Background Cardiovascular damage is a common complication in patients with chronic kidney disease (CKD), and left ventricular longitudinal strain (GLS) is superior to LVEF in evaluating systolic function. However, it has not been widely adopted clinically because it requires proficiency and is time-consuming. This study aimed to investigate the feasibility, reproducibility, and predictive value of automated GLS compared with manual GLS, providing a reference for clinical evaluation and reduction of cardiovascular events in CKD patients. Methods A total of 285 CKD patients (aged 52 +/- 12.85) without dialysis were enrolled from Hainan Provincial People's Hospital. GLS was measured using three methods on identical apical three-, two-, and four-chamber views: (1) fully automatic GLS analyzed by machine functions, (2) semi-automatic GLS corrected by researchers, and (3) manual GLS measured by experts. Five cases were excluded due to poor image quality. Clinical outcomes were followed up by telephone and outpatient visits. Results About 35% of automatic GLS results required manual correction, with significant differences among the three methods (P < 0.01). The correlation and consistency between semi-automatic and manual GLS were higher than those of automatic GLS (P < 0.01). During 2-year follow-up, 55 patients (19.6%) experienced cardiovascular events. Automated GLS predicted events but with lower accuracy than semi-automatic GLS. The analysis time for automatic (15.23 +/- 0.75 s) and semi-automatic GLS (75.06 +/- 19.01 s) was markedly shorter than manual analysis (236.81 +/- 45.41 s, P < 0.01). Conclusions Automated GLS assessment in CKD patients is feasible and reproducible. As some images still require manual correction, the semi-automated approach currently offers the optimal balance between efficiency and predictive value.
Objective We aimed to clarify the impact of early enteral nutrition support combined with comfort nursing on the prognosis of critically ill patients in the intensive care unit (ICU) who received ventilator-assisted ventilation. Methods 100 critically ill patients admitted to our ICU were selected and randomly divided into the control group (CG) and the observation group (OG). The OG initiated early enteral nutrition support within 24 h after admission to ICU and received comfort nursing. The CG initiated enteral nutrition support after admission to the ICU based on monitoring biochemical indicators and received routine ICU nursing. The nutritional status, immune function, total malnutrition rate, incidence of pulmonary infection, ventilator weaning time and ICU hospitalization time of the two groups were measured and compared. Results The levels of albumin (ALB), total protein (TP), and globulin (GLB) in both groups were higher than those at admission to the ICU, while OG group were higher than CG group (P < 0.05). The PCT levels of both groups decreased compared to the levels during the period from admission to the ICU, while OG group was greater decrease than CG group (P < 0.05). The overall malnutrition rate in OG group was lower than that in CG group (P < 0.05). The incidence of pulmonary infection in OG group was lower than that in CG group (P < 0.05). The time to weaning from the ventilator and the ICU stay time in OG group were shorter than those in CG group (P < 0.05). Conclusion For critically ill ICU patients undergoing ventilator assisted ventilation, early enteral nutrition support combined with comfort nursing can effectively reduce risk of malnutrition and pulmonary infection, enhance immune function, create convenient conditions for early weaning and early conversion to general wards, with broad clinical application prospects.
Background Gestational diabetes mellitus (GDM) is characterized by systemic immune dysregulation and chronic inflammation that contribute to insulin resistance and beta-cell dysfunction. The long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) has been implicated in several inflammatory disorders; however, its role in GDM-related immune and metabolic disturbances remains unclear. Methods A mouse model of GDM and insulin-resistant trophoblast cells were used to evaluate MALAT1 expression and its effects on inflammatory cytokines and beta-cell apoptosis. Gene expression was analyzed by qRT-PCR and Western blotting, while histological and biochemical assays assessed pancreatic morphology, serum glucose, and inflammatory cytokine levels. Functional and rescue experiments were performed to explore the molecular interaction between MALAT1, miR-576-5p, and HNRNPU. Results MALAT1 expression was markedly elevated in GDM mice and insulin-resistant trophoblasts, correlating with increased levels of TNF-alpha, IL-1 beta, and IL-6, as well as enhanced beta-cell apoptosis. Silencing MALAT1 alleviated hyperglycemia, preserved pancreatic islet structure, and reduced inflammatory mediator secretion. Mechanistically, MALAT1 acted as a competing endogenous RNA by sponging miR-576-5p to upregulate HNRNPU, thereby promoting NF-kappa B activation. HNRNPU overexpression reversed the antiinflammatory and anti-apoptotic effects of MALAT1 knockdown. Conclusion MALAT1 promotes immune-metabolic dysfunction in GDM through the miR-576-5p/HNRNPU/NF-kappa B axis. Targeting this pathway may offer a novel therapeutic strategy for reducing inflammation-associated complications in GDM.
Objective To investigate the role of microRNA-27b-3p (miR-27b-3p) in regulating ferroptosis in non-small cell lung cancer (NSCLC) cells and to elucidate the underlying molecular mechanism, with a focus on its interaction with SLC7A11. Methods The expression levels of miR-27b-3p and SLC7A11 were examined in NSCLC cell lines. Gain-of-function experiments were performed by overexpressing miR-27b-3p to assess its effects on NSCLC cell proliferation, migration, invasion, apoptosis, and ferroptosis. Ferroptosis was evaluated by measuring intracellular free iron, lipid peroxidation, and reactive oxygen species (ROS) levels in erastin-treated NSCLC cells. The targeting relationship between miR-27b-3p and SLC7A11 was analyzed, and rescue experiments were conducted by overexpressing SLC7A11 in miR-27b-3p-overexpressing cells. Results miR-27b-3p expression was significantly downregulated, while SLC7A11 expression was upregulated in NSCLC cells. Overexpression of miR-27b-3p inhibited NSCLC cell proliferation, migration, and invasion, and enhanced apoptosis and ferroptosis, as indicated by increased free iron, lipid peroxidation, and ROS levels in erastin-treated cells. SLC7A11 was identified as a target of miR-27b-3p, and its overexpression reversed the inhibitory effects of miR-27b-3p on proliferation, migration, and invasion, as well as the promoting effects on apoptosis and ferroptosis in NSCLC cells. Conclusion miR-27b-3p acts as a tumor suppressor in NSCLC by inducing ferroptosis and inhibiting malignant behaviors of NSCLC cells through direct targeting and negative regulation of SLC7A11. These findings suggest that the miR-27b-3p/SLC7A11 axis may represent a potential therapeutic target for NSCLC.
Background Parkinson's disease (PD) is a progressive neurodegenerative disorder associated with metabolic abnormalities. Serum biomarkers such as uric acid (UA), homocysteine (Hcy), and cystatin C (Cys-C) may be involved in its pathogenesis and progression. Objective To evaluate the associations between serum UA, Hcy, and Cys-C levels and disease duration, severity, and cognitive function in patients with PD. Methods From January 2023 to December 2024, sixty patients diagnosed with PD and sixty age-and sex-matched healthy controls were enrolled. PD patients were further stratified by disease duration (<5 years vs. >= 5 years), Hoehn and Yahr (H&Y) stage (mild vs. moderate-to-severe), and Montreal Cognitive Assessment (MoCA) score (normal cognition vs. cognitive impairment). Serum levels of UA, Hcy, and Cys-C were compared among groups, and Pearson correlation analysis was performed to examine their relationships with disease duration, H&Y stage, and MoCA score. Results Compared with healthy controls, PD patients exhibited significantly higher serum Hcy and Cys-C levels and lower UA levels (all P<0.01). Patients with longer disease duration, higher H&Y stage, or cognitive impairment showed elevated Hcy and Cys-C levels and reduced UA levels (P<0.01 for all comparisons). Pearson correlation analysis revealed that UA was negatively correlated with disease duration (r = -0.757, P<0.001), H&Y stage (r = -0.869, P<0.001), and MoCA score (r = -0.606, P<0.001), while Hcy and Cys-C were positively correlated with these indicators (all P<0.01). Conclusion Elevated serum Hcy and Cys-C and reduced UA levels are closely associated with PD progression and cognitive decline. These biomarkers may serve as valuable indicators for monitoring disease severity and guiding clinical management.
