Annals of clinical and laboratory science最新文献

{"title":"uPAR Is Regulated via miR-561-3p and Affects the Progression and Aggressiveness of CRC Cells.","authors":"Xi Yang, Xuelian Wang, Lu Sang","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Objective: </strong>Urokinase plasminogen activator (uPA), its receptor uPAR, and plasminogen activator inhibitor type 1 (PAI-1), constitute the plasminogen urokinase activation system that is thought to be associated with the malignant biology of cancer cells. Nevertheless, the regulation mechanism of uPAR expression in colorectal cancer remains unclear.</p><p><strong>Methods: </strong>The effect of uPAR and miR-516-3p on CRC cells was explored through Methyl thiazolyl tetrazolium (MTT) assay, colony formation, Transwell, and Apoptosis assays. Dual-luciferase reporter assays, reverse transcription quantitative PCR (RT-qPCR), and Western blot assay were carried out to determine that uPAR is directly regulated by miR-561-3p. Levels of protein expression were analyzed by Western blot assay.</p><p><strong>Results: </strong>In the study, we showed that uPAR was upregulated in serum samples from CRC patients and associated with the more advanced stage and distant metastasis in patients with CRC. In CRC cells, uPAR promotes cell growth, migration, and invasion, while inhibiting cell apoptosis. In addition, the expression of uPAR is negatively regulated by miR-561-3p through binging its 3' UTR.</p><p><strong>Conclusion: </strong>uPAR is downregulated by miR-561-3p, contributing to tumorigenesis in colorectal cancer.</p>","PeriodicalId":8228,"journal":{"name":"Annals of clinical and laboratory science","volume":"55 6","pages":"929-938"},"PeriodicalIF":0.9,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146112096","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":"Clinical Analysis of Primary Prostatic Diffuse Large B-Cell Lymphoma.","authors":"Shao-Juan Cui, Hang Yin, Qiong Liu, Dong-Ping Huang, Yu Chen","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Objective: </strong>Given the extreme rarity of primary diffuse large B-cell lymphoma of the prostate (P-DLBCL-P), medical institutions face challenges in accumulating a sufficient number of cases. Thus, investigating the clinical manifestations of this disease and exploring potential therapeutic strategies holds significant importance.</p><p><strong>Case report: </strong>We present three cases of P-DLBCL-P, all admitted to our hospital with symptoms of lower urinary tract obstruction. Following pathological examination of the prostate, all three patients were definitively diagnosed with P-DLBCL-P.</p><p><strong>Discussion: </strong>Case 1 discharged himself from the hospital after refusing treatment. Case 2 received eight courses of R-CDOP regimen chemotherapy but died of rectovesical fistula. Case 3 developed obstructive nephropathy due to urinary tract obstruction and died soon after emergency dialysis.</p><p><strong>Conclusions: </strong>P-DLBCL-P is an extremely rare disease that is prone to misdiagnosis, emphasizing the need to pay close attention to its clinical manifestations for prompt and accurate diagnosis. All three patients in this study received timely diagnoses, but one refused treatment, and the other two experienced disease progression despite appropriate intervention. Given the limited clinical data on this disease, more cases are required to explore the prognosis of patients and the efficacy of various therapeutic strategies, including emerging treatment options.</p>","PeriodicalId":8228,"journal":{"name":"Annals of clinical and laboratory science","volume":"55 6","pages":"988-994"},"PeriodicalIF":0.9,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146111901","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":"Establishing Age-Specific Reference Intervals for Serum Lung Cancer Biomarkers in the Chinese Elderly Population.","authors":"Guang Li, Hengchuan Shi, Xingyue Chen, Shan Kong","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Objective: </strong>Lung cancer's high global burden necessitates early diagnosis. Serum biomarkers (NSE, CYFRA 21-1, SCC) aid screening, but accurate interpretation requires reliable reference intervals (RIs). Most Chinese labs use Western population-based RIs, lacking age-stratification for the elderly and increasing misdiagnosis risk. This study established age- and sex-specific RIs for these biomarkers in Chinese elderly.</p><p><strong>Methods: </strong>A cohort of 77,123 healthy individuals undergoing physical examinations was screened using strict exclusion criteria to identify healthy reference individuals. Serum biomarker levels were measured using the Roche Cobas e801 fully automated immunoassay analyzer. RIs were established using the nonparametric percentile method (P2.5-P97.5), stratified by sex (Male vs. Female) and age group (50-59, 60-69, 70-79, 80-100 years).</p><p><strong>Results: </strong>Results revealed that NSE levels increased stepwise with age and were higher in females than males. CYFRA 21-1 levels increased linearly with age, while SCC exhibited a sharp rise in the 80-100-year group. The current manufacturer-provided standards significantly increased misdiagnosis rates in the elderly, highlighting the necessity for localized RIs.</p><p><strong>Conclusion: </strong>The newly established RIs demonstrated excellent performance in an independent validation cohort, significantly outperforming existing standards. This study provides the first age- and sex-stratified RIs for lung cancer serum biomarkers in the Chinese elderly population, filling a critical gap. These results offer a reliable tool for precise diagnosis and provide essential evidence for optimizing early lung cancer screening and clinical decision-making in the elderly.</p>","PeriodicalId":8228,"journal":{"name":"Annals of clinical and laboratory science","volume":"55 5","pages":"816-823"},"PeriodicalIF":1.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145547790","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":"Dexmedetomidine Regulates HMGB1 Transferred by HK-2 Cell-Derived Exosomes to Suppress Myocardial Cell Pyroptosis by Activating the TLR4 Signaling Pathway.","authors":"Jingjing Zhang, Qiang Geng, Jinhui Sun, Yuanming Zhang, Bing Zhang","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the effect of Dexmedetomidine (Dex) on myocardial cell pyroptosis by regulating HK-2 cell-derived exosomes and analyze its underlying mechanism.</p><p><strong>Methods: </strong>An <i>in vitro</i> model of Renal ischemia-reperfusion injury (RIRI) was created by exposing human proximal renal tubule epithelial cells (HK-2) to hypoxia/reoxygenation (H/R) and Dex treatment. We extracted HK-2 cell-derived exosomes using a kit and distinguished them through transmission electron microscopy and nanoparticle tracking analysis. These exosomes were co-cultured with cardiomyocytes AC16. The uptake of AC16 cell-derived exosomes was observed using fluorescent labeling. Cell activity and death rates were examined utilizing cell counting kit-8 and flow cytometry, respectively. The enzyme-linked immunosorbent assay was adopted for the evaluation of the release of inflammatory factors in the cell culture supernatant. Western blot was employed to assess the expression levels of HK-2 cell-derived exosome marker protein, AC16 cell pyroptosis-related protein, high mobility group box 1 (HMGB1), and the TLR4 signaling pathway.</p><p><strong>Results: </strong>H/R considerably hindered the activity and elevated the death rate of HK-2 cells, elevated the release of inflammatory factors, and significantly up-regulated HMGB1 expression in HK-2 cells. Dex exhibited a protection influence on HK-2 cells under H/R conditions, partially restoring cell activity, reducing cell death rate and the secretion of inflammatory molecules, and down-regulating HMGB1 expression in HK-2 cell-derived exosomes. AC16 cells could internalize exosomes derived from HK-2 cells, and the HMGB1 carried by these exosomes affected the activity of AC16 cells. Dex treatment down-regulated HMGB1 expression in HK-2 cell-derived exosomes under H/R conditions, thereby enhancing AC16 cell activity, reducing AC16 cell death rate and inflammatory factor release, and inhibiting AC16 cell pyroptosis. Furthermore, the use of cell pyroptosis inhibitor VX-765 and the TLR4 signaling pathway inhibitor Resatorvid proved that Dex exerted its protective properties on AC16 cells by modulating the TLR4 signaling pathway through its effects on HMGB1 carried by HK-2 cell-derived exosomes.</p><p><strong>Conclusion: </strong>Dex can significantly inhibit the expression of HMGB1 in HK-2 cell-derived exosomes exposed to H/R and inhibit AC16 cell pyroptosis through exosome uptake and the effect of HMGB1 on the TLR4 signaling pathway.</p>","PeriodicalId":8228,"journal":{"name":"Annals of clinical and laboratory science","volume":"55 5","pages":"639-650"},"PeriodicalIF":1.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145547655","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":"Annals of Clinical and Laboratory Science: Information for Authors.","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":8228,"journal":{"name":"Annals of clinical and laboratory science","volume":"55 5","pages":"840-841"},"PeriodicalIF":1.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145547666","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":"MTERF1 Regulates Podocyte Mitochondrial DNA Replication Impairment and Mitochondrial Dysfunction in Diabetic Nephropathy through the AMPK/mTOR Pathway.","authors":"Haiying Tao, Ling'an Yu","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Objective: </strong>This study was carried out with an objective to clarify the mechanism of mitochondrial transcription termination factor 1 (MTERF1) in regulating mitochondrial DNA (mtDNA) replication and mitochondrial function of podocytes in diabetic nephropathy (DN).</p><p><strong>Methods: </strong>To establish a type I diabetes model, C57BL/6J mice were injected intraperitoneally with streptozotocin (STZ). Eight weeks after STZ injection, blood glucose levels and renal function were assessed in mice. Mouse renal tissues were analyzed via hematoxylin-eosin, periodic acid-Schiff, and TdT-mediated dUTP nick-end labeling staining. Immunohistochemistry/Western blot were employed for the detection of MTERF1 expression. MPC-5 cells were treated with high glucose (HG) (30 mM) to establish the cellular model. MTERF1-overexpressing MPC-5 cells were constructed and treated with HG and the AMP-activated protein kinase (AMPK) inhibitor compound C (CC) for 24 h. Cell apoptosis was assessed by flow cytometry, cell viability by the cell counting kit-8 assay, mtDNA copy number by real-time quantitative PCR, adenosine triphosphate (ATP) production by ultraviolet spectrophotometric method, mitochondrial reactive oxygen species (mtROS) by MitoSox, and mitochondrial membrane potential (MMP) by JC-1. MTERF1 protein expression and AMPK/mammalian target of rapamycin (mTOR) signaling pathway activity were measured via Western blot.</p><p><strong>Results: </strong>The model group (relative to the control group) exhibited a significant rise in blood glucose, urine volume, urinary albumin, and urine albumin-creatinine ratio, along with significantly aggravated glomerular injury and markedly increased glycogen deposition and decreased MTERF1 expression in mouse renal tissue. In <i>in vitro</i> experiments, compared with the normal glucose (NG) group, the HG group showed increased apoptosis and reduced cell activity, accompanied by significantly decreased MTERF1 protein expression, mtDNA copy number, and ATP content. Compared to the HG+oe-NC group, the HG+oe-MTERF1 group showed significant increases in mtDNA copy number, ATP content, MMP, and AMPK/mTOR signaling pathway activity, while demonstrating decreased mtROS production. The HG+oe-MTERF1+CC group exhibited significant reductions in mtDNA copy number, ATP production, and AMPK/mTOR signaling pathway activity compared to the HG+oe-MTERF1 group, but displayed elevated mtROS levels.</p><p><strong>Conclusion: </strong>Over-expression of MTERF1 can alleviate HG-induced damage of mtDNA replication and mitochondrial dysfunction in podocytes via activating the AMPK/mTOR signaling pathway, thus improving DN.</p>","PeriodicalId":8228,"journal":{"name":"Annals of clinical and laboratory science","volume":"55 5","pages":"663-671"},"PeriodicalIF":1.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145547898","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":"X-Linked Sideroblastic Anemia Induced by a Novel ALAS2 Nonsense Mutation: A Case Report and Literature Review.","authors":"Hang Yin, Qing Shen, Chun-Li Xu, Dong-Ping Huang, Yu Chen","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Objective: </strong>To clarify the clinical manifestations of X-linked sideroblastic anemia (XLSA) and the mutational profiles of the aminolevulinate synthase 2 (<i>ALAS2</i>) gene, thereby optimizing treatment and prognosis.</p><p><strong>Case report: </strong>The proband, a 16-year-old male student, presented with microcytic hypochromic anemia, with hemoglobin (Hb) 55 g/L, red cell distribution width (RDW) 22.5%, mean corpuscular hemoglobin concentration (MCHC) 314 g/L, mean corpuscular hemoglobin (MCH) 23.9 pg, and mean corpuscular volume (MCV) 76.1 fL. Next-generation sequencing followed by Sanger sequencing of his family identified a de novo heterozygous nonsense mutation in <i>ALAS2</i> (c.224C>A); this identification led to the final diagnosis of XLSA with a novel <i>ALAS2</i> mutation.</p><p><strong>Discussion: </strong>Incorporating genetic analyses into diagnostic algorithms can improve the precision of XLSA diagnosis and support personalized treatment strategies for patients and families.</p><p><strong>Conclusions: </strong>Our findings expand the mutational spectrum of <i>ALAS2</i> and highlight that integrating next-generation sequencing (NGS) with Sanger validation into diagnostic workflows can significantly improve the diagnostic accuracy of XLSA.</p>","PeriodicalId":8228,"journal":{"name":"Annals of clinical and laboratory science","volume":"55 5","pages":"827-830"},"PeriodicalIF":1.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145548015","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":"FAM111B as a Multi-Omics Biomarker for Diagnosis, Prognosis, and Immune Modulation in Colorectal Cancer.","authors":"Zhiqiang Zhu","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Objective: </strong>Colorectal cancer (CRC) remains a leading cause of cancer mortality globally, necessitating novel biomarkers for early intervention. Although FAM111B - a gene implicated in DNA repair and cell cycle control - exhibits dysregulation in multiple malignancies, its CRC-specific relevance is underexplored.</p><p><strong>Methods: </strong>Integrative analysis of five CRC cohorts (TCGA/GEO) was conducted. Differential FAM111B expression was assessed using Wilcoxon tests (paired/unpaired samples). Spearman's correlation determined associations with clinical/molecular features. Prognostic performance of FAM111B combined with AJCC-TNM staging was evaluated via univariate/multivariate Cox regression. Functional characterization employed PPI networks, GO/KEGG, GSEA, and immune deconvolution (ssGSEA).</p><p><strong>Results: </strong>FAM111B demonstrated consistent overexpression in tumors versus controls across all datasets (<i>P</i><0.001), showing diagnostic capability (AUC=0.87). Elevated expression independently predicted poor survival (HR=1.82; 95%CI:1.3-2.5). Its integration with TNM staging improved prognostic stratification (ΔAUC=0.17; <i>P</i>=0.006). Functional studies linked FAM111B to oncogenesis through: 1. DNA damage response dysregulation; 2. Metabolic reprogramming (lipid/RNA metabolism); 3. Immunosuppressive microenvironment (reduced CD8+ T-cell infiltration; <i>P</i>=0.003).</p><p><strong>Conclusion: </strong>This multilevel analysis establishes FAM111B as a CRC biomarker with dual diagnostic-prognostic utility. Its roles in genomic stability, metabolic adaptation, and immune evasion highlight therapeutic potential. Clinical validation using probe ID1557129_a_at is warranted.</p>","PeriodicalId":8228,"journal":{"name":"Annals of clinical and laboratory science","volume":"55 5","pages":"745-763"},"PeriodicalIF":1.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145547824","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":"Mesenchymal Hamartoma of the Gingiva of an Infant: A Case Report.","authors":"Nasim Haghandish, Adel Kauzman, Nabil Ouatik, Consolato M Sergi","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>We present an 18-month-old boy with an exophytic mass in an unusual location, the right anterior-superior gingiva between deciduous teeth 5.3 and 5.4. Histopathologic and immunohistochemical investigations revealed a mesenchymal hamartoma (MH). Collagen fibers were haphazardly distributed in the dermis, admixed with nerve twigs and inflammatory cells. Twelve months of follow-up did not disclose any local relapse or evidence of oncological disease. To the best of our knowledge, this is the first case of gingival MH in an infant.</p>","PeriodicalId":8228,"journal":{"name":"Annals of clinical and laboratory science","volume":"55 5","pages":"824-826"},"PeriodicalIF":1.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145547905","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":"Suppression of PCBP1 Enhances PPARγ via TAK1 Modulation to Improve Glycemic and Lipid Metabolism Disorders in Gestational Diabetes Mellitus.","authors":"Xuemei Xia, Yan Chen","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Objective: </strong>Gestational diabetes mellitus (GDM) affects the health of pregnant women and their fetuses. Poly(C)-binding protein 1 (PCBP1), a multifunctional RNA-binding protein, is pivotal in maintaining cytosolic iron homeostasis. This study aims to explore the role and mechanism of PCBP1 in glucose and lipid metabolism dysregulation in GDM.</p><p><strong>Methods: </strong>To establish via a high-fat diet-induced GDM mouse model and a palmitic acid (PA)-triggered insulin resistance (IR) model in HepG2 cells, glucose tolerance and insulin tolerance tests were performed in GDM mice, with lipid metabolism evaluated via hematoxylin-eosin (HE) staining, Oil Red O staining, as well as biochemical assay kits. Glucose content was quantified using the glucose oxidase method, while cell viability was evaluated trough the cell counting kit-8(CCK-8) assay. Apoptotic activity was examined through Terminal deoxynucleotidyl transferase dutp nick end labeling (TUNEL) staining, and the expression levels of key proteins, including phosphorylated AKT (p-AKT), phosphorylated IRS1 (p-IRS1), PCBP1, transforming growth factor β-activated kinase 1(TAK1), and Peroxisome proliferator-activated receptor gamma (PPAR<i>γ</i>), were analyzed through Western blotting.</p><p><strong>Results: </strong>The results demonstrated that GDM mice exhibited profound glucose and lipid metabolism disorders, characterized by significant lipid droplet accumulation in hepatic cells and disrupted insulin signaling pathways. Furthermore, hepatic expression of PCBP1 and TAK1 was notably upregulated, whereas PPAR<i>γ</i> expression was significantly reduced. <i>In vitro</i> experiments revealed that silencing PCBP1 alleviated glucose and lipid metabolism abnormalities and improved insulin signaling in PA-induced insulin-resistant HepG2 (IR-HepG2) cells. This intervention also enhanced cell viability and suppressed apoptosis. Further mechanistic studies indicated that inhibition of TAK1 expression facilitated PPAR<i>γ</i> upregulation, while TAK1 overexpression negated these effects. Additionally, silencing PPAR<i>γ</i> in TAK1-silenced cells reversed the metabolic improvements in IR-HepG2 cells, whereas overexpression of PPAR<i>γ</i> mitigated the adverse effects of PCBP1 overexpression.</p><p><strong>Conclusion: </strong>The foregoing findings demonstrate that PCBP1 exerts its effects on glucose and lipid metabolism in GDM via the TAK1/PPAR<i>γ</i> signaling axis. Our study highlights the important function of the PCBP1/TAK1/PPAR<i>γ</i> signaling pathway in mediating glucose and lipid metabolism in GDM, providing valuable insights into possible therapeutic targets for GDM treatment.</p>","PeriodicalId":8228,"journal":{"name":"Annals of clinical and laboratory science","volume":"55 5","pages":"651-662"},"PeriodicalIF":1.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145547937","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}