We carried out parallel design and development of two differently structured auto sampler based on a multi-axis and multi-mode high-precision closed-loop servo control system. An integrated embedded control drive module was developed based on the idea of compatibility and inter-changeability, so that DC motor and encoder were standardized into uniform models. Meanwhile, electric and mechanical interfaces were uniformed to a same standard. This allows the direct exchange of above-mentioned components between the two models. A 1-μL manual sample injection syringe was installed on both standard 110-sample and platform 40-sample liquid auto sample injectors connected with gas chromatographer. Approximately 0. 5μL of cetane-isooctyl was sampled for 6 consecutive times at six different positions in the sample bottle. The repeatability RSDs of the injection peak areas of the two systems were 1. 1% and 1. 5%, respectively. A linear correlation coefficient (0. 9947) of peak area with injection volume was achieved based on the gradient sampling volume of 0. 1, 0. 3, 0. 5, 0. 7 and 0. 9 μL.

Objective: To establish a hydrogen peroxide (H₂O₂) induced injury model of pulmonary artery endothelial cells (PAECs) and explore the molecular mechanisms of oxidative stress on the structure and function of PAECs in this model. Methods: Human PAECs were treated with H₂O₂ at different concentrations (25, 50, 100, 200, 400, 800, 1 600, 3 200, 6 400 μmol/L) for 4 and 24 h, respectively. The PAECs survival curve was obtained according to the cell viability measured by CCK-8 assay. The cell apoptosis of PAECs was detected by flow cytometry. The reactive oxygen species (ROS) generation and mitochondrial activity were measured using small molecule fluorescent probes. Proteins were extracted and the phosphorylation levels of signal molecules in PAECs were detected by Western blot assays. Results: (1) The effect of H₂O₂ at various concentrations on cell viability of PAECs: cell viability of PAECs decreased in proportion to increasing concentration of H₂O₂ after incubation for 4 h. The half maximal inhibitory concentration (IC₅₀) of PAECs exposed to H₂O₂ for 4 and 24 h were 397.00 and 488.77 μmol/L, respectively. (2) The effect of H₂O₂ on cell apoptosis of PAECs: After H₂O₂ incubation for 4 h, proportions of PAECs at late-apoptosis ((22.58±3.69) %) and necrotic stage( (11.86±4.27)%) were significantly higher than those of control PAECs at late-apoptosis stage( (3.41±1.44)%, P<0.01) and at necrotic stage ((1.94±1.15) % , P<0.05). The survival rate of PAECs post H₂O₂ was dramatically lower than that of control PAECs ((7.98±3.21)% vs. (48.89±8.08)%, P<0.01). However, there is no statistical difference between both groups regarding to the early apoptosis. (3) The effect of H₂O₂ on mitochondrial activity and ROS production of PAECs: the mitochondrial activity and ROS generation of PAECs treated by H₂O₂ were significantly increased compared to those in control PAECs (P<0.01). (4) The effect of H₂O₂ on signaling molecules in PAECs: there was a significant increase in phosphorylation level of Akt in PAECs incubated with H₂O₂ for 30 minutes compared to that in control PAECs (P<0.01), while there was no significant difference in levels of Akt between H₂O₂ treated PAECs and control PAECs. Phosphorylation level of JNK as well as p38 were also significantly upregulated in H₂O₂ treated PAECs (P<0.01). Conclusion H₂O₂ at the concentration of 400 μmol/L could induce human PAECs injuries via the regulation of Akt and MAPK signaling pathways.