Bosnian Journal of Basic Medical Sciences (BJBMS)
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Association between diabetes mellitus and tinnitus: A meta-analysis
Get PDFDiabetes mellitus (DM) has been suggested as a potential risk factor for tinnitus, but evidence remains inconclusive. This meta-analysis aimed to evaluate the association between DM and tinnitus by systematically reviewing and synthesizing data from observational studies. A comprehensive literature search was conducted in PubMed, Embase, and Web of Science up to August 16, 2024. Observational studies with a sample size of at least 100 participants that assessed the relationship between DM and tinnitus were included. Studies involving populations with specific diseases were excluded. Odds ratios (ORs) and 95% confidence intervals (CIs) were pooled using a random-effects model. Study quality was assessed using the Newcastle-Ottawa Scale (NOS), and sensitivity and subgroup analyses were performed. Publication bias was evaluated using funnel plots and Egger’s regression test. Twelve studies comprising 2,277,719 participants were included. The pooled analysis revealed a significant association between DM and tinnitus (OR: 1.18, 95% CI: 1.06–1.31, P = 0.002), with moderate heterogeneity (I² = 51%). Sensitivity analyses confirmed the robustness of these findings. Subgroup analyses showed no significant differences by geographical region, mean age, sex distribution, tinnitus diagnosis method, or model used for association estimation. Publication bias was not detected (Egger’s test P = 0.29). These findings suggest that DM is significantly associated with an increased risk of tinnitus. Further research is warranted to explore underlying mechanisms and causal relationships. Nonetheless, the results underscore the importance of monitoring tinnitus in patients with diabetes
Clinical profile and risk factors for respiratory failure in children with Mycoplasma pneumoniae infection
Get PDFMycoplasma pneumoniae (MP) is a common cause of community-acquired pneumonia (CAP) in children and can lead to severe complications, including respiratory failure. A retrospective analysis of 2084 children diagnosed with CAP and treated in our hospital from January 2022 to January 2023 was conducted. A comprehensive dataset of patient demographics, clinical symptoms, and laboratory findings was initially assembled. Subsequent statistical analyses were carried out to elucidate the clinical characteristics of MP pneumonia (MPP) in children. Additionally, the study identified high-risk factors for respiratory failure in the context of MPP. Among the hospitalized MPP cases, 15.8% progressed to respiratory failure. Statistical analysis identified D-dimer level as a significant risk factor for respiratory failure in children with MPP. A predictive model was developed using D-dimer levels, yielding an area under the curve (AUC) of 0.818 with a cutoff value of 1.015 mg/L. The model demonstrated a sensitivity of 62.4% and a specificity of 91.3%, proving effective in predicting respiratory failure caused by MPP. Respiratory failure remains a critical complication in children with MPP, and D-dimer levels serve as a key predictive risk factor. Vigilant monitoring of coagulation function, particularly D-dimer levels, is essential for the early identification of patients at risk of developing respiratory failure in MPP cases
Study on the mechanism of Wnt/β-catenin pathway mediated by pterostilbene to reduce cerebral ischemia-reperfusion injury
Get PDFCerebral ischemia-reperfusion injury (CIRI) is the primary cause of damage following ischemic stroke, with ferroptosis serving as a key pathophysiological factor in CIRI. Pterostilbene (PTE) has been shown to reduce cerebral ischemic injury, but whether its mechanism of action involves ferroptosis remains unclear. In this study, an in vitro model of mouse hippocampal neuron (HT22) cell injury and an in vivo mouse CIRI model were established. Treatments included PTE, the ferroptosis activator Erastin, and the Wnt signaling pathway inhibitor (Dkk-1). Cell damage was assessed using flow cytometry, MTT assay, lactate dehydrogenase (LDH) release assay, and Calcein-AM/PI staining. Oxidative stress and ferroptosis in cells and tissues were evaluated using biochemical kits and fluorescence staining. Additionally, histopathological staining was performed to assess brain tissue damage, while qRT-PCR and Western blot analyses were used to measure ferroptosis-related factors and Wnt/β-catenin pathway-related proteins in both cells and tissues. HT22 cells subjected to injury exhibited decreased viability and increased cell death (P < 0.05). Similarly, CIRI mice demonstrated pronounced cerebral infarction and neuronal damage. Ferroptosis, characterized by elevated levels of iron ions, lipid peroxides (ROS and MDA), and reduced antioxidant enzymes (GSH and GPX4), was significantly increased in both cells and tissues (P < 0.05). Correspondingly, ferroptosis-related protein levels were elevated (P < 0.05), while Wnt/β-catenin pathway-related protein levels were significantly decreased (P < 0.05). Treatment with Erastin and Dkk-1 exacerbated neuronal damage, intensified ferroptosis, and inhibited the Wnt/β-catenin pathway. Conversely, PTE treatment activated the Wnt/β-catenin pathway, reduced ferroptosis, and improved neuronal damage. Specifically, PTE upregulated the Wnt/β-catenin pathway, decreased peroxide accumulation, and antagonized ferroptosis, ultimately mitigating CIRI. These findings suggest that PTE protects against CIRI by modulating the Wnt/β-catenin pathway and alleviating ferroptosis-induced damage
Lymphocyte subsets predict mortality in acute paraquat poisoning
Get PDFParaquat (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
UPP1 and AHSA1 as emerging biomarkers and targets in pancreatic cancer: A proteomic approach
Get PDFThe specific protein targets involved in pancreatic cancer (PC) pathogenesis and its varying levels of differentiation remain incompletely understood. Advanced proteomic methodologies provide a powerful means of identifying key regulatory proteins and signaling pathways central to cancer progression. In this study, proteomic analyses were performed on PC tissue samples of different differentiation grades, along with adjacent non-cancerous (para-PC) tissues. Bioinformatics techniques were used to identify differentially expressed proteins (DEPs) and their associated pathways. Key target proteins were validated using the Gene Expression Profiling Interactive Analysis (GEPIA) database, reverse transcription-quantitative polymerase chain reaction (RT-qPCR), Western blotting, immunohistochemistry (IHC), and immunofluorescence (IF). A total of 431 DEPs were identified between PC and para-PC tissues, while 470 DEPs distinguished poorly differentiated (PD) from moderately differentiated (MD) PCs. Functional enrichment analysis revealed that these DEPs participate in various biological processes and signaling pathways. Five DEPs were common to both comparisons, with Uridine Phosphorylase 1 (UPP1), Lactamase Beta, and Activator of HSP90 ATPase Activity 1 (AHSA1) showing particularly notable differences. UPP1 and AHSA1 were significantly upregulated in PC tissues relative to adjacent tissues and exhibited even higher expression in PD-PCs compared to MD ones. These findings were consistently supported by GEPIA, RT-qPCR, Western blotting, IHC, and IF analyses. This study identifies UPP1 and AHSA1 as key proteins linked to PC differentiation and progression, highlighting their potential as diagnostic markers and therapeutic targets. These insights enhance our understanding of the molecular mechanisms underlying PC and open new avenues for precision treatment strategies
Identification and validation of TUBB, CLTA, and FBXL5 as potential diagnostic markers of postmenopausal osteoporosis
Get PDFPostmenopausal osteoporosis (PMOP) is recognized as the most prevalent bone disease worldwide. N6-methyladenosine (m6A) is one of the most common RNA modifications influencing the progression of various disorders; however, its specific role in PMOP remains unexplored. This study aims to investigate the expression profiles of m6A-related genes and their impact on the prognosis of PMOP patients. We utilized the GSE56815 expression analysis dataset obtained from the Gene Expression Omnibus (GEO) database and extracted m6A-related genes for further examination. Our analysis revealed that m6A-related genes exhibited differential expression between PMOP patients and healthy controls. We employed consensus clustering to identify subgroups within the PMOP cohort and conducted immunological analyses on these clusters. Additionally, we intersected the clusters to identify differentially expressed genes (DEGs) and analyzed potential diagnostic markers for PMOP using support vector machine recursive feature elimination (SVM-RFE), LASSO, and random forest (RF) algorithms, which were subsequently validated in the GSE56116 dataset. The receiver operating characteristic (ROC) curve was employed to assess the diagnostic significance of these markers. Furthermore, quantitative PCR (qPCR) was performed to validate the expression of the identified genes. In the GSE56815 dataset, we identified three subtypes associated with m6A modifications, leading to the identification of 302 shared DEGs among these subtypes. Gene ontology (GO) analysis indicated that the DEGs were predominantly enriched in nuclear specks, the nuclear envelope, and nucleocytoplasmic transport processes. Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis further revealed that DEGs were primarily associated with endocytosis and nucleocytoplasmic transport pathways. Through the application of SVM, LASSO, and RF algorithms, we identified three potential diagnostic markers: TUBB, CLTA, and FBXL5, which demonstrated promising diagnostic capabilities when tested against an independent dataset. qPCR validation confirmed significant expression differences of these genes between the control and PMOP groups. The genetic markers identified in this study hold potential for accurately predicting the risk of PMOP in patients. The findings contribute to understanding the underlying molecular mechanisms of CLTA, TUBB, and FBXL5 in PMOP and may facilitate the development of novel therapeutic strategies and improved monitoring of the disease
TCF12 enhances angiogenesis and affects sorafenib response in liver cancer via HIF-1α interaction
Get PDFTranscription factor 12 (TCF12), a member of the basic Helix-Loop-Helix (bHLH) protein family, plays a crucial role in regulating cell growth and differentiation. It has been implicated in the development and progression of malignant tumors; however, its specific mechanisms in vascularization and drug resistance in liver cancer remain poorly understood. This study aims to explore how the interaction between TCF12 and Hypoxia-Inducible Factor 1-alpha (HIF-1α) affects vascularization and drug sensitivity in liver cancer. Using bioinformatics analysis (n = 374 TCGA samples and n = 50 clinical specimens), we assessed TCF12 expression levels in liver cancer and evaluated their association with patient prognosis. Gene Set Enrichment Analysis (GSEA) was employed to identify related signaling pathways. The expression of TCF12 in liver cancer tissues was examined via Western blotting and immunohistochemistry, while Kaplan-Meier survival analysis was used to analyze the relationship between TCF12 expression and overall survival. Functional assays—including scratch wound repair, tube formation, and endothelial cell permeability tests—were conducted to assess TCF12’s role in angiogenesis. Cell viability assays were performed to evaluate the impact of TCF12 on sorafenib sensitivity, and co-immunoprecipitation experiments were carried out to investigate the interaction between TCF12 and HIF-1α. Our bioinformatics analysis revealed that both TCF12 and HIF-1α are significantly overexpressed in liver cancer and are associated with poor prognosis. Immunohistochemical staining showed a positive correlation between TCF12 expression and the vascularization marker CD31. Furthermore, survival analysis demonstrated that patients with elevated TCF12 expression had significantly shorter overall survival. Functional assays indicated that TCF12 knockdown suppressed blood vessel formation and reduced endothelial cell permeability. Moreover, reducing TCF12 expression increased the sensitivity of liver cancer cells to sorafenib. Notably, overexpression of HIF-1α reversed these effects, and co-immunoprecipitation experiments confirmed a direct interaction between TCF12 and HIF-1α. In summary, this study demonstrates that TCF12 is highly expressed in liver cancer and is associated with poor prognosis. TCF12 promotes angiogenesis by stabilizing HIF-1α and modulates tumor sensitivity to sorafenib, highlighting its potential as a therapeutic target in liver cancer
Immunogenic cell death-related risk signature for tumor microenvironment profiling and prognostic prediction in colorectal cancer
Get PDFImmunogenic cell death (ICD) reshapes the tumor immune microenvironment and activates the adaptive immune response. However, the clinical significance of ICD-associated genes in colorectal cancer (CRC) remains unclear. In this study, we used weighted gene co-expression network analysis (WGCNA) to identify ICD-related gene modules. An ICD-related risk score (ICDRS) was then constructed using Cox regression modeling and LASSO analysis. Immune cell infiltration in patients with different risk levels was assessed using the ESTIMATE and single-sample Gene Set Enrichment Analysis algorithms (GSEA). The oncoPredict package was employed to explore the association between the ICDRS and chemotherapy drug sensitivity. Finally, the expression levels of ICD-related genes were validated through in vitro cellular experiments. Three CRC prognostic genes—CLMP, Neuropilin-1 (NRP1), and PLEKHO1—were identified from a set of 34 ICD-associated genes based on WGCNA and LASSO analyses. These genes were used to construct the ICDRS model. Notably, a high ICDRS was found to be an independent predictor of poorer overall survival (OS) in CRC patients. High-risk patients also exhibited increased immune cell infiltration. Moreover, the ICDRS was significantly correlated with sensitivity to conventional chemotherapeutic drugs, suggesting its potential utility in guiding personalized chemotherapy. Cellular assays confirmed that CLMP, NRP1, and PLEKHO1 were differentially expressed between normal and cancerous cells, and that NRP1 specifically promoted the proliferation, migration, and invasion of CRC cells. In conclusion, the ICDRS may serve as a reliable predictor of CRC prognosis and offers a promising direction for the clinical management of CRC patients
Emerging insights into mesenchymal stem cells and exosome-based therapies for liver injury
Get PDFHepatic ischemia-reperfusion injury, fatty liver, liver fibrosis, liver peroxidative injury, and drug-induced liver injury are among the most common liver diseases. Mesenchymal stem cells (MSCs) possess multi-lineage differentiation potential and immunomodulatory functions. In the treatment of liver injury, MSCs can promote repair through homing effects, direct differentiation into hepatocyte-like cells (HLCs), immunomodulation, and anti-fibrotic mechanisms. Clinically, MSCs contribute to liver injury repair either directly or indirectly via the secretion of exosomes. Beyond their reparative role, MSC-derived exosomes can also serve as molecular biomarkers for the diagnosis and prognosis of liver diseases. Establishing higher-quality standards, robust auditing and evaluation systems, and conducting deeper mechanistic studies are essential prerequisites for the future clinical application of MSCs in the treatment of liver diseases
Erratum: Rab8a/SNARE complex activation promotes vesicle anchoring and transport in spinal astrocytes to drive neuropathic pain
Get PDFIn the article “Rab8a/SNARE complex activation promotes vesicle anchoring and transport in spinal astrocytes to drive neuropathic pain” (Xiao et al., DOI: https://doi.org/10.17305/bb.2024.10441), published on 6 September 2024, an incorrect version of Figure 2 was inadvertently published due to an editorial oversight. The article has been corrected online to include the accurate figure. This correction does not affect the study’s results, interpretations, or conclusions. We apologize for the error and thank the authors for bringing it to our attention