ABSTRACT
Objective Based on the existing clinical drainage device, two novel mechanisms were designed for the connection between the drainage tube of the patient and the drainage tube of the drainage bag, so as to compare such two mechanisms and validate whether the mechanisms can meet the design requirements for clinical use. Methods Mechanism 1 used the method of electromagnetic drive to pull in and Mechanism 2 used the magnetization method of permanent magnet to pull in. The finite element model of static electromagnetic field was established. The force of the two mechanisms under different currents was compared, and the distribution of magnetic field lines and magnetic induction intensity was analyzed. Simulation experiments were designed for preliminary experimental research. Results Under the pull-in state, the maximum magnetic induction of Mechanism 1 and Mechanism 2 at the closed end surface was found in contact area of the two iron cores. The suction force of Mechanism 1 could be adjusted by the current. When the current was 1 A, the maximum magnetic induction intensity at the closed end was 0.76 T, the electromagnetic force measured by the experiment was 6.08 N, the magnetic force of Mechanism 2 was 6.68 N, which was smaller than the 8 N suture tension. Mechanism 2 was separated by supplying the driving coil with a reverse magnetic field. Conclusions When the current was 1 A, Mechanism 1 could meet the magnetic attraction requirements, and Mechanism 2 could be separated when the current reached 1.8 A. Both mechanisms met the requirements of clinical design, but Mechanism 2 was more secure in the process of application. The feasibility of the mechanism structure was verified by finite element analysis and experimental test.
ABSTRACT
Objective@#To explore effect of AMP-activated protein kinase (AMPK) /mammalian target of rapamycin (mTOR) /ribosomal protein S6 kinase-1 (S6K1) signaling pathways and the insulin-sensitizing effect by adiponectin in endometrial cancer HEC-1B cells.@*Methods@#The experiments were divided into 4 groups, adiponectin (Ad) group (HEC-1B cells treated with 20 μg/ml adiponectin for 30 minutes) , inhibitor group (HEC-1B cells treated with 10 μmol/L compound C for 30 minutes) , inhibitor+ Ad group (HEC-1B cells treated with 10 μmol/L compound C for 30 minutes following incubation with 20 μg/ml adiponectin for 30 minutes) , control group (only added the culture medium without serum DMEM) . (1) Real-time quantitative PCR and western blot analysis were used to detect the level of mRNA and protein of adiponectin receptor (AdipoR) 1 and AdipoR2. (2) Western blot analysis were used to detect phosphorylation of AMPK, mTOR, S6K1 or insulin receptor substrate 1 (IRS1) protein expression with stimulation in different concentrations of adiponectin (2.5, 5, 10, and 20 μg/ml) , or following incubation with insulin 50 nmol/L for 5 minutes; or treated with 20 μg/ml adiponectin for different times (15, 30, 45, and 60 minutes) , or following incubation with insulin 50 nmol/L for 5 minutes. (3) Cell counting kit-8 (CCK-8) assay was performed to investigate the cell proliferation, and transwell chamber assay was used to detect the cell migration in different groups.@*Results@#(1) The relative expression level of AdipoR1 mRNA and protein were higher than AdipoR2 in HEC-1B cell (8.50±0.09 to 1.00±0.00, and 0.91±0.03 to 0.69±0.03; P<0.05) . (2) The phosphorylation level of p-AMPK was significantly induced, and the phosphorylation level of p-mTOR and p-S6K1 proteins, and 20 μg/ml adiponectin at 30 minutes, AMPK protein had the highest level of activation. (3) Adiponectin induces increased tyrosine phosphorylation of IRS1 in a time-and concentration-dependent manner. (4) The proliferation inhibition ratio in Ad group (0.68±0.34) % was much more than that in inhibitor+Ad group (0.24±0.04) % (t=17.88, P<0.05) . The number of cell migration in Ad group (77±8) was much more than that in inhibitor+Ad group (132±13; t=-7.34, P<0.05) .@*Conclusions@#Adiponectin maybe inhibit proliferation and migration of endometrial cancer cells through AMPK/mTOR/S6K1 signal pathway. Adiponectin insensitizes insulin signaling may by regulating by the AMPK/S6K1/IRS1 pathway.