF":4.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147269413","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":"Calcineurin inhibition mitigates activation of enteric glia in vitro and affects their crosstalk with macrophages","authors":"Aurora Patti ,&nbsp;Cristiana Lucia Rita Lipari ,&nbsp;Armando Genazzani ,&nbsp;Maria Angela Sortino ,&nbsp;Sara Merlo","doi":"10.1016/j.neuint.2026.106123","DOIUrl":"10.1016/j.neuint.2026.106123","url":null,"abstract":"<div><div>Multiple factors contribute to the physiopathology of inflammatory bowel diseases (IBD) and the enteric nervous system is emerging as a key player in this context. In particular, enteric glial cells (EGCs) share very similar properties with central astrocytes, play a homeostatic function under basal conditions, but can be activated by inflammatory stimuli further contributing to mucosal damage. Calcineurin (CN) is an important mediator of astrocyte inflammation and has been described also in EGCs. The aim of this study was to establish an <em>in vitro</em> model of EGCs challenged with an inflammatory insult to better delineate the role of CN in their inflammatory reaction and interaction with immune cells. EGCs stimulated with LPS + ATP (5 μg/mL-2 mM) for 24 h showed typical inflammatory features with increased expression of the astrocyte marker GFAP, the inflammasome component NLRP3 and the alarmin HMGB1. Inhibition of CN by cyclosporin A (CsA, 1 μM) counteracted these effects and increased the expression of nuclear HMGB1. Nuclear translocation of NF-κB p65 induced by LPS + ATP was also blunted by CsA pre-treatment. The migration of RAW 264.7 macrophages co-cultured with LPS + ATP-stimulated EGCs was enhanced, an effect prevented by CsA. This was accompanied by activation of macrophages to a pro-inflammatory phenotype, as shown by increased COX-2, IL-1β and TNF-α gene expression. Inhibition of CN in EGCs reduced this response while increasing the phagocytic capacity of macrophages. Altogether the results here reported identify a central role for CN in the inflammatory response of EGCs and their crosstalk with cells of the immune system, supporting potential new sites of intervention for drugs targeting CN.</div></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"194 ","pages":"Article 106123"},"PeriodicalIF":4.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146123164","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":"Activation of 5-HT1A receptors in the ventrolateral orbital cortex alleviates neuropathic pain-induced depressive-like behaviors via GABAergic neurons in male rats","authors":"Yu-long Zhao ,&nbsp;Hui-yuan Yi ,&nbsp;Xue-mei Hou ,&nbsp;Xiao-chen La ,&nbsp;Sani Sa'idu Baba ,&nbsp;Yi-xiao Guo ,&nbsp;Rong-rong Yao ,&nbsp;Xiao-cui Yuan ,&nbsp;Qi-rui Zhang ,&nbsp;Hong Jia ,&nbsp;Yu-ying Wang ,&nbsp;Fu-quan Huo","doi":"10.1016/j.neuint.2026.106133","DOIUrl":"10.1016/j.neuint.2026.106133","url":null,"abstract":"<div><div>Neuropathic pain is frequently comorbid with depression, which exacerbates patient suffering and complicates clinical management. Although the ventrolateral orbital cortex (VLO) is involved in pain processing and emotional regulation, its specific role in neuropathic pain-induced depression remains unclear. Emerging evidence implicates 5-HT_1A receptors in modulating both pain and mood disorders via GABAergic transmission, yet their specific contributions in the VLO are not fully understood. Here, we aimed to investigate whether and how VLO 5-HT_1A receptors mediate depressive-like behaviors associated with neuropathic pain in male rats. Using a spared nerve injury (SNI) model, combined with neuropharmacological, chemogenetic, and cell-type-specific adeno-associated virus (AAV) approaches, we found that activating VLO 5-HT_1A receptor produced dose-dependent antidepressant effects, which were blocked by a selective antagonist. Mechanistically, 5-HT_1A receptor-mediated antidepressant effects were enhanced by a GABA_A receptor antagonist and suppressed by a GABA_A receptor agonist. Chemogenetic activation of VLO GABAergic neurons abolished the antidepressant effects of 5-HT_1A receptor stimulation. Furthermore, SNI-induced depressive-like behaviors correlated with reduced 5-HT_1A receptor expression in the VLO. AAV-mediated 5-HT_1A receptor overexpression specifically on GABAergic neurons alleviated depressive-like behaviors in SNI rats, while knockdown induced depressive-like phenotypes in wild-type rats. In conclusion, our findings demonstrate that 5-HT_1A receptors in the VLO alleviate neuropathic pain-induced depressive-like behaviors through a GABAergic disinhibition mechanism. This study highlights 5-HT_1A receptors in the VLO as promising therapeutic targets for mood disturbances associated with neuropathic pain, offering a cortical framework for comorbid pain-depression pathophysiology.</div></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"194 ","pages":"Article 106133"},"PeriodicalIF":4.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146256939","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}