Pd-Doped SnO 2

Methane (CH4), ethane (C2H6), ethylene (C2H4), and acetylene (C2C2) are important fault characteristic hydrocarbon gases dissolved in power transformer oil. Online monitoring these gaseous components and their generation rates can present the operational state of power transformer timely and effectively. Gas sensing technology is the most sticky and tricky point in online monitoring system. In this paper, pure and Pd-doped SnO2 nanoparticles were synthesized by hydrothermal method and characterized by X-ray powder diffraction, field-emission scanning electron microscopy, and energy dispersive X-ray spectroscopy, respectively. The gas sensors were fabricated by side-heated preparation, and their gas sensing properties against CH4, C2H6, C2H4, and C2H2 were measured. Pd doping increases the electric conductance of the prepared SnO2 sensors and improves their gas sensing performances to hydrocarbon gases. In addition based on the frontier molecular orbital theory, the highest occupied molecular orbital energy and the lowest unoccupied molecular orbital energy were calculated. Calculation results demonstrate that C2H4 has the highest occupied molecular orbital energy among CH4, C2H6, C2H4, and C2H2, which promotes charge transfer in gas sensing process, and SnO2 surfaces capture a relatively larger amount of electric charge from adsorbed C2H4

Gas Sensing Properties and Mechanism of Nano-SnO 2

Nano-SnO2 powder was prepared by the hydrothermal method in this paper. X-ray powder diffraction (XRD) and scanning electron microscopy (SEM) were used to characterize the composition of the crystalline phase and the morphology of the prepared gas-sensitive materials, respectively. In particular, the study focused on the sensing behaviors of nano-SnO2-based sensor towards power transformer fault gases such as hydrogen and carbon monoxide. The optimum working temperature for hydrogen and carbon monoxide is about 400∘C and 360∘C, separately. Further investigations into the adsorption process of gas molecule on SnO2 (110) surface based on the first principles were conducted. The calculations indicated that 1σ orbits of H2 split into several new electronic peaks and 5σ orbits of CO almost degenerated completely in the adsorption process, which promoted charge transfer between gas molecule and SnO2 (110) surface. It provides a qualitative explanation for the prepared nano-SnO2-based sensor exhibiting different gas sensing properties towards H2 and CO

Facile Hydrothermal Synthesis and Basic Gas-Sensing Properties of Two Three-Dimensional Nanostructures of SnO 2

The hierarchical SnO2 sphere-like architecture, consisting of numerous thin nanosheets, was successfully synthesized via a facile hydrothermal method. The structures and morphologies of this hierarchical architecture were characterized in detail by means of powder X-ray diffraction (XRD), field-emission scanning electron microscopy (FE-SEM), and Brunauer-Emmett-Teller (BET). Further comparative experiments of gas-sensing performances of the as-prepared SnO2 were investigated towards ethanol. It shows this three-dimensional, sheet-spheres, SnO2 as a potential gas-sensing material for a broad range of future sensor applications, like sensitive response to other gases such as hydrogen, carbonic oxide, and methane

PARP inhibitor veliparib and HDAC inhibitor SAHA synergistically co-target the UHRF1/BRCA1 DNA damage repair complex in prostate cancer cells

Abstract Background The poly ADP ribose polymerase (PARP) inhibitor olaparib has been approved for treating prostate cancer (PCa) with BRCA mutations, and veliparib, another PARP inhibitor, is being tested in clinical trials. However, veliparib only showed a moderate anticancer effect, and combination therapy is required for PCa patients. Histone deacetylase (HDAC) inhibitors have been tested to improve the anticancer efficacy of PARP inhibitors for PCa cells, but the exact mechanisms are still elusive. Methods Several types of PCa cells and prostate epithelial cell line RWPE-1 were treated with veliparib or SAHA alone or in combination. Cell viability or clonogenicity was tested with violet crystal assay; cell apoptosis was detected with Annexin V-FITC/PI staining and flow cytometry, and the cleaved PARP was tested with western blot; DNA damage was evaluated by staining the cells with γH2AX antibody, and the DNA damage foci were observed with a fluorescent microscopy, and the level of γH2AX was tested with western blot; the protein levels of UHRF1 and BRCA1 were measured with western blot or cell immunofluorescent staining, and the interaction of UHRF1 and BRCA1 proteins was detected with co-immunoprecipitation when cells were treated with drugs. The antitumor effect of combinational therapy was validated in DU145 xenograft models. Results PCa cells showed different sensitivity to veliparib or SAHA. Co-administration of both drugs synergistically decreased cell viability and clonogenicity, and synergistically induced cell apoptosis and DNA damage, while had no detectable toxicity to normal prostate epithelial cells. Mechanistically, veliparib or SAHA alone reduced BRCA1 or UHRF1 protein levels, co-treatment with veliparib and SAHA synergistically reduced BRCA1 protein levels by targeting the UHRF1/BRCA1 protein complex, the depletion of UHRF1 resulted in the degradation of BRCA1 protein, while the elevation of UHRF1 impaired co-treatment-reduced BRCA1 protein levels. Co-administration of both drugs synergistically decreased the growth of xenografts. Conclusions Our studies revealed that the synergistic lethality of HDAC and PARP inhibitors resulted from promoting DNA damage and inhibiting HR DNA damage repair pathways, in particular targeting the UHRF1/BRCA1 protein complex. The synergistic lethality of veliparib and SAHA shows great potential for future PCa clinical trials

Additional file 1: of PARP inhibitor veliparib and HDAC inhibitor SAHA synergistically co-target the UHRF1/BRCA1 DNA damage repair complex in prostate cancer cells

Table S1. Genes Confirmed to Induce BRCAness in Prostate Non- and Cancerous Cell Lines. (DOC 51 kb

Additional file 2: of PARP inhibitor veliparib and HDAC inhibitor SAHA synergistically co-target the UHRF1/BRCA1 DNA damage repair complex in prostate cancer cells

Figure S1. Co-treatment with SAHA and veliparib enhanced cell apoptosis in PCa cells. LNCaP (A) and C4–2(B) cells were treated with SAHA and veliparib alone or in combination for 3 days. Cells were stained with PI, and the apoptotic cells (sub-G1 population) were analyzed by flow cytometry. Graphs show the mean percentage of cells in sub-G1. (TIF 2355 kb

Additional file 3: of PARP inhibitor veliparib and HDAC inhibitor SAHA synergistically co-target the UHRF1/BRCA1 DNA damage repair complex in prostate cancer cells

Figure S2. (A) LNCaP, PC-3, CWR22Rv1 and C4–2 cells were treated with SAHA and veliparib alone or in combination for 3 days. The protein levels of RAD51 were assessed by western blot. (B) LNCaP, C4–2, VCaP, CWR22Rv1 and PC-3 cells were treated with SAHA and veliparib alone or in combination for 3 days. The protein levels of DNA damage repair molecules (Ku-70, ERCC1,MSH2 and MSH6) were assessed by western blot. (TIF 2690 kb

Differential Regulation of Dihydroceramide Desaturase by Palmitate versus Monounsaturated Fatty Acids: IMPLICATIONS FOR INSULIN RESISTANCE*

Much data implicate saturated fatty acids in deleterious processes associated with obesity, diabetes, and the metabolic syndrome. Many of these changes may be due to aberrant generation of bioactive lipids when saturated fatty acid availability to tissues is increased. On the other hand, studies are emerging that implicate the monounsaturated fatty acid oleate in protection from saturated fat mediated toxicity; however, the mechanisms are not well understood. Our data demonstrate a novel role for palmitate in increasing mRNA encoding DES1, which is the enzyme responsible for generating ceramide from its precursor dihydroceramide and thus controls synthesis of the bioactive lipid ceramide. Moreover, co-treatment with oleate prevented the increase in ceramide, and this occurred through attenuation of the increase in message and activity of DES1. Knockdown of DES1 also protected from palmitate-induced insulin resistance, and overexpression of this enzyme ameliorated the protective effect of oleate. Together, these findings provide insight into the mechanisms of oleate-mediated protection against metabolic disease and provide novel evidence for fatty acid-mediated regulation of a key enzyme of ceramide biosynthesis