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The viewing angle characteristics and light extraction efficiency of organic light-emitting diodes (OLEDs) with a micro-cavity structure were enhanced. This was accomplished by inserting a diffusion layer composed of nano-sized structures of a transparent polymer poly(methyl methacrylate) (PMMA) combined with a zinc oxide (ZnO) semi-planarization layer with a high refractive index (n = 2.1) into the devices. The PMMA nanostructures were fabricated by employing a reactive ion etching (RIE) process. The height and density of the PMMA nanostructures were controlled by varying the speed at which the PMMA was spin-coated onto the substrate. The insertion of the diffusion layer into the micro-cavity OLEDs (MC-OLEDs) improved the external quantum efficiency (EQE) by as much as 17% when compared to that of a MC-OLED without a diffusion layer. Furthermore, adjustment of the viewing angle from 0° to 60° halved the peak shift distance of the electroluminescence (EL) spectra from 42 to 20 nm. Additionally, changing the viewing angle from 0° to 60° changed the color coordinate movement distance of the MC-OLED with the diffusion layer to 0.078, less than half of the distance of the MC-OLED without the diffusion layer (0.165).

In this study, we report highly efficient green phosphorescent organic light-emitting diodes (OLEDs) with ultra-thin emission layers (EMLs). We use tris[2-phenylpyridinato-C2,N]iridium(III) (Ir(ppy) 3 ), a green phosphorescent dopant, for creating the OLEDs. Under systematic analysis, the peak external quantum efficiency (EQE) of an optimized device based on the ultra-thin EML structure is found to be approximately 24%. This result is highest EQE among ultra-thin EML OLEDs and comparable to the highest efficiency achieved by OLEDs using Ir(ppy) 3 that are fabricated via conventional doping methods. Moreover, this result shows that OLEDs with ultra-thin EML structures can achieve ultra-high efficiency.

In this study, an external light extraction layer with a micro-nano hybrid structure was applied to improve the external light extraction efficiency of organic light-emitting diodes (OLEDs). A reactive ion-etching (RIE) process, using O2 and CHF3 plasma, was performed on the surface of the micro-scale pattern to form micro-nano hybrid structures. According to the results of this study, the nanostructures formed by the treatment of O2 and CHF3 were different, and the efficiency according to the structures was analyzed experimentally and theoretically. As a result, the OLED, to which the micro-nano hybrid structure, manufactured through a simple process, is applied, improved the external light extraction efficiency by up to 38%, and an extended viewing angle profile was obtained. Additionally, an effective method for enhancing the out-coupling efficiency of OLEDs was presented by optimizing the micro-nano hybrid structure according to process conditions.

In this study, various diffusers are applied to highly efficient ultra-thin emission layer (EML) structure-based blue phosphorescent organic light-emitting diodes (PHOLEDs) to improve the electroluminescence (EL) characteristics and viewing angle. To achieve highly efficient blue PHOLEDs, the EL characteristics of ultra-thin EML PHOLEDs with the various diffusers having different structures of pattern–shape (hemisphere/sphere), size (4~75 μm), distribution (surface/embedded), and packing (close-packed/random) were systematically analyzed. The diffusers showed different enhancements in the overall EL characteristics of efficiencies, viewing angle, and others. The EL characteristics showed apparent dependency on their structure. The external quantum efficiency (EQE) was enhanced mainly by following the orders of pattern, size, and shape. Following the pattern size, the EQE enhancement gradually increased; the largest-sized diffuser with a 75 μm closed-packed hemisphere (diffuser-1) showed a 1.47-fold EQE improvement, which was the highest. Meanwhile, the diffuser with a ~7 μm random embedded sphere with a low density (diffuser 5) showed the lowest 1.02-fold-improved EQE. The reference device with ultra-thin EML structure-based blue PHOLEDs showed a maximum EQE of 16.6%, and the device with diffuser 1 achieved a maximum EQE of 24.3% with a 5.1% wider viewing angle compared to the reference device without a diffuser. For the in-depth analysis, the viewing angle profile of the ultra-thin EML PHOLED device and fluorescent green OLEDs were compared. As a result, the efficiency enhancement characteristics of the diffusers show a difference in the viewing angle profile. Finally, the application of the diffuser successfully demonstrated that the EL efficiency and viewing angle could be selectively improved. Additionally, we found that it was possible to realize a wide viewing angle and achieve considerable EQE enhancement by further investigations using high-density and large-sized embedded structures of light-extraction film.

In this study, we fabricated a random nanostructure (RNS) external light extraction composite layer containing high-refractive-index nanoparticles through a simple and inexpensive solution process and a low-temperature mask-free process. We focused on varying the shape and density of the RNSs and adjusted the concentration of the high-refractive-index nanoparticles to control the optical properties. The RNSs fabricated using a low-temperature mask-free process can use the distance between the nanostructures and various forms to control the diffraction and scattering effects in the visible light wavelength range. Consequently, our film exhibited a direct transmittance of ~85% at a wavelength of 550 nm. Furthermore, when the RNSs’ composite film, manufactured using the low-temperature mask-free process, was applied to organic light-emitting diodes (OLEDs), it exhibited an external quantum efficiency improvement of 32.2% compared with the OLEDs without the RNSs. Therefore, the randomly distributed high-refractive-index nanoparticles on the polymer film can reduce the waveguide mode and total reflection at the substrate/air interface. These films can be used as a scattering layer to reduce the loss of the OLED substrate mode.

Dermatofibrosarcoma protuberans (DFSP) is a very rare soft tissue sarcoma. DFSP often reveals a specific chromosome translocation, t(17;22)(q22;q13), which results in the fusion of collagen 1 alpha 1 (COL1A1) gene and platelet-derived growth factor-B (PDGFB) gene. The COL1A1-PDGFB fusion protein activates the PDGFB receptor and resultant constitutive activation of PDGFR receptor is essential in the pathogenesis of DFSP. Thus, blocking PDGFR receptor activation with imatinib has shown promising activity in the treatment of advanced and metastatic DFSP. Despite the success with targeted agents in cancers, acquired drug resistance eventually occurs. Here, we tried to identify potential drug resistance mechanisms against imatinib in a 46-year old female with DFSP who initially responded well to imatinib but suffered rapid disease progression. We performed whole-genome sequencing of both pre-treatment and post-treatment tumor tissue to identify the mutational events associated with imatinib resistance. No significant copy number alterations, insertion, and deletions were identified during imatinib treatment. Of note, we identified newly emerged 8 non-synonymous somatic mutations of the genes (ACAP2, CARD10, KIAA0556, PAAQR7, PPP1R39, SAFB2, STARD9, and ZFYVE9) in the imatinib-resistant tumor tissue. This study revealed diverse possible candidate mechanisms by which imatinib resistance to PDGFRB inhibition may arise in DFSP, and highlights the usefulness of whole-genome sequencing in identifying drug resistance mechanisms and in pursuing genome-directed, personalized anti-cancer therapy.

Oncogenic mutations in gastrointestinal stromal tumors (GISTs) predict prognosis and therapeutic responses to imatinib. In wild-type GISTs, the tumor-initiating events are still unknown, and wild-type GISTs are resistant to imatinib therapy. We performed an association study between copy number alterations (CNAs) identified from array CGH and gene expression analyses results for four wild-type GISTs and an imatinib-resistant PDGFRA D842V mutant GIST, and compared the results to those obtained from 27 GISTs with KIT mutations. All wild-type GISTs had multiple CNAs, and CNAs in 1p and 22q that harbor the SDHB and GSTT1 genes, respectively, correlated well with expression levels of these genes. mRNA expression levels of all SDH gene subunits were significantly lower (P≤0.041), whereas mRNA expression levels of VEGF (P=0.025), IGF1R (P=0.026), and ZNFs (P<0.05) were significantly higher in GISTs with wild-type/PDGFRA D842V mutations than GISTs with KIT mutations. qRT-PCR validation of the GSTT1 results in this cohort and 11 additional malignant GISTs showed a significant increase in the frequency of GSTT1 CN gain and increased mRNA expression of GSTT1 in wild-type/PDGFRA D842V GISTs than KIT-mutant GISTs (P=0.033). Surprisingly, all four malignant GISTs with KIT exon 11 deletion mutations with primary resistance to imatinib had an increased GSTT1 CN and mRNA expression level of GSTT1. Increased mRNA expression of GSTT1 and ZNF could be predictors of a poor response to imatinib. Our integrative approach reveals that for patients with wild-type (or imatinib-resistant) GISTs, attempts to target VEGFRs and IGF1R may be reasonable options.

Alzheimer’s disease (AD) is a form of dementia associated with abnormal glucose metabolism resulting from amyloid-beta (Aβ) plaques and intracellular neurofibrillary tau protein tangles. In a previous study, we confirmed that carboxy-dehydroevodiamine∙HCl (cx-DHED), a derivative of DHED, was effective at improving cognitive impairment and reducing phosphorylated tau levels and synaptic loss in an AD mouse model. However, the specific mechanism of action of cx-DHED is unclear. In this study, we investigated how the cx-DHED attenuates AD pathologies in the 5xFAD mouse model, focusing particularly on abnormal glucose metabolism. We analyzed behavioral changes and AD pathologies in mice after intraperitoneal injection of cx-DHED for 2 months. As expected, cx-DHED reversed memory impairment and reduced Aβ plaques and astrocyte overexpression in the brains of 5xFAD mice. Interestingly, cx-DHED reversed the abnormal expression of glucose transporters in the brains of 5xFAD mice. In addition, otherwise low O-GlcNac levels increased, and the overactivity of phosphorylated GSK-3β decreased in the brains of cx-DHED-treated 5xFAD mice. Finally, the reduction in synaptic proteins was found to also improve by treatment with cx-DHED. Therefore, we specifically demonstrated the protective effects of cx-DHED against AD pathologies and suggest that cx-DHED may be a potential therapeutic drug for AD.

Dermatofibrosarcoma protuberans (DFSP) is a very rare soft tissue sarcoma. DFSP often reveals a specific chromosome translocation, t(17; 22)(q22; q13), which results in the fusion of collagen 1 alpha 1 (COL1A1) gene and platelet-derived growth factor-B (PDGFB) gene. The COL1A1-PDGFB fusion protein activates the PDGFB receptor and resultant constitutive activation of PDGFR receptor is essential in the pathogenesis of DFSP. Thus, blocking PDGFR receptor activation with imatinib has shown promising activity in the treatment of advanced and metastatic DFSP. Despite the success with targeted agents in cancers, acquired drug resistance eventually occurs. Here, we tried to identify potential drug resistance mechanisms against imatinib in a 46-year old female with DFSP who initially responded well to imatinib but suffered rapid disease progression. We performed whole-genome sequencing of both pre-treatment and post-treatment tumor tissue to identify the mutational events associated with imatinib resistance. No significant copy number alterations, insertion, and deletions were identified during imatinib treatment. Of note, we identified newly emerged 8 non-synonymous somatic mutations of the genes (ACAP2, CARD10, KIAA0556, PAAQR7, PPP1R39, SAFB2, STARD9, and ZFYVE9) in the imatinib-resistant tumor tissue. This study revealed diverse possible candidate mechanisms by which imatinib resistance to PDGFRB inhibition may arise in DFSP, and highlights the usefulness of whole-genome sequencing in identifying drug resistance mechanisms and in pursuing genome-directed, personalized anti-cancer therapy.