Neurotherapeutics最新文献

{"title":"Shared and unique therapeutic targets of KarXT and clozapine for schizophrenia treatment revealed by network pharmacology and molecular docking analyses: Implications for differential clinical responses.","authors":"Chuanjun Zhuo, Chao Li, Hongjun Tian, Lina Wang, Xiaoyan Ma, Ranli Li, Ximing Chen, Yachen Li, Qiuyu Zhang, Lei Yang","doi":"10.1016/j.neurot.2025.e00714","DOIUrl":"https://doi.org/10.1016/j.neurot.2025.e00714","url":null,"abstract":"<p><p>Xanomeline plus trospium (KarXT) is a combination drug targeting muscarinic receptors with demonstrated efficacy against positive, negative, and cognitive symptoms of schizophrenia, although therapeutic effects on positive and negative symptoms do not differ significantly from risperidone and olanzapine. Clozapine remains the most effective treatment for schizophrenia unresponsive to other antipsychotics and demonstrates superior efficacy for positive and negative symptoms compared to risperidone and olanzapine. However, the common and distinct molecular targets underlying these different clinical responses to KarXT and clozapine are not fully understood. Potential xanomeline and clozapine targets were identified by searching PharmMapper, SwissTargetPrediction, GeneCards, and SuperPred, and schizophrenia-related targets by searching GeneCards, OMIM, and TTD. Protein-protein interaction (PPI) networks were constructed to identify hub targets, and GO and KEGG pathway enrichment analyses were conducted for the top 25 targets using DAVID. Cytoscape was used to build a network linking drugs, pathways, targets, and disease. Molecular docking simulations were conducted to assess drug binding affinities to core targets. Combined database searches identified 103 overlapping targets for xanomeline and schizophrenia, and 285 overlapping targets for clozapine and schizophrenia. PPI network and KEGG pathway analyses identified FOS, CASP3, NFKB1, AKT1, IGF1, KDR, and CDC42, proteins related to apoptosis, inflammation, neuroprotection, and MAPK signaling, as core xanomeline targets, and FOS, CASP3, NFKB1, TNF, IL6, IFNG, and CXCL8, proteins involved in apoptosis, inflammation, immune responses, and IL-17 signaling, as core clozapine targets. Molecular docking confirmed strong binding between drugs and core targets. KarXT and clozapine share core targets FOS, CASP3, and NFKB1. Distinct KarXT targets such as AKT1, IGF1, KDR, and CDC42, and clozapine targets including TNF, IL6, IFNG, and CXCL8 may explain differences in therapeutic efficacy. These bioinformatics findings support recent meta-analyses and provide guidance for more appropriate drug selection.</p>","PeriodicalId":19159,"journal":{"name":"Neurotherapeutics","volume":" ","pages":"e00714"},"PeriodicalIF":6.9,"publicationDate":"2025-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144799742","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reticuline modulates astrocyte and microglial responses to enhance prognosis after traumatic brain injury.","authors":"Shuhui Xu, Jue Zhu, Jiajia Wen, Chenxing Wang, Xuanfeng Chen, Weiquan Liao, Zhichao Lu, Ziheng Wang, Peipei Gong","doi":"10.1016/j.neurot.2025.e00709","DOIUrl":"https://doi.org/10.1016/j.neurot.2025.e00709","url":null,"abstract":"<p><p>Traumatic brain injury (TBI) poses a serious threat to public health due to its high disability and mortality rates. Therefore, it is crucial to explore effective therapeutic strategies. Studies have shown that reticuline may exert a cardioprotective effect by blocking the JAK-STAT signaling pathway, but its effect in TBI has not been explored. Therefore, this study aimed to evaluate the potential clinical value of reticuline after TBI and its impact on the inflammatory quiescent state. This study assessed the therapeutic effect of reticuline administered intraperitoneally using the controlled cortical impact (CCI) model in adult rats. In addition, to clarify the mechanism of action of reticuline, we used Colivelin, a STAT3 agonist, to restore the function of related signal pathways and explore its intervention effect. The study showed that reticuline inhibited neuroinflammation and promoted neurological function recovery after TBI by regulating the JAK-STAT signaling pathway, reducing the toxic response of astrocytes and microglia while retaining its neuroprotective effect. In summary, this study reveals that reticuline may promote neural repair after TBI through a JAK-STAT-dependent anti-inflammatory effect. Our findings further expand its potential application value in brain injury treatment and provide new ideas for intervention strategies for TBI.</p>","PeriodicalId":19159,"journal":{"name":"Neurotherapeutics","volume":" ","pages":"e00709"},"PeriodicalIF":6.9,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144794963","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aberrant S-nitrosylation in the TCA cycle contributes to mitochondrial dysfunction, energy compromise, and synapse loss in neurodegenerative diseases.","authors":"Tomohiro Nakamura, Anamika Sharma, Stuart A Lipton","doi":"10.1016/j.neurot.2025.e00708","DOIUrl":"10.1016/j.neurot.2025.e00708","url":null,"abstract":"<p><p>Neuronal synaptic activity relies heavily on mitochondrial energy production, as synaptic transmission requires substantial ATP. Accordingly, mitochondrial dysfunction represents a key underlying factor in synaptic loss that strongly correlates with cognitive decline in Alzheimer's disease and other neurocognitive disorders. Increasing evidence suggests that elevated nitro-oxidative stress impairs mitochondrial bioenergetic function, leading to synaptic degeneration. In this review, we highlight the pathophysiological roles of nitric oxide (NO)-dependent posttranslational modifications (PTMs), particularly S-nitrosylation of cysteine residues, and their impact on mitochondrial metabolism. We focus on the pathological S-nitrosylation of tricarboxylic acid cycle enzymes, particularly α-ketoglutarate dehydrogenase, as well as electron transport chain proteins. This aberrant PTM disrupts mitochondrial energy production. Additionally, we discuss the consequences of aberrant protein S-nitrosylation on mitochondrial dynamics and mitophagy, further contributing to mitochondrial dysfunction and synapse loss. Finally, we examine current strategies to ameliorate S-nitrosylation-mediated mitochondrial dysfunction in preclinical models of neurodegenerative diseases and explore future directions for developing neurotherapeutics aimed at restoring mitochondrial metabolism in the context of nitro-oxidative stress.</p>","PeriodicalId":19159,"journal":{"name":"Neurotherapeutics","volume":" ","pages":"e00708"},"PeriodicalIF":6.9,"publicationDate":"2025-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144743323","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of gasotransmitters in Parkinson's disease: Interplay of nitric oxide, carbon monoxide, and hydrogen sulfide.","authors":"Jennifer L O'Connor, Dionisia M Fountos, Bita Firouzan, Fateme Azizi, Rasoul Ghasemi, Khosrow Kashfi","doi":"10.1016/j.neurot.2025.e00710","DOIUrl":"https://doi.org/10.1016/j.neurot.2025.e00710","url":null,"abstract":"<p><p>Parkinson's disease (PD) is a progressive neurodegenerative condition marked by dopaminergic neuron loss and α-synuclein accumulation. In recent years, a growing body of work has explored the roles of endogenous gasotransmitters-namely nitric oxide (NO), carbon monoxide (CO), and hydrogen sulfide (H₂S)-in pathways relevant to PD pathology. Though traditionally viewed as toxic, these molecules may, under regulated conditions, influence oxidative stress, neuroinflammation, and mitochondrial function in ways that could be therapeutically significant. NO illustrates this complexity. At physiological concentrations, it supports synaptic function and cerebral blood flow. Yet, when overproduced, it promotes oxidative damage and disrupts mitochondrial processes. Therapeutic strategies include NOS enzyme inhibition and controlled-release NO donors. Nanoparticle-based delivery systems have also been proposed to fine-tune local NO availability, though their clinical relevance remains to be fully validated. CO, produced via heme oxygenase-1 (HO-1), has shown cytoprotective and anti-inflammatory effects. While promising in modulating redox signaling and apoptosis, any therapeutic use of CO requires careful dose regulation to avoid toxicity. H₂S, whose levels appear diminished in PD models, has demonstrated antioxidant, anti-inflammatory, and mitochondrial-supportive effects in preclinical studies. As with NO and CO, maintaining balanced levels of H₂S is critical-both too little and too much can cause harm, making precise delivery essential. This review examines the involvement of NO, CO, and H₂S in PD-related stress responses, emphasizing how their effects vary across experimental models and remain only partially understood.</p>","PeriodicalId":19159,"journal":{"name":"Neurotherapeutics","volume":" ","pages":"e00710"},"PeriodicalIF":5.6,"publicationDate":"2025-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144718155","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Redox modulation of the complement cascade contributes to synapse loss in Alzheimer's disease.","authors":"Chang-Ki Oh, Yubo Wang, Stuart A Lipton","doi":"10.1016/j.neurot.2025.e00707","DOIUrl":"10.1016/j.neurot.2025.e00707","url":null,"abstract":"<p><p>Neuroinflammation is characterized by activation of the immune response in the central nervous system (CNS). In Alzheimer's disease (AD), this involves stimulation of glial cells, including microglia and astrocytes, that surround senile plaques and affected neurons. The complement system is a crucial component of the innate immune system, responsible for rapidly eliminating pathogens and dead or dying cells, while also influencing the magnitude and duration of the inflammatory immune response. Moreover, the complement system plays both neuroprotective and neurodestructive roles. In AD, dysregulation of the complement system contributes to excessive microglial phagocytosis of synapses, with such synaptic loss representing the major correlate to cognitive decline in the course of the disease. However, the detailed mechanism for complement activation in AD had remained poorly understood until the discovery that complement factors were aberrantly S-nitrosylated, representing a redox-mediated posttranslational modification that controls the complement cascade. Nitrosative stress, caused by excessive generation of reactive nitrogen species (RNS), including nitric oxide (NO)-related species, had been recognized as a critical factor in the pathogenesis and progression of AD. Recent publications highlighted in this review support the notion that the NO-related species support aberrant S-nitrosylation of complement proteins, leading to pathological activation of the complement system, thus contributing to synaptic loss in AD.</p>","PeriodicalId":19159,"journal":{"name":"Neurotherapeutics","volume":" ","pages":"e00707"},"PeriodicalIF":6.9,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144718230","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting macro- and micro-nutrient regulation of H₂S signaling for the aging brain.","authors":"Matthew Godwin, Christopher Hine","doi":"10.1016/j.neurot.2025.e00638","DOIUrl":"https://doi.org/10.1016/j.neurot.2025.e00638","url":null,"abstract":"<p><p>Global growth in aged population demographics is a testament to medical and societal innovations over the past 100 years. However, with advanced age comes declines in various organs and tissues, thus limiting quality of life in one's later years. There are numerous hypotheses for what the driving and causative factors are for biological aging, with each proposing molecular targets and their therapeutic strategies. One such hypothesis is that dysfunctions in cellular and systemic redox homeostasis are to blame, in that aging-related increases in oxidative stress and diminished thiol-mediated protections and signaling activity drive macromolecular damage leading to tissue failure, particularly in the brain. Addressing redox dysfunction has been somewhat a challenge clinically, as antioxidant supplementation has not shown to be universally effective at slowing the aging process. Thus, geroscience interventions that can bolster our endogenous redox machinery may be more effective. In this review, we highlight hydrogen sulfide (H₂S) and its associated metabolism and gasotransmitter signaling as potent redox mechanisms that can be leveraged via macro- and/or micro-nutrient interventions. Specifically, dietary restriction (DR) and iron status greatly impact the enzymatic and non-enzymatic production, metabolism, and thiol modifications of H₂S. As both DR and iron status can have profound impacts on redox homeostasis and aging in the brain, we discuss how all these factors are intertwined in glioblastoma (GBM) and neurodegeneration, two of the most significant aging-related disorders of the brain that limit both lifespan and healthspan.</p>","PeriodicalId":19159,"journal":{"name":"Neurotherapeutics","volume":" ","pages":"e00638"},"PeriodicalIF":5.6,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144659690","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Yin-Yang of sulfur dioxide: Effect on cognitive function.","authors":"Prakashkumar Dobariya, Joshua Smith, Swati S More","doi":"10.1016/j.neurot.2025.e00633","DOIUrl":"10.1016/j.neurot.2025.e00633","url":null,"abstract":"<p><p>Gaseous neurotransmitters drive numerous physiological processes, rendering important their study in pathophysiology. One such gasotransmitter, sulfur dioxide (SO₂), is abundantly produced by the cardiovascular system. SO₂ influences hemodynamics and vascular structure, protects from myocardial ischemia and reperfusion, myocardial injury, respiratory complications, and atherosclerosis. This being said, it is an air pollutant with central effects. Current effort is directed largely at elucidating the pathophysiological role of SO₂ in neurological conditions such as effects on aging, ischemic stroke, seizure, neurodegeneration, and memory loss. Newer studies examine its neuroprotective effect and the advantages of correcting SO₂ imbalance during oxidative stress and inflammation, in turn positively affecting cognition. A deep understanding of the molecular players in the pathophysiologic balance of SO₂, or lack thereof, may open therapeutic avenues into disorders of cognition and aging that stem from redox imbalance. This account portrays extant understanding of the role of SO₂ in neurocognition and the underlying molecular mechanisms.</p>","PeriodicalId":19159,"journal":{"name":"Neurotherapeutics","volume":" ","pages":"e00633"},"PeriodicalIF":6.9,"publicationDate":"2025-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144564944","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Indole-3-propionic acid promotes Schwann cell proliferation following peripheral nerve injury by activating the PI3K/AKT pathway","authors":"Huimei Zhang ,&nbsp;Sijia Wang ,&nbsp;Qi Zhang ,&nbsp;Xinyu Du ,&nbsp;Danyang Xu ,&nbsp;Jinkun Wen ,&nbsp;Mingrui Jin ,&nbsp;Jing Liu ,&nbsp;Xiaobao Jin ,&nbsp;Mengxia Wang ,&nbsp;Li Luo ,&nbsp;Lixia Li","doi":"10.1016/j.neurot.2025.e00578","DOIUrl":"10.1016/j.neurot.2025.e00578","url":null,"abstract":"<div><div>The proliferation of Schwann cells (SCs) is integral for axonal regeneration following peripheral nerve injury, and enhancing their proliferation can accelerate axonal regeneration. Indole-3-propionic acid (IPA), a metabolite of tryptophan synthesized by the intestinal microbiota, has potential in accelerating axonal regeneration in peripheral nerves. Nonetheless, the capacity of IPA to promote SC proliferation remains undetermined. Consequently, this study aimed to investigate the effects of IPA on SC proliferation and the underlying mechanisms. Therefore, we cultured RSC96 ​cells in vitro and used a Cell Counting Kit-8 (CCK8), an EdU Cell Proliferation Detection Kit (EdU), and a Cell Cycle and Apoptosis Assay Kit for the analyses. Additionally, we established a rat sciatic nerve crush injury model in vivo and performed immunofluorescence staining. These findings indicated that IPA enhanced SC proliferation. We further investigated the potential mechanism by which IPA promotes SC proliferation by conducting Western blotting and observed that IPA increased the levels of phosphorylated phosphatidylinositol 3-kinase/phosphatidylinositol 3-kinase (p-PI3K/PI3K) and phosphorylated protein kinase B/protein kinase B (p-AKT/AKT) in RSC96 ​cells, which suggested that IPA may promote the proliferation of RSC96 ​cells by activating the PI3K/AKT pathway. We cultured RSC96 ​cells in vitro, established a sciatic nerve crush model in vivo, and administered a PI3K inhibitor (LY294002) in combination with IPA treatment to validate this hypothesis. Our results revealed a reduction in the proliferation rate of RSC96 ​cells or SCs following the inhibition of p-PI3K/PI3K and p-AKT/AKT expression, as evidenced by the results of the EdU, CCK8 and immunofluorescence staining assays. These findings indicated that IPA may indeed promote SC proliferation through the activation of the PI3K/AKT pathway.</div></div>","PeriodicalId":19159,"journal":{"name":"Neurotherapeutics","volume":"22 4","pages":"Article e00578"},"PeriodicalIF":6.9,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143730940","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Maternal oxytocin administration mitigates nociceptive, social, and epigenetic impairments in adolescent offspring exposed to perinatal trauma","authors":"Sydney Harris ,&nbsp;Zoe Kodila ,&nbsp;Sabrina Salberg ,&nbsp;Marissa Sgro ,&nbsp;Elaina Vlassopoulos ,&nbsp;Crystal N. Li ,&nbsp;Madeleine J. Smith ,&nbsp;Sandy R. Shultz ,&nbsp;Glenn R. Yamakawa ,&nbsp;Melanie Noel ,&nbsp;Richelle Mychasiuk","doi":"10.1016/j.neurot.2025.e00598","DOIUrl":"10.1016/j.neurot.2025.e00598","url":null,"abstract":"<div><div>Adverse childhood experiences (ACEs) alter brain development, leading to vulnerability for chronic pain, mental health disorders, and suicidality. These effects often emerge during adolescence. Importantly, ACEs can occur prenatally, including when exposed to <em>in utero</em> intimate partner violence (IPV) or postnatally as maternal neglect. Maternal social support has demonstrated promise in the mitigation of ACE-related deficits. Oxytocin, which has a role in social-bonding and stress regulation, serves as a suitable surrogate for social support in preclinical studies. Therefore, we aimed to explore the effects of oxytocin on alleviating social deficits, nociception, and epigenetic changes resulting from models that aimed to mimic the stress normally induced following exposure to two ACEs: IPV <em>in utero</em> and maternal neglect. During pregnancy, dams were randomly assigned to experience the model of IPV or a sham insult. Following birth, offspring from the IPV group underwent 10 days of maternal separation. Dams received three days of oxytocin therapy while nursing. In adolescence, half of the offspring underwent a plantar surgery to induce pain. Overall, in adolescence, rats exposed to the ACEs exhibited increased nociceptive sensitivity and aberrant social interactions, particularly among males, further suggesting that ACEs can increase an individual's risk for chronic pain. The ACEs changed gene expression related to social behaviour and neuroplasticity. Maternal oxytocin normalized pain, social, and gene changes, while oxytocin levels in offspring correlated with nociceptive sensitivity. Although ACEs have enduring consequences, the outcomes are modifiable, and oxytocin may be a robust and implementable therapeutic capable of attenuating early adversity.</div></div>","PeriodicalId":19159,"journal":{"name":"Neurotherapeutics","volume":"22 4","pages":"Article e00598"},"PeriodicalIF":6.9,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144021647","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of Age on Switching or Stopping Disease Modifying Therapies in Multiple Sclerosis","authors":"Areeba Siddiqui ,&nbsp;Le H. Hua","doi":"10.1016/j.neurot.2025.e00603","DOIUrl":"10.1016/j.neurot.2025.e00603","url":null,"abstract":"<div><div>Older patients age ≥55 account for almost half of the total MS population. While focal inflammatory demyelinating processes and progressive processes such as compartmentalized CNS inflammation, neurodegeneration, and failure of compensatory mechanisms co-occur from disease onset, there is a shift in the predominant disease processes with notable clinical progression occurring in the fifth decade of life. Clinically, this manifests in reduction in clinical relapses and MRI activity as persons with MS age, with an increase in slow disability progression independent of relapses. As disease modifying therapies have demonstrated efficacy on relapse reduction, but not centrally mediated progressive processes, the benefit of DMT wanes with age due to change in underlying biological disease processes. Contrastingly, risks of DMTs increase due to biological changes related with age, setting up a scenario where considerations on switching or stopping DMT become more clinically important based on risk-benefit ratios. This review will cover evidence regarding DMT use in older patients with MS and discuss age considerations in the management of patients with MS.</div></div>","PeriodicalId":19159,"journal":{"name":"Neurotherapeutics","volume":"22 4","pages":"Article e00603"},"PeriodicalIF":6.9,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144020128","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}