RESUMO
Using the diaphragm-type air spring as the research object. The ratio of the vertical stiffness change caused by compressed air to the total vertical stiffness change was calculated, and it was determined that the nonlinearity of air spring vertical stiffness was mainly caused by the deformation stiffness of the rubber airbag. The variation law of vertical dynamic stiffness of air spring was predicted by theory: due to the material's viscoelasticity, the vertical dynamic stiffness rises as the excitation frequency rises, and the vertical dynamic stiffness decreases with the increase of excitation amplitude due to the damping of the material. An air spring finite element analysis (FEA) and experiment were conducted. The results show that the vertical dynamic stiffness obtained through simulation and experiment is consistent with the theoretical prediction, when various factors such as material nonlinearity, element coupling, and stiffness value sensitivity were considered. This proves that the predicted vertical dynamic stiffness variation law is reliable. The vertical dynamic stiffness obtained from both simulation and experiment showed a strong correlation in numerical values, which verified the accuracy of the FEA model of air spring established in this paper.
RESUMO
A previously identified anti-rheumatic compound α-mangostin (MAN) possesses notable metabolism regulatory properties. In this study, we investigated the immune implication of MAN-altered fat metabolism on adjuvant-induced arthritis (AIA) in rats. Seven days after AIA induction, the rats received oral treatment of MAN at 50 mg/kg/day for 30 days. Metabolic indicators and basic clinical parameters were evaluated using samples collected on day 20 and 38 since immunization. Expression of nicotinamide phosphoribosyltransferase (NAMPT), sirtuin 1 (SIRT1), peroxisome proliferator activated receptor gamma (PPAR-γ), stearoyl-coa desaturase 1 (SCD-1), toll like receptor 4 (TLR4), prostaglandin-endoperoxide synthase 2 (COX-2), (p)-JNK, (p)-p65 and IL-1ß were investigated by either RT-qPCR or immunobloting methods. In in vitro experiments, we treated (pre)-adipocytes with monocytes/macrophages and MAN, and investigated the changes of macrophages brought by pre-adipocytes co-culture. Generally, MAN restored the impaired fat anabolism in AIA rats, indicated by increased fat reservoir, leptin and adiponectin secretion, and PPAR-γ and SCD-1 expression. Meanwhile, it decreased circulating IL-1ß and IL-6 levels, restored serological lipid profile changes, and relieved oxidative stresses, demonstrating potent therapeutic effects on AIA. AIA rats-derived monocytes inhibited mRNA PPAR-γ and SCD-1 expression in pre-adipocytes. Contrarily, MAN facilitated adipocyte differentiation in vitro, and increased free fatty acids production. It also significantly increased PPAR-γ and SCD-1 expression, which can be abrogated by PPAR-γ inhibitor T0070907. Similarly, lipopolysaccharide-primed macrophages inhibited PPAR-γ expression in the co-cultured pre-adipocytes, which was reversed by MAN. In the same co-culture system, lipopolysaccharide-induced inflammation was amplified by the co-existence of pre-adipocytes. More secretion of IL-1ß and IL-6 and higher levels expression of COX-2, p-JNK, p-p65 and TLR4 were observed in lipopolysaccharide-treated macrophages when co-cultured by pre-adipocytes. The intensified inflammatory situation was eased by MAN. The treatment with pre-adipocytes culture medium achieved similar effects. Medium from lipopolysaccharide-treated adipocytes promoted IL-1ß, IL-6 and MCP-1 production in separately cultured macrophages, and COX-2, p-JNK, p-p65 and TLR4 expression were increased at the meantime. MAN treatment on pre-adipocytes impaired these changes. It suggests that fat anabolism in AIA rats was deficient due to increased energy expenditure caused by inflammatory conditions. MAN restored fat metabolism homeostasis by up-regulating PPAR-γ, and reshaped secretion profile of adipocytes.
RESUMO
BACKGROUND: The bilayer gelatin sealing sheet was developed as a safe, effective, easy-to-handle and low-cost hemostatic agent. OBJECTIVE: To examine the feasibility of gelatin sealing sheets using a canine arterial hemorrhage model. METHODS: In vivo degradation of gelatin sealing sheets was examined by implanting subcutaneously in rats. For the hemostatic and anti-adhesion efficacy investigations, femoral arteries of dogs were pricked with syringe needle to make a small hole and a gelatin (i.e. experimental group) or fibrin glue sealing sheet (i.e. control group) was applied on the hole to stop bleeding (n=8). After discontinuation of the bleeding, the skin incisions were closed and re-examined 4 weeks postoperatively. RESULTS: From the degradation study, 4 h thermally treated gelatin sheet which degraded within 3 weeks in vivo was chosen for the further hemostatic study. In all cases of gelatin and fibrin glue sealing sheets, bleeding from the needle hole on canine femoral arteries was effectively stopped. Postoperative adhesions and inflammation at the site in the experimental group were significantly less than those in the control group (P<0.01 for adhesion scores). CONCLUSIONS: The gelatin sealing sheet was found to be as effective as the fibrin glue sealing sheet as a surgical hemostatic agent, and more effective in preventing postoperative adhesions.
