Physical Properties of Sputtered Germanium-Doped Indium Tin Oxide Films (ITO: Ge) Obtained at Low Deposition Temperature

Undoped and Ge-doped ITO films (ITO: Ge) deposited at low temperature (70℃) have been studied. Although both samples have the same carrier concentration, a higher carrier mobility occurs for ITO: Ge. An evaluation of the relative position of the dopant associated energy states has been carried out

Extracellular matrix degradation pathways and fatty acid metabolism regulate distinct pulmonary vascular cell types in Pulmonary Arterial Hypertension

Pulmonary arterial hypertension (PAH) describes a group of diseases characterized by raised pulmonary vascular resistance, resulting from vascular remodelling in the pre-capillary resistance arterioles. Left untreated, patients die from right heart failure. Pulmonary vascular remodelling involves all cell types but to date the precise roles of the different cells is unknown. This study investigated differences in basal gene expression between PAH and controls using both human pulmonary microvascular endothelial (HPMEC) and pulmonary artery smooth muscle cells (HPASMC). HPMEC and HPASMC from PAH patients and controls were cultured to confluence, harvested and RNA extracted. Whole genome sequencing was performed and after transcript quantification and normalization, we examined differentially expressed genes (DEGs) and applied gene set enrichment analysis (GSEA) to the DEGs to identify putative activated pathways. HPMEC displayed 1008 significant (p≤0.0001) DEGs in PAH samples compared to controls. In HPASMC there were 229 significant (p≤0.0001) DEGs between PAH and controls. Pathway analysis revealed distinctive differences: HPMEC display down-regulation of extracellular matrix organisation, collagen formation and biosynthesis, focal- and cell- adhesion molecules suggesting severe endothelial barrier dysfunction and vascular permeability in PAH pathogenesis. In contrast pathways in HPASMC were mainly up-regulated, including those for fatty acid metabolism, biosynthesis of unsaturated fatty acids, cell-cell and adherens junction interactions suggesting a more energy-driven proliferative phenotype. This suggests that the two cell types play different mechanistic roles in PAH pathogenesis and further studies are required to fully elucidate the role each plays and the interactions between these cell types in vascular remodelling in disease progression

Wear behaviour of cemented carbide tools in dry machining of aluminium alloy

Several causes of tool wear have been investigated in dry machining of aluminium alloy with cemented carbide insert; some of the most important are: adhesion and diffusion. The formation of built-up edge (BUE) and adhesive layer on the tool rake face degrades on the one hand, the shape and efficiency of cutting tool and on the other hand, the surface quality and dimensional accuracy of the finished product. This paper describes tool wear mechanisms in dry machining of a usual aluminium–copper alloy (2024) with an uncoated cemented carbide tool (WC–Co). Orthogonal cutting tests were performed using an instrumented planer machine. The morphology of chips, cutting forces and contact lengths were analyzed for several cutting conditions. The tool–chip interface temperature and the average pressure were calculated by conducting calibration–cutting experiments in conjunction with FEM simulations. This allowed to define the contact parameters associated with different cutting conditions on the tool rake face. High-speed camera movies (CCD), white light interferometry, scanning electron microscopy (SEM) equipped with energy dispersive X-ray spectrometer (EDS) and Auger electron spectroscopy (AES) were investigated to show the development of the built-up edge and the adhesive layer on the tool rake face during machining process. The results confirmed that the wear mechanisms involve the activation of the chemical and the diffusional phenomenon

Low temperature, fast deposition of metallic titanium nitride films using plasma activated reactive evaporation

Titanium and titanium nitride thin films were deposited on silica glass and W substrates at a high coating growth rate by plasma-activated reactive evaporation (ARE). The crystal structure, preferred orientation and grain size of the coatings were determined by x-ray diffraction (XRD) technique using Cu-Kalpha x rays. The analysis of the coating morphology was performed by field-emission scanning electron microscopy (FE-SEM). The composition of the films was analyzed by Auger electron spectroscopy (AES) and electron-probe microanalysis (EPMA). The titanium and titanium nitride condensates were collected on a carbon-coated collodion film then characterized by transmission electron microscopy (TEM) in order to study the structures of the deposits at very short deposition times. The resistivity of the films was measured by using the four-point-probe method. The titanium coatings were found to consist of very fine particles (40 nm in grain size) and to exhibit a strong (002) texture. The titanium nitride coatings were substoichiometric (TiNx,x<1), with an oxygen content ranging from 7 to 15 at. % depending on the deposition conditions. The deposits were found to exhibit a (111) preferred orientation. This behavior became stronger with coating thickness. In spite of the presence of oxygen, all the TiNx coatings obtained at low temperature and a high growth rate in this work exhibited a rather high electrical conductivity

Targeting peptidyl-prolyl isomerase 1 in experimental pulmonary arterial hypertension

Background Pulmonary arterial hypertension (PAH) is a progressive disease characterised by pro -proliferative and anti-apoptotic phenotype in vascular cells, leading to pulmonary vascular remodelling and right heart failure. Peptidyl-prolyl cis/trans isomerase, NIMA interacting 1 (Pin1), a highly conserved enzyme, which binds to and catalyses the isomerisation of specific phosphorylated Ser/Thr-Pro motifs, acts as a molecular switch in multiple coordinated cellular processes. We hypothesised that Pin1 plays a substantial role in PAH, and its inhibition with a natural organic compound, Juglone, would reverse experimental pulmonary hypertension.Results We demonstrated that the expression of Pin1 was markedly elevated in experimental pulmonary hypertension (i.e. hypoxia-induced mouse and Sugen/hypoxia-induced rat models) and pulmonary arterial smooth muscle cells of patients with clinical PAH. In vitro Pin1 inhibition by either Juglone treatment or short interfering RNA knockdown resulted in an induction of apoptosis and decrease in proliferation of human pulmonary vascular cells. Stimulation with growth factors induced Pin1 expression, while its inhibition reduced the activity of numerous PAH-related transcription factors, such as hypoxia-inducible factor (HIF)-alpha and signal transducer and activator of transcription (STAT). Juglone administration lowered pulmonary vascular resistance, enhanced right ventribular function, improved pulmonary vascular and cardiac remodelling in the Sugen/hypoxia rat model of PAH and the chronic hypoxia-induced pulmonary hypertension model in mice.Conclusion Our study demonstrates that targeting of Pin1 with small molecule inhibitor, Juglone, might be an attractive future therapeutic strategy for PAH and right heart disease secondary to PAH

Gusev photometric variability as seen from orbit by hrsc/mars-express

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