Neuroscience最新文献

{"title":"Therapeutic potential of dopamine and serotonin in inflammation and cancer: Insights into immune regulation.","authors":"Hamid Norioun, Ramin Hossein Baki, Saeedeh Ghiasvand, Noushika Sahandifar","doi":"10.1016/j.neuroscience.2024.12.014","DOIUrl":"https://doi.org/10.1016/j.neuroscience.2024.12.014","url":null,"abstract":"<p><strong>Introduction: </strong>This review explores the significant roles of neurotransmitters, focusing on dopamine and serotonin, in inflammation and cancer. These neurotransmitters are vital for neural signaling and play crucial roles in various physiological and pathological processes.</p><p><strong>Materials and methods: </strong>We conducted an extensive literature review, focusing on studies published between 2013 and 2024, using databases such as PubMed, Google Scholar, and Scopus. Studies were selected based on relevance to neurotransmitter synthesis, receptor function, and their involvement in diseases like cancer and neurodegenerative disorders. The key search terms included \"dopamine\", \"serotonin\", \"inflammation\", and \"cancer\".</p><p><strong>Results: </strong>Dopamine and serotonin are synthesized intracellularly and function as pivotal signaling molecules within the central nervous system (CNS) and peripheral systems. Through their respective receptors, dopamine and serotonin influence immune responses and the functionality of various bodily systems. Dysregulation in their signaling pathways is associated with a range of cancers and imbalances within the immune system.</p><p><strong>Discussion: </strong>The interplay between dopamine and serotonin systems extends beyond neural communication, significantly affecting immune responses and inflammation. Dopamine's role in modulating immune cell activity highlights its potential in treating inflammatory conditions and cancer. Similarly, serotonin's extensive physiological impact underscores the importance of targeting 5-HT pathways in various disorders. Future research should focus on developing therapeutic strategies that leverage these neurotransmitters' regulatory functions in both the CNS and peripheral systems.</p>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2024-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142828690","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":"HO-1 represses NF-κB signaling pathway to mediate microglia polarization and phagocytosis in intracerebral hemorrhage.","authors":"Weiping Chen, Zhiping Wu, Zhijuan Cheng, Yangbo Zhang, Qinghua Luo, Min Yin","doi":"10.1016/j.neuroscience.2024.12.020","DOIUrl":"10.1016/j.neuroscience.2024.12.020","url":null,"abstract":"<p><strong>Background: </strong>Microglia polarization plays a crucial role in inflammatory injury of brain following intracerebral hemorrhage (ICH). Heme oxygenase-1 (HO-1) has demonstrated protective properties against inflammation and promote hematoma clearance after ICH. The objective of this study was to explore impacts of HO-1 on microglia polarization and phagocytosis after ICH, along with the underlying mechanism.</p><p><strong>Methods: </strong>ICH model was constructed in C57BL/6 mice. Neurological deficit of ICH mice was evaluated. HE detected pathological changes of mouse brain tissue. Immunofluorescence staining tested co-localization between HO-1 or NF-κB p65 and IBA1. The expressions of gene and proteins were detected by RT-qPCR and Western blot, respectively. Flow cytometry determined microglial polarization phenotype and neuron apoptosis. Cell viability of neuron was assessed by CCK-8. Red blood cells labeled by PKH-26 and co-cultured with microglia for examining microglial erythrophagocytosis.</p><p><strong>Results: </strong>Both HO-1 and NF-κB p65 phosphorylation were elevated in brain tissues of ICH mice. ZnPP, a HO-1 inhibitor, could exacerbate microglial M1 polarization and nerve injury, as well as repress microglial erythrophagocytosis in vitro and hematoma clearance in vivo. On the contrary, Tat-NBD, a NF-κB inhibitor, greatly suppressed microglial M1 polarization, and induced M2 polarization and microglial erythrophagocytosis, thus improving nerve injury and hematoma clearance after ICH. Notably, it was observed that NF-κB p65 could be activated by ZnPP treatment, and the regulatory roles of ZnPP on microglial polarization and erythrophagocytosis after ICH in vivo and in vitro were all diminished by Tat-NBD.</p><p><strong>Conclusion: </strong>Therefore, our data demonstrated that HO-1 alleviated nerve injury and induced M2 polarization and phagocytosis of microglia after ICH via inhibiting NF-κB signaling pathway, which could provide deepen the pathological understanding of ICH and provide potential intervention targets and drug candidate for ICH.</p>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":" ","pages":"17-27"},"PeriodicalIF":2.9,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142822319","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":"Beauty and the brain - Investigating the neural and musical attributes of beauty during naturalistic music listening.","authors":"E Brattico, A Brusa, M J Dietz, T Jacobsen, H M Fernandes, G Gaggero, P Toiviainen, P Vuust, A M Proverbio","doi":"10.1016/j.neuroscience.2024.12.008","DOIUrl":"https://doi.org/10.1016/j.neuroscience.2024.12.008","url":null,"abstract":"<p><p>Beauty judgments are common in daily life, but rarely studied in cognitive neuroscience. Here, in three studies, we searched for the neural mechanisms of musical beauty using a naturalistic free-listening paradigm applied to behavioral and neuroimaging recordings and validated by experts' judgments. In Study 1, 30 adults continuously rated the perceived beauty of three musical pieces using a motion sensor. This served to identify the musical passages that were inter-subjectively judged as more or less beautiful ('beautiful' vs. 'not-beautiful' passages). For identifying the consistent neural determinants of the perception of musical beauty, we utilized these ratings to Study 2, where 36 adults were recorded with functional magnetic resonance imaging (fMRI) while they listened attentively to the same pieces of Study 1. In Study 3, to identify the musicological features characterizing the beautiful and not-beautiful passages of Studies 1-2, we collected post-hoc questionnaires from 12 music-composition experts. Results from Study 2 evidenced focal activity in the orbitofrontal cortex when listening to beautiful passages whereas the not-beautiful passages were associated with bilateral supratemporal activity. Effective connectivity analysis discovered inhibition of auditory activation and neural communication with the right orbitofrontal cortex for listening to beautiful passages vs. intrinsic activation of auditory cortices and decreased coupling to orbitofrontal cortex for not-beautiful passages. Experts' questionnaires indicated that the beautiful passages were more melodic, calm, sad, slow, tonal, traditional, and simple than the ones rated negatively. In sum, we identified neural and psychological underpinnings of musical beauty, irrespectively of individual taste and listening biography.</p>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2024-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142813701","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":"Bayesian brain theory: Computational neuroscience of belief.","authors":"Hugo Bottemanne","doi":"10.1016/j.neuroscience.2024.12.003","DOIUrl":"10.1016/j.neuroscience.2024.12.003","url":null,"abstract":"<p><p>Bayesian brain theory, a computational framework grounded in the principles of Predictive Processing (PP), proposes a mechanistic account of how beliefs are formed and updated. This theory assumes that the brain encodes a generative model of its environment, made up of probabilistic beliefs organized in networks, from which it generates predictions about future sensory inputs. The difference between predictions and sensory signals produces prediction errors, which are used to update belief networks. In this article, we introduce the fundamental principles of Bayesian brain theory, and show how the brain dynamics of prediction are associated with the generation and evolution of beliefs.</p>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":" ","pages":"198-204"},"PeriodicalIF":2.9,"publicationDate":"2024-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142792020","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":"Repeated exposure to high-dose nicotine induces prefrontal gray matter atrophy in adolescent male rats.","authors":"Xi Chen, Kehong Long, Sijie Liu, Yue Cai, Linlin Cheng, Wei Chen, Fuchun Lin, Hao Lei","doi":"10.1016/j.neuroscience.2024.11.059","DOIUrl":"https://doi.org/10.1016/j.neuroscience.2024.11.059","url":null,"abstract":"<p><p>Incidences of seizure after e-cigarette use in adolescents and young adults have been reported, raising the concern about the risk of nicotine overconsumption. Few previous studies have investigated the effects of nicotine at high doses on brain and behavior in adolescent animals. In this study, the effects of a 15-day repeated nicotine treatment at a daily dose of 2 mg/kg body weight were investigated in adolescent and adult male rats. Nicotine treatment abolished body weight gain in the adults, but did not affect the body weight significantly in the adolescents. Only the nicotine-treated adolescents showed significant changes in brain anatomy 1 day post-treatment, which manifested as a significant reduction of whole-brain gray matter (GM) volume, a further reduction of regional GM volume in the medial prefrontal cortex (mPFC) and altered GM volume covariations between the mPFC and a number of brain regions. The mPFC of nicotine-treated adolescent rats did not exhibit evident signs of neuronal degeneration and reactive astrocytosis, but showed a significantly decreased expression of presynaptic marker synaptophysin (SYN), along with a significantly increased oxidative stress and a significantly elevated expressions of microglial marker ionized calcium binding adaptor molecule 1 (IBA1). Together, these results suggested that repeated nicotine overdosing may shift regional redox, modulate microglia-mediated pruning, and give rise to structural/connectivity deficits in the mPFC of adolescent male rats.</p>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2024-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142780541","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":"Cerebral blood flow in attention deficit hyperactivity disorder: A systematic review.","authors":"Johanna Berthier, Francky Teddy Endomba, Michel Lecendreux, Sibylle Mauries, Pierre A Geoffroy","doi":"10.1016/j.neuroscience.2024.11.075","DOIUrl":"https://doi.org/10.1016/j.neuroscience.2024.11.075","url":null,"abstract":"<p><strong>Background and objectives: </strong>Attention deficit hyperactivity disorder (ADHD) is one of the most frequent and disabling neurodevelopmental disorders. Recent research on cerebral blood flow (CBF) has enhanced understanding of the underlying pathophysiology in neuropsychiatric disorders. This systematic review aims to synthesize the existing literature on CBF anomalies among individuals with ADHD in comparison to controls.</p><p><strong>Methods: </strong>Following the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) approach, a systematic literature search was conducted using PubMed, PsycInfo, and Web of Science to identify relevant studies on CBF in ADHD.</p><p><strong>Results: </strong>Twenty studies, encompassing a total of 1652 participants with ADHD and 580 controls, were included, employing measurements from SPECT (n = 9), ASL (n = 6), PET (n = 4), and BOLD-derived quantitative maps (n = 1). In individuals with ADHD during resting state, hypoperfusion was frequently observed in the right orbitofrontal gyrus, temporal cortex, basal ganglia and putamen. Conversely, hyperperfusion was noted in frontal lobes, left postcentral gyrus, and occipital lobes. During cognitive tasks, hyperperfusion was observed in frontal areas, temporal regions, cingulate cortex and the precuneus. Furthermore, the administration of methylphenidate was associated with increased CBF in striatal and posterior periventricular regions, the right thalamus, and the precentral gyrus.</p><p><strong>Conclusion: </strong>This review highlights diverse CBF anomalies in ADHD. The most consistently reported findings suggest hypoperfusion during resting state in prefrontal and temporal areas, along with the basal ganglia, while there is a hyperperfusion in frontal, parietal and occipital regions. Further research, including longitudinal studies, is essential to develop a comprehensive understanding of CBF implications in ADHD.</p>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2024-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142780534","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":"Beyond digestion: Exploring how the gut microbiota modulates human social behaviors","authors":"Mohammad Abavisani ,&nbsp;Navid Faraji ,&nbsp;Negar Ebadpour ,&nbsp;Prashant Kesharwani ,&nbsp;Amirhossein Sahebkar","doi":"10.1016/j.neuroscience.2024.11.068","DOIUrl":"10.1016/j.neuroscience.2024.11.068","url":null,"abstract":"<div><div>For a long time, traditional medicine has acknowledged the gut’s impact on general health. Contemporary science substantiates this association through investigations of the gut microbiota, the extensive community of microorganisms inhabiting our gastrointestinal system. These microscopic residents considerably improve digestive processes, nutritional absorption, immunological function, and pathogen defense. Nevertheless, a variety of gastrointestinal and extra-intestinal disorders can result from dysbiosis, an imbalance of the microbial composition of the gut microbiota. A groundbreaking discovery is the gut-brain axis, a complex communication network that links the enteric and central nervous system (CNS). This bidirectional communication allows the brain to influence gut activities and vice versa, impacting mental health and mood disorders like anxiety and depression. The gut microbiota can influence this communication by creating neurotransmitters and short-chain fatty acids, among other biochemical processes. These factors may affect our mental state, our ability to regulate our emotions, and the hypothalamic–pituitary–adrenal (HPA) axis. This study aimed to explore the complex interrelationships between the brain and the gut microbiota. We also conducted a thorough examination of the existing understanding in the area of how microbiota affects social behaviors, including emotions, stress responses, and cognitive functions. We also explored the potential of interventions that focus on the connection between the gut and the brain, such as using probiotics to treat diseases of the CNS. This research opens up new possibilities for addressing mental health and neurological conditions in an innovative manner.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"565 ","pages":"Pages 52-62"},"PeriodicalIF":2.9,"publicationDate":"2024-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142757601","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":"Long-term potentiation in the hippocampus: From magnesium to memory.","authors":"Graham L Collingridge","doi":"10.1016/j.neuroscience.2024.11.069","DOIUrl":"https://doi.org/10.1016/j.neuroscience.2024.11.069","url":null,"abstract":"<p><p>Long-term potentiation (LTP) is a widely studied phenomenon since the underlying molecular mechanisms are widely believed to be critical for learning and memory and their dysregulation has been implicated in many brain disorders affecting cognitive functions. Central to the induction of LTP, in most pathways that have been studied in the mammalian CNS, is the N-methyl-D-aspartate receptor (NMDAR). Philippe Ascher discovered that the NMDAR is subject to a rapid, highly voltage-dependent block by Mg²⁺. Here I describe how my own work on NMDARs has been so profoundly influenced by this seminal discovery. This personal reflection describes how the voltage-dependent Mg²⁺ block of NMDARs was a crucial component of the understanding of the molecular mechanisms responsible for the induction of LTP. It explains how this unusual molecular mechanism underlies the Hebbian nature of synaptic plasticity and the hallmark features of NMDAR-LTP (input specificity, cooperativity and associativity). Then the role of the Mg²⁺ block of NMDARs is discussed in the context of memory and dementia. In particular, the idea that alterations in the voltage-dependent block of the NMDAR is a component of cognitive decline during normal ageing and neurodegenerative disorders, such as Alzheimer's disease, is discussed.</p>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2024-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142769905","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":"Serpina3n in neonatal microglia mediates its protective role for damaged adult microglia by alleviating extracellular matrix remodeling-induced tunneling nanotubes degradation in a cell model of traumatic brain injury","authors":"Gengfan Ye ,&nbsp;Zhigang Wang ,&nbsp;Pandi Chen ,&nbsp;Junyi Ye ,&nbsp;Shiwei Li ,&nbsp;Maosong Chen ,&nbsp;Jiugeng Feng ,&nbsp;Hongcai Wang ,&nbsp;Wei Chen","doi":"10.1016/j.neuroscience.2024.11.066","DOIUrl":"10.1016/j.neuroscience.2024.11.066","url":null,"abstract":"<div><div>Traumatic brain injury (TBI) induces significant neuroinflammation, primarily driven by microglia. Neonatal microglia (NMG) may have therapeutic potential by modulating the inflammatory response of damaged adult microglia (AMG). This study investigates the influence of NMG on AMG function through extracellular matrix (ECM) remodeling and the formation of tunneling nanotubes (TnTs), with a focus on the role of Serpina3n. We established an <em>in vitro</em> TBI model using a 3D Transwell system, co-culturing damaged AMG with NMG. Viral vector transfection was employed to manipulate Serpina3n expression in NMG. Quantitative real-time PCR, Western blotting, and ELISA were utilized to assess inflammatory markers, ECM remodeling proteins, and TnTs-related proteins. Co-culturing with NMG significantly inhibited M1 polarization of AMG and reduced the release of pro-inflammatory cytokines while promoting M2 polarization and increasing the production of anti-inflammatory cytokines. NMG expressed higher levels of Serpina3n, which played a crucial role in reducing Granzyme B, matrix metalloproteinase (MMP) 2 and MMP9 expression, thereby mitigating ECM remodeling. Inhibition of Serpina3n in NMG increased pro-inflammatory markers and decreased TnTs formation proteins, whereas overexpression of M−sec in AMG counteracted these effects. This highlights the importance of TnTs in maintaining microglial function and promoting an anti-inflammatory environment. In conclusion, NMG improve the function of damaged AMG by modulating ECM remodeling and promoting TnTs formation through the action of Serpina3n.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"565 ","pages":"Pages 1-9"},"PeriodicalIF":2.9,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142755039","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":"Emerging biophysical techniques for probing synaptic transmission in neurodegenerative disorders","authors":"Mayur B. Kale ,&nbsp;Nitu L. Wankhede ,&nbsp;Ashok Kumar Bishoyi ,&nbsp;Suhas Ballal ,&nbsp;Rishiv Kalia ,&nbsp;Renu Arya ,&nbsp;Sachin Kumar ,&nbsp;Mohammad Khalid ,&nbsp;Monica Gulati ,&nbsp;Mohit Umare ,&nbsp;Brijesh G. Taksande ,&nbsp;Aman B. Upaganlawar ,&nbsp;Milind J. Umekar ,&nbsp;Spandana Rajendra Kopalli ,&nbsp;Mohammad Fareed ,&nbsp;Sushruta Koppula","doi":"10.1016/j.neuroscience.2024.11.055","DOIUrl":"10.1016/j.neuroscience.2024.11.055","url":null,"abstract":"<div><div>Plethora of research has shed light on the critical role of synaptic dysfunction in various neurodegenerative disorders (NDDs), including Alzheimer’s disease (AD), Parkinson’s disease (PD), Amyotrophic lateral sclerosis (ALS), and Huntington’s disease (HD). Synapses, the fundamental units for neural communication in the brain, are highly vulnerable to pathological conditions and are central to the progression of neurological diseases. The presynaptic terminal, a key component of synapses responsible for neurotransmitter release and synaptic communication, undergoes structural and functional alterations in these disorders. Understanding synaptic transmission abnormalities is crucial for unravelling the pathophysiological mechanisms underlying neurodegeneration. In the quest to probe synaptic transmission in NDDs, emerging biophysical techniques play a pivotal role. These advanced methods offer insights into the structural and functional changes occurring at nerve terminals in conditions like AD, PD, HD &amp; ALS. By investigating synaptic plasticity and alterations in neurotransmitter release dynamics, researchers can uncover valuable information about disease progression and potential therapeutic targets. The review articles highlighted provide a comprehensive overview of how synaptic vulnerability and pathology are shared mechanisms across a spectrum of neurological disorders. In major neurodegenerative diseases, synaptic dysfunction is a common thread linking these conditions. The intricate molecular machinery involved in neurotransmitter release, synaptic vesicle dynamics, and presynaptic protein regulation are key areas of focus for understanding synaptic alterations in neurodegenerative diseases.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"565 ","pages":"Pages 63-79"},"PeriodicalIF":2.9,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142751394","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}