Bosnian Journal of Basic Medical Sciences
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Correction: LKB1 suppression promotes cardiomyocyte regeneration via LKB1-AMPK-YAP axis
Full text linkCorrected article: https://www.bjbms.org/ojs/index.php/bjbms/article/view/7225
In the published article [Qu S, et al. LKB1 suppression promotes cardiomyocyte regeneration via LKB1-AMPK-YAP axis. Bosn J Basic Med Sci. 2022; DOI: 10.17305/bjbms.2021.7225], an error was identified in Figure 4D1. Specifically, the immunofluorescence image originally belonging to the "vector" group was mistakenly used for the "LKB1 OE" group during figure preparation. This was an inadvertent error in image placement.The corrected version of Figure 4 is shown below. This correction does not affect the statistical analysis, interpretation, or the overall conclusions of the study
Iliac vein stenting outcomes in non-thrombotic and thrombotic diseases: A systematic review and meta-analysis
Full text linkIliac vein stenting (IVS) is an endovascular revascularization procedure for iliac venous outflow obstruction. We aimed to synthesize the efficacy and safety of IVS across iliac vein disease phenotypes and follow-up horizons. Following a pre-registered protocol (PROSPERO CRD42024606701), we systematically searched Embase, Scopus, PubMed, Web of Science, and Cochrane Library on October 5, 2024. Without restricting study design, we included English-language reports with at least 10 patients that reported at least one prespecified outcome (or convertible data) and excluded studies with additional core therapies or duplicated cohorts. Diseases were classified as non-thrombotic iliac vein compression syndrome (NIVCS), post iliac vein thrombotic syndrome (PIVTS), chronic iliac vein obstruction (CIVO, that is, NIVCS or PIVTS), and acute thrombotic iliac vein obstruction (ATIVO, that is, a CIVO patient with acute ipsilateral thrombosis). The primary outcome was cumulative primary patency (CPP); secondary outcomes comprised ulcer healing, edema and pain relief, quality-of-life improvement, revised Venous Clinical Severity Score change, and adverse events. CPPs at prespecified intervals were extracted for each disease category and pooled in separate meta-analyses. Twenty-seven studies (4,782 patients) were included; demographic, intraoperative, and outcome data were systematically abstracted. Pooled CPPs were consistently high, particularly for NIVCS, and were lower when thrombotic components were present (PIVTS and ATIVO), while other efficacy outcomes generally improved and serious complications were uncommon. In conclusion, across diverse iliac vein diseases and follow-up periods, IVS demonstrates good efficacy and safety; this unfunded study supports IVS as a prominent treatment option
Low expression of CADPS predicts poor prognosis in pediatric acute lymphoblastic leukemia without fusion genes
Full text linkPediatric acute lymphoblastic leukemia (ALL) is among the most prevalent hematological malignancies in children. Despite an overall cure rate approaching 90%, a subset of patients still experiences relapse, even with advanced therapeutic interventions. Research into the molecular characteristics and prognostic markers of fusion gene-negative (FG-negative) pediatric ALL remains limited. To address this gap, we performed whole-exome sequencing (WES) and whole-transcriptome sequencing (RNA-seq) on 54 FG-negative ALL cases from our center. Our results indicated that neither specific mutations nor tumor mutational burden significantly influenced relapse risk. Notably, we identified a significant downregulation of CADPS in FG-negative pediatric ALL patients who relapsed. The expression levels and prognostic significance of CADPS were further validated using data from the Therapeutically Applicable Research to Generate Effective Treatments (TARGET) cohort, where lower CADPS expression was associated with reduced event-free survival (EFS) and overall survival (OS) (P < 0.001 for both). Cox regression analyses were subsequently employed to identify OS-related factors and to construct a prognostic prediction model. Notably, this model demonstrated a significant correlation with therapeutic targets. In conclusion, our findings support the potential of CADPS expression as a novel biomarker for prognostic stratification in FG-negative pediatric ALL patients
From BJBMS to Biomolecules and Biomedicine: A new chapter
Full text linkThe scientific community is continually evolving, driven by advancements, shifting priorities, and growing demands for global dissemination of knowledge. A clear example of successfully adapting to these demands is the transition from the Bosnian Journal of Basic Medical Sciences (BJBMS) to Biomolecules and Biomedicine (BB) in 2023. This strategic move symbolizes a significant step forward, expanding the journal’s global reach and scientific scope.
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Genetic determinants of lipid metabolism in cardioprotection: From mechanisms to clinical practice
Full text linkAtherosclerotic cardiovascular diseases continue to be the leading causes of morbidity and mortality globally. Disorders of lipoprotein metabolism contribute significantly to the development of atherosclerosis, which begins with the subendothelial retention of plasma-derived apolipoprotein B-containing lipoproteins, particularly low-density lipoprotein (LDL) and its remnants. Elevated LDL cholesterol levels and triglycerides, coupled with low high-density lipoprotein (HDL) cholesterol levels, are critical risk factors for atherosclerotic cardiovascular diseases. Landmark epidemiological studies have identified dyslipidemia as a key modifiable risk factor for these diseases, elucidating the essential role of lipid abnormalities in atherogenesis and highlighting significant opportunities for cardiovascular disease prevention and risk stratification. Genetic epidemiology studies have shown that lifelong low levels of LDL due to genetic variations markedly reduce the risk of atherosclerotic cardiovascular diseases. Recent advancements in lipid-lowering pharmacology are increasingly informed by genetic studies that reveal naturally occurring mutations offering lifelong cardioprotection. Furthermore, these genetic studies have facilitated the development of novel therapeutics and enhanced the prediction of potential side effects, variability in individual drug responses, and improved risk stratification. This narrative review article aims to summarize key genetic variants that influence lipid metabolism and examine their therapeutic potential in cardiovascular therapy. Given the central role of atherosclerosis in determining cardiovascular risk, it is vital to consider lipid metabolism in the context of genetic factors that affect individual susceptibility to hyperlipidemia. Defining cardioprotective genetic determinants is equally important, as it may provide a foundation for therapeutic strategies by emphasizing protective mechanisms
Long-term smoking contributes to aging frailty and inflammatory response
Full text linkIn recent years, the health challenges linked to frailty in the elderly, particularly those worsened by cigarette smoke, have become more pronounced. However, quantitative studies examining the impact of smoking dosage on frailty in this population remain limited. To address this gap, we developed a model using smoke-exposed elderly mice. Fifteen-month-old C57BL/6J mice were exposed to smoke from two burning cigarettes for 15 min in a whole-body chamber. This exposure occurred 4, 6, and 8 times daily for 30 days, representing low, medium, and high smoking dosages, respectively. Frailty levels were assessed through rotation and grip strength tests, alongside lung histopathology and inflammatory factor protein expression analyses across the three dosage groups. Additionally, we used the Gene Expression Omnibus (GEO) database to validate the correlation between frailty and inflammation in elderly smokers, facilitating cross-comparisons between animal model findings and human sample data. Our results show that mice exposed to high-dose smoking were significantly more prone to frailty, with notable reductions in maximal grip strength (P < 0.01) and drop time (P < 0.001). Among human samples, 69.2% of elderly smokers exhibited a frailty phenotype, compared to just 15.4% of nonsmokers. Both smoking-exposed mice and elderly smokers demonstrated upregulation of tumor necrosis factor-α (TNF-α) and interleukin-1 β (IL-1β) in lung tissue and serum. Mechanistically, this upregulation activates the NF-κB signaling pathway. Our findings quantitatively link smoking-induced frailty to increased levels of TNF-α and IL-1β, providing experimental evidence for the diagnosis and prevention of frailty in elderly populations
Trends in noninvasive ocular nanoparticle drug delivery: A bibliometric analysis (2004–2023)
Full text linkThis study presents a bibliometric analysis of research on noninvasive nanoparticle drug delivery systems for the transocular surface from 2004 to 2023. Relevant publications were retrieved from the Web of Science Core Collection. VOSviewer and CiteSpace were used to map contributions by countries/regions, authors, institutions, journals, keywords, keyword clusters, and timeline trends. A total of 695 articles were analyzed, showing a steady year-by-year increase in publications. China, the United States, and Spain were the leading contributors. Among authors, Alvarez-Lorenzo, Carmen was the most prolific, while Chanhan, Anuj’s work received the most citations among the top 10 prolific researchers. The International Journal of Pharmaceutics published the highest number of articles in this field, whereas the Journal of Controlled Release was the most frequently cited among the top 10 most productive journals. The University of Santiago de Compostela and the University of Florida were among the most active institutions in this research area. Keyword analysis identified recent key themes, such as controlled release, cell interaction, dry eye, mechanisms, gene expression, and ocular drug delivery. The growing interest in transocular surface nanoparticle drugs is driven by their advantages, including increased solubility, improved stability, reduced administration frequency, sustained therapeutic concentrations, enhanced corneal penetration, and prolonged ocular surface residence time
The influence of sodium-glucose co-transporter-2 inhibitors on the risk of cancer therapy-related cardiac dysfunction: A meta-analysis
Full text linkCancer therapy-related cardiac dysfunction (CTRCD) is a major concern for patients undergoing cardiotoxic cancer treatments. Sodium-glucose co-transporter-2 (SGLT2) inhibitors have shown cardioprotective effects in both diabetic and non-diabetic populations. However, their impact on CTRCD risk remains uncertain. This meta-analysis aimed to assess the association between SGLT2 inhibitor use and CTRCD in cancer patients receiving cardiotoxic treatments. A systematic search of PubMed, Embase, and Web of Science was conducted to identify relevant studies. Cohort studies comparing CTRCD incidence in cancer patients with and without SGLT2 inhibitor use were included. Risk ratios (RRs) were pooled using a random-effects model, and subgroup and meta-regression analyses were performed to explore potential effect modifiers. Ten cohort studies involving 34,847 cancer patients met the inclusion criteria. Overall, SGLT2 inhibitor use was associated with a significantly reduced risk of CTRCD (RR: 0.47, 95% confidence interval: 0.33–0.68, P < 0.001), though significant heterogeneity was observed (I² = 70%). Subgroup analysis indicated a stronger protective effect in patients receiving anthracyclines (RR: 0.26) compared to those undergoing other treatments (RR: 0.73, P for subgroup difference = 0.001). Additionally, the cardioprotective effect was more pronounced in cohorts with a lower proportion of men (<55%, RR: 0.27) compared to those with a higher proportion (≥55%, RR: 0.75, P < 0.001). Sensitivity analyses, conducted by excluding one study at a time, consistently supported these findings, reinforcing their robustness. In conclusion, SGLT2 inhibitor use is associated with a lower risk of CTRCD in cancer patients, particularly those receiving anthracyclines. These findings highlight the potential role of SGLT2 inhibitors in mitigating cardiotoxicity during cancer therapy
Silencing CACYBP suppresses lung adenocarcinoma growth via CDK1 inhibition
Full text linkCalcyclin-binding protein (CACYBP) is a multidomain adaptor protein implicated in the development of various cancers. However, its molecular and biological roles in lung adenocarcinoma (LUAD) remain unclear. In this study, we aimed to elucidate the biological impact of CACYBP in LUAD. Immunohistochemistry was used to assess CACYBP expression in LUAD tissues. Lentivirus-mediated CACYBP knockdown was established in LUAD cell lines, and target gene expression was analyzed via Western blotting and qRT-PCR. Cell proliferation, apoptosis, and migration were evaluated using flow cytometry, colony formation assays, cell counting kit-8 (CCK 8) assays, Celigo cell counting, wound healing assays, Transwell assays, and mouse xenograft models. Co-immunoprecipitation was performed to verify the interaction between CACYBP and cyclin-dependent kinase 1 (CDK1). Additionally, the phosphoinositide 3-kinase (PI3K) inhibitor LY294002 was used to investigate the involvement of CDK1 in the PI3K/AKT pathway. Our findings revealed that CACYBP was upregulated in LUAD tissues and correlated with advanced disease stages and poor prognosis. CACYBP knockdown inhibited LUAD progression and metastasis, promoted cell apoptosis in vitro, and reduced tumorigenicity in vivo. Mechanistically, we identified CDK1 as a direct interacting partner of CACYBP. CDK1 overexpression enhanced the malignant phenotype of LUAD cells and partially reversed the inhibitory effects of CACYBP knockdown. Furthermore, inhibition of the PI3K/AKT pathway using LY294002 significantly suppressed CDK1-mediated LUAD cell growth. In conclusion, CACYBP appears to function as a tumor promoter in LUAD, at least in part through CDK1-mediated activation of the PI3K/AKT pathway. These findings suggest that CACYBP could serve as a promising therapeutic target and a novel biomarker for LUAD prognosis
Lymphocyte subsets predict mortality in acute paraquat poisoning
Full text linkParaquat (PQ) is a highly effective herbicide widely used in agricultural production, known for its strong herbicidal power, rapid action, and minimal environmental pollution. However, it is also highly toxic to humans and animals, with acute lung injury (ALI) being the primary cause of death. While the toxic mechanisms of PQ have been studied from various perspectives, its effects on lymphocytes and their subsets remain unclear. This study aimed to explore the relationship between lymphocyte dysfunction and mortality in acute PQ poisoning. A total of 92 patients with PQ poisoning who visited the emergency department of The Affiliated Lihuili Hospital of Ningbo University between January 1, 2016, and September 30, 2021, were included. Basic demographic and laboratory data within 24 h of admission were collected. Peripheral blood lymphocyte subsets were analyzed using flow cytometry. To identify independent risk factors for mortality, patients were followed up for 90 days. COX proportional hazards models and LASSO regression were applied to screen for predictive variables and develop a predictive model. All participants provided informed consent, and the study was approved by the relevant ethics committee. Among the 92 patients, 36 died. Compared with the survival group, the death group showed significantly higher white blood cell and neutrophil counts, lymphocyte counts, and CD4+/CD8+ T cell ratios, while the percentage of natural killer (NK) cells was significantly lower (P < 0.001). COX regression analysis identified these factors as independent risk factors for mortality: lymphocyte count: hazard ratio (HR) = 1.59; 95% confidence interval (CI), 1.02–2.47; P = 0.04 neutrophil count: HR = 1.12; 95% CI, 1.06–1.18; P = 0.04 CD4+/CD8+ T cell ratio: HR = 2.01; 95% CI, 1.03–3.92; P = 0.04 NK cell percentage: HR = 0.88; 95% CI, 0.82–0.95; P = 0.002. These findings suggest that lymphocyte count, neutrophil count, CD4+/CD8+ T cell ratio, and NK cell percentage are all associated with mortality in PQ poisoning cases