Solution-Processed Chloroaluminum Phthalocyanine (ClAlPc) Ammonia Gas Sensor with Vertical Organic Porous Diodes.

In this research work, the gas sensing properties of halogenated chloroaluminum phthalocyanine (ClAlPc) thin films were studied at room temperature. We fabricated an air-stable ClAlPc gas sensor based on a vertical organic diode (VOD) with a porous top electrode by the solution process method. The surface morphology of the solution-processed ClAlPc thin film was examined by field emission scanning electron microscopy (FESEM) and atomic force microscopy (AFM). The proposed ClAlPc-based VOD sensor can detect ammonia (NH3) gas at the ppb level (100~1000 ppb) at room temperature. Additionally, the ClAlPc sensor was highly selective towards NH3 gas compared to other interfering gases (NO2, ACE, NO, H2S, and CO). In addition, the device lifetime was tested by storing the device at ambient conditions. The effect of relative humidity (RH) on the ClAlPc NH3 gas sensor was also explored. The aim of this study is to extend these findings on halogenated phthalocyanine-based materials to practical electronic nose applications in the future.

Pemetrexed induces both intrinsic and extrinsic apoptosis through ataxia telangiectasia mutated/p53-dependent and -independent signaling pathways.

Pemetrexed, a new-generation antifolate, has demonstrated promising single-agent activity in front- and second-line treatments of non-small cell lung cancer. However, the molecular mechanism of pemetrexed-mediated antitumor activity remains unclear. The current study shows that pemetrexed induced DNA damage and caspase-2, -3, -8, and -9 activation in A549 cells and that treatment with caspase inhibitors significantly abolished cell death, suggesting a caspase-dependent apoptotic mechanism. The molecular events of pemetrexed-mediated apoptosis was associated with the activation of ataxia telangiectasia mutated (ATM)/p53-dependent and -independent signaling pathways, which promoted intrinsic and extrinsic apoptosis by upregulating Bax, PUMA, Fas, DR4, and DR5 and activating the caspase signaling cascade. Supplementation with dTTP allowed normal S-phase progression and rescued apoptotic death in response to pemetrexed. Overall, our findings reveal that the decrease of thymidylate synthase and the increase of Bax, PUMA, Fas, DR4, and DR5 genes may serve as biomarkers for predicting responsiveness to pemetrexed.

First Order Rate Law Analysis for Reset State in Vanadium Oxide Thin Film Resistive Random Access Memory Devices.

In the reset state, the decay reaction mechanism and bipolar switching properties of vanadium oxide thin film RRAM devices for LRS/HRS are investigated and discussed here. To discover the properties of I-V switching curves, the first order rate law behaviors of the reset state between the resistant variety properties and the reaction time were observed. To verify the decay reaction mechanism in the reset state, vanadium oxide thin films from RRAM devices were measured by different constant voltage sampling and exhibited the same decay reaction rate constant. Finally, the electrical conduction transfer mechanism and metallic filament forming model described by I-V switching properties of the RRAM devices were proven and investigated.

Multicolor Emission from Ultraviolet GaN-Based Photonic Quasicrystal Nanopyramid Structure with Semipolar InxGa1-xN/GaN Multiple Quantum Wells.

In this study, we demonstrated large-area high-quality multi-color emission from the 12-fold symmetric GaN photonic quasicrystal nanorod device which was fabricated using the nanoimprint lithography technology and multiple quantum wells regrowth procedure. High-efficiency blue and green color emission wavelengths of 460 and 520 nm from the regrown InxGa1-xN/GaN multiple quantum wells were observed under optical pumping conditions. To confirm the strong coupling between the quantum well emissions and the photonic crystal band-edge resonant modes, the finite-element method was applied to perform a simulation of the 12-fold symmetry photonic quasicrystal lattices.

Hydrophobic and Hydrophilic Conjugated Polymer Dots as Binary Photocatalysts for Enhanced Visible-Light-Driven Hydrogen Evolution through Förster Resonance Energy Transfer.

Organic semiconducting polymers exhibited promising photocatalytic behavior for hydrogen (H2) evolution, especially when prepared in the form of polymer dots (Pdots). However, the Pdot structures were formed using common nonconjugated amphiphilic polymers, which have a negative effect on charge transfer between photocatalysts and reactants and are unable to participate in the photocatalytic reaction. This study presents a new strategy for constructing binary Pdot photocatalysts by replacing the nonconjugated amphiphilic polymer typically employed in the preparation of polymer nanoparticles (Pdots) with a low-molecular-weight conjugated polyelectrolyte. The as-prepared polyelectrolyte/hydrophobic polymer-based binary Pdots truly enhance the electron transfer between the Pt cocatalyst and the polymer photocatalyst with good water dispersibility. Moreover, unlike the nonconjugated amphiphilic polymer, the photophysics and mechanism of this photocatalytic system through time-correlated single-photon counting (TCSPC) and transient absorption (TA) measurements confirmed the Förster resonance energy transfer (FRET) between the polyelectrolyte as a donor and the hydrophobic polymer as an acceptor. As a result, the designated binary Pdot photocatalysts significantly enhanced the hydrogen evolution rate (HER) of 43 900 µmol g-1 h-1 (63.5 µmol h-1, at 420 nm) for PTTPA/PFTBTA Pdots under visible-light irradiation.

Pemetrexed induces S-phase arrest and apoptosis via a deregulated activation of Akt signaling pathway.

Pemetrexed is approved for first-line and maintenance treatment of patients with advanced or metastatic non-small-cell lung cancer (NSCLC). The protein kinase Akt/protein kinase B is a well-known regulator of cell survival which is activated by pemetrexed, but its role in pemetrexed-mediated cell death and its molecular mechanisms are unclear. This study showed that stimulation with pemetrexed induced S-phase arrest and cell apoptosis and a parallel increase in sustained Akt phosphorylation and nuclear accumulation in the NSCLC A549 cell line. Inhibition of Akt expression by Akt specific siRNA blocked S-phase arrest and protected cells from apoptosis, indicating an unexpected proapoptotic role of Akt in the pemetrexed-mediated toxicity. Treatment of A549 cells with pharmacological inhibitors of phosphatidylinositol 3-kinase (PI3K), wortmannin and Ly294002, similarly inhibited pemetrexed-induced S-phase arrest and apoptosis and Akt phosphorylation, indicating that PI3K is an upstream mediator of Akt and is involved in pemetrexed-mediated cell death. Previously, we identified cyclin A-associated cyclin-dependent kinase 2 (Cdk2) as the principal kinase that was required for pemetrexed-induced S-phase arrest and apoptosis. The current study showed that inhibition of Akt function and expression by pharmacological inhibitors as well as Akt siRNA drastically inhibited cyclin A/Cdk2 activation. These pemetrexed-mediated biological and molecular events were also observed in a H1299 cell line. Overall, our results indicate that, in contrast to its normal prosurvival role, the activated Akt plays a proapoptotic role in pemetrexed-mediated S-phase arrest and cell death through a mechanism that involves Cdk2/cyclin A activation.

Sustained activation of ERK and Cdk2/cyclin-A signaling pathway by pemetrexed leading to S-phase arrest and apoptosis in human non-small cell lung cancer A549 cells.

Pemetrexed, a multitargeted antifolate with the ability to inhibit several enzymes involved in purine and pyrimidine syntheses, has demonstrated clinical activity in non-small cell lung cancer cells, as well as in a broad array of other solid tumors. In this study, we show that inducing cell cycle S-phase arrest and apoptosis in human lung adenocarcinoma A549 cells with pemetrexed is associated with increased cyclin-A and cyclin-dependent kinase 2 (Cdk2) protein and Cdk2/cyclin-A kinase activity. Knockdown of cyclin-A using small interfering RNA (siRNA), and inhibiting Cdk2 activity with flavopiridol, strikingly reduced S-phase arrest and apoptosis. Moreover, pemetrexed induced sustained activation of extracellular signal-regulated kinase1/2 (ERK1/2). Knockdown of ERK1/2 using specific siRNA, as well as known inhibitors (PD98059 and U0126), effectively suppressed the expression of cyclin-A and Cdk2, and reduced S-phase arrest and apoptosis induced by pemetrexed. These data provide the first evidence that pemetrexed-induced S-phase arrest and apoptosis is associated with an increase in Cdk2 and cyclin-A expression and activation, which is ERK-dependent and upstream of caspase-3. Our findings suggest that the ERK-mediated Cdk2/cyclin-A signaling pathway is an important regulator of pemetrexed-induced S-phase arrest and apoptotic cell death.