Developmental Neuroscience最新文献

{"title":"Region-Specific Brain Volume Changes Emerge in Adolescence in the Valproic Acid Model of Autism and Parallel Human Findings.","authors":"Cole King, Ivina Mali, Hunter Strating, Elizabeth Fangman, Jenna Neyhard, Macy Payne, Stefan H Bossmann, Bethany Plakke","doi":"10.1159/000538932","DOIUrl":"10.1159/000538932","url":null,"abstract":"<p><strong>Introduction: </strong>Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by social and communication deficits, cognitive dysfunction, and stereotyped repetitive behaviors. Regional volume changes are commonly observed in individuals with ASD. To examine volumetric dysregulation across adolescence, the valproic acid (VPA) model was used to induce ASD-like phenotypes in rats.</p><p><strong>Method: </strong>Regional volumes were obtained via magnetic resonance imaging at either postnatal day 28 or postnatal day 40 (P40), which correspond to early and late adolescence, respectively.</p><p><strong>Results: </strong>Consistent with prior research, VPA animals had reduced total brain volume compared to control animals. A novel outcome was that VPA animals had overgrown right hippocampi at P40. Differences in the pattern of development of the anterior cingulate cortex were also observed in VPA animals. Differences for the posterior cingulate were only observed in males, but not females.</p><p><strong>Conclusion: </strong>These results demonstrate differences in region-specific developmental trajectories between control and VPA animals and suggest that the VPA model may capture regional volume changes consistent with human ASD.</p>","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140858865","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":"Left OFC activation in fNIRS during an inhibitory control task in an early years sample: integrating stress responses with cognitive function and brain activation.","authors":"Mirela Ramacciotti, Raimundo da Silva Soares Junior, João Ricardo Sato, M. Gualtieri","doi":"10.1159/000539023","DOIUrl":"https://doi.org/10.1159/000539023","url":null,"abstract":"INTRODUCTION\u0000Previous functional near-infrared (fNIRS) studies using Go/No-Go (GNG) tasks have focused on brain activation in relation to cognitive processes, particularly inhibitory control (IC). The results of these studies commonly describe right hemispheric engagement of the dorsolateral, ventromedial or inferior frontal regions of the prefrontal cortex (PFC). Considering that typical healthy cognitive development is negatively correlated with higher cortisol levels (which may alter brain development), the overarching aim of the current study was to investigate how elevated stress (due to unforeseeable events such as the pandemic) impacts early cognitive development.\u0000\u0000\u0000METHOD\u0000In this study, we examined fNIRS data collected from a sample of children (aged 2 - 4 years) during a GNG task relative to the response to stressors measured via hair cortisol concentrations. We acquired data in an ecological setting (Early Childhood Education and Care) during the coronavirus pandemic.\u0000\u0000\u0000RESULTS\u0000We found that children with higher stress levels and a less efficient inhibitory control recruited more neural terrain and our group-level analysis indicated activation in the left orbitofrontal area during IC performance.\u0000\u0000\u0000CONCLUSIONS\u0000A contextual stressor may disrupt accuracy in the executive function of inhibitory control early in development. More research efforts are needed to understand better how an orbitofrontal network subserves goal-directed behavior.","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140655023","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":"TFEB overexpression through GFAP promoter disrupts neuronal lamination by dysregulating neurogenesis during embryonic development.","authors":"Lei Wang, Jiaxin Cao, Haichao Chen, Yuezhang Ma, Yishu Zhang, Xiaomei Su, Yuhong Jing, Yonggang Wang","doi":"10.1159/000538656","DOIUrl":"https://doi.org/10.1159/000538656","url":null,"abstract":"INTRODUCTION\u0000Transcription factor EB (TFEB), a key regulator of autophagy and lysosomal biogenesis, has diverse roles in various physiological processes. Enhancing lysosomal function by TFEB activation has recently been implicated in restoring neural stem cells (NSCs) function. Overexpression of TFEB can inhibit the cell cycle of newborn cortical NSCs. It has also been found that TFEB regulates the pluripotency transcriptional network in mouse embryonic stem cells independent of autophagy lysosomal biogenesis. This study aims to explore the effects of TFEB activation on neurogenesis in vivo through transgenic mice.\u0000\u0000\u0000METHODS\u0000We developed a GFAP-driven TFEB overexpression mouse model (TFEB GoE) by crossing the floxed TFEB overexpression mice and hGFAP-cre mice. We performed immunohistochemical and fluorescence staining on brain tissue from newborn mice to assess neurogenesis changes, employing markers such as GFAP, Nestin, Ki67, DCX, Tbr1 and Neun to trace different stages of neural development and cell proliferation.\u0000\u0000\u0000RESULTS\u0000TFEB GoE mice exhibited premature mortality, dying at 10-20 days after birth. Immunohistochemical analysis revealed significant abnormalities, including disrupted hippocampal structure and cortical layering. Compared to control mice, TFEB GoE mice showed a marked increase in radial glial cells (RGCs) in the hippocampus and cortex, with Ki67 staining indicating these cells were predominantly in a quiescent state. This suggests that TFEB overexpression suppresses RGCs proliferation. Additionally, abnormal distributions of migrating neurons and mature neurons were observed, highlighted by DCX, Tbr1 and Neun staining, indicating a disruption in normal neurogenesis.\u0000\u0000\u0000CONCLUSION\u0000This study, using transgenic animals in vivo, revealed that GFAP-driven TFEB overexpression leads to abnormal neural layering in the hippocampus and cortex by dysregulating neurogenesis. Our study is the first to discover the detrimental impact of TFEB overexpression on neurogenesis during embryonic development, which has important reference significance in future TFEB overexpression interventions in NSCs for treatment.","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140737499","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":"Timing of methamphetamine exposure during adolescence differentially influences parvalbumin and perineuronal net immunoreactivity in the medial prefrontal cortex of female, but not male, rats.","authors":"Amara S Brinks, Lauren K Carrica, Dominic J Tagler, Joshua M Gulley, Janice M Juraska","doi":"10.1159/000538608","DOIUrl":"10.1159/000538608","url":null,"abstract":"<p><strong>Introduction: </strong>Adolescence involves significant reorganization within the medial prefrontal cortex (mPFC), including modifications to inhibitory neurotransmission that may be mediated through parvalbumin (PV) interneurons and their surrounding perineuronal nets (PNNs). These developmental changes, which can result in increased PV neuron activity in adulthood, may be disrupted by drug use resulting in lasting changes in mPFC function and behavior. Methamphetamine (METH), which is a readily available drug used by some adolescents, increases PV neuron activity and could influence the activity-dependent maturational process of these neurons.</p><p><strong>Methods: </strong>In the present study, we used male and female Sprague Dawley rats to test the hypothesis that METH exposure influences PV and PNN expression in a sex- and age-specific manner. Rats were injected daily with saline or 3.0 mg/kg METH from early adolescence (EA; 30-38 days old), late adolescence (LA; 40-48 days old), or young adulthood (60-68 days old). One day following exposure, effects of METH on PV cell and PNN expression were assessed using immunofluorescent labeling within the mPFC.</p><p><strong>Results: </strong>METH exposure did not alter male PV neurons or PNNs. Females exposed in early adolescence or adulthood had more PV expressing neurons while those exposed in later adolescence had fewer, suggesting distinct windows of vulnerability to changes induced by METH exposure. In addition, females exposed to METH had more PNNs and more intense PV neuron staining, further suggesting that METH exposure in adolescence uniquely influences development of inhibitory circuits in the female mPFC.</p><p><strong>Conclusions: </strong>This study indicates that the timing of METH exposure, even within adolescence, influences its neural effects in females.</p>","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140319851","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":"Development of A New Scoring System in Higher Animals for Testing Cognitive Function in the Newborn Period: Effect of Prenatal Hypoxia-Ischemia.","authors":"Zhongjie Shi, Nadiya Sharif, Kehuan Luo, Sidhartha Tan","doi":"10.1159/000538607","DOIUrl":"10.1159/000538607","url":null,"abstract":"<p><p>Introduction Enhanced models for assessing cognitive function in the neonatal period are imperative in higher animals. Postnatal motor deficits, characteristic of cerebral palsy, emerge in newborn kits within our prenatal-rabbit model of hypoxia-ischemia (HI). In humans, prenatal HI leads to intellectual disability and cerebral palsy. In a study examining cognitive function in newborn rabbits, we explored several questions. Is there a distinction between conditioned and unconditioned kits? Can the kits discern the human face or the lab coat? Do motorically-normal kits, born after prenatal HI, exhibit cognitive deficits? Methods The conditioning protocol was randomly assigned to kits from each litter. For conditioning, the same human, wearing a lab coat, fed the rabbit kits for 9 days before the cognitive test. The 6-arm radial maze was chosen for its simplicity and ease of use. Normally appearing kits, born after uterine ischemia at 79% or 92% term in New Zealand White rabbits, were compared to Naïve kits. On postpartum day 22/23 or 29/30, the 6-arm maze helped determine if the kits recognized the original feeder from bystander (Test-1) or the lab coat on bystander (Test-2). The use of masks of feeder/bystander (Test-3) assessed confounding cues. A weighted score was devised to address variability in entry to maze arms, time, and repeated-trial learning. Results In conditioned kits, both Naïve and HI kits exhibited a significant preference for the face of the feeder, but not the lab coat. Cognitive deficits were minimal in normal-appearing HI kits. Conclusion The weighted score system was amenable to statistical manipulation.</p>","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140319850","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":"The Intersection of Epigenetic Alterations and Developmental State in Pediatric Ependymomas.","authors":"Alisha Simone Kardian, Stephen Mack","doi":"10.1159/000537694","DOIUrl":"10.1159/000537694","url":null,"abstract":"<p><strong>Background: </strong>Ependymomas are the third most common brain cancer in children and have no targeted therapies. They are divided into at least 9 major subtypes based on molecular characteristics and major drivers and have few genetic mutations compared to the adult form of this disease, leading to investigation of other mechanisms.</p><p><strong>Summary: </strong>Epigenetic alterations such as transcriptional programs activated by oncofusion proteins and alterations in histone modifications play an important role in development of this disease. Evidence suggests these alterations interact with the developmental epigenetic programs in the cell of origin to initiate neoplastic transformation and later disease progression, perhaps by keeping a portion of tumor cells in a developmental, proliferative state.</p><p><strong>Key messages: </strong>To better understand this disease, research on its developmental origins and associated epigenetic states needs to be further pursued. This could lead to better treatments, which are currently lacking due to the difficult-to-drug nature of known drivers such as fusion proteins. Epigenetic and developmental states characteristic of these tumors may not just be potential therapeutic targets, but used as a tool to find new avenues of treatment.</p>","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140289465","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":"Upstream stimulating factor 2 aggravates neuropathic pain induced in spinal nerve ligation-induced mice via regulating SNHG5/miR-181b-5p.","authors":"Mi Chen, Yang Yang, Jiatian Cui, Li Qiu, Xiaohua Zou, Xianggang Zeng","doi":"10.1159/000538178","DOIUrl":"https://doi.org/10.1159/000538178","url":null,"abstract":"<p><strong>Background: </strong>Upstream stimulating factor 2 (USF2) belongs to basic-Helix-Loop-Helix-Leucine Zipper transcription factor family, regulating expression of genes involved in immune response or energy metabolism network. Role of USF2 in neuropathic pain was evaluated.</p><p><strong>Methods: </strong>Mice were intraspinally injected with adenovirus for knockdown of USF2 (Ad-shUSF2), and then subjected to spinal nerve ligation (SNL) to induce neuropathic pain. Distribution and expression of USF2 was detected by western blot and immunofluorescence. Mechanical and thermal pain sensitivity were examined by paw withdrawal thresholds (PWT) and paw withdrawal latency (PWL). Chromatin immunoprecipitation (ChIP) and luciferase activity assays were performed to detect binding ability between USF2 and SNHG5.</p><p><strong>Results: </strong>The expression of USF2 was elevated and colocalized with astrocytes and microglia in L5 dorsal root ganglion (DRG) of SNL-induced mice. Injection of Ad-shUSF2 attenuated SNL-induced decrease of PWT and PWL in mice. Knockdown of USF2 increased level of IL-10, but decreased TNF-α, IL-1β, and IL-6 in SNL-induced mice. Silence of USF2 enhanced protein expression of CD206, while reduced expression of CD16 and CD32 in SNL-induced mice. USF2 bind to promoter of SNHG5, and weakened SNL-induced up-regulation of SNHG5. SNHG5 bind to miR-181b-5p, and miR-181b-5p to interact with CXCL5.</p><p><strong>Conclusion: </strong>Silence of USF2 ameliorated neuropathic pain, suppressed activation of M1 microglia and inhibited inflammation in SNL-induced mice through regulation of SNHG5/miR-181b-5p/CXCL5 axis. Therefore, USF2/SNHG5/miR-181b-5p/CXCL5 might be a promising target for neuropathic pain. However, the effect of USF2/SNHG5/miR-181b-5p/CXCL5 on neuropathic pain should also be investigated in further research.</p>","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140112098","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":"Identification of differentially expressed miRNA in the rat hippocampus during adolescence through an epigenome-wide analysis.","authors":"Ana Vázquez-Ágredos, Paula Rovira, Blanca Gutiérrez, Fernando Gámiz, Milagros Gallo","doi":"10.1159/000538168","DOIUrl":"https://doi.org/10.1159/000538168","url":null,"abstract":"<p><strong>Introduction: </strong>Epigenetic mechanisms involving microRNAs (miRNAs) play a fundamental role in many biological processes, particularly during prenatal and early postnatal development. Their role in adolescent brain development, however, has been poorly described. The present study aims to explore miRNA expression in the hippocampus during adolescence compared to adulthood in rats.</p><p><strong>Method: </strong>The brains of female and male Wistar rats were extracted and the hippocampus was freshly dissected at postnatal day 41 (adolescence) and postnatal day 98 (adulthood). An epigenome-wide analysis was conducted to identify the miRNAs significantly expressed in adolescence compared to adulthood. Additionally, target genes of such miRNAs were considered to perform an exploratory gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis.</p><p><strong>Results: </strong>We identified 16 differentially expressed miRNAs in adolescent male rats compared with adult male rats, and 4 differentially expressed miRNAs in adolescent females compared with adult females. Enrichment analysis reinforced that the target genes found are related to neurodevelopmental processes such as cell proliferation, cell migration and nervous system development.</p><p><strong>Conclusion: </strong>Our findings suggest a complex pattern of miRNA expression during adolescence, which differs from that in adulthood. The differential expression of miRNA in the hippocampus during adolescence may be associated with the late developmental changes occurring in this brain region. Furthermore, the observed sex differences in miRNA expression patterns indicate potential sexual differentiation in hippocampal development. Further comprehensive investigations are needed to elucidate the roles of miRNA in normal brain development.</p>","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140029498","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":"Septotemporal variation of information processing in the hippocampus of Fmr1 KO rat.","authors":"Leonidas J Leontiadis, Panagiotis Felemegkas, George Trompoukis, Giota Tsotsokou, Athina Miliou, Evangelia Karagianni, Pavlos Rigas, Costas Papatheodoropoulos","doi":"10.1159/000537879","DOIUrl":"https://doi.org/10.1159/000537879","url":null,"abstract":"<p><p>Introduction Fragile X messenger ribonucleoprotein (FMRP) is a protein involved in many neuronal processes in the nervous system including the modulation of synaptic transmission. Loss of FMRP produces the fragile X syndrome (FXS), a neurodevelopmental disorder affecting synaptic and neuronal function and producing cognitive impairments. However, the effects of FXS on short-term processing of synaptic inputs and neuronal outputs in the hippocampus have not yet been sufficiently clarified. Furthermore, it is not known whether dorsal and ventral hippocampus are affected similarly or not in FXS. Method We used a Fmr1 knock-out (KO) rat model of FXS and recordings of evoked field potentials from the CA1 field of transverse slices from both the dorsal and the ventral hippocampus of adult rats. Results Following application of a frequency stimulation protocol consisting of a ten-pulse train and recordings of fEPSP, we found that the dorsal but not ventral KO hippocampus shows altered short-term synaptic plasticity. Furthermore, applying the frequency stimulation protocol and recordings of population spikes, both segments of the KO hippocampus display altered short-term neuronal dynamics. Conclusions These data suggest that short-term processing of synaptic inputs is affected in the dorsal, not ventral FXS hippocampus, while short-term processing of neuronal output is affected in both segments of the FXS hippocampus in a similar way. These FXS-associated changes may have significant impact on the functions of the dorsal and ventral hippocampus in individuals with FXS.</p>","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139900732","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":"Sex-specific behavioural deficits in adulthood following acute activation of the GABAA receptor in the neonatal mouse.","authors":"Ane Goikolea-Vives, Cathy Fernandes, Michael S C Thomas, Claire Thornton, Helen B Stolp","doi":"10.1159/000536641","DOIUrl":"10.1159/000536641","url":null,"abstract":"<p><strong>Introduction: </strong>Sex differences exist in the prevalence of neurodevelopmental disorders (NDDs). Part of the aetiology of NDDs has been proposed to be alterations in the balance between excitatory and inhibitory neurotransmission, leading to the question of whether males and females respond differently to altered neurotransmitter balance. We investigated whether pharmacological alteration of GABAA signalling in early development results in sex-dependent changes in adult behaviours associated with NDDs.</p><p><strong>Methods: </strong>Male and female C57BL/6J mice received intraperitoneal injections of 0.5mg/kg muscimol or saline on postnatal days (P) 3-5 and were subjected to behavioural testing, specifically open field, light dark box, marble burying, sucralose preference, social interaction and olfactory habituation/dishabituation tests between P60-90.</p><p><strong>Results: </strong>Early postnatal administration of muscimol resulted in reduced anxiety in the light dark box test in both male and female adult mice. Muscimol reduced sucralose preference in males, but not females, whereas female mice showed reduced social behaviours. Regional alterations in cortical thickness were observed in the weeks following GABAA receptor activation, pointing to an evolving structural difference in the brain underlying adult behaviour.</p><p><strong>Conclusions: </strong>We conclude that activation of the GABAA receptor in the first week of life resulted in long-lasting changes in a range of behaviours in adulthood following altered neurodevelopment. Sex of the individual affected the nature and severity of these abnormalities, explaining part of the varied pathophysiology and neurodevelopmental diagnosis that derive from excitatory/inhibitory imbalance.</p>","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139703904","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}