Constructing Highly Efficient Blue OLEDs with External Quantum Efficiencies up to 7.5 % Based on Anthracene Derivatives.

Acquiring desirable device performance with deep-blue color purity that fulfills practical application requirements is still a challenge. Bipolar fluorescent emitters with hybrid local and charge transfer (HLCT) state may serve to address this issue. Herein, by inserting anthracene core in the deep-blue building blocks, the authors successfully developed two highly twisted D-π-A fluorescent emitters, ICz-An-PPI and IP-An-PPI, featuring different acceptor groups. Both exhibited superb thermal stabilities, high photo luminescent quantum yields and excellent bipolar transport capabilities. The non-doped OLEDs using ICz-An-PPI and IP-An-PPI as the emitting layers showed efficient blue emission with an external quantum efficiency (EQEmax ) of 4.32 % and 5.41 %, and the CIE coordinates of (0.147, 0.180) and (0.149, 0.150), respectively. In addition, the deep blue doped device based on ICz-An-PPI was achieved with an excellent CEmax of 5.83 cd A-1 , EQEmax of 4.6 % and the CIE coordinate of (0.148, 0.078), which is extremely close to the National Television Standards Committee (NTSC) standard. Particularly, IP-An-PPI-based doped device had better performance, with an EQEmax of 7.51 % and the CIE coordinate of (0.150, 0.118), which was very impressive among the recently reported deep-blue OLEDs with the CIEy <0.12. Such high performance may be attributed to the hot exciton HLCT mechanism via T7 to S2 . Our work may provide a new approach for designing high-efficiency deep-blue materials.

DNA methylation status of imprinted H19 and KvDMR1 genes in human placentas after conception using assisted reproductive technology.

BACKGROUND: Assisted reproductive technologies (ARTs), such as in vitro fertilization (IVF) and intracytoplasmic sperm injection (ICSI), are thought to destabilize genomic imprints. Previous studies examining the association between ART and aberrant DNA methylation have been inconclusive. METHOD: The DNA methylation status of H19 and KvDMR1was compared between newborns conceived through ART and those conceived naturally to evaluate the safety of ART. Placental tissues from 6 full-term, naturally conceived pregnancies (no gestational comorbidities) and six full-term ART pregnancies (no gestational complication) were collected. Genomic DNA (gDNA) and RNA were extracted from both groups. Real-time PCR was used to analyze the mRNA expression levels of H19 and KvDMR1 in the placenta for both groups. A whole-genome DNA methylation microarray was used to examine three placentas from full-term, naturally conceived pregnancies and three placentas from full-term IVF pregnancies. RESULT: The expression level of H19 in the IVF group was significantly higher than that in the natural pregnancy group, whereas the expression level of KvDMR1 was significantly lower in the ART group than in the natural pregnancy group. Also, human ART manipulation resulted in placental gDNA methylation modifications. Conclusion: Abnormal methylation patterns were detected in phenotypically normal phenotype conceived by ART, which may occur due to imprinting errors in sperm/oocyte cells or side effects of in vitro embryo culture procedures. Further investigation is necessary to determine whether imprinted gene expression and DNA methylation can be regulated through other mechanisms. KEYWORDS: Assisted reproductive technology (ART); placenta; methylation; H19; KvDMR1.

Metformin improved oxidized low-density lipoprotein-impaired mitochondrial function and increased glucose uptake involving Akt-AS160 pathway in raw264.7 macrophages.

BACKGROUND: Macrophage accumulation in the vascular wall is a hallmark of atherosclerosis. Studies showed that shifting of oxidized lipids-induced inflammatory macrophages towards an anti-inflammatory phenotype by promoting oxidative metabolism attenuated atherosclerosis progression. Therefore, this study aimed to investigate whether metformin, which has ameliorated atherosclerosis in animal models and clinical trials, modulated oxidized low-density lipoprotein (Ox-LDL) induced inflammatory status in macrophages by regulating cellular oxidative metabolism. METHODS: Murine raw264.7 macrophages were incubated with Ox-LDL (50 µg/mL) in the presence or absence of metformin (15 µmol/L) for 24 h. Real-time polymerase chain reaction was used to quantify the transcription of classically activated (M1) pro-inflammatory and alternatively activated (M2) anti-inflammatory markers and mitochondrial DNA copy numbers. Cellular reactive oxygen species (ROS) production and mitochondrial membrane potential were detected by immunofluorescence. Cellular adenosine triphosphate (ATP) synthesis, glucose uptake, and lactic acid production were measured by commercial kit and normalized to cellular lysates. Western blotting analysis was performed to detect the expression of mitochondrial fusion/fission related proteins, enzymes mediating lipid metabolism and signaling pathway of glucose transport. Differences between groups were analyzed using one-way analysis of variance. RESULTS: Metformin improved Ox-LDL-impaired anti-inflammatory phenotype in raw264.7 macrophages as shown by up-regulated transcription of anti-inflammatory markers including interleukin 10 (0.76 ±â€Š0.04 vs. 0.94 ±â€Š0.01, P = 0.003) and Resistin-like molecule alpha (0.67 ±â€Š0.08 vs. 1.78 ±â€Š0.34, P = 0.030). Conversely, Ox-LDL-diminished phosphorylation of Akt was up-regulated by metformin treatment (0.47 ±â€Š0.05 vs. 1.02 ±â€Š0.08, P = 0.040), associated with an improvement of mitochondrial function, characterized by decreased ROS generation (2.50 ±â€Š0.07 vs. 2.15 ±â€Š0.04, P = 0.040), increased lipid oxidation, and elevated cellular ATP production (0.026 ±â€Š0.001 vs. 0.035 ±â€Š0.003, P = 0.020). Moreover, metformin-mediated Akt activation increased Akt substrate of 160 kDa (AS160) phosphorylation (0.51 ±â€Š0.04 vs. 1.03 ±â€Š0.03, P = 0.0041), promoted membrane translocation of glucose transporter 1, and increased glucose influx into the cells (4.78 ±â€Š0.04 vs. 5.47 ±â€Š0.01, P < 0.001). CONCLUSION: This study suggested that targeting macrophage metabolism with new or existing drugs had therapeutic potential for the prevention and treatment of diabetes-accelerated atherosclerosis.