Current Neuropharmacology最新文献

{"title":"Venlafaxine and Delirium: Understanding the Association.","authors":"Francisco Epelde","doi":"10.2174/011570159X378277250702051515","DOIUrl":"https://doi.org/10.2174/011570159X378277250702051515","url":null,"abstract":"<p><p>Delirium represents a significant clinical, economic, and societal challenge, frequently arising in hospitalized patients due to multiple factors, including pharmacological triggers. Recognizing and preventing delirium is crucial to improving patient outcomes and reducing healthcare costs. This review focuses on the association between venlafaxine, a commonly used antidepressant, and delirium. We explore potential mechanisms, clinical presentations, and risk factors linked to venlafaxine-induced delirium, emphasizing the need for heightened awareness among clinicians. The findings underscore the importance of vigilance during drug initiation, dosage adjustment, or withdrawal to mitigate the risk of this neuropsychiatric condition.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144648724","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":"Neural Networks of Knowledge: Ontologies Pioneering Precision Medicine In Neurodegenerative Diseases.","authors":"Pooja Mittal, Rupesh Kumar Gautam, Himanshu Sharma, Rajat Goyal, Garima Malik, Ramit Kapoor, Dileep Kumar Sharma, Mohammad Amjad Kamal, Haque Shafiul, Siva Gajula Nageswara Rao","doi":"10.2174/011570159X353727250314065140","DOIUrl":"https://doi.org/10.2174/011570159X353727250314065140","url":null,"abstract":"<p><p>The review focuses on the ways that ontologies are revolutionising precision medicine in their effort to understand neurodegenerative illnesses. Ontologies, which are structured frameworks that outline the relationships between concepts in a certain field, offer a crucial foundation for combining different biological data. Novel insights into the construction of a precision medicine approach to treat neurodegenerative diseases (NDDs) are given by growing advancements in the area of pharmacogenomics. Affected parts of the central nervous system may develop neurological disorders, including Alzheimer's, Parkinson's, autism spectrum, and attention-deficit/hyperactivity disorder. These models allow for standard and helpful data marking, which is needed for crossdisciplinary study and teamwork. With case studies, you can see how ontologies have been used to find biomarkers, understand how sicknesses work, and make models for predicting how drugs will work and how the disease will get worse. For example, problems with data quality, meaning variety, and the need for constant changes to reflect the growing body of scientific knowledge are discussed in this review. It also looks at how semantic data can be mixed with cutting-edge computer methods such as artificial intelligence and machine learning to make brain disease diagnostic and prediction models more exact and accurate. These collaborative networks aim to identify patients at risk, identify patients in the preclinical or early stages of illness, and develop tailored preventative interventions to enhance patient quality of life and prognosis. They also seek to identify new, robust, and effective methods for these patient identification tasks. To this end, the current study has been considered to examine the essential components that may be part of precise and tailored therapy plans used for neurodegenerative illnesses.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144636479","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":"Therapeutic Approaches Interfering with Nuclear Localization Signals: An Emerging Strategy for CNS-Related Diseases.","authors":"Margrate Anyanwu, Matteo Giannangeli, Alessandra Gianoncelli, Giovanni Ribaudo","doi":"10.2174/011570159X384321250627071259","DOIUrl":"https://doi.org/10.2174/011570159X384321250627071259","url":null,"abstract":"<p><p>Although medicinal chemistry is constantly looking for new therapeutic approaches against pathological conditions affecting the central nervous system (CNS), such as neurodegeneration and cancer, this quest has not been fully successful yet. The lack of understanding of all the complex mechanisms underlying these conditions makes the identification of new effective drugs challenging. A wide variety of pathophysiological events are regulated at both nuclear and cytoplasmic levels, and in this context, targeting the shuttle system composed of the karyopherin superfamily and their cargoes may provide an alternative strategy. Molecular recognition is highly specific and strictly related to the presence of special \"tag\" regions, known as nuclear localization signals, that are localized in the amino acid sequences of cargoes. Importantly, their trafficking is involved in various pathophysiological processes, including CNS diseases. Curiously, although this system has been studied intensively, much remains to be discovered to date. Throughout the years, drug discovery allowed the identification of small molecules and peptides able to target karyopherin-cargo complexes to provide new potential pharmacological treatments. Indeed, the first examples of drug candidates targeting this mechanism that reached clinical trials are appearing in the literature. With this mini-review, this study aims at presenting an updated overview on the most recent reports investigating the use of the karyopherin shuttle system as a new therapeutic target especially for CNS-related diseases.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144636495","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 the cGAS-STING Pathway: Modulating Inflammation, Oxidative Stress, and Autophagy for Novel Depression Therapies.","authors":"Wen Ma, Shanshan Chu, Yumei Ma, Sutian Wang, Xuehai Ma","doi":"10.2174/011570159X386374250623095520","DOIUrl":"https://doi.org/10.2174/011570159X386374250623095520","url":null,"abstract":"<p><p>The pathological mechanisms underlying depression, a prevalent mental disorder, remain only partially elucidated despite extensive research efforts. Recent advancements have underscored the pivotal roles of multiple biological processes in the onset and progression of depression, including inflammation, oxidative stress, and autophagy. Inflammation is associated with the disruption of neurotransmitter systems and neural plasticity, whereas oxidative stress contributes to neuronal damage and impaired brain function. Moreover, moderate autophagy is essential for maintaining neuronal health. Dysregulation of autophagy may lead to the accumulation of damaged proteins and organelles, which can exacerbate depressive symptoms. Among the various molecular pathways involved, the cGAS-STING signalling pathway has emerged as a key regulator of these processes. Traditionally known for its role in detecting cytosolic DNA and initiating innate immune defences against pathogens, the cGAS-STING pathway has recently been implicated in regulating inflammatory responses, oxidative stress levels, and autophagy in the central nervous system. This dual function positions the cGAS-STING pathway as a potential link between immune dysregulation and the neurobiological foundations of depression. This paper offers a systematic overview of existing studies on the role of the cGAS-STING pathway in inflammation, oxidative stress, and autophagy within the central nervous system, particularly in the context of depression. The review reveals how modulation of the cGAS-STING pathway may influence these critical biological processes and thereby ameliorate depressive symptoms. Furthermore, the review discusses the therapeutic potential of targeting the cGAS-STING pathway and offers promising research directions. Ultimately, this paper aims to provide novel insights and approaches for developing more effective treatments for depression.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144636480","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":"Emerging Therapeutic Targets for Spontaneous Intracerebral Hemorrhage.","authors":"Alessandro Pezzini","doi":"10.2174/011570159X390388250708063345","DOIUrl":"https://doi.org/10.2174/011570159X390388250708063345","url":null,"abstract":"","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144636478","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":"Assessment Value of Electromyography for Bortezomib-Related Peripheral Neuropathy.","authors":"Yijun Shen, Zhen Zhang, Yuchen Liu, Siyuan Song, Tian Li, Jihong Dong, Guanru Niu","doi":"10.2174/011570159X376896250624070328","DOIUrl":"https://doi.org/10.2174/011570159X376896250624070328","url":null,"abstract":"<p><strong>Introduction: </strong>This study investigates the relationship between National Cancer Institute Common Terminology Criteria (NCI-CTC) for grading bortezomib-induced peripheral neuropathy (BIPN) and objective motor/sensory nerve dysfunctions assessed by nerve conduction studies (NCS). It also evaluates the correlation between specific nerve conduction abnormalities and progression- free survival (PFS).</p><p><strong>Methods: </strong>Thirty-three patients with multiple myeloma developing peripheral neuropathy during bortezomib treatment were enrolled. Participants were grouped based on NCI-CTC toxicity scores (< 2, n=17; ≥ 2, n=16). Comprehensive NCS were performed, assessing compound muscle action potentials (CMAP), motor conduction velocities (MCV), sensory nerve action potentials (SNAP), and sensory conduction velocities (SCV) across ulnar, median, tibial, peroneal, sural, and superficial peroneal nerves. Correlation analyses were used to examine the association between NCS parameters and PFS.</p><p><strong>Results: </strong>Patients with higher NCI-CTC grades (≥ 2) exhibited significant reductions in motor and sensory nerve conduction parameters. Notably, the peroneal nerve showed significant decreases in CMAP (p=0.0059) and MCV (p=0.0223). The superficial peroneal nerve displayed a significant reduction in SCV (p=0.0189). A strong positive correlation was found between median nerve SNAP and longer PFS (r=0.558, p=0.001).</p><p><strong>Discussion: </strong>The findings indicate that higher clinical grades of BIPN (NCI-CTC ≥ 2) are associated with objective neurophysiological evidence of worsened nerve function, with the peroneal nerve being particularly affected. The correlation between median nerve SNAP and PFS suggests that NCS parameters could potentially serve as prognostic markers in patients with BIPN.</p><p><strong>Conclusion: </strong>Bortezomib-induced neurotoxicity leads to significant impairments in both motor and sensory nerve conduction. Median nerve SNAP shows promise as a predictor for PFS, underscoring the potential value of NCS in monitoring neurotoxicity and guiding clinical management in patients receiving bortezomib.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144607758","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":"Diabetes, Alzheimer's Disease Risk Factors, and the Cafeteria Diet: A Comprehensive Review.","authors":"Md Abubakar, Aditi Giri, Falguni Goel, Manshad Khan, Janmejay Gupta, Daksh Kumar, Monika Kaushik, Sachchida Nand Rai, Nitesh Kumar","doi":"10.2174/011570159X384737250626094315","DOIUrl":"https://doi.org/10.2174/011570159X384737250626094315","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is a progressive neurodegenerative disorder with multifaceted risk factors, including diet and metabolic dysfunction. The rising prevalence of AD and diabetes has drawn attention to their shared pathophysiological mechanisms. The \"cafeteria diet,\" characterized by high-fat, high-sugar, and energy-dense foods, has emerged as a significant contributor to metabolic dysfunctions, including obesity and insulin resistance, which are risk factors for both diabetes and neurodegenerative diseases. This study explores the effects of the cafeteria diet on cognitive impairment, AD pathology, and its potential role in exacerbating diabetes-related neurological complications. Animal models were subjected to cafeteria diets, mimicking human dietary patterns, to investigate changes in brain structure, amyloid-beta accumulation, tau hyperphosphorylation, and cognitive function. Additionally, metabolic profiling demonstrated the development of insulin resistance and other hallmarks of diabetes, which were closely correlated with the severity of cognitive deficits. Neuropathological analyses revealed exacerbated amyloid-beta accumulation and increased neuroinflammation, linking dietary-induced diabetes to AD pathophysiology. These findings underscore the critical role of dietary habits in modulating the risk and progression of AD, highlighting the importance of interventions targeting metabolic health to mitigate cognitive decline. This study emphasizes the need for further research to unravel the molecular mechanisms underlying the diet-diabetes- AD axis and develop targeted therapeutic strategies.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144599689","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":"Experimental Evaluation of QY-69: A Butyrylcholinesterase Inhibitor with Anti-Glioblastoma Efficacy.","authors":"Kaixuan Wang, Ziyao Lu, Yuetong Duan, Siyu He, Weiping Lyu, Qinghong Liao, Qi Li, Xuehong Chen, Huanting Li","doi":"10.2174/011570159X394797250701074055","DOIUrl":"https://doi.org/10.2174/011570159X394797250701074055","url":null,"abstract":"<p><strong>Introduction: </strong>Glioblastoma multiforme (GBM) is the most aggressive malignant primary brain tumor, characterized by poor prognosis. Moreover, cognitive impairment from the tumor and its treatments compromises patients' quality of life. Butyrylcholinesterase (BChE) inhibition enhances cognitive function. Notably, BCHE is overexpressed in GBM tissues; its downregulation suppresses tumor cell proliferation, migration, and invasion. This study aimed to identify a BChE inhibitor with dual functionality: anti-GBM efficacy and cognitive protection via modulation of neuro-inflammation.</p><p><strong>Methods: </strong>QY-69 was identified from an in-house BChE inhibitor library through cytotoxicity-based screening. Its anti-GBM effects were evaluated through colony formation, wound healing, and transwell assays. Orthotopic GBM mice were treated with QY-69 orally for 15 days. Tumor progression, cognitive function (Morris water maze), and neuroinflammation (microglia and astrocyte immunofluorescence) were analyzed.</p><p><strong>Results: </strong>QY-69 exhibited significant antiproliferative activity at micromolar concentrations. In vitro assays demonstrated significant inhibition of GBM cell growth, migration, and invasion. Behavioral impairment in mice was improved, and the activation of astrocytes and microglia in peritumoral tissues was reduced, indicating a decrease in neuroinflammation.</p><p><strong>Discussion: </strong>QY-69 demonstrated dual therapeutic potential in GBM by inhibiting tumor progression and alleviating cognitive impairment. However, its precise molecular mechanisms remain to be elucidated. Future research should employ transcriptomic and proteomic approaches to elucidate the molecular basis of its anti-GBM activity.</p><p><strong>Conclusion: </strong>QY-69, a BChE inhibitor, exhibits potent anti-GBM activity and confers cognitive protection, positioning it as a promising dual-action therapeutic candidate. By inhibiting tumor progression and reducing neuro-inflammation, it may enhance both survival and quality of life in GBM patients.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144583334","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":"Peroxiredoxin 6 Alone or in Combination with Fingolimod Ameliorates EAE.","authors":"Lunin S M, Novoselova E G, Glushkova O V, Parfenyuk S B, Kuzekova A A, Novoselova T V, Sharapov M G, Mubarakshina E K, Goncharov R G, Khrenov M O","doi":"10.2174/011570159X372166250619064636","DOIUrl":"https://doi.org/10.2174/011570159X372166250619064636","url":null,"abstract":"<p><strong>Introduction: </strong>Multiple Sclerosis (MS) is characterized by the infiltration of leukocytes into the nervous tissue, and disruption of the Blood-Brain Barrier (BBB) is one of the main factors in the progression of MS and its model, Experimental Autoimmune Encephalomyelitis (EAE). Furthermore, some anti-lymphocytic drugs against MS may inherently produce BBB disruption as their side effect. This study hypothesized that drugs restoring the BBB may be useful for the treatment of MS and EAE, as well as for ameliorating the side effects of modern anti-lymphocytic drugs.</p><p><strong>Methods: </strong>EAE was induced in SJL/J mice. EAE progression was evaluated by a severity score and a plasma cytokine profile, while a BBB condition was evaluated by the Evans dye method, Tight Junction Proteins (TJPs) content, and leukocyte infiltration.</p><p><strong>Results: </strong>The mice with EAE demonstrated neurological symptoms, a cytokine response, and BBB deterioration, which was associated with upregulation of the NADPH oxidases NOX1 and NOX4 in the brain. Administration of the anti-lymphocyte drug fingolimod to EAE mice caused lymphopenia, improved animal health, enhanced the BBB function during the administration period, and decreased the pro-inflammatory response, but it was accompanied by a \"withdrawal effect,\" defined as a sharp increase in the IL-17 and IFN-gamma to levels higher than those in untreated animals, lymphocyte hyperactivation, worsening symptoms, and increasing BBB permeability after discontinuation of fingolimod. Administration of peroxiredoxin 6 (Prdx6) to EAE mice also improved BBB, decreased lymphocyte infiltration and NADPH oxidase expression, and ameliorated symptoms. Preliminary administration of Prdx6 before the fingolimod treatment eliminated the \"withdrawal effect\" of fingolimod and led to full recovery of the EAE mice. This Prdx6 effect was associated with the activation of anti-proliferative and pro-apoptotic signaling cascades in lymphocytes.</p><p><strong>Discussion and conclusion: </strong>Both fingolimod and Prdx6 produced beneficial effects, while Prdx6 may be useful for ameliorating the side effects of anti-lymphocytic drugs. Accounting for literature data that discontinuation of MS treatment is very likely to lead to a severe MS rebound, a drug that prevents the rebound should be useful.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144583335","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":"In vivo Effects of Disease-modifying Therapies on Immunological Subsets in Patients with Relapsing-Remitting Multiple Sclerosis.","authors":"Chiara Finocchiaro, Clara Grazia Chisari, Salvatore Lo Fermo, Emanuele D'Amico, Nunziatina Laura Parrinello, Alessandra Romano, Giuseppe Alberto Palumbo, Sara Marino, Anna Maria Corsale, Francesco Di Raimondo, Mario Zappia, Francesco Patti","doi":"10.2174/011570159X360729250319064959","DOIUrl":"https://doi.org/10.2174/011570159X360729250319064959","url":null,"abstract":"<p><strong>Background: </strong>Disease-modifying therapies (DMTs) are aimed at controlling Multiple Sclerosis disease by modulating or suppressing the immune system. However, there is limited data on changes in immune cell subsets induced by these treatments.</p><p><strong>Objective: </strong>To assess differences in myeloid, T-, and B-cell subsets in the peripheral blood of relapsing- remitting MS (RR-MS) patients treated with different DMTs.</p><p><strong>Methods: </strong>This longitudinal study enrolled all RR-MS patients treated with cladribine (CLAD), dimethyl fumarate (DMF), and natalizumab (NTZ) between July 2022 and September 2022. All patients underwent blood sample collection with flow cytometry at baseline (T0; before starting treatment) and 24 ± 3 months after treatment initiation (T1).</p><p><strong>Results: </strong>Forty-three RR-MS patients (83.7% women; mean age 34.7 ± 11.1 years; median EDSS: 2.0, IQR: 1.0-2.8) were enrolled. Among them, 24 (55.8%) were treated with DMF, 10 (23.3%) with NTZ, and 9 (20.9%) with CLAD. At T1, patients assigned to CLAD showed a reduction in B-cell memory-switched (p = .029), B-cell memory-unswitched (p = .08), and B-cell naïve resting (p = .029). Additionally, the T and NK cell compartments showed a reduction in the percentage of CD3/CD4/ CD127/CD45RA/CD161+ (p = .057). In the NTZ group, a significant decrease in the percentage of CD3/CD4/CD127/CD45RA/CD161+ (p = .029) was observed. A reduced percentage of mature naïve B cells (p = .057) and B memory-unswitched (p = .059) was observed in the DMF group. No significant differences were found in the myeloid subsets.</p><p><strong>Conclusion: </strong>DMTs induced significant modifications in B- and T-cell compartments. Characterizing these immunologic changes could deepen our understanding of the mechanisms of action of different therapies.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144575013","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}