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1.
ACS Omega ; 7(32): 28646-28657, 2022 Aug 16.
Artigo em Inglês | MEDLINE | ID: mdl-35990452

RESUMO

As micropower devices, microfluidic fuel cells (MFCs) have gained much attention due to their simple configurations and high power densities. MFCs exploit the parallel laminar flowing of two electrolytes in a microchannel with a characteristic length from 1 to 1000 µm to separate the anolyte and catholyte, without the proton exchange membranes in the traditional fuel cells. These membrane-less configurations can avoid a series of technical problems related to the membranes. To achieve an MFC with high power density and low cost, we constructed the direct formate MFCs with two catalyst-free oxidants containing FeCl3 and Na2S2O8 solutions, respectively, and compared the performance of the two MFCs. Due to Na2S2O8 being an oxidant with some distinctive advantages, including its high theoretical potential, high solubility of itself and its reduction product, and environmental friendliness, the Na2S2O8-based MFC showed a higher open-circuit voltage (>2.0 V) and better performance. Then, we studied the effects of oxidant concentrations, flow rates, and fuel concentrations on the performance of the Na2S2O8-based MFC. The results showed the optimum performance of the Na2S2O8-based MFC with the peak power density of 214.95 mW cm-2 and the limiting current density of 700.13 mA cm-2 under the conditions of 1.5 M HCOONa, 2 M Na2S2O8, and 300 µL min-1 at an anolyte/catholyte flow ratio of 2:1. The performance was also the highest among the direct formate MFCs reported up to now. Moreover, the Na2S2O8-based MFC could stably discharge for about 4 h under a constant voltage. All of the results demonstrated that Na2S2O8 was a suitable oxidant and that the Na2S2O8-based MFC could realize the goals of high power density and low cost for the actual application of MFCs.

2.
ACS Omega ; 6(29): 19153-19161, 2021 Jul 27.
Artigo em Inglês | MEDLINE | ID: mdl-34337253

RESUMO

Membraneless microfluidic fuel cells (MFCs) have garnered tremendous interest as micropower devices, which exploit the colaminar nature of two aqueous electrolytes to separate the anode and cathode and avoid the membrane usually used in a fuel cell. Our previous research shows that the performance of FeCl3-based MFCs with catalyst-free cathodes is mainly limited by the cathode. To improve the power output of these MFCs, we activated the carbon paper cathode by an electrochemical method in the three solutions (Na2SO4, NaOH, and H2SO4) to improve the electrochemical characteristics of the carbon paper cathode. The surface functionalities and defects, reduction activation of iron ions as the oxidant, cathode resistance, and performance of FeCl3-based MFCs were measured and compared. Our work shows that the electrochemical activation of the carbon paper in different solutions is a simple and effective method to enhance the electrochemical characteristics of the carbon paper cathode and improve the performance of the FeCl3-based MFC. Also, the MFC with the carbon paper cathode activated in the H2SO4 solution reaches the optimum performance: 235.6 mW cm-3 in volumetric power density and 1063.33 mA cm-3 in volumetric limiting current density, which are 1.58 and 1.52 times as much as that of a MFC with an untreated carbon paper cathode, respectively. This best performance can be attributed to the cathode activated in the H2SO4 solution with the largest number of oxygen-containing functional groups, the largest electrochemical active surface area, strongest reduction of iron ions, and least resistance of the cathode.

3.
Front Immunol ; 9: 878, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-29760701

RESUMO

Atherosclerosis is the major cause of cardiovascular diseases. Current evidences indicate that inflammation is involved in the pathogenesis of atherosclerosis. Human gingiva-derived mesenchymal stem cells (GMSC) have shown anti-inflammatory and immunomodulatory effects on autoimmune and inflammatory diseases. However, the function of GMSC in controlling atherosclerosis is far from clear. The present study is aimed to elucidate the role of GMSC in atherosclerosis, examining the inhibition of GMSC on macrophage foam cell formation, and further determining whether GMSC could affect the polarization and activation of macrophages under different conditions. The results show that infusion of GMSC to AopE-/- mice significantly reduced the frequency of inflammatory monocytes/macrophages and decreased the plaque size and lipid deposition. Additionally, GMSC treatment markedly inhibited macrophage foam cell formation and reduced inflammatory macrophage activation, converting inflammatory macrophages to anti-inflammatory macrophages in vitro. Thus, our study has revealed a significant role of GMSC on modulating inflammatory monocytes/macrophages and alleviating atherosclerosis.


Assuntos
Aterosclerose , Gengiva/citologia , Macrófagos/fisiologia , Células-Tronco Mesenquimais , Animais , Diferenciação Celular/fisiologia , Células Espumosas/fisiologia , Xenoenxertos , Humanos , Ativação de Macrófagos/fisiologia , Transplante de Células-Tronco Mesenquimais , Camundongos , Camundongos Knockout , Monócitos
4.
FEBS Open Bio ; 6(7): 720-8, 2016 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-27398311

RESUMO

Exposure to concentrated ambient fine particulate matter (PM2.5) has been associated with cardiovascular diseases (CVDs). The barrier function of vascular endothelial cells is critical for the development of CVDs. Here, we employed human umbilical vein endothelial cells to clarify the function of ambient PM2.5 pollution in the regulation of membrane permeability of vascular endothelial cells. The results show that a high concentration of PM2.5, which mainly includes heavy metals and polycyclic aromatic hydrocarbons, induces barrier dysfunction of vascular endothelial cells. This was mediated in part by promoting IL-6 expression, which then increases the transcriptional activity of HIF-1α by promoting its translocation to the nucleus. Our findings indicate that concentrated PM2.5 can destroy membrane integrity and promote permeability in vascular endothelial cells, thereby contributing to the development of CVDs.

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