A new small-molecular thermally cross-linkable material {[4-(9-phenyl-9H-carbazol-4-yl)phenyl]-bis-(4′-vinylbiphenyl-4-yl)-amine} (PCP-bis-VBPA, PbV) containing the styrene moiety was synthesized for hole transport layers in wet processed organic light-emitting diodes (OLEDs). It was found that PbV exhibited relatively high glass temperatures above 154 °C and a triplet energy (T 1 ) greater than 2.81 eV. This new synthetic hole transport material (HTM) forms very uniform films after crosslinking reaction with little pin-holes, although it was smallmolecule-based cross-linkable HTM. However, to solve the certain minor non-uniformity caused by pinholes with various sizes, a semi-interpenetrating network was formed with well-known polymeric HTM with high mobility [e.g., poly(9,9-dioctylfluorene-co-N-(4-butylphenyl)diphenyl amine), TFB, or poly(N,N′-bis-4-butylphenyl-N,N′-bisphenyl)benzidine, poly-TPD]. As a result, we successfully fabricated red phosphorescent OLED showing an efficiency of about 16.7 cd/A and 12.4% (external quantum efficiency) if we applied PbV blended with 20% of TFB or poly-TPD. In particular, the efficiency and lifetime are significantly improved by 1.5 and 4.5 times, respectively, compared to those of the control device without using blended HTM.

No abstract

Apoptosis is a process of active cell death characterized by cell surface blebbing, changes in membrane permeability, nuclear DNA condensation, and internucleosomal fragmentation.1) Several apoptotic pathways exist in cells responsive to apoptotic stimuli, and although each pathway is initiated by different mechanisms, they share a common final phase of apoptosis, which involves the activation of executioner caspases and the dismantling of substrates critical for cell survival.2) Classical apoptosis can be initiated via two distinct biochemical mechanisms, both of which result in caspase activation: (i) the extrinsic pathway that involves ligation of cell surface death receptors by their respective ligands, and (ii) the intrinsic mitochondrial pathway, which is largely controlled by the Bcl-2 family of pro-and anti-apoptotic proteins. It has been well established that the expressions of many gene products, such as Bid, Bax and Bcl-2, are critical for programmed cell death. Bcl-2 and Bcl-xl have anti-apoptotic functions, whereas Bid, Bax, Bim and Bcl-xs promote apoptosis. The balance between these two groups of genes determines the fate of cells in many systems, 3) and in particular, determines the depolarization of the mitochondrial membrane and the release of cytochrome c from mitochondria into the cytosol.4) This released cytochrome c then binds to apoptotic protease activating factor-1 (Apaf-1), which causes its oligomerization. 5) Procaspase-9 then binds to Apaf-1 oligomers to form a high-molecular-mass complex called apoptosome.6) In addition, this interaction activates caspase-9, which activates caspase-3 and thus triggers the irreversible apoptotic program. 7)Donepezil (R,S-1-benzyl-4-[(5,6-dimethoxy-1-indanon)-2-yl]methylpiperidine hydrochloride) is prescribed for the treatment of cognitive dysfunction in Alzheimer's disease (AD).8) It prevents the hydrolysis of acetylcholine (ACh) and elevates ACh concentrations in the synaptic cleft, which increases cholinergic transmission.9) Previous studies haveshown that donepezil has neuroprotective effects in addition to its AChE-inhibiting action, and that these effects are due to the stimulation of nicotinic acetylcholine receptors, the activation of the phosphoinositide-3 kinase/Akt pathway, and the up-regulation of the anti-apoptotic protein Bcl-2. 10,11) However, no report has been issued on the molecular mechanism underlying the anti-proliferative effects of donepezil.In the present study, we demonstrate that donepezilinduced apoptosis involves the mitochondrial pathway via loss of mitochondrial membrane potential, a hallmark of permeability transition, and that this causes the release of cytochrome c to cytosol, and the sequential activations of caspases-8, -9, and -3 via the modulation of Bcl-2 in human promyelocytic leukemia HL-60 cells. Furthermore, this is the first report to show that donepezil induces apoptosis through a mitochondria-mediated caspase-dependent pathway. Hoegi-dong, Dongdaemun-gu, Seoul 130-701, Republic of Korea: and d Eisai Korea ...

DMAC-DPS showing AIE behavior increased TTA and STA, whereas Ph-OBNA showing ACQ behavior showed relatively small TTA and STA values due to the generation of excimers.

Previously, we reported that (E)-8-acetoxy-2-[2-(3,4-diacetoxyphenyl)ethenyl]-quinazoline (8-ADEQ), a synthetic analogue of resveratrol had anti-inflammatory and G2/M cell cycle arrest activities, but the underlying molecular mechanism of cytotoxic effects of this compound was not determined. In this study, 8-ADEQ displayed potent cytotoxicity and triggered apoptosis in HL-60 cells as evidenced by DNA fragmentation, DNA ladder formation, and the externalization of Annexin V-targeted phosphatidylserine residues in HL-60 cells. In addition, 8-ADEQ triggered activation of caspases-8, -9, -6 and -3 and cleavage of their substrates such as poly(ADP-ribose) polymerase (PARP). Moreover, 8-ADEQ induced loss of mitochondrial membrane potential (MMP) and release of cytochrome c to the cytosol. Caspase-3 inhibitor (z-DEVD-fmk), caspase-8 inhibitor (z-IETD-fmk), caspase-9 inhibitor (z-LEHD), and broad caspase inhibitor (z-VAD‑fmk) significantly suppressed the 8-ADEQ-induced DNA fragmentation. Interestingly, pretreatment with z-IETD-fmk, a caspase-8 inhibitor, completely abolished 8-ADEQ-induced caspase-3 and -9 activation, and subsequent DNA fragmentation. 8-ADEQ also increased the expression of Fas, Fas-associated death domain (FADD) and FasL, and formation of death-inducing signaling complex (DISC). Further analysis revealed that 8-ADEQ-induced apoptosis was mediated by upregulation of reactive oxidative species (ROS) generation. Taken together, our data indicated that 8-ADEQ-stimulated apoptosis in HL-60 leukemia cells is due to a Fas-mediated caspase-8-dependent pathway via ROS generation, but also, to a lesser extent cytochrome c release and caspase-9 activation.