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Polyurethane (PU) has become one of the most widely used materials in the industrial field due to its excellent performance and wide range of applications. The increasing consumption of polyurethane materials has resulted in significant polyurethane waste. We can recycle waste polyurethane to obtain recycled polyurethane, but to make the recycled polyurethane meet different performance requirements in terms of utility and cost and enable the recycled polyether polyol to be further applied to high-end applications, it is necessary to improve the use value of recycled polyether polyol. In this paper, self-made Fluorodiol was added to the degradation process of waste polyurethane to obtain fluorinated regenerated polyether polyol. Recycled fluorinated polyurethane with excellent performance was prepared using fluorine-containing recycled polyether polyol. The regenerated fluorinated polyether polyols were characterized by infrared spectroscopy, viscosity, hydroxyl value, and GPC molecular weight distribution. The density, apparent morphology, water absorption, mechanical strength, thermal conductivity, and thermal stability of RFPU rigid foams with different fluorine contents were studied by scanning electron microscopy. The results show that when the addition of Fluorodiol was 8% of the mass of waste polyurethane, the density was 41.2 kg/m3, the immersion loss rate was 2.125%, the compressive strength was 0.315 Mpa, and the thermal conductivity was 0.0227 W/m·K. The RFPU prepared by Fluorodiol has low surface energy, good compressive strength, hydrolysis resistance, and is expected to be widely used in special insulation materials. Thus, the sustainable recycling of polyurethane is achieved.

Previous studies show that several pathways are involved in sanguinarine-induced apoptotic cell death, including AKT downregulation, inhibition of NF-kB activation, mediation of ROS production, downregulation of anti-apoptosis proteins XIAP and cIAP-1, upregulation of BAX, and downregulation of BCL2. In this study, we found out that the quenching of ROS generation by N-acetyl-l-cysteine (NAC), a scavenger of ROS, reversed sanguinarine-induced apoptosis effects, also we found out that sanguinarine-induced rat hepatic stellate T6 cells (HSC-T6 cells) apoptosis was correlated with the generation of increased ROS, which was followed by the activation of caspase-8 (-3, -6, and -9), and the decreasing in the miltochondrial membrane potential (MMP) and the down-regulation of anti-apoptotic protein Bcl-2. It is not clear whether BCL2's downregulation relates to its promoter methylation and miR-15a/16-1 expression which can bind to BCL2 3'-UTR (un-translation reagon). We showed that sanguinarine-induced down regulation of BCL2 was associated with the increased methylation rate of BCL2 promotor district and the increased expression of miR-15a/16-1. HSC-T6 cells treatment with 5-Aza-2'-deoxycytidine (5'-Aza-CdR) impeded sanguinarine-induced BCL2 promotor district methylation and recovered BCL2's expression. Over expression of BCL2 using pEGFP-N1 vector decreased sanguinarine-induced HSC-T6 cells apoptotic death significantly but not completely. These observations clearly showed that BCL2 down regulation was associated with its promoter methylation and miR-15a/16-1 upregulation in sanguinarine-induced Rat HSC-T6 cells.

Although sanguinarine (SANG) can be transformed to dihydrosanguinarine (DHSA) in human and animals, the enzyme involved in the imine bond reduction of SANG is still unknown. In this study, we found that rat NAD(P)H:quinone oxidoreductase 1 expressed by prokaryotic system can transform SANG to DHSA in an NADPH dependent manner. We also found out that there was more DHSA in rAAV-NQO1 infected than rAAV-CYP1A1 and rAAV-control infected BRL cells. SANG decreased rat BRL cell proliferation and augmented cell apoptosis in a time and dose dependent manner. However, the influence of DHSA to BRL cells is not significant difference than SANG. SANG-induced apoptosis was correlated with the up-regulation of Bax/Bcl2 ratio and the down-regulation of Bcl2. SANG can also dose dependently down regulate NQO1 expression, but CYP1A1 expression was a little up regulated. Since CYP1A1 involving in SANG oxidative reactions and NQO1 involving in the transform of SANG to DHSA, we hypothesized that up regulation of NQO1 could reduce SANG cytotoxicity and up regulation of CYP1A1 could increase SANG cytotoxitity. Our further study showed that recombinant adeno-associated virus (rAAV) mediated overexpression of NQO1 significantly increased cell proliferation and decreased Bax/Bcl2 ratio, apoptosis, and cytotoxicity, whereas rAAV mediated CYP1A1 overexpression had opposite effects. These data illustrated that NQO1 involved in the imine bond reduction of sanguinarine and this was a less toxic metabolizing pathway than CYP1A1-metabolizing pathway.

The purpose of this study was to investigate the possibility that oxidative stress was involved in danofloxacin-induced toxicity in renal tubular cells epithelial cell line (LLC-PK1). Confluent LLC-PK1 cells were incubated with various concentrations of danofloxacin. The extent of oxidative damage was assessed by measuring the reactive oxygen species (ROS) level, lipid peroxidation, cell apoptosis and antioxidative enzyme activities. Danofloxacin induced a concentration-dependent increase in the ROS production, not even cytotoxic conditions. Similarly, danofloxacin caused an about 4 times increase in the level of thiobarbituric acid reactive substances at the concentration of 400 μM for 24 hr, but it did not induce cytotoxicity and apoptosis. Antioxidant enzymes activities, such as superoxide dismutase (SOD) and catalase (CAT), were increased after treatment with 100, 200 and 400 μM of danofloxacin for 24 hr. The activity of glutathione peroxidase (GPX) was significantly decreased in a concentration-dependent manner. In addition, ROS production, lipid peroxidation and GPX decline were inhibited by additional glutathione and N-acetyl cysteine. These data suggested that danofloxacin could not induce oxidative stress in LLC-PK1 cells at the concentration (≤400 μM) for 24 hr. The increase levels of ROS and lipid peroxidation could be partly abated by the increase activities of SOD and CAT.

Background Inhibiting the action of proprotein convertase subtilisin/kexin type 9 (PCSK9) on the low-density lipoprotein receptor (LDLR) has emerged as a novel therapeutic target for hypercholesterolemia. Here we investigated the effect of berberine, natural plant extracts, on PCSK9-LDLR pathway in C57BL/6 mice with lipopolysaccharide (LPS) induced inflammation. Methods Forty female mice were divided into four groups (n = 10): control, LPS (5 mg/kg), LPS + berberine 10 (5 mg/kg LPS plus 10 mg/kg berberine), and LPS + berberine 30 (5 mg/kg LPS plus 30 mg/kg berberine). Changes in the levels of blood lipids [total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C)]; pro-inflammatory cytokines [interferon-γ (IFNγ), tumor necrosis factor α (TNFα), and interleukin-1α (IL-1α)], 8-isoprostane, hepatic expressions of PCSK9 and LDLR were determined. Results Berberine pretreatment reduced the expression of hepatic PCSK9, decreased the plasma TC, TG, LDL-C, IFNγ, TNFα, IL-1α, and 8-isoprostane concentrations; increased HDL-C level and LDLR expression in mice. Conclusion The present results suggest that berberine inhibits dyslipidemia in C57BL/6 mice with LPS induced inflammation through regulating PCSK9-LDLR pathway.

In order to analyze the different construction program under the tunnel surrounding rock stress, strain and plastic zone changes, we take water tunnel group of nuclear power plant as basic project and the application of software FLACIS3D numerical simulation.The results show that: During the tunnel excavation and support group process, the different rock tunnel construction program can produce different stress, displacement and plastic zone extended range of distribution and other aspects.To interval-type excavation program,although previously disturbing effect of the excavation of the tunnel construction and tunnel excavation of rock, it can generate less impact on the stability of surrounding rock. For the latter excavation of the tunnel, the tunnel project area affected by the first digging,the stress can be released, the stability of the first excavation of the tunnel effect is also small.Comparing to sequential and parallel program-type excavation program, the use of interval-style group of rock tunnel excavation will help stabilize the body.

In order to study the rule of highway subgrade settlement, both on-site experiments and theoretical analysis methods were used to analysis high fill embankment settlement. Gray model theory can be effectively forecasted the embankment of the different stages and the final settlement. According to the measured data of deposition tests, the comparative analysis of predicted results was carried out and some conclusions were drawn: 1) It is feasible that gray model theory is used to predict the settlement of the subgrade; 2) gray theory predictions adapt to these situations that similar information is less known, uncertainties and some rock deformation issues; 3)gray prediction accuracy is higher. The prediction model of GM established (1, 1) is reliable.

Mastitis is the inflammation of the mammary gland. Recent research has shown that Angiopoietin-like protein 2 (ANGPTL2) is a key inflammatory mediator. In the present study, we tested whether there is a correlation between increased ANGPTL2 expression and inflammation in response to Staphylococcus aureus in murine mastitis and the mechanisms involved. Thirty mice were divided into two groups: blank control group, challenged group. The entire infused mammary glands were removed to observe the changes of histopathology, myeloperoxidase (MPO) activity, production of tumour necrosis factor-α (TNF-α) and interleukin (IL)-6, and genes expression of ANGPTL2, TNF-α and IL-6. In challenged group, the structure of mammary glands was damaged and the large areas of cell fragments were observed. The MPO activity, IL-6 and TNF-α concentrations, ANGPTL2, IL-6, and TNF-α mRNA levels were significantly elevated in challenged group compared with blank control group. The present findings indicate ANGPTL2 may mediate the inflammation in murine mastitis through the activation of IL-6 and TNF-α.