Stretchable electroluminescent device is a compliant form of light-emitting device to expand the application areas of conventional optoelectronics on rigid wafers. Currently, practical implementations are impeded by the high operating voltage required to achieve sufficient brightness. In this study, we report the fabrication of an intrinsically stretchable electroluminescent device based on silver nanowire electrodes and high-k thermoplastic elastomers. The device exhibits a bright emission with a low driving voltage by using polar elastomer as a dielectric matrix of the electroluminescent layer. Highly stretchable silver nanowire electrodes contribute to the exceptional elasticity and durability of the device in spite of bending, stretching, twisting, puncturing, and cutting. Stretchable electroluminescent devices developed here may find potential uses in wearable displays, deformable lightings, and soft robotics.

Stretchable alternating current electroluminescent display is an emerging form of light-emitting device by combining elasticity with optoelectronic properties. The practical implementations are currently impeded by the high operating voltages required to achieve sufficient brightness. In this study, we report the development of dielectric nanocomposites by filling surface-modified ceramic nanoparticles into polar elastomers, which exhibit a series of desirable attributes, in terms of high permittivity, mechanical deformability, and solution processability. Dielectric nanocomposite effectively concentrates electric fields onto phosphor to enable low-voltage operation of stretchable electroluminescent display, thereby alleviating safety concerns toward wearable applications. The practical feasibility is demonstrated by an epidermal stopwatch that allows intimate integration with the human body. The high-permittivity nanocomposites reported here represent an attractive building block for stretchable electronic systems, which may find broad range of applications in intrinsically stretchable transistors, sensors, light-emitting devices, and energy-harvesting devices.

In response to a growing demand for subnational and spatially explicit data on China's future population, this study estimates China's provincial population from 2010 to 2100 by age (0-100+), sex (male and female) and educational levels (illiterate, primary school, junior-high school, senior-high school, college, bachelor's, and master's and above) under different shared socioeconomic pathways (SSPs). The provincial projection takes into account fertility promoting policies and population ceiling restrictions of megacities that have been implemented in China in recent years to reduce systematic biases in current studies. The predicted provincial population is allocated to spatially explicit population grids for each year at 30 arc-seconds resolution based on representative concentration pathway (RCP) urban grids and historical population grids. The provincial projection data were validated using population data in 2017 from China's Provincial Statistical Yearbook, and the accuracy of the population grids in 2015 was evaluated. These data have numerous potential uses and can serve as inputs in climate policy research with requirements for precise administrative or spatial population data in China.

Histone acetylation has been linked to developmental changes in gene expression and is a validated drug target of apicomplexan parasites, but little is known about the roles of individual histone modifying enzymes and how they are recruited to target genes. The protozoan parasite Toxoplasma gondii (phylum Apicomplexa) is unusual among invertebrates in possessing two GCN5-family lysine acetyltransferases (KATs). While GCN5a is required for gene expression in response to alkaline stress, this KAT is dispensable for parasite proliferation in normal culture conditions. In contrast, GCN5b cannot be disrupted, suggesting it is essential for Toxoplasma viability. To further explore the function of GCN5b, we generated clonal parasites expressing an inducible HA-tagged dominant-negative form of GCN5b containing a point mutation that ablates enzymatic activity (E703G). Stabilization of this dominant-negative GCN5b was mediated through ligand-binding to a destabilization domain (dd) fused to the protein. Induced accumulation of the ddHAGCN5b(E703G) protein led to a rapid arrest in parasite replication. Growth arrest was accompanied by a decrease in histone H3 acetylation at specific lysine residues as well as reduced expression of GCN5b target genes in GCN5b(E703G) parasites, which were identified using chromatin immunoprecipitation coupled with microarray hybridization (ChIP-chip). Proteomics studies revealed that GCN5b interacts with AP2-domain proteins, apicomplexan plant-like transcription factors, as well as a “core complex” that includes the co-activator ADA2-A, TFIID subunits, LEO1 polymerase-associated factor (Paf1) subunit, and RRM proteins. The dominant-negative phenotype of ddHAGCN5b(E703G) parasites, considered with the proteomics and ChIP-chip data, indicate that GCN5b plays a central role in transcriptional and chromatin remodeling complexes. We conclude that GCN5b has a non-redundant and indispensable role in regulating gene expression required during the Toxoplasma lytic cycle.

Cancer stem cells (CSCs) have recently been linked to new treatment strategies for gastric cancer due to the critical role which they play as the 'heartbeat' of cancer. In the present study, we explored the effects of quercetin, an anti-inflammatory and antiviral compound, on gastric CSCs (GCSCs). We noted that quercetin exerted pronounced inhibitory effects on GCSC survival. Moreover, quercetin induced cell apoptosis in a mitochondrial-dependent manner, as shown by the reduction in mitochondrial membrane potential, the activation of caspase-3 and -9, and the downregulation of Bcl-2, as well as the upregulation of Bax and cytochrome c (Cyt-c). Additionally, a marked decrease in Akt phosphorylation levels was observed following treatment with quercetin, whereas pre-treatment with fumonisin B1 (FB1, Akt activator) significantly attenuated the inhibitory effects of quercetin on cell growth and its promoting effects on mitochondrial-dependent apoptosis. Notably, FB1 enhanced the expression of Bcl-2, which was inhibited by quercetin, and prevented the decrease in mitochondrial membrane potential induced by quercetin. However, the increase in the levels of caspases, Bax and Cyt-c induced by quercetin was also attenuated by the addition of FB1 to the GCSCs. Therefore, our results demonstrate that quercetin triggers mitochondrial apoptotic-dependent growth inhibition via the blockade of phosphoinositide 3-kinase (PI3K)-Akt signaling in GCSCs, indicating a potential target for the treatment of gastric cancer.

In Gram-positive bacteria, the RNA transcripts of many amino acid biosynthetic and aminoacyltRNA synthetase genes contain 5' untranslated regions, or leader RNAs, that function as riboswitches. These T bxo riboswitches bind cognate tRNA molecules and regulate gene expression by a transcription attenuation mechanism. The Specifier Loop domain of the leader RNA contains nucleotides that pair with nucleotides in the tRNA anticodon loop and is flanked on one side by a kink-turn, or GA, sequence motif. We have determined the solution NMR structure of the kink-turn (K-turn) sequence element within the context of the Specifier Loop domain. The K-turn sequence motif has several non-canonical base pairs typical of K-turn structures but adopts an extended conformation. The Specifier Loop domain contains a loop E structural motif and the single strand Specifier nucleotides stack with their Watson-Crick edges displaced toward the minor groove. Mg 2+ leads to significant bending of the helix axis at the base of the Specifier Loop domain, but does not alter the K-turn. ITC indicates that the K-turn sequence causes a small enhancement of the interaction between tRNA anticodon arm with the Specifier Loop domain. One possibility is that the K-turn structure is formed and stabilized when tRNA binds the T box riboswitch and interacts with Stem I and the antiterminator helix. This motif in turn anchors the orientation of Stem I relative to the 3' half of the leader RNA, further stabilizing the tRNA-T box complex.

The conversion of excess ammonia N into harmless N2 is a primary challenge for wastewater treatment. We present here a method to generate ClO• directionally for quick and efficient decomposition of NH4 + N to N2. ClO• was produced and enhanced by a bifacial anode, a front WO3 photoanode and a rear Sb–SnO2 anode, in which HO• generated on WO3 reacts with HClO generated on Sb–SnO2 to form ClO•. Results show that the ammonia decomposition rate of Sb–SnO2/WO3 is 4.4 times than that of WO3 and 3.3 times than that of Sb–SnO2, with achievement of the removal of NH4 + N on Sb–SnO2/WO3 and WO3 being 99.2 and 58.3% in 90 min, respectively. This enhancement is attributed to the high rate constant of ClO• with NH4 + N, which is 2.8 and 34.8 times than those of Cl• and HO•, respectively. The steady-state concentration of ClO• (2.5 × 10–13 M) is 102 times those of HO• and Cl•, and this is further confirmed by kinetic simulations. In combination with the Pd–Cu/NF cathode to form a denitrification exhaustion system, Sb–SnO2/WO3 shows excellent total nitrogen removal (98.4%), which is more effective than WO3 (47.1%) in 90 min. This study provides new insight on the directed ClO• generation and its application on ammonia wastewater treatment.

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