Annals of clinical and laboratory science最新文献

{"title":"Morroniside Attenuates Rheumatoid Arthritis by Inhibiting Rheumatoid Synoviocytes Invasion through the NF-κB/MMPs Pathway.","authors":"Yan Wang, Ruili Yin, Xin Li, Baoyu Zhang, Yuan Wang, Lijie Zhang, Yanan Cheng, Dong Zhao","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Objective: </strong>Morroniside (MOR) has been reported to ameliorate inflammation in cardiovascular and cerebrovascular disease; however, its impact and mechanism on rheumatoid arthritis (RA) remains unclear. This study aimed to investigate the beneficial role of morroniside in treating RA and explore the anti-invasive mechanism of morroniside on joint destruction.</p><p><strong>Methods: </strong><i>In vitro</i> (using primary rat articular fibroblast-like synoviocytes (FLSs)) a wound healing assay was used to detect the migration of primary rat FLSs. Quantitative RT-PCR was used to measure the transcription of matrix metalloproteinase (MMP) MMP2 and MMP9. Western blot was used to measure the expression of MMP2, MMP9, p65, phosphorylated-p65 (p-p65), inhibitor of nuclear factor (NF)-[Formula: see text]B<i>α</i> (I[Formula: see text]B<i>α</i>), I[Formula: see text]B kinase <i>α</i>/β (IKK<i>α</i>/β), and phosphorylated-IKK<i>α</i>/β. Immunofluorescence assay was used to measure the nuclear translocation of p65. <i>In vivo</i> (using rats with collagen-induced arthritis), the joint histopathological changes were detected by routine hematoxylin and eosin. Immunohistochemistry assay was used to measure the expression MMP2 and MMP9.</p><p><strong>Results: </strong>Morroniside diminished tumor necrosis factor (TNF)<i>α</i>-stimulated migration of primary rat articular FLSs. Morroniside also attenuated RA-FLSs invasion into joint and joint destruction in rats with collagen-induced arthritis (CIA). Further analysis revealed that morroniside inhibited the overexpression of matrix metalloproteinase MMP2 and MMP9 in TNF<i>α</i>-stimulated primary rat articular FLSs and joints of CIA rats. Mechanistically, morroniside suppressed the activation of I[Formula: see text]B kinase <i>α</i>/β, which resulted in elevated levels of the inhibitor of nuclear factor (NF)-[Formula: see text]B.</p><p><strong>Conclusion: </strong>The present study suggested that morroniside can prevent joint destruction by suppressing the activation of the NF-[Formula: see text]B/MMPs pathway, thereby preventing FLSs invasion.</p>","PeriodicalId":8228,"journal":{"name":"Annals of clinical and laboratory science","volume":"54 5","pages":"604-617"},"PeriodicalIF":1.1,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142613826","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":"Biomarkers Identification of Early Rheumatoid Arthritis via Bioinformatics Approach and Experimental Verification.","authors":"Caifang Shen, Bin Gu, Maodan Tang, Ke Ma, Kaili Du, Jianping Wu, Youlong Xiong, Dong Zhan","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Objective: </strong>To screen and identify potential biomarker for early rheumatoid arthritis (RA) by bioinformatic analysis and experimental investigation.</p><p><strong>Methods: </strong>Transcriptome data of RA synovium was downloaded from GEO. Differentially expressed genes (DEGs), gene ontology (GO) functional annotation, and KEGG pathway were analyzed to inspect significative target genes. The protein-protein interaction was constructed using STRING database and Cytoscape to screen hub genes with least absolute shrinkage and selection operator (LASSO). The diagnostic effectivity of screened hub genes was analyzed with receiver operating characteristic (ROC). RA synovial fibroblast (SF) was treated with TNF-<i>α</i> (20ng/mL for 24h). RT-qPCR and Western blotting were used to measure mRNA and protein for screened hub gene.</p><p><strong>Results: </strong>A total of 271 DEGs were found in GEO dataset. GO analysis indicated that DEGs mainly involved in phagocytosis, recognition and complement activation, etc. KEGG analysis suggested that DEGs were mostly enriched in the cytokine-cytokine receptor interaction, regulation of lipolysis in adipocytes, PPAR signaling pathway. LASSO regression and ROC curve indicated that ADIPOQ, CIDEA, FABP4, AQP7, LOC102723407, PLIN4, LIPE, CIDEC, PLIN1, and LEP had excellent diagnostic value. The area under ROC was 0.734. The level of ADIPOQ, LEP, LIPE, PLIN1, and PLIN4 were lower in RA group rather than that of control group (<i>p</i><0.01). The higher expressions of CIDEC and FABP4 were found in RA group comparing to control group (<i>p</i><0.001).</p><p><strong>Conclusions: </strong>Identified hub genes might be valuable biomarkers for early RA diagnosis to promote precise and personal therapy.</p>","PeriodicalId":8228,"journal":{"name":"Annals of clinical and laboratory science","volume":"54 5","pages":"661-670"},"PeriodicalIF":1.1,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142613778","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":"Escitalopram Relieves Sleep Anxiety in Patients with Cerebral Small Vessel Disease Sleep Disorder by Downregulating the Nrf2/ARE Signaling Pathway.","authors":"Lifei Xing, Lihua Sun, Hongliang Yan, Heyangzi Gong, Min Wang, Jianying Lv, Haiying Wang, Yanhong Wang","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Objective: </strong>Nrf2/ARE signaling pathway is reported to alleviate sleep anxiety in patients with sleep disorders. This study aimed at exploring the effect of escitalopram (ESC) on sleep anxiety in patients with cerebral small vessel disease (CSVD) and sleep disorder and its correlation with the Nrf2/ARE signaling pathway.</p><p><strong>Methods: </strong>In the present study, we enrolled 80 CSVD patients (disease group) and 40 healthy patients (control group) in our hospital. The CSVD patients were classified into ESC treatment group and conventional treatment group and administered ESC and diazepam, respectively. After treatment, the patients' sleep quality was monitored within three months, and their symptoms were evaluated. Additionally, a mouse model of CSVD was set up, and the rats received intragastric administration of low, moderate, and high dosage of ESC or thymoquinone. The morphology of nerve cells and cognitive functions in the rat hippocampus were seen. TUNEL staining was conducted to detect nerve cell apoptosis and RT-qPCR, and Western blot analyses determined the expression levels of Nrf2 and ARE.</p><p><strong>Results: </strong>Compared with conventional treatment group, the patients of ESC treatment group had shorter symptom improvement time and better sleep quality with a lower AHI and PSQI score. On the other hand, in the animal model, ESC treatment alleviated sleep disorders in CSVD rats, improved cognition and serum TNF-<i>α</i> levels, and protected nerve cells. Administration of ESC eliminated the expressions of Nrf2 and ARE and reduced nerve cell apoptosis dose-dependently. Moreover, Nrf2/ARE pathway activator (Danshensu) decreased rat sleep time and the level of serum TNF-<i>α</i> with more cell atrophy, while Nrf2/ARE pathway inhibitor (ML385) greatly improved sleep quality of CSVD rats.</p><p><strong>Conclusion: </strong>ESC can effectively relieve sleep anxiety in patients with CSVD and sleep disorders through downregulating the Nrf2/ARE signaling pathway. ESC treatment increases patient's sleep time and serum TNF-<i>α</i> levels and attenuates nerve cell damage, further improving the patient's sleep quality.</p>","PeriodicalId":8228,"journal":{"name":"Annals of clinical and laboratory science","volume":"54 5","pages":"577-587"},"PeriodicalIF":1.1,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142613795","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":"LNCRNA 1197 Promotes the Progression of Fibroblast-Like Synovial Cells by Targeting miR-206 in Rheumatoid Arthritis Patients: A Pilot Study.","authors":"Xiang Lu, Shanle Yan, Xiaoli Li, Yuan Xue, Liyun Zhang","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Objective: </strong>We studied the role of LNCRNA 1197 in rheumatoid arthritis (RA) and its underlying mechanism.</p><p><strong>Methods: </strong>We detected expression of LNCRNA 1197 in RA fibroblast-like synovial cells (RA-FLS) by RT-qPCR. Functional experiments were conducted to assess the impact of LNCRNA on cells as demonstrated by a Transwell assay. In addition, Western blot analysis was conducted to analyze the expression of proliferation-related proteins and flow cytometry and CCK-8 to analyze cell cycle and cell proliferation. We also identified the potential downstream target miRNA of LNCRNA 1197.</p><p><strong>Results: </strong>LNCRNA 1197 was highly expressed in RA-FLS. When LNCRNA 1197 was knocked down, the cell proliferation, migration, and invasion of RA-FLS were alleviated, and pro-inflammatory cytokines were significantly downregulated. Interestingly, LNCRNA 1197 was indicated to target miR-206 and promoted progression of FLS by inhibiting miR-206.</p><p><strong>Conclusion: </strong>Taken altogether, LNCRNA 1197 promotes the progression of RA-FLSs by miR-206 inhibition.</p>","PeriodicalId":8228,"journal":{"name":"Annals of clinical and laboratory science","volume":"54 5","pages":"588-596"},"PeriodicalIF":1.1,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142613802","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-16-5p Promotes the Progression of Esophageal Squamous Cell Carcinoma via Regulating AMPK/mTOR Signaling Pathway.","authors":"Wen-Xiu Yu, Min Zhou, Zhi-Jing Yin, Na Ji, Hai-Lin Yu","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Objective: </strong>Esophageal squamous cell carcinoma (ESCC) is commonly diagnosed with high mortality worldwide. Cell proliferation and cell apoptosis are essential biological processes for the development of cancers. MiR-16-5p, a critical member of miRNAs family, is involved in cell apoptosis and tumor progression. However, the role of miR-16-5p in regulating esophageal squamous cell carcinoma and the underlying mechanism remain unclear.</p><p><strong>Methods: </strong>In this study, we used human ESCC tissue samples and human esophageal cells to determine the expression level of miR-16-5p in ESCC tissues and cells. Cell Counting Kit-8 assay and flow cytometry were used to test cell proliferation and apoptosis. Western blotting was used to detect protein expression levels. The scratch assay was used to analyze the level of cell migration, and the transwell assay was used to analyze the invasive ability of tumor cells.</p><p><strong>Results: </strong>The expression of miR-16-5p was up-regulated in ESCC tissues and cells. Knockdown of miR-16-5p significantly inhibited cell proliferation and promoted cell apoptosis. The knockdown of miR-16-5p also restrained cell migration and invasion. We revealed that AMPK/mTOR signaling pathway participated in the regulation of ESCC progression.</p><p><strong>Conclusion: </strong>miR-16-5p may promote the proliferation, migration, and invasion of ESCC through modulating AMPK/mTOR signaling pathway.</p>","PeriodicalId":8228,"journal":{"name":"Annals of clinical and laboratory science","volume":"54 5","pages":"569-576"},"PeriodicalIF":1.1,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142613808","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":"Information About The Association of Clinical Scientists.","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":8228,"journal":{"name":"Annals of clinical and laboratory science","volume":"54 5","pages":"715"},"PeriodicalIF":1.1,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142613816","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":"Sysmex XN-9000 Hematology Analyzer Can Provide Reference for the Classification of Nucleated Cells in Body Fluid and Detect Malignant Serous Effusion.","authors":"Yabin Chen, Jian Huang, Huidan Chen, Linghui Ma, Min Dou, Qiurong Zhao, Zhishan Zhang, Xiaomei Wen","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Objective: </strong>The purpose of this study is to evaluate the accuracy of Sysmex XN-9000 hematology analyzer (XN-9000) in detecting nucleated cell classifications in serous effusion and to further evaluate whether it can be used for screening malignant serous effusion.</p><p><strong>Methods: </strong>The consistency between XN-9000 and manual microscopy in the classification of nucleated cells was evaluated using Passing-Bablok regression and Bland-Altman plot. ROC analysis was applied to evaluate the value of HF-BF% in screening malignant specimens.</p><p><strong>Results: </strong>In the serous effusion of the group with nucleated cell count of (0-150) ×10⁶/μL, high consistency between XN-9000 and manual microscopy was found in detecting NE-BF% and LY-BF%. In the group with nucleated cell count >150×10⁶/μL, there was high consistency in detecting NE-BF%, LY-BF%, and HF-BF%. ROC analysis showed that HF-BF% can be used for screening malignant serous effusion, with an area under the curve (AUC) of 0.572 (95%CI=0.504~0.639).</p><p><strong>Conclusion: </strong>If XN-9000 detection results are mainly NE-BF% and LY-BF%, the classification can be effectively referred to and reported regardless of the number of nucleated cells in the serous effusion. HF-BF% has certain value in screening malignant serous effusion with a nuclear cell count >150×10⁶/μL. The optimal cut-off value is 13.15%.</p>","PeriodicalId":8228,"journal":{"name":"Annals of clinical and laboratory science","volume":"54 5","pages":"671-678"},"PeriodicalIF":1.1,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142613840","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":"<i>Letter to the Editor</i>. Evaluation of Swab: Direct Extraction Kit, Comparing with AdvanSure E3 System for Nucleic Acid Extraction in Identification of SARS-CoV-2.","authors":"Chang-Hun Park, Heeyoung Kwon","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":8228,"journal":{"name":"Annals of clinical and laboratory science","volume":"54 5","pages":"706-709"},"PeriodicalIF":1.1,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142613764","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":"Mesoporous Silica Nano-Modified Ginsenoside Rh2 Promote Tumor Immunosuppression and Inhibit Lung Cancer Development through the PD-1/PD-L1 Pathway.","authors":"Boxiong Cao, Qiang Wei, Hao Feng, Zemin He","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Objective: </strong>To explore the mechanism for mesoporous silica nano-modified ginsenoside Rh2 promoting tumor immunosuppression in lung cancer through PD-1/PD-L1 pathway.</p><p><strong>Methods: </strong>Firstly, G-Rh2-MSN were prepared and lung cancer A549 cells were cultured. The following groups were set up to analyze whether G-Rh2-MSN down-regulates PD-1/PD-L1 to promote tumor immunity, inhibit activities of lung cancer cells, and promote apoptosis: Model control group, G-Rh2 group, G-Rh2-MSN group, G-Rh2-MSN+PT001 group, G-Rh2-MSN+nivolumab group, G-Rh2-MSN+Durvalumab group, G-Rh2-MSN+atezolizumab group, and G-Rh2-MSN+nivolumab+Durvalumab group.</p><p><strong>Results: </strong>G-Rh2-MSN was successfully prepared and found to promote tumor immunity, inhibit the behaviors of lung cancer cells, and accelerate apoptosis. Down-regulation of PD-1/PD-L1 pathway by G-Rh2-MSN can accelerate development of tumor immunosuppressive lung cancer. G-Rh2-MSN promoted tumor immunity by downregulating PD-1/PD-L1, inhibiting activities of lung cancer cells, and promoting apoptosis.</p><p><strong>Conclusion: </strong>We clarified the mechanism for G-Rh2-MSN in lung cancer A549 cells, showing that it can significantly down-regulate PD-1/PD-L1 signaling, thereby promoting tumor immunity. G-Rh2-MSN modified material inhibits immune escape and reduces behaviors of lung cancer A549 cells by affecting PD-1 and PD-L1 expression, which has potential clinical application prospects.</p>","PeriodicalId":8228,"journal":{"name":"Annals of clinical and laboratory science","volume":"54 5","pages":"597-603"},"PeriodicalIF":1.1,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142613807","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 Role of STEAP3 in Pathogenesis of Gliomas: An Independent Prognostic Factor and Regulator of Ferroptosis.","authors":"Hong Cheng, Fang Ling, Xiaoli Hou, Jing Wang, Yingjie Zhao, Yixia Wang, Yasen Cao","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Objective: </strong>Gliomas are common intracranial tumors with high malignancy and poor prognosis, classified into glioblastomas (GBM) and low-grade glioma (LGG). However, the regulatory mechanisms of glioma tumorigenesis remain unclear. This study aimed to investigate the role of six-transmembrane epithelial antigen of the prostate 3 (STEAP3) in glioma prognosis and explore its potential as a therapeutic target, as well as the ferroptosis-related molecular mechanism in progression of gliomas.</p><p><strong>Methods: </strong>Cox regression analyses were used to identify prognostic factors of gliomas patients from Cancer Genome Atlas (TCGA) database and DESeq2 package was used for differential gene expression comparisons between Grade 2 and Grade 4 gliomas. Wilcoxon rank-sum test was used to compare the STEAP3 expression levels between glioma tissues and normal controls in Xiantao platform, as well as between TCGA glioma samples and GTEx normal samples. A protein-protein interaction (PPI) network was constructed using STRING database information, with hub genes identified through Cytoscape software. Cell viability was determined by MTT assay. Cell proliferation was determined by BrdU incorporation and clone formation assay. GSH and MDA concentration was determined according to kit protocols. The expression of STEAP3, Nrf2, GPX4 was determined by western blotting analysis.</p><p><strong>Results: </strong>Our results revealed that STEAP3 is overexpressed in glioma tissues compared to normal counterparts and correlates with poor overall survival (OS). High STEAP3 expression significantly correlates with various clinical-pathological features such as age, histological type, treatment response, World Health Organization (WHO) grade, isocitrate dehydrogenase (IDH) status, and survival events. Knockdown STEAP3 inhibited cell proliferation and enhanced erastin-induced ferroptosis in U87 and U138 cells. Moreover, knockdown STEAP3 in glioma cells decreased the GSH levels and increased the production of MDA probably by inhibiting the Nrf2/GPX4 related signaling pathway.</p><p><strong>Conclusion: </strong>STEAP3 serves as an independent biomarker for glioma prognosis with significant diagnostic value. High STEAP3 expression was correlated with poor overall outcomes of glioma patients. Knockdown of STEAP3 significantly suppressed the proliferation of glioma cells and increased erastin-induced ferroptosis via Nrf2/GPX4 pathway.</p>","PeriodicalId":8228,"journal":{"name":"Annals of clinical and laboratory science","volume":"54 5","pages":"618-632"},"PeriodicalIF":1.1,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142613845","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}