Metal β-diketoiminate precursor use in aerosol assisted chemical vapour deposition of gallium- and aluminium-doped zinc oxide

Aerosol assisted chemical vapour deposition (AACVD) has been used to deposit thin films of ZnO from the single-source precursor [Zn(OC(Me)CHC(Me)N( i Pr)) 2 ] (1) affording highly transparent ( > 80%) and conductive films (sheet resistance ∼70 KΩ/sq). Extension of this AACVD method whereby related precursors of the type, [R 2 M(OC(Me)CHC(Me)N( i Pr))] (R = Et, M = Al (2); R = Me, M = Ga (3)), isolated as oils, were added to the precursor solution allowed for the deposition of aluminium- and gallium-doped ZnO (AZO and GZO) films, respectively. Complexes 1–3 were characterised by elemental analysis, NMR and mass spectrometry. Films were deposited in under 30 min at 400 °C, from CH 2 Cl 2 /toluene solutions with a N 2 carrier gas. Herein we report the bulk resistivity, ρ, of AZO (0.252 Ω cm) and GZO (0.756 Ω cm) films deposited from this novel approach. All the films transparency exceeded 80% in the visible, X-ray diffraction (XRD) showed all films to crystallise in the wurtzite phase whilst X-ray photoemission spectroscopy (XPS) confirmed the presence of the Al and Ga dopants in the films, and highlighted the low C-contamination ( < 5%) this route offers. Investigation of a mechanism analogous to the Kirkendall effect confirmed that heating of GZO films at 1000 °C produced the spinel structure GaZn 2 O 4

Loss of Endometrial Plasticity in Recurrent Pregnancy Loss

© 2015 AlphaMed Press.Menstruation drives cyclic activation of endometrial progenitor cells, tissue regeneration, and maturation of stromal cells, which differentiate into specialized decidual cells prior to and during pregnancy. Aberrant responsiveness of human endometrial stromal cells (HESCs) to deciduogenic cues is strongly associated with recurrent pregnancy loss (RPL), suggesting a defect in cellular maturation. MeDIP-seq analysis of HESCs did not reveal gross perturbations in CpG methylation in RPL cultures, although quantitative differences were observed in or near genes that are frequently deregulated in vivo. However, RPL was associated with a marked reduction in methylation of defined CA-rich motifs located throughout the genome but enriched near telomeres. Non-CpG methylation is a hallmark of cellular multipotency. Congruently, we demonstrate that RPL is associated with a deficiency in endometrial clonogenic cell populations. Loss of epigenetic stemness features also correlated with intragenic CpG hypomethylation and reduced expression of HMGB2, coding high mobility group protein 2. We show that knockdown of this sequence-independent chromatin protein in HESCs promotes senescence and impairs decidualization, exemplified by blunted time-dependent secretome changes. Our findings indicate that stem cell deficiency and accelerated stromal senescence limit the differentiation capacity of the endometrium and predispose for pregnancy failure. Stem Cells 2016;34:346-356 Recurrent pregnancy loss is caused by endometrial stem cell deficiency, triggering heightened tissue senescence and impaired decidualization

Large-Scale Selective Sweep among Segregation Distorter Chromosomes in African Populations of Drosophila melanogaster

Segregation Distorter (SD) is a selfish, coadapted gene complex on chromosome 2 of Drosophila melanogaster that strongly distorts Mendelian transmission; heterozygous SD/SD+ males sire almost exclusively SD-bearing progeny. Fifty years of genetic, molecular, and theory work have made SD one of the best-characterized meiotic drive systems, but surprisingly the details of its evolutionary origins and population dynamics remain unclear. Earlier analyses suggested that the SD system arose recently in the Mediterranean basin and then spread to a low, stable equilibrium frequency (1–5%) in most natural populations worldwide. In this report, we show, first, that SD chromosomes occur in populations in sub-Saharan Africa, the ancestral range of D. melanogaster, at a similarly low frequency (∼2%), providing evidence for the robustness of its equilibrium frequency but raising doubts about the Mediterranean-origins hypothesis. Second, our genetic analyses reveal two kinds of SD chromosomes in Africa: inversion-free SD chromosomes with little or no transmission advantage; and an African-endemic inversion-bearing SD chromosome, SD-Mal, with a perfect transmission advantage. Third, our population genetic analyses show that SD-Mal chromosomes swept across the African continent very recently, causing linkage disequilibrium and an absence of variability over 39% of the length of the second chromosome. Thus, despite a seemingly stable equilibrium frequency, SD chromosomes continue to evolve, to compete with one another, or evade suppressors in the genome

LiBiNorm: an htseq-count analogue with improved normalisation of Smart-seq2 data and library preparation diagnostics

Protocols for preparing RNA sequencing (RNA-seq) libraries, most prominently “Smart-seq” variations, introduce global biases that can have a significant impact on the quantification of gene expression levels. This global bias can lead to drastic over- or under-representation of RNA in non-linear length-dependent fashion due to enzymatic reactions during cDNA production. It is currently not corrected by any RNA-seq software, which mostly focus on local bias in coverage along RNAs. This paper describes LiBiNorm, a simple command line program that mimics the popular htseq-count software and allows diagnostics, quantification, and global bias removal. LiBiNorm outputs gene expression data that has been normalized to correct for global bias introduced by the Smart-seq2 protocol. In addition, it produces data and several plots that allow insights into the experimental history underlying library preparation. The LiBiNorm package includes an R script that allows visualization of the main results. LiBiNorm is the first software application to correct for the global bias that is introduced by the Smart-seq2 protocol. It is freely downloadable at http://www2.warwick.ac.uk/fac/ sci/lifesci/research/libinorm