Polymerization of styrene in alcoholic media in the presence of poly(jV-vinylpyrrolidone) (PVP) produces monodisperse latex particles from 1 to 18 µ in size. The results are rationalized in the context of a mechanism involving grafting of polystyrene chains to PVP steric stabilizer. Increasing the initial styrene concentration from 5 to 40% by volume increases the particle size obtained. Comparison of this effect to that of added toluene suggests that the primary effect of monomer concentration is a solvent effect: the more soluble the polystyrene is in the reaction medium, the larger the particles. The influence of PVP concentration and molecular weight was found to obey the approximate relationship dso = 90.4[PVP]~°'31MW~°•18. The power law dependence of diameter on initiator concentration was found to be 0.39, in good agreement with prior work. The addition of a chain-transfer agent produced polydisperse particles with molecular weight dispersities (Mw/Mn) of ca. 100, modifying the power law dependence of size on initiator concentration to a slope of 0.19. A maximum in particle size was found in a series of solvents varying from 80% ethanol/water to ethanol and from methanol to decanol, with 4-µ particles obtained in butanol and pentanol, 1.2-µ particles in 80% ethanol/water, and 1.6-µ particles in decanol. The molecular weights correlated inversely with particle size and could be semiquantitatively rationalized on the basis of the locus of polymerization shifting from particle capture of growing oligomers from the continuous phase in the case of smaller particles to particle capture of dead polymer in the case of large particles.

The major hurdle in the fight against cancer is the non-specific nature of current treatments. The search for specific drugs that are non-cytotoxic to normal cells and can effectively target cancer cells has lead some researchers to investigate the potential anti-cancer activity of natural compounds. Some natural compounds, such as Taxol, have been shown to possess some anti-cancer potential. Pancratistatin (PST) is a natural compound that was isolated from the spider lily Pancratium littorale and shown to exhibit antineoplastic activity. The specificity of PST to cancer cells and the mechanism of PST's action remain unknown. This study provides a detailed look at the effect of PST treatment on cancerous and normal cells. Our results indicate that PST induced apoptosis selectively in cancer cells and that the mitochondria may be the site of action of PST in cancer cells. A biochemical target available specifically in cancer cells may lead to the development of new and more effective cancer fighting agents.

Recently a major research effort has been focused on the development of anticancer drugs by targeting the components of a biochemical pathway to induce apoptosis in cancerous cells. Some of the natural products (e.g. paclitaxel) have been proven to be useful in inducing apoptosis in cancer cells with limited specificity. Pancratistatin, a natural product isolated and characterized over a decade ago, has been shown to be cytostatic and antineoplastic. We investigated the specificity and biochemical mechanism of action of pancratistatin. Pancratistatin seemed to show more specificity than VP-16 or paclitaxel as an efficient inducer of apoptosis in human lymphoma (Jurkat) cells, with minimal effect on normal nucleated blood cells. Caspase-3 activation and exposure of phosphatidyl serine on the outer leaflet of the plasma membrane were earlier events than the generation of ROS and DNA fragmentation observed following pancratistatin treatment. This indicates a possible involvement of caspase-3 and plasma membrane proteins in the induction phase of apoptosis. Our results indicate that pancratistatin does not cause DNA double-strand breaks or DNA damage prior to the execution phase of apoptosis in cancer cells. Parallel experimentation with VP-16, a currently used medication for cancer treatment, indicated that VP-16 causes substantial DNA damage in normal non-cancerous blood cells, while pancratistatin does not cause any DNA double-strand breaks or DNA damage in non-cancerous cells. Taken together, our finding that pancratistatin induces apoptosis in cancer cells using non-genomic targets, and more importantly does not seem to have any affect non-cancerous cells, presents a significant platform to develop non-toxic anticancer therapies.

The discovery of a complex-induced proximity effect and scope of regioselective ylide formation on acetal- and ketal-functionalized trialkylphosphine-derived phosphonium salts is explored as a route to homologated unsaturated carbonyl derivatives.

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