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Background The relationship between venous congestion in cardiopulmonary bypass (CPB) and acute kidney injury (AKI) in cardiac surgery has not utterly substantiated. This study aimed at investigate the relationship between CVP in CPB and the occurrence of AKI. Methods We retrospectively reviewed 2048 consecutive patients with cardiovascular disease undergoing cardiac procedure with CPB from January 2018 to December 2022. We used the median CVP value obtained during CPB for our analysis and patients were grouped according to this parameter. The primary outcomes were AKI and renal replacement therapy(RRT). Multivariable logistic regression was used to explore the association between CVP and AKI. Results A total of 2048 patients were enrolled in our study and divided into high CVP group (CVP ≥ 6.5 mmHg) and low CVP group (CVP < 6.5 mmHg) according to the median CVP value. Patients in high CVP group had the high AKI and RRT rate when compared to the low CVPgroup[(367/912,40.24%)vs.(408/1136,35.92%), P  = 0.045;(16/912,1.75%vs.9/1136;0.79%), P  = 0.049]. Multivariate logistic regression analysis displayed CVP played an indispensable part in development of renal failure in surgical. Conclusions Elevated CVP(≥ 6.5mmH 2 OmmHg) in CPB during cardiac operation is associated with an increased risk of AKI in cardiovascular surgery patients. Clinical attention should be paid to the potential role of CVP in predicting the occurrence of AKI.

The physical world around us is inherently curvy, dynamic, and variable, yet modern industrial civilization is grounded in the planar, rigid paradigms of science and technology. This fundamental disconnect between two‐dimensional (2D) techniques and three‐dimensional (3D) realities significantly restricts our ability to fully perceive and to understand the complexity of real‐world objects. Over the past several decades, driven by application demands across various industries, advancements in high‐speed, high‐accuracy, and high‐resolution sensors, as well as ever‐increasing AI algorithms and computational power, curvy surface reconstruction that can reconstruct continuous, smooth geometrical and physical fields from discrete data by algorithms and mathematics have experienced tremendous developments. However, previous reviews in this field have primarily focused on geometric shapes, optical measurement techniques, or reconstruction algorithms, leaving a comprehensive overview that integrates both geometric and physical dimensions still lacking. Here, for the first time, we bridge this gap by expanding the scope from special curvy imaging to general curvy reconstruction incorporating physical fields, with a particular emphasis on measurement techniques, especially the emerging opportunities from advanced techniques. Initially, a brief overview starts with introducing the theoretical underpinnings and primary issues of curvy surface reconstruction. Next, an in‐depth discussion of the main non‐contact and contact measurement methods is presented, detailing their operational principles, progress, merits and demerits, and future efforts. Following that, several reconstruction algorithms and their applications are discussed. Finally, our insights on the ongoing challenges and opportunities in this field are summarized. This review introduces the concept of “general curvy surface reconstruction,” which incorporates both geometric and physical dimensions, representing an upgrade over conventional geometric reconstruction that focuses solely on spatial relationships. Particular emphasis is placed on the emerging opportunities enabled by advanced measurement techniques, rapidly evolving AI algorithms, and increasing computational power.

Objectives Endoscopic vein harvesting (EVH) is an alternative technique to obtain the saphenous vein for coronary artery bypass grafting (CABG) surgery. We aimed to evaluate the early and mid-term outcomes of patients with EVH in CABG. Methods This cohort study included consecutive isolated CABG patients in Nanjing First Hospital from July 2020 to December 2022 using propensity score matching methods. Patients were classified to EVH group and open vein harvesting (OVH) group according to the vein harvesting methods. The primary outcome was the all-cause death, and the secondary outcomes were major adverse cardiovascular events (MACEs) including cardiovascular death, heart failure, myocardial infarction and revascularization and asymptomatic survival in the follow-up. Results Totally 1247 patients were included in the study with 849 in OVH group and 398 in EVH group. Patients with EVH were more female, diabetes, higher body mass index, more multi-vessel and left main diseases. 308 pairs were formed after the matching. There was no significant difference in the rates of in-hospital death (EVH vs. OVH, 2.3% vs. 1.3%, P  = 0.543). During the 3 years follow-up, EVH grafts were considered not inferior to OVH grafts, no differences were found in all-cause death [8.5% vs. 5.0%, hazard ratio (HR) 1.565, 95% confidence interval (CI): 0.77–3.17, P  = 0.21], MACEs (8.1% vs. 7.1%, HR 1.165, 95CI: 0.51–2.69, P  = 0.71) and asymptomatic survival (66.7% vs. 72.5%, HR 1.117, 95%CI: 0.65–1.92, P  = 0.68). Conclusions EVH grafts were considered comparable to OVH grafts in patients following CABG in the 3 years follow-up.

Abdominal aortic aneurysm (AAA) is a vascular disorder that is considered a chronic inflammatory disease. However, the precise molecular mechanisms involved in AAA have not been fully elucidated. Recently, significant progress has been made in understanding the function and mechanism of action of inhibitor of kappa B kinase epsilon (IKKε) in inflammatory and metabolic diseases. The angiotensin II- (Ang II-) induced or pharmacological inhibitors were established to test the effects of IKKε on AAA in vivo. After mice were continuously stimulated with Ang II for 28 days, morphologically, we found that knockout of IKKε reduced AAA formation and drastically reduced maximal diameter and severity. We also observed a decrease in elastin degradation and medial destruction, which were independent of systolic blood pressure or plasma cholesterol concentrations. Western blot analyses and immunohistochemical staining were carried out to measure IKKε expression in AAA tissues and cell lines. AAA phenotype of mice was measured by ultrasound and biochemical indexes. In zymography, immunohistology staining, immunofluorescence staining, and reactive oxygen species (ROS) analysis, TUNEL assay was used to examine the effects of IKKε on AAA progression in AAA mice. IKKε deficiency significantly inhibited inflammatory macrophage infiltration, matrix metalloproteinase (MMP) activity, ROS production, and vascular smooth muscle cell (VSMC) apoptosis. We used primary mouse aortic VSMC isolated from apolipoprotein E (Apoe) −/− and Apoe−/−IKKε−/− mice. Mechanistically, IKKε deficiency blunted the activation of the ERK1/2 pathway. The IKKε inhibitor, amlexanox, has the same impact in AAA. Our results demonstrate a critical role of IKKε in AAA formation induced by Ang II in Apoe−/− mice. Targeting IKKε may constitute a novel therapeutic strategy to prevent AAA progression.

In this work, the corrosion behavior of copper in a simulated organic acid environment containing formic acid and acetic acid was investigated by electrochemical testing and surface characterization. In addition to deducing the corrosion mechanism of copper in the organic acid corrosion environment, the corrosion inhibitor BTA was also used to slow down the corrosion of copper by organic acid. The results show that the corrosion rate of copper in the two groups of organic acids first decreases and then increases with the immersion time. Microelectrochemical (Scanning Vibrating Electrode Technique) results shows that the anodic peak of the sample is higher in formic acid. Formic acid is more corrosive. The corrosion products of red copper gradually increased in the two groups of organic acid atmospheres, and the final corrosion products were cuprous oxide, copper formate particles and copper acetate hydrate, respectively. When the concentration of BTA is 0.5 g/L, the electrochemical activity of TP2 copper is weakened, the surface of the sample is relatively smooth, there are no large corrosion pits, and the corrosion rate is reduced.

A topological insulator with large bulk-insulating behavior and high electron mobility of the surface state is needed urgently, not only because it would be a good platform for studying topological surface states but also because it is a prerequisite for potential future applications. In this work, we demonstrated that tin (Sn) or indium (In) dopants could be introduced into a BiSbTeSe[sub.2] single crystal. The impacts of the dopants on the bulk-insulating property and electron mobility of the surface state were systematically investigated by electrical transport measurements. The doped single crystals had the same crystal structure as the pristine BiSbTeSe[sub.2], no impure phase was observed, and all elements were distributed homogeneously. The electrical transport measurements illustrated that slight Sn doping could improve the performance of BiSbTeSe[sub.2] a lot, as the longitudinal resistivity (ρ [sub.xx]), bulk carrier density (n [sub.b]), and electron mobility of the surface state (μ [sub.s]) reached about 11 Ωcm, 7.40 × 10[sup.14] cm[sup.−3], and 6930 cm[sup.2]/(Vs), respectively. By comparison, indium doping could also improve the performance of BiSbTeSe[sub.2] with ρ [sub.xx], n [sub.b], and μ [sub.s] up to about 13 Ωcm, 1.29 × 10[sup.15] cm[sup.−3], and 4500 cm[sup.2]/(Vs), respectively. Our findings suggest that Sn- or indium-doped BiSbTeSe[sub.2] crystals should be good platforms for studying novel topological properties, as well as promising candidates for low-dissipation electron transport, spin electronics, and quantum computing.

A topological insulator with large bulk-insulating behavior and high electron mobility of the surface state is needed urgently, not only because it would be a good platform for studying topological surface states but also because it is a prerequisite for potential future applications. In this work, we demonstrated that tin (Sn) or indium (In) dopants could be introduced into a BiSbTeSe single crystal. The impacts of the dopants on the bulk-insulating property and electron mobility of the surface state were systematically investigated by electrical transport measurements. The doped single crystals had the same crystal structure as the pristine BiSbTeSe , no impure phase was observed, and all elements were distributed homogeneously. The electrical transport measurements illustrated that slight Sn doping could improve the performance of BiSbTeSe a lot, as the longitudinal resistivity ( ), bulk carrier density ( ), and electron mobility of the surface state ( ) reached about 11 Ωcm, 7.40 × 10 cm , and 6930 cm /(Vs), respectively. By comparison, indium doping could also improve the performance of BiSbTeSe with , , and up to about 13 Ωcm, 1.29 × 10 cm , and 4500 cm /(Vs), respectively. Our findings suggest that Sn- or indium-doped BiSbTeSe crystals should be good platforms for studying novel topological properties, as well as promising candidates for low-dissipation electron transport, spin electronics, and quantum computing.

A topological insulator with large bulk-insulating behavior and high electron mobility of the surface state is needed urgently, not only because it would be a good platform for studying topological surface states but also because it is a prerequisite for potential future applications. In this work, we demonstrated that tin (Sn) or indium (In) dopants could be introduced into a BiSbTeSe2 single crystal. The impacts of the dopants on the bulk-insulating property and electron mobility of the surface state were systematically investigated by electrical transport measurements. The doped single crystals had the same crystal structure as the pristine BiSbTeSe2, no impure phase was observed, and all elements were distributed homogeneously. The electrical transport measurements illustrated that slight Sn doping could improve the performance of BiSbTeSe2 a lot, as the longitudinal resistivity (ρxx), bulk carrier density (nb), and electron mobility of the surface state (μs) reached about 11 Ωcm, 7.40 × 1014 cm−3, and 6930 cm2/(Vs), respectively. By comparison, indium doping could also improve the performance of BiSbTeSe2 with ρxx, nb, and μs up to about 13 Ωcm, 1.29 × 1015 cm−3, and 4500 cm2/(Vs), respectively. Our findings suggest that Sn- or indium-doped BiSbTeSe2 crystals should be good platforms for studying novel topological properties, as well as promising candidates for low-dissipation electron transport, spin electronics, and quantum computing.

Doxorubicin (DOX) is a chemotherapeutic agent used to treat solid tumors and hematologic malignancies, though DOX-induced cardiomyopathy poses a risk of severe cardiac impairment and poor prognosis. Immune cells have been increasingly implicated in cardiovascular inflammation, with overproduction of inflammatory cytokines and macrophage accumulation. However, its molecular mechanism remains unclear and needs to be further investigated. This study investigated the involvement of IKKα in regulating cardiac function in response to early-stage DOX stimulation. Results indicated that IKKα Lyz2−Cre mice were more susceptible to DOX-induced cardiac injury than IKKα flox/flox mice, showing reduced heart function, extensive cardiac fibrosis, and elevated inflammatory markers. Single-cell transcriptomic analysis revealed cellular heterogeneity in DOX-induced cardiomyopathy tissue between IKKα flox/flox and IKKα Lyz2−Cre mice, identifying 11 cell types, 8 of which were immune cells. Bar plots and cell density analysis showed a higher proportion of T cells in IKKα flox/flox mice, while IKKα Lyz2−Cre mice had increased monocytes and macrophages. Notably, IKKα deletion promoted a shift in macrophage polarization from Fcna + M2 to Jaml + M1 and impaired T cell activation and differentiation. Additionally, IKKα played a critical role in mediating macrophage-T cell interactions. Loss of macrophage IKKα activated T cells through Jaml + M1 macrophage, and activated T cells subsequently enhanced M1 macrophage activation via IFN-γ and IL-6. These findings highlight the potential of targeting immune cell interactions as a therapeutic strategy.

Caspase activation and recruitment domain 3 (CARD3) is a caspase recruitment domain (CARD)-containing serine/threonine kinase and plays a pivotal role in apoptosis, immunity, tissue development and proliferation. To date, the causal relationship between CARD3 and myocardial infarction (MI) remains largely unexplored. This study aimed to identify the functional significance of CARD3 in the regulation of cardiac remodelling after MI and the underlying mechanisms of its effects. The levels of CARD3 expression were up-regulated in failing human and mouse post-infarction hearts. In addition, CARD3-knockout (KO) mice and transgenic mice overexpressing CARD3 in the heart were then generated and subjected to MI. Compared with wild-type (WT) control mice, CARD3-KO mice developed smaller infarct sizes, improved survival rates, and preserved left ventricle (LV) function after MI. Significantly, CARD3-KO hearts had less cardiomyocyte apoptosis and inflammatory cell infiltration in the infarct border zone. Attenuated LV remodelling was also observed in the KO hearts following MI, with reduced cardiac hypertrophy and fibrosis. Conversely, CARD3 overexpression resulted in the opposite MI-induced phenotype. Similar results were observed in ex vivo-cultured neonatal rat cardiomyocytes exposed to hypoxia. Mechanistically, we discovered that the CARD3-mediated detrimental effects of MI were associated with the activation of the NF-κB and p38 signalling cascades. Taken together, these data demonstrate that CARD3 serves as a novel positive modulator of ventricular remodelling after MI via the regulation of the NF-κB and p38 signalling. Thus, CARD3 may be a promising therapeutic target for the treatment of heart failure after MI.