HIGH STRENGTH-GEOPOLYMER BUILDING MATERIAL

New geopolymer concrete with high mechanical strength - 58.9 MPa after 28 days of curing - was experimentally made under environmental friendly and economic conditions. The high-strength-geopolymer is baed on coal fly ash and building concrete waste as geopolymer materials suitable for completely substituting the cement in concrete structure. The alumino-silicate geopolymer materials with binder role were activated in liquid alkaline medium (sodium silicate and sodium hydroxide) for facilitating the polymerization reaction that turns the alumino-silicate wastes into geopolymer concrete. The use for the first time in this experiment of recycled building concrete waste from demolition is the work originality

HIGH STRENGTH-GEOPOLYMER BUILDING MATERIAL

New geopolymer concrete with high mechanical strength - 58.9 MPa after 28 days of curing - was experimentally made under environmental friendly and economic conditions. The high-strength-geopolymer is baed on coal fly ash and building concrete waste as geopolymer materials suitable for completely substituting the cement in concrete structure. The alumino-silicate geopolymer materials with binder role were activated in liquid alkaline medium (sodium silicate and sodium hydroxide) for facilitating the polymerization reaction that turns the alumino-silicate wastes into geopolymer concrete. The use for the first time in this experiment of recycled building concrete waste from demolition is the work originality

LOW-CEMENT DOSAGE REFRACTORY CONCRETE WITH LOW THERMAL CONDUCTIVITY

Super-aluminous refractory concrete (over 94 % Al2O3) with low dosage of cement (9 %) was made, its physical, thermal, and mechanical characteristics being considered suitable for the intermediate layer of a steel casting ladle: porosity of 29.31 %, the apparent density of 2.32 g·cm-3 thermal conductivity of 1.45 W·m-1·K-1, and compressive strength of 34.8 MPa (after heat treatment at 1500 ºC). The aim of the research was achieving a super-aluminous concrete with low-cement dosage, which would have acceptable thermal insulation properties, so that the heat loss through this refractory lining layer would be significantly reduced compared to the reference situation

LOW-CEMENT DOSAGE REFRACTORY CONCRETE WITH LOW THERMAL CONDUCTIVITY

Super-aluminous refractory concrete (over 94 % Al2O3) with low dosage of cement (9 %) was made, its physical, thermal, and mechanical characteristics being considered suitable for the intermediate layer of a steel casting ladle: porosity of 29.31 %, the apparent density of 2.32 g·cm-3 thermal conductivity of 1.45 W·m-1·K-1, and compressive strength of 34.8 MPa (after heat treatment at 1500 ºC). The aim of the research was achieving a super-aluminous concrete with low-cement dosage, which would have acceptable thermal insulation properties, so that the heat loss through this refractory lining layer would be significantly reduced compared to the reference situation

miR449 Protects Airway Regeneration by Controlling AURKA/HDAC6-Mediated Ciliary Disassembly

Airway mucociliary regeneration and function are key players for airway defense and are impaired in chronic obstructive pulmonary disease (COPD). Using transcriptome analysis in COPD-derived bronchial biopsies, we observed a positive correlation between cilia-related genes and microRNA-449 (miR449). In vitro, miR449 was strongly increased during airway epithelial mucociliary differentiation. In vivo, miR449 was upregulated during recovery from chemical or infective insults. miR0449−/− mice (both alleles are deleted) showed impaired ciliated epithelial regeneration after naphthalene and Haemophilus influenzae exposure, accompanied by more intense inflammation and emphysematous manifestations of COPD. The latter occurred spontaneously in aged miR449−/− mice. We identified Aurora kinase A and its effector target HDAC6 as key mediators in miR449-regulated ciliary homeostasis and epithelial regeneration. Aurora kinase A is downregulated upon miR449 overexpression in vitro and upregulated in miR449−/− mouse lungs. Accordingly, imaging studies showed profoundly altered cilia length and morphology accompanied by reduced mucociliary clearance. Pharmacological inhibition of HDAC6 rescued cilia length and coverage in miR449−/− cells, consistent with its tubulin-deacetylating function. Altogether, our study establishes a link between miR449, ciliary dysfunction, and COPD pathogenesis

miR449 Protects Airway Regeneration by Controlling AURKA/HDAC6-Mediated Ciliary Disassembly

Airway mucociliary regeneration and function are key players for airway defense and are impaired in chronic obstructive pulmonary disease (COPD). Using transcriptome analysis in COPD-derived bronchial biopsies, we observed a positive correlation between cilia-related genes and microRNA-449 (miR449). In vitro, miR449 was strongly increased during airway epithelial mucociliary differentiation. In vivo, miR449 was upregulated during recovery from chemical or infective insults. miR0449-/- mice (both alleles are deleted) showed impaired ciliated epithelial regeneration after naphthalene and Haemophilus influenzae exposure, accompanied by more intense inflammation and emphysematous manifestations of COPD. The latter occurred spontaneously in aged miR449-/- mice. We identified Aurora kinase A and its effector target HDAC6 as key mediators in miR449-regulated ciliary homeostasis and epithelial regeneration. Aurora kinase A is downregulated upon miR449 overexpression in vitro and upregulated in miR449-/- mouse lungs. Accordingly, imaging studies showed profoundly altered cilia length and morphology accompanied by reduced mucociliary clearance. Pharmacological inhibition of HDAC6 rescued cilia length and coverage in miR449-/- cells, consistent with its tubulin-deacetylating function. Altogether, our study establishes a link between miR449, ciliary dysfunction, and COPD pathogenesis

miR449 Protects Airway Regeneration by Controlling AURKA/HDAC6-Mediated Ciliary Disassembly

Airway mucociliary regeneration and function are key players for airway defense and are impaired in chronic obstructive pulmonary disease (COPD). Using transcriptome analysis in COPD-derived bronchial biopsies, we observed a positive correlation between cilia-related genes and microRNA-449 (miR449). In vitro, miR449 was strongly increased during airway epithelial mucociliary differentiation. In vivo, miR449 was upregulated during recovery from chemical or infective insults. miR0449−/− mice (both alleles are deleted) showed impaired ciliated epithelial regeneration after naphthalene and Haemophilus influenzae exposure, accompanied by more intense inflammation and emphysematous manifestations of COPD. The latter occurred spontaneously in aged miR449−/− mice. We identified Aurora kinase A and its effector target HDAC6 as key mediators in miR449-regulated ciliary homeostasis and epithelial regeneration. Aurora kinase A is downregulated upon miR449 overexpression in vitro and upregulated in miR449−/− mouse lungs. Accordingly, imaging studies showed profoundly altered cilia length and morphology accompanied by reduced mucociliary clearance. Pharmacological inhibition of HDAC6 rescued cilia length and coverage in miR449−/− cells, consistent with its tubulin-deacetylating function. Altogether, our study establishes a link between miR449, ciliary dysfunction, and COPD pathogenesis

Septins and Bacterial Infection

Septins, a unique cytoskeletal component associated with cellular membranes, are increasingly recognized as having important roles in host defense against bacterial infection. A role for septins during invasion of Listeria monocytogenes into host cells was first proposed in 2002. Since then, work has shown that septins assemble in response to a wide variety of invasive bacterial pathogens, and septin assemblies can have different roles during the bacterial infection process. Here we review the interplay between septins and bacterial pathogens, highlighting septins as a structural determinant of host defense. We also discuss how investigation of septin assembly in response to bacterial infection can yield insight into basic cellular processes including phagocytosis, autophagy, and mitochondrial dynamics