Enhanced performance in fluorene-free organometal halide perovskite light-emitting diodes using tunable, low electron affinity oxide electron injectors.

Fluorene-free perovskite light-emitting diodes (LEDs) with low turn-on voltages, higher luminance and sharp, color-pure electroluminescence are obtained by replacing the F8 electron injector with ZnO, which is directly deposited onto the CH3NH3PbBr3 perovskite using spatial atmospheric atomic layer deposition. The electron injection barrier can also be reduced by decreasing the ZnO electron affinity through Mg incorporation, leading to lower turn-on voltages.The authors would like to acknowledge funding from the Cambridge Commonwealth, European and International Trusts, Rutherford Foundation of New Zealand, A*STAR National Science Scholarship, Girton College Cambridge, Gates Cambridge Scholarship, EPSRC (Reference: EP/G060738/1), the ERC Advanced Investigator Grant, Novox, ERC-2009-adG 247276 and Cambridge Display Technology.This is the final version of the article. It was first published by Wiley at http://onlinelibrary.wiley.com/doi/10.1002/adma.201405044/abstract

Identifying and Reducing Interfacial Losses to Enhance Color-Pure Electroluminescence in Blue-Emitting Perovskite Nanoplatelet Light-Emitting Diodes.

Perovskite nanoplatelets (NPls) hold promise for light-emitting applications, having achieved photoluminescence quantum efficiencies approaching unity in the blue wavelength range, where other metal-halide perovskites have typically been ineffective. However, the external quantum efficiencies (EQEs) of blue-emitting NPl light-emitting diodes (LEDs) have reached only 0.12%. In this work, we show that NPl LEDs are primarily limited by a poor electronic interface between the emitter and hole injector. We show that the NPls have remarkably deep ionization potentials (≥6.5 eV), leading to large barriers for hole injection, as well as substantial nonradiative decay at the NPl/hole-injector interface. We find that an effective way to reduce these nonradiative losses is by using poly(triarylamine) interlayers, which lead to an increase in the  EQE of the blue (464 nm emission wavelength) and sky-blue (489 nm emission wavelength) LEDs to 0.3% and 0.55%, respectively. Our work also identifies the key challenges for further efficiency increases

MiR-128 Inhibits Tumor Growth and Angiogenesis by Targeting p70S6K1

MicroRNAs are a class of small noncoding RNAs that function as critical gene regulators through targeting mRNAs for translational repression or degradation. In this study, we showed that miR-128 expression levels were decreased in glioma, and identified p70S6K1 as a novel direct target of miR-128. Overexpression of miR-128 suppressed p70S6K1 and its downstream signaling molecules such as HIF-1 and VEGF expression, and attenuated cell proliferation, tumor growth and angiogenesis. Forced expression of p70S6K1 can partly rescue the inhibitory effect of miR-128 in the cells. Taken together, these findings will shed light to the role and mechanism of miR-128 in regulating glioma tumor angiogenesis via miR-128/p70S6K1 axis, and miR-128 may serve as a potential therapeutic target in glioma in the future

Evidence that talin alternative splice variants from Ciona intestinalis have different roles in cell adhesion

BACKGROUND: Talins are large, modular cytoskeletal proteins found in animals and amoebozoans such as Dictyostelium discoideum. Since the identification of a second talin gene in vertebrates, it has become increasingly clear that vertebrate Talin1 and Talin2 have non-redundant roles as essential links between integrins and the actin cytoskeleton in distinct plasma membrane-associated adhesion complexes. The conserved C-terminal I/LWEQ module is important for talin function. This structural element mediates the interaction of talins with F-actin. The I/LWEQ module also targets mammalian Talin1 to focal adhesion complexes, which are dynamic multicomponent assemblies required for cell adhesion and cell motility. Although Talin1 is essential for focal adhesion function, Talin2 is not targeted to focal adhesions. The nonvertebrate chordate Ciona intestinalis has only one talin gene, but alternative splicing of the talin mRNA produces two proteins with different C-terminal I/LWEQ modules. Thus, C. intestinalis contains two talins, Talin-a and Talin-b, with potentially different activities, despite having only one talin gene. RESULTS: We show here that, based on their distribution in cDNA libraries, Talin-a and Talin-b are differentially expressed during C. intestinalis development. The I/LWEQ modules of the two proteins also have different affinities for F-actin. Consistent with the hypothesis that Talin-a and Talin-b have different roles in cell adhesion, the distinct I/LWEQ modules of Talin-a and Talin-b possess different subcellular targeting determinants. The I/LWEQ module of Talin-a is targeted to focal adhesions, where it most likely serves as the link between integrin and the actin cytoskeleton. The Talin-b I/LWEQ module is not targeted to focal adhesions, but instead preferentially labels F-actin stress fibers. These different properties of C. intestinalis the Talin-a and Talin-b I/LWEQ modules mimic the differences between mammalian Talin1 and Talin2. CONCLUSION: Vertebrates and D. discoideum contain two talin genes that encode proteins with different functions. The urochordate C. intestinalis has a single talin gene but produces two separate talins by alternative splicing that vary in a domain crucial for talin function. This suggests that multicellular organisms require multiple talins as components of adhesion complexes. In C. intestinalis, alternative splicing, rather than gene duplication followed by neo-functionalization, accounts for the presence of multiple talins with different properties. Given that C. intestinalis is an excellent model system for chordate biology, the study of Talin-a and Talin-b will lead to a deeper understanding of cell adhesion in the chordate lineage and how talin functions have been parceled out to multiple proteins during metazoan evolution

Physicochemical, textural and viscoelastic properties of palm diacylglycerol bakery shortening during storage

BACKGROUND: Diacylglycerol (DAG), which has health-enhancing properties, is sometimes added to bakery shortening to produce baked products with enhanced physical functionality. Nevertheless, the quantity present is often too little to exert any positive healthful effects. This research aimed to produce bakery shortenings containing significant amounts of palm diacyglycerol (PDG). Physicochemical, textural and viscoelastic properties of the PDG bakery shortenings during 3 months storage were evaluated and compared with those of commercial bakery shortening (CS). RESULTS: PDG bakery shortenings (DS55, DS64 and DS73) had less significant increments in slip melting point (SMP), solid fat content (SFC) and hardness during storage as compared to CS. Unlike CS, melting behaviour and viscoelastic properties of PDG bakery shortenings remained unchanged during storage. As for polymorphic transformation, CS contained only β crystals after 8 weeks of storage. PDG bakery shortenings managed to retard polymorphic transformation for up to 10 weeks of storage in DS55 and 12 weeks of storage in DS64 and DS73. CONCLUSION: PDG bakery shortenings had similar if not better storage stability as compared to CS. This is mainly due to the ability of DAG to retard polymorphic transformation from β′ to β crystals. Thus, incorporation of DAG improved physical functionality of bakery shortening

Glucuronidation by UGT1A1 Is the Dominant Pathway of the Metabolic Disposition of Belinostat in Liver Cancer Patients

10.1371/journal.pone.0054522PLoS ONE81

Role and Mechanism of Arsenic in Regulating Angiogenesis

Arsenic is a wide spread carcinogen associated with several kinds of cancers including skin, lung, bladder, and liver cancers. Lung is one of the major targets of arsenic exposure. Angiogenesis is the pivotal process during carcinogenesis and chronic pulmonary diseases, but the role and mechanism of arsenic in regulating angiogenesis remain to be elucidated. In this study we show that short time exposure of arsenic induces angiogenesis in both human immortalized lung epithelial cells BEAS-2B and adenocarcinoma cells A549. To study the molecular mechanism of arsenic-inducing angiogenesis, we find that arsenic induces reactive oxygen species (ROS) generation, which activates AKT and ERK1/2 signaling pathways and increases the expression of hypoxia-inducible factor 1 (HIF-1) and vascular endothelial growth factor (VEGF). Inhibition of ROS production suppresses angiogenesis by decreasing AKT and ERK activation and HIF-1 expression. Inhibition of ROS, AKT and ERK1/2 signaling pathways is sufficient to attenuate arsenic-inducing angiogenesis. HIF-1 and VEGF are downstream effectors of AKT and ERK1/2 that are required for arsenic-inducing angiogenesis. These results shed light on the mechanism of arsenic in regulating angiogenesis, and are helpful to develop mechanism-based intervention to prevent arsenic-induced carcinogenesis and angiogenesis in the future

Coaction of Spheroid-Derived Stem-Like Cells and Endothelial Progenitor Cells Promotes Development of Colon Cancer

Although some studies described the characteristics of colon cancer stem cells (CSCs) and the role of endothelial progenitor cells (EPCs) in neovascularization, it is still controversial whether an interaction exists or not between CSCs and EPCs. In the present study, HCT116 and HT29 sphere models, which are known to be the cells enriching CSCs, were established to investigate the roles of this interaction in development and metastasis of colon cancer. Compared with their parental counterparts, spheroid cells demonstrated higher capacity of invasion, higher tumorigenic and metastatic potential. Then the in vitro and in vivo relationship between CSCs and EPCs were studied by using capillary tube formation assay and xenograft models. Our results showed that spheroid cells could promote the proliferation, migration and tube formation of EPCs through secretion of vascular endothelial growth factor (VEGF). Meanwhile, the EPCs could increase tumorigenic capacity of spheroid cells through angiogenesis. Furthermore, higher microvessel density was detected in the area enriching cancer stem cells in human colon cancer tissue. Our findings indicate that spheroid cells possess the characteristics of cancer stem cells, and the coaction of CSCs and EPCs may play an important role in the development of colon cancer

A functional variant in the Stearoyl-CoA desaturase gene promoter enhances fatty acid desaturation in pork

There is growing public concern about reducing saturated fat intake. Stearoyl-CoA desaturase (SCD) is the lipogenic enzyme responsible for the biosynthesis of oleic acid (18:1) by desaturating stearic acid (18:0). Here we describe a total of 18 mutations in the promoter and 3′ non-coding region of the pig SCD gene and provide evidence that allele T at AY487830:g.2228T>C in the promoter region enhances fat desaturation (the ratio 18:1/18:0 in muscle increases from 3.78 to 4.43 in opposite homozygotes) without affecting fat content (18:0+18:1, intramuscular fat content, and backfat thickness). No mutations that could affect the functionality of the protein were found in the coding region. First, we proved in a purebred Duroc line that the C-T-A haplotype of the 3 single nucleotide polymorphisms (SNPs) (g.2108C>T; g.2228T>C; g.2281A>G) of the promoter region was additively associated to enhanced 18:1/18:0 both in muscle and subcutaneous fat, but not in liver. We show that this association was consistent over a 10-year period of overlapping generations and, in line with these results, that the C-T-A haplotype displayed greater SCD mRNA expression in muscle. The effect of this haplotype was validated both internally, by comparing opposite homozygote siblings, and externally, by using experimental Duroc-based crossbreds. Second, the g.2281A>G and the g.2108C>T SNPs were excluded as causative mutations using new and previously published data, restricting the causality to g.2228T>C SNP, the last source of genetic variation within the haplotype. This mutation is positioned in the core sequence of several putative transcription factor binding sites, so that there are several plausible mechanisms by which allele T enhances 18:1/18:0 and, consequently, the proportion of monounsaturated to saturated fat.This research was supported by grants from the Spanish Ministry of Science and Innovation (AGL2009-09779 and AGL2012-33529). RRF is recipient of a PhD scholarship from the Spanish Ministry of Science and Innovation (BES-2010-034607). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of manuscript