1-Phenyl-1H-tetrazol as corrosion inhibitor for pipeline steel in sulfuric acid solution

1-Phenyl-1H-tetrazol (PHT) has been studied as an efficient corrosion inhibitor for X65 steel in sulfuric acid corrosion environment. Atomic force microscope test results show that PHT can effectively inhibit the corrosion of X65 steel in 0.5 M sulfuric acid solution. Quantum chemical calculations and molecular dynamics simulations show that PHT has a small energy gap value and a large dipole moment value, which is an excellent corrosion inhibitor. In addition, the adsorption of PHT on the Fe(110) surface adopts parallel adsorption and a large binding energy value, which shows that PHT can effectively inhibit the corrosion of X65 steel. Potentiodynamic polarization test results show that as the PHT concentration increases, the value of the corrosion current density decreases significantly. When the PHT concentration is 1 mM, the corrosion inhibition efficiency can reach 92.1%. In addition, the adsorption of PHT on the surface of X65 steel conforms to Langmuir adsorption, and the adsorption process is spontaneous

Arctigenin-induced reversal of drug resistance in cisplastin-resistant cell line A549/DDP, and the mechanism involved

Purpose: To investigate the drug resistance reversal effect of arctigenin (ARG) on cisplatin-insensitive A549/DDP cancer cells, and to elucidate the underlying mechanism(s). Methods: Four groups of cells: control, DDP, ARG and ADP were used. The degrees of inhibition of proliferation, drug resistance and apoptotic changes were measured using MTT assay, CCK-8 assay and flow cytometry, respectively. Expressions of PTEN and STAT3 proteins were determined by Western blotting. Results: At ARG concentration of 5 μmol/L, A549/DDP cells were significantly inhibited (p < 0.05). The combination therapy was more effective in reversing A549/DDP cells resistance than the single therapy. The expression level of PTEN protein increased with increase in ARG concentration, while STAT3 protein expression decreased with increase in ARG concentration. ADP group up-regulated PTEN but decreased STAT3 expression levels. Conclusion: ARG regulates drug resistance in A549/DDP cells, possibly via a mechanism involving reduction of A549/DDP cell sensitivity to DDP, thereby regulating the stress pathways associated with PTEN and STAT3. The combination of ARG and DDP effectively reduces A549/DDP cells resistance

Adsorption kinetics and thermodynamics of water-insoluble crosslinked β-cyclodextrin polymer for phenol in aqueous solution

A water-insoluble β-cyclodextrin (β-CD) polymer was synthesized by reacting β-CD with hexamethyl- ene diisocyanate, and its adsorption kinetics and thermodynamics for phenol from aqueous solution was investi- gated. The kinetics of adsorption followed the pseudo-second-order model and the adsorption isotherms could be well fitted by the Freundlich adsorption equation. The values of thermodynamic parameters demonstrated that the adsorption was a physisorption in a spontaneous and exothermic process

CDK4 regulation by TNFR1 and JNK is required for NF-κB–mediated epidermal growth control

Nuclear factor κB (NF-κB) mediates homeostatic growth inhibition in the epidermis, and a loss of NF-κB function promotes proliferation and oncogenesis. To identify mechanisms responsible for these effects, we impaired NF-κB action in the epidermis by three different genetic approaches, including conditional NF-κB blockade. In each case, epidermal hyperplasia was accompanied by an increase in both protein levels and tissue distribution of the G1 cell cycle kinase, CDK4. CDK4 up-regulation required intact TNFR1 and c-Jun NH2-terminal kinase (JNK) function. Cdk4 gene deletion concomitant with conditional NF-κB blockade demonstrated that CDK4 is required for growth deregulation. Therefore, epidermal homeostasis depends on antagonist regulation of CDK4 expression by NF-κB and TNFR1/JNK

Panax notoginseng

To investigate the therapeutic effects of PN on intestinal inflammation and microvascular injury and its mechanisms, dextran sodium sulfate- (DSS-) or iodoacetamide- (IA-) induced rat colitis models were used. After colitis model was established, PN was orally administered for 7 days at daily dosage of 1.0 g/kg. Obvious colonic inflammation and mucosal injuries and microvessels were observed in DSS- and IA-induced colitis groups. DAI scores, serum concentrations of VEGFA121, VEGFA165, VEGFA165/VEGFA121, IL-6, and TNF-α, and expression of Rap1GAP and TSP1 proteins in the colon were significantly higher while serum concentrations of IL-4 and IL-10 and MVD in colon were significantly lower in the colitis model groups than in the normal control group. PN promoted repair of colonic mucosal injury and microvessels, attenuated inflammation, and decreased DAI scores in rats with colitis. PN also decreased the serum concentrations of VEGFA121, VEGFA165, VEGFA165/VEGFA121, IL-6, and TNF-α and increased the serum concentrations of IL-4 and IL-10, with the expression of Rap1GAP and TSP1 proteins in colonic mucosa being downregulated. The constituents of PN were identified with HPLC-DAD. To sum up, PN could promote repair of injuries of colonic mucosa and microvessels via downregulating VEGFA isoforms and inhibiting Rap1GAP/TSP1 signaling pathway

New advances in catalysts for polystyrene hydrogenation

Polystyrene is one of the most widely used plastics, and could be catalytic hydrogenated to polycyclohexylethylene with improved physical properties. The research progress in the efficiency palladium catalyst for polystyrene hydrogenation was illustrated and reviewed, further development was discussed

New advances in catalysts for C9 petroleum resin hydrogenation

C9 petroleum resin is a thermoplastic polymer produced by polymerization of C9 fraction obtaining from the steam cracking unit, and could be catalytic hydrogenated to remove the ethylenic C=C bond, aromatic ring with improved physical properties. The research progress in the efficiency supported nickel or/and palladium catalysts for C9 petroleum resin hydrogenation was illustrated and reviewed, further development was discussed

Accelerated structural evolution of galaxies in a starbursting cluster at z=2.51

Structural properties of cluster galaxies during their peak formation epoch, $z \sim 2-4$ provide key information on whether and how environment affects galaxy formation and evolution. Based on deep HST/WFC3 imaging towards the z=2.51 cluster, J1001, we explore environmental effects on the structure, color gradients, and stellar populations of a statistical sample of cluster SFGs. We find that the cluster SFGs are on average smaller than their field counterparts. This difference is most pronounced at the high-mass end ($M_{\star} > 10^{10.5} M_{\odot}$) with nearly all of them lying below the mass-size relation of field galaxies. The high-mass cluster SFGs are also generally old with a steep negative color gradient, indicating an early formation time likely associated with strong dissipative collapse. For low-mass cluster SFGs, we unveil a population of compact galaxies with steep positive color gradients that are not seen in the field. This suggests that the low-mass compact cluster SFGs may have already experienced strong environmental effects, e.g., tidal/ram pressure stripping, in this young cluster. These results provide evidence on the environmental effects at work in the earliest formed clusters with different roles in the formation of low and high-mass galaxies.Comment: 13 pages, 10 figures, 1 tabl

PRIMA-1Met suppresses colorectal cancer independent of p53 by targeting MEK

This work was supported by Grant No. 81201779 (Hua Xiong) from the National Natural Science Youth Foundation; Grant No. 81502118 (Yanmei Zou) from the National Natural Science Youth Foundation; Grant No. 2014CFB250 (Yanmei Zou) from the Natural Science Foundation of Hubei Province; Grant No. 81372434 (Huihua Xiong) from the National Natural Science Foundation.PRIMA-1Met is the methylated PRIMA-1 (p53 reactivation and induction of massive apoptosis) and could restore tumor suppressor function of mutant p53 and induce p53 dependent apoptosis in cancer cells harboring mutant p53. However, p53 independent activity of PRIMA-1Met remains elusive. Here we reported that PRIMA-1Met attenuated colorectal cancer cell growth irrespective of p53 status. Kinase profiling revealed that mitogen-activated or extracellular signal-related protein kinase (MEK) might be a potential target of PRIMA-1Met. Pull-down binding and ATP competitive assay showed that PRIMA-1Met directly bound MEK in vitro and in cells. Furthermore, the direct binding sites of PRIMA-1Met were explored by using a computational docking model. Treatment of colorectal cancer cells with PRIMA-1Met inhibited p53-independent phosphorylation of MEK, which in turn impaired anchorage-independent cell growth in vitro. Moreover, PRIMA-1Met suppressed colorectal cancer growth in xenograft mouse model by inhibiting MEK1 activity. Taken together, our findings demonstrate a novel p53-independent activity of PRIMA-1Met to inhibit MEK and suppress colorectal cancer growth.Publisher PDFPeer reviewe