Presence Of 2c Research Articles

Elevated temperature performance and creep behavior of Y2O3 reinforced Ti-48Al-6Nb alloy at the brittle-ductile transition temperature

This study investigated the elevated temperature properties and creep behavior of Y2O3-bearing Ti-48Al-6Nb alloy. Tensile and creep tests of Ti-48Al-6Nb and Ti-48Al-6Nb-0.05Y2O3 alloys were performed. The results show that the brittle-ductile transition temperatures (BDTTs) of both alloys are determined to be 825–850 ℃ by tensile tests at the strain rate of 5 × 10−4 s−1. And the BDTTs of both alloys are determined to be 800–825 ℃ by creep tests under a constant stress of 325 MPa, reducing about 25 ℃ due to the slower creep rates. Y2O3 improves the creep properties of the alloys by refining α2/γ lamellar spacing, decreasing segregation and preventing dislocation movement. Furthermore, creep deformation behavior of α2 phases at the BDTT was discussed. Deformation of α2 laths during creep is mainly provided by a→ type dislocations below the BDTT. While above the BDTT, 2c→+a→ type dislocations were activated due to the active thermal activation and decreasing Peierls-Nabarro stress. The presence of 2c→+a→ slip systems in α2 laths contributes to ductile deformation during creep.

Adsorption and inhibition mechanism of (Z)-4-((4-methoxybenzylidene)amino)-5-methyl-2,4-dihydro-3H-1,2,4-triazole-3-thione on carbon steel corrosion in HCl: Experimental and theoretical insights

Although the number of reported corrosion inhibitors has increased steeply in recent years, global corrosion damages raised the need for highly effective, new promising compounds for corrosion protection of metals and their alloys. Herein, chemical and electrochemical testing methods like weight loss, electrochemical impedance spectroscopy (EIS) and potentiodynamic polarization (PDP) measurements were applied to evaluate the inhibition performance and adsorption mechanism of (Z)-4-((4-methoxybenzylidene)amino)-5-methyl-2,4-dihydro-3H-1,2,4-triazole-3-thione (2C) against carbon steel (CS) corrosion 1.0 M HCl. Together, electrochemical results and morphological evidence from scanning electron microscope (SEM) demonstrated that, in the presence of 2C, the inhibition efficiency reaches a maximum of 86% at 10−3, forming a compact protective layer on CS surface. On the other hand, corrosion inhibition decreases a little with the rise of the temperature. The investigated compound was classified as a mixed class inhibitor, affecting both anodic and cathodic reactions, while its adsorption followed the Langmuir adsorption isotherm. Molecular dynamics (MD) simulations and quantum chemical calculations were used to give further insights into the inhibiting action of 2C and to explain its mechanism of action. Scanning electron microscopy (SEM) reveals an enhanced surface morphology of carbon steel after the addition of the tested compound to the electrolyte.

Enterovirus 2C Protein Suppresses IKKα Phosphorylation by Recruiting IKKβ and IKKα into Viral Inclusion Bodies.

The nuclear factor-kappa B (NF-κB) signaling network constitutes a first line of defense against the invading viruses. However, viruses also adopted multiple strategies to interfere with NF-κB activation. Enterovirus 71 (EV71), in the family Picornaviridae, has become the main pathogen responsible for hand, foot, and mouth disease. Recent studies have reported that the nonstructural protein 2C of EV71 inhibits TNF-α induced NF-κB activation by suppressing IKKβ phosphorylation. In our study, we found that 2C can form inclusion bodies (IBs) in infected and transfected cells. Furthermore, 2C was able to sequester IKKβ into IBs through direct interaction with IKKβ. Although 2C did not directly interact with IKKα, viral protein 2C was able to sequester the IKKα into the IBs mediated by IKKβ. Our in vitro data further demonstrated that EV71 2C could suppress IKKα phosphorylation. These all together support a novel mechanism for EV71 to escape from NF-κB response, in which the phosphorylation of IKKα was suppressed by being recruited into viral IBs in the presence of 2C and IKKβ.

The identification of a small molecule compound that reduces HIV-1 Nef-mediated viral infectivity enhancement.

Nef is a multifunctional HIV-1 protein that accelerates progression to AIDS, and enhances the infectivity of progeny viruses through a mechanism that is not yet understood. Here, we show that the small molecule compound 2c reduces Nef-mediated viral infectivity enhancement. When added to viral producer cells, 2c did not affect the efficiency of viral production itself. However, the infectivity of the viruses produced in the presence of 2c was significantly lower than that of control viruses. Importantly, an inhibitory effect was observed with Nef+ wild-type viruses, but not with viruses produced in the absence of Nef or in the presence of proline-rich PxxP motif-disrupted Nef, both of which displayed significantly reduced intrinsic infectivity. Meanwhile, the overexpression of the SH3 domain of the tyrosine kinase Hck, which binds to a PxxP motif in Nef, also reduced viral infectivity. Importantly, 2c inhibited Hck SH3-Nef binding, which was more marked when Nef was pre-incubated with 2c prior to its incubation with Hck, indicating that both Hck SH3 and 2c directly bind to Nef and that their binding sites overlap. These results imply that both 2c and the Hck SH3 domain inhibit the interaction of Nef with an unidentified host protein and thereby reduce Nef-mediated infectivity enhancement. The first inhibitory compound 2c is therefore a valuable chemical probe for revealing the underlying molecular mechanism by which Nef enhances the infectivity of HIV-1.

Synthetic 3-Arylidenefl avanones as Inhibitors of the Initial Stages of Biofilm Formation by Staphylococcus aureus and Enterococcus faecalis

The antimicrobial activity of twenty two synthetic flavonoids is reported. Among them three 3-arylideneflavanones, 2b, 2c, and 2i, were shown to be highly active against Staphylococcus aureus, S. epidermidis, and Enterococcus faecalis reference strains, with MIC (minimal inhibitory concentration) values ranging from 4.68 microg/ml (14.3 microM) to 37.5 microg/ml (119.7 microM). The synergy of oxacillin and vancomycin with 2c, evaluated as fractional inhibitory concentration index (FICI) was shown (against planktonic culture of S. aureus A3 and E. faecium 138/09 clinical strains). The presence of 2c in the culture medium diminished the initial adhesion of bacteria to an abiotic surface. Such an effect resulted in a decrease in biofilm formation during prolonged culture. Unfortunately, 2e failed to eradicate the S. aureus mature biofilm which was already preformed, however, decreased the number of live biofilm cells. The biofilm of E. faecalis was more susceptible to the action of 3-arylideneflavanone 2c than the S. aureus biofilm. The finding that 3-arylideneflavanones are lipophilic, cause bacterial aggregation, and influence the integrity of membranes making them permeable to SYTO 9/propidium iodide dyes may implicate the cytoplasmic membrane as a target site for these compounds activity.

THE ROLE OF ??4 INTEGRIN/FIBRONECTIN INTERACTIONS IN ALLOSPECIFIC CYTOTOXIC CELL ACTIVATION AND HOMING-INITIAL STUDIES IN THE 2C T-CELL RECEPTOR TRANSGENIC

431 For allograft rejection to occur, alloreactive T cells must become activated and migrate to the graft site. Interactions between integrin adhesion molecules and their ligands are believed to be important in both processes. The purpose of this study was to develop a model in which T cell activation and homing could be monitored independently in vivo. We then tested the model using a peptide inhibitor of α4 integrin/fibronectin (FN) interactions thought to specifically inhibit T cell homing without affecting activation. Methods. The 2C T cell receptor transgenic provides a purified alloreactive CD8+ cytotoxic T cell(CTL) population (B6 background) with specificity for the Class I MHC(Ld) of the BALB/c mouse. To study allorejection in vivo, we used an adoptive transfer model of allograft rejection. B6-scid recipients were made diabetic with streptozotocin and transplanted with BALB/c islets under the renal capsule. Islets in non-reconstituted recipients survived indefinitely. The adoptive transfer of 2 × 106 2C splenic CTL led to rejection within 14 days. CTL homing was defined as the presence of 2C+ T cells in the islet allograft both histologically and by flow cytometry of the graft 10 days after transplantation. CTL activation was defined as the phenotypic expression of activation markers(IL2-receptor and LFA-1) on 2C+ cells in reconstituted animals in vivo 10 days after transplantation. Since naive 2C CTL express α4 integrin (as measured by flow cytometry), we chose to study α4/FN interactions in homing and activation using a specific pentapeptide inhibitor of α4/FN adhesion termed connecting segment 1 peptide (CSI-P) via continuous infusion Alzet pumps (15mg/kg/d × 14 days). Results. Prior to injection, the 2C T cells expressed very low, but detectable levels of IL2R and LFA-1. In B6-scid mice who did not receive a BALB/c graft, adoptively-transferred 2C cells did not show phenotypic signs of activation (negative control). In B6-scid recipients of BALB/c islet allografts (positive control), the 2C cells in the spleen showed signs of activation (high expression of IL2R and LFA-1). In addition, the islet allograft was infiltrated with large numbers of 2C+ T cells. CS1-P completely blocked 2C CTL homing to the islet allograft at 10 days after transplantation. In contrast, CS1-P did not block 2C CTL activation eitherin vivo (phenotypic evidence of 2C activation was found in CS1-P treated B6-scid recipients of BALB/c islet grafts) or in vitro (2C CTL proliferation in response to BALB/c stimulator cells was not blocked by CS1-P). Importantly, CS1-P treatment significantly delayed the 2C-mediated rejection of BALB/c islet grafts (14.7±3.3 controls vs 29.5±4.4 d, p<0.01). Conclusion. We conclude that this 2C adoptive transfer model of allograft rejection is useful in assessing both CTL activation and homingin vivo. These data suggest that α4/FN interactions are critically important for CTL homing to the graft, but do not significantly affect activation. Thus, CS1-P may represent a unique class of immunosuppressive agents that prolongs allograft survival by inhibiting CTL homing.

THE ROLE OF α4 INTEGRIN/FIBRONECTIN INTERACTIONS IN ALLOSPECIFIC CYTOTOXIC T CELL ACTIVATION AND HOMING-INITIAL STUDIES IN THE 2C T-CELL RECEPTOR TRANSGENIC.

431 For allograft rejection to occur, alloreactive T cells must become activated and migrate to the graft site. Interactions between integrin adhesion molecules and their ligands are believed to be important in both processes. The purpose of this study was to develop a model in which T cell activation and homing could be monitored independently in vivo. We then tested the model using a peptide inhibitor of α4 integrin/fibronectin (FN) interactions thought to specifically inhibit T cell homing without affecting activation. Methods. The 2C T cell receptor transgenic provides a purified alloreactive CD8+ cytotoxic T cell (CTL) population (B6 background) with specificity for the Class I MHC (Ld) of the BALB/c mouse. To study allorejection in vivo, we used an adoptive transfer model of allograft rejection. B6-scid recipients were made diabetic with streptozotocin and transplanted with BALB/c islets under the renal capsule. Islets in non-reconstituted recipients survived indefinitely. The adoptive transfer of 2× 106 2C splenic CTL led to rejection within 14 days. CTL homing was defined as the presence of 2C+ T cells in the islet allograft both histologically and by flow cytometry of the graft 10 days after transplantation. CTL activation was defined as the phenotypic expression of activation markers (IL2-receptor and LFA-1) on 2C+ cells in reconstituted animals in vivo 10 days after transplantation. Since naive 2C CTL express α4 integrin (as measured by flow cytometry), we chose to study α4/FN interactions in homing and activation using a specific pentapeptide inhibitor of α4/FN adhesion termed connecting segment 1 peptide (CS1-P) via continuous infusion Alzet pumps (15mg/kg/d× 14 days). Results. Prior to injection, the 2C T cells expressed very low, but detectable levels of IL2R and LFA-1. In B6-scid mice who did not receive a BALB/c graft, adoptively-transferred 2C cells did not show phenotypic signs of activation (negative control). In B6-scid recipients of BALB/c islet allografts (positive control), the 2C cells in the spleen showed signs of activation (high expression of IL2R and LFA-1). In addition, the islet allograft was infiltrated with large numbers of 2C+ T cells. CS1-P completely blocked 2C CTL homing to the islet allograft at 10 days after transplantation. In contrast, CS1-P did not block 2C CTL activation either in vivo(phenotypic evidence of 2C activation was found in CS1-P treated B6-scid recipients of BALB/c islet grafts) or in vitro (2C CTL proliferation in response to BALB/c stimulator cells was not blocked by CS1-P). Importantly, CS1-P treatment significantly delayed the 2C-mediated rejection of BALB/c islet grafts (14.7±3.3 controls vs 29.5±4.4 d, p<0.01). Conclusion. We conclude that this 2C adoptive transfer model of allograft rejection is useful in assessing both CTL activation and homingin vivo. These data suggest that α4/FN interactions are critically important for CTL homing to the graft, but do not significantly affect activation. Thus, CS1-P may represent a unique class of immunosuppressive agents that prolongs allograft survival by inhibiting CTL homing.

Influence of Hexasulfonated Calix[6]arenes on the Reactivities of Arenediazonium Ions in an Aqueous System

Abstract The pKa of Phenol Blue shifted from 4.6 to 6.2 because of complexation of protonated Phenol Blue in the cavity of hexasulfonated calix[6]arene with dodecyl substituents (2C12). The finding stimulated us to examine whether the analogs (2C) suppress the dediazoniation of arenediazonium ions in an aqueous system as crown ethers do in organic solvents. We have found that 2C can suppress the dediazoniation in an aqueous system where neither 18-crown-6 nor anionic micelles are effective. The magnitude of the inhibition effect was 4–5 fold. The reaction rate of the diazo coupling with N,N-dimethylaniline was significantly suppressed in the presence of 2C, suggesting that arenediazonium ions are deactivated through complexation with 2C. The novel stabilization effects were explained by the strong anionic reaction field which neither 18-crown-6 nor anionic micelles have: that is, 2C has a peculiar architecture that six sulfonato groups are circularly arranged on the edge of the calixarene cavity.