Zn anodes suffer from poor Coulombic efficiency (CE) and serious dendrite formation due to the unstable anode/electrolyte interface (AEI). The electrical double layer (EDL) structure formed before cycling is of great significance for building stable solid electrolyte interphase (SEI) on Zn surface but barely discussed in previous research about the stabilization of Zn anode. Herein, saccharin (Sac) is introduced as electrolyte additive for regulating the EDL structure on the AEI. It is found that Sac derived anions are preferentially adsorbed on the Zn metal surface instead of water dipole, creating a new H2O‐poor EDL structure. Moreover, the unique SEI is also detected on the Zn surface due to the decomposition of Sac anions. Both are proved to be capable of modulating Zn deposition behavior and preventing side reactions. Encouragingly, Zn|Zn symmetric cells using Sac additive deliver a high cumulative plated capacity of 2.75 Ah cm−2 and a high average CE of 99.6% under harsh test condition (10 mA cm−2, 10 mAh cm−2). The excellent stability is also achieved at a high rate of 40 mA cm−2. The effectiveness of this Sac additive is further demonstrated in the Zn‐MnO2 full cells.
In this study, a novel Co 3 O 4 /Co(OH) 2 heterostructure is obtained via electrodeposition on nickel (Ni) foam, forming sandwich-like structure and freestanding electrode. The outer Co(OH) 2 with layered structure can provide sufficient absorption sites and enable facile ion intercalation, meanwhile the presence of a conductive and robust interfacial Co 3 O 4 layer between Ni foam and Co(OH) 2 is found effectively minimizes the charge transfer resistance and stabilizes the interface, thus improving the electrode's rate and cycling performance with high capacity preserved synergistically. Furthermore, the structural evolution of Co(OH) 2 and Co 3 O 4 upon cycling are elucidated systematically using a series of in situ and ex situ techniques. The Co(OH) 2 is found irreversibly changed to CoOOH upon first charge, which is then reversibly converted to CoO 2 during the subsequent charge-discharge cycles. The Co 3 O 4 exhibits negligible phase changes of the bulk upon cycling, indicating its good structural integrity that contributes to the significantly improved cyclability. In general, this work not only offers an ease and effective approach to optimize the charge storage properties of Co 3 O 4 /Co(OH) 2 heterostructure via interfacial layer control, but also provides valuable insights in understanding their charge storage mechanisms, which may inspire the development of more heterostructures or extend to other applications.
Potassium-ion batteries (PIBs) are attractive for grid-scale energy storage due to the abundant potassium resource and high energy density. The key to achieving high-performance and large-scale energy storage technology lies in seeking eco-efficient synthetic processes to the design of suitable anode materials. Herein, a spherical sponge-like carbon superstructure (NCS) assembled by 2D nanosheets is rationally and efficiently designed for K+ storage. The optimized NCS electrode exhibits an outstanding rate capability, high reversible specific capacity (250 mAh g−1 at 200 mA g−1 after 300 cycles), and promising cycling performance (205 mAh g−1 at 1000 mA g−1 after 2000 cycles). The superior performance can be attributed to the unique robust spherical structure and 3D electrical transfer network together with nitrogen-rich nanosheets. Moreover, the regulation of the nitrogen doping types and morphology of NCS-5 is also discussed in detail based on the experiments results and density functional theory calculations. This strategy for manipulating the structure and properties of 3D materials is expected to meet the grand challenges for advanced carbon materials as high-performance PIB anodes in practical applications.
Background: Recent studies suggest the involvement of the adenosine monophosphate-activated serine/threonine protein kinase (AMPK) pathway in the pathogenesis of diabetic nephropathy (DN). Resveratrol, an agent that activates AMPK, may have the potential to protect against the development of DN. This study was designed to investigate the therapeutic effects of resveratrol on renal hypertrophy in early-stage diabetes and the underlying mechanisms. Method: Molecular and structural changes involved in the pathogenesis of DN were tested in a rat model of early-stage diabetes. Renal mesangial cells (RMCs) were cultured in media containing different concentrations of glucose with or without resveratrol. Cellular DNA synthesis was assayed by measuring 3H-thymidine incorporation. The phosphorylation status of AMPK, eukaryotic translation initiation factor 4E binding protein 1 (4E-BP1), and phospho- ribosomal protein S6 (S6) was analyzed by Western blot. Results: Resveratrol reduced plasma creatinine and urinary albumin excretion and attenuated renal hypertrophy without affecting blood glucose levels. Moreover, resveratrol activated AMPK and inhibited phosphorylation of 4E-BP1 and S6 in diabetic rat kidneys. In vitro, resveratrol blocked high glucose-induced dephosphorylation of AMPK and phosphorylation of 4E-BP1 and S6 and strongly inhibited both the DNA synthesis and proliferation of RMCs. Conclusion: These findings suggest the possibility that resveratrol exerts antiproliferative, antihypertrophic effects by activating AMPK and reducing 4E-BP1 and S6 phosphorylation, thus suppressing the development and progression of DN.
Oxygen-containing functional groups were found to effectively boost the K+ storage performance of carbonaceous materials, however, the mechanism behind the performance enhancement remains unclear. Herein, we report higher rate capability and better long-term cycle performance employing oxygen-doped graphite oxide (GO) as the anode material for potassium ion batteries (PIBs), compared to the raw graphite. The in situ Raman spectroscopy elucidates the adsorption-intercalation hybrid K+ storage mechanism, assigning the capacity enhancement to be mainly correlated with reversible K+ adsorption/desorption at the newly introduced oxygen sites. It is unraveled that the C=O and COOH rather than C-O-C and OH groups contribute to the capacity enhancement. Based on in situ Fourier transform infrared (FT-IR) spectra and in situ electrochemical impedance spectroscopy (EIS), it is found that the oxygen-containing functional groups regulate the components of solid electrolyte interphase (SEI), leading to the formation of highly conductive, intact and robust SEI. Through the systematic investigations, we hereby uncover the K+ storage mechanism of GO-based PIB, and establish a clear relationship between the types/contents of oxygen functional groups and the regulated composition of SEI.
Fibroblasts play a pivotal role in the process of cutaneous wound repair, whereas their migratory ability under diabetic conditions is markedly reduced. In this study, we investigated the effect of basic fibroblast growth factor (bFGF) on human dermal fibroblast migration in a high-glucose environment. bFGF significantly increased dermal fibroblast migration by increasing the percentage of fibroblasts with a high polarity index and reorganizing F-actin. A significant increase in intracellular reactive oxygen species (ROS) was observed in dermal fibroblasts under diabetic conditions following bFGF treatment. The blockage of bFGF-induced ROS production by either the ROS scavenger N-acetyl-L-cysteine (NAC) or the NADPH oxidase inhibitor diphenylene iodonium chloride (DPI) almost completely neutralized the increased migration rate of dermal fibroblasts promoted by bFGF. Akt, Rac1 and JNK were rapidly activated by bFGF in dermal fibroblasts, and bFGF-induced ROS production and promoted dermal fibroblast migration were significantly attenuated when suppressed respectively. In addition, bFGF-induced increase in ROS production was indispensable for the activation of focal adhesion kinase (FAK) and paxillin. Therefore, our data suggested that bFGF promotes the migration of human dermal fibroblasts under diabetic conditions through increased ROS production via the PI3K/Akt-Rac1-JNK pathways.
The development of aqueous zinc metal batteries (AZMBs) is significantly impeded by the poor cycle stability of Zn anodes due to the uncontrolled dendrite growth and low Coulombic efficiency (CE). Herein, for the first time, SeO 2 additives are introduced into ZnSO 4 electrolyte to enhance the stability of the Zn anode. According to the experimental results, the protective ZnSe layer is initially in-situ formed on the Zn surface prior to the Zn plating, which acts as a shield for inhibiting the parasitic reactions and dendrite formation. Moreover, this additive strategy yields the unique characteristic of self-healing for recovering the cracks in the consequence of huge volume change, ensuring the durability of ZnSe layer. Consequently, Zn|Zn symmetric cell using SeO 2 additive delivers an enhanced cumulative plated capacity of 2.1 Ah cm −2 under practical test conditions, which far exceeds the previously reported works. Meanwhile, the average CE of 99.6% for 250 cycles is also demonstrated in Zn|Cu half cells with the presence of the SeO 2 additive. In addition, the positive effect of the SeO 2 additive is further illustrated in the Zn-MnO 2 full cells with a limited Zn.
Background and purpose: Thioredoxin (Trx) is an oxidoreductase that prevents free radical-induced cell death in cultured cells. Here we assessed the mechanism(s) underlying the cardioprotective effects of Trx in vivo. Experimental approach: The effects of myocardial ischemia (30 min) and reperfusion were measured in mice, with assays of myocardial apoptosis, superoxide production, NOx and nitrotyrosine content, and myocardial infarct size. Recombinant human Trx (rhTrx, 0.7-20 mg kg -1 , i.p.) was given 10 min before reperfusion. Key results: Treatment with 2 mg kg -1 rhTrx significantly decreased myocardial apoptosis and reduced infarct size (Po0.01). Nitrotyrosine content of cardiomyocytes was markedly reduced in rhTrx-treated animals (Po0.01). To further identify the mechanisms by which rhTrx may exert its anti-nitrative effect, iNOS expression and production of NOx and superoxide were determined. Treatment with rhTrx had no significant effect on iNOS expression or NOx content in the ischemic/reperfused heart. However, it markedly upregulated mSOD and reduced tissue superoxide content. To further establish a causative link between the anti-peroxynitrite effect and the cardioprotective effect of rhTrx, cultured adult cardiomyocytes were incubated with SIN-1, a peroxynitrite donor, (50 mM for 3 h) resulting in a nitrotyrosine content comparable to that seen in the ischemic/ reperfused heart and causing significant cardiomyocyte apoptosis (Po0.01). Treatment with rhTrx markedly decreased SIN-1 induced apoptosis (Po0.01). Conclusions and implications:These results demonstrate that Trx is a novel anti-apoptotic and cardioprotective molecule that exerts its cardioprotective effects by reducing ischemia/reperfusion-induced oxidative/nitrative stress.
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