Effect of upflow and downflow baffle configuration on particulate matter removal in a mirror-symmetrical multi-compartment scrubber.

Control over particulate matter (PM) emission from grilling is required for improving public health and air quality. The performance of mirror-symmetrical multi-compartment scrubbers with an upflow (U-type) and downflow baffle (D-type) configuration was evaluated for PM emission control from grilling at a flow rate of 30 m3 min-1. The PM removal efficiency of the U-type scrubber was the highest when the water level was 8 cm (95.6%), and the pressure drops recorded at the water levels of 6, 8 and 10 cm were 103, 122 and 153 mmH2O, respectively. Although PM removal efficiency of the D-type scrubber was over 91.0% at the water levels of 8, 10 and 12 cm, the pressure drops were 124, 142 and 185 mmH2O, respectively. A comprehensive evaluation of the water volume, pressure drop and PM removal performance, as well as device size, revealed that the U-type scrubber with a PM removal efficiency of 92% or higher and a pressure drop of 122 mmH2O or lower at the water levels of 6-8 cm was more economical for removing PM from grilling gas than the D-type scrubber.

Diphenylaminoarylvinyl-Substituted Diphenylanthracenes for Organic Light-Emitting Diodes.

Two blue fluorescent materials based on diphenylaminoarylvinyl-substituted diphenylanthracene have been synthesized. Multilayered organic light-emitting diodes (OLED) with the following sequence; ITO/NPB (50 nm)/Blue materials (30 nm)/Bphen (30 nm)/Liq (2 nm)/Al (100 nm) were fabricated using these materials as emitters. Two devices exhibited blue electroluminescence. Particularly, a device using 6-(4-(10-phenylanthracen-9-yl)styryl)-N,N-diphenylnaphthalen-2-amine (2) exhibited blue emission with a luminance efficiency, a power efficiency, an external quantum efficiency and CIE coordinates of 5.69 cd/A, 1.99 lm/W, 3.39% at 100 mA/cm² and (x = 0.19, y =0.31) at 8.0 V, respectively.

Synthesis of Benzo[g]quinoline Derivatives and Their Electroluminescent Properties.

Two fluorescent benzo[g]quinoline derivatives were synthesized via Friedländer synthesis. Multilayered OLEDs using benzo[g]quinoline derivatives as the emitters showed unexpected emissions by electroplexes. Particularly, a device using 2-(naphthalen-3-yl)-4-phenylbenzo[g]quinoline as an emitting material exhibited efficient emission with a luminous efficiency, a power efficiency, an external quantum efficiency, and CIE coordinates of 3.58 cd/A, 1.11 lm/W, 1.08% at 20 mA/cm², and (0.36, 0.56) at 1,000 cd/m², respectively.

Effects of intramuscular morphine in men and women with temporomandibular disorder with myofascial pain.

OBJECTIVES: This placebo-controlled randomized double-blinded clinical study assessed the analgesic efficacy of intramuscular morphine in TMD patients with myofascial pain and sex-dependent responses of the morphine treatment. SUBJECTS AND METHODS: Men and women with TMD were treated with morphine (1.5 or 5 mg), lidocaine, or saline in the masseter muscle. VAS of pain intensity, PPT, and PPtol were compared between treatment groups and gender. An additional group was treated with morphine in the trapezius muscle to evaluate the systemic effect of morphine that may reduce pain in the masseter muscle. RESULTS: There was a significant difference in VAS scores between the morphine 5 mg group and the saline group favoring morphine, but not between the morphine 5 mg and lidocaine. Morphine 1.5 and 5 mg treatments led to consistently and significantly elevated PPT and PPtol measures in men, but not in women. Morphine administered in the trapezius muscle did not affect the outcome measures. CONCLUSION: A single dose intramuscular morphine produced analgesic effects up to 48 hr in patients with myofascial pain. Intramuscular morphine elevated mechanical pain threshold and tolerance in the masseter only in male patients, suggesting sex differences in local morphine effects. No systemic effect of intramuscular morphine was detected.

Effects of Melatonin and Its Underlying Mechanism on Ethanol-Stimulated Senescence and Osteoclastic Differentiation in Human Periodontal Ligament Cells and Cementoblasts.

The present study evaluated the protective effects of melatonin in ethanol (EtOH)-induced senescence and osteoclastic differentiation in human periodontal ligament cells (HPDLCs) and cementoblasts and the underlying mechanism. EtOH increased senescence activity, levels of reactive oxygen species (ROS) and the expression of cell cycle regulators (p53, p21 and p16) and senescence-associated secretory phenotype (SASP) genes (interleukin [IL]-1ß, IL-6, IL-8 and tumor necrosis factor-α) in HPDLCs and cementoblasts. Melatonin inhibited EtOH-induced senescence and the production of ROS as well as the increased expression of cell cycle regulators and SASP genes. However, it recovered EtOH-suppressed osteoblastic/cementoblastic differentiation, as evidenced by alkaline phosphatase activity, alizarin staining and mRNA expression levels of Runt-related transcription factor 2 (Runx2) and osteoblastic and cementoblastic markers (glucose transporter 1 and cementum-derived protein-32) in HPDLCs and cementoblasts. Moreover, it inhibited EtOH-induced osteoclastic differentiation in mouse bone marrow⁻derived macrophages (BMMs). Inhibition of protein never in mitosis gene A interacting-1 (PIN1) by juglone or small interfering RNA reversed the effects of melatonin on EtOH-mediated senescence as well as osteoblastic and osteoclastic differentiation. Melatonin blocked EtOH-induced activation of mammalian target of rapamycin (mTOR), AMP-activated protein kinase (AMPK), mitogen-activated protein kinase (MAPK) and Nuclear factor of activated T-cells (NFAT) c-1 pathways, which was reversed by inhibition of PIN1. This is the first study to show the protective effects of melatonin on senescence-like phenotypes and osteoclastic differentiation induced by oxidative stress in HPDLCs and cementoblasts through the PIN1 pathway.

N-methyl-D-aspartate (NMDA) impairs myogenesis in C2C12 cells.

INTRODUCTION: N-methyl-d-aspartate (NMDA) is expressed in sensory neurons and plays important roles in peripheral pain mechanisms. The aim of this study was to examine the effects and molecular mechanisms of NMDA on C2C12 myoblast proliferation and differentiation. METHODS: Cytotoxicity and differentiation were examined by the MTT assay, reverse transcription-polymerase chain reaction, and immunofluorescence. RESULTS: NMDA had no cytotoxicity (10-500 µM) and inhibited myoblastic differentiation of C2C12 cells, as assessed by F-actin immunofluorescence and levels of mRNAs encoding myogenic markers such as myogenin and myosin heavy-chain 2. It inhibited phosphorylation of mammalian target of rapamycin (mTOR) by inactivating mitogen-activated protein kinases (MAPKs), including extracellular signal-regulated kinase, c-Jun N-terminal kinase, and p38. It induced reactive oxygen species production. Furthermore, NMDA-suppressed expression of F-actin was reversed by adding the antioxidant N-acetylcysteine. CONCLUSIONS: Collectively, these results indicate that NMDA impairs myogenesis or myogenic differentiation in C2C12 cells through the mTOR/MAPK signaling pathways and may lead to skeletal muscle degeneration. Muscle Nerve 56: 510-518, 2017.

HIF-2 Inhibition Supresses Inflammatory Responses and Osteoclastic Differentiation in Human Periodontal Ligament Cells.

Recent reports suggest that hypoxia inducible factor-2α (HIF-2α) is a key regulator of osteoarthritis cartilage destruction. However, the precise role of HIF-2α in the inflammatory response and osteoclast differentiation remains unclear. The purpose of this study was to investigate the effect of HIF-2α on inflammatory cytokines, extracellular matrix (ECM) destruction enzymes, and osteoclastic differentiation in nicotine and lipopolysaccharide (LPS)-stimulated human periodontal ligament cells (PDLCs). HIF-2α was upregulated in chronically inflamed PDLCs of periodontitis patients, and in nicotine- and LPS-exposed PDLC in dose- and time-dependent manners. HIF-2α inhibitor and HIF-2α siRNA attenuated the nicotine- and LPS- induced production of NO and PGE2 , upregulation of iNOS, COX-2, pro-inflammatory cytokines (IL-1ß, TNF-α, IL-1ß, IL-6, IL-8, IL-10, IL-11, and IL-17), and matrix metalloproteinases (MMPs; MMP-1, -8, -13, -2 and -9), and reversed the effect on TIMPs (TIMP-1 and -2) in PDLCs. The conditioned medium produced by nicotine and LPS-treated PDLCs increased the number of TRAP-stained osteoclasts, TRAP activity and osteoclast-specific genes, which has been blocked by HIF-2α inhibition and silencing. HIF-2α inhibitor and HIF-2α siRNA inhibited the effects of nicotine and LPS on the activation of Akt, JAK2 and STAT3, ERK and JNK MAPK, nuclear factor-κB, c-Jun, and c-Fos. Taken together, this study is the first to demonstrate that HIF-2α inhibition exhibits anti-inflammatory activity through the inhibition of inflammatory cytokines and impairment of ECM destruction, as well as blocking of osteoclastic differentiation in a nicotine- and periodontopathogen-stimulated PDLCs model. Thus, HIF-2α inhibition may be a novel molecular target for therapeutic approaches in periodontitis.

Muramyl dipeptide activates human beta defensin 2 and pro-inflammatory mediators through Toll-like receptors and NLRP3 inflammasomes in human dental pulp cells.

PURPOSE: The expression levels of intracellular pyrin domain-containing 3 (NLRP3) and microbial pattern-recognition receptors, such as nucleotide-binding oligomerization domain 2 (NOD2), have been reported in human dental pulp cells (HDPCs) and inflamed dental pulp tissue, but the role of NLRP3 and Toll-like receptors (TLRs) in the production of human beta defensin 2 (hBD2) and inflammatory cytokines against invading pathogens remains poorly defined. The aim of this study was to determine whether the NOD2 ligand muramyl dipeptide (MDP) upregulates hBD2 and inflammatory cytokines and whether this response is dependent on TLRs and NLRP inflammasomes in HDPCs. METHODOLOGY: The effects of MDP on the expression of hBD2, TLRs, inflammasomes, and pro-inflammatory mediators in HDPCs were examined using Western blotting and reverse transcription-polymerase chain reaction. Levels of pro-inflammatory cytokines, such as nitric oxide (NO) and prostaglandin E2 (PGE2), were determined by enzyme-linked immunosorbent assay. RESULTS: MDP upregulated hBD2, TLR2, and TLR4 mRNAs and protein levels in a dose- and time-dependent manner. TLR2 and TLR4 neutralizing blocking antibodies and NOD2- and hBD2-specific small interfering RNAs (siRNAs) attenuated the MDP-induced production of NO, PGE2, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and IL-8 and upregulated inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX2) in HDPCs. Additionally, MDP activated inflammasome-related genes, such as NLRP3, caspase 1, apoptotic speck protein containing a caspase recruitment domain, and IL-1ß. Furthermore, silencing of the NLRP3 gene using a siRNA significantly decreased the MDP-induced expression of hBD2 and cytokines, such as iNOS-derived NO, COX2, PGE2, TNF-α, IL-6, and IL-8. CONCLUSION: These results suggest that NOD2 activates the TLR2, TLR4, and NLRP3 inflammasome-signaling pathways in HDPCs to induce the production of multiple inflammatory mediators and antimicrobial peptides, which in turn promote pulp immune defense against microbial challenge. CLINICAL RELEVANCE: The TLR and NLRP3 inflammasome pathways may represent an important modulatory mechanism of immune defense responses during the progression of pulpitis. Our results suggest that local inhibition of NLRP3 and TLRs may reduce the impact of cytokine-mediated host destructive processes in pulpitis.

Combined effects of dentin sialoprotein and bone morphogenetic protein-2 on differentiation in human cementoblasts.

The aim of this study is to determine the effects of the combination of recombinant human BMP-2 (rh-BMP-2) and dentin sialoprotein (rh-DSP) on growth and differentiation in human cementoblasts and determine the underlying signal transduction mechanism. Compared to treatment of cementoblasts with either rh-BMP-2 or rh-DSP alone, the combination of rh-BMP-2 and rh-DSP synergistically increased cell growth, ALP activity, nodule formation and expression of differentiation markers. The differentiation-promoting effect was also observed in periodontal ligament cells and an osteoblastic cell line. Likewise, combination of rh-DSP and rh-BMP-2 increased BMP-2 mRNA expression and Smad1/5/8 phosphorylation, which was blocked by the BMP antagonist noggin. The expression levels of α2ß1 integrin and RhoA, as well as the phosphorylation status of FAK and Akt, were increased by the combination of rh-BMP-2 and rh-DSP in a time-dependent manner. In addition, rh-BMP-2 and rh-DSP enhanced expression of Wnt ligands, ß-catenin activation and GSK-3ß phosphorylation, all of which were inhibited by the Wnt receptor antagonist DKK1. Furthermore, treatment with rh-DSP plus rh-BMP-2 resulted in phosphorylation of extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38 and also induced the nuclear translocation of the NF-κB p65 subunit, which was blocked by noggin. This study demonstrates for the first time that rh-DSP and rh-BMP-2 act synergistically, enhancing each other's ability to stimulate cementoblastic cell growth and differentiation in vitro via autocrine BMP, integrin, Wnt/ß-catenin, MAP kinase and NF-κB pathways. These results support the therapeutic potential of a combination strategy for aiding periodontal regeneration.

MBD6 is a direct target of Oct4 and controls the stemness and differentiation of adipose tissue-derived stem cells.

Argonaute 2 (Ago2) is a pivotal regulator of cell fate in adult stem cells. Its expression is significantly downregulated in late passages of cells, concomitant with a prominent increase in Ago2 cytosolic localization in single cells. Nuclear localization of Ago2 is crucial for the survival, proliferation, and differentiation of hATSCs (human adipose tissue-derived stem cells), mediated by the specific binding of the regulatory regions of functional genes, which positively or negatively altered gene expression. Ago2 targets genes that control stemness, reactive oxygen species scavenging, and microRNA expression, all of which are crucial for hATSC survival and self-renewal. Ago2 promotes cell proliferation and self-renewal by activating the expression of octamer-binding transcription factor 4 (Oct4). We confirmed the direct regulation of Oct4 activity by Ago2, as indicated by the results of the ChIP analysis. Methyl-CpG-binding protein 6 (MBD6) was detected as an Oct4 regulatory gene. As predicted, knockdown of MBD6 expression attenuated cell proliferation and eventually induced cell death. We hypothesized that MBD6 functions downstream of Oct4 in the regulation of stemness-related genes, cell proliferation, self-renewal activity, and survival. MBD6 also promoted cell transdifferentiation into neural and endodermal ß-cells while significantly attenuating differentiation into the mesodermal lineage. We demonstrate that MBD6 is regulated by Ago2 via an interaction with Oct4, which alters self-renewal and gene expression in hATSCs. MBD6 was promoted cell proliferation through a novel set of signal mediators that may influence differentiation by repressing MBD2 and MBD3, which are possibly recruited by germ cell nuclear factor (GCNF).

CD49f enhances multipotency and maintains stemness through the direct regulation of OCT4 and SOX2.

CD49f (integrin subunit α6) regulates signaling pathways in a variety of cellular activities. However, the role of CD49f in regulating the differentiation and pluripotency of stem cells has not been fully investigated. Therefore, in this study, human mesenchymal stem cells (hMSCs) were induced to form spheres under nonadherent culture conditions, and we found that the CD49f-positive population was enriched in MSC spheres compared with MSCs in a monolayer. The expression of CD49f regulated the ability of hMSCs to form spheres and was associated with an activation of the phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway. Furthermore, the forced expression of CD49f modulated the proliferation and differentiation potentials of hMSCs through prolonged activation of PI3K/AKT and suppressed the level of p53. We showed that the pluripotency factors OCT4 and SOX2 were recruited to the putative promoter region of CD49f, indicating that OCT4 and SOX2 play positive roles in the expression of CD49f. Indeed, CD49f expression was upregulated in human embryonic stem cells (hESCs) compared with hMSCs. The elevated level of CD49f expression was significantly decreased upon embryoid body formation in hESCs. In hESCs, the knockdown of CD49f downregulated PI3K/AKT signaling and upregulated the level of p53, inducing differentiation into three germ layers. Taken together, our data suggest that the cell-surface protein CD49f has novel and dynamic roles in regulating the differentiation potential of hMSCs and maintaining pluripotency.

MicroRNA 486 is a potentially novel target for the treatment of spinal cord injury.

MicroRNAs have been shown to effectively regulate gene expression at the translational level. Recently, we identified novel microRNAs that were upregulated in a mouse model of spinal cord injury. Among those, we have focused on microRNA 486, which directly represses NeuroD6 expression through a conserved sequence in its untranslated region. We correlated the overexpression of microRNA 486 in motor neurons with a poor outcome due to progressive neurodegeneration and a pathophysiology that is mediated by reactive oxygen species. The expression of microRNA 486 was induced by reactive oxygen species that were produced by inflammatory factors, and reactive oxygen species were accumulated in response to the knockdown of NeuroD6, which enhances the downregulation of glutathione peroxidase 3 and thioredoxin-like 1 after traumatic spinal cord injury. NeuroD6 directly bound to regulatory regions of thioredoxin-like 1 and glutathione peroxidase 3 in motor neurons and activated their expression, which promoted reactive oxygen species scavenging. Moreover, knocking down microRNA 486 induced the expression of NeuroD6, which effectively ameliorated the spinal cord injury and allowed the mice to recover motor function. The infusion of exogenic NeuroD6 in spinal cord injury lesions effectively blocked apoptosis by reactivating thioredoxin-like 1 and glutathione peroxidase 3, which was accompanied by a recovery of motor function. Collectively, these findings have identified a novel microRNA in spinal cord injury lesions called microRNA 486, demonstrating a new role for NeuroD6 in neuroprotection, and suggest a potential therapeutic target for spinal cord injuries.

Growth inhibition and apoptosis-inducing effects of cudraflavone B in human oral cancer cells via MAPK, NF-κB, and SIRT1 signaling pathway.

The goal of this study was to investigate the effect and molecular mechanism of cudraflavone B, a prenylated flavonoid isolated from the root bark of Cudrania tricuspidata, against oral squamous cell carcinoma cells. We observed that cudraflavone B inhibited proliferation of these cells in a time- and dose-dependent manner. At 15 µM, cudraflavone B induced cell death via apoptosis (characterized by the appearance of nuclear morphology) and increased the accumulation of the sub-G1 peak (portion of apoptotic annexin V positive cells). Treatment with cudraflavone B triggered the mitochondrial apoptotic pathway (indicated by induction of the proapoptotic protein p53 and the p21 and p27 effector proteins), downregulation of cell cycle regulatory proteins (e.g., p-Rb, changing Bax/Bcl-2 ratios, cytochrome-c release), and caspase-3 activation. Cudraflavone B time-dependently activated NF-κB, the MAP kinases p38, and ERK, and induced the expression of SIRT1. SIRT1 activator, resveratrol, dose-dependently attenuated the growth-inhibitory and apoptosis-inducing effect of cudraflavone B and blocked cudraflavone B-induced regulatory protein expressions in the mitochondrial pathway such as p53, p21, p27, Bax, caspase-3, and cytochrome-c. Conversely, treatment with SIRT1 inhibitor sirtinol caused opposite effects. These results demonstrate for the first time that the molecular mechanism underlying the antitumor effect in oral squamous cell carcinoma cells is related to the activation of MAPK/and NF-κB as well as of the SIRT1 pathway. Therefore, cudraflavone B may be a lead for the development of a potential candidate for human oral squamous cell carcinoma cells.

New culture system for human embryonic stem cells: autologous mesenchymal stem cell feeder without exogenous fibroblast growth factor 2.

Human embryonic stem (hES) cells have been successfully maintained using human-cell feeder systems or feeder-free systems. However, despite advances in culture techniques, hES cells require supplementation with fibroblast growth factor 2 (FGF-2), an exogenous stemness factor, which is needed to sustain the authentic undifferentiated status. We developed a new culture system for hES cells; this system does not require supplementation with FGF-2 to obtain hES cells that are suitable for tissue engineering and regenerative medicine. This culture system employed mesenchymal stem cells derived from hES cells (hESC-MSCs) as autologous human feeder cells in the absence of FGF-2. The hES cell line SNUhES3 cultured in this new autologous feeder culture system maintained the typical morphology of hES cells and expression of pluripotency-related proteins, SSEA-4, TRA-1-60, OCT4, and alkaline phosphatase, without development of abnormal karyotypes after more than 30 passages. RNA expression of the pluripotency-related genes OCT4 and NANOG was similar to the expression in SNUhES3 cells maintained on xenofeeder STO cells. To identify the mechanism that enables the cells to be maintained without exogenous FGF-2, we checked the secretion of FGF-2 from the mitomycin-C treated autofeeder hESC-MSCs versus xenofeeder STO cells, and confirmed that hESC-MSCs secreted FGF-2 whereas STO cells did not. The level of FGF-2 in the media from the autofeeder system without exogenous FGF-2 was comparable to that from the xenofeeder system with addition of FGF-2. In conclusion, our new culture system for hES cells, which employs a feeder layer of autologous hESC-MSCs, supplies sufficient amounts of secreted FGF-2 to eliminate the requirement for exogenous FGF-2.

Histone deacetylase regulates high mobility group A2-targeting microRNAs in human cord blood-derived multipotent stem cell aging.

Cellular senescence involves a reduction in adult stem cell self-renewal, and epigenetic regulation of gene expression is one of the main underlying mechanisms. Here, we observed that the cellular senescence of human umbilical cord blood-derived multipotent stem cells (hUCB-MSCs) caused by inhibition of histone deacetylase (HDAC) activity leads to down-regulation of high mobility group A2 (HMGA2) and, on the contrary, to up-regulation of p16(INK)4(A), p21(CIP)¹(/WAF)¹ and p27(KIP)¹. We found that let-7a1, let-7d, let-7f1, miR-23a, miR-26a and miR-30a were increased during replicative and HDAC inhibitor-mediated senescence of hUCB-MSCs by microRNA microarray and real-time quantitative PCR. Furthermore, the configurations of chromatins beading on these miRNAs were prone to transcriptional activation during HDAC inhibitor-mediated senescence. We confirmed that miR-23a, miR-26a and miR-30a inhibit HMGA2 to accelerate the progress of senescence. These findings suggest that HDACs may play important roles in cellular senescence by regulating the expression of miRNAs that target HMGA2 through histone modification.

Histone deacetylase controls adult stem cell aging by balancing the expression of polycomb genes and jumonji domain containing 3.

Aging is linked to loss of the self-renewal capacity of adult stem cells. Here, we observed that human multipotent stem cells (MSCs) underwent cellular senescence in vitro. Decreased expression of histone deacetylases (HDACs), followed by downregulation of polycomb group genes (PcGs), such as BMI1, EZH2 and SUZ12, and by upregulation of jumonji domain containing 3 (JMJD3), was observed in senescent MSCs. Similarly, HDAC inhibitors induced cellular senescence through downregulation of PcGs and upregulation of JMJD3. Regulation of PcGs was associated with HDAC inhibitor-induced hypophosphorylation of RB, which causes RB to bind to and decrease the transcriptional activity of E2F. JMJD3 expression regulation was dependant on histone acetylation status at its promoter regions. A histone acetyltransferase (HAT) inhibitor prevented replicative senescence of MSCs. These results suggest that HDAC activity might be important for MSC self-renewal by balancing PcGs and JMJD3 expression, which govern cellular senescence by p16(INK4A) regulation.

Platinum(II) Complexes Based on Phenylbenzoazole-Derived Ligands for Phosphorescent Organic Light-Emitting Diodes.

Phosphorescent Pt(II) complexes based on phenylbenzoazole ligands were synthesized and their photophysical properties were investigated for OLEDs. Multilayered OLEDs devices using these complexes as emitters showed the efficient emissions, which are very sensitive to the structural and photophysical properties of Pt(II) complexes. In particularly, a device C using Pt(II) complex 2 based on phenylbenzoazole ligand as the dopant exhibited efficient emission with a luminous efficiency, a power efficiency, an external quantum efficiency, and CIE coordinates of 8.03 cd/A, 2.79 lm/W, 4.84% at 20 mA/cm², and (0.63, 0.35) at 10.0 V, respectively.

Erratum to "Isocudraxanthone K Induces Growth Inhibition and Apoptosis in Oral Cancer Cells via Hypoxia Inducible Factor-1α".

[This corrects the article DOI: 10.1155/2014/934691.].

Red Phosphorescent Platinum(II) Complexes with Tetradentate Pyridine-Containing Ligands for Organic Light Emitting Diodes.

Here, red phosphorescent platinum(II) complexes based on tetradentate pyridine-containing lig-ands are studied. To investigate their electroluminescent properties, multilayer devices were fabricated in the following sequence; ITO (180 nm)/4,4',4″-Tris[2-naphthyl(phenyl)amino]triphenylamine (2-TNATA) (30 nm)/N, N'-di(1-naphthyl)-N,N'-diphenyl-1,1'-biphenyl)4,4'-diamine (NPB) (20 nm)/ Tris(4-carbazoyl-9-ylphenyl)amine (TCTA) (10 nm)/4,4'-Bis(N-carbazolyl)-1,1'-biphenyl (CBP) (20 nm)/Platinum(II) complex (20 nm)/1,3,5-Tris(1-Phenyl-1H-benzimidazol-2-yl)benzene) (TPBi) (40 nm)/Liq (2 nm)/Al (100 nm). In particularly, a device using platinum(II) complex based on N-(3,5-di-tert-butylphenyl)-3-(pyridin-2-yl)-N-(3-(pyridin-2-yl)phenyl)benzenamineligand showed the efficient red emission, with a luminous efficiency, power efficiency, and external quantum efficiency of, and the Commission International de LEclairge (CIE) coordinates of 27.26 cd/A, 10.54 lm/W, 8.50% at 20 mA/cm², and (0.65, 0.33) at 11.0 V, respectively.

Platinum (II) Complexes Based on Tetradentate Pyridine-Containing Ligands for Phosphorescent Organic Light-Emitting Diodes.

In this study, we designed and synthesized two phosphorescent emitting materials based on tetradentate pyridine-containing ligands. Their photophysical properties were examined for OLEDs and multilayer devices using these materials were fabricated in the following sequence; ITO (180 nm)/4,4',4″-Tris[2-naphthyl(phenyl)amino]triphenylamine (2-TNATA) (30 nm)/N,N'-di(1-naphthyl)-N,N'-diphenyl-1,1'-biphenyl)4,4'-diamine (NPB) (20 nm)/Tris(4-carbazoyl-9-ylphenyl)amine (TCTA) (10 nm)/4,4'-Bis(N-carbazolyl)-1,1'-biphenyl(CBP): 5, 8, 15% Platinum (II) complexes (20 nm)/1,3,5-Tris(1-Phenyl-1H-benzimidazol-2-yl)benzene) (TPBi) (40 nm)/Liq (2 nm)/Al (100 nm). In particularly, a device using Platinum (II) complex based on A/-(3,5-di-tert-butylphenyl)-6-phenyl-N-(6-phenylpyridin-2-yl)pyridin-2-amine ligand showed the efficient emission, with luminous efficiency, power efficiency, and external quantum efficiency, and the Commission International de LEclairge (CIE) coordinates of 29.29 cd/A, 9.37 lm/W, 8.66% at 20 mA/cm2, and (0.32, 0.62) at 8.0 V, respectively.