In order to achieve high-precision pneumatic cylinder friction test, this paper proposes a new direct measurement method based on electric cylinder in which the axially acting forces from the compressed air in the two facing pneumatic cylinders cancel each other out and the detected value of the force transducer is just friction. For the sake of the implementation of the method, a new low-cost test method for identifying deadband of proportional directional valve was proposed, and a set of fuzzy PI constant pressure control system was designed to cope with a certain degree of leakage in the chamber. Based on the above, a friction test platform with two pneumatic cylinders facing each other was eventually built to study the influence of pressure, pressure difference, and piston speed on the friction of two commonly used different types of pneumatic cylinders. Through multiple sets of tests, it is found that when the lip seals are used in pairs between the piston and the inner wall of the cylinder, the friction between the piston and the cylinder is only related to the sum of the two chamber pressures, but not to the pressure difference between the two chambers; When the O-ring seal is used between the piston and the inner wall of the cylinder, the friction between the piston and the cylinder is related not only to the pressure of the two chambers, but also to the pressure difference between the two chambers. In addition, a series of comparative tests with the traditional single-cylinder friction test method directly demonstrate the effectiveness of the proposed new method.

No abstract

No abstract

Background The resistance to epidermal growth factor receptor (EGFR)- tyrosine kinase inhibitors (TKIs) therapy is currently the major clinical challenge in the treatment of lung cancer. This study aims to reveal the role of glucagon-like peptide (GLP) 2 and GLP-2 receptor (GLP2R) signaling on the EGFR-TKIs and cisplatin resistance of lung cancer cells. Methods The common differentially expressed genes in PC9 and HCC827 cells that were individually resistant to one of the three EGFR-TKIs (dacomitinib, osimertinib and afatinib) were screened. The data were from GSE168043 and GSE163913. The expression of GLP2R in drug-resistant cells was detected by western blot. The effect of GLP2R expression down- or up-regulation on resistance to dacomitinib, osimertinib, afatinib or cisplatin was measured by CCK-8 and flow cytometry assays. The long-acting analog of GLP-2, teduglutide, treated the parental cells. Results A total of 143 common differentially expressed genes were identified. Compared with the parent cells, the GLP2R expression in drug-resistant cell lines was significantly up-regulated. The exogenous expression of GLP2R in parental cells enhanced cell viability, while knockdown of GLP2R levels in drug-resistant cell lines inhibited cell viability. In addition, teduglutide treatment also enhanced the viability of lung cancer cells. Conclusion GLP2-GLP2R signal may change the sensitivity of cells to EGFR-TKIs and cisplatin. The development of GLP-2 or GLP2R inhibitors may be beneficial to the clinical treatment of lung cancer.

No abstract