Archives of Medical Science最新文献

{"title":"Virtual reality technology improves the gait and balance function of the elderly: a meta-analysis of randomized controlled trials.","authors":"Junyu Chen, Shuxia Yan, Haiyan Yin, Dan Lin, Ziqi Mei, Zichun Ding, Meng Wang, Yamei Bai, Guihua Xu","doi":"10.5114/aoms/186353","DOIUrl":"10.5114/aoms/186353","url":null,"abstract":"<p><strong>Introduction: </strong>Improving the gait and balance function is an important part of the health of the elderly. This study aimed to conduct a meta-analysis to evaluate the effects of virtual reality (VR) technology on the gait and balance function of the elderly.</p><p><strong>Material and methods: </strong>Two authors independently searched EMBASE, PubMed, Web of Science, ClinicalTrials, Cochrane Library, China National Knowledge Infrastructure (CNKI), Wanfang and Weipu databases up to October 20, 2023 for randomized controlled trials (RCTs) on the application of VR in improving the gait and balance function in the elderly. We screened the literature, extracted data and evaluated the bias risk of included RCTs, and used RevMan software for meta-analysis.</p><p><strong>Results: </strong>Fourteen RCTs were finally included in this meta-analysis. A total of 662 elderly adults were included, of whom 336 underwent VR intervention. The results of the meta-analysis showed that the gait and balance function of the elderly in the VR group were significantly better than those in the traditional intervention group (all <i>p</i> < 0.05). There was no significant difference in terms of increasing the muscle strength of the lower extremities or alleviating the fear of falling between groups (all <i>p</i> > 0.05).</p><p><strong>Conclusions: </strong>VR can effectively improve the gait and dynamic and static balance function of the elderly. However, the effect of VR on increasing the muscle strength of lower extremities and reducing the fear of falling in the elderly is still not obvious.</p>","PeriodicalId":8278,"journal":{"name":"Archives of Medical Science","volume":"20 6","pages":"1918-1929"},"PeriodicalIF":3.0,"publicationDate":"2024-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11831358/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143447744","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PPAR-α regulates metabolic remodelling and participates in myocardial fibrosis in patients with atrial fibrillation of rheumatic heart disease.","authors":"Xiaoying Hu, Daisong Jiang, Zheng Zhang, Zhenmei An","doi":"10.5114/aoms/181134","DOIUrl":"10.5114/aoms/181134","url":null,"abstract":"<p><strong>Introduction: </strong>This study will explore the correlation of peroxisome proliferator activated receptor-α (PPAR-α) regulation of metabolic remodelling in the myocardial fibrosis of atrial fibrillation (AF) in rheumatic heart disease.</p><p><strong>Material and methods: </strong>The left atrial appendage tissues were evaluated by Masson staining for fibrosis degree, and Western Blot was used to detect the expression of proteins related to glucose metabolism disorder, lipid metabolism abnormality, and mitochondrial dysfunction. The myocardial fibroblasts were established by stimulation with ANG II, and the PPAR-α agonist GW7647 was administered. The changes of phenotype transformation of myocardial fibroblasts were detected by cellular immunofluorescence, the secretion level of supernatant collagen was detected by ELISA. Finally, the correlation between PPAR-α protein expression and myocardial fibrosis was analysed and a conclusion was drawn.</p><p><strong>Results: </strong>Masson staining showed that the degree of myocardial fibrosis in patients with AF was significantly increased; WB analysis showed that there were statistically significant differences in protein expression related to glucose metabolism disorder, lipid metabolism abnormality, and mitochondrial dysfunction. There was a correlation between PPAR-α protein expression and myocardial fibrosis (<i>r</i> = -0.5322, <i>p</i> < 0.0001). After stimulation with PPAR-α agonist GW7647, the phenotypic differentiation of myocardial fibro-blasts into myofibroblasts was inhibited. The protein expression related to mitochondrial dysfunction was statistically different.</p><p><strong>Conclusions: </strong>This study found that there is a negative correlation between the expression of PPAR-α protein and myocardial fibrosis in rheumatic heart disease AF, which plays a protective role. PPAR-α may participate in the pathogenesis of myocardial fibrosis in rheumatic heart disease AF by regulating glucose metabolism, lipid metabolism, and mitochondrial function.</p>","PeriodicalId":8278,"journal":{"name":"Archives of Medical Science","volume":"20 5","pages":"1461-1471"},"PeriodicalIF":3.0,"publicationDate":"2024-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11623188/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142793999","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Good efficacy achieved by telitacicept in treatment of systemic lupus erythematosus with alopecia areata.","authors":"Fangling Yao, Shenyi Yu, Zheng Liao, Li Deng","doi":"10.5114/aoms/188860","DOIUrl":"https://doi.org/10.5114/aoms/188860","url":null,"abstract":"","PeriodicalId":8278,"journal":{"name":"Archives of Medical Science","volume":"20 3","pages":"1050-1052"},"PeriodicalIF":3.0,"publicationDate":"2024-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11264150/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141756819","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Combretastatin A4 phosphate encapsulated in hyaluronic acid nanoparticles is highly cytotoxic to oral squamous cell carcinoma.","authors":"Chuanxi Sun, Ziqi Zhou, Fangqiang Liu, Hong Li, Zhe Liu","doi":"10.5114/aoms/189535","DOIUrl":"https://doi.org/10.5114/aoms/189535","url":null,"abstract":"<p><strong>Introduction: </strong>To investigate the toxicity of combretastatin A4 phosphate (CA4P) hyaluronic acid (HA) gel nanoparticles (HA-CA4P-NPs) in OSCC (oral squamous cell carcinoma).</p><p><strong>Methods: </strong>Toxicity was investigated using fluorescence microscopy, MTT assay, flow cytometry, and OSCC xenograft mouse models.</p><p><strong>Results: </strong>Compared with CA4P, HA-CA4P-NPs generated nearly 10 times more fluorescence in OSCC cells. Cytotoxicity assays showed that HACA4P-NPs were more toxic to SCC-4 cells but not to HNECs. Remarkable necrosis was induced in SCC-4 cells after exposure to HA-CA4P-NPs, and related proteins were upregulated. Furthermore, HA-CA4P-NPs significantly reduced the tumour size.</p><p><strong>Conclusions: </strong>HA-CA4P-NPs improved drug release and delivery, and increased cytotoxicity to cancer cells.</p>","PeriodicalId":8278,"journal":{"name":"Archives of Medical Science","volume":"20 3","pages":"1022-1028"},"PeriodicalIF":3.0,"publicationDate":"2024-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11264095/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141756816","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The mediating effect of depression on the association between lung disease and cardiovascular health.","authors":"Feng Chen, Hao Lin, Yuansi Zhang, Yu Zhang, Enhui Yang","doi":"10.5114/aoms/189973","DOIUrl":"https://doi.org/10.5114/aoms/189973","url":null,"abstract":"<p><strong>Introduction: </strong>In this study, we investigated the effect of depression on the interaction between lung disease and cardiovascular health (CVH).</p><p><strong>Methods: </strong>Utilising data from the National Health and Nutrition Examination Survey (2013-2018), we employed multivariate regression and bootstrap mediation analysis to explore the relationships among lung diseases, depression, and CVH scores.</p><p><strong>Results: </strong>Complex and significant associations were identified among lung diseases, depression, and CVH scores, with depression mediating 9.42% of the effect on CVH, especially for chronic bronchitis patients.</p><p><strong>Conclusions: </strong>Depression significantly mediated the relationship between lung disease and reduced CVH scores, highlighting the importance of mental health management in lung disease patients.</p>","PeriodicalId":8278,"journal":{"name":"Archives of Medical Science","volume":"20 3","pages":"1029-1033"},"PeriodicalIF":3.0,"publicationDate":"2024-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11264099/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141756825","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LINC00847 drives pancreatic cancer progression by targeting the miR-455-3p/HDAC4 axis.","authors":"Shunxin Hao, Zhi Yao, Yifeng Liu","doi":"10.5114/aoms/171672","DOIUrl":"https://doi.org/10.5114/aoms/171672","url":null,"abstract":"<p><strong>Introduction: </strong>Pancreatic cancer (PC) is a common malignant tumor of the digestive system, posing a serious threat to the life of patients. This study aims to investigate the role of LINC00847 and the LINC00847/miR-455-3p/HDAC4 mechanism in PC progression.</p><p><strong>Material and methods: </strong>The RNA levels of LINC00847, miR-455-3p and HDAC4 were determined by RT-qPCR. HDAC4 protein level was assessed by western blotting. Colony formation and CCK-8 assays were employed to test the proliferation of PC cells. Transwell and scratch assays were conducted to evaluate the cell invasive and migratory abilities, respectively. The effect of LINC00847 silencing on PC cells <i>in vivo</i> was verified using a mouse xenograft model. The correlation among LINC00847, miR-455-3p and HDAC4 was ascertained by dual-luciferase reporter (DLR) assay and Pearson's correlation analysis.</p><p><strong>Results: </strong>The result showed that LINC00847 mainly localized in the cytoplasm was upregulated in PC cells and tissues. Downregulating LINC00847 hindered migration, proliferation, and invasion of PC cells <i>in vitro</i>. Moreover, it also suppressed tumor growth in an <i>in vivo</i> xenograft model. LINC00847 was found to directly target miR-455-3p. miR-455-3p overexpression inhibited cell proliferation and invasion. In addition, HDAC4 was confirmed to be a target gene of miR-455-3p, and HDAC4 overexpression overturned the impact of LINC00847 knockdown on PC cell progression.</p><p><strong>Conclusions: </strong>Our findings reveal that LINC00847 potentially plays a key role in the carcinogenesis of PC progression. This effect may be mediated via regulating the miR-455-3p/HDAC4 axis. This study provides insights into the intricate molecular mechanisms underlying PC and opens avenues for potential therapeutic interventions.</p>","PeriodicalId":8278,"journal":{"name":"Archives of Medical Science","volume":"20 3","pages":"847-862"},"PeriodicalIF":3.0,"publicationDate":"2024-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11264153/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141756822","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Efficacy of linezolid in the treatment of tuberculous meningitis: a meta-analysis.","authors":"Xiaoshu Liu, Daoyan Tang, Min Qi, Jian-Qing He","doi":"10.5114/aoms/189905","DOIUrl":"https://doi.org/10.5114/aoms/189905","url":null,"abstract":"<p><strong>Introduction: </strong>Tuberculous meningitis (TBM) is a severe extra-pulmonary tuberculosis with high fatality. This meta-analysis aimed to assess the impact of linezolid on TBM treatment outcomes.</p><p><strong>Methods: </strong>We searched multiple databases for studies published up to May 18, 2024 comparing the effects of linezolid on TBM. Meta-analysis was conducted using Review Manager 5.4.</p><p><strong>Results: </strong>Our findings indicated that linezolid may reduce treatment failure risk (RR = 0.42 (0.20, 0.89), <i>p</i> = 0.02) and improve temperature recovery (RR = 1.56 (1.21, 2.02), <i>p</i> < 0.001) in TBM patients.</p><p><strong>Conclusions: </strong>The analysis suggests a positive association between linezolid treatment and therapeutic improvements, with no significant adverse reactions reported.</p>","PeriodicalId":8278,"journal":{"name":"Archives of Medical Science","volume":"20 3","pages":"1038-1042"},"PeriodicalIF":3.0,"publicationDate":"2024-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11264080/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141756817","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Licorice-induced severe hypokalemic rhabdomyolysis.","authors":"Haihong Wang, Zhenhua Wen, Miao You","doi":"10.5114/aoms/188909","DOIUrl":"https://doi.org/10.5114/aoms/188909","url":null,"abstract":"","PeriodicalId":8278,"journal":{"name":"Archives of Medical Science","volume":"20 3","pages":"1048-1049"},"PeriodicalIF":3.0,"publicationDate":"2024-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11264147/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141756821","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circular RNA circ_001621 acts as a tumor promoter in lung cancer by regulating the miR-199a-3p/GREM1 axis.","authors":"Jun Lei, Song Qiao","doi":"10.5114/aoms/174052","DOIUrl":"https://doi.org/10.5114/aoms/174052","url":null,"abstract":"<p><strong>Introduction: </strong>Investigating how circular RNAs (circRNAs) function during tumorigenesis may help uncover novel diagnostic markers for cancer treatment. The oncogenic role of circ_001621 has been verified in osteosarcoma, but its role in lung cancer has yet to be reported. This research is the first to investigate the circ_001621 expression and regulatory mechanism in lung cancer.</p><p><strong>Material and methods: </strong>RT-qPCR was performed to assess the circ_001621 expression levels in lung cancer cells and tissues. The influence of circ_001621 on the viability, invasive ability, and apoptosis of lung cancer cells was investigated through CCK-8, transwell, and caspase-3 activity experiments, respectively. A xenograft nude mouse model was designed to evaluate how circ_001621 functions <i>in vivo</i>. The RIP and luciferase reporter experiments confirmed the binding among circRNA, miRNA, and mRNA.</p><p><strong>Results: </strong>Circ_001621 was dramatically upregulated in lung cancer tissues and cells. Silencing circ_001621 in lung cancer cells reduced their viability and invasive ability but stimulated apoptosis. The nude mice experiment demonstrated that circ_001621 downregulation considerably stunted tumor growth <i>in vivo</i>. Additionally, circ_001621 could sponge miR-199a-3p. The inhibitor of miR-199a-3p improved the viability and invasion of cells while inhibiting apoptosis. Moreover, it offset the impact of circ_001621 on lung cancer cells. MiR-199a-3p was observed to target GREM1, and the downregulation of GREM1 could counteract miR-199a-3p-induced effects on lung cancer cells.</p><p><strong>Conclusions: </strong>The circ_001621/miR-199a-3p/GREM1 axis exhibits an association with the development of lung cancer, suggesting its potential as a future therapeutic target for the disease.</p>","PeriodicalId":8278,"journal":{"name":"Archives of Medical Science","volume":"20 3","pages":"876-886"},"PeriodicalIF":3.0,"publicationDate":"2024-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11264106/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141756807","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cinobufagin disrupts the stability of lipid rafts by inhibiting the expression of caveolin-1 to promote non-small cell lung cancer cell apoptosis.","authors":"Zhongqing Xu, Jinwei Li, Shuyu Fang, Mingzhu Lian, Changxiao Zhang, Jiahuan Lu, Kai Sheng","doi":"10.5114/aoms/174578","DOIUrl":"https://doi.org/10.5114/aoms/174578","url":null,"abstract":"<p><strong>Introduction: </strong>The study was designed to explore how cinobufagin (CB) regulates the development of non-small cell lung cancer (NSCLC) cells through lipid rafts.</p><p><strong>Material and methods: </strong>The effects of CB at gradient concentrations (0, 0.5, 1 and 2 µM) on NSCLC cell viability, apoptosis, reactive oxygen species (ROS) level, phosphorylation of Akt, and apoptosis- and lipid raft-related protein expression were assessed by MTT assay, flow cytometry and Western blot. Cholesterol and sphingomyelin were labeled with BODIPY to evaluate the effect of CB (2 µM) on them. Sucrose density gradient centrifugation was used to extract lipid rafts. The effect of CB on the expression and distribution of caveolin-1 was determined by immunofluorescence, quantitative reverse transcription polymerase chain reaction and Western blot. After overexpression of caveolin-1, the above experiments were performed again to observe whether the regulatory effect of CB was reversed.</p><p><strong>Results: </strong>CB inhibited NSCLC cell viability while promoting apoptosis and ROS level. CB redistributed the lipid content on the membrane surface and reduced the content of caveolin-1 in the cell membrane. In addition, CB repressed the activation of AKT. However, caveolin-1 overexpression reversed the effects of CB on apoptosis, AKT activation and lipid raft.</p><p><strong>Conclusions: </strong>CB regulates the activity of Akt in lipid rafts by inhibiting caveolin-1 expression to promote NSCLC cell apoptosis.</p>","PeriodicalId":8278,"journal":{"name":"Archives of Medical Science","volume":"20 3","pages":"887-908"},"PeriodicalIF":3.0,"publicationDate":"2024-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11264083/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141756806","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}