Publications by authors named "Yang-Chih Cheng"

In this study, we have investigated the improvements in the performance of an all-solid-state complementary electrochromic device (ECD) by using the proposed high pressure treatment (HPT). The Li:TaOelectrolyte layer was recrystallized by the HPT utilizing pressurized COgas (∼200 atm) and at low temperature (<60 °C), which enhanced the coloration performance of the WO/Li:TaO/NiO complementary ECD by ∼20%. The reliability and durability of the ECD were confirmed by long term transmittance retention measurements, which indicated an improvement in the coloration performance by ∼14% upon the release of the bias voltages.

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Metastatic melanoma is challenging to clinically address. Although standard-of-care targeted therapy has high response rates in patients with BRAF-mutant melanoma, therapy relapse occurs in most cases. Intrinsically resistant melanoma cells drive therapy resistance and display molecular and biologic properties akin to neural crest-like stem cells (NCLSC) including high invasiveness, plasticity, and self-renewal capacity.

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Recent studies have profiled the innate immune signatures in patients infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and suggest that cellular responses to viral challenge may affect disease severity. Yet the molecular events that underlie cellular recognition and response to SARS-CoV-2 infection remain to be elucidated. Here, we find that SARS-CoV-2 replication induces a delayed interferon (IFN) response in lung epithelial cells.

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Unlabelled: Disrupted antiviral immune responses are associated with severe COVID-19, the disease caused by SAR-CoV-2. Here, we show that the 73-amino-acid protein encoded by of the viral genome contains a putative transmembrane domain, interacts with membrane proteins in multiple cellular compartments, and impairs antiviral processes in a lung epithelial cell line. Proteomic, interactome, and transcriptomic analyses, combined with bioinformatic analysis, revealed that expression of only this highly unstable small viral protein impaired interferon signaling, antigen presentation, and complement signaling, while inducing IL-6 signaling.

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In this work, a high-density hydrogen (HDH) treatment is proposed to reduce interface traps and enhance the efficiency of the passivated emitter rear contact (PERC) device. The hydrogen gas is compressed at pressure (~ 70 atm) and relatively low temperature (~ 200 °C) to reduce interface traps without changing any other part of the device's original fabrication process. Fourier-transform infrared spectroscopy (FTIR) confirmed the enhancement of Si-H bonding and secondary-ion mass spectrometry (SIMS) confirmed the SiN/Si interface traps after the HDH treatment.

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The cellular stress response triggers a cascade of events leading to transcriptional reprogramming and a transient inhibition of global protein synthesis, which is thought to be mediated by phosphorylation of eukaryotic initiation factor-2α (eIF2α). Using mouse embryonic fibroblasts (MEFs) and the fission yeast S. pombe, we report that rapid translational arrest and cell survival in response to hydrogen peroxide-induced oxidative stress do not rely on eIF2α kinases and eIF2α phosphorylation.

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Cold forging is often applied in the fastener industry. Wires in coil form are used as semi-finished products for the production of billets. This process usually requires preliminarily drawing wire coil in order to reduce the diameter of products.

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An emerging therapeutic strategy for cancer is to induce selective lethality in a tumor by exploiting interactions between its driving mutations and specific drug targets. Here we use a multi-species approach to develop a resource of synthetic lethal interactions relevant to cancer therapy. First, we screen in yeast ∼169,000 potential interactions among orthologs of human tumor suppressor genes (TSG) and genes encoding drug targets across multiple genotoxic environments.

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Many tumors become addicted to autophagy for survival, suggesting inhibition of autophagy as a potential broadly applicable cancer therapy. ULK1/Atg1 is the only serine/threonine kinase in the core autophagy pathway and thus represents an excellent drug target. Despite recent advances in the understanding of ULK1 activation by nutrient deprivation, how ULK1 promotes autophagy remains poorly understood.

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SRC kinase is activated in castration resistant prostate cancer (CRPC), phosphorylates the androgen receptor (AR), and causes its ligand-independent activation as a transcription factor. However, activating SRC mutations are exceedingly rare in human tumors, and mechanisms of ectopic SRC activation therefore remain largely unknown. Performing a functional genomics screen, we found that downregulation of SRC inhibitory kinase CSK is sufficient to overcome growth arrest induced by depriving human prostate cancer cells of androgen.

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NKX3.1 is a homeobox transcription factor whose function as a prostate tumor suppressor remains insufficiently understood because neither the transcriptional program governed by NKX3.1, nor its interacting proteins have been fully revealed.

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This study investigates how to adjust the transmit power of femto base station (FBS) to mitigate interference problems between the FBSs and mobile users (MUs) in the 2-tier heterogeneous femtocell networks. A common baseline of deploying the FBS to increase the indoor access bandwidth requires that the FBS operation will not affect outdoor MUs operation with their quality-of-service (QoS) requirements. To tackle this technical problem, an FBS transmit power adjustment (FTPA) algorithm is proposed to adjust the FBS transmit power (FTP) to avoid unwanted cochannel interference (CCI) with the neighboring MUs in downlink transmission.

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Background: Itraconazole is believed to carry a low risk of hepatic toxicity owing to its low affinity for the human P-450 enzyme. Therefore, hepatic failure caused by itraconazole is exceedingly rare.

Objectives: We report the case of a 46-year-old woman who developed hepatic failure related to itraconazole that was administered for the treatment of onychomycosis.

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A 25-pixel illumination system composed of a 5 × 5 dielectric liquid-lens (DLL) zoom module array, 25 light-emission diodes (LEDs), and a secondary optical lens demonstrates 3D light field manipulation. LEDs function as 2D illumination pixels while the DLL module array performs longitudinal illuminance adjustability by zooming each illumination pixel. A test on the similarity of two illuminance patterns between experiments and simulations shows a normalized cross correlation (NCC) higher than 0.

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This study presents packaged microscale liquid lenses actuated with liquid droplets of 300-700 μm in diameter using the dielectric force manipulation. The liquid microlens demonstrated function focal length tunability in a plastic package. The focal length of the liquid lens with a lens droplet of 500 μm in diameter is shortened from 4.

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Background: The cyclin-dependent kinase (CDK) inhibitor p27(Kip)¹ is downregulated in a majority of human cancers due to ectopic proteolysis by the ubiquitin-proteasome pathway. The expression of p27 is subject to multiple mechanisms of control involving several transcription factors, kinase pathways and at least three different ubiquitin ligases (SCF(SKP)², KPC, Pirh2), which regulate p27 transcription, translation, protein stability and subcellular localization. Using a chemical genetics approach, we have asked whether this control network can be modulated by small molecules such that p27 protein expression is restored in cancer cells.

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WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT Reflux oesophagitis is a common clinical disorder associated with significant morbidity. Proton pump inhibitors are the current pharmacotherapy of choice, but not all treated patients achieve symptom relief. Little is known about the efficacy of mosapride, a prokinetic agent which decreases episodes of gastro-oesophageal reflux, as an adjunct to proton pump inhibitors in improving the symptoms of reflux oesophagitis.

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Aim: The optimal dosage of proton pump inhibitor in bleeding peptic ulcers remains controversial. The aim was to compare the clinical effectiveness of two doses of infusional pantoprazole in peptic ulcer bleeding.

Methods: Peptic ulcer patients (n= 120) with bleeding stigmata were enrolled after successful endoscopic therapy.

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Macrophage infiltration and inflammatory cytokines are powerful drivers of tumorigenesis and metastasis. Wu et al., in this issue of Cancer Cell, show that TNFalpha-dependent NFkappaB activation induces COP9 signalosome-mediated inhibition of GSK3beta and the SCF(beta-TRCP) ubiquitin ligase, thus leading to stabilization of the transcription factor Snail and promoting cell migration and metastasis.

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Exocytosis of a single bovine adrenal chromaffin cell, triggered by histamine stimulation, was investigated via the electric responses detected with single-walled carbon-nanotube field-effect transistors (SWCNT-FET) and the morphological changes acquired by atomic force microscopy (AFM). Secretion of chromogranin A (CgA), stored in the vesicles of a single chromaffin cell, can be monitored in situ by the antibody against CgA (CgA-antibody) functionalized on the SWCNT-FET devices. The SWCNT-FET can further discriminate the amount of released CgA with different levels of histamine stimulations.

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Preexisting and acquired resistance to epidermal growth factor receptor (EGFR) inhibitors limits their clinical usefulness in patients with advanced non-small cell lung cancer (NSCLC). This study characterizes the efficacy and mechanisms of the combination of gefitinib or erlotinib with OSU-03012, a celecoxib-derived antitumor agent, to overcome EGFR inhibitor resistance in three NSCLC cell lines, H1155, H23, and A549. The OSU-03012/EGFR inhibitor combination induced pronounced apoptosis in H1155 and H23 cells, but not in A549 cells, suggesting a correlation between drug sensitivity and basal phospho-Akt levels independently of EGFR expression status.

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Calcium binding protein-1 (CaBP1) is a calmodulin like protein shown to modulate Ca2+ channel activities. Here, we explored the functions of long and short spliced CaBP1 variants (L- and S-CaBP1) in modulating stimulus-secretion coupling in primary cultured bovine chromaffin cells. L- and S-CaBP1 were cloned from rat brain and fused with yellow fluorescent protein at the C-terminal.

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Considering the role of aberrant beta-catenin signaling in tumorigenesis, we investigated the mechanism by which the peroxisome proliferator-activated receptor gamma (PPARgamma) agonist troglitazone facilitated beta-catenin down-regulation. We demonstrate that troglitazone and its more potent PPARgamma-inactive analogs Delta2TG and STG28 mediated the proteasomal degradation of beta-catenin in prostate cancer cells by up-regulating the expression of beta-transducin repeat-containing protein (beta-TrCP), an F-box component of the Skp1-Cul1-F-box protein E3 ubiquitin ligase. Evidence indicates that although small interfering RNA-mediated beta-TrCP knockdown protected cells against STG28-facilitated beta-catenin ablation, ectopic beta-TrCP expression enhanced the degradation.

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This study reports a histone deacetylation-independent mechanism whereby histone deacetylase (HDAC) inhibitors sensitize prostate cancer cells to DNA-damaging agents by targeting Ku70 acetylation. Ku70 represents a crucial component of the nonhomologous end joining repair machinery for DNA double-strand breaks (DSB). Our data indicate that pretreatment of prostate cancer cells with HDAC inhibitors (trichostatin A, suberoylanilide hydroxamic acid, MS-275, and OSU-HDAC42) led to increased Ku70 acetylation accompanied by reduced DNA-binding affinity without disrupting the Ku70/Ku80 heterodimer formation.

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