4-isopropyl-2,6-bis(1-phenylethyl)aniline 1 (KTH13-AD1) is a metabolite of Cordyceps bassiana that has been traditionally used to treat various inflammatory disease. Even though it has the magnificent pharmaceutical potential, there was not much understanding on its anti-inflammatory actions. Therefore, this study was aimed to determine the anti-inflammatory effects of KTH13-AD1. We found that KTH13-AD1 suppressed nitric oxide (NO) and reactive oxygen species (ROS) production in lipopolysaccharide (LPS)- or sodium nitroprusside (SNP)-treated macrophages (RAW264.7 cells). Similarly, mRNA expression of inducible NO synthase (iNOS) and tumor necrosis factor-a (TNF-a) analyzed by RT-PCR and real-time PCR was also reduced by this compound. Interestingly, KTH13-AD1 also strongly diminished the levels of NF-kB-mediated luciferase activities and nuclear translocated NF-kB family proteins. In agreement with these, KTH13-AD1 suppressed the upstream signaling pathway for NF-kB activation including IkBa, IKKa/b, AKT, p85/PI3K and Src in time- and dose-dependent manners. Therefore, these results strongly suggest that KTH13-AD1 has a strong anti-inflammatory activity via suppression of the NF-kB signaling pathway.

A series of noble poly(amide-imide)s and copoly(amide-imide)s bearing 1,2-bis(4-phenoxy)benzene units were synthesized by the direct polycondensation of 1,2-bis(4-trimellitimidophenoxy)benzene[1,2-PTPB] with a combination of commercially available aromatic diamines and diacids such as m-phenylene diamine, p-phenylene diamine(PPD), isophthalic acid and terephthalic acid(TA) in N-methyl-2-pyrrolidone(NMP) using triphenyl phosphite and pyridine as a condensing agent in the presence of dehydrating agent (CaCl2). The resulting polymers had inherent viscosities in the range of 0.37~0.78 dL/g and most of them were soluble m common organic solvents including NMP, dimethylacetamide, dimethylsulfoxide, dimethylformamide, and m-cresol. Wide-angle X-ray diffractograms revealed that the copoly(amide-imide) derived from PPD with mixed acids of 1,2-BTPB and TA, showed crystalline nature, whereas all of the other polymers were found to be amorphous. The glass transition temperatures of the polymers occurred over the temperature range of 270~323℃ in their differential scanning calorimetry curves and their 10% weight loss temperature, determined by thermogravimetric analysis in air and nitrogen atmosphere, were in the range 465~535℃, 500~550℃, respectively, indicating their good thermal stability.

The authors have demonstrated white oraganic light-emitting diodes (WOLED) using 1,4-bis[2-(4'-diphenylaminobiphenyl-4-yl)vinyl]benzene as fluorescent blue emitter and iridium(III) bis(5-acetyl-2-phenylpyridinato-N,C2') acetylacetonate as phosphorescent red emitter. The optimized WOLED using red host material as bis(2-methyl-8-quinolinato) -4-phenylphenolate exhibited proper color stability in comparison with the control device using 4,4'-N,N'-dicarbazole-biphenyl as red host. The white device showed a maximum luminance of 21100 cd/m2 at 14 V, luminous efficiency of 9.7 cd/A at 20 mA/cm2, and Commission Internationale de I'Eclairage (CIEx,y)coordinates of (0.32, 0.34) at 1000 cd/m2. The devices also exhibited the color shift with δCIEx,y coordinates of ± (0.01,0.01) from 100 to 20000 cd/m2.

The Maillard Reaction Products (MRPs) such as Glucose-tyrosine (Glu-Tyr) and Xylose-arginine (Xyl-Arg) have antioxidant, antimutagenic, and antibacterial effects. However, to date, still little is known about the other biological effects of the MRPs. In this study, we investigated whether the fructose-tyrosine MRP, 2,4-bis(p-hydroxyphenyl)-2-butenal (Fru-Tyr), could modulate cell cycle progression and NF-κB activity, and thereby induce apoptotic cell death of colon cancer cells. Treatment with different concentrations (10-40 μg/ ml) of Fru-Tyr for 24 h inhibited colon cancer cell (SW620 and HCT116) growth followed by induction of G₂/M phase cell cycle arrest and apoptosis in a dose-dependent manner. We also found that Fru-Tyr suppressed tumor necrosis factor-alpha (TNF-α)-induced NF-κB transcriptional activity. Moreover, Fru-Tyr induced the expression of apoptotic gene, cleaved caspse-3. These results suggest that Fru-Tyr inhibited colon cancer cell growth through induction of G₂/M phase cell cycle arrest and apoptotic cell death by modulating of NF-κB.