Improved diffusion and storage of lithium ions via recrystallization induced conducting pathways in a Li:TaO-based electrolyte for all-solid-state electrochromic devices with enhanced performance.

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.

Neural Crest-Like Stem Cell Transcriptome Analysis Identifies LPAR1 in Melanoma Progression and Therapy Resistance.

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.

SARS-CoV-2 ORF9c Is a Membrane-Associated Protein that Suppresses Antiviral Responses in Cells.

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.

Reducing Interface Traps with High Density Hydrogen Treatment to Increase Passivated Emitter Rear Contact Cell Efficiency.

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.

Cross Talk between eIF2α and eEF2 Phosphorylation Pathways Optimizes Translational Arrest in Response to Oxidative Stress.

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.

Improvement of the Mechanical Properties of 1022 Carbon Steel Coil by Using the Taguchi Method to Optimize Spheroidized Annealing Conditions.

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.

A Network of Conserved Synthetic Lethal Interactions for Exploration of Precision Cancer Therapy.

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.

Small Molecule Inhibition of the Autophagy Kinase ULK1 and Identification of ULK1 Substrates.

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.

Downregulation of c-SRC kinase CSK promotes castration resistant prostate cancer and pinpoints a novel disease subclass.

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.

Systems analysis of the prostate tumor suppressor NKX3.1 supports roles in DNA repair and luminal cell differentiation.

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.

An MBS-assisted femtocell transmit power control scheme with mobile user QoS guarantee in 2-tier heterogeneous femtocell networks.

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.

Three-dimensional illumination system using dielectric liquid lenses.

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.

Chemical genetics approach to restoring p27Kip1 reveals novel compounds with antiproliferative activity in prostate cancer cells.

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.

Inflamed snail speeds metastasis.

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.

Exocytosis of a single bovine adrenal chromaffin cell: the electrical and morphological studies.

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.

Targeting endoplasmic reticulum stress and Akt with OSU-03012 and gefitinib or erlotinib to overcome resistance to epidermal growth factor receptor inhibitors.

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.

Ca2+ binding protein-1 inhibits Ca2+ currents and exocytosis in bovine chromaffin cells.

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.

Histone deacetylase inhibitors sensitize prostate cancer cells to agents that produce DNA double-strand breaks by targeting Ku70 acetylation.

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.

Peroxisome proliferator-activated receptor gamma-independent suppression of androgen receptor expression by troglitazone mechanism and pharmacologic exploitation.

Previously, we showed that the peroxisome proliferator-activated receptor gamma (PPARgamma) agonist troglitazone at high doses was able to suppress androgen receptor (AR) expression in LNCaP prostate cancer cells independently of PPARgamma. Pharmacologic exploitation of this finding led to STG28, a PPARgamma-inactive analogue of troglitazone with substantially higher potency in AR repression. Considering the pivotal role of AR in prostate tumorigenesis, this study investigates the mechanism by which troglitazone and derivatives suppress AR expression in LNCaP cells.

alpha-Tocopheryl succinate induces apoptosis in prostate cancer cells in part through inhibition of Bcl-xL/Bcl-2 function.

Although the antitumor effect of alpha-tocopheryl succinate (vitamin E succinate) has been well demonstrated, its underlying mechanism remains elusive. This study provides evidence that inhibition of Bcl-xL/Bcl-2 function represents a major pathway whereby alpha-tocopheryl succinate mediates apoptosis induction in prostate cancer cells. In vitro data indicate that alpha-tocopheryl succinate was able to disrupt the binding of Bak BH3 peptide to Bcl-xL and Bcl-2 with IC50 of 26 microm, in line with its potency in antiproliferation.

Peroxisome proliferator-activated receptor gamma-independent repression of prostate-specific antigen expression by thiazolidinediones in prostate cancer cells.

In light of the potential use of the thiazolidinedione family of peroxisome proliferator-activated receptor-gamma (PPARgamma) agonists in prostate cancer treatment, this study assessed the mechanism by which these agents suppress prostate-specific antigen (PSA) secretion in prostate cancer cells. Two lines of evidence indicate that the effect of thiazolidinediones on PSA down-regulation is independent of PPARgamma activation. First, this thiazolidinedione-mediated PSA down-regulation is structure-specific irrespective of the relative PPARgamma agonist potency.

Thiazolidenediones mediate apoptosis in prostate cancer cells in part through inhibition of Bcl-xL/Bcl-2 functions independently of PPARgamma.

Certain members of the thiazolidenedione family of the peroxisome proliferator-activated receptor gamma (PPARgamma) agonists, such as troglitazone and ciglitazone, exhibit antitumor effects; however, the underlying mechanism remains inconclusive. This study shows that the effect of these thiazolidenedione members on apoptosis in prostate cancer cells is independent of PPARgamma activation. First, close structural analogues of thiazolidenediones, whereas devoid of PPARgamma activity, retain the ability to induce apoptosis with equal potency.