Background: Acute kidney injury (AKI) is a common and serious complication in the intensive care unit (ICU), and continuous renal replacement therapy (CRRT) is an important treatment option. However, there is no clear standard for the optimal time to stop CRRT. The cardiorenal interaction effect suggests that there may be a potential link between cardiac function and CRRT. This study aimed to investigate the left ventricular diastolic function for predicting CRRT discontinuation.
Methods: This is a prospective cohort study.
Results: The study included 154 AKI patients admitted to ICUs undergoing CRRT from February 2023 to August 2024, which were divided into the successful downtime group (87 patients) and the failure group (67 patients), and their baseline data, laboratory indices, and ultrasound parameters were analyzed. The results showed that serum creatinine, urea nitrogen, and E/e' measured at the time of CRRT discontinuation were significantly lower in the successful group than in the unsuccessful group (all P < 0.05). A higher E/e' measured at the time of CRRT discontinuation was associated with a lower likelihood of successful CRRT discontinuation (OR 0.71, 95% CI 0.61-0.83). Receiver operating characteristic analysis showed that E/e' at the time of CRRT discontinuation had good discriminative ability for successful discontinuation (AUC 0.832), with an empirically derived cut-off value of 8.62.
Conclusion: Our findings suggest that left ventricular diastolic function is associated with successful CRRT discontinuation in patients with AKI, and that E/e' may serve as a supportive, noninvasive parameter to complement clinical assessment at the time of CRRT discontinuation.
ESCC is highly aggressive. The patients with advanced disease have a poor prognosis, making it the main type of EC in China. Glycolytic metabolic reprogramming supports the occurrence, malignant progression, and drug resistance of ESCC. This may lead to late cancer detection and treatment difficulties. However, the specific mechanisms driving this phenomenon remain a mystery. In this study, we found that VPS4A had high expression in ESCC tissues. It was an independent factor affecting patient prognosis. In vivo and in vitro experiments demonstrated that VPS4A activated glycolysis in ESCC to promote tumor malignant progression and radioresistance. Mechanistically, VPS4A upregulated MYO1C expression to enhance glycolytic metabolism in ESCC cells, increasing glucose uptake and lactate production, thereby enhancing the radioresistance of tumor. Moreover, lactate produced by glycolysis could also enhance the VPS4A and MYO1C expression. Overall, our study indicated that VPS4A is a valuable therapeutic target for ESCC, highlighting the significance of the VPS4A/MYO1C/glycolysis axis in ESCC progression.
Magnetic nanoparticles (MNP) have gained significant attention for their potential in cancer therapy, particularly in targeted drug delivery, imaging, and hyperthermia treatments due to their unique magnetic properties, biological compatibility and applicability. This literature review focuses on recent progress in the green-synthesized MNP, explores their mechanisms of drug delivery, and critically evaluates their clinical applicability. The gaps in the literature that this review addresses include the inconsistency in nanoparticle size and surface properties, the limitations in achieving sustained and predictable drug release, and the difficulties in maintaining long-term stability in physiological conditions. It also discusses potential future development, including smart nanotechnology, individual medicine, and AI-acquired platforms. These findings show how MNPs can increase precise oncology by increasing medical effect, reducing toxicity and lightweight real-time monitoring of treatments.
Objective: Idiopathic inflammatory myopathy (IIM) is a collection of autoimmune disorders marked by muscle inflammation, with heart failure (HF) being a common and deadly complication. Exploring the underlying mechanisms and diagnostic markers for HF in IIM has significant clinical value.
Methods: We identified shared differentially expressed genes (DEGs) between HF and IIM using transcriptome data from the Gene Expression Omnibus (GEO). DEGs underwent functional enrichment analysis via Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO). Key genes were screened using two machine-learning algorithms and a protein-protein interaction network. Immune cell infiltration was estimated using the CIBERSORT algorithm, and its correlation with key genes was assessed. The key gene-related regulatory transcription factors (TFs) and miRNAs were predicted using miRNet, followed by validation through both online datasets and clinical samples.
Results: Seventy DEGs were shared by IIM and HF, primarily involved in immune and inflammatory responses. Key genes, including DDX60, CCL5, and IFIT3, exhibited strong diagnostic potential in both IIM and HF cohorts. Expression of IFIT3 and CCL5 was negatively associated with Tregs. In order to uncover the control of important genes, we also constructed TF-gene and miRNA-gene networks. Lastly, we confirmed that IIM with HF had higher levels of miR-100-5p expression than those without HF.
Conclusion: DDX60, CCL5, and IFIT3 are likely central to the development of HF in IIM. Additionally, serum levels of miR-100-5p may serve as a potential biomarker for detecting HF in IIM patients.
Aims: This study aimed to investigate the potential efficacy and safety of conduction system pacing (CSP) upgrades in patients indicated for elective replacement (ERI) with a left ventricular ejection fraction (LVEF) of less than 50% including those with heart failure with mildly reduced ejection fraction (HFmrEF).
Methods: This observational, retrospective cohort study included all patients with an LVEF < 50% who had a right ventricular pacing percentage of ≥ 40% prior to pulse generator replacement from January 2018 to October 2021. Cardiac performance and lead outcomes were compared across different LVEF groups based on whether they received CSP upgrades.
Results: A total of 60 patients were enrolled in this study, comprising 29 patients who successfully underwent CSP upgrades (29/32, 90.46%) and 31 patients who declined the upgrades. Comparable improvements in LVEF (9.00 ± 5.90% vs. 5.90 ± 3.72%, P = 0.325) and LVEDD (2.80 ± 1.95 mm vs. 3.10 ± 2.60 mm, P = 0.835) were noted in patients with HFmrEF. However, the final LVEF (53.50 ± 6.06 vs. 40.10 ± 10.20, P = 0.031) and LVEDD (48.60 ± 4.79 vs. 55.67 ± 9.80, P = 0.040) were more favorable in patients with HFmrEF compared to those with heart failure with reduced ejection fraction (HFrEF). In patients who declined CSP upgrades, NYHA grade (2.92 ± 0.79 vs. 2.75 ± 0.45, P = 0.010) and LVEF (29.50 ± 8.19% vs. 32.92 ± 5.25%, P = 0.018) decreased in patients with HFrEF, while comparable reductions in LVEF (45.84 ± 3.00% vs. 39.89 ± 10.83%, P = 0.001) and LVEDD (55.86 ± 9.62 mm vs. 50.11 ± 6.26 mm, P = 0.044) were observed in patients with HFmrEF. No complications, including thrombosis, infection, lead dislodgement, perforation, or stroke, were reported. The pacing threshold (1.25 ± 0.45 V vs. 1.57 ± 0.55 V, P = 0.129) did not differ significantly between patients with CSP upgrades and those without, following a follow-up period of 40.57 ± 8.21 months.
Conclusion: CSP upgrade during pulse generator replacement for battery depletion was associated with improved cardiac performances in patients with LVEF less than 50%. The final cardiac performance in patients with HFmrEF is more favorable. Larger-scale randomized controlled studies are therefore necessary to validate these findings, confirm the efficacy of CSP upgrade, and establish its optimal timing.
Background: On a global scale, coronary artery disease (CAD) continues to be one of the leading causes of morbidity and death. Glycosylation, a vital post-translational modification, has been linked to a range of cardiovascular conditions, including CAD. This study aims to systematically identify and validate glycosylation-based prognostic biomarkers for CAD, with the ultimate goal of developing a novel clinical diagnostic tool.
Methods: We sourced and pre-processed CAD data sets (GSE20680, GSE20681, GSE42148) from the Gene Expression Omnibus (GEO) database, which comprised 199 CAD samples and 162 control samples post batch effect removal. DE analysis was executed using the R software to pinpoint glycosylation-related differentially expressed genes (GRDEGs), whose functional enrichment analysis was conducted subsequently. Risk scores were calculated using a diagnostic model that was built employing logistic regression (LR), support vector machine (SVM) algorithms, and least absolute shrinkage and selection operator (LASSO) regression analysis. The model further underwent validation employing receiver operating characteristic (ROC) curves, calibration plots, as well as decision curve analysis (DCA). The infiltrated abundance of the immune cells between the high-risk group (HRG) and low-risk group (LRG) was then analyzed by ssGSEA to explore the effect of the GRDEG-based prognostic signatures on the immune response. Furthermore, the interaction networks were constructed to explore the potential regulatory mechanisms and therapy approaches based on the GRDEGs. Finally, the levels of the GRDEG-based prognostic signatures in CAD samples were detected using qRT-PCR and western blotting.
Results: Thirty-nine GRDEGs were significantly and differently expressed between the CAD and control groups, which predominantly participate in protein glycosylation and N-Glycan biosynthesis pathways. Among these genes, seven GRDEGs were identified as the prognostic risk signatures, including F5, MGAT4A, HSPG2, ARSB, TUBB3, ST6GAL1, and CAMLG. Based on these genes, the CAD samples were separated into HRG and LRG, and the ICI between HRG and LRG were shown to be significantly different. The constructed interaction networks further suggested that the seven GRDEGs were regulated by several microRNAs (miRNAs), transcription factors (TFs), and RNA-binding proteins (RBPs), and they were the target genes of some chemical drugs. Finally, the outcomes of qRT-PCR and western blotting demonstrated that there were significant variations in expressing these seven key genes in CAD.
Conclusions: This study establishes the critical role of GRDEGs in CAD pathogenesis and presents a robust diagnostic model with potential clinical utility. Furthermore, our findings reveal novel molecular targets that may inform future therapeutic strategies for CAD.
Background: Effective pain management following hip arthroplasty is critical for patient recovery. As a key component of multimodal analgesia strategies, nerve blocks are widely utilized for postoperative analgesia. However, the comparative efficacy of different nerve block techniques remains unclear. This study employs a Bayesian network meta-analysis (NMA) to compare analgesic outcomes among six commonly used nerve block techniques after hip arthroplasty.
Methods: Randomized controlled trials (RCTs) comparing postoperative pain outcomes among six nerve block techniques-supra-inguinal fascia iliaca block (FIB), erector spinae plane block (ESPB), quadratus lumborum block (QLB), pericapsular nerve group block (PENG), lumbar plexus block (LPB), and circum-psoas block (CPB)-after hip arthroplasty were systematically searched in PubMed, Embase, Web of Science, and the Cochrane Library from inception to October 15, 2024. 15 RCTs involving 1,068 patients were included. Methodological quality and evidence certainty were assessed using Cochrane RoB 2.0 and GRADE framework. A Bayesian NMA with random/fixed-effects models integrated direct and indirect evidence. Interventions were ranked using the surface under the cumulative ranking curve (SUCRA). Outcomes included static/dynamic pain scores at 12 and 24 h, 24-h intravenous morphine consumption, and postoperative adverse effects (nausea, vomiting, and dizziness).Data were analyzed using R 4.4.1 and Stata 15.
Results: 15 RCTs (n = 1068) comparing six nerve block techniques were included. The NMA showed no statistically significant differences in static or dynamic pain scores at 12 or 24 h. For 24-h morphine consumption, CPB was associated with significantly lower use compared to QLB and FIB. Statistically significant differences were found for postoperative adverse effects. SUCRA rankings consistently indicated CPB had the highest probability of being among the most effective options across outcomes, followed by PENG. The overall certainty of evidence was moderate.
Conclusions: This NMA found no significant differences in analgesia among six nerve blocks after hip arthroplasty, but SUCRA rankings suggest CPB may be optimal for analgesia, morphine-sparing and postoperative adverse effects, while PENG may serve as an alternative in selected clinical contexts.
Registration: PROSPERO (CRD420251101790).
Background: The triglyceride glucose (TyG) index, a surrogate marker of insulin resistance, has been linked to cardiovascular risk. However, its prognostic role in critically ill patients with atherosclerotic cardiovascular disease (ASCVD) remains unclear.
Methods: In this retrospective cohort study using the MIMIC-IV database, we identified 2,493 ASCVD patients and stratified them into TyG tertiles upon Intensive Care Unit (ICU) admission. Primary outcomes were 30-, 90-, and 365-day mortality. Secondary outcomes included the use and timing of mechanical ventilation (MV) and vasopressors. Cox regression, restricted cubic spline, and Fine-Gray competing risk models were applied. Propensity score matching (PSM) was performed as a sensitivity analysis. Subgroup analyses were conducted by age, sex, race, hypertension, diabetes, and statin use. Mediation analysis using white blood cell (WBC) count explored systemic inflammation.
Results: Higher TyG tertiles were consistently associated with increased mortality: 30-day (HR 1.85, 95% CI 1.46-2.36, P < 0.001), 90-day (HR 1.73, 95% CI 1.39-2.15, P < 0.001), and 365-day (HR 1.66, 95% CI 1.37-2.03, P < 0.001). These associations remained robust in propensity score-matched (PSM) analyses. Elevated TyG was also linked to greater need for MV (OR 1.93, 95% CI 1.66-2.24, P < 0.001) and vasopressor support (OR 1.58, 95% CI 1.35-1.86, P < 0.001) within the first 24 h, and to earlier initiation of these interventions in competing risk models (MV): sHR (subdistribution hazard ratio) 1.46, 95% CI 1.35-1.57, P < 0.001; vasopressor use: sHR 1.41, 95% CI 1.30-1.53, P < 0.001. WBC count partially mediated the TyG-mortality association, accounting for 22.18% of the total effect (P < 0.001) for 30-day mortality. In exploratory subgroup analyses, the association between TyG and mortality appeared more pronounced in nondiabetic patients (30-day HR 1.58, 95% CI 1.35-1.84) than in diabetic patients (HR 1.13, 95% CI 0.94-1.36), although these findings should be interpreted cautiously.
Conclusion: In critically ill patients with ASCVD, higher TyG index was associated with adverse outcomes, including increased mortality and earlier initiation of organ-supportive interventions. These findings suggest that TyG could serve as a practical biomarker for early risk stratification in this high-risk population, though prospective studies are warranted to confirm its clinical utility.
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