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Abstract Aims Prior evidence has shown a significant link between inflammation and the development of myocarditis. This study aimed to investigate the causal relationship between inflammation‐related genes (IRGs) and myocarditis. Methods and results In this study, the causal relationship between 167 IRGs and myocarditis were investigated using datasets from the Gene Set Enrichment Analysis and Integrative Epidemiology Unit open genome‐wide association study (IEU OpenGWAS) databases. The GWAS data (finn‐b‐I9 MYOCARD) contained single nucleotide polymorphisms (SNPs) data from 117 755 myocarditis samples (16 379 455 SNPs, 829 cases vs. 116 926 controls). Five algorithms [MR‐Egger, weighted median, inverse variance weighted (IVW), simple mode, and weighted mode regression] were employed for the MR analysis, with IVW as the primary method, and sensitivity analysis was conducted. Subcellular localization and protein–protein interaction (PPI) network analyses were performed for selected biomarkers. Results were verified in ebi‐a‐GCST90018882 (24 180 570 SNPs, 633 cases vs. 427 278 controls) and finn‐b‐I9 MYOCARD EXNONE (16 380 466 SNPs, 829 cases vs. 217 963 controls) to enhance reliability. Results IRF7 and ADORA2B were shown to be two exposure factors after screening. Univariable MR (UVMR) analysis revealed that IRF7 was a risk factor for myocarditis [IVW: odd ratio (OR) = 1.041, 95% confidence interval (CI) = 1.018–1.955, P = 0.039], while ADORA2B was a protective factors for myocarditis (IVW: OR = 0.799, 95% CI = 0.640–0.997, P = 0.047). Sensitivity analysis confirmed the robustness of these findings. Multivariable MR (MVMR) analysis further demonstrated a direct causal role of ADORA2B in preventing myocarditis. Subcellular localization analysis indicated predominant cytoplasmic expression and limited mitochondrial expression for both genes. The results of PPI analysis showed that 20 genes were predicted to be associated with IRF7 function, such as response to type I interferon, pattern recognition receptor signalling pathway, and toll‐like receptor signalling pathway. The results in finn‐b‐I9 MYOCARD EXNONE were consistent with MR analysis. Conclusions The findings indicated there was a causal connection between IRGs (IRF7 and ADORA2B) and myocarditis, which offered a crucial point of reference and guidance for future studies and myocarditis treatment.

Abstract Background Hyperglycemia upon admission is associated with poor prognosis of many cardiovascular diseases. However, the relationship of stress hyperglycemia ratio (SHR), admission blood glucose (ABG), and hemoglobin A1c (HbA1c) with pulmonary hypertension has not been reported. This study aimed to explore the association of hyperglycemia indices with disease severity and long-term adverse outcomes in patients with idiopathic pulmonary arterial hypertension (IPAH). Methods This multi-center cohort study included 625 consecutive patients diagnosed with or treated for IPAH between January 2015 and June 2023. SHR was calculated using the followings: ABG (mmol/L)/(1.59 × HbA1c [%] − 2.59). The primary endpoint was defined as clinical worsening events. Multivariable Cox regression and restricted cubic spline analyses were employed to evaluate the association of SHR, ABG, and HbA1c with endpoint events. The mediating effect of pulmonary hemodynamics was evaluated to investigate the potential mechanism between hyperglycemia and clinical outcomes. Results During a mean follow-up period of 3.8 years, 219 (35.0%) patients experienced all-cause death or clinical worsening events. Hyperglycemia indices correlated with well-validated variables that reflected the severity of IPAH, such as the World Health Organization functional class, 6-min walk distance, and N-terminal pro-brain natriuretic peptide levels. Multivariable Cox regression analyses indicated that SHR (hazard ratio [HR] 1.328, 95% confidence intervals [CI]: 1.185, 1.489 per 0.1-unit increment, P

Summary: Heart failure (HF) is a global concern, particularly HF with preserved ejection fraction (HFpEF), lacking effective treatments. Understanding the differences of metabolic profiles between HFpEF and HFrEF (heart failure with reduced ejection fraction) patients is crucial for therapeutic advancements. In this study, pseudotargeted metabolomics was employed to analyze for disparities of plasma metabolic profiles between HFpEF and HFrEF in two cohorts: discovery (n = 514) and validation (n = 3368). Plasma-free carnitine levels were significant changed in HF patients. A non-linear and U-shaped (for HFpEF) or J-shaped (for HFrEF) association between circulating free carnitine levels and the composite risk of cardiac events were observed. Interestingly, HFpEF patients with low free carnitine (≤40.18 μmol/L) displayed a poorer survival, contrasting with HFrEF where higher levels (≥35.67 μmol/L) were linked to poorer outcomes, indicating distinct metabolism pathways. In conclusion, these findings offer insights into HFpEF metabolic profiles, suggesting potential therapeutic targets.

Abstract Background Insulin resistance (IR) plays an important role in the pathophysiology of cardiovascular disease. Recent studies have shown that diabetes mellitus and impaired lipid metabolism are associated with the severity and prognosis of idiopathic pulmonary arterial hypertension (IPAH). However, the relationship between IR and pulmonary hypertension is poorly understood. This study explored the association between four IR indices and IPAH using data from a multicenter cohort. Methods A total of 602 consecutive participants with IPAH were included in this study between January 2015 and December 2022. The metabolic score for IR (METS-IR), triglyceride to high-density lipoprotein cholesterol (TG/HDL-C) ratio, triglyceride and glucose (TyG) index, and triglyceride-glucose-body mass index (TyG-BMI) were used to quantify IR levels in patients with IPAH. The correlation between non-insulin-based IR indices and long-term adverse outcomes was determined using multivariate Cox regression models and restricted cubic splines. Results During a mean of 3.6 years’ follow-up, 214 participants experienced all-cause death or worsening condition. Compared with in low to intermediate-low risk patients, the TG/HDL-C ratio (2.9 ± 1.7 vs. 3.3 ± 2.1, P = 0.003) and METS-IR (34.5 ± 6.7 vs. 36.4 ± 7.5, P

Abstract Background Metals have been linked to a diverse spectrum of age-related diseases; however, the effects of metal exposure on health span remains largely unknown. This cohort study aims to determine the association between plasma metal and health span in elder adults aged ≥ 90 years. Methods The plasma concentrations of seven metals were measured at baseline in 300 elder adults. The end of the health span (EHS) was identified as the occurrence of one of eight major morbidities or mortality events. We used Cox regression to assess hazard ratios (HR). The combined effects of multiple metal mixtures were estimated using grouped-weighted quantile sum (GWQS), quantile g-computation (Q-gcomp), and Bayesian kernel machine regression (BKMR) methods. Results The estimated HR for EHS with an inter-quartile range (IQR) increment for selenium (Se) was 0.826 (95% confidence interval [CI]: 0.737–0.926); magnesium (Mg), 0.806 (95% CI: 0.691–0.941); iron (Fe), 0.756 (95% CI: 0.623–0.917), and copper (Cu), 0.856 (95% CI: 0.750–0.976). The P for trend of Se, Mg, and Fe were all

Copper/stainless steel composite is often used for preparation of superconducting busbar “double box” lap joints. However, it is a challenge for the large thickness T2 copper/316L stainless steel composite is fabricated by explosive welding, because of the bonding interface is always present many problems such as large ripple size, many microscopic defects, low bonding strength and poor sealing etc. In this paper, the big-thickness T2 copper/316L stainless steel composite with small size wavy interface was successfully fabricated by explosive welding. Microstructure of bonding interface indicated that the welding process could be divided into three stages: detonation growth stage, detonation stabilization stage, detonation descent stage. The morphology of bonding interface presented a regular wavy interface and no defects such as cracks, voids and intermetallic compound were formed in the stable stage, which was consistent with the results of ultrasonic and permeability quality inspection. The hardness of copper side and stainless steel side close to the bonding interface reached 131HV and 432HV, respectively. Dynamic recrystallization and fine grain generated in the bonding interface. The mechanical properties of tensile strength, pull-off strength and shear strength in the stable detonation stage is greater than 110 MPa, which is meeting the requirements of preparation of superconducting busbar “double box” lap joints. The deformation failure mainly occurred in the copper side near the bonding interface, which presented a higher bonding strength than copper. Some dimples and tearing edges with different sizes on the fracture surfaces, indicating that the fracture was a typical ductile fracture.

Steel-like density HfZrTiTa0.2Al0.8 high entropy alloy (HEA) with a density of 7.78 g/cm3 is designed and fabricated as a novel energetic structural material (ESM). The microstructure, thermal analysis, compressive mechanical properties, ignition and energy release under dynamic loading are systemically investigated. The experimental results show that the HfZrTiTa0.2Al0.8 HEA has a single BCC solid solution structure, and spinodal decomposition with elements segregation in the nanoscale is observed. Thermal analysis shows the HEA keeps stable in the Ar atmosphere and the oxidizing reaction occurs in the Air atmosphere. The mechanical properties show brittle characteristics with maximum strength with 1520 MPa and fracture strain 0.07 and strain rate effect from 0.001s−1 to 3000s−1 is observed. Under high strain rate loading, the fracture-induced spark is observed, which is caused by an oxidizing reaction due to the rise. By direct ballistic test, the energy release velocity threshold is measured as 980 m/s, and the energy release intensity is more violent in higher velocity impact conditions. Moreover, the impact reaction degree is increased with increasing fragmentation degree and adiabatic temperature rise induced by impact. The designed HEA-ESM is a promising candidate that simultaneously possesses both high strength, high reactive heat and excellent energetic characteristics in the application field of high-strength ESM fragment.

Large-depth and multiscale gradient microstructure in dual-phase Al0.6CoCrFeNi high entropy alloy (HEA) were fabricated by explosion hardening (EH) technique. The gradient microstructure evolution was investigated in detail. The microhardness distribution and tensile properties near EH affected surface were also determined. The formation and strengthening mechanisms of gradient microstructure after EH treatment were subsequently analyzed. Experimental results showed that the multiscale gradient microstructure in terms of grain size, phase morphology, dislocation structure, texture was induced in dual-phase (BCC + FCC) HEA by EH technique. The closer to EH affected surface, the finer grain size, higher dislocation density and stronger texture intensity. The deformation and break of spinodal decomposition and formation of new grain boundaries by dislocation structure contributed to grain refinement and transition of equiaxed grains to dendritic grains from lower area to EH affected surface. After EH treatment, the microhardness generally increased with a maximum increase of ∼67% within 5 mm from EH affected surface, the tensile yield stress increased from 320 MPa to maximum of 700 MPa. The strengthening mechanism is different at various depth positions: near EH affected surface, the main strengthening mechanism is high-density dislocations, stacking faults and grain refinement; in areas relatively far from EH affected surface, only dislocation structure contributed to the strengthening of mechanical properties.

Abstract Aims Left ventricular (LV) remodelling after acute myocardial infarction (AMI) is associated with heart failure and increased mortality. There was no consensus on the definition of LV remodelling, and the prognostic value of LV remodelling with different definitions has not been compared. We aimed to find the optimal definition and develop a prediction nomogram as well as online calculator that can identify patients at risk of LV remodelling. Methods and results This prospective, observational study included 829 AMI patients undergoing percutaneous coronary intervention from January 2015 to January 2020. Echocardiography was performed within the 48 h of admission and at 6 months after infarction to evaluate LV remodelling, defined as a 20% increase in LV end‐diastolic volume (LVEDV), a 15% increase in LV end‐systolic volume (LVESV), or LV ejection fraction (LVEF)

Explosive welding interface commonly show wavy shapes, makes microstructure anisotropic. The effects of microstructure and different loading directions on shear properties of bonding interfaces at dynamic loading conditions are still unclear. In this work, characteristics on transverse and longitudinal sections of TA2/Q235 welding interface was characterized by optical microscopy. It was found that the transverse sections of bonding interface showed wavy shapes with wavelength and amplitude of 1200 μm and 400 μm. The longitudinal sections of bonding interfaces were composed of wavy interface, dislocation shaped interface and stacking fault shaped interface, which was explained by non-equilibrium theory. A small-size S-shaped specimens was processed to investigate shear properties of bonding interface varied with orientation angles (0°, 45°and 90°) at both quasi-static (0.001 s−1) and dynamic (5000∼7000 s−1) loadings. Meanwhile, fracture mechanism of interfaces was analyzed by scanning electron microscopy coupled with energy dispersive spectrometer. The results indicated that the maximum shear strength of joining interfaces (380 MPa–410 MPa under quasi-static loading, and 450 MPa–600 MPa under dynamic loading) was obtained along 90° orientation angle. Fluctuation of explosive detonation pressure was the fundamental cause of the interface inhomogeneity, and strength of joining interfaces increases with increasing strain rates, indicating positive strain rate sensitivity. Fracture mainly occurred in bonding interfaces near TA2 side at quasi-state loading, and failure occurred in interface waves at dynamic loading because of TA2 showed more obvious strain rate sensitivity than Q235. Fracture morphology indicated the ductile-brittle mixed fracture occurred in both quasi-static and dynamic tests.

As a kind of promising aerospace material, TiAl alloys need to withstand extreme conditions such as high-rate impact loads and high temperatures. The mechanism on the failure and fracture of TiAl alloys under extreme conditions is related with the microstructure, including phase and grain size. In the present research, two kinds of TiAl alloys tailored with different microstructures, near lamellar (NL) and near gamma (NG), were fabricated by thermo-mechanical treatment. Microstructural characterization was analyzed by XRD and EBSD. The dynamic behavior of the TiAl alloys under different temperatures ranging from 293 K–873 K was investigated by a split Hopkinson pressure bar. The strain rate sensitivity and temperature sensitivity was analyzed. The microstructural evolution was concerned to understand the failure mechanism of the two kinds of the TiAl alloys. The NG-TiAl had the homogeneous deformation with synergy effect between homogeneous equiaxed grain and lamellar structure, and no failure occurred in NG-TiAl. However, the NL-TiAl showed heterogeneous deformation with both “orange peel effect” and cracks, which was attributed to large equiaxed grain and brittle γ-lamellae with similar orientation. Further, the cracks were easily nucleated and propagated from the interface between γ-lamellae structures, especially in the γ-lamellae structures parallel with the loading direction. Finally, the modified Johnson–Cook constitutive model was proposed to describe the deformation behavior, in which both strain rate hardening and temperature softening terms were expressed as a function of strain and strain rate.

Background: Long-term ambient particulate matter (PM) exposure exerts detrimental effects on cardiovascular health. Evidence on the relation of chronically exposed ambient PM10 and PM2.5 with coronary stenosis remains lacking. Our aim was to investigate the association of PM10 and PM2.5 with coronary stenosis in patients undergoing coronary angiography. Methods: We performed a retrospective cohort study consisting of 7513 individuals who underwent coronary angiography in Fujian Province, China, from January 2019 to December 2021. We calculated a modified Gensini score (GS) to represent the degree of stenosis in coronary arteries by selective coronary angiography. We fitted linear regressions and logistic models to assess the association of PM10 and PM2.5 with coronary stenosis. We employed restricted cubic splines to describe the exposure-response curves. We performed mediation analyses to assess the potential mediators. Results: Long-term ambient PM10 and PM2.5 (prior three years average) exposure was significantly associated with the GS, with a breakpoint concentration of 47.5 μg/m3 and 25.8 μg/m3 for PM10 and PM2.5, respectively, above which we found a linear positive exposure-response relationship of ambient PM with GS. Each 10 µg /m3 increase in PM10 exposure (β: 4.81, 95 % CI: 0.44–9.19) and PM2.5 exposure [β: 10.50, 95 % CI: 3.14–17.86] were positively related to the GS. The adjusted odds ratio (OR) for each 10 µg/m3 increment in PM10 exposure on severe coronary stenosis was 1.33 (95 % CI: 1.04–1.76). Correspondingly, the adjusted OR for PM2.5 was 1.87 (95 % CI: 1.24–2.99). The mediation analysis indicated that the effect of PM10 on coronary stenosis may be partially mediated through total cholesterol, low-density lipoprotein cholesterol, apolipoprotein B, serum creatinine and blood urea nitrogen, and the effect of PM2.5 may be mediated in part by hemoglobin A1c. Conclusion: Our study provides the first evidence that chronic ambient PM10 and PM2.5 exposure was associated with coronary stenosis assessed by GS in patients with suspected coronary artery disease and reveals its potential mediators.

Abstract Objective To explore the clinical outcomes and effect on intraoperative blood loss and postoperative pain of patients undergoing the retroperitoneal laparoscopic partial nephrectomy (RLPN) for complex renal tumors. Methods Fifty patients with complex renal tumor admitted to our hospital from February 2017 to February 2019 were selected as the research object and divided into the RLPN group (given the retroperitoneal laparoscopic partial nephrectomy, n = 24) and the OPN group (given the open partial nephrectomy, n = 26) by number table method to compare their various perioperative indicators and serum stress response and analyze the clinical effect of different surgical methods on the complex renal tumor. Results The clinical information of patients in both groups were not significantly different (P > 0.05); in addition to the operative time, the intraoperative blood loss, hospital stay, warm ischemia time, and numerical rating scale (NRS) scores of the RLPN group were clearly lower than those of the OPN group (P < 0.05); after treatment, patients in the RLPN group obtained significantly lower white blood cell (WBC) count, cortisol, and c-reactive protein (CRP) levels than the OPN group (P < 0.05); the renal glomerular filtration rate (GFR) of the affected side, quality of life scores, and 3-year overall survival rate of treated patients in the RLPN group were obviously higher than those in the OPN group (P < 0.05); and patients in the RPLN group had significantly lower incidence rate (P < 0.05). Conclusion Compared with OPN, RLPN is more worthy of promotion and application, because it has better treatment outcomes, significantly reduces intraoperative blood loss, alleviates the body stress response and postoperative pain, and improves the quality of life.

Abstract Iron tailings have few macropores which severely inhibit infiltration and transport of soil water. Polyacrylamide (PAM) can regulate soil water, but it is rarely used when remediating tailings matrix. In this research, PAM of four molecular weights of 300w, 600w, 800w, and 1000w were selected as amendments, and were each applied at five mass concentrations of 0% (CK), 0.01%, 0.04%, 0.08%, and 0.16% to observe their effects on water transport in iron tailings using column simulations in the laboratory. After adding PAM, the water retention and saturated water content of iron tailings increased significantly (P

Abstract Background The relationships of renal dysfunction (RD) and chronic kidney disease (CKD) with prognosis have been well established among non-ST elevation acute coronary syndrome (NSTE-ACS) patients who receive percutaneous coronary intervention (PCI), but the efficacy of different estimated glomerular filtration rate (eGFR) formulas for predicting the prognosis is unknown. Methods The cohort originated from a retrospective data, which consecutively enrolled 8197 patients. The eGFR was calculated by the Cockcroft-Gault, Modification of Diet in Renal Disease (MDRD), CKD Epidemiology Collaboration-creatinine, CKD Epidemiology Collaboration-Cys-C, CKD Epidemiology Collaboration-Cys-C-creatinine and a modified abbreviated MDRD (c-aGFR) equations in Chinese CKD patients. Patients were excluded if the eGFR could not be obtained by one of the formulas. Patients were categorized as having normal renal function, mild RD, moderate RD, severe RD, or kidney failure to compare prognosis. The primary outcome was the in-hospital net adverse clinical events (NACE). The secondary outcomes were NACE and all-cause death during follow-up. Results In total, 2159 NSTE-ACS patients (age: 64.23 ± 10.25 years; males: 73.7%) were enrolled. 39 (1.8%) patients with in-hospital NACE were observed. During the 3.23 ± 1.55-year follow-up, 1.7% death and 4.2% NACE were observed in 1 year. The percentage of severe RD patients ranged from 15.4 to 39.2% according to different calculation formulas. A high prevalence of in-hospital NACE was observed in the severe RD groups (ranging from 8 to 14.3% for different formulas). Multiple regression analysis showed that a high eGFR is a protect factor against NACE and all-cause death regardless of the formula use. Receiver operating characteristic curves showed similar predictive performance of the c-aGFR when compared to other formulas (in-hospital NACE: AUC = 0.612, follow-up NACE: AUC = 0.622, and follow-up death: AUC = 0.711). Conclusions Severe RD results in a high prevalence of in-hospital NACE in NSTE-ACS patients after PCI regardless of the formulas use. Different formulas have a similar ability to predict in-hospital and long-term prognosis in NSTE-ACS patients. The c-aGFR formula is the simplest and a more convenient formula for use in practice.

During the explosive welding, the bonding interface of welded materials was fast heated due to high strain rate and drastic plastic deformation. The periodical wave interface, with an amplitude of ~300 μm and a period wavelength of ~800 μm, was identifiable as a uniform wave interface formed in the bonding interface. The details of the formation of melting zone and mixing zone of welding materials at the interface were observed. Combined with the Ti-Fe binary phase diagram and the principle of diffusion welding, the phase composition and evolution process of the melting and mixing zone of the bonding interface were investigated by transmission electron microscopy (TEM) and energy dispersive spectrometer (EDS). Significance of the intermetallic compound was found in the mixing zone and melting zone, which was mainly TiFe, TiFe2, TiO2, Fe2O3 and some other intermetallic oxides. Meanwhile, the phenomenon of the titanium agglomeration and oxygen precipitation was observed in the melting zone. The bonding interface could be determined as a mixing welding of mechanical mixing, melting, diffusion and solidification that occurred in the mixing zone, and melting welding and diffusion welding mainly occurred in the melting region.

Explosive hardening of commercial pure titanium plate was conducted by a thin-layer high-detonation-velocity explosive. The nanoindentation and Vickers hardness tests of the treated titanium plates along the depth of shock loading were performed. The microstructures along the depth were characterized by using different methods, including X-Ray Diffraction, Optical Microscopy, Electron Back-Scattered Diffraction and Transmission Electron Microscopy. Experimental results showed that large-depth gradient hardness distribution with depth of 2.5 mm was produced in CP titanium by explosive hardening. There are two gradient hardened layers, ultra-hardened layer with a depth of 0–40 μm and a hardness increase of ∼400%, sub-hardened layer with a depth of 40 μm-2500 μm and a hardness increase of 54.3%. Gradient microstructures with different characteristics were observed, including gradient α-ω phase transition, gradient grain size, gradient twining and gradient dislocation. The area of gradient microstructure is consistence with that of gradient hardness distribution. Grain refinement/α-ω phase transition mainly contributed to hardness sharply increasing in ultra-hardened layer. High-density dislocation/twining mainly contributed to hardness increasing in the sub-hardened layer. Finally, the formation mechanism of gradient microstructures and grain refinement mechanism was detailly discussed.

Background: Contrast-associated acute kidney injury (CA-AKI) is responsible for a substantial proportion of the observed mortality that occurs after percutaneous coronary intervention (PCI), particularly in elderly patients. However, there has been significant and debate over whether the optimal definition of CA-AKI persists over prolonged periods due to variations in the prevalence and effects on prognosis. In this study, we aimed to identify whether different definitions of CA-AKI exert differential impacts on long-term mortality when compared between elderly and non-elderly patients receiving elective PCI.Methods: We prospectively investigated 5,587 consenting patients undergoing elective PCI between January 2012 and December 2018. We considered two classical definitions of CA-AKI from the European Society of Urogenital Radiology (ESUR) and the Acute Kidney Injury Network (AKIN). Multivariable Cox regression analysis was used to investigate the association between CA-AKI and long-term mortality. We also performed interaction and stratified analyses according to age (≤75 or >75 years).Results: The incidence of CA-AKI according to the ESUR and AKIN definitions was 18.7 and 6.1%, respectively. After a median follow-up of 2.1 years, multivariable Cox regression analysis indicated that CA-AKI according to the AKIN definition was a risk factor for long-term mortality in the overall population [hazard ratio (HR) = 2.20; 95% confidential interval (CI): 1.51–3.22; p < 0.001]; however, this was not the case for the ESUR definition (HR = 1.27; 95% CI: 0.92–1.76; p = 0.153). Further interaction analysis identified a significant interaction between age and the ESUR definition (p = 0.040). Stratified analyses also found an association between the ESUR definition and long-term mortality in patients >75 years of age (p = 0.011), but not in patients ≤75 years of age (p = 0.657).Conclusion: As a stringent definition of CA-AKI, the AKIN definition was significantly associated with long-term mortality in both non-elderly and elderly patients. However, in elderly patients, the more lenient definition provided by the ESUR was also significantly correlated with long-term mortality, which could sensitively identify high-risk elderly patients and may provide a better alternative.

Background: Coronary heart disease is a highly prevalent inflammatory disease caused by coronary atherosclerosis. Numerous studies have revealed that perivascular adipose tissue is closely associated with atherosclerosis. Here, we conducted a comprehensive analysis of long non-coding RNAs and mRNAs differentially expressed in perivascular adipose tissue in patients with coronary heart disease. Methods: We conducted Gene Ontology term and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses of the differentially expressed genes. Furthermore, single sample gene set enrichment analysis, immune infiltration analysis, and co-expression analysis of differentially expressed long non-coding RNAs and immune gene sets were performed. Finally, the starBase and miRTarBase databases were used to construct a competing endogenous RNA network. Results: The results show that aortic perivascular adipose tissue has higher inflammation and immune infiltration levels in patients with coronary heart disease. Dysregulated long non-coding RNAs may be related to immunity, inflammation, and hypoxia. Conclusions: The findings of this study provide new insights into atherosclerosis and coronary heart disease.

Aim: Accumulating evidence suggests that MELD-XI score holds the ability to predict the prognosis of congestive heart failure. However, most of the evidence is based on the end-stage heart failure population; thus, we aim to explore the association between the MELD-XI score and the prognosis in heart failure with preserved ejection fraction (HFpEF).Methods: A total of 30,096 patients hospitalized for HFpEF in Fujian Provincial Hospital between January 1, 2014 and July 17, 2020 with available measures of creatinine and liver function were enrolled. The primary endpoint was 60-day in-hospital all-cause mortality. Secondary endpoints were 60-day in-hospital cardiovascular mortality and 30-day rehospitalization for heart failure.Results: A total of 222 patients died within 60 days after admission, among which 75 deaths were considered cardiogenic. And 73 patients were readmitted for heart failure within 30 days after discharge. Generally, patients with an elevated MELD-XI score tended to have more comorbidities, higher NYHA class, and higher inflammatory biomarkers levels. Meanwhile, the MELD-XI score was positively correlated with NT-pro BNP, left atrial diameter, E/e' and negatively correlated with LVEF. After adjusting for conventional risk factors, the MELD-XI score was independently associated with 60-day in-hospital all-cause mortality [hazard ratio(HR) = 1.052, 95% confidential interval (CI) 1.022–1.083, P = 0.001], 60-day in-hospital cardiovascular mortality (HR = 1.064, 95% CI 1.013–1.118, P = 0.014), and 30-day readmission for heart failure (HR = 1.061, 95% CI 1.015–1.108, P = 0.009). Furthermore, the MELD-XI score added an incremental discriminatory capacity to risk stratification models developed based on this cohort.Conclusion: The MELD-XI score was associated with short-term adverse events and provided additional discriminatory capacity to risk stratification models in patients hospitalized for HFpEF.

Objectives To develop a model of in-hospital mortality using medical record front page (MRFP) data and assess its validity in case-mix standardisation by comparison with a model developed using the complete medical record data.Design A nationally representative retrospective study.Setting Representative hospitals in China, covering 161 hospitals in modelling cohort and 156 hospitals in validation cohort.Participants Representative patients admitted for acute myocardial infarction. 8370 patients in modelling cohort and 9704 patients in validation cohort.Primary outcome measures In-hospital mortality, which was defined explicitly as death that occurred during hospitalisation, and the hospital-level risk standardised mortality rate (RSMR).Results A total of 14 variables were included in the model predicting in-hospital mortality based on MRFP data, with the area under receiver operating characteristic curve of 0.78 among modelling cohort and 0.79 among validation cohort. The median of absolute difference between the hospital RSMR predicted by hierarchical generalised linear models established based on MRFP data and complete medical record data, which was built as ‘reference model’, was 0.08% (10th and 90th percentiles: −1.8% and 1.6%). In the regression model comparing the RSMR between two models, the slope and intercept of the regression equation is 0.90 and 0.007 in modelling cohort, while 0.85 and 0.010 in validation cohort, which indicated that the evaluation capability from two models were very similar.Conclusions The models based on MRFP data showed good discrimination and calibration capability, as well as similar risk prediction effect in comparison with the model based on complete medical record data, which proved that MRFP data could be suitable for risk adjustment in hospital performance measurement.

Endothelial dysfunction is involved in the pathophysiological processes of contrast media (CM)–induced acute kidney injury (CI-AKI) after vascular angiography or intervention. Previous study found that apolipoprotein A-I (apoA-I) mimetic peptide, D-4F, alleviates endothelial impairments via upregulating heme oxygenase-1 (HO-1) expression and scavenging excessively generated reactive oxygen species (ROS). However, whether D-4F could ameliorate oxidative injuries in endothelial cells through suppressing ROS production remains unclear. In this study, a representative nonionic iodinated CM, iodixanol, was chosen for the in vitro and in vivo studies. Endothelial cell viability was assayed using micrographs, lactate dehydrogenase (LDH) activity, and cell counting kit-8 (CCK-8). Apoptosis was detected using flow cytometry analysis and caspase-3 activation. Endothelial inflammation was tested using monocyte adhesion assay and adhesion molecule expression. ROS production was detected by measuring the formation of lipid peroxidation malondialdehyde (MDA) through the thiobarbituric acid reactive substance (TBARS) assay. Peroxynitrite (ONOO⁻) formation was tested using the 3-nitrotyrosine ELISA kit. Iodixanol impaired cell viability, promoted vascular cell adhesion molecule-1 (VCAM-1) and intercellular cell adhesion molecule-1 (ICAM-1) expression, and induced cell apoptosis in human umbilical vein endothelial cells (HUVECs). However, D-4F mitigated these injuries. Furthermore, iodixanol induced the phosphorylation of protein kinase C (PKC) beta II, p47, Rac1, and endothelial nitric oxide synthase (eNOS) at Thr495, which elicited ROS release and ONOO⁻ generation. D-4F inhibited NADPH oxidase (NOX) activation, ROS production, and ONOO⁻ formation via the AMP-activated protein kinase (AMPK)/PKC pathway. Additionally, after an intravascular injection of iodixanol in Sprague Dawley rats, iodixanol induced a remarkable inflammatory response in arterial endothelial cells, although significant apoptosis and morphological changes were not observed. D-4F alleviated the vessel inflammation resulting from iodixanol in vivo. Collectively, besides scavenging ROS, D-4F could also suppress ROS production and ONOO⁻ formation through the AMPK/PKC pathway, which ameliorated oxidative injuries in endothelial cells. Hence, D-4F might serve as a potential agent in preventing CI-AKI.

Abstract Background A great number of studies reported that 12/15-lipoxygenase (12/15-LO) played an important role in atherosclerosis. And its arachidonic acid(AA) metabolite, 15(S)-hydroperoxy-5,8,11,13-(Z,Z,Z,E)-eicosatetraenoic acid (15(S)-HETE), is demonstrated to mediate endothelial dysfunction. 15-oxo-5,8,11,13-(Z,Z,Z,E)-eicosatetraenoic acid (15-oxo-ETE) was formed from 15-hydroxyprostaglandin dehydrogenase (PGDH)-mediated oxidation of 15(S)-HETE. However, relatively little is known about the biological effects of 15-oxo-ETE in cardiovascular disease. Here, we explore the likely role of 15-lipoxygenase (LO)-1-mediated AA metabolism,15-oxo-ETE, in the early pathogenesis of atherosclerosis. Methods The 15-oxo-ETE level in serum was detected by means of liquid chromatography and online tandem mass spectrometry (LC-MS/MS). And the underlying mechanisms were illuminated by molecular techniques, including immunoblotting, MTT assay, immunocytochemistry and Immunohistochemistry. Results Increased 15-oxo-ETE level is found in in patients with acute myocardial infarction (AMI). After 15-oxo-ETE treatment, Human umbilical vein endothelial cells (HUVECs) showed more attractive to monocytes, whereas monocyte adhesion is suppressed when treated with PKC inhibitor. In ex vivo study, exposure of arteries from C57 mice and ApoE−/−mice to 15-oxo-ETE led to significantly increased E-selectin expression and monocyte adhesion. Conclusions This is the first report that 15-oxo-ETE promotes early pathological process of atherosclerosis by accelerating E-selectin expression and monocyte adhesion. 15-oxo-ETE -induced monocyte adhesion is partly attributable to activation of PKC.

Apolipoprotein A-I (apoA-I) mimetic peptide, D-4F, exhibits anti-atherogenic effects similar to high-density lipoprotein (HDL). However, it remains elusive whether D-4F and HDL share similar molecular mechanisms underlying anti-atherogenic effects and endothelial cell protections. We here compared the metabolic changes in endothelial cells induced by D-4F and HDL against oxidized low-density lipoprotein (ox-LDL), which may be of benefit to understanding the protective mechanisms of HDL and D-4F. Functional assays, including wound healing, transwell migration, and tube formation, were used to evaluate the pro-angiogenic effects of HDL and D-4F. NMR-based metabolomic analysis was employed to explore the protective mechanisms underlying HDL and D-4F. Partial least-squares discriminant analysis (PLS-DA) was performed to assess metabolic profiles, and orthogonal PLS-DA (OPLS-DA) was carried out to identify characteristic metabolites. Moreover, significantly altered metabolic pathways were also analyzed. We found that ox-LDL impaired the migration and tube formation of endothelial cells. Metabolomic analysis showed that ox-LDL triggered oxidative stress, impaired glycolysis, and enhanced glycerophospholipid metabolism. Both HDL and D-4F improved the migration and angiogenesis of endothelial cells, alleviated oxidative stress, and ameliorated disordered glycolysis impaired by ox-LDL. Strikingly, HDL partially attenuated the disturbed glycerophospholipid metabolism, whereas D-4F did not show this effect. In summary, although D-4F shared the similar protective effects with HDL on the migration and angiogenesis of endothelial cells, it could not deduce the molecular mechanisms of HDL completely. Nevertheless, D-4F possesses the potentiality to be exploited as clinically applicable agent for endothelial cell protection and cardiovascular disease treatment.

Endothelial dysfunction plays key roles in the pathological process of contrast media (CM)-induced acute kidney injury (CI-AKI) in patients undergoing vascular angiography or intervention treatment. Previously, we have demonstrated that an apolipoprotein A-I (apoA-I) mimetic peptide, D-4F, inhibits oxidative stress and improves endothelial dysfunction caused by CM through the AMPK/PKC pathway. However, it is unclear whether CM induce metabolic impairments in endothelial cells and whether D-4F ameliorates these metabolic impairments. In this work, we evaluated vitalities of human umbilical vein endothelial cells (HUVECs) treated with iodixanol and D-4F and performed nuclear magnetic resonance (NMR)-based metabolomic analysis to assess iodixanol-induced metabolic impairments in HUVECs, and to address the metabolic mechanisms underlying the protective effects of D-4F for ameliorating these metabolic impairments. Our results showed that iodixanol treatment distinctly impaired the vitality of HUVECs, and greatly disordered the metabolic pathways related to energy production and oxidative stress. Iodixanol activated glucose metabolism and the TCA cycle but inhibited choline metabolism and glutathione metabolism. Significantly, D-4F pretreatment could improve the iodixanol-impaired vitality of HUVECs and ameliorate the iodixanol-induced impairments in several metabolic pathways including glycolysis, TCA cycle and choline metabolism in HUVECs. Moreover, D-4F upregulated the glutathione level and hence enhanced antioxidative capacity and increased the levels of tyrosine and nicotinamide adenine dinucleotide in HUVECs. These results provided the mechanistic understanding of CM-induced endothelial impairments and the protective effects of D-4F for improving endothelial cell dysfunction. This work is beneficial to further exploring D-4F as a potential pharmacological agent for preventing CM-induced endothelial impairment and acute kidney injury.

High entropy alloys (HEAs) are usually fabricated using arc melting which has the disadvantages of diseconomy, and the limitations in the shape and size of final products. However, recently, quite a large amount of research has been carried out to find the fabrication techniques for HEAs with better properties such as mechanical alloying and rapid solidification. In this paper, an AlCoCrFeNi high entropy alloy was successfully fabricated by the shock consolidation technique. In this method, the starting powders were mixed by mechanical alloying and then the shock wave was imposed to the compacted powders by explosion. High levels of residual stress existed in samples fabricated by the shock consolidation method. Due to this, after fabrication of the sample, heat treatment was used to eliminate the residual stress and improve the mechanical properties. The microstructure of the samples before and after heat treatment were examined by XRD, SEM and electron backscatter diffraction (EBSD). The shock consolidated sample and sample with heat treatment both showed the nano-structure. After heat treatment the hardness of the sample was decreased from 715 HV to the 624 HV, however the failure strength increased, and as expected the ductility of the sample was improved after heat treatment.

A new S-shaped specimen geometry is developed in this study to investigate the shear behavior of materials under dynamic shear condition. Traditionally, hat-shaped geometry is used to study the dynamic shear of materials by a conventional split Hopkinson pressure bar apparatus. However, in this geometry, the force equilibrium on the two sides of the sample is difficult to fulfill, and the stress field in the shear region is not homogeneous. Hence, the calculated shear stress−strain curve from this geometry is not precise. To overcome this problem, the new S-shaped specimen is designed to achieve accurate shear stress−strain curve. This geometry can be used in a wide range of strain rates and does not require additional machining process for microstructure observation. The new S-shaped specimen is successfully coupled with digital image correlation method because of the flat surface. Digital image correlation results indicate that the fracture patterns of the new S-shaped specimen occur with maximum shear strains in the shear region in the middle of the sample. This result is also validated by finite element model simulation. The new S-shaped specimen geometry can be used to study the dynamic shear behavior of various metals.