Boride Coating on Titanium Alloys as Biomaterial in Wear and Fretting Applications

The issue taken into account is the lifespan and potential toxicity of arthroprostheses with a focus on metal-polyethylene coupling. The gold standard for hip prostheses is a femoral component made of Ti6Al4V alloy, a head made of Co-Cr-Mo alloy and an insert made of UHMWPE while for knee prostheses the gold standard is a tibial component made of Co-Cr-Mo alloy, a femoral component made of Ti6Al4V and an insert made of UHMWPE. Open issues are wear of UHMWPE, toxicity of Co alloys and low fretting/wear resistance of Ti alloys. The aim of this research is to focus on the most biocompatible material (Ti6Al4V alloy) in order to improve its bio-tribological characteristics. A ceramic surface conversion by thermal treatment was used to obtain a borided coating on the titanium alloy surface in order to combine high hardness, good wettability and lubricant behavior of ceramics with good mechanical properties of Ti metal alloys. The coatings were characterized by means of optical microscope observation, FESEM analysis, XRD analysis, microindentation, scratch, friction and wear tests in order to identify the thermal treatment most suitable to obtain a coating with the required properties (thickness, hardness, roughness, wear resistance, friction coefficient and scratch resistance, surface lubrication ability in contact with human fluids) without significant modification of the microstructure of the substrate

Fragility in the 14q21q translocation region

Aphidicolin (APC)-induced chromosomal breakage was analyzed for women representing three generations of a single family and carrying a Robertsonian translocation rob(14q21q). Fluorescence in situ hybridization (FISH) analysis confirmed the dicentric constitution of the derived chromosome and indicated the absence of beta-satellite signal at the translocation region. Per-individual analysis of metaphases from APC-treated peripheral blood lymphocyte cultures identified significantly nonrandom chromosomal breakage at the translocation region in all three individuals examined. The APC-inducible fragility at the 14q21q translocation region suggests that this rearrangement was the result of chromosomal mutation at fragile site(s) in the progenitor chromosomes, or that this fragility was the result of the fusion of nonfragile progenitor chromosomes

Ubiquitination and the Ubiquitin-Proteasome System as regulators of transcription and transcription factorsin epithelial mesenchymal transition of cancer.

Epithelial to Mesenchymal Transition (EMT) in cancer is a process that allows cancer cells to detach from neighboring cells, become mobile and metastasize and shares many signaling pathways with development. Several molecular mechanisms which regulate oncogenic properties in neoplastic cells such as proliferation, resistance to apoptosis and angiogenesis through transcription factors or other mediators are also regulators of EMT. These pathways and downstream transcription factors are, in their turn, regulated by ubiquitination and the Ubiquitin-Proteasome System (UPS). Ubiquitination, the covalent link of the small 76-amino acid protein ubiquitin to target proteins, serves as a signal for protein degradation by the proteasome or for other outcomes such as endocytosis, degradation by the lysosome or directing these proteins to specific cellular compartments. This review discusses aspects of the regulation of EMT by ubiquitination and the UPS and underlines its complexity focusing on transcription and transcription factors regulating EMT and are being regulated by ubiquitination