Frontiers in Cellular Neuroscience最新文献

{"title":"Voluntary running reduces loss of PTEN-deficient Purkinje cells, modulates their metabolic signaling, and improves motor deficits in mice.","authors":"Siena R Brazier, Kathryn L Ditrano, David S Betancourt-Trompa, Grace A Belt, Olivia R Barbarini, Ursula M Pena, Izabella M Espinal-San Miguel, Ana V Rodriguez, Carly N Immerman, Cameron J Petrelli, Reagan R Dennett, Rohan Reddy, Daniel J Greenspan, Lindsay J Walsh, Connor Enestvedt, Campbell M Bridges, Pamela A Snodgrass-Belt, Ileana Soto","doi":"10.3389/fncel.2026.1865302","DOIUrl":"10.3389/fncel.2026.1865302","url":null,"abstract":"<p><p>Dysregulation of the PTEN-mTORC1 signaling pathway disrupts cellular metabolism and contributes to neurodevelopmental disorders, including autism spectrum disorder (ASD). In cerebellar Purkinje cells (PCs), PTEN deficiency leads to hyperactivation of mTORC1, impaired energy homeostasis, and progressive neuronal degeneration. Given that physical exercise is a potent modulator of metabolic signaling, we investigated whether voluntary running could restore metabolic balance and ameliorate cellular and behavioral deficits in a mouse model of PC-specific PTEN deficiency. Using <i>Pten</i> conditional knockout (cKO) mice, we evaluated the effects of voluntary running on motor coordination, metabolic signaling, neuronal morphology and preservation, and social and non-social behaviors. Behavioral analyses revealed that running significantly improved motor performance in <i>Pten</i> cKO mice. At the cellular level, voluntary running increased phosphorylated AMP-activated protein kinase (pAMPK) and restored mitochondrial and lysosomal content in PC dendrites from <i>Pten</i> cKO mice. Unexpectedly, running further enhanced mTORC1 activity in <i>Pten</i> cKO mice, as indicated by increased pS6R immunoreactivity, suggesting a complex interplay between anabolic and catabolic pathways. Behavioral analyses further revealed that voluntary running reduced sex-dependent differences in social and non-social behaviors observed in sedentary <i>Pten</i> cKO mice. Despite persistent dendritic hypertrophy and synaptic VGLUT2 alterations, running reduced PC loss and partially normalized microglial morphology and activation. Together, these findings demonstrate that voluntary running improves metabolic homeostasis and neuronal preservation in <i>Pten</i> cKO mice, even in the presence of sustained mTORC1 activation. Our results highlight the therapeutic potential of physical activity in modulating metabolic pathways and mitigating neurodevelopmental pathology.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1865302"},"PeriodicalIF":4.4,"publicationDate":"2026-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13437335/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148677704","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: TAT-HSP27 peptide improves neurologic deficits and reduces apoptosis after experimental subarachnoid hemorrhage.","authors":"Xiao-Yan Zhou, Jing-Yi Sun, Wei-Qi Wang, Shu-Xian Li, Han-Xia Li, Hui-Juan Yang, Ming-Feng Yang, Hui Yuan, Zong-Yong Zhang, Bao-Liang Sun, Jin-Xiang Han","doi":"10.3389/fncel.2026.1911280","DOIUrl":"10.3389/fncel.2026.1911280","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.3389/fncel.2022.878673.].</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1911280"},"PeriodicalIF":4.4,"publicationDate":"2026-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13435768/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148673316","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial: Role of microbiota in neurocognitive disorders: a developmental origin perspective.","authors":"Nouha Bouayed Abdelmoula, Hayet Sellami, Sourour Neji, Fabian M Feiguin, Balkiss Abdelmoula","doi":"10.3389/fncel.2026.1917819","DOIUrl":"https://doi.org/10.3389/fncel.2026.1917819","url":null,"abstract":"","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1917819"},"PeriodicalIF":4.4,"publicationDate":"2026-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13429453/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148668512","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gut-brain axis mechanisms of remote brain dysfunction after traumatic spinal cord injury: immune inflammation, the vagus nerve, and neuroendocrine pathways.","authors":"Yutong Liu, Haifeng Zhang, Bingkai Ren","doi":"10.3389/fncel.2026.1879641","DOIUrl":"10.3389/fncel.2026.1879641","url":null,"abstract":"<p><p>Traumatic spinal cord injury (SCI) has traditionally been regarded as a central nervous system injury mainly confined to the injured segment. However, increasing evidence indicates that SCI can also induce neuroinflammation, cognitive decline, and emotional disorders in remote brain regions, suggesting that its pathological impact is systemic rather than purely local. Remote brain dysfunction after SCI is unlikely to be driven by a single pathway, but may arise from the combined effects of systemic inflammation, autonomic imbalance, neuroendocrine dysregulation, and disruption of intestinal homeostasis. Unlike previous reviews that mainly discuss SCI-associated gut dysbiosis, neuroinflammation, or gut-brain communication separately, this review organizes SCI-related intestinal abnormalities around the concept of \"gut-derived pathological signals\" and further distinguishes direct SCI evidence from cross-disease mechanistic evidence and proposed mechanistic inference. Specifically, we summarize how intestinal dysmotility, microbial metabolic remodeling, abnormalities in short-chain fatty acids (SCFAs), barrier vulnerability, and mucosal immune imbalance after SCI may generate persistent pathological signals. We then analyze how these signals may affect the central nervous system through an immune-inflammatory main axis, a vagal neural relay branch, and a neuroendocrine modulatory branch, ultimately converging on a common downstream brain effector stage characterized by blood-brain barrier impairment, neuroinflammation, synaptic plasticity deficits, and dysfunction of key brain regions such as the hippocampus and medial prefrontal cortex (mPFC). Based on this cascade, we propose a stratified intervention framework involving upstream restoration of intestinal homeostasis, midstream regulation of interorgan transmission pathways, and downstream protection of brain effector mechanisms. Overall, this review provides an evidence-stratified gut-brain axis framework for understanding remote brain dysfunction after SCI and highlights the need for SCI-specific temporal mapping and pathway-selective causal validation.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1879641"},"PeriodicalIF":4.4,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13414276/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148619075","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial: Emerging mechanisms in neuroinflammation: potential therapeutic targets for neurodegenerative diseases.","authors":"Junhui Wang, Hongxing Wang, Dirk M Hermann","doi":"10.3389/fncel.2026.1908534","DOIUrl":"10.3389/fncel.2026.1908534","url":null,"abstract":"","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1908534"},"PeriodicalIF":4.4,"publicationDate":"2026-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13395715/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148583867","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Case Report: A case of paraneoplastic autoimmune encephalitis with concurrent anti-GABABR and anti-SOX1 antibody positivity.","authors":"Feng Liu, Ye-Han Jiang, Yu-Fang Hu, Jin-Guan Qin, Guang-Sheng Liu","doi":"10.3389/fncel.2026.1816167","DOIUrl":"10.3389/fncel.2026.1816167","url":null,"abstract":"<p><strong>Background: </strong>Paraneoplastic autoimmune encephalitis (PAE) is most commonly associated with small cell lung cancer (SCLC). Anti-<i>γ</i>-aminobutyric acid B receptor (GABABR) antibodies underlie a treatable limbic syndrome, whereas anti-SRY-box transcription factor 1 (SOX1) antibodies serve as high-specificity onconeural biomarkers of SCLC-driven autoimmunity. The sequential emergence of these two antibodies during the longitudinal course of a single patient has rarely been documented.</p><p><strong>Case presentation: </strong>A 75-year-old man presented with episodic impaired consciousness, behavioural disturbance and rapid cognitive decline. Brain MRI showed bilateral hippocampal signal abnormalities. A cell-based assay (CBA) detected anti-GABABR antibodies at high titre in serum (1:3200) and cerebrospinal fluid (CSF; 1:1000), while a tissue-based assay (TBA) on rat brain confirmed a neuronal cell-surface staining pattern; the full paraneoplastic panel, including anti-SOX1, was negative, and initial tumour screening was unrevealing. A diagnosis of anti-GABABR encephalitis (initially regarded as non-paraneoplastic) was made and the patient improved with intravenous immunoglobulin (IVIG), high-dose corticosteroids and maintenance mycophenolate mofetil. During a refractory second relapse 5 months later, repeat CBA showed rising anti-GABA_BR titres (serum 1:10,000; CSF 1:1000) and newly positive anti-SOX1 antibodies (serum 1:100; CSF 1:1); a previously occult right superior mediastinal mass radiologically compatible with SCLC was identified on repeat chest CT. The diagnosis was revised to anti-GABA_BR/anti-SOX1 dual-antibody PAE (probable PNS by 2021 PNS-Care criteria). The family declined biopsy, PET/CT and antitumour therapy because of advanced age and frailty; repeated IVIG with continued immunosuppression achieved partial clinical stabilisation with persistent cognitive impairment.</p><p><strong>Conclusion: </strong>Apparently isolated anti-GABA_BR encephalitis can evolve into dual anti-GABABR/anti-SOX1 paraneoplastic disease, with the second antibody heralding an occult SCLC. Repeating both CBA-based and intracellular antibody panels at every clinical relapse, together with repeat thoracic imaging, is essential to avoid missing an evolving paraneoplastic aetiology.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1816167"},"PeriodicalIF":4.4,"publicationDate":"2026-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13391288/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148577577","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial: Cell therapy in the central nervous system and its crosstalk with the immune system.","authors":"María Norte-Munoz, Raquel Boia, David García-Bernal, Marta Agudo-Barriuso","doi":"10.3389/fncel.2026.1916972","DOIUrl":"https://doi.org/10.3389/fncel.2026.1916972","url":null,"abstract":"","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1916972"},"PeriodicalIF":4.4,"publicationDate":"2026-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13391314/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148577553","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ethanol selectively disrupts neuronal microexon regulation and chromatin marks in PC12 cells.","authors":"Montserrat Olivares-Costa, Pascal Jorratt, Camila Morales, Sebastián F Estay, Adrian R Krainer, María Estela Andrés, Paola A Haeger","doi":"10.3389/fncel.2026.1854045","DOIUrl":"10.3389/fncel.2026.1854045","url":null,"abstract":"<p><strong>Introduction: </strong>Exposure to alcohol (ethanol) is the most common toxic insult during human development and is a teratogenic agent associated with abnormalities ranging from behavioral disorders to fetal alcohol syndrome. Ethanol disrupts gene regulatory programs crucial for neuronal identity, including alternative splicing. A distinctive feature of developing neuronal transcriptomes is the high prevalence of microexon inclusion, which consists of short exonic sequences ranging from 3 to 51 nucleotides. However, the impact of ethanol on microexon inclusion remains poorly understood.</p><p><strong>Methods: </strong>In this study, we investigated whether ethanol exposure disrupts neuron-specific alternative splicing programs during neuronal differentiation. To this end, PC12 cells were exposed to 50 mM ethanol throughout five days of NGF-induced differentiation, alongside undifferentiated control cells, to analyze mRNA and protein expression dynamics of key splicing regulators and neurodevelopmental targets.</p><p><strong>Results: </strong>Our data show that in undifferentiated cells, ethanol exposure resulted in a significant reduction in <i>Srrm4</i> expression, while concomitantly increasing <i>Srrm3</i> mRNA levels, consistent with reduced neuron-specific microexon inclusion of the intersectin 1 (<i>Itsn</i>1) mRNA. While undifferentiated PC12 cells primarily express the canonical variants of lysine-specific demethylase 1 (LSD1) and PHD finger protein 21A (PHF21A), differentiation triggers the inclusion of microexons 8a and 14, generating the neuron-specific isoforms neuronal LSD1 and PHF21A, respectively. Under differentiated conditions, ethanol exposure increased neurite length but did not affect the mRNA levels of the neuronal variants of <i>Lsd1</i>, <i>Phf21a,</i> or <i>Itsn1</i>. Notably, ethanol exposure significantly increased the levels of LSD1 protein and its associated histone substrate, H3K4me2, in differentiated PC12 cells.</p><p><strong>Discussion: </strong>Taken together, these findings suggest that ethanol exposure modulates post-transcriptional and chromatin-based mechanisms during neuronal commitment and differentiation. This selective disruption highlights distinct molecular pathways that may contribute to persistent neurodevelopmental alterations relevant to alcohol use disorder, providing new insights into the teratogenic mechanisms of ethanol on the developing nervous system.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1854045"},"PeriodicalIF":4.4,"publicationDate":"2026-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13388176/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148561284","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Up regulated hippocampal insulin pathway and oxidative stress are related to opposite changes in olfaction and episodic memory in a compensatory metabolic syndrome model in rats.","authors":"Pedro Isauro Clavel-Pérez, Bryan V Phillips-Farfán, Luz Camacho-Castillo, Ana Laura Calderón-Garcidueñas, Karla Carvajal","doi":"10.3389/fncel.2026.1845387","DOIUrl":"10.3389/fncel.2026.1845387","url":null,"abstract":"<p><p>Insulin resistance, a major component of metabolic syndrome (MetS), is involved in phosphorylated tau and beta amyloid buildup, linking MetS to neurodegenerative processes, e.g., Alzheimer's disease. One of the initial signs of neurodegeneration, in diseases such as Parkinson's and Alzheimer's, is olfactory dysfunction. Accordingly, in previous reports we found that high carbohydrate diet based on 30% sucrose in drinking water, increased visceral fat and insulin resistance, leading to an augment of oxidative stress and reduced brain energy metabolism, upregulating amyloidogenic genes (<i>APP</i> and <i>BACE1</i>) in hypothalamus and hippocampus. Thus, herein we comparatively evaluated the effect of sucrose induced MetS on episodic memory, olfaction, protein expression in amyloidogenic and insulin pathways, lipoperoxidation, antioxidant and BACE1 enzymatic activity between the hippocampus and olfactory bulb in male Wistar rats. Also, cellular structure of the olfactory bulb was analyzed. After 24 weeks of 30% sucrose consumption, we found preserved performance in a memory test; decreased hippocampal expression of APP and hyperactivation of the insulin pathway, low levels of lipoperoxidation, and high activity of antioxidant and BACE1 enzymes. Olfactory dysfunction was present in MetS rats, accompanied by morphological alterations in the olfactory bulb along with BACE1 increased activity. Thus, chronic high-sucrose consumption may prime the brain for neurodegenerative processes by modulating insulin signaling, oxidative stress homeostasis and amyloidogenic pathways in a region-dependent manner, with the olfactory system emerging as an early and sensitive target of metabolic dysfunction.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1845387"},"PeriodicalIF":4.4,"publicationDate":"2026-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13384890/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148548580","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Blood-brain barrier integrity disruption linked to brain lesions and relapse prediction in Southern Chinese anti-NMDAR encephalitis patients.","authors":"Lingling Tong, Hui Chen, Yanzhen Huang, Wenlin Jiang, Wen Huang","doi":"10.3389/fncel.2026.1872425","DOIUrl":"10.3389/fncel.2026.1872425","url":null,"abstract":"<p><strong>Objective: </strong>This study aims to investigate the characteristic brain abnormalities in Southern Chinese patients with anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis and to explore their association with blood-brain barrier (BBB) disruption and clinical implications.</p><p><strong>Methods: </strong>This study retrospectively analyzed 80 cases of anti-NMDAR encephalitis. Patients were divided into a group with abnormal brain MRI (<i>n</i> = 35) and a group with normal brain MRI (<i>n</i> = 45). The extent of BBB disruption was assessed using the albumin quotient (Qalb), defined as the cerebrospinal fluid (CSF)-to-serum albumin ratio. Disease severity was evaluated using the modified Rankin Scale (mRS). Patients were further categorized into a relapse group and a non-relapse group based on post-discharge relapse status. Key predictive factors were identified through multivariate regression analysis.</p><p><strong>Results: </strong>Brain MRI abnormalities were observed in 43.75% (35/80) of the anti-NMDAR encephalitis patients. Among these, typical MRI findings of anti-NMDAR encephalitis abnormalities were present in 26 patients (32.5% of the total cohort). Brain MRI abnormalities were significantly associated with abnormal BBB permeability (42.9% vs. 13.3%, <i>p</i> = 0.003). Multivariate logistic regression analysis identified two independent predictive factors for brain MRI abnormalities: BBB dysfunction (OR = 4.088, 95% CI: 1.031-16.213, <i>p</i> = 0.045) and time from symptom onset to first-line immunotherapy (OR = 1.041, 95% CI: 1.001-1.083, <i>p</i> = 0.045). Furthermore, receiver operating characteristic (ROC) curve analysis demonstrated that the combined model of BBB dysfunction and time from symptom onset to first-line immunotherapy exhibited favorable predictive performance, with an area under the curve (AUC) of 0.745 (95% CI: 0.634-0.857). BBB dysfunction was closely associated with multi-regional cerebral involvement (<i>p</i> = 0.002). Further Spearman correlation analysis showed that impaired BBB integrity correlated with greater MRI lesion severity and broader lesional distribution (<i>p</i> = 0.003). In binary logistic regression analysis adjusting for mRS score, positive oligoclonal bands (OCBs) were identified as a potential predictor of relapse, with an OR of 7.991 (95% CI: 1.242-51.411, <i>p</i> = 0.029). The AUC was 0.730 (95% CI: 0.542-0.918), indicating moderate predictive performance.</p><p><strong>Conclusion: </strong>Abnormal BBB permeability is an independent risk factor for structural abnormalities on brain MRI and is positively correlated with the extent of MRI abnormalities. CSF OCB positivity is a risk factor for disease relapse. These findings may inform brain injury assessment, relapse risk stratification, and individualized treatment in patients with anti-NMDAR encephalitis.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1872425"},"PeriodicalIF":4.4,"publicationDate":"2026-07-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13381047/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148520044","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}