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Objective Postoperative acute kidney injury (PO-AKI) is a common complication after cardiac surgery. We aimed to evaluate whether machine learning algorithms could significantly improve the risk prediction of PO-AKI. Methods The retrospective cohort study included 2310 adult patients undergoing cardiac surgery in a tertiary teaching hospital, China. Postoperative AKI and severe AKI were identified by the modified KDIGO definition. The sample was randomly divided into a derivation set and a validation set based on a ratio of 4:1. Exploiting conventional logistic regression (LR) and five ML algorithms including decision tree, random forest, gradient boosting classifier (GBC), Gaussian Naive Bayes and multilayer perceptron, we developed and validated the prediction models of PO-AKI. We implemented the interpretation of models using SHapley Additive exPlanation (SHAP) analysis. Results Postoperative AKI and severe AKI occurred in 1020 (44.2%) and 286 (12.4%) patients, respectively. Compared with the five ML models, LR model for PO-AKI exhibited the largest AUC (0.812, 95% CI : 0.756, 0.860, all P  < 0.05), sensitivity (0.774, 95% CI : 0.719, 0.813), accuracy (0.753, 95% CI : 0.719, 0.781) and Youden index (0.513, 95% CI : 0.451, 0.573). Regarding severe AKI, GBC algorithm showed a significantly higher AUC than the other four ML models (all P  < 0.05). Although no significant difference ( P  = 0.173) was observed in AUCs between GBC (0.86, 95% CI : 0.808, 0.902) and conventional logistic regression (0.803, 95% CI : 0.746, 0.852), GBC achieved greater sensitivity, accuracy and Youden index than conventional LR. Notably, SHAP analyses showed that preoperative serum creatinine, hyperlipidemia, lipid-lowering agents and assisted ventilation time were consistently among the top five important predictors for both postoperative AKI and severe AKI. Conclusion Logistic regression and GBC algorithm demonstrated moderate to good discrimination and superior performance in predicting PO-AKI and severe AKI, respectively. Interpretation of the models identified the key contributors to the predictions, which could potentially inform clinical interventions.

There are potential issues in Fig 4 in Biol. Open (2017) 6, 489-495 (doi:10.1242/bio.024133).

Objective. Long noncoding RNAs (lncRNAs), including some members of small nucleolar RNA host gene (SNHG), are important regulators in myocardial injury, while the role of SNHG4 in myocardial infarction (MI) is rarely known. This study is aimed at exploring the regulatory role and mechanisms of SNHG4 on MI. Methods. Cellular and rat models of MI were established. The expression of relating genes was measured by qRT-PCR and/or western blot. In vitro, cell viability was detected by MTT assay, and cell apoptosis was assessed by caspase-3 level, Bax/Bcl-2 expression, and/or flow cytometry. The inflammation was evaluated by TNF-α, IL-1β, and IL-6 levels. The myocardial injury in MI rats was evaluated by echocardiography, TTC/HE/MASSON/TUNEL staining, and immunohistochemistry (Ki67). DLR assay was performed to confirm the target relationships. Results. SNHG4 was downregulated in hypoxia-induced H9c2 cells and MI rats, and its overexpression enhanced cell viability and inhibited cell apoptosis and inflammation both in vitro and in vivo. SNHG4 overexpression also decreased infarct and fibrosis areas, relieved pathological changes, and improved heart function in MI rats. In addition, miR-148b-3p was an action target of SNHG4, and its silencing exhibited consistent results with SNHG4 overexpression in vitro. DUSP1 was a target of miR-148b-3p, which inhibited the apoptosis of hypoxia-induced H9c2 cells. Both miR-148b-3p overexpression and DUSP1 silencing weakened the effects of SNHG4 overexpression on protecting H9c2 cells against hypoxia. Conclusions. Overexpression of SNHG4 relieved MI through regulating miR-148b-3p/DUSP1, providing potential therapeutic targets.

The profound inhibitory effect of Tanshinone IIA (Tan IIA) on atherosclerosis has been demonstrated, whereas the latent mechanism is not completely cleared. This study aimed to investigate the cellular and molecular mechanisms underlying Tan IIA protecting against atherosclerosis. Oil Red O staining and ELISA assay showed that Tan IIA suppressed the progress of atherosclerosis and reduced the levels of inflammatory cytokines in serum of apolipoprotein E deficient (ApoE–/–) mice. Flow cytometry assay revealed that Tan IIA inhibited oxidized LDL (ox-LDL)-induced apoptosis of VSMCs. MTT and transwell assay indicated that Tan IIA suppressed the ox-LDL-stimulated proliferation and migration of RAW264.7 cells. Moreover, Tan IIA ameliorated inflammatory cytokine upregulation elicited by ox-LDL in RAW264.7 cells. Additionally, Tan IIA inhibited the apoptosis of VSMCs and decreased the levels of MMP-2, MMP-9 in ApoE–/– mice. In conclusion, our study demonstrated Tan IIA suppressed the progression of atherosclerosis by inhibiting vascular inflammation, apoptosis of VSMCs and proliferation and migration of macrophages induced by ox-LDL.

Invasive cardiac lipoma is a rare type of primary cardiac tumor that is composed of adipose tissue but infiltrating the adjacent structures. It is a benign tumor that can cause significant morbidity and mortality due to its size and location within the heart. We describe a giant invasive intracardiac lipoma across atrial wall extending to the ascending aorta and the superior vena cava. This review will provide an overview of invasive cardiac lipoma, including its clinical presentation, diagnosis, and management.

Background Obstruction of the left or right coronary artery is a rare but lethal complication during transcatheter aortic valve implantation (TAVI). The new J-Valve™ prosthesis is a new second generation TAVI device which has several features to avoid the coronary obstruction such as low profile design and clip fixation of the native leaflets. The aim of this study is to report our initial experience of using this valve in treating patient with high risk factors for coronary obstruction during TAVI procedure. Case presentation Three high surgical risk patients (All females with 77, 76, and 75 years old) with symptomatic aortic stenosis were enrolled. All patients have the common feature of low coronary ostium height (< 10 mm) with narrowed aortic sinus (< 30 mm) on CT angiogram and marked leaflet calcification. Three 25 mm J-Valve prostheses were successfully implanted through trans-apical approach. No coronary obstruction was noted for these patients. Effective aortic open area was significantly increased after valve implantation (Preoperative 0.7, 0.7 and 0.65 cm 2 – Postoperative 1.8, 1.9 and 2.0 cm 2 ). Only one patient was noted to have trivial degree paravalvular leakage. Conclusion The new J-Valve prosthesis is a new second generation TAVI device. This system may provide another safety treatment option for patient with high risk factor for coronary obstruction underwent TAVI procedure.

Tricuspid regurgitation (TR) may occur late after left-sided valve surgery (LSVS). Isolated tricuspid regurgitation after left-sided valve surgery (iTR-LSVS) refers to isolated TR without significant lesions in the mitral and/or aortic position late after mitral and/or aortic replacement or repair. Severe TR has a negative impact on long-term prognosis and requires surgical or transcatheter treatment. However, there is no clear recommendation on when and how intervention should be performed for patients with iTR-LSVS in the current guidelines for the management of valvular heart disease. The historically high operative mortality may be reduced by current minimally invasive techniques and transcatheter therapy. To further understand iTR-LSVS, standardize the treatment, improve the prognosis, and promote the collaboration, the Chinese Minimally Invasive Cardiovascular Surgery Committee (CMICS) wrote this expert consensus on the management of iTR-LSVS from the aspects of etiology, preoperative evaluation, indications for intervention, surgical treatment, transcatheter therapy, and postoperative management.

Bisphenol A (BPA) is a widely used industrial chemical with potential endocrine‐disrupting effects on metabolic processes. This study investigates the impact of BPA on hepatic function and transcriptional regulation in mouse livers and AML12 cells. Male mice were exposed to low (5 g/kg) and high (50 g/kg) doses of BPA for six weeks. Transcriptomic analysis was performed on liver tissues, and histological examinations were conducted. AML12 cells were treated with varying BPA concentrations, and PPARG transcriptional activity was assessed using a luciferase reporter assay. Additionally, molecular docking, molecular dynamics (MD) simulations, drug affinity responsive target stability (DARTS), cellular thermal shift assay (CETSA), MM‐PBSA calculations, and multi‐species protein structure comparative analysis were employed to analyse the interaction between BPA and PPARG. Transcriptomic analysis revealed a decrease in differentially expressed genes with higher BPA doses, with low‐dose exposure significantly downregulating hepatic Cpt1a mRNA levels. Histological examination indicated lipid vacuole formation at high doses without collagen deposition. BPA consistently inhibited PPARG activity in both MCF7 cells and mouse livers. BPA exposure disrupts hepatic lipid metabolism and PPARG activity, highlighting its role as an endocrine disruptor. Further research is needed to elucidate the long‐term effects of BPA on liver health.

BackgroundHigh-sugar, high-fat diets (HSDFD) can lead to hepatic dysfunction, but the molecular mechanisms underlying protective compounds like sesamin remain unclear MethodsWe employed a multi-faceted approach combining in silico and in vivo techniques. Utilizing the AlphaFold database, we screened multi-species proteomes to identify potential sesamin targets. Molecular dynamics simulations and MM-PBSA analysis were used to characterize sesamin-protein interactions. In vivo studies included single-cell RNA sequencing of hepatocytes from HSDFD-fed mice. We validated our findings using cellular thermal shift assays (CETSA), drug affinity responsive target stability (DARTS) assays, Western blotting, and qPCR. ResultsHSDFD induced significant redistribution of hepatocyte subpopulations with high CYP1A2 abundance. Computational analysis identified CYP1A2 as a direct target of sesamin, with species-specific interaction patterns. Sesamin exhibited stable binding to CYP1A2, modulating its activity through subtle conformational changes. Key residues F451 and I386 were crucial for sesamin's regulation of CYP1A2-mediated ROS production. Sesamin supplementation ameliorated HSDFD-induced hepatic dysfunction by modulating fatty acid metabolism and oxidative stress responses. ConclusionOur study unveils CYP1A2 as a key molecular target of sesamin in HSDFD-induced hepatic dysfunction, providing new insights into potential therapeutic strategies for metabolic liver disorders.