Hexane extract of Persea schiedeana Ness as green corrosion inhibitor for the brass immersed in 0.5 M HCl.

The hexane extract of Persea schiedeana Ness (PSN) was analyzed as corrosion inhibitor for the brass surface immersed in 0.5 M HCl. Fourier-transform infrared spectroscopy and a gas chromatographic (GC) and mass spectrometric (MS) were used to identify the PSN extract's functional groups and compound constituents. The functional groups identified were CH 3 and CH 2 functional alkyl groups, C=O stretching vibration of aldehydes, ketones, and carbonyl groups. The GC/MS determined the presence of fatty acids in the PSN extract, where palmitic acid, oleic acid, and ethyl oleate were the major constituents. Electrochemical characterizations were conducted to observe the effect of PSN as corrosion inhibitor on the brass surface. The Rp and Rn calculated from EIS and ENA give the same behavior. Based on the OCP behavior, it was determined that the PSN works as a mix inhibitor, affecting both anodic and cathodic reactions. The corrosion current density (Icorr) suggests that the extract of PSN reduces the corrosion rate of the brass with efficiencies above 90% for all concentrations. The efficiency obtained for each PSN concentration was attributed to forming a corrosion scale of CuO and Cu 2 O , which reacted with the carboxyl group to form copper carboxylates on the metal surface.

TGF-ß1 signaling inhibit the in vitro apoptotic, infection and stimulatory cell response induced by influenza H1N1 virus infection on A549 cells.

Influenza A virus (IAV) infection induces host cell responses that could derive in inflammatory and apoptotic response. In this respect, in multiple pathological situations, TGF-ß1 has shown anti-inflammatory effect, but its role during IAV infection is poorly understood. Interestingly, recent profiling expression studies have suggested that the TGF-ß1 pathway could be functionally related to the IAV infection's host response. To gain an understanding of the involvement of TGF-ß1's signaling pathway during IAV infection, we compared different apoptotic proteins such as TNFR1, Fas ligand, XIAP, cIAP, among others proteins, and pro-inflammatory elements like IL-1ß in the A549 cells during IAV infection (H1N1/NC/99), with and without 1 h of pre-treatment with TGF-ß1. Pre-incubation with TGF-ß1 significantly inhibited apoptosis and the presence of pro-apoptotic factors. Moreover, the relative abundance of immunodetected IAV M1 protein along 24 -h post-infection period was abridged, which correlated with a disminished infectious viral progeny Additionally, caspase 1 activation and increase of IL-1ß induced by IAV infection was also reduced by TGF-ß1 signaling activation. Whereas IAV infection increase of Smad-7 and, as consequence, partially inhibiting Smad2/3 phosphorylation, pre-treatment with TGF-ß1 blocked IAV-dependent Smad7 induction and prevented Smad2/3 signaling shutdown. All these data suggest the role of TGF-ß1 signaling pathway in the control of host cell response induced by the IAV infection and identify a potential clinical target to modulate acute cell death.