9 research outputs found

    Additional file 1: of Facile fabrication of self-assembled ZnO nanowire network channels and its gate-controlled UV detection

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    Figure S1. Home-made pulling system consisted of syringe pump, stirrer. The substrate was pulled vertically. Figure S2. Energy dispersive spectroscopy (EDS) mapping image of ZnO NWs network. (a) SEM image of ZnO NWs network. (b) EDS mapping of Zn. (c) EDS data of ZnO NW network channel fixed on SiO2 wafer. The peaks show the Zn and O element, respectively. The Si peak is due to SiO2 wafer. Figure S3. ZnO NWs network electrical properties by controlled pulling speed 0.5 mm min− 1. (a) current-voltage characteristics of various back-gate voltage. Vg ranged from − 60 V to 60 V in 20 V steps. (b) Ids vs Vg relations of ZnO NWs network channel fabricated at various Vds. Vds ranged from 0 to 7 V in 1 V steps. Figure S4. Resistance distribution of ZnO NWs network devices at different pulling speeds. Figure S5. Thermal treatment process of ZnO NW network FET in vacuum condition. The thermal treatment process gives the flow of the Ar gas of 100 sccm rate. Two step raises of the temperature 110 °C to 300 °C. Figure S6. Transconductance vs Vg. The maximum transconductance gm value is 47 nS at Vds 7 V. Figure S7. I-V characteristics before (blue) and after (red) UV illumination (Vg = − 60 V). The signal increased by ~ 104 orders. Inset shows a log scale. Figure S8. Comparison of performances of ZnO NW network based UV sensors. Figure S9. Schematic diagram depicting the carrier generation and transportation processes in the ZnO NW network channel before (left) and after (right) UV illumination. Band diagram of the devices under different gate bias conditions and UV illumination. (DOC 1567 kb

    Additional file 2 of Development and characterization of a Nannochloropsis mutant with simultaneously enhanced growth and lipid production

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    Additional file 2: Fig. S1. Whole gel Southern blot result. Lane 1, WT (no digestion); lane 2, Mut68 (no digestion); Lane 3, WT (digested by NheI); lane 4, Mut68 (digested by NheI); Lane 5, WT (digested by NheI and XhoI); lane 6, Mut68 (digested by NheI and XhoI)

    MOESM1 of 1-Palmitoyl-2-linoleoyl-3-acetyl-rac-glycerol (PLAG) attenuates gemcitabine-induced neutrophil extravasation

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    Additional file 1. Figure S1. Analysis of Differentiation of BMDM and human neutrophil-like HL-60 cells by flow cytometry. A, FACS analysis illustrates the purity of BMDM at day 7 using a macrophage marker F4/80-PE. B, Differentiation of HL-60 cells into human neutrophil-like cells confirmed by flow cytometry and a CD11b-PE marker. Figure S2. Neutrophil counts of the blood and peritoneum in mice treated with PLAG, reparixin or NAC. Male balb/c mice of 6 to 8 weeks of age were orally administered with 250mg/kg of PLAG (in PBS), or intraperitoneally injected with 50mg/kg of reparixin (in mineral oil) or with 50mg/kg of NAC (in PBS). After 15h, blood and peritoneal fluid samples were collected for CBC analysis. The number of neutrophils from the blood and the peritoneal fluid of (A) PLAG, (B) reparixin and (C) NAC-treated mice. Each group contains five mice, and bars represent the mean ± SD. ns, not significant. Figure S3. PLAG inhibits other chemotherapeutic agents-induced neutrophil migration. Male balb/c mice of 6-8 weeks of age were orally administrated with 250mg/kg PLAG, and then intraperitoneally injected with (A) 100mg/kg 5-fluouracil or (B) AC regimen (2.5mg/kg of adriamycin and 100mg/kg of cyclophosphamide) for 24h. The number of blood neutrophils were determined by CBC analysis. Each group contains five mice, and bars represent the mean ± SD. * p<0.05, ** p<0.01, *** p<0.001. Figure S4. Gemcitabine induces a neutrophil-attracting chemokine CXCL8 production via MAPK activation in THP-1 cells. The mRNA level of CXCL8 in human monocytic THP-1 stimulated with (A) various doses and (B) different time points of gemcitabine treatment. The protein concentration of CXCL8 in THP-1 stimulated with (C) various doses and (D) different time points of gemcitabine treatment. E, Gemcitabine induces phosphorylation of ERK, p38 MAPK and JNK analyzed by western blot in THP-1 cells. The transmigration of differentiated HL-60 cells towards the conditioned medium of THP-1 stimulated with (F) various doses and (G) different time points of gemcitabine treatment. * p<0.05, ** p<0.01, *** p<0.001. Figure S5. Gemcitabine increases intracellular reactive oxygen species (ROS) levels in a time-dependent manner. A and B, THP-1 cells were treated with 10ug/ml of gemcitabine for different time points, and then the level of intracellular ROS in the cells was stained with CM-H2DCFDA and analyzed by flow cytometry. C, CM-H2DCFDA fluorescence imaging of ROS in THP-1 cells using a confocal microscope. The bars represent the mean ± SD. * p<0.05, ** p<0.01, *** p<0.001. Figure S6. PLAG does not interfere with the anti-cancer effect of gemcitabine in athymic nude mice implanted with a human myeloma cell line RPMI8226. A, The treatment design and schedule using a human RPMI8226 xenograft mice model. B, The tumor weights of the treatment groups at day 40. ns; not significant, *p < 0.05

    Additional file 6 of Development and characterization of a Nannochloropsis mutant with simultaneously enhanced growth and lipid production

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    Additional file 6: Fig. S3. Predicted protein crystal structure of WT (a) and truncated (b) TPS based on the template-based prediction tool RaptorX. Yellow, TPSWT and TPS Tr domain; cyan, TPPWT and TPPTr domain; purple, N-terminalWT and N-terminalTr domain; orange, C-terminalWT; grey, disordered region

    Additional file 5 of Development and characterization of a Nannochloropsis mutant with simultaneously enhanced growth and lipid production

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    Additional file 5: Fig. S2. Coding DNA sequence of truncated TPS in Mut68. Inserted pNsShble was highlighted in green and stop codon generated by insertion of pNsShble was underlined
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