Enhanced electrical properties of electrospun nylon66 nanofibers containing carbon nanotube fillers and Ag nanoparticles

In this study, we describe the preparation and characterization of electrospun Nylon66 composite nanofibers incorporated with carbon nanotubes (CNT) fillers and silver nanoparticles. We have incorporated the composites in to Nylon66 nanofibers to enhance the characteristics of the resultant composite nanofibers. The resultant composite nanofibers were characterized by using field-emission scanning electron microscopy, energy dispersive X-ray analysis, high-resolution transmission electron microscopy, X-ray diffraction, and current-voltage (I–V) measurement analysis. The morphology of the composite nanofibers exhibited densely arranged mesh-like ultrafine nanofibers which were strongly bound in between the main fibers. From I–V characteristics, it was observed that the incorporation of CNT fillers and Ag nanoparticles in to electrospun Nylon66 composite nanofibers can be significantly enhanced the electrical properties.     

PTP1B Inhibitory and Anti-Inflammatory Effects of Secondary Metabolites Isolated from the Marine-Derived Fungus Penicillium sp. JF-55

Protein tyrosine phosphatase 1B (PTP1B) plays a major role in the negative regulation of insulin signaling, and is thus considered as an attractive therapeutic target for the treatment of diabetes. Bioassay-guided investigation of the methylethylketone extract of marine-derived fungus Penicillium sp. JF-55 cultures afforded a new PTP1B inhibitory styrylpyrone-type metabolite named penstyrylpyrone (1), and two known metabolites, anhydrofulvic acid (2) and citromycetin (3). Compounds 1 and 2 inhibited PTP1B activity in a dose-dependent manner, and kinetic analyses of PTP1B inhibition suggested that these compounds inhibited PTP1B activity in a competitive manner. In an effort to gain more biological potential of the isolated compounds, the anti-inflammatory effects of compounds 1–3 were also evaluated. Among the tested compounds, only compound 1 inhibited the production of NO and PGE₂, due to the inhibition of the expression of iNOS and COX-2. Penstyrylpyrone (1) also reduced TNF-α and IL-1β production, and these anti-inflammatory effects were shown to be correlated with the suppression of the phosphorylation and degradation of IκB-α, NF-κB nuclear translocation, and NF-κB DNA binding activity. In addition, using inhibitor tin protoporphyrin (SnPP), an inhibitor of HO-1, it was verified that the inhibitory effects of penstyrylpyrone (1) on the pro-inflammatory mediators and NF-κB DNA binding activity were associated with the HO-1 expression. Therefore, these results suggest that penstyrylpyrone (1) suppresses PTP1B activity, as well as the production of pro-inflammatory mediators via NF-κB pathway, through expression of anti-inflammatory HO-1.