Using angle-selective optical film to enhance the light extraction of a thin-film encapsulated 3D reflective pixel for OLED displays.

Light extraction improvement is still an important issue for active-matrix organic light-emitting diode displays (AMOLEDs). In our previous work, a three-dimensional (3D) reflective pixel configuration embedding the OLED in the concave 3D reflector and patterned high-index filler had been proposed for significant enhancement of the pixel light extraction. In this work, influences of thin film encapsulation (TFE) on light extraction of such reflective 3D OLED pixels are considered as well by simulation studies. Unfortunately, the optical simulation reveals strong reduction of the light extraction efficiency induced by TFE layers. As such, an additional angle-selective optical film structure between the pixel and the encapsulation layers is introduced to control the angular distribution of the light coupled into the encapsulation layers and to solve TFE-induced optical losses. As a result, TFE-induced losses can be substantially reduced to retain much of light extraction efficiency. The results of this study are believed to provide useful insights and guides for developing even more efficient and power-saving AMOLEDs.

Comprehensive Investigation of Electrical and Optical Characteristics of InGaN-Based Flip-Chip Micro-Light-Emitting Diodes.

Micro-light-emitting diodes (micro-LEDs) have been regarded as the important next-generation display technology, and a comprehensive and reliable modeling method for the design and optimization of characteristics of the micro-LED is of great use. In this work, by integrating the electrical simulation with the optical simulation, we conduct comprehensive simulation studies on electrical and optical/emission properties of real InGaN-based flip-chip micro-LED devices. The integrated simulation adopting the output of the electrical simulation (e.g., the non-uniform spontaneous emission distribution) as the input of the optical simulation (e.g., the emission source distribution) can provide more comprehensive and detailed characteristics and mechanisms of the micro-LED operation than the simulation by simply assuming a simple uniform emission source distribution. The simulated electrical and emission properties of the micro-LED were well corroborated by the measured properties, validating the effectiveness of the simulation. The reliable and practical modeling/simulation methodology reported here shall be useful to thoroughly investigate the physical mechanisms and operation of micro-LED devices.

Proteasome inhibitors restore the STAT1 pathway and enhance the expression of MHC class I on human colon cancer cells.

BACKGROUND: A new strategy, particularly a novel combination, for immunotherapy in microsatellite stable metastatic colorectal cancer (mCRC) treatment needs to be formulated. Studies on the interferon-γ (IFN-γ)/ Janus kinase (JAK)/ signal transducer and activator of transcription (STAT)1 pathway provide new directions in this regard. METHODS: Our study applies three colon cancer cell lines, including microsatellite stable (MSS) cell lines, which are SW480 and SW620, and microsatellite instability-high (MSI-H) cell line, which is DLD-1. We compared the expressions of immune surface markers on colon cancer cells in response to IFN-γ. We elucidated these mechanisms, which involved the upregulation of immune surface markers. Furthermore, we examined real-world clinical samples using the PerkinElmer Opal multiplex system and NanoString analysis. RESULTS: We established that the baseline expression of major histocompatibility complex (MHC) class I alleles and programmed death-ligand 1 (PD-L1) were generally low in cell line models. The immune surface markers were significantly increased after IFN-γ stimulation on SW480 but were notably unresponsive on the SW620 cell line. We discovered that STAT1 and phosphorylated STAT1 (pSTAT1) were downregulated in the SW620 cell line. We verified that the STAT1/pSTAT1 could be restored through the application of proteasome inhibitors, especially bortezomib. The expression of MHC class I as downstream signals of STAT1 was also up-regulated by proteasome inhibitors. The similar results were reproduced in DLD-1 cell line, which was also initially unresponsive to IFN-γ. In real-world samples of patients with mCRC, we found that higher STAT1 expression in tumor cells was strongly indicative of a highly immunogenic microenvironment, with significantly higher expression levels of MHC class I and PD-L1, not only on tumor cells but also on non-tumor cells. Furthermore, tumor infiltrating lymphocytes (TILs) were increased in the positive-STAT1 group. Through NanoString analysis, we confirmed that the mRNA expressions of IFN-γ, human leukocyte antigen (HLA)-A, HLA-E, and HLA-G were also significantly higher in the positive-STAT1 group than those in the negative-STAT1 group. CONCLUSION: Our study provides a novel rationale for the addition of bortezomib, a proteasome inhibitor, into new immunotherapy combinations.

Chemotherapy agents stimulate dendritic cells against human colon cancer cells through upregulation of the transporter associated with antigen processing.

Single immunotherapy fails to demonstrate efficacy in patients with microsatellite stable (MSS) metastatic colorectal cancer (mCRC). Research on immune reactions before and after systemic agents for mCRC is warranted. Our study examined cell line models to compare the expression of immune surface markers on colon cancer cells before and after chemotherapy agents. We also elucidated mechanisms underlying the effects of chemotherapy agents on immune surface markers. We used real-world clinical samples with NanoString analysis and the Perkin-Elmer Opal multiplex system. We established that chemotherapy agents, particularly 7-ethyl-10-hydroxycamptothecin (SN-38), the active metabolite of irinotecan, stimulated the expression of stimulatory MHC class I alleles through stimulation the pathway of transporters associated with antigen processing 1 and 2 (TAP1 and TAP2) in cell line models. Application of infected cell protein 47 (ICP-47), a specific inhibitor of the TAP1/TAP2, significantly inhibited expression of TAP1/TAP2 and also inhibited the expression of the downstream MHC class I. In the functional assay, SN-38 significantly promoted the phagocytosis of colon cancer cells by monocyte-derived dendritic cells (MoDCs). We confirmed that the expression of major histocompatibility complex (MHC) class I, significantly increased after first-line chemotherapy and targeted therapy in the samples of real-world patients with de novo mCRC. Our study provides new insights for novel immunotherapy combinations.