Comparative study on the predictive value of TG/HDL-C, TyG and TyG-BMI indices for 5-year mortality in critically ill patients with chronic heart failure: a retrospective study.

BACKGROUND: The triglyceride glucose (TyG) index, TyG-body mass index (TyG-BMI), and triglyceride-density lipoprotein cholesterol ratio (TG/HDL-C) are substitute indicators for insulin resistance (IR). This study aimed to compare the predictive value of these indicators for 5-year mortality in critically ill patients with chronic heart failure (CHF). METHODS: Critically ill patients with CHF were identified from the Multiparameter Intelligent Monitoring in Intensive Care (MIMIC) III and IV databases. The primary outcome was 5-year mortality. The relationship between the three indices and mortality risk was determined using multivariate Cox proportional hazards models, Kaplan-Meier (K‒M) analysis and restricted cubic splines analysis. A receiver operating characteristic (ROC) curve was generated to compare the ability of the three indices to predict mortality. Finally, whether the IR indices would further increase the predictive ability of the basic model including baseline variables with a significance level between survivors and non-survivors was evaluated by ROC curve. RESULTS: Altogether, 1329 patients with CHF were identified from the databases. Cox proportional hazards models indicated that the TyG index was independently associated with an elevated risk of 5-year mortality (hazard ratio [HR], 1.56; 95% confidence interval [CI] 1.29-1.9), while the TyG-BMI index and TG/HDL-C level were significantly associated with 5-year mortality, with an HR (95% CI) of 1.002 (1.000-1.003) and 1.01 (1.00-1.03), respectively. The K-M analysis revealed that the cumulative incidence of all-cause 5-year death increased with increasing quartiles of the TyG index, TyG-BMI index, or TG/HDL-C ratio. According to the ROC curve, the TyG index outperformed the TyG-BMI and TG/HDL-C ratio at predicting all-cause 5-year mortality (0.608 [0.571-0.645] vs. 0.558 [0.522-0.594] vs. 0.561 [0.524-0.598]). The effect of the TyG index on all-cause mortality was consistent across subgroups, with no significant interaction with randomized factors. Furthermore, adding the TyG index to the basic model for 5-year mortality improved its predictive ability (area under the curve, 0.762 for the basic model vs. 0.769 for the basic model + TyG index); however, the difference was not statistically significant. CONCLUSION: As continuous variables, all three indices were significantly associated with 5-year mortality risk in critically ill patients with CHF. Although these IR indices did not improve the predictive power of the basic model in patients with CHF, the TyG index appears to be the most promising index (vs. TyG-BMI and TG/HDL-C ratio) for prevention and risk stratification in critically ill patients with CHF.

Shared Genetic Features of Psoriasis and Myocardial Infarction: Insights From a Weighted Gene Coexpression Network Analysis.

BACKGROUND: Increasing evidence suggests a higher propensity for acute myocardial infarction (MI) in patients with psoriasis. However, the shared mechanisms underlying this comorbidity in these patients remain unclear. This study aimed to explore the shared genetic features of psoriasis and MI and to identify potential biomarkers indicating their coexistence. METHODS AND RESULTS: Data sets obtained from the gene expression omnibus were examined using a weighted gene coexpression network analysis approach. Hub genes were identified using coexpression modules and validated in other data sets and through in vitro cellular experiments. Bioinformatics tools, including the Human microRNA Disease Database, StarBase, and miRNet databases, were used to construct a ceRNA network and predict potential regulatory mechanisms. By applying weighted gene coexpression network analysis, we identified 2 distinct modules that were significant for both MI and psoriasis. Inflammatory and immune pathways were highlighted by gene ontology enrichment analysis of the overlapping genes. Three pivotal genes-Src homology and collagen 1, disruptor of telomeric silencing 1-like, and feline leukemia virus subgroup C cellular receptor family member 2-were identified as potential biomarkers. We constructed a ceRNA network that suggested the upstream regulatory roles of these genes in the coexistence of psoriasis and MI. CONCLUSIONS: As potential therapeutic targets, Src homology and collagen 1, feline leukemia virus subgroup C cellular receptor family member 2, and disruptor of telomeric silencing 1-like provide novel insights into the shared genetic features between psoriasis and MI. This study paves the way for future studies focusing on the prevention of MI in patients with psoriasis.

The effect of cardiac rehabilitation on cardiopulmonary function after coronary artery bypass grafting: A systematic review and meta-analysis.

We carried out a meta-analysis on the effect of cardiac rehabilitation (CR) on cardiopulmonary function after coronary artery bypass grafting (CABG). Four databases were searched for studies comparing CR with control. A random-effects model was used to pool mean difference (MD). The meta-analysis showed an increase in peak oxygen consumption (peak VO2) (MD = 1.93 mL/kg/min, p = 0.0006), and 6-min walk distance (6MWD) (MD = 59.21 m, p < 0.00001), and a decrease in resting heart rate (resting HR) (MD = 5.68 bpm, p < 0.0001) in the CR group. The subgroup analysis revealed aerobic exercise could further improve resting HR and peak HR, and physical/combination with aerobic exercise could further increase 6MWD. The improvement of peak VO2, workload, resting HR, peak HR, and 6MWD regarding CR performed within one week after CABG is greater than that one week after CABG. CR after CABG can improve the cardiopulmonary function, which is reflected by the improvement of peak VO2, 6MWD, and resting HR.

Association between insulin resistance and uncontrolled hypertension and arterial stiffness among US adults: a population-based study.

BACKGROUND: Prior research has established the correlation between insulin resistance (IR) and hypertension. While the association between triglyceride-glucose (TyG) index, a reliable surrogate marker of IR, and uncontrolled hypertension as well as arterial stiffness among individuals with hypertension remains undisclosed. METHODS: In this study, a total of 8513 adults diagnosed with hypertension from the National Health and Nutrition Examination Survey 1999-2018 were included. The primary outcome of the study are arterial stiffness (represented with estimated pulse wave velocity, ePWV) and uncontrolled hypertension. Logistic regression model, subgroup analysis, restricted cubic spine, and smooth curve fitting curve were conducted to evaluate the association between the IR indicators and uncontrolled hypertension and arterial stiffness in individuals with hypertension. RESULTS: Among included participants, the overall prevalence of uncontrolled hypertension was 54.3%. After adjusting for all potential covariates, compared with the first quartile of TyG index, the risk of uncontrolled hypertension increased about 28% and 49% for participants in the third quartile (OR, 1.28; 95% CI 1.06-1.52) and the fourth quartile (OR, 1.49; 95% CI 1.21-1.89) of TyG index, respectively. The higher OR of TyG index was observed in participants taking antihypertensive medication [fourth quartile versus first quartile (OR, 2.03; 95% CI 1.37-3.11)]. Meanwhile, we explored the potential association between TyG index and arterial stiffness and found that TyG index was significantly associated with increased arterial stiffness (ß for ePWV, 0.04; 95% CI 0.00-0.08; P = 0.039). However, traditional IR indicator HOMA-IR showed no significant positive correlation to uncontrolled hypertension as well as arterial stiffness in US adults with hypertension. CONCLUSION: Elevated levels of the TyG index were positive associated with prevalence of uncontrolled hypertension and arterial stiffness among US adults with hypertension.

A fusion of VGG-16 and ViT models for improving bone tumor classification in computed tomography.

Background and Objective: Bone tumors present significant challenges in orthopedic medicine due to variations in clinical treatment approaches for different tumor types, which includes benign, malignant, and intermediate cases. Convolutional Neural Networks (CNNs) have emerged as prominent models for tumor classification. However, their limited perception ability hinders the acquisition of global structural information, potentially affecting classification accuracy. To address this limitation, we propose an optimized deep learning algorithm for precise classification of diverse bone tumors. Materials and Methods: Our dataset comprises 786 computed tomography (CT) images of bone tumors, featuring sections from two distinct bone species, namely the tibia and femur. Sourced from The Second Affiliated Hospital of Fujian Medical University, the dataset was meticulously preprocessed with noise reduction techniques. We introduce a novel fusion model, VGG16-ViT, leveraging the advantages of the VGG-16 network and the Vision Transformer (ViT) model. Specifically, we select 27 features from the third layer of VGG-16 and input them into the Vision Transformer encoder for comprehensive training. Furthermore, we evaluate the impact of secondary migration using CT images from Xiangya Hospital for validation. Results: The proposed fusion model demonstrates notable improvements in classification performance. It effectively reduces the training time while achieving an impressive classification accuracy rate of 97.6%, marking a significant enhancement of 8% in sensitivity and specificity optimization. Furthermore, the investigation into secondary migration's effects on experimental outcomes across the three models reveals its potential to enhance system performance. Conclusion: Our novel VGG-16 and Vision Transformer joint network exhibits robust classification performance on bone tumor datasets. The integration of these models enables precise and efficient classification, accommodating the diverse characteristics of different bone tumor types. This advancement holds great significance for the early detection and prognosis of bone tumor patients in the future.

Placental MRI segmentation based on multi-receptive field and mixed attention separation mechanism.

OBJECTIVE: To reduce the occurrence of massive bleeding during placental abruption in patients with placenta accrete, we established a medical imaging based on multi-receptive field and mixed attention separation mechanism (MRF-MAS) model to improve the accuracy of MRI placenta segmentation and provide a basis for subsequent placenta accreta. METHODS: We propose a placenta MRI segmentation technology using the MRF-MAS framework to develop a medical image diagnostic technique. The model first uses the multi-receptive field feature structure to obtain multi-level information, and improves the expression of features at differing scales. Note that the hybrid attention mechanism combines channel attention and spatial attention, separates the input feature sets and computes the attention separately, and finally reorganizes the feature maps. To show that the model can improve the accuracy of segmenting the placenta, we adopt mean Intersection over Union (IoU), Dice similarity coefficient (Dice) and area under the receiver operating characteristic curve (AUC) with U-Net, Mask RCNN, Deeplab v3 for comparison. RESULTS: The four models achieved different outcomes based on our placenta dataset, with our model IoU and Dice up to 0.8169 and 0.8992, which are 5.51% and 3.03% higher than the average of the three comparison models. CONCLUSION: The model proposed by us is helpful to assist the imaging diagnosis and at the same time provides a quantitative reference for the precise treatment of placenta accreta, assists the Equationtion of the clinical operation plan of the physician, and promotes the precision medicine of placenta accreta.

Serum ferritin and the risk of short-term mortality in critically ill patients with chronic heart failure: a retrospective cohort study.

Background: Serum ferritin levels are associated with a higher risk of incident heart failure (HF). Whether serum ferritin levels, either increased or decreased, predict the risk of mortality in individuals with chronic heart failure (CHF) remains unknown. Objectives: This study aimed to clarify the potential predictive significance of serum ferritin levels in assessing the short-term mortality in critically ill patients with chronic heart failure (CHF). Methods: Critically ill patients with CHF were identified from the Multiparameter Intelligent Monitoring in Intensive Care III and IV (MIMIC III and IV) databases. Linear and logistic regression models and Cox proportional hazards models were applied to assess the associations between serum ferritin and survival. Results: A total of 1,739 and 2,322 patients with CHF identified from the MIMIC III and IV databases, respectively, fulfilled the inclusion criteria. In the MIMIC III group, compared with the reference group (serum ferritin ≥70 and <500 ng/mL), serum ferritin ≥1000 ng/mL was a significant predictor of 28-day (odds ratio [OR], 1.76; 95% confidence interval [CI], 1.14-2.72) and 90-day mortality (OR, 1.64; 95% CI, 1.13-2.39). The results from the Cox regression and Kaplan-Meier curves revealed similar results. In the MIMIC IV group, serum ferritin ≥1000 ng/mL was a significant predictor of in-hospital (OR, 1.70; 95% CI, 1.18-2.46), 28-day (OR, 1.83; 95% CI, 1.24-2.69), and 90-day mortality (OR, 1.57; 95% CI, 1.11-2.22) after adjusting for confounding factors. Conclusion: High ferritin levels (≥1000 ng/mL) were associated with increased short-term mortality in critically ill patients with CHF, indicating that serum ferritin may serve as a useful prognostic marker for CHF.

Brain image segmentation of the corpus callosum by combining Bi-Directional Convolutional LSTM and U-Net using multi-slice CT and MRI.

BACKGROUND AND OBJECTIVE: Traditional disease diagnosis is usually performed by experienced physicians, but misdiagnosis or missed diagnosis still exists. Exploring the relationship between changes in the corpus callosum and multiple brain infarcts requires extracting corpus callosum features from brain image data, which requires addressing three key issues. (1) automation, (2) completeness, and (3) accuracy. Residual learning can facilitate network training, Bi-Directional Convolutional LSTM (BDC-LSTM) can exploit interlayer spatial dependencies, and HDC can expand the receptive domain without losing resolution. METHODS: In this paper, we propose a segmentation method by combining BDC-LSTM and U-Net to segment the corpus callosum from multiple angles of brain images based on computed tomography (CT) and magnetic resonance imaging (MRI) in which two types of sequence, namely T2-weighted imaging as well as the Fluid Attenuated Inversion Recovery (Flair), were utilized. The two-dimensional slice sequences are segmented in the cross-sectional plane, and the segmentation results are combined to obtain the final results. Encoding, BDC- LSTM, and decoding include convolutional neural networks. The coding part uses asymmetric convolutional layers of different sizes and dilated convolutions to get multi-slice information and extend the convolutional layers' perceptual field. RESULTS: This paper uses BDC-LSTM between the encoding and decoding parts of the algorithm. On the image segmentation of the brain in multiple cerebral infarcts dataset, accuracy rates of 0.876, 0.881, 0.887, and 0.912 were attained for the intersection of union (IOU), dice similarity coefficient (DS), sensitivity (SE), and predictive positivity value (PPV). The experimental findings demonstrate that the algorithm outperforms its rivals in accuracy. CONCLUSION: This paper obtained segmentation results for three images using three models, ConvLSTM, Pyramid-LSTM, and BDC-LSTM, and compared them to verify that BDC-LSTM is the best method to perform the segmentation task for faster and more accurate detection of 3D medical images. We improve the convolutional neural network segmentation method to obtain medical images with high segmentation accuracy by solving the over-segmentation problem.

Association of iron status with non-alcoholic fatty liver disease and liver fibrosis in US adults: a cross-sectional study from NHANES 2017-2018.

Aims: Non-alcoholic fatty liver disease (NAFLD) is a widely prevalent hepatic disorder resulting in a high risk of adverse prognosis, and its presence has been considered a cause or an outcome of metabolic syndrome. But the relative factors and mechanism of NAFLD are still unclear. The aim of this study is to explore the association between iron status indicators and NAFLD as well as liver fibrosis. Methods: This study evaluated whether serum iron status indicators are independently related to the risk of NAFLD. The independent variable was each one of the iron status indicators (iron intake, ferritin, iron, unsaturated iron binding force (UIBC), total iron binding capacity (TIBC), transferrin saturation, transferrin receptor, hemoglobin, and mean cell hemoglobin), and the dependent variables were NAFLD and advanced liver fibrosis. A multivariable logistic regression analysis and subgroup analysis were performed to evaluate the association between iron status indicators and NAFLD as well as liver fibrosis. Results: A total of 3727 patients were included. After adjusting for other covariates in multiple logistic regression models, the serum ferritin, UIBC, TIBC, and hemoglobin had a significant positive association with the NAFLD (odds ratio [OR] = 1.16, 95% confidence interval [CI]: 1.09, 1.23; 1.31, 95% CI: 1.06, 1.62; 1.82, 95% CI: 1.23, 2.67; 2.67, 95% CI: 1.48, 4.82, separately), and the risk of NAFLD diagnosed by VCTE or ALT/AST further increased in the fourth quartile group of serum ferritin (diagnosed by VCTE OR = 1.93, 95% CI: 1.49, 2.50; diagnosed by ALT/AST OR = 5.76, 95% CI: 3.96, 8.38). Moreover, the main positive correlation between serum ferritin and NAFLD was found in females, participants aged >41 years, with no diabetes. Conclusion: Our results indicated that iron status indicators were closely associated with the occurrence of advanced liver fibrosis, which may indicate that iron status indicators could be potential biomarkers of NAFLD and advanced liver fibrosis.

Inhibition of Th17 cells by donepezil ameliorates experimental lung fibrosis and pulmonary hypertension.

Rationale: Pulmonary hypertension (PH) secondary to lung fibrosis belongs to WHO Group III, one of the most common subgroups of PH; however, it lacks effective treatment options. Cholinesterase inhibitor donepezil (DON) has been shown to effectively improve Group I PH. However, its effects on Group III PH are unknown. Methods: A lung fibrosis-induced PH mouse model was constructed using a single intratracheal instillation of bleomycin (BLM), after which DON was administered daily. Pulmonary artery and right ventricle (RV) remodeling were evaluated at the end of the study. Lung tissue in each group was analyzed using RNA sequencing, and the results were further verified with datasets from patients with PH. The mechanisms underlying DON-induced effects on PH were verified both in vivo and in vitro. Results: DON effectively improved pulmonary artery and RV remodeling in the BLM-induced mouse model. Transcriptomic profiles of lung tissue indicated that the expression of inflammatory and fibrotic genes was significantly changed in this process. In the animal model and patients with PH, T helper 17 lymphocytes (Th17) were the most common inflammatory cells infiltrating the lung tissue. DON significantly inhibited lung fibroblast activation; thus, preventing lung fibrosis and reducing the inflammatory response and Th17 cell infiltration in the BLM-induced lung tissue. In addition, Th17 cells could activate lung fibroblasts by secreting IL17A, and DON-mediated inhibition of Th17 cell differentiation was found to depend on the α7nAchR-JAK2-STAT3 pathway. Conclusion: DON can alleviate lung fibrosis and PH in an experimental mouse model. It inhibited pro-inflammatory Th17 cell differentiation, which is dependent on a cholinergic receptor pathway, thereby regulating fibroblast activation.

Association of preoperative monocyte/lymphocyte ratio with postoperative oxygenation impairment in patients with acute aortic syndrome.

BACKGROUND: Postoperative oxygenation impairment represents a common complication in patients with the acute aortic syndrome (AAS). The study aimed to explore the relationship between inflammatory indicators and AAS patients with oxygenation impairment after operation. METHODS: In this study, 330 AAS patients who underwent surgery were enrolled and divided into 2 groups based on postoperative oxygenation impairment (non-oxygenation impairment group and oxygenation impairment group). Regression analysis was performed to assess the relationship between inflammatory indicators and postoperative oxygenation impairment. A smooth curve and interaction analysis were further conducted. Stratified analysis was used according to preoperative monocyte/lymphocyte ratio (MLR) (Tertiles). RESULTS: Multivariate analysis showed that preoperative MLR was independently related to oxygenation impairment after surgery in AAS patients (OR, 95% CI, P: 2.77, 1.10-7.00, 0.031). The smooth curve indicated the risk of postoperative oxygenation impairment was higher with the elevated preoperative MLR. Interaction analysis revealed that patients with AAS with high preoperative MLR who had coronary artery disease (CAD) had a higher risk of oxygenation impairment after operation. Moreover, stratified analysis was performed according to baseline MLR (Tertiles), and a higher baseline MLR level in AAS patients was correlated with a lower arterial oxygen tension (PaO2) / inspiratory oxygen fraction (FiO2) ratio perioperatively. CONCLUSIONS: In AAS patients, preoperative MLR level was independently related to postoperative oxygenation impairment.

Desipramine enhances the stability of atherosclerotic plaque in rabbits monitored with molecular imaging.

Acid sphingomyelinase (ASM) promotes atherogenesis and acute cardiovascular events. We previously demonstrated ASM inhibitor desipramine attenuated oxidized-LDL-induced macrophage apoptosis in vitro. Here, we aim to determine whether ASM-mediated apoptosis in plaque improves stability in vivo. In this study, rabbits with abdominal aorta balloon injury and a 12-week high-cholesterol diet (HCD) were used to simulate an atherosclerotic plaque model. Atherosclerotic rabbits received oral administration of saline (Control group), atorvastatin (Ator group), or desipramine (DES group). ASM activity and ceramide level were measured by ultra-performance liquid chromatography (UPLC). Plaque morphology was assessed by histochemistry and immunohistochemistry. Apoptosis was evaluated by SPECT/CT imaging of 99mTc-duramycin uptake and TUNEL. We found that increasing ASM activity and ceramide level in atherosclerotic rabbits was abated by additional atorvastatin and desipramine treatment. Meanwhile, the DES and Ator groups were similar in plaque stability, with smaller plaque size, areas of macrophages, higher smooth muscle cell content, and decreased apoptosis and matrix metalloproteinase (MMP) activities relative to the Control group. 99mTc-duramycin uptake of rabbit aorta was significantly higher in Control than in the Normal group, while it was reduced by desipramine and atorvastatin administration. Moreover, the uptake of 99mTc-duramycin positively correlated with apoptotic cell number, macrophage infiltration, and plaque instability. The present study demonstrated that desipramine exerted plaque-stabilizing effects partially by suppressing apoptosis and MMP activity in a rabbit model. And 99mTc-duramycin SPECT/CT imaging allowed noninvasively monitoring of atherosclerotic disease and evaluation of anti-atherosclerotic therapy.

A comprehensive overview of cellular senescence from 1990 to 2021: A machine learning-based bibliometric analysis.

Background: As a cellular process, senescence functions to prevent the proliferation of damaged, old and tumor-like cells, as well as participate in embryonic development, tissue repair, etc. This study aimed to analyze the themes and topics of the scientific publications related to cellular senescence in the past three decades by machine learning. Methods: The MeSH term "cellular senescence" was used for searching publications from 1990 to 2021 on the PubMed database, while the R platform was adopted to obtain associated data. A topic network was constructed by latent Dirichlet allocation (LDA) and the Louvain algorithm. Results: A total of 21,910 publications were finally recruited in this article. Basic studies (15,382, 70.21%) accounted for the most proportion of publications over the past three decades. Physiology, drug effects, and genetics were the most concerned MeSH terms, while cell proliferation was the leading term since 2010. Three senolytics were indexed by MeSH terms, including quercetin, curcumin, and dasatinib, with the accumulated occurrence of 35, 26, and 22, separately. Three clusters were recognized by LDA and network analyses. Telomere length was the top studied topic in the cluster of physiological function, while cancer cell had been a hot topic in the cluster of pathological function, and protein kinase pathway was the most popular topic in the cluster of molecular mechanism. Notably, the cluster of physiological function showed a poor connection with other clusters. Conclusion: Cellular senescence has obtained increasing attention over the past three decades. While most of the studies focus on the pathological function and molecular mechanism, more researches should be conducted on the physiological function and the clinical translation of cellular senescence, especially the development and application of senotherapeutics.

Blood and urine manganese exposure in non-alcoholic fatty liver disease and advanced liver fibrosis: an observational study.

Manganese was the key activator of biological enzymes-mediated metabolic diseases (Mets)-associated pathophysiological process. Non-alcoholic fatty liver disease (NAFLD), which was the hepatic manifestation of Mets, development remained a mystery. We aimed to explore the association between blood/urine manganese exposure and NAFLD and liver fibrosis diagnosed by vibration-controlled transient elastography (VCTE). All data were extracted from National Health and Nutrition Examination Survey database (2017-2018). A total of 3580 participants with blood manganese data were enrolled and divided into four groups according to the quartile of blood manganese exposure level. In multiple logistic regression models, the higher blood manganese exposure level (groups 2, 3, and 4) had a significant positive association with NAFLD (ß = 1.58, 1.30, and 1.69). In subgroup analysis, the main inversely correlation between blood manganese and NAFLD was found in participants with normal/high body mass index and high blood manganese exposure level. Moreover, in 1179 participants with urine manganese data, urine manganese exposure level presented as significantly associated with advanced liver fibrosis in models 1 and 2 (ß = 2.00 and 2.02). This study showed that manganese exposure level was positively associated with NAFLD and advanced liver fibrosis among the US population. We suggested that manganese exposure level was a biomarker of the development of NAFLD.

The association between body mass index and risk of preoperative oxygenation impairment in patients with the acute aortic syndrome.

Objective: The study aimed to determine the relationship between body mass index (BMI) and the risk of acute aortic syndrome (AAS) with preoperative oxygenation impairment. Methods: A meta-analysis of published observational studies involving BMI and AAS with preoperative oxygenation impairment was conducted. A total of 230 patients with AAS were enrolled for retrospective analysis. All patients were divided into 2 groups (Non-oxygenation impairment group and Oxygenation impairment group). Logistic regression analysis was performed to assess the relation between BMI and the risk of preoperative oxygenation impairment after the onset of AAS. Dose-response relationship curve and subgroup analysis were conducted to test the reliability of BMI as an independent factor of it. Results: For the meta-analysis, the quantitative synthesis indicated that excessive BMI increased the risk of preoperative oxygenation impairment (OR: 1.30, 95% CI: 1.05-1.60, P heterogeneity = 0.001). For the retrospective analysis, a significant association was observed after adjusting for a series of variables. BMI was significantly related to preoperative oxygenation impairment after the onset of AAS (OR: 1.34, 95% CI: 1.15-1.56, p <0.001), and compared with normal weight group (18.5 kg/m2 ≤ BMI < 23.0 kg/m2), the individuals with excessive BMI were at higher risk of preoperative oxygenation impairment for the obese group (BMI ≥ 25 kg/m2) (OR: 17.32, 95% CI: 4.03-74.48, p <0.001). A J-shape curve in dose-response relationship analysis further confirmed their positive correlation. Subgroup analysis showed that diastolic blood pressure (DBP) ≥ 90mmHg carried an excess risk of preoperative oxygenation impairment in obese patients. Conclusion: Excessive BMI was an independent risk factor for AAS with preoperative oxygenation impairment.

Identification and exploration of novel M2 macrophage-related biomarkers in the development of acute myocardial infarction.

Background: Acute myocardial infarction (AMI), one of the most severe and fatal cardiovascular diseases, is a major cause of morbidity and mortality worldwide. Macrophages play a critical role in ventricular remodeling after AMI. The regulatory mechanisms of the AMI progression remain unclear. This study aimed to identify hub regulators of macrophage-related modules and provide translational experiments with potential therapeutic targets. Materials and methods: The GSE59867 dataset was downloaded from the Gene Expression Omnibus (GEO) database for bioinformatics analysis. The expression patterns of 22 types of immune cells were determined using CIBERSORT. GEO2R was used to identify differentially expressed genes (DEGs) through the limma package. Then, DEGs were clustered into different modules, and relationships between modules and macrophage types were analyzed using weighted gene correlation network analysis (WGCNA). Further functional enrichment analysis was performed using significantly associated modules. The module most significantly associated with M2 macrophages (Mϕ2) was chosen for subsequent analysis. Co-expressed DEGs of AMI were identified in the GSE123342 and GSE97320 datasets and module candidate hub genes. Additionally, hub gene identification was performed in GSE62646 dataset and clinical samples. Results: A total of 8,760 DEGs were identified and clustered into ten modules using WGCNA analysis. The blue and turquoise modules were significantly related to Mϕ2, and 482 hub genes were discerned from two hub modules that conformed to module membership values > 0.8 and gene significance values > 0.25. Subsequent analysis using a Venn diagram assessed 631 DEGs in GSE123342, 1457 DEGs in GSE97320, and module candidate hub genes for their relationship with Mϕ2 in the progression of AMI. Finally, four hub genes (CSF2RB, colony stimulating factor 2 receptor subunit beta; SIGLEC9, sialic acid-binding immunoglobulin-like lectin 9; LRRC25, leucine-rich repeat containing 25; and CSF3R, colony-stimulating factor-3 receptor) were validated to be differentially expressed and to have high diagnostic value in both GSE62646 and clinical samples. Conclusion: Using comprehensive bioinformatics analysis, we identified four novel genes that may play crucial roles in the pathophysiological mechanism of AMI. This study provides novel insights into the impact of macrophages on the progression of AMI and directions for Mϕ2-targeted molecular therapies for AMI.

Outcomes of hyperlactatemia on admission in critically ill patients with acute myocardial infarction: A retrospective study from MIMIC-IV.

Background: It has not been verified whether there is a correlation between admission hyperlactatemia and outcomes in critically ill patients with acute myocardial infarction (AMI), especially in large data studies, which we aimed to do in this study. Methods: For this retrospective study, we extracted analysis data from a famous online intensive care unit database, the Medical Information Mart for Intensive Care (MIMIC)-IV. Included patients were divided into four groups according to the serum lactate level on admission. Hospital mortality and mortality over time were the main outcomes. To explore the relationship between admission hyperlactatemia and outcomes in critically ill patients with AMI, logistic regression, Cox regression, Kaplan-Meier curves, and subgroup analyses were used. Results: 2171 patients matching the selection criteria were enrolled in this study. After adjusting for potential confounding factors, hyperlactatemia on admission contributed to increased short-term mortality in critically ill patients with AMI. The adjusted odds ratio for hospital mortality were 1.62, 3.46 and 5.28 in the mild, moderate, and severe hyperlactatemia groups (95% CI: 1.20-2.18, 2.15-5.58, and 2.20-12.70, respectively). The adjusted hazard ratio for 7-day and 30-day mortality were 1.99 and 1.35 (95% CI: 1.45-2.73 and 1.09-1.67) in the mild hyperlactatemia group, 3.33 and 2.31 (95% CI: 2.22-4.99 and 1.72-3.10) in the moderate hyperlactatemia group, 4.81 and 2.91 (95% CI: 2.86-8.08 and 1.88-4.50) in the severe hyperlactatemia group. The adjusted hazard ratio for 1-year and 5-year mortality were 2.03 and 1.93 (95% CI: 1.58-2.62 and 1.52-2.47) in the moderate hyperlactatemia group, 1.92 and 1.74 (95% CI: 1.28-2.89 and 1.17-2.59) in the severe hyperlactatemia group. Subgroup analyses indicated that the positive correlation between serum lactate level on admission and short-term mortality of critically ill patients with AMI was similar in the subgroups of cardiogenic shock and acute heart failure (P for interaction > 0.05). Conclusion: Hyperlactatemia, especially moderate and severe hyperlactatemia, on admission is closely related to higher short-term mortality incidence in critically ill patients with AMI. The relationship between serum lactate level on admission and short-term mortality of critical AMI patients is stable in subgroups of cardiogenic shock and acute heart failure.

COVID-19 is associated with the risk of cardiovascular disease death: A two-sample Mendelian randomization study.

Objective: This study aimed to estimate the causal effects of Coronavirus disease 2019 susceptibility and hospitalization on cardiovascular disease death using two-sample Mendelian randomization analysis. Methods: We used statistics from a genome-wide association study. A total of 2,568,698 participants were assessed in this study, including 1,299,010 in Coronavirus disease 2019 susceptibility databases, 908,494 in Coronavirus disease 2019 hospitalization database, and 361,194 in a cardiovascular disease death database. We performed two-sample Mendelian randomization analysis using the inverse variance weighted method. As sensitivity analysis techniques, Mendelian randomization-Egger regression, heterogeneity analyses, and Leave-one-out analysis were employed. Reverse Mendelian randomization analysis was used to detect reverse causality. Statistical significance was defined as P < 0.05. Results: Coronavirus disease 2019 susceptibility may be a causal factor for cardiovascular disease death (ß = 2.188 × 10-3, P = 0.002), which involves five common single nucleotide polymorphisms. Similarly, Coronavirus disease 2019 hospitalization may also be a causal factor for cardiovascular disease death (ß = 8.626 × 10-4, P = 0.010), which involves nine common single nucleotide polymorphisms. Furthermore, sensitivity and reverse Mendelian randomization analysis suggested that no heterogeneity, horizontal pleiotropy or reverse causality was found between Coronavirus disease 2019 and cardiovascular disease death. Conclusion: Our bidirectional Mendelian randomization analysis showed a causal relationship between Coronavirus disease 2019 susceptibility and hospitalization associated with an increased risk of cardiovascular disease death.

Impact of body mass index on postoperative oxygenation impairment in patients with acute aortic syndrome.

Objective: Oxygenation impairment is a common complication of acute aortic syndrome (AAS) patients after surgical repair. The aim of this study is to identify the relationship between body mass index (BMI) and the risk of postoperative oxygenation impairment in AAS patients. Methods: A total of 227 consecutive patients who were diagnosed as AAS and underwent surgical repair were recruited. They were divided into two groups based on the postoperative oxygenation impairment (non-oxygenation impairment group and oxygenation impairment group). Logistic regression was conducted to evaluate the association between BMI and the risk of oxygenation impairment after surgery. Dose-response curve and subgroup analysis were used to test the reliability of the results of regression analysis. A meta-analysis was then performed to further confirm these results using Pubmed, Embase, and Web of Science databases. Results: For the retrospective study, a significant association was observed after adjusting for a series of variables. BMI was significantly correlated with postoperative oxygenation impairment in patients with AAS (OR, 95% CI, P: 1.27, 1.17-1.46, 0.001). Compared with the normal weight group (18.5 kg/m2 ≤ BMI <23.0 kg/m2), patients with excessive BMI were at a higher risk of oxygenation impairment for the overweight group (23.0 kg/m2 ≤ BMI <25 kg/m2) and obesity group (BMI ≥25 kg/m2) (OR, 95% CI, P: 4.96, 1.62-15.15, 0.005; 9.51, 3.06-29.57, <0.001). The dose-response curve showed that the risk of oxygenation impairment after surgery increased with the increased BMI. Besides, subgroup analysis showed that AAS patients who have an excess weight with a TNF-α ≥ 8.1 pg/ml carried an excess risk of postoperative oxygenation impairment. For the meta-analysis, the pooled result also indicated that AAS patients with high BMI had a significantly increased risk of oxygenation impairment after surgery (OR, 95% CI, P: 1.40, 1.18-1.66, 0.001). Conclusion: Excessive BMI was an independent risk factor for AAS with postoperative oxygenation impairment.

The association between non-alcoholic fatty liver disease (NAFLD) and advanced fibrosis with blood selenium level based on the NHANES 2017-2018.

BACKGROUND & OBJECTIVE: Selenium was one of the essential trace elements that played a pivotal role in human health. Although previous studies have investigated the relationship between selenium and non-alcoholic fatty liver disease (NAFLD) and fibrosis, these findings were still inconclusive. Our study was aimed to explore the association between blood selenium level and NAFLD and advanced liver fibrosis diagnosed by vibration controlled transient elastography (VCTE) in US adults. METHODS: All data were extracted from National Health and Nutrition Examination Survey database (2017-2018). Participants were divided into four groups according to quartile of blood selenium level. Liver stiffness and controlled attenuation parameter (CAP) were measured by VCTE. Multiple logistic regression models and subgroup analyses were conducted to determine the association between blood selenium level and NAFLD and advanced liver fibrosis diagnosed by a variety of methods. RESULTS: A total of 3336 participants were enrolled in main analysis. In multiple logistic regression models, the higher blood selenium level (>205.32, ≤453.62 µg/L) had a significant positive association with NAFLD (ß = 1.31). Moreover, high blood selenium level had significantly inversely association to advanced liver fibrosis (ß = 0.61). In subgroup analysis, the main inversely correlation between blood selenium and advanced liver fibrosis was found in males with high blood selenium level. Despite dietary selenium intake being adjusted or in different subgroups, the associations between blood selenium level and NAFLD/advanced liver fibrosis remained significant. CONCLUSIONS: This study showed that blood selenium level were positively association with NAFLD among US population. Participants with lower blood selenium level showed a higher percentage of advanced liver fibrosis. Blood selenium is more likely to cause NAFLD and liver fibrosis due to imbalances in selenium homeostasis rather than dietary selenium intake.Key messagesHigh blood selenium level was association with NAFLD diagnosed by vibration controlled transient elastography.Participants with lower blood selenium level had high percentage of advanced liver fibrosis.NAFLD and liver fibrosis are caused by an imbalance of selenium homeostasis, not by dietary selenium intake.