Archives of Medical Science最新文献

{"title":"Sport-related entheseal adaptation and damage in elite athletes: a cross-sectional ultrasound study.","authors":"Sibel Bakirci, Tuba Melekoglu, Güfat Arslan, Seyyid B Acıkgoz, Yılmaz Sungur, Sibel Z Aydin","doi":"10.5114/aoms/217517","DOIUrl":"https://doi.org/10.5114/aoms/217517","url":null,"abstract":"<p><strong>Introduction: </strong>Entheses, the sites where tendons, ligaments, and joint capsules insert into bone, are highly susceptible to mechanical stress. While enthesitis is a cardinal feature of spondyloarthritis (SpA), repetitive mechanical loading in elite athletes can also induce entheseal changes. High-resolution ultrasound (US) allows for detailed assessment of entheseal inflammation and structural damage. However, the specific impact of sport-specific loading patterns on differentiating physiological entheseal adaptation from early pathology in asymptomatic elite athletes remains a critical area for investigation.</p><p><strong>Material and methods: </strong>This cross-sectional study evaluated 87 elite athletes from various sports (athletics, basketball, cycling, golf, handball, climbing, archery) and 49 sedentary controls. Elite status was defined as training > 10 h/week for over 5 years. All participants underwent US evaluation of 20 bilateral entheseal sites. US findings were scored semi-quantitatively (0-3) for inflammation (hypoechogenicity, thickening, power Doppler [PD] signals) and damage (calcifications, erosions, enthesophytes) according to OMERACT definitions. Athletes were grouped by dominant extremity use (upper, lower, or both). Statistical comparisons and linear regression analyses were performed to identify associations between entheseal scores and demographic/training variables.</p><p><strong>Results: </strong>Elite athletes exhibited significantly higher entheseal inflammation and damage scores compared to sedentary controls (<i>p</i> < 0.05). Athletes practicing upper extremity-dominant sports (e.g., archery, climbing) showed significantly higher upper extremity inflammation (median [IQR], 1 [0-3] vs. 0 [0-1.5]; <i>p</i> = 0.010) and damage scores (median [IQR], 0 [0-3] vs. 0 [0-0]; <i>p</i> < 0.001) than controls. Similarly, lower extremity-dominant athletes (e.g., athletics, cycling) had significantly higher lower extremity inflammation scores (median [IQR], 2 [1-4] vs. 0 [0-1]; <i>p</i> < 0.001). Linear regression revealed that upper extremity inflammation was independently associated with age and weekly training duration, while lower extremity inflammation was solely associated with body mass index (BMI). Notably, a high prevalence of US abnormalities was observed despite many athletes being asymptomatic.</p><p><strong>Conclusions: </strong>Sport-specific mechanical loading is strongly associated with localized entheseal changes detectable by US in elite athletes. These findings underscore the importance of contextualizing US results within an athlete's specific sport and loading history to distinguish between subclinical entheseal adaptation and true pathology.</p>","PeriodicalId":8278,"journal":{"name":"Archives of Medical Science","volume":"22 4","pages":"2154-2162"},"PeriodicalIF":3.6,"publicationDate":"2026-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13663641/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149191038","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":"Remnant cholesterol inflammatory index and mortality in cardiovascular-kidney-metabolic syndrome: a national study.","authors":"Lele Wang, Haoran Li, Lili Wang, Ji Hao, Qingdui Zhang, Qiang Zhou, Jing Wang, Chunmei Qi","doi":"10.5114/aoms/218809","DOIUrl":"10.5114/aoms/218809","url":null,"abstract":"<p><strong>Introduction: </strong>Cardiovascular-kidney-metabolic (CKM) syndrome reflects the interconnected progression of metabolic dysfunction, kidney impairment, and cardiovascular disease. The remnant cholesterol inflammatory index (RCII), integrating remnant cholesterol and C-reactive protein, may capture combined metabolic-inflammatory stress, but its association with mortality in CKM populations is unclear.</p><p><strong>Material and methods: </strong>Using NHANES 1999-2018, we included adults aged ≥ 18 years with complete CKM staging and RCII measurements. All-cause mortality was the primary outcome, and cardiovascular mortality the secondary outcome. Kaplan-Meier analysis, Cox models, restricted cubic splines (RCS), and subgroup analyses were performed to evaluate associations between RCII and mortality.</p><p><strong>Results: </strong>Among 11,917 CKM participants (median follow-up: 157 months), 2,474 all-cause and 774 cardiovascular deaths occurred. Elevated RCII was associated with increased mortality. In the fully adjusted model, each SD increase in RCII corresponded to a 7% higher risk of all-cause (HR = 1.07, 95% CI: 1.05-1.09) and 8% higher cardiovascular mortality (HR = 1.08, 95% CI: 1.05-1.12) (both <i>p</i> < 0.001). Compared to the lowest RCII quartile (Q1 < 1.61), the highest quartile (Q4 ≥ 13.42) had a 41% higher risk of all-cause (HR = 1.41, 95% CI: 1.24-1.60) and 34% higher cardiovascular mortality (HR = 1.34, 95% CI: 1.06-1.69). RCS analysis revealed significant nonlinear relationships, with consistent associations across subgroups and no significant interactions.</p><p><strong>Conclusions: </strong>Elevated RCII is strongly and consistently associated with increased all-cause and cardiovascular mortality risks among individuals with CKM. Further studies are warranted to validate its incremental predictive value and to explore targeted interventions for populations with high RCII.</p>","PeriodicalId":8278,"journal":{"name":"Archives of Medical Science","volume":"22 2","pages":"672-683"},"PeriodicalIF":3.6,"publicationDate":"2026-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13266776/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148262955","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":"NBPF1 acts as a tumor suppressor in prostate cancer by regulating the PI3K/AKT pathway.","authors":"Zhihao Yao, Mingquan Chen, Junming Bi, Zhaoqiang Jiang, Weinan Zeng, Bowen Yang, Hangyu Liao, Xiaokang Gu, Ping Zhu, Cheng Zhang, Yanjun Liu, Yuming Yu","doi":"10.5114/aoms/214433","DOIUrl":"10.5114/aoms/214433","url":null,"abstract":"<p><strong>Introduction: </strong>Prostate cancer (PCa) is a leading malignancy in men, yet the roles of many candidate regulators remain unclear. Neuroblastoma breakpoint family member 1 (NBPF1) has been implicated as a tumor suppressor in other cancers; however, its function and clinical relevance in PCa remain undefined.</p><p><strong>Material and methods: </strong>NBPF1 expression was examined in tissue microarrays (TMAs) comprising 77 PCa tumors and 73 normal prostate tissues using immunohistochemistry, and its correlation with clinicopathological features and outcomes was assessed. NBPF1 gain- and loss-of-function models were established in PCa cell lines (LNCaP, DU145, PC3, 22RV1) and compared with RWPE-1 cells. Proliferation (CCK-8, EdU, colony formation), migration/invasion (wound healing, Transwell), and protein expression (qRT-PCR, Western blot) were assessed. <i>In vivo</i> oncogenic effects were evaluated using PC3 xenografts (<i>n</i> = 5 per group). RNA-seq of NBPF1-silenced PC3 cells, as well as KEGG analysis, was used to identify downstream pathways.</p><p><strong>Results: </strong>NBPF1 was markedly downregulated in PCa compared with normal prostate, and low expression was associated with adverse features (e.g., higher Gleason grade) and poorer prognosis. NBPF1 overexpression suppressed proliferation, migration, and invasion, whereas NBPF1 knockdown had the opposite effects. In mice, NBPF1 loss accelerated tumor growth. Transcriptomic profiling implicated the PI3K/AKT signaling pathway as a key downstream pathway; concordantly, NBPF1 loss increased p-AKT and elevated MMP2/MMP9 expression, while NBPF1 overexpression reduced pathway activation and protease expression.</p><p><strong>Conclusions: </strong>NBPF1 functions as a tumor suppressor in PCa, inhibiting progression at least partly through modulation of the PI3K/AKT pathway. NBPF1 may serve as a prognostic biomarker and a potential therapeutic target in prostate cancer.</p>","PeriodicalId":8278,"journal":{"name":"Archives of Medical Science","volume":"22 3","pages":"1748-1773"},"PeriodicalIF":3.6,"publicationDate":"2026-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13426230/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148652987","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":"Global co-occurrence patterns of cancer and cardiovascular disease: a comprehensive analysis based on the Global Burden of Disease Study 2021.","authors":"Xiaohan Qiu, Ben Hu, Jiahan Ke, Jun Gu","doi":"10.5114/aoms/216397","DOIUrl":"10.5114/aoms/216397","url":null,"abstract":"<p><strong>Introduction: </strong>Cardiovascular disease (CVD) and neoplasms are the two leading causes of death worldwide. Previous research has predominantly addressed these conditions separately or focused on specific regions. We aimed to characterize the global co-occurrence pattern of CVD and neoplasms from spatial and temporal perspectives and identify corresponding risk factors across different epidemiological contexts.</p><p><strong>Material and methods: </strong>Using GBD 2021 data, we extracted age-standardized disability-adjusted life year (DALY) rates of CVD and neoplasms and modifiable risk factor exposure from 204 countries and territories (1990-2021). We identified four epidemiological patterns: low-burden, neoplasm-dominant, CVD-dominant, and dual-burden regions. We calculated population attributable fractions (PAF) and integrated machine learning with SHAP values to distinguish intervention priorities. Average annual percentage changes (AAPC) were used to evaluate temporal trends.</p><p><strong>Results: </strong>Each pattern comprised 50-52 countries. Spatial distribution overlapped with socioeconomic development stages and risk factor exposure. Temporal analysis revealed widening global inequality: low-burden regions achieved 3-4% annual reductions while dual-burden regions experienced an increasing burden, creating a 5.8 percentage point gap. High systolic blood pressure was the universal dominant CVD risk factor, accounting for 49.7% of the global burden (49.2-52.4% across patterns). For neoplasms, smoking contributed 18.5% globally but varied dramatically by pattern (10.4-23.4%). Modifiable risk factors' specific combinations greatly influenced global disparities.</p><p><strong>Conclusions: </strong>The co-occurrence of CVD and neoplasms represents interconnected manifestations of different epidemiological transition stages, with concerning divergence between regions. Interventions targeting hypertension control and tobacco cessation, combined with pattern-specific strategies, can fundamentally reduce the global disease burden.</p>","PeriodicalId":8278,"journal":{"name":"Archives of Medical Science","volume":"22 2","pages":"760-781"},"PeriodicalIF":3.6,"publicationDate":"2026-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13266533/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148262660","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":"Evaluating the potential causal relationship between carnitine-related metabolites and breast cancer: a Mendelian randomization and transcriptomic analysis.","authors":"Feifeng Ran, Lilin Que, Lan Luo, Mei Gan, Rensheng Wang, Leifeng Liang","doi":"10.5114/aoms/216186","DOIUrl":"10.5114/aoms/216186","url":null,"abstract":"<p><strong>Introduction: </strong>Breast cancer (BC) is the most common malignancy among women worldwide. Although observational studies have linked carnitine-related metabolites (CRMs) to BC, causal inference has been limited by confounding and reverse causality. This study used Mendelian randomization (MR) analysis to investigate the potential causal link between CRMs and BC.</p><p><strong>Material and methods: </strong>MR analysis was conducted using the Cancer Genome Atlas-BC and CRM-related datasets to explore the potential causal relationship between CRMs and BC. Variants were screened based on criteria encompassing genome-wide significance (<i>p</i> < 5×10^-8), independence (<i>r</i> ² < 0.001, kb=10000), and sufficient strength (F-statistic > 10). Various MR techniques, including inverse-variance weighted, MR-Egger, simple mode, weighted mode, and weighted median approaches, were applied to assess these potential causal associations. Single-cell RNA sequencing (scRNA-seq) was employed to investigate the expression and biological functions of biomarkers linked to metabolites.</p><p><strong>Results: </strong>The MR analysis suggested that genetically predicted elevated levels of octanoylcarnitine and decanoylcarnitine were associated with increased risk of BC. Functional enrichment analysis identified 12 candidate genes associated with these metabolites, which are involved in fatty acid β-oxidation (FAO) pathways. ScRNA-seq analysis revealed eight distinct cell subpopulations, with macrophages exhibiting the highest intercellular communication. Six biomarkers were identified as potential contributors to BC development: ACADM, FNIP2, RAPGEF2, RABGGTB, PPID, and ST6GALNAC3.</p><p><strong>Conclusions: </strong>This study provides evidence supporting potential causal associations between octanoylcarnitine and decanoylcarnitine and BC risk. Integrative single-cell transcriptomics revealed six CRM-associated biomarkers and their dynamic expression within tumor microenvironments. Additional experimental and clinical studies are needed to validate these observations and clarify their biological and translational relevance.</p>","PeriodicalId":8278,"journal":{"name":"Archives of Medical Science","volume":"22 3","pages":"1688-1705"},"PeriodicalIF":3.6,"publicationDate":"2026-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13426160/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148652871","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":"Epstein-Barr virus-related antibody traits and idiopathic pulmonary fibrosis: a bidirectional Mendelian randomization study.","authors":"Wentao Wu, Huiying Zhang, Zhe Peng, Shuohao Wang, Xiaozhao Li, Gaojun Xu, Yiqiang Yuan","doi":"10.5114/aoms/214291","DOIUrl":"10.5114/aoms/214291","url":null,"abstract":"<p><strong>Introduction: </strong>Previous studies have suggested an association between herpesvirus infections and idiopathic pulmonary fibrosis (IPF), but the causal relationship remains largely unclear. We used bidirectional Mendelian randomization (MR) to investigate the associations between genetically predicted antibody responses to herpesviruses and IPF risk.</p><p><strong>Material and methods: </strong>The data for different antibodies against herpes simplex virus (HSV), cytomegalovirus (CMV), and Epstein-Barr virus (EBV) were obtained from the IEU GWAS database (https://gwas.mrcieu.ac.uk/datasets/), and the data for IPF were obtained from the FinnGen GWAS database (https://r7.finngen.fi/). We selected eligible single nucleotide polymorphisms (SNPs) from summary-level data of GWAS as instrumental variables. The generalized summary data-based MR (GSMR) method was used as the main analysis method, complemented by inverse-variance weighted (IVW), MR-Egger, and weighted median analyses. Sensitivity analyses were conducted to check the robustness of the MR results, and reverse MR analyses were performed to assess potential reverse causation.</p><p><strong>Results: </strong>Genetically predicted antibody responses to EBV viral capsid antigen (VCA) p18 were associated with IPF risk. However, GSMR and IVW results indicated that anti-EBV IgG levels were significantly negatively associated with IPF. Sensitivity analyses suggested limited influence of horizontal pleiotropy.</p><p><strong>Conclusions: </strong>Genetically predicted EBV-related immune responses show heterogeneous associations with IPF risk. These findings suggest a potential role of EBV-related immune mechanisms in IPF, although causal interpretation should be made cautiously. Further studies are needed to clarify underlying biological mechanisms.</p>","PeriodicalId":8278,"journal":{"name":"Archives of Medical Science","volume":"22 3","pages":"1811-1821"},"PeriodicalIF":3.6,"publicationDate":"2026-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13426140/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148652728","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":"Irisin may be involved in exendin-4 mitochondrial action in human adipocytes.","authors":"Agnieszka Dziewońska, Anna Polus, Anna Gruca, Bogdan Solnica, Joanna Góralska","doi":"10.5114/aoms/214730","DOIUrl":"10.5114/aoms/214730","url":null,"abstract":"<p><strong>Introduction: </strong>Disturbed mitochondrial activity in adipocytes has been proposed as one of the mechanisms involved in metabolic dysfunction in obesity. Glucagon-like peptide receptor agonists (GLP-1RAs) are used to normalize glucose level and reduce body weight. GLP-1 activates intracellular pathways similar to those of irisin, a peptide that modulates metabolism by stimulating the 'browning' of adipocytes. The aim of the study was to investigate the mechanisms of action of the GLP-1RA exendin-4 at the mRNA, protein, and mitochondrial levels in human adipocytes.</p><p><strong>Material and methods: </strong>Human Chub-S7 preadipocytes were differentiated <i>in vitro</i> to mature adipocytes and then stimulated with exendin-4 at 100 nM for 24 h. Expression levels of mRNA and proteins (irisin, adiponectin, visfatin/NAMPT) were measured. Oxygen consumption rates and intracellular ATP content were determined.</p><p><strong>Results: </strong>Exendin-4 enhanced the secretion of irisin and visfatin by adipocytes. Upregulated expression of FNDC5, NAMPT, and UCP2 genes was accompanied by modest changes in mitochondrial activity in exendin-4-treated adipocytes. Exendin-4 exerted a similar effect on mitochondrial oxygen consumption rates as irisin, including increased maximum mitochondrial respiration and reserve capacity with unchanged intracellular ATP.</p><p><strong>Conclusions: </strong>Increasing energy expenditure by exendin-4 may be associated with upregulation of irisin in human adipocytes. Clinical studies are necessary to confirm the hypothesis that nutrients, by stimulating the secretion of GLP-1, may influence the expression of irisin and thus modulate the mitochondrial metabolism of adipocytes.</p>","PeriodicalId":8278,"journal":{"name":"Archives of Medical Science","volume":"22 2","pages":"958-967"},"PeriodicalIF":3.6,"publicationDate":"2026-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13266781/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148263014","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":"Exploring the potential causal role of IgG N-glycosylation in urological cancers: a two-sample Mendelian randomization study using European ancestry datasets.","authors":"Yatfaat Ho, Manchun Chao","doi":"10.5114/aoms/214288","DOIUrl":"10.5114/aoms/214288","url":null,"abstract":"<p><strong>Introduction: </strong>Urological cancers pose a significant global health burden. Alterations in immunoglobulin G(IgG) N-glycosylation are implicated in cancer pathogenesis, but their causal role remains unclear. This study aimed to explore the potential causal associations between 77 specific IgG N-glycan traits (IGPs) and the risks of bladder, kidney, and prostate cancer.</p><p><strong>Material and methods: </strong>We conducted a two-sample Mendelian randomization (MR) study using summary-level data. Genetic instruments for IGPs were obtained from a genome-wide association study (GWAS) of European descent. Outcome data were sourced from the FinnGen consortium. The inverse-variance weighted (IVW) method was the primary analysis, supplemented by multiple sensitivity analyses (MR-Egger, weighted median, MR-PRESSO, and MR-RAPS). The Steiger test was used to confirm causal direction.</p><p><strong>Results: </strong>After false discovery rate (FDR) correction, one association remained statistically significant. Using the IVW method, genetically predicted higher levels of IGP23 were significantly associated with a decreased risk of bladder cancer (OR = 0.78, <i>p</i> = 4.7e-04, FDR = 0.037). Thirteen additional nominal associations (<i>p</i> < 0.05) were observed for urological cancers (e.g., IGP10 for prostate cancer; IGP52, IGP73 for kidney cancer), although these did not withstand multiple testing correction. Sensitivity analyses showed no evidence of directional pleiotropy.</p><p><strong>Conclusions: </strong>Our study provides evidence supporting a potential causal association between the IgG N-glycan trait IGP23 and the risk of bladder cancer. Other nominal associations require further investigation. These findings highlight IGP23 as a candidate for future mechanistic and translational research in bladder cancer.</p>","PeriodicalId":8278,"journal":{"name":"Archives of Medical Science","volume":"22 3","pages":"1738-1747"},"PeriodicalIF":3.6,"publicationDate":"2026-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13426189/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148652830","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":"Understanding the link between lipid and ocular disorders for effective therapy.","authors":"Muhammad Zulfiqah Sadikan, Haryati Ahmad Hairi, Lidawani Lambuk","doi":"10.5114/aoms/216374","DOIUrl":"10.5114/aoms/216374","url":null,"abstract":"<p><p>Cholesterol is an essential lipid for cellular integrity and metabolic homeostasis; however, dysregulated cholesterol metabolism is increasingly recognized as a key contributor to multiple ocular diseases. Beyond its established role in cardiovascular pathology, emerging evidence implicates altered lipoprotein balance, impaired cholesterol transport, and lipid-driven inflammation in the pathogenesis of age-related macular degeneration, retinal vascular diseases, cataracts, and glaucoma. This review integrates current knowledge on cholesterol synthesis, transport, and regulation with ocular-specific mechanisms, emphasizing the differential roles of low-density lipoprotein, high-density lipoprotein, and triglyceride-rich lipoproteins. Key molecular pathways, including the mevalonate-SREBP axis, ABCA1/ABCG1-mediated reverse cholesterol transport, VEGF-driven angiogenesis, oxidative stress signaling, and inflammatory cascades, are critically discussed. Clinical and translational implications are highlighted, particularly the potential ocular benefits of lipid-modulating therapies such as statins, fenofibrate, and antioxidant supplementation. Understanding cholesterol as a modifiable determinant of ocular health may enable integrated preventive strategies and guide future therapeutic innovation in vision-threatening diseases.</p>","PeriodicalId":8278,"journal":{"name":"Archives of Medical Science","volume":"22 2","pages":"583-601"},"PeriodicalIF":3.6,"publicationDate":"2026-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13266743/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148263162","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":"Combining the PI-RADS v2.1 score with PSAD improves the diagnostic accuracy of transition zone prostate cancer.","authors":"Jinman Zhong, Jianke Ding, Yuelang Zhang, Quanxin Yang","doi":"10.5114/aoms/213307","DOIUrl":"10.5114/aoms/213307","url":null,"abstract":"<p><strong>Introduction: </strong>Transition zone (TZ) prostate cancer poses diagnostic challenges due to overlapping imaging features with benign prostatic hyperplasia (BPH). This study aimed to investigate whether Prostate Imaging Reporting and Data System (PI-RADS) v2.1 combined with prostate-specific antigen density (PSAD) can enhance diagnostic accuracy in distinguishing TZ cancer from BPH.</p><p><strong>Material and methods: </strong>The retrospective study included 377 patients divided into two groups: the TZ cancer group (<i>n</i> = 139) and the BPH group (<i>n</i> = 238). Two radiologists independently reviewed prostate MR images of each patient and assigned a PI-RADS score for the TZ lesion. Clinical characteristics were compared between the two groups using the χ² test, <i>t</i>-test, or Mann-Whitney <i>U</i>-test. The diagnostic performance of PI-RADS scores, PSAD, and the combined parameters was determined by ROC curve analysis.</p><p><strong>Results: </strong>Statistically significant differences were found in PSA, prostate volume, PSAD, and PI-RADS scores between the two groups (all <i>p</i> < 0.0001). No difference in age was observed between the two groups (<i>p</i> = 0.602). The area under the curve (AUC) for PI-RADS v2.1 alone was 0.802 (95% CI: 0.759-0.841) with a sensitivity of 79.14% and specificity of 74.37% at a cutoff of ≥ 4. The AUC for PSAD alone was 0.808 (95% CI: 0.765-0.847) with a sensitivity of 79.14% and specificity of 77.31% at a cutoff of 0.22 ng/ml/ml. Combining PI-RADS and PSAD yielded an AUC of 0.873 (95% CI: 0.835-0.905), with a sensitivity of 79.26% and specificity of 86.55%.</p><p><strong>Conclusions: </strong>The combination of PI-RADS v2.1 and PSAD enhances the diagnostic accuracy for TZ cancer, thereby reducing unnecessary invasive procedures.</p>","PeriodicalId":8278,"journal":{"name":"Archives of Medical Science","volume":"22 2","pages":"884-891"},"PeriodicalIF":3.6,"publicationDate":"2026-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13266513/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148263124","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}