Al-, Ga-, and In-doped ZnO thin films via aerosol assisted CVD for use as transparent conducting oxides

Al-, Ga-, and In-doped ZnO thin films were deposited on glass substrates by aerosol assisted chemical vapour deposition (AACVD) at a deposition temperature of 450 °C. The air-stable compound zinc acetylacetonate [Zn(acac)2] was used as a Zn source, whilst for the dopants of Al, Ga and In, the corresponding trichloride was used. Methanol solutions of the metal salts were used as precursor solutions and N2 carrier gas was used for the aerosol. Films were grown in approximately 30 min and were synthesised using dopant values of 5, 10, 15 and 20 mol.% (with respect to the Zn) in the precursor solution. XRD analysis showed that the films were wurtzite ZnO. XPS analysis confirmed the presence of the dopants in the films. Several of the films showed high transparency (>80%) in the visible range, and low resistivity (∼10−3 Ω cm)

Scaling aerosol assisted chemical vapour deposition: Exploring the relationship between growth rate and film properties

Thin films of fluorine doped tin oxide were deposited, by an aerosol assisted chemical vapour deposition route, to study the effect of scaling the growth rate. The effect of precursor concentration on the growth rate of the films and the properties of deposited films were compared. The films were characterised by X-ray diffraction, scanning electron microscopy, UV/vis spectroscopy, X-ray photoelectron spectroscopy and Hall effect measurements. A maximum film growth rate of ca. 100 nm min− 1 was observed, which is significantly faster than previously reported aerosol assisted studies. This method shows the ability of aerosol assisted methods to deliver high growth rates whilst maintaining the ease of doping and control over stoichiometry

Transparent conducting oxide thin films of Si-doped ZnO prepared by aerosol assisted CVD

For the first time, aerosol assisted chemical vapour deposition (AACVD) was used to deposit Si-doped ZnO thin films on glass. Depositions were done at a temperature of 450 °C. The precursor solution was made by dissolving the air-stable compounds zinc acetylacetonate and tetraethyl orthosilicate in methanol with a small addition of acetic acid to aid solubility. The dopant concentration in the precursor solution was optimised to find the best optoelectronic properties. The incorporation of Si into the ZnO lattice was confirmed by unit cell volumes calculated from X-ray diffraction (XRD) data and by X-ray photoelectron spectroscopy (XPS). The films consisted of pure phase wurtzite ZnO, with preferred orientation in the (002) plane. Scanning electron microscopy (SEM) was used to examine the surface morphology of the films. The optical properties of the films were analysed using UV/vis spectroscopy and indicated that the average transmittance in the visible part of the spectrum (400-700 nm) varied between 72% and 80%. The electrical properties of the films were obtained from Hall effect measurements using the van der Pauw method. The incorporation of Si into the films resulted in a decrease in resistivity down to a minimum value of 2.0 × 10−2 Ω cm for the film deposited from a 4 mol% Si : Zn ratio in the precursor solution. This conductive film was a significant improvement over the non-conductive undoped ZnO film

Targeted inhibition of gut bacterial β-glucuronidase activity enhances anticancer drug efficacy

Irinotecan treats a range of solid tumors, but its effectiveness is severely limited by gastrointestinal (GI) tract toxicity caused by gut bacterial β-glucuronidase (GUS) enzymes. Targeted bacterial GUS inhibitors have been shown to partially alleviate irinotecan-induced GI tract damage and resultant diarrhea in mice. Here, we unravel the mechanistic basis for GI protection by gut microbial GUS inhibitors using in vivo models. We use in vitro, in fimo, and in vivo models to determine whether GUS inhibition alters the anticancer efficacy of irinotecan. We demonstrate that a single dose of irinotecan increases GI bacterial GUS activity in 1 d and reduces intestinal epithelial cell proliferation in 5 d, both blocked by a single dose of a GUS inhibitor. In a tumor xenograft model, GUS inhibition prevents intestinal toxicity and maintains the antitumor efficacy of irinotecan. Remarkably, GUS inhibitor also effectively blocks the striking irinotecan-induced bloom of Enterobacteriaceae in immune-deficient mice. In a genetically engineered mouse model of cancer, GUS inhibition alleviates gut damage, improves survival, and does not alter gut microbial composition; however, by allowing dose intensification, it dramatically improves irinotecan’s effectiveness, reducing tumors to a fraction of that achieved by irinotecan alone, while simultaneously promoting epithelial regeneration. These results indicate that targeted gut microbial enzyme inhibitors can improve cancer chemotherapeutic outcomes by protecting the gut epithelium from microbial dysbiosis and proliferative crypt damage

IL2 Inducible T-cell Kinase, a Novel Therapeutic Target in Melanoma

PURPOSE: IL2 inducible T-cell kinase (ITK) promoter CpG sites are hypomethylated in melanomas compared with nevi. The expression of ITK in melanomas, however, has not been established and requires elucidation. EXPERIMENTAL DESIGN: An ITK-specific monoclonal antibody was used to probe sections from deidentified, formalin-fixed paraffin-embedded tumor blocks or cell line arrays and ITK was visualized by IHC. Levels of ITK protein differed among melanoma cell lines and representative lines were transduced with four different lentiviral constructs that each contained an shRNA designed to knockdown ITK mRNA levels. The effects of the selective ITK inhibitor BI 10N on cell lines and mouse models were also determined. RESULTS: ITK protein expression increased with nevus to metastatic melanoma progression. In melanoma cell lines, genetic or pharmacologic inhibition of ITK decreased proliferation and migration and increased the percentage of cells in the G0-G1 phase. Treatment of melanoma-bearing mice with BI 10N reduced growth of ITK-expressing xenografts or established autochthonous (Tyr-Cre/Pten(null)/Braf(V600E)) melanomas. CONCLUSIONS: We conclude that ITK, formerly considered an immune cell-specific protein, is aberrantly expressed in melanoma and promotes tumor development and progression. Our finding that ITK is aberrantly expressed in most metastatic melanomas suggests that inhibitors of ITK may be efficacious for melanoma treatment. The efficacy of a small-molecule ITK inhibitor in the Tyr-Cre/Pten(null)/Braf(V600E) mouse melanoma model supports this possibility