The viscoelasticity of a fluid was tuned with the Faradaic reaction of (11-ferrocenylundecyl)trimethylammonium bromide (FTMA), a "redox-switchable" surfactant. An aqueous solution of the reduced form of FTMA exhibited a remarkable viscoelasticity in the presence of sodium salicylate (NaSal) because of the formation of three-dimensional entanglement of wormlike micelles. Electrolytic oxidation of FTMA caused the viscosity of the system to dramatically decrease and the elasticity to disappear. This drastic decrease in viscoelasticity arose from the disruption of wormlike micelles. This novel electrorheological phenomenon is expected to be applicable to ink for inkjet printers, the electrochemically controlled release of substances entrapped in wormlike micelles of FTMA, and fluid flow rate control using electric signals.

We report a reversible photoinduced fluid viscosity change. A small amount of a "photoswitchable" azobenzene-modified cationic surfactant (4-butylazobenzene-4'-(oxyethyl)trimethylammonium bromide, AZTMA) was added to a wormlike micellar solution of cetyltrimethylammonium bromide (CTAB) containing sodium salicylate (NaSal). The trans-AZTMA solution had a remarkably high viscosity as a result of the entangled network of wormlike micelles. UV light irradiation on the trans-AZTMA solution remarkably decreased the viscosity of the solution because the bulky structure of cis-AZTMA is likely to disrupt the network structure of wormlike micelles. This photoinduced viscosity change is perfectly reversible between the trans- and cis-AZTMA solutions.

No abstract

No abstract

We report on the design and synthesis of a green-emitting iridium complex–peptide hybrid (IPH) 4, which has an electron-donating hydroxyacetic acid (glycolic acid) moiety between the Ir core and the peptide part. It was found that 4 is selectively cytotoxic against cancer cells, and the dead cells showed a green emission. Mechanistic studies of cell death indicate that 4 induces a paraptosis-like cell death through the increase in mitochondrial Ca2+ concentrations via direct Ca2+ transfer from ER to mitochondria, the loss of mitochondrial membrane potential (ΔΨm), and the vacuolization of cytoplasm and intracellular organelle. Although typical paraptosis and/or autophagy markers were upregulated by 4 through the mitogen-activated protein kinase (MAPK) signaling pathway, as confirmed by Western blot analysis, autophagy is not the main pathway in 4-induced cell death. The degradation of actin, which consists of a cytoskeleton, is also induced by high concentrations of Ca2+, as evidenced by costaining experiments using a specific probe. These results will be presented and discussed.