Colas (Canada)

The aim of this paper is to analyse sewage sludge production at the level of Medimurje and Varazdin counties with economic analysis of acceptable technical/technological solutions for sludge management routes. The topic is very broad, so the focus was placed on four variants of sludge disposal, which were determined by preliminary analysis to be the most applicable for the area in question. These are: 1) disposal of sewage sludge in agriculture, 2) incineration of sludge in a central mono-incinerator, 3) composting for the area of Varazdin County and at the same time use of sludge reed beds for the area of Medimurje County, and 4) export of sludge outside the state borders. Based on the analysis carried out for the described four variants, sludge incineration in a regional mono-incinerator turned out as the economically most advantageous solution, while the variant that includes disposal of sludge in agriculture has showed as the most expensive one. The last one also showed the largest range of costs uncertainties, but the mentioned facts are greatly influenced by unfavourable legislation, the changes of which in a more rational direction would greatly contribute to the greater competitiveness of this variant. Overall, taking into account the lowest cost and uncertainties in the predicted unit costs, the sludge composting in the Varazdin County and the construction of a reed beds for the Medimurje County, turned out to be the optimal variant. This solution is also the one that was ultimately adopted in practice.

RationaleAutopsy and biomarker studies suggest that endotheliopathy contributes to coronavirus disease (COVID-19)-associated acute respiratory distress syndrome. However, the effects of COVID-19 on the lung endothelium are not well defined. We hypothesized that the lung endotheliopathy of COVID-19 is caused by circulating host factors and direct endothelial infection by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).ObjectivesWe aimed to determine the effects of SARS-CoV-2 or sera from patients with COVID-19 on the permeability and inflammatory activation of lung microvascular endothelial cells.MethodsHuman lung microvascular endothelial cells were treated with live SARS-CoV-2; inactivated viral particles; or sera from patients with COVID-19, patients without COVID-19, and healthy volunteers. Permeability was determined by measuring transendothelial resistance to electrical current flow, where decreased resistance signifies increased permeability. Inflammatory mediators were quantified in culture supernatants. Endothelial biomarkers were quantified in patient sera.Measurements and Main ResultsViral PCR confirmed that SARS-CoV-2 enters and replicates in endothelial cells. Live SARS-CoV-2, but not dead virus or spike protein, induces endothelial permeability and secretion of plasminogen activator inhibitor 1 and vascular endothelial growth factor. There was substantial variability in the effects of SARS-CoV-2 on endothelial cells from different donors. Sera from patients with COVID-19 induced endothelial permeability, which correlated with disease severity. Serum levels of endothelial activation and injury biomarkers were increased in patients with COVID-19 and correlated with severity of illness.ConclusionsSARS-CoV-2 infects and dysregulates endothelial cell functions. Circulating factors in patients with COVID-19 also induce endothelial cell dysfunction. Our data point to roles for both systemic factors acting on lung endothelial cells and viral infection of endothelial cells in COVID-19–associated endotheliopathy.

Rationale: The 17q12-21.1 locus is one of the most highly replicated genetic associations with asthma. Individuals of African descent have lower linkage disequilibrium in this region, which could facilitate identifying causal variants.Objectives: To identify functional variants at 17q12-21.1 associated with early-onset asthma among African American individuals.Methods: We evaluated African American participants from SAPPHIRE (Study of Asthma Phenotypes and Pharmacogenomic Interactions by Race-Ethnicity) (n = 1,940), SAGE II (Study of African Americans, Asthma, Genes and Environment) (n = 885), and GCPD-A (Study of the Genetic Causes of Complex Pediatric Disorders-Asthma) (n = 2,805). Associations with asthma onset at ages under 5 years were meta-analyzed across cohorts. The lead signal was reevaluated considering haplotypes informed by genetic ancestry (i.e., African vs. European). Both an expression-quantitative trait locus analysis and a phenome-wide association study were performed on the lead variant.Measurements and Main Results: The meta-analyzed results from SAPPHIRE, SAGE II, and the GCPD-A identified rs11078928 as the top association for early-onset asthma. A haplotype analysis suggested that the asthma association partitioned most closely with the rs11078928 genotype. Genetic ancestry did not appear to influence the effect of this variant. In the expression-quantitative trait locus analysis, rs11078928 was related to alternative splicing of GSDMB (gasdermin-B) transcripts. The phenome-wide association study of rs11078928 suggested that this variant was predominantly associated with asthma and asthma-associated symptoms.Conclusions: A splice-acceptor polymorphism appears to be a causal variant for asthma at the 17q12-21.1 locus. This variant appears to have the same magnitude of effect in individuals of African and European descent.

Abstract The control of monolayer concrete armour units on coastal protection breakwaters can be time and cost consuming, especially underwater. Such controls occur frequently on construction projects which last for several years, or during the operation and maintenance of such structures. On top of that, the complexity of this type of projects - usually coastal constructions such a dike easily exceeds 6000 units/km - requires precision and productivity for the control inspections. As a result, specific control solutions have been developed on the NRL project to inspect the breakwater during its construction.