{"title":"Colony Stimulating Factor 1 Receptor/c-Myc Axis Promotes Microglial M2 Polarization to Augment Proliferation of Glioma Cells","authors":"F. Fu, C. H. Du, Q. Chen, L. Tian","doi":"10.1134/s1819712425700953","DOIUrl":"https://doi.org/10.1134/s1819712425700953","url":null,"abstract":"M2-polarized microglial phenotype has been demonstrated to exert a pro-tumor immune response. However, its underlying mechanism in the development and growth of glioma remains unclear. Here, we studied the regulation and mechanism of colony stimulating factor 1 receptor (CSF-1R)/c-Myc axis on microglial polarization, as well as the proliferation of glioma cells. In this study, the abundance of CSF-1R was boosted in glioma tissues, and level of CSF-1R was connected with the prognosis of patients with glioma. Lack of CSF-1R expression abridged M2 polarization in microglia. Besides, repression of CSF-1R expression blocked the promotive effect of M2 microglia on proliferation of glioma cells. In addition, c-Myc knockdown could neutralize the effect of CSF-1R overexpression on microglial polarization and proliferation of glioma cells. The CSF-1R/c-Myc axis could stimulate secretion of pro-tumoral factors by M2 microglia. Downregulation of CSF-1R restrained the promoting effect of M2 microglia on the proliferation of glioma cells in vivo. In conclusion, these data suggested that CSF-1R/c-Myc axis promoted microglial M2 phenotype to boost proliferation of glioma cells, which further deepens our understanding on the role of microglia-associated tumor microenvironment in tumorigenesis of glioma.","PeriodicalId":19119,"journal":{"name":"Neurochemical Journal","volume":"19 4","pages":"916-925"},"PeriodicalIF":0.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147921595","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}
I. I. Babkina, I. G. Savinkova, A. S. Artyukhov, L. R. Gorbacheva
{"title":"Effect of Gestational Diabetes in Female Rats on Brain Astrocyte Functions in Their Offspring","authors":"I. I. Babkina, I. G. Savinkova, A. S. Artyukhov, L. R. Gorbacheva","doi":"10.1134/s1819712425700837","DOIUrl":"https://doi.org/10.1134/s1819712425700837","url":null,"abstract":"Gestational diabetes mellitus (GDM) in the mother may impair fetal brain development through epigenetic mechanisms and metabolic dysregulation of glial cells. The present study aims to investigate functional changes in astrocytes derived from the brains of neonatal rats born to females with streptozotocin-induced GDM. It was found that maternal GDM not only led to hypoglycemia in newborn pups but also increased the proliferation of primary cortical astrocytes under glucose deprivation compared to control. Astrocyte proliferation in response to activation of protease-activated receptor 1 (PAR1) by a peptide agonist did not differ in the GDM and control groups. Astrocyte proliferation was increased in glucose-containing medium, while glucose deprivation either had no effect or suppressed proliferation. Interestingly, noticeable lipopolysaccharide (LPS)-induced activation of primary astrocytes observed in the control group was completely abolished in the GDM group, as indicated by IL-6 secretion levels. These findings suggest that intrauterine exposure to GDM may program long-term alterations in the metabolic and immune activity of fetal astrocytes.","PeriodicalId":19119,"journal":{"name":"Neurochemical Journal","volume":"19 4","pages":"791-799"},"PeriodicalIF":0.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147905185","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}
Min Cheng, Yue Yu, Chun Xiao, Hongbin Liu, Shanjun Chen, Fei‐Ji Sun
{"title":"Expression of CD200 and Its Influences on Epileptogenesis in a Mouse Model of Focal Cortical Dysplasia","authors":"Min Cheng, Yue Yu, Chun Xiao, Hongbin Liu, Shanjun Chen, Fei‐Ji Sun","doi":"10.1134/s1819712425700230","DOIUrl":"https://doi.org/10.1134/s1819712425700230","url":null,"abstract":"Focal cortical dysplasia (FCD) is one of the major causes of refractory epilepsy. Evidence suggests that neuroinflammation contributes to the epileptogenesis of FCD. Downregulation of cluster of differentiation 200 (CD200) leads to neuroinflammation. We previously reported decreased expression of CD200 in brain lesions of FCD patients. In this study, we examined the expression and influences of CD200 on epileptogenesis in a mouse model of FCD. Video monitoring revealed an increased number of motor seizures in cd200 knockout (cd200–/–) FCD mice compared to the wild-type (WT) FCD mice, and CD200 fusion protein (CD200 Fc) downregulated the number of motor seizures in WT FCD mice. Western blotting results displayed a decreased protein expression of CD200 in FCD mice versus the control groups (CTX), and the relative protein level of CD200 is negatively correlated with motor seizure occurrence. Immunohistochemistry and double-labeled immunofluorescence showed that CD200 was expressed in neurons and astrocytes, not in microglia. Correlation analysis revealed a negative correlation between the immunoreactivity (IR) scores of CD200 and the number of ionized calcium binding adaptor molecule 1 (IBA1)-positive microglia. Enzyme-linked immune sorbent assays (ELISAs) showed that the production of interleukin-1β (IL-1β), IL-6, and IL-17 was upregulated in cd200–/– FCD compared to the CTX. In addition, CD200 Fc could downregulate the expression of IL-1β, IL-6, and IL-17, and up-regulate the expression of downstream of tyrosine kinase 2 (Dok2), which is the downstream molecular of the CD200 pathway. Our findings suggest that CD200 may play a pivotal role in the epileptogenesis of FCD.","PeriodicalId":19119,"journal":{"name":"Neurochemical Journal","volume":"19 2","pages":"196-205"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147897908","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}
Lingli Yang, Duo Gao, Yao Wang, Minghong Xu, Yingchao Wang
{"title":"Diagnostic Significance of Serum miR-483-5p in Cerebrovascular Disease and Its Role in the Prognosis of Interventional Therapy","authors":"Lingli Yang, Duo Gao, Yao Wang, Minghong Xu, Yingchao Wang","doi":"10.1134/s1819712425700308","DOIUrl":"https://doi.org/10.1134/s1819712425700308","url":null,"abstract":"Cerebrovascular disease (CVD) represents the primary contributor to disability and premature mortality among the population of China. The investigation of particular biomarkers aims to forecast the occurrence of ischemic CVD (ICVD), indicate the disease severity and identify individuals of poor prognosis so as to develop effective molecular tools. This study employed quantitative PCR and Pearson correlation analysis to assess the expression levels of miR-483-5p in the serum of ICVD patients and its association with the NIHSS score. The Chi-square test was utilized to investigate the relationship between miR-483-5p and clinical features. The logistic regression and ROC analysis were conducted to identify risk factors associated with the ICVD occurrence and the diagnostic efficacy of miR-483-5p. The prognostic outcome of ICVD patients was analyzed using the Chi-square test. A Cox regression model was employed to identify impact factors of poor prognosis. Survival curves for ICVD patients categorized by different levels of miR-483-5p were generated using the Kaplan–Meier method. miR-483-5p exhibited a significant upregulation in the serum of ICVD patients and demonstrated a strong positive correlation with the NIHSS score. The expression levels of miR-483-5p were significantly associated with both blood pressure and lipids in ICVD individuals, and miR-483-5p was the most influential risk factor for ICVD occurrence. Additionally, miR-483-5p possessed considerable discriminatory power in identifying ICVD. Both the NIHSS and miR-483-5p levels were significantly linked to poor prognosis in ICVD patients, with those who exhibited lower levels of miR-483-5p tending to have better prognoses. The miR-483-5p could potentially be a promising biomarker for ICVD. It could be applied in both the diagnosis of ICVD and the identification of individuals at risk for poor prognosis.","PeriodicalId":19119,"journal":{"name":"Neurochemical Journal","volume":"19 2","pages":"245-255"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147902335","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}
Peng-Hui Du, Qiqi Wu, Zihui Xu, Zhihong Xu, Qing-Liu Zheng
{"title":"Diagnostic and Prognostic Value of miR-140-5p in Patients with ICU-Acquired Weakness","authors":"Peng-Hui Du, Qiqi Wu, Zihui Xu, Zhihong Xu, Qing-Liu Zheng","doi":"10.1134/s1819712425700138","DOIUrl":"https://doi.org/10.1134/s1819712425700138","url":null,"abstract":"There is a lack of comprehensive research on intensive care unit acquired weakness (ICU-AW), which hinders the early detection and diagnosis of this condition. This study aims to investigate the diagnostic and prognostic significance of miR-140-5p in ICU-AW patients and assess its potential utility as a biomarker for ICU-AW. The expression level of miR-140-5p was assessed using real-time quantitative PCR in ICU-AW patients. The diagnostic and prognostic value of miR-140-5p in ICU-AW patients was evaluated through ROC curve, correlation, Cox regression, and Kaplan–Meier survival analysis. Additionally, the target gene of miR-140-5p was predicted, followed by enrichment analysis on the Gene Ontology (GO) function and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway. The expression of miR-140-5p was up-regulated in ICU-AW patients and showed a significant association with MRC and SOFA sores. miR-140-5p demonstrated potential diagnostic utility in discriminating ICU-AW patients from the controls. ICU-AW patients exhibiting low miR-140-5p expression levels tended to have a more favorable prognosis. Enrichment analyzed based on GO and KEGG suggested miR-140-5p might facilitate intercellular communication via exosomes. The miR-140-5p exhibits promise as a potential biomarker for diagnosing and prognosticating the outcomes of ICU-AW.","PeriodicalId":19119,"journal":{"name":"Neurochemical Journal","volume":"19 1","pages":"116-123"},"PeriodicalIF":0.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147894302","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}
Hongwen Xiao, Yan Huang, Jianrong Zhang, Yue Wu, Qingping Huang, Ying Gao, Jingqin Wang, Chengchen Guo, Shuqing Zhang, Lin Zhang
{"title":"Circulating lncRNA SNHG5 in Cerebral Ischemic Stroke Patients and Its Relationship with Cell Apoptosis and Inflammatory Response","authors":"Hongwen Xiao, Yan Huang, Jianrong Zhang, Yue Wu, Qingping Huang, Ying Gao, Jingqin Wang, Chengchen Guo, Shuqing Zhang, Lin Zhang","doi":"10.1134/s1819712424700545","DOIUrl":"https://doi.org/10.1134/s1819712424700545","url":null,"abstract":"Ischemic stroke is the second leading cause of death and disability after cardiovascular disease worldwide. LncRNA SNHG5 has been studied in acute coronary syndrome and diabetic nephropathy. The specific role of SNHG5 in ischemic stroke is elusive. This study aimed to assess the clinical significance and functional role of SNHG5 in ischemic stroke. Serum expression of SNHG5 in all participants was measured by RT-qPCR. The diagnostic and prognostic potential of SNHG5 in ischemic stroke was assessed by ROC and Kaplan–Meier curve analysis. CCK-8 assay, cell apoptotic assay, and ELISA assays were performed to evaluate the role of SNHG5 on cell proliferation, apoptosis, and inflammation response in the PC12 ischemic stroke cell model, respectively. Compared to non-ischemic stroke individuals, serum SNHG5 expression was increased in ischemic stroke patients. The raised expression of SNHG5 could differentiate ischemic stroke patients from non-ischemic stroke individuals with a relatively high sensitivity and specificity. SNHG5 was positively associated with NIHSS score and patients’ poor prognosis. SNHG5 expression was a risk factor for ischemic stroke. Furthermore, silencing SNHG5 could effectively ameliorate cell proliferation, apoptosis, and inflammatory response caused by ischemic stroke. Circulating serum SNHG5 expression is upregulated and has potential as a diagnostic and prognostic marker in ischemic stroke. Silencing SNHG5 may alleviate the damage and inflammation response of the ischemic stroke cell model.","PeriodicalId":19119,"journal":{"name":"Neurochemical Journal","volume":"18 4","pages":"895-902"},"PeriodicalIF":0.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147907156","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":"miR-92b-3p Regulates Cell Progression and Drug Resistance through Upregulation of CXCL5 in Glioma","authors":"Hao Shen, Ling Xu, Ping Zhang, Chaozhi Yang, Jie Yu, H.T. Wu","doi":"10.1134/s1819712424700120","DOIUrl":"https://doi.org/10.1134/s1819712424700120","url":null,"abstract":"As malignant central nervous system tumors, glioma have strong aggressiveness and drug resistance, which reduces the survival of patients. This study explores the molecular mechanisms that influence the progression and drug resistance of glioma cells, promoting the progress of glioma research. In this study, miR-92b-3p and CXCL5 expression were determined using real-time quantitative polymerase chain reaction in glioma tissues and cells. Pearson correlation analysis was performed for both. Luciferase activity reports were utilized to confirm the targeted association between miR-92b-3p and CXCL5. The effects of miR-92b-3p and CXCL5 on the proliferation and metastasis of glioma cells were investigated by Transwell and CCK-8 assay. Finally, the Temozolomide (TMZ) drug-resistant cell lines were constructed, and apoptosis experiments were conducted to explore the drug-resistant mechanism of glioma cells. It was found that miR-92b-3p was down-regulated in glioma tissues and cells, while CXCL5 expression was up-regulated, with a negative correlation between the two and a targeting of miR-92b-3p to CXCL5. Up-regulation of miR-92b-3p inhibited the invasive activity of glioma cells, while overexpression of CXCL5 reversed this phenomenon. There was a negative correlation between miR-92b-3p expression and the IC50 value of TMZ in glioma. Up or downregulation of miR-92b-3p promoted and inhibited TMZ-induced apoptosis in glioma cells, respectively, whereas regulation of CXCL5 expression reversed this phenomenon. miR-92b-3p can exert anticancer effect by targeting CXCL5. Upregulating miR-92b-3p can inhibit the activity of glioma cells, and promote the apoptosis of glioma cells induced by TMZ.","PeriodicalId":19119,"journal":{"name":"Neurochemical Journal","volume":"18 3","pages":"538-547"},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147883767","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}
M. Yu. Zhanina, T. A. Druzhkova, N. V. Ierusalimsky, E. E. Vladimirova, N. N. Eremina, A. B. Guekht, N. V. Gulyaeva
{"title":"Decreased Volumes of Selected Cortical and Limbic Structures of the Brain Are Associated with Post-Stroke Cognitive and Affective Disorders: Multiple Hit Scenarios?","authors":"M. Yu. Zhanina, T. A. Druzhkova, N. V. Ierusalimsky, E. E. Vladimirova, N. N. Eremina, A. B. Guekht, N. V. Gulyaeva","doi":"10.1134/s1819712424020193","DOIUrl":"https://doi.org/10.1134/s1819712424020193","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Abstract</h3><p>Post-stroke depressive disorders (PSD) and post-stroke cognitive impairments (PCI) are frequent consequences of ischemic stroke (IS). The study was focused on exploring possible associations between relative volumes of cortical and limbic brain structures during the acute period of IS, and changes in biochemical indices of hypothalamic-pituitary-adrenal, sympathoadrenal medullary and inflammatory systems, with the development of PSD or PCI after mild or moderate IS. Patients developing PSD later on had significantly smaller relative volumes of the hippocampus, entorhinal cortex, and temporal pole versus patients without depressive symptoms. PCI development was associated with significantly smaller volumes of temporal pole and supramarginal gyrus versus patients without cognitive changes. Multiple logistic regression analysis showed higher likelihood of developing PSD in patients with smaller temporal pole volume (β0 = 10.9; β = –4.27; <i>p</i> = 0.04) and in-creased salivary α-amylase activity (β0 = –3.55; β = 2.68e-05; <i>p</i> = 0.02). PCI likelihood was higher in patients with smaller supramarginal gyrus volume (β0 = 3.41; β = –0.99; <i>p</i> = 0.047), smaller temporal pole volume (β0 = 3.41; β = –3.12; <i>p</i> = 0. 06), and increased hair cortisol concentration at admission (index of accumulated stress load within a month before IS; β0 = 3.41; β = –0.05; <i>p</i> = 0.08). The data support the hypothesis suggesting predisposition to PSD and PCI and multi hit scenarios of their pathogenesis with IS providing a final hit.</p>","PeriodicalId":19119,"journal":{"name":"Neurochemical Journal","volume":"46 1","pages":""},"PeriodicalIF":0.5,"publicationDate":"2024-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141166422","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":"Changes in the Level of Neurotransmitters and Markers of Neurodegeneration in the Brain of Rats with Experimental Parkinson’s Disease after Therapy with Steroid Glycoalkaloids","authors":"V. A. Voronov, D. I. Pozdnyakov","doi":"10.1134/s1819712424020168","DOIUrl":"https://doi.org/10.1134/s1819712424020168","url":null,"abstract":"<p><b>Abstract</b><i>—</i>Parkinson’s disease is a chronic neurodegenerative disease, one of the pathobiochemical manifestations of which is an imbalance of neurotransmitters in the brain. The aim of this work was to study the effect of glycoalkaloids on changes in the level of neurotransmitters and markers of brain neurodegeneration in rats with experimental Parkinson’s disease. Parkinson’s disease was modeled in animals by intracerebral administration of rotenone. The studied glycoalkaloids were administered orally at a dose of 0.06 mg/kg for 28 days after pathology modeling. The study found that the use of the analyzed glycoalkaloids did not affect the concentration of dopamine and serotonin and also significantly (<i>p</i> < 0.05) reduced the level of ACh by 35.9% and increased the level of GABA by 55.1%, reduced the concentration of S100ß protein by 68.6%, and increased the level of BDNF by 52.4%.</p>","PeriodicalId":19119,"journal":{"name":"Neurochemical Journal","volume":"22 1","pages":""},"PeriodicalIF":0.5,"publicationDate":"2024-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141166494","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":"Effects of Intrathecal Administration of Prostaglandin-D2 on Stress-Induced Analgesia: Involvements of DP2 Receptors","authors":"Mona Paknia, Mohammad Zarei, Safoura Raoufi, Parisa Habibi, Fatemeh Ramezani‑Aliakbari, Seyed Asaad Karimi","doi":"10.1134/s1819712424020119","DOIUrl":"https://doi.org/10.1134/s1819712424020119","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Abstract</h3><p>Prostaglandin D<sub>2</sub> is the most abundant prostaglandin in the mammalian brain. Exposure to stressful stimuli is often accompanied by reduced pain sensitivity, termed “stress-induced analgesia” (SIA). In the present study, the possible modulatory role of prostaglandin-D2 (PGD2) in the acute or chronic type of SIA was examined in male and female rats. Acute and chronic (long-term) restraint stress (RS) in male and female rats was performed prior to intraplantar injections of formalin, a noxious inflammatory agent. The involvements of specific PGD2 receptors in the modulatory role of PGD2 on SIA also investigated by specific antagonists (DP1 or DP2). Corticosterone levels were assessed in groups of rats following exposure to stress. Acute or chronic restraint stress altered formalin-induced spontaneous behaviors in male and female rats. Furthermore, intrathecal microinjection of PGD2 (10 µg/mL) could reverse acute SIA in male but not in female rats. DP2 antagonist of PGD2 (CAY10471) attenuated pain score in the acute RS-induced analgesia in male rats. Administration of PGD2 increases the phospho-extracellular signal regulated kinase 2 (pERK2) levels in the spinal cord of male RS rats. Sex differences were also seen in plasma corticosterone concentrations post injection of PGD2 in acute SIA in male rats. The outcome suggests that not only central microinjection of PGD2 could attenuate acute SIA in male rats, but also its antagonist could turn over this effect.</p>","PeriodicalId":19119,"journal":{"name":"Neurochemical Journal","volume":"65 1","pages":""},"PeriodicalIF":0.5,"publicationDate":"2024-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141173437","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}