Archives of Medical Science最新文献

{"title":"Serum total bile acids are associated with coronary artery calcification as assessed by non-gated chest computed tomography: a multicenter study.","authors":"Yuxuan Tong, Xiao Chen, Dongdong Wang, Xuefei Zhang, Yuxin Pan, Mengjia Chen, Hangyi Zhou, Jianhua Wang, Dongling Lv","doi":"10.5114/aoms/216044","DOIUrl":"10.5114/aoms/216044","url":null,"abstract":"<p><strong>Introduction: </strong>Coronary artery calcification (CAC) is a risk factor for cardiovascular disease (CVD). The association between serum total bile acid (TBA) concentration and CAC has not been investigated, even though bile acid may act as a mediator between gut microbiota and CVD. We examined this relationship in a general Chinese population.</p><p><strong>Material and methods: </strong>This cross-sectional study included 2133 people who underwent computed tomography (CT) scans for lung cancer screening between 2018 and 2020. Information on medical history, laboratory test results, and demographics was collected from medical records. CAC was assessed on non-gated chest CT images. Multivariable logistic regression analysis and restricted triple spline analysis were applied to examine the correlation between TBA and CAC risk.</p><p><strong>Results: </strong>CACs were detected in 426 of 2133 participants. Participants with higher TBA concentrations had a considerably higher prevalence of CAC (33.4% in the fourth quartile and 11.5% in the first quartile, <i>p</i> < 0.001). TBA was closely associated with CAC, as determined by multivariable logistic regression analysis (OR = 1.05, 95% CI: 1.00-1.10). The fourth TBA quartile was significantly associated with a high incidence of CAC in the general population (OR = 1.76, 95% CI: 1.02-3.06), in older adults (OR = 1.66, 95% CI: 1.03-2.68), and in subjects without diabetes (OR = 1.62, 95% CI: 1.07-2.45) or hypertension (OR = 1.74, 95% CI: 1.16-2.63) when compared to the first TBA quartile.</p><p><strong>Conclusions: </strong>A substantial and positive correlation was found between elevated TBA and CAC. The causal relationship between TBA and CAC risk should be investigated in longitudinal studies.</p>","PeriodicalId":8278,"journal":{"name":"Archives of Medical Science","volume":"22 3","pages":"1381-1388"},"PeriodicalIF":3.6,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13426178/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148653100","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":"&lt;i&gt;Slc6a4&lt;/i&gt; silencing alleviates ropivacaine-induced injury in myocardial infarction cell models","authors":"Jing Wan, Xiaonan Du, Peiwen Luo, S. Li","doi":"10.5114/aoms/211891","DOIUrl":"https://doi.org/10.5114/aoms/211891","url":null,"abstract":"Introduction Myocardial infarction (MI), often caused by atherosclerotic plaque rupture, leads to severe myocardial ischemia and necrosis. Despite advancements in treatment, its molecular mechanisms remain incompletely understood. Local anesthetics such as ropivacaine, while beneficial for pain control, may induce cardiotoxicity, complicating MI management. This study aimed to explore the effects of ropivacaine on H9c2 cardiomyocytes and the protective potential of Slc6a4 silencing against ropivacaine-induced cellular damage. Material and methods Bioinformatics analysis of the GSE97320 dataset identified MI-associated differentially expressed genes (DEGs), which overlapped with ropivacaine-related genes. H9c2 cells were cultured and treated with ropivacaine to induce myocardial injury. The effects on cell cycle, apoptosis, and oxidative stress were assessed, and the role of Slc6a4 silencing under hypoxia/reoxygenation (H/R) conditions was investigated. Results Ropivacaine induced G1 phase arrest and apoptosis in H9c2 cells, with increased Bax and caspase 3 levels and decreased Bcl-2. Oxidative stress was elevated, as evidenced by increased ROS, MDA, and LDH levels and reduced SOD, GSH, and ATP. Slc6a4 silencing under H/R conditions mitigated these effects, reducing cell cycle dysregulation and apoptosis by 40%, lowering NLRP3 inflammasome expression, and promoting Nrf2 nuclear translocation. Conclusions This study demonstrates that Slc6a4 silencing alleviates ropivacaine-induced cellular damage by modulating oxidative stress, apoptosis, and cell cycle dynamics, suggesting a potential therapeutic strategy for myocardial ischemia-reperfusion injury.","PeriodicalId":8278,"journal":{"name":"Archives of Medical Science","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.archivesofmedicalscience.com/pdf-211891-135124?filename=Slc6a4-silencing-alleviat.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147917070","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":"Diabetes risk assessment in Polish community pharmacies. Results from a pilot national screening campaign.","authors":"Magdalena Jasińska-Stroschein, Magdalena Waszyk-Nowaczyk, Olga Sierpniowska, Artur Jędra, Aleksandra Uruska, Jacek Jóźwiak","doi":"10.5114/aoms/216396","DOIUrl":"10.5114/aoms/216396","url":null,"abstract":"","PeriodicalId":8278,"journal":{"name":"Archives of Medical Science","volume":"22 1","pages":"527-530"},"PeriodicalIF":3.6,"publicationDate":"2026-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13154790/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147866562","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":"2025: The year in cardiovascular disease - the year of triglyceride lowering therapies. Can we effectively reduce triglyceride-related residual cardiovascular disease and pancreatitis risk?","authors":"Peter P Toth, Maciej Banach","doi":"10.5114/aoms/216960","DOIUrl":"10.5114/aoms/216960","url":null,"abstract":"<p><p>This state-of-the-art review surveys the rapidly advancing field of triglyceride-lowering therapies as of 2025, positioning hypertriglyceridemia (HTG) as both a residual driver of atherosclerotic cardiovascular disease (ASCVD) and a key precipitant of acute pancreatitis. After outlining the pathophysiological role of elevated triglycerides - via remnant lipoproteins, inflammation and endothelial dysfunction, often within the lipid triad of low high-density lipoprotein-cholesterol (HDL-C) and small, dense low-density lipoprotein (LDL) - we evaluate established and emerging pharmacologic options. Fenofibrate, a PPAR-α activator, remains a cornerstone for mixed dyslipidemia, improving micro- and macrovascular outcomes in diabetes. Purified eicosapentaenoic acid (icosapent ethyl) is highlighted for its robust reduction of major adverse cardiovascular events despite neutral triglyceride thresholds, albeit with a modest increase in atrial fibrillation risk. Novel agents targeting apolipoprotein C-III (volanesorsen, olezarsen, plozasiran) achieve profound triglyceride declines and substantially mitigate pancreatitis in familial chylomicronemia syndrome (FCS), while angiopoietin-like 3 (ANGPTL3) inhibitors and fibroblast growth factor 21 (FGF21) agonists demonstrate early promise in broad atherogenic-lipid reduction and metabolic modulation. The paper emphasizes the importance of genetic testing to differentiate FCS from multifactorial chylomicronemia syndrome, guiding personalized therapy. Current guidelines endorse icosapent ethyl and fenofibrate for high-risk HTG, with apoC-III inhibitors poised to become first-line for FCS as access improves. Ongoing trials of ANGPTL3 inhibitors, FGF21 agonists and gene-editing approaches may soon redefine lifelong lipid management.</p>","PeriodicalId":8278,"journal":{"name":"Archives of Medical Science","volume":"21 6","pages":"2229-2245"},"PeriodicalIF":3.3,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12887957/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146163935","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":"CYP2J2 links metabolic reprogramming to colorectal cancer progression.","authors":"Guowen Lu, Yier Qiu, Zhongchen Liu","doi":"10.5114/aoms/216416","DOIUrl":"10.5114/aoms/216416","url":null,"abstract":"","PeriodicalId":8278,"journal":{"name":"Archives of Medical Science","volume":"21 6","pages":"2872-2875"},"PeriodicalIF":3.3,"publicationDate":"2025-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12887966/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146163929","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":"Curcumin ameliorates ulcerative colitis via inhibiting STAT3-mediated angiogenesis.","authors":"Su Xu, Zixuan Zhou, Aoxun Zhu, Yurong Guo, Shengnan Jin, Maozhen Zhang, Yanping Hao","doi":"10.5114/aoms/215559","DOIUrl":"10.5114/aoms/215559","url":null,"abstract":"<p><strong>Introduction: </strong>Ulcerative colitis (UC) is a chronic and persistent inflammatory bowel disease with limited clinical treatment options and significant therapeutic challenges. This study aimed to evaluate whether the therapeutic effect of curcumin against ulcerative colitis is positively correlated with its inhibition of angiogenesis and to elucidate the underlying angiogenesis-related molecular mechanism.</p><p><strong>Material and methods: </strong>A multi-database analysis was performed to predict the possible targets involved in curcumin inhibition of UC. Tube formation and aortic ring assays were used to evaluate angiogenesis <i>in vitro</i>. A dextran sulfate sodium (DSS)-induced ulcerative colitis mouse model was used to evaluate curcumin's effect on UC.</p><p><strong>Results: </strong>We first employed a comprehensive multi-database analysis to identify overlapping targets connecting curcumin, ulcerative colitis, and angiogenesis, leading to the identification of signal transducer and activator of transcription 3 (STAT3) as a potential mediator of this process. <i>In vitro</i> experimental results demonstrated that curcumin significantly inhibited tube formation in human umbilical vein endothelial cells (HUVEC) and suppressed endothelial sprouting in rat aortic rings. Furthermore, curcumin downregulated the expression of vascular endothelial growth factor (VEGF) in HUVEC cells and concurrently inhibited the expression of phosphorylated JAK2 and phosphorylated STAT3 (Y705). Notably, the addition of VEGF partially reversed curcumin's inhibitory effects on p-JAK2 and p-STAT3. <i>In vivo</i> studies using a DSS-induced mouse model of ulcerative colitis revealed that curcumin ameliorated DSS-induced colon shortening and various disease symptoms. It also suppressed serum levels of TNF-α and IL-6 and inhibited the expression of STAT3 and VEGF in colonic tissues.</p><p><strong>Conclusions: </strong>Curcumin ameliorates ulcerative colitis through inhibition of the VEGF-mediated JAK2/STAT3 signaling pathway. These findings position curcumin as a potential clinical candidate drug for the treatment of ulcerative colitis.</p>","PeriodicalId":8278,"journal":{"name":"Archives of Medical Science","volume":"22 2","pages":"926-939"},"PeriodicalIF":3.6,"publicationDate":"2025-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13266764/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148263137","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":"Association between maternal pre-pregnancy body mass index, health and socioeconomic factors and neonatal birthweight, preterm birth and onset of delivery, double-center case-control study.","authors":"Iwona Jańczewska, Alicja Jańczewska-Twardowska, Natalia K Mazur-Ejankowska, Małgorzata Szczurek-Gierczak, Jolanta Wierzba","doi":"10.5114/aoms/216395","DOIUrl":"10.5114/aoms/216395","url":null,"abstract":"","PeriodicalId":8278,"journal":{"name":"Archives of Medical Science","volume":"21 6","pages":"2876-2881"},"PeriodicalIF":3.3,"publicationDate":"2025-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12887981/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146163907","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":"&lt;i&gt;JAG1&lt;/i&gt;-Notch signaling drives M1 macrophage polarization in osteoarthritis","authors":"Shufeng Yang, Li Jiao, Chengcheng Jiang, Guang Li, Fan Sun","doi":"10.5114/aoms/210615","DOIUrl":"https://doi.org/10.5114/aoms/210615","url":null,"abstract":"Introduction Osteoarthritis (OA) is characterized by chronic synovial inflammation, in which synovial macrophages (SMs) play a crucial role. The contribution of JAG1 to macrophage polarization in OA remains unclear. Material and methods Differentially expressed genes (DEGs) were identified by analyzing the GSE64394, GSE55457, and GSE1919 datasets. An in vitro OA model was created. The effects on Notch signaling and macrophage polarization were assessed in IL-1-treated fibroblast-like synoviocytes (FLS) co-cultured with SMs. JAG1 expression was manipulated by siRNA knockdown and overexpression, and downstream effects were assessed using quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blotting (WB). Results Eleven overlapping DEGs, including JAG1, IL6, TGFB2, CX3CL1, and MMP1 were identified. Through the construction of cellular models, these genes were found to be potentially associated with inflammation, immune regulation, and extracellular matrix remodeling in OA. Additionally, the OA model was shown to induce polarization of SMs toward the M1 phenotype. In vitro experiments revealed that JAG1 was significantly upregulated in OA samples. JAG1 knockdown in the co-culture model reduced M1 markers (NOS2, PTGS2, CD64, CD86), increased M2 markers (CD206, CD163), and suppressed Notch signaling, while JAG1 overexpression reversed these effects. Conclusions JAG1 promotes the polarization of SMs toward M1 in OA by activating the Notch signaling pathway, providing preliminary evidence that the JAG1/Notch axis may serve as a potential therapeutic target for regulating inflammation and tissue remodeling in OA.","PeriodicalId":8278,"journal":{"name":"Archives of Medical Science","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.archivesofmedicalscience.com/pdf-210615-134226?filename=JAG1-Notch-signaling-driv.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147883614","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":"Mortality trends related to cardiac arrest in patients with diabetes mellitus aged 25 and older across the United States: an analysis using the CDC WONDER database from 1999 to 2024.","authors":"Muhammad Abdullah Naveed, Ahila Ali, Muhammad Ahmed, Muhammad Junaid Razzak, Omer Rehan Muhammad, Muhammad Naveed Uz Zafar, Muhammad Hasan, Rabia Iqbal, Bazil Azeem, Hamza Naveed, Harigopal Sandhyavenu, Muhammad Bilal Munir, Wael Almahmeed, Sivaram Neppala, Maciej Banach","doi":"10.5114/aoms/215585","DOIUrl":"10.5114/aoms/215585","url":null,"abstract":"<p><strong>Introduction: </strong>Cardiac arrest (CA) is a leading cause of death in the US, with over 600,000 cases annually. People with diabetes mellitus (DM) have higher CA risk and worse outcomes due to factors such as obesity, hypertension, and dyslipidemia. This study examined the mortality trends of CA among adults with diabetes from 1999 to 2024.</p><p><strong>Material and methods: </strong>We analyzed data from the CDC WONDER multiple-cause-of-death database, identifying decedents aged ≥ 25 years with both CA and DM listed as underlying or contributing causes of death (ICD-10: I46.0 to I46.9 for CA; E10-E14 for DM). Annual crude and age-adjusted mortality rates were calculated. Joinpoint regression was used to identify trend changes and calculate annual percent changes (APC) and average annual percent changes (AAPC).</p><p><strong>Results: </strong>Between 1999 and 2024, a total of 1,146,259 deaths were recorded. Overall, the age-adjusted mortality rate (AAMR) decreased from 21.3 per 100,000 in 1999 to 18.3 in 2024 with an AAPC of -0.69. However, a significant increase occurred from 2018 to 2021 (APC: +11.02), coinciding with the COVID-19 pandemic. Men exhibited higher AAMRs than women (23.9 and 16.1, respectively), and non-Hispanic Black individuals had the highest racial AAMRs at 37.1. Geographic disparities revealed the Western U.S. to have the highest mortality rate at 29, and urban areas to have slightly higher AAMRs than rural areas (19.4 vs. 18.7).</p><p><strong>Conclusions: </strong>While CA-related mortality among diabetic adults decreased from 1999 to 2018, a rise between 2018 and 2021 highlights vulnerabilities, especially among men, non-Hispanic Black populations, and high-burden regions. Continued efforts are necessary to address healthcare disparities and enhance emergency responses, thereby reducing mortality gaps.</p>","PeriodicalId":8278,"journal":{"name":"Archives of Medical Science","volume":"22 1","pages":"75-86"},"PeriodicalIF":3.6,"publicationDate":"2025-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13154751/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147866197","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":"Factors influencing the risk of cardiovascular complications following COVID-19 - clinical implications. The LATE-COVID study.","authors":"Joanna Lewek, Bożena Sosnowska, Agata Bielecka-Dąbrowa, Maciej Banach","doi":"10.5114/aoms/188090","DOIUrl":"10.5114/aoms/188090","url":null,"abstract":"","PeriodicalId":8278,"journal":{"name":"Archives of Medical Science","volume":"21 6","pages":"2882-2887"},"PeriodicalIF":3.3,"publicationDate":"2025-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12887968/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146163881","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}