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For centrifugal casting 27Cr44Ni5W3Al+MA alloy used in ethylene pyrolysis furnace, its creep behaviours at 1050°C are investigated. The results show that the alloy undergoes three stages during the creep tests under different stress levels ranging from 18 MPa to 30 MPa. The apparent stress index n of the alloy is 6.11, and the creep deformation mechanism is mainly dislocation climbing. During the creep test, the fishbone-like M7C3 inside eutectic precipitates in casted alloy gradually transform to massive M23C6 at the edge of the precipitate. Creep induced voids germinate and connect at the interface of austenite/M23C6 and austenite/Ni3Al, the cavities expand along the M23C6 and Ni3Al, forming micro-cracks and the alloy eventually cracks. [ABSTRACT FROM AUTHOR]

Medial vascular calcification, associated with enhanced mortality in chronic kidney disease (CKD), is fostered by osteo-/chondrogenic transdifferentiation of vascular smooth muscle cells (VSMCs). Here, we describe that serum- and glucocorticoid-inducible kinase 1 (SGK1) was upregulated in VSMCs under calcifying conditions. In primary human aortic VSMCs, overexpression of constitutively active [SGK1.sup.S422D], but not inactive [SGK1.sup.K127N], upregulated osteo-/chondrogenic marker expression and activity, effects pointing to increased osteo-/chondrogenic transdifferentiation. [SGK1.sup.S422D] induced nuclear translocation and increased transcriptional activity of NF-[kappa]B. Silencing or pharmacological inhibition of IKK abrogated the osteoinductive effects of [SGK1.sup.S422D]. Genetic deficiency, silencing, and pharmacological inhibition of SGK1 dissipated phosphate-induced calcification and osteo-/chondrogenic transdifferentiation of VSMCs. Aortic calcification, stiffness, and osteo-/chondrogenic transdifferentiation in mice following cholecalciferol overload were strongly reduced by genetic knockout or pharmacological inhibition of Sgk1 by EMD638683. Similarly, Sgk1 deficiency blunted vascular calcification in apolipoprotein E-deficient mice after subtotal nephrectomy. Treatment of human aortic smooth muscle cells with serum from uremic patients induced osteo-/chondrogenic transdifferentiation, effects ameliorated by EMD638683. These observations identified SGK1 as a key regulator of vascular calcification. SGK1 promoted vascular calcification, at least partly, via NF-[kappa]B activation. Inhibition of SGK1 may, thus, reduce the burden of vascular calcification in CKD., Introduction Medial vascular calcification is associated with cardiovascular events and mortality (1) of patients with chronic kidney disease (CKD) (2). In contrast to intimal atherosclerosis, vascular calcification is fostered by [...]

Keywords: computational fluid dynamics; degradation; Swirling vortex cavitator; tetracycline EN computational fluid dynamics degradation Swirling vortex cavitator tetracycline 955 963 9 09/20/22 20220901 NES 220901 1 Introduction Antibiotics are commonly utilized for treatment and prevention of deadly infections in humans and animals. Nevertheless, the absolute degradation amount of tetracycline at higher initial concentration of tetracycline was larger than that of tetracycline at low concentration owing to the fuller utilization of hydroxyl radicals. When the initial concentration of tetracycline increases, the degradation efficiency of tetracycline decreases accordingly due to the limited amount of tetracycline degradation. 3.5 Degradation of tetracycline at different reaction times Figure 10 shows the degradation efficiency of tetracycline by the vortex cavitator at different degradation times. [Extracted from the article]

In the present study, the microstructure evolution of 35Cr45NiNb+MA ethylene cracking furnace tubes during service and its effect on the properties were investigated. According to the results, in the early stage of service, the skeletal M7C3 and vermicular NbC were transformed into blocky M23C6 and G phase (Ni16Nb6Si7), respectively, accompanied with many dispersed M23C6 secondary carbides. With the extension of service time, M23C6 carbides on the grain boundaries were transformed into M7C3 with high stacking fault structure and coarsened, and the blocky G phase was transformed into granular NbC. The yield strength and ultimate tensile strength of the aging furnace tubes decreased by 9%-18%, yet the elongation after fracture decreased significantly from 10.0%-14.0% to 3.0%-5.0%. The hardness of the carburized zone of the carburized tubes increased by 10%-17%, and the rupture time decreased by 45%-75% under the test condition of 1100℃ and 16MPa. Finally, the evolution map was summarized. [ABSTRACT FROM AUTHOR]

Abstract Autonomic dysreflexia (AD), a syndrome caused by loss of supraspinal control over sympathetic activity and amplified vascular reflex upon sensory stimuli below injury level, is a major health problem in high-level spinal cord injury (SCI). After supraspinal sympathetic control of the vasculature below the lesion is lost, the renin-angiotensin system (RAS) is thought to be involved in AD by regulating blood pressure and vascular reactivity. In this study, we aimed to assess the role of different RAS receptors during AD following SCI. Therefore, we induced AD by colorectal distention (CRD) in wild-type mice and mice deficient in the RAS components angiotensin (Ang) II type 1a receptor (AT1a) (Agtr1a −/− ) and Ang-(1–7) receptor Mas (Mas −/− ) four weeks after complete transection of spinal cord at thoracic level 4 (T4). Systemic blood pressure measurements and wire myography technique were performed to assess hemodynamics and the reactivity of peripheral arteries, respectively. CRD increased mean arterial blood pressure (MAP) and decreased heart rate (HR) in all three animal groups. However, we found less increases in MAP in Mas −/− mice compared to control mice after CRD, whereas AT1a deficiency did not affect the hemodynamic response. We found that the reactivity of wild-type and Mas −/− mesenteric arteries, which are innervated from ganglia distal but close to thoracic level T4, was diminished in response to Ang II in AD after T4-SCI, but this difference was not observed in the absence of AT1a receptors. CRD did not influence the reactivity of femoral arteries which are innervated from ganglia more distal to thoracic level T4, in response to Ang II in AD. In conclusion, we identified a specific role of the Ang-(1–7) receptor Mas in regulating the systemic blood pressure increase in AD in T4-SCI mice. Furthermore, AT1a signaling is not involved in this hemodynamic response, but underlies increased vascular reactivity in mesenteric arteries in response to Ang II, where it may contribute to adaptive changes in regional blood flow. Highlights • AT1 and Mas receptors play differential roles in AD in T4-SCI mice. • AD had less effect on mean arterial pressure in Mas−/− mice. • T4-SCI decreased reactivity to Ang II in mesenteric arteries. • T4-SCI did not affect femoral artery tension in response to Ang II. • MAS-AT1 complexes could be novel targets for AD in SCI patients. [ABSTRACT FROM AUTHOR]

Endothelial nitric oxide synthase (eNOS)-related vessel relaxation is a highly coordinated process that regulates blood flow and pressure and is dependent on caveolae. Here, we investigated the role of caveolar plasma membrane stabilization by the dynamin-related ATPase EHD2 on eNOS-nitric oxide (NO)-dependent vessel relaxation. Loss of EHD2 in small arteries led to increased numbers of caveolae that were detached from the plasma membrane. Concomitantly, impaired relaxation of mesenteric arteries and reduced running wheel activity were observed in EHD2 knockout mice. EHD2 deletion or knockdown led to decreased production of nitric oxide (NO) although eNOS expression levels were not changed. Super-resolution imaging revealed that eNOS was redistributed from the plasma membrane to internalized detached caveolae in EHD2-lacking tissue or cells. Following an ATP stimulus, reduced cytosolic Ca2+ peaks were recorded in human umbilical vein endothelial cells (HUVECs) lacking EHD2. Our data suggest that EHD2-controlled caveolar dynamics orchestrates the activity and regulation of eNOS/NO and Ca2+ channel localization at the plasma membrane., Competing Interests: The authors have declared that no competing interests exist.

Caveolae, flask-shaped cholesterol-, and glycosphingolipid-rich membrane microdomains, contain caveolin 1, 2, 3 and several structural proteins, in particular Cavin 1-4, EHD2, pacsin2, and dynamin 2. Caveolae participate in several physiological processes like lipid uptake, mechanosensitivity, or signaling events and are involved in pathophysiological changes in the cardiovascular system. They serve as a specific membrane platform for a diverse set of signaling molecules like endothelial nitric oxide synthase (eNOS), and further maintain vascular homeostasis. Lack of caveolins causes the complete loss of caveolae; induces vascular disorders, endothelial dysfunction, and impaired myogenic tone; and alters numerous cellular processes, which all contribute to an increased risk for hypertension. This brief review describes our current knowledge on caveolae in vasculature, with special focus on their pathophysiological role in hypertension.

Background: Relaxins are small peptide hormones, which are novel candidate molecules that play important roles in cardiometablic syndrome. Relaxins are structurally related to the insulin hormone superfamily, which provide vasodilatory effects by activation of G-protein-coupled relaxin receptors (RXFPs) and stimulation of endogenous nitric oxide (NO) generation. Recently, relaxin could be demonstrated to activate G i proteins and phosphoinositide 3-kinase (PI3K) pathways in cultured endothelial cells in vitro . However, the contribution of the G i -PI3K pathway and their individual components in relaxin-dependent relaxation of intact arteries remains elusive. Methods: We used Gα i2 - ( Gnai2 -/- ) and Gα i3 -deficient ( Gnai3 -/- ) mice, pharmacological tools and wire myography to study G-protein-coupled signaling pathways involved in relaxation of mouse isolated mesenteric arteries by relaxins. Human relaxin-1, relaxin-2, and relaxin-3 were tested. Results: Relaxin-2 (∼50% relaxation at 10 -11 M) was the most potent vasodilatory relaxin in mouse mesenteric arteries, compared to relaxin-1 and relaxin-3. The vasodilatory effects of relaxin-2 were inhibited by removal of the endothelium or treatment of the vessels with N (G)-nitro-L-arginine methyl ester (L-NAME, endothelial nitric oxide synthase (eNOS) inhibitor) or simazine (RXFP1 inhibitor). The vasodilatory effects of relaxin-2 were absent in arteries of mice treated with pertussis toxin (PTX). They were also absent in arteries isolated from Gnai2 -/- mice, but not from Gnai3 -/- mice. The effects were not affected by FR900359 (Gα q protein inhibitor) or PI-103 (PI3Kα inhibitor), but inhibited by TGX-221 (PI3Kβ inhibitor) or AS-252424 (PI3Kγ inhibitor). Simazine did not influence the anti-contractile effect of perivascular adipose tissue. Conclusion: Our data indicate that relaxin-2 produces endothelium- and NO-dependent relaxation of mouse mesenteric arteries by activation of RXFP1 coupled to G i2 -PI3K-eNOS pathway. Targeting vasodilatory G i -protein-coupled RXFP1 pathways may provide promising opportunities for drug discovery in endothelial dysfunction and cardiometabolic disease.