Photocatalytic fuel cell based on integrated silicon nanowire arrays/zinc oxide heterojunction anode for simultaneous wastewater treatment and electricity production.

Photocatalytic fuel cells (PFCs) convert organic waste into electricity, thereby providing a potential solution for remediating environmental pollution and solving energy crises. Most PFCs for energy generation applications use powder photocatalysts, which have poor mechanical stability, high internal resistance, and may detach from the substrate during reactions, leading to unstable performance. Integrated photoelectrodes can overcome the drawbacks of powder catalysts. In this study, an integrated photoanode was prepared based on a silicon nanowire arrays/zinc oxide (Si NWs/ZnO) heterojunction by combining metal-assisted chemical etching (MACE) and hydrothermal methods. The resulting photoanode was used to assemble a PFC for simultaneous electricity generation and Rhodamine (RhB) dye wastewater degradation. This PFC showed excellent cell performance under irradiation, with a short-circuit current density of 0.183 Am-2, an open-circuit voltage (OCV) of 0.72 V, and a maximum power density of 0.87 W m-2. It could also be used continuously 20 times while degrading > 90% of RhB. This performance was ascribed to the three-dimensional (3D) structure and large surface area of Si NWs, as well as the matched band structure of ZnO, which facilitated the efficient separation and transport of photogenerated carriers in Si NWs/ZnO. The integrated structure also shortened the carrier transport pathways and suppressed carrier recombination. This research provides a foundation for the development of efficient, stable, low-cost, small-scale PFCs.

Palmitic acid induces nDNA release to cytosol and promotes microglial M1 polarization via cGAS-STING signaling pathway.

Palmitic acid (PA), the most common statured fatty acid in diets, is involved in peripheral as well as central inflammation. The M1 polarization of microglia plays an important role in PA-induced neuroinflammation. However, it is still unclear on the key factor and molecule mechanism of microglial polarization among it. Thus, we investigated whether the release of self-DNA into the cytoplasm of microglia was a consequence of PA treatment, as in aortic endothelial cells and adipocytes. RT-qPCR and immunofluorescence were performed to detect the status of cytosolic DNA and microglial polarization after PA treatment. We found that the content of cytosolic nDNA rather than mtDNA increased after PA treatment and the M1 polarization of microglia was associated with this. Moreover, the knockdown of cGAS in BV2 microglial cells demonstrated that the cGAS-STING pathway is involved in polarization process. Our results revealed that nDNA and cGAS-STING pathway are critically involved in PA-induced microglial M1 polarization. This mechanism may pose a new insight on targeting microglia may be a promising way to mitigate diet-induced early neuroinflammation.

The effects of activin A on the migration of human breast cancer cells and neutrophils and their migratory interaction.

Activin A belongs to the superfamily of transforming growth factor beta (TGFß) and is a critical regulatory cytokine in breast cancer and inflammation. However, the role of activin A in migration of breast cancer cells and immune cells was not well characterized. Here, a microfluidic device was used to examine the effect of activin A on the migration of human breast cancer cell line MDA-MB-231 cells and human blood neutrophils as well as their migratory interaction. We found that activin A promoted the basal migration but impaired epidermal growth factor (EGF)-induced migration of breast cancer cells. By contrast, activin A reduced neutrophil chemotaxis and transendothelial migration to N-Formyl-Met-Leu-Phe (fMLP). Finally, activin A promoted neutrophil chemotaxis to the supernatant from breast cancer cell culture. Collectively, our study revealed the different roles of activin A in regulating the migration of breast cancer cells and neutrophils and their migratory interaction. These findings suggested the potential of activin A as a therapeutic target for inflammation and breast cancers.

A dual-docking microfluidic cell migration assay (D2-Chip) for testing neutrophil chemotaxis and the memory effect.

Chemotaxis is a classic mechanism for guiding cell migration and an important topic in both fundamental cell biology and health sciences. Neutrophils are a widely used model to study eukaryotic cell migration and neutrophil chemotaxis itself can lead to protective or harmful immune actions to the body. While much has been learnt from past research about how neutrophils effectively navigate through a chemoattractant gradient, many interesting questions remain unclear. For example, while it is tempting to model neutrophil chemotaxis using the well-established biased random walk theory, the experimental proof was challenged by the cell's highly persistent migrating nature. A special experimental design is required to test the key predictions from the random walk model. Another question that has interested the cell migration community for decades concerns the existence of chemotactic memory and its underlying mechanism. Although chemotactic memory has been suggested in various studies, a clear quantitative experimental demonstration will improve our understanding of the migratory memory effect. Motivated by these questions, we developed a microfluidic cell migration assay (so-called dual-docking chip or D2-Chip) that can test both the biased random walk model and the memory effect for neutrophil chemotaxis on a single chip enabled by multi-region gradient generation and dual-region cell alignment. Our results provide experimental support for the biased random walk model and chemotactic memory for neutrophil chemotaxis. Quantitative data analyses provide new insights into neutrophil chemotaxis and memory by making connections to entropic disorder, cell morphology and oscillating migratory response.

Involvement of TGF-ß1/Smad3 Signaling in Carbon Tetrachloride-Induced Acute Liver Injury in Mice.

Transforming growth factor-beta1 (TGF-ß1) is a major factor in pathogenesis of chronic hepatic injury. Carbon tetrachloride (CCl4) is a liver toxicant, and CCl4-induced liver injury in mouse is a classical animal model of chemical liver injury. However, it is still unclear whether TGF-ß1 is involved in the process of CCl4-induced acute chemical liver injury. The present study aimed to evaluate the role of TGF-ß1 and its signaling molecule Smad3 in the acute liver injury induce by CCl4. The results showed that CCl4 induced acute liver injury in mice effectively confirmed by H&E staining of liver tissues, and levels of not only liver injury markers serum ALT and AST, but also serum TGF-ß1 were elevated significantly in CCl4-treated mice, compared with the control mice treated with olive oil. Our data further revealed that TGF-ß1 levels in hepatic tissue homogenate increased significantly, and type II receptor of TGF-ß (TßRII) and signaling molecules Smad2, 3, mRNA expressions and Smad3 and phospho-Smad3 protein levels also increased obviously in livers of CCl4-treated mice. To clarify the effect of the elevated TGF-ß1/Smad3 signaling on CCl4-induced acute liver injury, Smad3 in mouse liver was overexpressed in vivo by tail vein injection of Smad3-expressing plasmids. Upon CCl4 treatment, Smad3-overexpressing mice showed more severe liver injury identified by H&E staining of liver tissues and higher serum ALT and AST levels. Simultaneously, we found that Smad3-overexpressing mice treated with CCl4 showed more macrophages and neutrophils infiltration in liver and inflammatory cytokines IL-1ß and IL-6 levels increment in serum when compared with those in control mice treated with CCl4. Moreover, the results showed that the apoptosis of hepatocytes increased significantly, and apoptosis-associated proteins Bax, cytochrome C and the cleaved caspase 3 expressions were up-regulated in CCl4-treated Smad3-overexpressing mice as well. These results suggested that TGF-ß1/Smad3 signaling was activated during CCl4-induced acute liver injury in mice, and Smad3 overexpression aggravated acute liver injury by promoting inflammatory cells infiltration, inflammatory cytokines release and hepatocytes apoptosis. In conclusion, the activation of TGF-ß signaling contributes to the CCl4-induced acute liver injury. Thus, TGF-ß1/Smad3 may serve as a potential target for acute liver injury therapy.