Search

Introduction: The present study was to investigate the clinical role of miR-330-3p in acute cerebral infarction (ACI), including its diagnostic and prognostic potential. Preliminary exploration of its target genes was archived by bioinformatics analysis. Methods: miR-330-3p in plasma of the patients with ACI and controls were quantified by real-time quantitative PCR. The 1-month prognosis of the ACI patients was evaluated by the Glasgow Outcome Scale (GOS). The correlation between the plasma levels of miR-330-3p and the GOS scores was tested by Pearson correlation analysis. The receiver operating characteristic (ROC) curves were established based on the expression level of miR-330-3p in different groups. The miR-330-3p-targeting genes were analyzed using Venn diagram, protein-protein interaction network, and Gene Ontology enrichment analysis. Results: miR-330-3p was significantly increased in the plasma of ACI patients compared with that in healthy controls, and ROC curve revealed its diagnostic value for ACI. miR-330-3p was significantly increased in the plasma of patients with poor 1-month prognosis compared with those with good 1-month prognosis. miR-330-3p expression was negatively correlated with GOS score, suggesting its potential to predict the 1-month prognosis for ACI. One-year survival analysis revealed surviving patients had lower levels of miR-330-3p than the deceased. miR-330-3p was proven to predict the death of patients with ACI. The miR-330-3p-targeting genes were associated with synapse-related Gene Ontology terms. Conclusion: miR-330-3p was upregulated in the plasma of patients with ACI, making it a promising diagnostic and prognostic marker for patients with ACI. miR-330-3p could facilitate synaptic plasticity following cerebral infarction. [ABSTRACT FROM AUTHOR]

Hematological malignant tumors (HMTs) are serious diseases that threaten human health and life with high mortality. Therefore, it is necessary to develop novel strategies for diagnosis and treatment. Human endogenous retroviruses (HERVs) have recently attracted increasing attention as potential targets for cancer diagnosis and therapy. In this study, we explored the association between HERV-K expression levels and HMTs development. Clinical data and peripheral blood samples were collected from 236 leukemia, 384 lymphoma patients, and 69 healthy controls. Quantitative polymerase chain reaction was used to detect the expression of HERV-K gag, pol, and env genes in peripheral blood mononuclear cells or different cell subpopulations. Differently expressed HERV-K genes were further tested by using deep sequencing method, and further analyzed with gene ontology (GO) annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment. B cell- and T cell-related cytokines in patients were also detected by enzyme-linked immunosorbent assay (ELISA). The results showed that the expression levels of the HERV-K gag, pol, and env genes in patients were significantly higher than in healthy controls. There was a correlation between the expression level of HERV-K and the clinicopathological parameters of leukemia patients. HERV-K expression was increased in the B lymphocytes of leukemia and lymphoma patients, but not in the T cells or neutrophils. The GO and KEGG analyses showed that abnormal expression of the HERV-K locus in patients affected immune regulation. The analysis of cytokines proved that the B cell-related cytokines, including interleukin (IL)-1β, IL-2, IL-4, IL-6, IL-10, tumor necrosis factor (TNF)-α, and interferon-gamma, were significantly decreased in patients, while the T cell-related cytokines, including IL-3, IL-12, and TNF-β, were not significantly changed. In conclusion, HERV-K genes might participate in the occurrence and development of leukemia and lymphoma, and might be biomarkers for the detection or evaluation of leukemia and lymphoma. [ABSTRACT FROM AUTHOR]

To date, the predictive role of laboratory indicators for the phenomenon of no flow is unclear. Hence, our objective was to conduct a meta‐analysis to investigate the association between laboratory parameters and the risk of the no‐reflow phenomenon in patients with ST‐elevation myocardial infarction (STEMI) following primary percutaneous coronary intervention (PCI). This, in turn, aims to offer valuable insights for early clinical prediction of no‐reflow. We searched Pubmed, Embase, and Cochrane Library from the establishment of the database to October 2023. We included case‐control or cohort study that patients with STEMI following primary PCI. We excluded repeated publication, research without full text, incomplete information or inability to conduct data extraction and animal experiments, reviews, and systematic reviews. STATA 15.1 was used to analyze the data. The pooled results indicated that elevated white blood cell (WBC) count (odds ratio [OR] = 1.061, 95% confidence interval [CI]: 1.013–1.112), neutrophil count (OR = 1.324, 95% CI: 1.128–1.553), platelet (PLT) (OR = 1.002, 95% CI: 1.000–1.005), blood glucose (OR = 1.005, 95% CI: 1.002–1.009), creatinine (OR = 1.290, 95% CI: 1.070–1.555), total cholesterol (TC) (OR = 1.022, 95% CI: 1.012–1.032), d‐dimer (OR = 1.002, 95% CI: 1.001–1.004), and fibrinogen (OR = 1.010, 95% CI: 1.005–1.015) were significantly associated with increased risk of no‐reflow. However, elevated hemoglobin was significantly associated with decreased risk of no‐reflow. In conclusion, our comprehensive analysis highlights the predictive potential of various parameters in assessing the risk of no‐reflow among STEMI patients undergoing PCI. Specifically, WBC count, neutrophil count, PLT, blood glucose, hemoglobin, creatinine, TC, d‐dimer, and fibrinogen emerged as significant predictors. This refined risk prediction may guide clinical decision‐making, allowing for more targeted and effective preventive measures to mitigate the occurrence of no‐reflow in this patient population. [ABSTRACT FROM AUTHOR]