A Study on Preparation and Property Evaluations of Composites Consisting of TPU/Triclosan Membranes and Tencel®/LMPET Nonwoven Fabrics.

This study investigated eco-friendly antibacterial medical protective clothing via the nonwoven process and characteristic evaluations. Firstly, Tencel® fibers and low melting point polyester (LMPET) fibers (re-sliced and granulated from recycled PET bottles) were mixed at different ratios and then needle punched at diverse needle rolling depths. The influences of manufacturing parameters on the Tencel®/LMPET nonwoven fabrics were examined in terms of mechanical properties, water vapor transmission rate, and stiffness. Next, Tencel®/LMPET nonwoven fabrics were combined with thermoplastic polyurethane (TPU)/Triclosan antibacterial membranes that contained different contents of triclosan using melt processing technology. The resulting Tencel®/LMPET/TPU/Triclosan composites were characterized via different measurements; an optimal bursting strength of 86.86 N, an optimal horizontal tensile strength of 41.90 N, and an optimal stiffness along the MD and CD of 8.60 cm were recorded. Furthermore, the Tencel®/LMPET/TPU/Triclosan composites exhibited a distinct inhibition zone in the antibacterial measurement, and the hydrostatic pressure met the requirements of the EN 14126:2003 and GB 19082-200 disposable medical protective gear test standards.

Thyroid hormone receptor-mediated regulation of the methionine adenosyltransferase 1 gene is associated with cell invasion in hepatoma cell lines.

The thyroid hormone T(3) regulates differentiation, growth, and development. We demonstrated that methionine adenosyltransferase 1A (MAT1A) was positively regulated by T(3) identified by cDNA microarray previously. The expression of the MAT1A was upregulated by T(3) in hepatoma cell lines overexpressing thyroid hormone receptors (TRs). Additionally, these findings indicate that MAT1A may be regulated by CCAAT/enhancer binding protein (C/EBP). The critical role of the C/EBP binding sites was confirmed by the reporter or chromatin immuno-precipitation (ChIP) assay. In addition, C/EBP was upregulated in hepatoma cells after T(3) treatment and ectopic expression of MAT1A inhibited cell migration and invasion in J7 hepatoma cells. Conversely, knockdown of MAT1A expression increased cell migration. Together, these findings suggest that the expression of the MAT1A gene is mediated by C/EBP and is indirectly upregulated by T(3). Finally, TR was downregulated in a small subset of hepatocellular carcinoma cells concomitantly reduced the expression of C/EBPalpha and MAT1A.