The design of highly active, stable, and low‐cost electrocatalysts for the oxygen evolution reaction (OER) in proton exchange membrane water electrolyzer remains a challenge. RuO2 shows relatively low cost but poor stability. Here, the critical role of sulfate anion doping in promoting OER activity and stability of RuO2 is reported. Coupled with the Fe cation doping, the sulfate‐functionalized RuFeOx (S‐RuFeOx) displays a remarkable OER performance with a low overpotential of 187 mV at 10 mA cm−2 in acid, and much enhanced stability. The excellent OER activity of S‐RuFeOx is attributed to the dual positive effects that the sulfate dopants weaken the adsorption of the *OOH intermediate, and Fe dopants promote the deprotonation of chemisorbed water molecules to form *OOH. The enhanced stability is in part due to the sulfate dopants which stabilize the lattice oxygen. These results demonstrate that the anion and cation co‐doped RuO2 is a promising candidate for highly efficient OER electrocatalysts.
Proton exchange membrane water electrolyzer can sustainably and environmentally friendly produce hydrogen. However, it is hindered by the lack of high-performance anode catalysts for oxygen evolution reaction (OER) in acid electrolyte. Herein, IrCuNi deeply concave nanocubes (IrCuNi DCNCs) are successfully synthesized from the selective etching of the facet of cubic nanoparticles, and they significantly boost the OER. The obtained IrCuNi DCNCs show high activity toward OER in the acidic electrolyte, which only requires an overpotential of 273 mV to achieve the OER current density of 10 mA cm −2 at a low Ir loading of 6.0 μg Ir cm −2 . The precious metal based mass activity is 6.6 A mg Ir −1 at 1.53 V, which is 19 times as high as that of pristine Ir. It demonstrates that the outstanding catalytic performance is beneficial from the well-defined multimetal concave nanostructures, which may shed light on the fabrication of efficient water electrolyzers.
BGN might play an important role on metastasis in human endometrial cancer and it might be a target marker for the molecular therapy of advanced and recurrence endometrial cancer.
Abstract. Silent information regulator 1 (SIRT1) is involved in a number of cellular regulatory mechanisms affecting cellular life span, stress resistance, apoptosis and cellular metabolism. Recent studies have revealed that SIRT1 plays a dual role as a tumor suppressor and a tumor promoter in multiple stages of carcinogenesis. Increased lipogenesis has been found in cancer cells, sterol regulatory element binding protein 1 (SREBP1) are nuclear lipogenic transcription factors, which mainly regulate lipogenic processes by activating genes involved in fatty acid and triglyceride biosynthesis. In the present study, we detected expression of SIRT1 in endometrial cancer (EC) and illustrated the relationship between SIRT1 and SREBP1, which indicated that SIRT1 could stimulate endometrial tumor growth through the lipogenic pathway. Gene expression levels of SIRT1 were assayed using quantitative real-time PCR and protein expression levels were detected by western blotting. RNA interference was conducted in order to explore the subsequent effect on tumor cells and on the expression of SREBP1. Expression levels of SIRT1 in EC were found to be significantly higher than in normal endometrium. Knockdown of SIRT1 could downregulate expression of SREBP1 and suppress cell proliferation. These results demonstrated that SIRT1 may play a role as a tumor promoter in EC and can promote endometrial tumor growth by promoting lipogenesis. Our findings suggest that targeting SIRT1 may provide a theoretical basis for the management of EC. IntroductionEndometrial cancer (EC) is the most common malignancy of the female reproductive tract and its incidence is on the increase (1). Approximately 40% of all cases can be attributed to obesity (2). Aberration in lipid metabolism contributes to different aspects of tumorigenesis (3); our research team focused on this domain of EC in recent years.NAD-dependent class III histone deacetylase silent information regulator 1 (SIRT1), that shares the highest degree of homology with the yeast protein SIR2, can deacetylate both histones and non-histone proteins (4). Its deacetylation activity enables it to interact with a variety of important transcription factors and transcriptional co-regulatory factors, to regulate gene transcription, chromosome stability and activity of target proteins, which are involved in tumor metabolism and development (5,6). The current results demonstrated that SIRT1 plays a dual role as a tumor promoter as well as a tumor suppressor (7). Its involvement in tumorigenesis may be due to its diverse distribution in different tissues and different upstream and downstream regulatory factors that regulate its function (8).Sterol regulatory element binding protein 1 (SREBP1) belongs to the family of the basic helix-loop-helix leucine zipper family of DNA binding transcription factors, which can regulate most enzymes involved in fatty acid biosynthesis, such as acetyl-CoA carboxylase, fatty acid synthase, Elovl-6 and stearoyl-CoA desaturase (9). Lipogenesis is increased in cancer cells...
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