NANOTUBES BIOLOGICALLY ACTIVE IN MEDIA WITH HIGH SALT CONCENTRATION

ABSTRAC

The Morphostructural, Compositional, and Electrochemical Characterization of Electrodeposited Nanolayers on a New Ti-15Ta-5Zr Alloy

A porous, homogeneous, phosphorous-enriched oxide nanolayer was realized on the new Ti-15Ta-5Zr alloy surface by the anodic galvanostatic electrodeposition in phosphoric acid solution. This nanolayer contains TiO2, ZrO2 oxides, tantalum suboxides, and PO43- ions incorporated in the time of the electrodeposition process and has a thickness of 15.5 nm (X-ray photoelectron spectroscopy data). Atomic force microscopy determined a homogeneous roughness. Scanning electron microscopy evinced a porous microstructure that can stimulate the growth of the bone tissue into pores. The presence of the PO43- anions promotes the electrostatic bonds between the nanolayer and different species from the biofluid, namely, osteoinduction. The anodic oxidation nanolayer improved all electrochemical and corrosion parameters conferring superior protection to the substrate by its higher resistance to the ion migration. Impedance spectra showed that the electrodeposited nanolayer is formed by an inner, dense, barrier layer and an outer porous layer. The nanolayer thickened in time, namely, is bioactive. The oxidized nanolayer is able to protect the alloy from ion release, to assure long-term corrosion resistance, to minimize adverse reactions, to increase alloy bioactivity, to stimulate cell growth, and to favor osseointegration

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Genetic mechanisms of critical illness in COVID-19.

Host-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10-8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10-8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 ×  10-12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10-8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

La Banque de Tissus de l'Hôpital Universitaire Erasme.

The evolution of the Tissue Bank belonging to the University Hospital Erasme is summarized during its 13 years of experience. In parallel with this evolution, the important modifications of the legislation, the selection criteria and the bone graft processing are reported. The significant improvement of the safety of the allograft related to the risk of infection is also mentioned. In constant progression, the ongoing research within the BTE studies the osteogenic activity of the graft, mostly of bone demineralized matrix.English AbstractHistorical ArticleJournal ArticleSCOPUS: sh.jinfo:eu-repo/semantics/publishe

Multi-stage pulsed laser deposition of aluminum nitride at different temperatures

We report on multi-stage pulsed laser deposition of aluminum nitride (AlN) on Si (1 0 0) wafers, at different temperatures. The first stage of deposition was carried out at 800 °C, the optimum temperature for AlN crystallization. In the second stage, the deposition was conducted at lower temperatures (room temperature, 350 °C or 450 °C), in ambient Nitrogen, at 0.1 Pa. The synthesized structures were analyzed by grazing incidence X-ray diffraction (GIXRD), transmission electron microscopy (TEM), atomic force microscopy and spectroscopic ellipsometry (SE). GIXRD measurements indicated that the two-stage deposited AlN samples exhibited a randomly oriented wurtzite structure with nanosized crystallites. The peaks were shifted to larger angles, indicative for smaller inter-planar distances. Remarkably, TEM images demonstrated that the high-temperature AlN "seed" layers (800 °C) promoted the growth of poly-crystalline AlN structures at lower deposition temperatures. When increasing the deposition temperature, the surface roughness of the samples exhibited values in the range of 0.4-2.3 nm. SE analyses showed structures which yield band gap values within the range of 4.0-5.7 eV. A correlation between the results of single- and multi-stage AlN depositions was observed. © 2015 Elsevier B.V. All rights reserved

Hydrophobic Carbonate Coatings on Pure Biodegradable Mg by Immersion in Carbonated Water: Formation Mechanism

Mg is one of the few materials of choice for biodegradable implants, despite its rapid degradation when used without surface protection treatment. This study presents the effect of carbonation time on the formation of hydrophobic carbonate coatings grown on pure magnesium using a simple, green chemical conversion method in carbonated water. The evolution of the coating with immersion time in carbonating solution was studied in order to ascertain the mechanistic of coating formation by Raman and EDS spectroscopy, XRD, SEM and AFM microscopy. Wettability was investigated by contact angle measurements. The formation mechanism of the hydrophobic coating involves the surface nucleation of carbonates mediated by the dissolution of the native corrosion product, brucite Mg(OH)2, surface conversion into hydroxycarbonates, surface calcite nucleation and growth by attachment of nanoparticles, leading to the lateral growth of a continuous carbonate coating layer of intertwined calcite microcrystals

Hydrophobic Carbonate Coatings on Pure Biodegradable Mg by Immersion in Carbonated Water: Formation Mechanism

Mg is one of the few materials of choice for biodegradable implants, despite its rapid degradation when used without surface protection treatment. This study presents the effect of carbonation time on the formation of hydrophobic carbonate coatings grown on pure magnesium using a simple, green chemical conversion method in carbonated water. The evolution of the coating with immersion time in carbonating solution was studied in order to ascertain the mechanistic of coating formation by Raman and EDS spectroscopy, XRD, SEM and AFM microscopy. Wettability was investigated by contact angle measurements. The formation mechanism of the hydrophobic coating involves the surface nucleation of carbonates mediated by the dissolution of the native corrosion product, brucite Mg(OH)2, surface conversion into hydroxycarbonates, surface calcite nucleation and growth by attachment of nanoparticles, leading to the lateral growth of a continuous carbonate coating layer of intertwined calcite microcrystals