Exciton-Scissoring Perfluoroarenes Trigger Photomultiplication in Full Color Organic Image Sensors.

An unprecedented but useful functionality of perfluoroarenes to enable exciton scissoring in photomultiplication-type organic photodiodes (PM-OPDs) is reported. Perfluoroarenes that are covalently connected to polymer donors via a photochemical reaction enable the demonstration of high external quantum efficiency and B-/G-/R-selective PM-OPDs without the use of conventional acceptor molecules. The operation mechanism of the suggested perfluoroarene-driven PM-OPDs, how covalently bonded polymer donor:perfluoroarene PM-OPDs can perform as effectively as polymer donor:fullerene blend-based PM-OPDs, is investigated. By employing a series of arenes and conducting steady-state/time-resolved photoluminescence and transient absorption spectroscopy analyses, it is found that interfacial band bending between the perfluoroaryl group and polymer donor is responsible for exciton scissoring and subsequent electron trapping, which induces photomultiplication. Owing to the acceptor-free and covalently interconnected photoactive layer in the suggested PM-OPDs, superior operational and thermal stabilities are observed. Finally, finely patterned B-/G-/R-selective PM-OPD arrays that enable the construction of highly sensitive passive matrix-type organic image sensors are demonstrated.

Magnetic interaction of Janus magnetic particles suspended in a viscous fluid.

We studied the magnetic interaction between circular Janus magnetic particles suspended in a Newtonian fluid under the influence of an externally applied uniform magnetic field. The particles are equally compartmentalized into paramagnetic and nonmagnetic sides. A direct numerical scheme is employed to solve the magnetic particulate flow in the Stokes flow regime. Upon applying the magnetic field, contrary to isotropic paramagnetic particles, a single Janus particle can rotate due to the magnetic torque created by the magnetic anisotropy of the particle. In a two-particle problem, the orientation of each particle is found to be an additional factor that affects the critical angle separating the nature of magnetic interaction. Using multiparticle problems, we show that the orientation of the particles has a significant influence on the dynamics of the particles, the fluid flow induced by the actuated particles, and the final conformation of the particles. Straight and staggered chain structures observed experimentally can be reproduced numerically in a multiple particle problem.

17beta-Estradiol inhibits calcium-dependent, but not calcium-independent, contraction in isolated rat aorta.

It is now well known that 17beta-estradiol has an endothelium-independent, non-genomic vasorelaxant effect. We hypothesized that 17beta-estradiol has its non-genomic effect on calcium-independent contraction in de-endothelialized rat aortic rings. Rat aortic ring preparations were mounted in organ baths and exposed to contractile agents. 17beta-Estradiol (8, 20 or 50 microM), but not 17alpha-estradiol, concentration-dependently decreased the tension induced by 1.0 microM phenylephrine (PE) in the presence, but not in the absence, of calcium in the solution. Pretreatment with 17beta-estradiol concentration-dependently inhibited vascular contractions induced by cumulative addition of PE or calcium and almost completely abolished those induced by cumulative addition of Bay K8644, a calcium channel opener. Furthermore, 17beta-estradiol also concentration-dependently decreased the tension induced by 0.3 microM phorbol 12,13-dibutyrate (PDBu), a protein kinase C activator, in the presence of calcium in the solution, but not in the absence of calcium in the solution. Pretreatment with 17beta-estradiol had little effect on vascular contractions induced by PDBu or PE or on PE-induced mitogen-activated protein kinase (MAPK) activation in calcium-free Krebs solution. These results suggest that 17beta-estradiol inhibits calcium-dependent, but not calcium-independent, vascular contraction.

Enhanced contractility of vascular smooth muscle after brief exposure to arsenate.

Epidemiological studies indicate that arsenic exposure induces hypertension. We hypothesized that arsenate exposure modulates the contractility of vascular smooth muscle through the stress response. Intraperitoneal injection of sodium arsenate (15mg/kg) 16h before increased not only the blood pressure of rats but also the pressor response to preganglionic nerve stimulation (2 and 16Hz) or to bolus injection of vasopressin or phenylephrine in pithed rats as compared with the control rats. Exposure of rat aortic rings to 4mM sodium arsenate for 60min enhanced the contractile responses to KCl or phenylephrine as well as the HSP 70 expression 8h later, but did not affect the relaxation responses to acetylcholine, histamine, or sodium nitroprusside. These results suggest that brief exposure to arsenate is associated with enhanced contractility of vascular smooth muscle through the stress response.

Endothelial dysfunction after exposure to cobalt chloride enhanced vascular contractility.

Brief exposure to cobalt chloride augmented vascular contractility. We hypothesized that endothelial dysfunction plays a role in the augmentation of aortic contractility, after brief exposure to cobalt chloride. Rat aortic ring preparations were mounted in organ baths, exposed to cobalt chloride (0.3-300µmol/L) for 30min, and then subjected to contractile agents or relaxants 1 and 5h after the end of exposure. Presence of cobalt chloride did not affect the contractile response to phenylephrine. Brief exposure to cobalt chloride, however, even at 5h after the end of exposure, not only augmented contractile responses to KCl or phenylephrine but also attenuated the relaxant response to acetylcholine. The mechanical denudation of endothelium or inhibition of endothelial nitric oxide synthase with 100µmol/L N(ω)-nitro-l-arginine methyl ester abolished the augmentation of contractile responses. Pre-treatment with 150units/mL of superoxide dismutase also abrogated the augmented contractile responses. Brief exposure to cobalt chloride did not affect the contractile response to phorbol dibutyrate in the presence or absence of calcium, or the expression of HSP70. In conclusion, endothelial dysfunction plays an important role in the augmentation of aortic contractility, after brief exposure to cobalt chloride.