MicroRNA-33b inhibits liver cancer cell proliferation, migration and invasion via down-regulation of Fli-1 and MMP-2 protein expressions

Purpose: To study the influence of microRNA-33b (miR-33b) on liver cancer cell proliferation, migration and invasiveness, and the mechanism involved. Methods: MicroRNA-33b or Fli-1 overexpression plasmid was transfected into liver cancer (SMMC7721) cells. Cell proliferation, migration, and invasiveness were determined using cell counting kit 8 (CCK-8), scratch test, and Transwell invasion assay, respectively. The amounts of miR-33b and Fli-1 in liver cancer tissues,  paracancerous normal tissues, and miR-33b overexpression and control groups were measured using qRT-PCR, while protein concentration of matrix metalloproteinase 2 (MMP-2) was assayed using Western blotting. Results: Fli-1 protein was markedly upregulated in liver cancerous cells, relative to paracancerous normal tissues (p < 0.05). MicroRNA-33b protein expression was also significantly upregulated in miR33b overexpression group, but the corresponding Fli-1 expression was downregulated in miR-33b overexpression group, relative to control (p < 0.05). MicroRNA-33b overexpression significantly and time-dependently inhibited SMMC7721 cell proliferation and migration, but it reduced the degree of apoptosis (p < 0.05). Liver cancer (SMMC7721) cells in miR-33b overexpression group were less invasive than the control group (p < 0.05). Similarly, miR-33b overexpression significantly downregulated MMP-2 protein expression in SMMC7721cells (p < 0.05). Conclusion: Overexpression of miR-33b suppresses the proliferation, migratory and invasive potential of hepatic cancer cells via down-regulation of Fli-1 and MMP-2 protein expression. This finding may be useful in the identification of new liver cancer drugs

Knowledge-Assisted Dual-Stage Evolutionary Optimization of Large-Scale Crude Oil Scheduling

With the scaling up of crude oil scheduling in modern refineries, large-scale crude oil scheduling problems (LSCOSPs) emerge with thousands of binary variables and non-linear constraints, which are challenging to be optimized by traditional optimization methods. To solve LSCOSPs, we take the practical crude oil scheduling from a marine-access refinery as an example and start with modeling LSCOSPs from crude unloading, transportation, crude distillation unit processing, and inventory management of intermediate products. On the basis of the proposed model, a dual-stage evolutionary algorithm driven by heuristic rules (denoted by DSEA/HR) is developed, where the dual-stage search mechanism consists of global search and local refinement. In the global search stage, we devise several heuristic rules based on the empirical operating knowledge to generate a well-performing initial population and accelerate convergence in the mixed variables space. In the local refinement stage, a repair strategy is proposed to move the infeasible solutions towards feasible regions by further optimizing the local continuous variables. During the whole evolutionary process, the proposed dual-stage framework plays a crucial role in balancing exploration and exploitation. Experimental results have shown that DSEA/HR outperforms the state-of-the-art and widely-used mathematical programming methods and metaheuristic algorithms on LSCOSP instances within a reasonable time

中国财政政策调整的宏观经济效应——基于消费者异质性的新凯恩斯模型

This paper construct the NK model with Cosummer’s Heterogeneity included three sectors, in which government is divided into three type of fiscal sector, social security department and central bank. The tax shocks, social security fees rate shock and fiscal expenditure shock are incorporated with the NK model to explord the contribution and the dynamic effect of the fiscal policy shocks on macroeconomic volatility. The results show that (1) the shocks of good taxation contribute most in real economy than the shocks of other fiscal policy, and the size of contribution on macroeconomic volatility is 65%; (2) reducing of the tax rates, social security fees rate and fiscal spending stimulate economic growth, and it is more important that cutting the tax rate of labour income and lowering social security fees rate are better measures; (3) cutting tax rates and lowering of social security fees rate improve the fiscal sustainability; (4)the inflation is a joint monetary-fiscal phenomenon. On this basis, this paper propose that government should adopt active tax and fee policies---cutting labour income taxation rate and lower social security fees rate, to spur stable economic growth, simultaneously raise benchmark interest rate to prevent inflation

中国财政政策调整的宏观经济效应——基于消费者异质性的新凯恩斯模型

This paper construct the NK model with Cosummer’s Heterogeneity included three sectors, in which government is divided into three type of fiscal sector, social security department and central bank. The tax shocks, social security fees rate shock and fiscal expenditure shock are incorporated with the NK model to explord the contribution and the dynamic effect of the fiscal policy shocks on macroeconomic volatility. The results show that (1) the shocks of good taxation contribute most in real economy than the shocks of other fiscal policy, and the size of contribution on macroeconomic volatility is 65%; (2) reducing of the tax rates, social security fees rate and fiscal spending stimulate economic growth, and it is more important that cutting the tax rate of labour income and lowering social security fees rate are better measures; (3) cutting tax rates and lowering of social security fees rate improve the fiscal sustainability; (4)the inflation is a joint monetary-fiscal phenomenon. On this basis, this paper propose that government should adopt active tax and fee policies---cutting labour income taxation rate and lower social security fees rate, to spur stable economic growth, simultaneously raise benchmark interest rate to prevent inflation

Progress in the clinical treatment of keloids

Keloid is a pathological scar that is higher than the skin surface following skin damage. Its lesion range often extends beyond the original damage boundary and does not naturally subside over time. Its pathogenesis is very complex, currently the main causes include fibroblast excessive proliferation, collagen and extracellular matrix (Extracellular matrix, ECM) excessive deposition, excessive angiogenesis, and so on. The traditional treatment method primarily involves surgical intervention, but it is associated with a high recurrence rate post-surgery. Consequently, many treatment methods are derived according to the different clinical characteristics of keloid. This paper will review the therapeutic progress in recent years from surgical treatment, physiotherapy, drug therapy, and biological therapy, with the goal of offering valuable insights for the clinical treatment of keloids

α-Mangostin protects against myocardial ischemia reperfusion injury by suppressing the activation of HIF-1α

Purpose: To investigate the cytoprotective effect of α-mangostin on myocardial tissues in ischemic rats, and the underlying mechanism.Methods: Histopathological changes in myocardial tissues were determined using inverted microscope. Protein expressions were measured by western blotting, while enzyme-linked immunosorbent assay (ELISA) was used to assay the expression levels of caspase-3, caspase-9 and caspase-8.Results: Treatment with α-mangostin (20 mg/kg) suppressed production of reactive oxygen species (ROS) and lipid peroxides in myocardial tissues of MI/R rats, and significantly alleviated MI/R injurymediated reduction in ATP levels in cardiac tissues (p < 0.05). α-Mangostin treatment of MI/R injury rats suppressed HIF-1α activation, and markedly elevated BNIP3 levels, relative to model group. Moreover, MI/R-induced cardiomyocyte apoptosis was significantly alleviated by α-mangostin treatment (p < 0.05). Treatment with α-mangostin also suppressed I/R-induced increases in caspase-8 and caspase-3 activation in myocardial tissues, improved Nrf-2 activation, and promoted HO-1 and GST levels in MI/R injury rats (p < 0.05).Conclusion: These results suggest that α-mangostin protects rat cardiac tissues from MI/R-induced oxidative damage via reduction of HIF-1α expression, inhibition of ROS generation and suppression of apoptosis. Therefore, α-mangostin may be of therapeutic importance for the management of myocardial ischemia in humans. Keywords: α-Mangostin, Hypoxia, Inflammation, Nrf-2, Oxidative stress, Reperfusio