Structural, Optical and Electrochromic Properties of Sol–Gel V

Vanadium pentoxide thin films are prepared by the sol–gel route by dissolving V2O5 powder (99.5% purity) in H2O2 solution. The solution is spin-coated on glass substrates for optical (UV–VIS–NIR) and XRD analysis, and on ITOcoated glass substrates for electrochromic measurements. The samples are then annealed at 150°C for 1 hour. The resulting films have a yellow-orange color, typical of polycrystalline V2O5. XRD measurements have shown that after annealing in air at 400°C the structure of the films has a c-axis preferred orientation, the (0 0 1)-type planes lying parallel to the substrate. SEM analysis revealed a smooth surface. The films’ optical and physical constants (n, α, Eg, the thickness d and the mean thickness inhomogeneity s) are calculated using a simple and accurate method based on the transmission spectrum alone. The films’ electrochromism is studied using cyclic voltammetry (CV) and chronoamperometry in propylene carbonate solution containing 1 mol/l LiCIO4. The films show reversible multichromism (yellow–green–blue) upon Li+ ion insertion/extraction. The absorbance of films colored at three different potentials is measured in the UV–VIS–PIR wavelength range, and this study shows that the changes in the optical absorption are consistent with the film color changes. Finally, the optical and electrochromic properties of the films prepared by this method are compared with those of our sputtered films already studied and with other works

Schottky Diodes and Thin Films Based on Copolymer: Poly(aniline-co-toluidine)

Poly(aniline-co-o-toluidine) (PANI-co-POT) thin films were deposited on indium tin oxide- (ITO-) coated glass substrates by electrochemical polymerization under cyclic voltammetric conditions from aniline-co-o-toluidine monomer in an aqueous solution of HCl as a supporting electrolyte. These measurements showed that the optical band gap of the copolymer films is on the order of 2.65 eV. On the other hand, ITO/PANI-co-POT/Al devices were fabricated by thermal evaporation of Aluminum circular electrodes on the as-deposited PANI-co-POT films. The Current-Voltage characteristics of these devices are nonlinear. The diode parameters were calculated from I-V characteristics using the modified Shockley equation. The C-F characteristics were also measured

Dielectric Behavior of Ceramic (BST)/Epoxy Thick Films

Composite materials were made by mixing powders of Ba1−xSrxTiO3 (x=0.2 and 0.4) ceramics and epoxy resin with various volume fractions (vol%). Dielectric measurements of these composites were performed as a function of filler ratio in the range 100–360°K at 10 KHz. The dielectric constant of the composite increased with increasing volume fraction varies slightly with temperature. The 20 vol% of BST(0.4)-epoxy composite had the highest dielectric constant of 19.4 and dielectric loss tangent of 0.027. Among the dielectric mixing models presented, the model of Lichtenecker shows the best fit to the experimental data for both composites

Structural, Optical and Electrochromic Properties of Nanocrystalline TiO

Nanocrystalline TiO2 thin filmswere prepared by spin coating on covered glass substrates with an indium tin oxide (ITO) layer. The structural, electrochromic and optical properties of the films were investigated. The films are crystallized predominantly in the anatase phase with lattice parameters a = b = 0.378 nm and c = 0.958 nm . The crystallite size was found to be of the order of 14 nm. The films showed reversible coloration/bleaching cycles as demonstrated by cyclic voltametry and current–time transients. The transmission of the blue colored films decreased and their absorption edge was less sharp and shifted to higher wavelengths as a result of the intercalation of Li+ ions

Warsaw Breakage Syndrome associated DDX11 helicase resolves G-quadruplex structures to support sister chromatid cohesion

Warsaw Breakage Syndrome (WABS) is a rare disorder related to cohesinopathies and Fanconi anemia, caused by bi-allelic mutations in DDX11. Here, we report multiple compound heterozygous WABS cases, each displaying destabilized DDX11 protein and residual DDX11 function at the cellular level. Patient-derived cell lines exhibit sensitivity to topoisomerase and PARP inhibitors, defective sister chromatid cohesion and reduced DNA replication fork speed. Deleting DDX11 in RPE1-TERT cells inhibits proliferation and survival in a TP53-dependent manner and causes chromosome breaks and cohesion defects, independent of the expressed pseudogene DDX12p. Importantly, G-quadruplex (G4) stabilizing compounds induce chromosome breaks and cohesion defects which are strongly aggravated by inactivation of DDX11 but not FANCJ. The DNA helicase domain of DD

Somatic genomic alterations in retinoblastoma beyond RB1 are rare and limited to copy number changes

Retinoblastoma is a rare childhood cancer initiated by RB1 mutation or MYCN amplification, while additional alterations may be required for tumor development. However, the view on single nucleotide variants is very limited. To better understand oncogenesis, we determined the genomic landscape of retinoblastoma. We performed exome sequencing of 71 retinoblastomas and matched blood DNA. Next, we determined the presence of single nucleotide variants, copy number alterations and viruses. Aside from RB1, recurrent gene mutations were very rare. Only a limited fraction of tumors showed BCOR (7/71, 10%) or CREBBP alterations (3/71, 4%). No evidence was found for the presence of viruses. Instead, specific somatic copy number alterations were more common, particularly in patients diagnosed at later age. Recurrent alterations of chromosomal arms often involved less than one copy, also in highly pure tumor samples, suggesting within-tumor heterogeneity. Our results show that retinoblastoma is among the least mutated cancers and signify the extreme sensitivity of the childhood retina for RB1 loss. We hypothesize that retinoblastomas arising later in retinal development benefit more from subclonal secondary alterations and therefore, these alterations are more selected for in these tumors. Targeted therapy based on these subclonal events might be insufficient for complete tumor control

Absence of the MGMT protein as well as methylation of the MGMT promoter predict the sensitivity for temozolomide

The DNA repair protein O(6)-methylguanine-DNA methyltransferase (MGMT) can cause resistance to the alkylating drug temozolomide (TMZ). The purpose of this study was to determine the relationship between the MGMT status, determined by means of several techniques and methods, and the cytotoxic response to TMZ in 11 glioblastoma multiforme (GBM) cell lines and 5 human tumour cell lines of other origins. Cell survival was analysed by clonogenic assay. The MGMT protein levels were assessed by western blot analysis. The MGMT promoter methylation levels were determined using methylation-specific multiplex ligation-dependent probe amplification (MS-MLPA) and quantitative real-time methylation-specific PCR (qMSP). On the basis of the results of these techniques, six GBM cell lines were selected and subjected to bisulphite sequencing. The MGMT protein was detected in all TMZ-resistant cell lines, whereas no MGMT protein could be detected in cell lines that were TMZ sensitive. The MS-MLPA results were able to predict TMZ sensitivity in 9 out of 16 cell lines (56%). The qMSP results matched well with TMZ sensitivity in 11 out of 12 (92%) glioma cell lines. In addition, methylation as detected by bisulphite sequencing seemed to be predictive of TMZ sensitivity in all six cell lines analysed (100%). The MGMT protein expression more than MGMT promoter methylation status predicts the response to TMZ in human tumour cell line

Genetic polymorphisms and susceptibility to lung disease

Susceptibility to infection by bacterium such as Bacillus anthracis has a genetic basis in mice and may also have a genetic basis in humans. In the limited human cases of inhalation anthrax, studies suggest that not all individuals exposed to anthrax spores were infected, but rather, individuals with underlying lung disease, particularly asthma, sarcoidosis and tuberculosis, might be more susceptible. In this study, we determined if polymorphisms in genes important in innate immunity are associated with increased susceptibility to infectious and non-infectious lung diseases, particularly tuberculosis and sarcoidosis, respectively, and therefore might be a risk factor for inhalation anthrax. Examination of 45 non-synonymous polymorphisms in ten genes: p47phox (NCF1), p67phox (NCF2), p40phox (NCF4), p22phox (CYBA), gp91phox (CYBB), DUOX1, DUOX2, TLR2, TLR9 and alpha 1-antitrypsin (AAT) in a cohort of 95 lung disease individuals and 95 control individuals did not show an association of these polymorphisms with increased susceptibility to lung disease

Mutations in KEOPS-Complex Genes Cause Nephrotic Syndrome with Primary Microcephaly

Galloway-Mowat syndrome (GAMOS) is an autosomal-recessive disease characterized by the combination of early-onset nephrotic syndrome (SRNS) and microcephaly with brain anomalies. Here we identified recessive mutations in OSGEP, TP53RK, TPRKB, and LAGE3, genes encoding the four subunits of the KEOPS complex, in 37 individuals from 32 families with GAMOS. CRISPR-Cas9 knockout in zebrafish and mice recapitulated the human phenotype of primary microcephaly and resulted in early lethality. Knockdown of OSGEP, TP53RK, or TPRKB inhibited cell proliferation, which human mutations did not rescue. Furthermore, knockdown of these genes impaired protein translation, caused endoplasmic reticulum stress, activated DNA-damage-response signaling, and ultimately induced apoptosis. Knockdown of OSGEP or TP53RK induced defects in the actin cytoskeleton and decreased the migration rate of human podocytes, an established intermediate phenotype of SRNS. We thus identified four new monogenic causes of GAMOS, describe a link between KEOPS function and human disease, and delineate potential pathogenic mechanisms