93 research outputs found

    Aldehyde Dehydrogenase-2 Attenuates Myocardial Remodeling and Contractile Dysfunction Induced by a High-Fat Diet

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    Background/Aims: Consumption of a high-fat (HF) diet exacerbates metabolic cardiomyopathy through lipotoxic mechanisms. In this study, we explored the role of aldehyde dehydrogenase-2 (ALDH2) in myocardial damage induced by a HF diet. Methods: Wild-type C57 BL/6J mice were fed a HF diet or control diet for 16 weeks. ALDH2 overexpression was achieved by injecting a lentiviral ALDH2 expression vector into the left ventricle. Results: Consumption of a HF diet induced metabolic syndrome and myocardial remodeling, and these deleterious effects were attenuated by ALDH2 overexpression. In addition, ALDH2 overexpression attenuated the cellular apoptosis and insulin resistance associated with a HF diet. Mechanistically, ALDH2 overexpression inhibited the expression of c-Jun N-terminal kinase (JNK)-1, activated protein 1 (AP-1), insulin receptor substrate 1 (IRS-1), 4- hydroxynonenal, caspase 3, transforming growth factor β1, and collagen I and III, and enhanced Akt phosphorylation. Conclusion: ALDH2 may effectively attenuate myocardial remodeling and contractile defects induced by a HF diet through the regulation of the JNK/AP-1 and IRS-1/Akt signaling pathways. Our study demonstrates that ALDH2 plays an essential role in protecting cardiac function from lipotoxic cardiomyopathy

    The First Case of Ischemia-Free Kidney Transplantation in Humans

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    Background: Ischemia-reperfusion injury (IRI) has been considered an inevitable event in organ transplantation since the first successful kidney transplant was performed in 1954. To avoid IRI, we have established a novel procedure called ischemia-free organ transplantation. Here, we describe the first case of ischemia-free kidney transplantation (IFKT). Materials and Methods: The kidney graft was donated by a 19-year-old brain-dead donor. The recipient was a 47-year-old man with end-stage diabetic nephropathy. The graft was procured, preserved, and implanted without cessation of blood supply using normothermic machine perfusion. Results: The graft appearance, perfusion flow, and urine production suggested that the kidney was functioning well-during the whole procedure. The creatinine dropped rapidly to normal range within 3 days post-transplantation. The levels of serum renal injury markers were low post-transplantation. No rejection or vascular or infectious complications occurred. The patient had an uneventful recovery. Conclusion: This paper marks the first case of IFKT in humans. This innovation may offer a unique solution to optimizing transplant outcomes in kidney transplantation

    Optimal time decay estimation for large-solution about 3D compressible MHD equations

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    This paper mainly focus on optimal time decay estimation for large-solution about compressible magnetohydrodynamic equations in 3D whole space, provided that (σ01,u0,M0)L1H2(\sigma_{0}-1,u_{0},M_{0})\in L^1\cap H^2. In [2](Chen et al.,2019), they proved time decay estimation of (σ1,u,M)H1\|(\sigma-1,u,M)\|_{H^1} being (1+t)34(1+t)^{-\frac{3}{4}}. Based on it, we obtained that of (σ1,u,M)H1\|\nabla(\sigma-1,u,M)\|_{H^1} being (1+t)54(1+t)^{-\frac{5}{4}} in [24]. Therefore, we are committed to improving that of 2(σ1,u,M)L2\|\nabla^2 (\sigma-1,u,M)\|_{L^2} in this paper. Thanks to the method adopted in [25] (Wang and Wen, 2021), we get the optimal time decay estimation to the highest-order derivative for space of solution, which means that time decay estimation of 2(σ1,u,M)L2\|\nabla^2 (\sigma-1,u,M)\|_{L^2} is (1+t)74(1+t)^{-\frac{7}{4}}

    Control of the Variable-Speed Pumped Storage Unit-Wind Integrated System

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    The integration of variable-speed pumped storage unit (VS-PSU) guarantees an efficient peak regulation and frequency modulation of the power grid. The present research analyzes the active power flow of the VS-PSU under synchronous, subsynchronous, and supersynchronous speed in both generation and pumping modes. The control strategy of the VS-PSU is realized by the dq-axis vector control method. Furthermore, the control of the VS-PSU integrated with wind power has been conducted using DIgSILENT platform with the VS-PSU of 300 kW capacity. Results show that the fluctuation of the power output of the wind power plant can be reduced effectively. The safe, economical, and stable operation of power system integrated with wind power can be achieved by the significant contribution of the VS-PSU

    Bone mesenchymal stem cells ameliorate ischemia/reperfusion-induced damage in renal epithelial cells via microRNA-223

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    Abstract Background Recent studies have indicated that microRNA-223 (miR-223) plays a role in the tissue-protective effect of mesenchymal stem cells (MSCs). NLR family-pyrin domain containing 3 (NLRP3) was reported to affect a renal ischemia/reperfusion (I/R) injury by exerting a direct effect on the renal tubular epithelium. Therefore, we investigated how miR-223 and NLRP3 might function in kidneys exposed to conditions of ischemia and subsequent reperfusion. Methods Hypoxia/reoxygenation (H/R) murine renal tubular epithelial cells (RTECs) were cocultured with either MSCs or hypoxia-pretreated MSCs (htMSCs), after which the RTECs were examined for their viability and evidence of apoptosis. Next, miR-223 expression in the MSCs was downregulated to verify that MSCs protected RTECs via the transport of miR-223. Kidney I/R KM/NIH mouse models were created and used for in vivo studies. Results The results showed that coculture with MSCs significantly increased the viability of RTECs and decreased their rates of apoptosis. The levels of hepatocyte growth factor (HGF), insulin-like growth factor-1 (IGF-1), transforming growth factor beta (TGF-β), and vascular endothelial growth factor (VEGF) in samples of coculture supernatants were higher than those in samples of non-coculture supernatants. A bioinformatics analysis revealed a targeting relationship between miR-223 and NLRP3. A dual luciferase assay showed that miR-223 inhibited NLRP3 expression. The htMSCs displayed a protective function associated with an upregulation of miR-223 as induced by Notch1 and the downregulation of NLRP3. Conversely, inhibition of miR-223 impeded the protective effect of MSCs. In the I/R mouse models, injection of either MSCs or htMSCs ameliorated the damage to kidney tissue, while suppression of miR-223 expression in MSCs reduced their protective effect on mouse kidneys. Conclusions Our results demonstrate that miR-223 and NLRP3 play important roles in the treatment of renal tissue injuries with transplanted MSCs

    Investigation on the Metal Transfer and Cavity Evolution during Submerged Arc Welding with X-ray Imaging Technology

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    The physical phenomena of submerged arc welding (SAW) conducted with a 1.6 mm flux-cored wire were investigated using X-ray imaging technique. Three kinds of metal transfer modes were confirmed in this paper, namely the front flux wall-guided droplet transfer, back flux wall-guided droplet transfer, and repelled droplet transfer, of which the corresponding percentages were 47.65%, 45.29%, and 7.06%, respectively. Although the average sizes of the droplets for SAW and FCAW (flux-cored wire welding) were 2.0 mm and 1.9 mm with an average droplet transfer time of 90.3 ms, it required 36.4% more time for the droplet of SAW to finish one metal transfer than it did in FCAW. In addition, the volume of the cavity was not constant but repeated a cycle mode of “expansion and contraction” during the whole process. Thus, the dynamics of the cavity and viscous resistance caused by the flux collectively slowed down the velocity of the droplets from the wire to the weld pool in SAW. Compared with FCAW, a smoother weld without pits and pores was manufactured during the SAW process. Due to the compression effect of the flux, the 14.5 mm average weld width of SAW was 2.9 mm shorter than that of the FCAW. Furthermore, the thickness of slag with a porous structure in SAW was 2.7 times of that in FCAW, indicating that it could provide better protection to the weld of SAW
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