Journal of integrative neuroscience最新文献

{"title":"Association Between White Matter Hyperintensity and Cognitive Impairment in Cerebral Small Vessel Disease: The Frequency-dependent Role of Brain Functional Activity.","authors":"Dongqiong Fan, Tingting Wang, Haichao Zhao, Chang Liu, Chenhui Liu, Tao Liu, Yilong Wang","doi":"10.31083/JIN36303","DOIUrl":"10.31083/JIN36303","url":null,"abstract":"<p><strong>Background: </strong>Cognitive dysfunction in cerebral small vessel disease (CSVD) patients is associated with white matter hyperintensity (WMH), which demonstrates frequency-dependent correlations with brain functional activities. However, the neural mechanisms underlying the relationship between these structural and functional abnormalities and cognitive impairment remain unclear.</p><p><strong>Methods: </strong>We recruited 34 CSVD patients (mean age 63.74 ± 4.85 years, 19 males) and 45 age-matched healthy controls (mean age 63.69 ± 6.15 years, 15 males). All participants underwent magnetic resonance imaging (MRI) scanning and comprehensive cognitive assessments, including three behavioral tasks and a cognitive questionnaire battery. Regional brain activity and network topological properties were separately compared between the two groups for each of the three frequency bands (slow-4, slow-5, and typical band) using two-sample <i>t</i>-tests. Simple and multiple mediation analyses were performed to examine the relationships among WMH, functional brain measures, and global cognition.</p><p><strong>Results: </strong>CSVD patients exhibited frequency-specific alterations in regional activity and reduced global functional organization in the slow-4 band. Frequency-dependent functional measures in the slow-4 band significantly mediated the relationship between deep WMH and cognitive performance.</p><p><strong>Conclusion: </strong>Our findings demonstrate the frequency-specific mediating role of abnormal brain functions in the pathophysiological pathway linking WMHs to cognitive impairment. This study provides new insight into the pathological mechanisms underlying WMH-related cognitive dysfunction.</p><p><strong>Clinical trial registration: </strong>ChiCTR2100043346, 02 November 2021, https://www.chictr.org.cn/showproj.html?proj=52285.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"24 4","pages":"36303"},"PeriodicalIF":2.5,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144008537","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibition of Neutrophil Extracellular Traps: A Potential Therapeutic Strategy for Hemorrhagic Stroke.","authors":"Rasit Dinc, Nurittin Ardic","doi":"10.31083/JIN26357","DOIUrl":"https://doi.org/10.31083/JIN26357","url":null,"abstract":"<p><p>Stroke is a major health problem with high mortality and morbidity rates, partly due to limited treatment options. Inflammation has a critical role in the secondary damage that occurs following a stroke event. Neutrophil extracellular traps (NETs) are released by neutrophils and contribute to the progression of neuroinflammation that further worsens brain damage. The prevention of NET formation at sites of brain damage has been reported to prevent neuroinflammation and improve neurological deficits. The aim of this article was to assess the importance of NETs as a treatment target for hemorrhagic stroke in light of the available evidence. NETs are network structures that consist of decondensed DNA strands coated with granule proteins such as citrullinated histones, neutrophile esterase (NE), myeloperoxidase (MPO), and high mobility group protein B1 (HMGB1). Peptidyl arginine deiminase type-IV (PAD4) plays a key role in the formation of NETs. Inhibitors of NET formation, such as the PAD4-specific inhibitor GSK484, are effective at preventing inflammation and thus ultimately reducing brain damage after stroke. In conclusion, inhibition of NETs offers a potential therapeutic strategy for hemorrhagic stroke, although further research is needed to clarify the role of NETs in this condition.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"24 4","pages":"26357"},"PeriodicalIF":2.5,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144029476","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of Auditory Evoked Potentials in Neuromyelitis Optica Spectrum Disorder.","authors":"Lucas Pinto Mielle, Liliane Aparecida Fagundes Silva, Dayane Aparecida Nascimento Barbosa, Glauciene Amaral Martins, Alessandra Giannella Samelli, Carla Gentile Matas","doi":"10.31083/JIN27733","DOIUrl":"https://doi.org/10.31083/JIN27733","url":null,"abstract":"<p><strong>Background: </strong>Neuromyelitis optica spectrum disorder (NMOSD) is a recurrent demyelinating neuroinflammatory disorder of the central nervous system. This study aimed to evaluate the neural conduction and sound information processing in individuals with NMOSD, through the analysis of auditory brainstem responses (ABRs) and cortical auditory evoked potentials (CAEPs).</p><p><strong>Methods: </strong>Twenty-four individuals (9-21 years old) were distributed into two groups: the study group (SG), diagnosed with NMOSD, and the control group, healthy individuals. Their ABRs and CAEPs were evaluated, and the results were examined alongside data from cranial magnetic resonance imaging (MRI).</p><p><strong>Results: </strong>Abnormal ABRs were observed in 33% of the SG and increased I-III interpeak was the most prevalent finding. The CAEPs showed abnormalities in 58% of the SG, mainly to P1 latency. SG subjects presented longer P1, N1, and N2 latencies and lower N2-P3 amplitude. MRI showed alterations mostly in the pons, midbrain, and IV ventricle.</p><p><strong>Conclusions: </strong>Alterations in neural conduction and sound information processing were observed in individuals with NMOSD when compared with their peers. Auditory evoked potentials are important instruments to identify central auditory dysfunction in this population as well as to monitor disease evolution.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"24 4","pages":"27733"},"PeriodicalIF":2.5,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143997512","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Attention Performance and Altered Amplitude of Low-frequency Fluctuations in the Attention Network of Patients with MCI: A Resting-state Functional MRI Study.","authors":"Jia Luo, Yi Zeng, Yuwei Ye, Yiping Xiao, Qiurong Xie, Jijing Zhang, Weilin Cai, Huanyun Xu, Shengxiang Liang, Jia Huang","doi":"10.31083/JIN36464","DOIUrl":"https://doi.org/10.31083/JIN36464","url":null,"abstract":"<p><strong>Background: </strong>This study aimed to explore attention alteration in mild cognitive impairment (MCI) patients and their association with abnormalities of autonomic brain activity within the attention network to reveal the neuroimaging basis behind these changes.</p><p><strong>Methods: </strong>A total of 25 MCI patients and 31 normal controls (NCs) were recruited for the study. The Test of Attention Performance (TAP) version 2.3 was used to evaluate alertness, selective attention, and divided attention in MCI patients and NCs. Subsequently, participants underwent resting-state magnetic resonance imaging (MRI) scans to compare whole-brain autonomic activity characteristics between groups using the amplitude of low-frequency fluctuation (ALFF). Data preprocessing and analysis were conducted using Data Processing & Analysis of Brain Imaging in MATLAB R2018b.</p><p><strong>Results: </strong>There were significant differences in omissions of intrinsic alertness, total omissions of divided attention, omissions and correct of visual divided attention between the two groups. Meanwhile, independent sample <i>t</i>-tests indicated that the MCI group exhibited higher <i>z</i>-scored ALFF (zALFF) in the left middle occipital gyrus, left superior frontal gyrus (orbital part), and right inferior frontal gyrus (orbital part) when compared with the NC group. The MCI group exhibited reduced zALFF in the left median cingulate and paracingulate gyrus, left precuneus, and right rolandic operculum. Notably, the decreased zALFF in the left precuneus showed a significant negative correlation with divided attention.</p><p><strong>Conclusions: </strong>Our findings suggest that patients with MCI exhibit relatively normal performance in selective attention and phase alertness tasks, while they demonstrate a decline in capacity for divided attention and intrinsic alertness tasks. Divided attention in MCI patients may be associated with abnormalities in spontaneous neural activity in the left precuneus. This study provides new and complementary insights into the neural basis of divided attention in patients with MCI.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"24 4","pages":"36464"},"PeriodicalIF":2.5,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143996012","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lactate-Dehydrogenase-5 May Play a Key Role in the Disturbance of Brain Energy Caused by Tuberculous Meningitis.","authors":"Qingdong Zhu, Huawei He, Qian Long, Cailing Wei, Jieling Chen, Lanwei Nong, Sijun Li","doi":"10.31083/JIN26741","DOIUrl":"https://doi.org/10.31083/JIN26741","url":null,"abstract":"<p><strong>Background: </strong>The conversion of pyruvate to lactate is primarily catalyzed by lactate-dehydrogenase-5 (LDH-5), which comprises four lactate-dehydrogenase-A (LDHA) subunits. However, the mechanism of LDH-5 in tuberculous meningitis (TBM) remains elusive.</p><p><strong>Methods: </strong>Thirty-two samples of cerebrospinal fluid (CSF) were collected, including 15 from individuals without central nervous system (CNS) infectious diseases (control group) and 17 from individuals with TBM (TBM group). Based on the results of brain imaging, nine patients with TBM with meningeal enhancement were included in the meninges group. Eight patients with TBM with lesions in the brain parenchyma were included in the brain parenchyma group. The levels of adenosine triphosphatase (ATP), lactate, LDH-1, pyruvate and LDH-5 in the CSF were assessed. Subsequently, the levels of ATP, pyruvate and lactate, as well as the amplitude and frequency of action potentials (APs) in neurons overexpressing LDHA, were investigated.</p><p><strong>Results: </strong>Reduced levels of pyruvate and ATP and elevated levels of lactate and LDH-5 were observed in the CSF of individuals with TBM. The ATP level was decreased in the brain parenchyma group. In neurons with LDHA overexpression, the lactate level increased, while ATP and pyruvate levels, as well as the amplitude and frequency of APs, decreased.</p><p><strong>Conclusion: </strong>Elevated levels of LDH-5 in the CNS of individuals with TBM may lead to a disturbance in brain energy and negatively affect neuronal activity.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"24 4","pages":"26741"},"PeriodicalIF":2.5,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143995772","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hippocampal Neuroplasticity and Adult Neurogenesis: Mechanisms and Implications.","authors":"Hyewon Jang, Poornima D E Weerasinghe-Mudiyanselage, Changjong Moon","doi":"10.31083/JIN36128","DOIUrl":"https://doi.org/10.31083/JIN36128","url":null,"abstract":"","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"24 4","pages":"36128"},"PeriodicalIF":2.5,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144025147","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"5-Fluorouracil Impairs Transmission of Acetylcholine in the Hippocampus and Induces Cognitive Impairments in Mice.","authors":"Xiwen Huang, Shunqing Peng, Yongquan Lan, Wenjun Chen, Jianlin Wu","doi":"10.31083/JIN26903","DOIUrl":"https://doi.org/10.31083/JIN26903","url":null,"abstract":"<p><strong>Background: </strong>Chemotherapy-induced cognitive impairments are a significant adverse sequela of cancer treatment. The potential mechanism of chemotherapy-induced cognitive impairments remains elusive. The present study evaluated the impact of a commonly utilized chemotherapy agent, 5-fluorouracil (5-FU), on acetylcholine (ACh) levels in the hippocampus.</p><p><strong>Methods: </strong>5-FU was injected into mice once a day for 10 days to create a mouse model of chemotherapy-induced cognitive impairment. Microdialysis and HPLC-MS/MS were used to determine hippocampal ACh levels. Biocytin injection and patch-clamp recordings were performed on cholinergic (ChAT) neurons in the medial septum (MS) to observe their morphological and electrophysiological changes. Chemogenetic tools were used to activate ChAT neurons in the MS. The acetylcholinesterase inhibitor donepezil was injected i.p. into mice to elevate ACh levels in the brain.</p><p><strong>Results: </strong>Cognitive performance in mice was impaired after 5-FU treatment, accompanied by reduced ACh release in the hippocampus. The administration of 5-FU led to compromised structural integrity and diminished activity of ChAT neurons in the MS. Chemogenetic stimulation of MS ChAT neurons ameliorated the cognitive impairments. The administration of donepezil also reduced the cognitive impairments caused by 5-FU.</p><p><strong>Conclusions: </strong>5-FU therapy caused cognitive impairments in mice by affecting the neuronal structure and activity of ChAT neurons in the MS. Inducing the increase of ACh levels could be a promising therapeutic approach for addressing 5-FU treatment-induced cognitive impairments.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"24 4","pages":"26903"},"PeriodicalIF":2.5,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144011190","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acute Restraint Stress Enhances Prosocial Behavior in Rats via Oxytocin and Fear-Related Circuits.","authors":"Sheng-Chiang Wang, Chen-Cheng Lin, Chun-Chuan Chen, Yia-Ping Liu","doi":"10.31083/JIN33400","DOIUrl":"https://doi.org/10.31083/JIN33400","url":null,"abstract":"<p><strong>Background: </strong>Stress is a critical determinant of social behavior, with oxytocin playing a key role in buffering stress effects and facilitating social bonding. However, the relationship between stress-induced fear and oxytocin-associated sociability remains unclear, particularly in contexts reminiscent of prior stress. This study investigates whether acute restraint stress (ARS) alters anxiety-related behaviors and prosocial choices, and whether these effects can be modulated by pharmacological intervention targeting the oxytocin and corticotropin-releasing hormone (CRH) systems.</p><p><strong>Methods: </strong>Sprague-Dawley rats were subjected to ARS and assessed for anxiety-like behavior using the elevated T-maze (ETM) and for prosocial behavior using the social choice test (SCT). The effects of the oxytocin receptor antagonist L-368899 and CRH receptor antagonist antalarmin were evaluated in this paradigm. Plasma corticosterone was checked peripherally and the tissue concentrations of serotonin (5-HT), dopamine (DA), and norepinephrine (NE) were measured in the hippocampus, medial prefrontal cortex (mPFC), and amygdala to assess stress-related neurochemical changes in the fear circuit.</p><p><strong>Results: </strong>(i) ARS rats showed a significant increase in prosocial preference compared to control, an effect blocked by L-368899 or antalarmin. (ii) ARS rats exhibited reduced corticosterone levels, together with shorter avoidance latency, and longer escape latency in the ETM. (iii) Neurochemically, ARS rats had decreased DA and increased NE levels in the mPFC, both of which were normalized by L-368899 treatment.</p><p><strong>Conclusions: </strong>Oxytocin modulates stress-induced alterations in monoaminergic activity within the mPFC, influencing social choice behavior. These findings provide new insights into the neurobiological mechanisms underlying stress-related sociability and the context-dependent role of oxytocin in fear memory and social behavior.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"24 4","pages":"33400"},"PeriodicalIF":2.5,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144022792","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Human Brain Inspired Artificial Intelligence Neural Networks.","authors":"Paschalis Theotokis","doi":"10.31083/JIN26684","DOIUrl":"https://doi.org/10.31083/JIN26684","url":null,"abstract":"<p><p>It is becoming increasingly evident that Artificial intelligence (AI) development draws inspiration from the architecture and functions of the human brain. This manuscript examines the alignment between key brain regions-such as the brainstem, sensory cortices, basal ganglia, thalamus, limbic system, and prefrontal cortex-and AI paradigms, including generic AI, machine learning, deep learning, and artificial general intelligence (AGI). By mapping these neural and computational architectures, I herein highlight how AI models progressively mimic the brain's complexity, from basic pattern recognition and association to advanced reasoning. Current challenges, such as overcoming learning limitations and achieving comparable neuroplasticity, are addressed alongside emerging innovations like neuromorphic computing. Given the rapid pace of AI advancements in recent years, this work underscores the importance of continuously reassessing our understanding as technology evolves exponentially.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"24 4","pages":"26684"},"PeriodicalIF":2.5,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143996286","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Resveratrol Alleviates Ischemia-Reperfusion-Induced Neuronal Damage by Inhibiting NR3C2-Mediated TRIM28 Expression.","authors":"Yan Li, Haiwei Xie, Shuang Liu, Zhongfan Ruan, Baiyun Wang","doi":"10.31083/JIN31375","DOIUrl":"https://doi.org/10.31083/JIN31375","url":null,"abstract":"<p><strong>Background: </strong>Cerebral ischemia-reperfusion injury (CIRI) exacerbates neuronal damage through mechanisms including apoptosis and autophagy dysregulation. Resveratrol (Res), a natural polyphenol with neuroprotective properties, may alleviate CIRI-induced damage by modulating key signaling pathways. This study investigates the therapeutic effects of Res on CIRI, focusing on its role in balancing apoptosis and autophagy via regulation of nuclear receptor subfamily 3 group C member 2 (NR3C2) and tripartite motif containing 28 (TRIM28).</p><p><strong>Method: </strong><i>In vivo</i>, cognitive impairment, neurological dysfunction, cerebral infarction, neuronal damage, and inflammatory response were assessed in Sprague Dawley (SD) rats subjected to middle cerebral artery occlusion/reperfusion (MCAO/R) using the morris water maze, Longa and Bederson scores, 2,3,5-tripheny ltetrazolium chloride (TTC) staining, hematoxylin and eosin staining, Nissl staining, and enzyme-linked immunosorbent assay (ELISA). The expression of NR3C2 and TRIM28 were analyzed by real time quantitative polymerase chain reaction (RT-qPCR) and western blot (WB). <i>In vitro</i>, Res effects on oxygen-glucose deprivation/reperfusion (OGD/R)-treated PC12 cells were evaluated using cell counting kit-8 (CCK-8), ELISA, terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling (TUNEL) staining, and WB. The relationship between NR3C2 and TRIM28 was validated using dual luciferase and chromatin immunoprecipitation followed by quantitative polymerase chain reaction (ChIP-qPCR).</p><p><strong>Result: </strong>Res treatment significantly improved cognitive performance in the morris water maze test, and the infarct area was reduced by 16.736%. It was accompanied by downregulation of NR3C2 and TRIM28 expression. <i>In vitro</i>, Res enhanced cell viability, reduced inflammatory responses and apoptosis (with a 17.70% decrease in cell apoptosis rate), and restored autophagy balance. Mechanistically, NR3C2 was shown to directly regulate TRIM28 transcription, mediating the observed neuroprotective effects.</p><p><strong>Conclusion: </strong>Res inhibits NR3C2 expression, which in turn directly regulates the transcription of TRIM28 through NR3C2, alleviating apoptosis and autophagy dysregulation induced by CIRI. This mechanism clearly demonstrates the important role of NR3C2 in CIRI and reveals its regulatory relationship with TRIM28. By uncovering the neuroprotective effects of Res, we provide new insights for the treatment of CIRI and lay the foundation for future targeted therapeutic strategies involving NR3C2 and TRIM28.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"24 4","pages":"31375"},"PeriodicalIF":2.5,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144016843","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}