Exciton binding energies in conjugated polyelectrolyte films.

Molecular design: The electronic structure of conjugated polyelectrolytes as a function of ionization potential (IP) and electron affinity (EA) is determined using X-ray absorption and emission spectroscopy (see figure). Different functional groups give rise to dissimilar transport gaps and exciton binding energies.

A Micellar Complex of a Conjugated Polyelectrolyte for Efficient FRET to Dye-Labeled DNA.

A polymer-surfactant micellar complex has been studied as a fluorescence resonance energy transfer (FRET) donor to fluorescein-labeled DNA (ssDNA-Fl). In water, the molar absorptivity and fluorescence quantum efficiency of cationic poly(fluorene-co-phenylene) (c-PFP) are substantially increased in the presence of non-ionic surfactants. A TEM microscopic study shows the formation of a nanowire micellar complex of c-PFP and the surfactants. About a 400% enhancement of the FRET signal is measured in c-PFP/ssDNA-Fl with Brij 30, relative to that without surfactants. The signal amplification is successfully modulated using different types of non-ionic surfactants which perturb the complexation, fine-structure of the complex (i.e., donor-acceptor separation), and the resulting energy transfer process.

Syntheses of hydroxy substituted 2-phenyl-naphthalenes as inhibitors of tyrosinase.

Oxyresveratrol and resveratrol, with hydroxy substituted trans-stilbene structure, exert potent inhibitory effects on cyclooxygenase, rat liver mitochondrial ATPase activity, and tyrosinase. As the isosteres of oxyresveratrol, a new family of hydroxyl substituted phenyl-naphthalenes were synthesized to show excellent inhibition of mushroom tyrosinase. Compound 10, which is isostere of resveratrol, showed IC50 value of 16.52 microM in mushroom tyrosinase activity. As compared to this, the reference compound, resveratrol, showed IC50 value of 55.61 microM. Compound 4, which is isostere of oxyresveratrol, showed IC50 value of 0.49 microM. Among the other three derivatives, compound 13 showed IC50 value of 0.034 microM.

Apoptosis and modulation of cell cycle control by synthetic derivatives of ursodeoxycholic acid and chenodeoxycholic acid in human prostate cancer cells.

The effects of synthetic derivatives of ursodeoxycholic acid (UDCA), HS-1183, and chenodeoxycholic acid (CDCA), HS-1199 and HS-1200, on the proliferation of human prostate carcinoma PC-3 cells were investigated. Whereas CDCA and UDCA had no effects on the growth of cells in a concentration range we have tested, HS-1199 and HS-1200 completely inhibited the cell proliferation, and HS-1183 showed a weak inhibitory activity. This proliferation-inhibitory effect of the synthetic bile acid derivatives was due to the induction of apoptosis, which was confirmed by observing DNA fragmentation, chromatin condensation and cleavage of PARP. Flow cytometric analysis also revealed that the synthetic bile acid derivatives arrested the cell cycle progression at the G1 phase, which effects were associated with inhibition of phosphorylation of pRB and enhanced binding of pRB and E2F-1. They also suppressed Cdk2 and cyclin E-dependent kinase activities without changes of their expressions. Furthermore, the synthetic bile acids increased the levels of Cdk inhibitor, p21WAF1/CIP1, expression and activated the reporter construct of p21WAF1/CIP1 promoter in p53-independent manner, and p21WAF1/CIP1 proteins induced by the synthetic bile acid derivatives were associated with Cdk2 and proliferating cell nuclear antigen. These distinctive features suggest that it is possible to create the new drugs useful for cancer therapy from the synthetic bile acid derivatives as lead compounds.