Very bright blue organic light emitting diodes were fabricated using highly fluorescent dipyrazolopyridine derivatives, 4-(4-substituted phenyl)-1,7-diphenyl-3,5-dimethyl-1,7dihydrodipyrazolo[3,4-b,4′,3′-e]pyridine (PAP–X, X=CN, Ph, and OMe), as emitter by doping the dye in an electron-transporting host, 2,2′,2″-(1,3,5-benzenetriyl)tris-[1-phenyl-1H-benzimidazole] (TPBI). Two hole-transporting layers, 4,4′-bis[N-(1-naphthyl-1-)-N-phenyl-amino]-biphenyl (NPB) and 4,4′-dicarbazolyl-1,1′-biphenyl (CBP) were used to achieve the emission from PAP–X. The devices with a general configuration of indium tin oxide/NPB/CBP/TPBI:PAP(2%)/Mg:Ag showed a bright blue emission. The PAP–CN-based device is exceptionally good, with a brightness of 11 200 cd/m2 at 14.2 V and the peak external quantum efficiency of 3.2%. The efficiency is the highest for the blue emission.

Starburst amorphous compounds as hole‐transporting materials in light‐emitting devices are investigated here. In addition, the synthesis by Stille's palladium‐catalyzed cross‐coupling reaction (see Figure) of these compounds—benzene molecules with six peripheral diarylthienylamine moieties—is reported as are their physical and electrochemical properties.

Star-shaped compounds containing a triphenylamine as the central core and three diphenylthienylamines (NAr 1 Ar 2 (th): 3a, Ar 1 ) Ar 2 ) Ph; 3b, Ar 1 ) Ph and Ar 2 ) 3-tolyl; 3c, Ar 1 ) Ph and Ar 2 ) 1-naphthyl; 3d, NAr 1 Ar 2 ) carbazolyl) as the peripheral functional groups have been synthesized and characterized. These compounds exhibit four successive reversible one-electron redox processes except for 3d in which only two one-electron reversible oxidation waves are observed. The compounds 3a-d can be used as hole transport materials, and electroluminescent devices ITO/3/Alq [tris(8-quinolinolato)aluminum]/Mg:Ag emit green light characteristic of Alq. The device ITO/3d/BCP (bathocuproine)/Alq/Mg:Ag is blue emitting, in which 3d is the luminophore.

Acetylcholinesterase inhibitors (AChEI's) are used to treat Alzheimer's disease (AD), and the putative mode of action is to increase acetylcholine (ACh) levels. Our goal is to evaluate competition of ACh with nicotinic alpha4beta2 receptor PET agonist radiotracer, 2-[(18)F]fluoro-3-[2-((S)-3-pyrrolinyl)methoxy]pyridine ((18)F-nifene). This ability to measure ACh-(18)F-nifene competition may have potential to assess efficacy of AChEI's in vivo. In vitro studies in rat brain slices used two AChEI's, physostigmine (PHY) and galanthamine (GAL). Brain slices were incubated with (18)F-nifene and various concentrations of PHY (0.2-20 microM) or GAL (0.4-4 microM) prior to (18)F-nifene treatment. For ACh competition, slices were also incubated with PHY + 100 nM ACh or GAL + 100 nM ACh or 100 nM ACh alone. Nonspecific binding of (18)F-nifene was determined using 300 microM nicotine. In the in vitro rat brain homogenate binding assay, ACh inhibited (3)H-cytisine binding to alpha4beta2 receptors with K(i) values of 19.2 nM (with PHY) and 34.7 microM (no PHY) indicating approximately 1.8 x 10(3) weaker binding of ACh in the absence of AChEI. Binding of (18)F-nifene was not affected by PHY (0.2-20 microM) or ACh 100 nM alone but decreased substantially by PHY + ACh 100 nM in all brain regions (down by >40% of control in thalamus). Similarly, for GAL (4 microM) no effect on (18)F-nifene binding occurred but GAL (0.4-4 microM) + ACh 100 nM showed a reduction of (18)F-nifene binding in all brain regions (down by approximately 15%). The reduction in both cases is a result of ACh competition with (18)F-nifene in the presence of AChEI. These preliminary in vitro results suggest that ACh is able to compete with (18)F-nifene at the alpha4beta2 receptors in the presence of PHY or GAL. The effect is AChEI-concentration dependent and is greater for PHY than GAL. Thus (18)F-nifene has promise for assessing ACh levels and AChEI effects in vivo.