Cybersecurity awareness framework for academia.
A conceptual outcome-based framework for the design and delivery of real-time virtual courses.
Background: The prevalence of Candida glabrata healthcare-associated infections is on the rise worldwide and in Lebanon, Candida glabrata infections are difficult to treat as a result of their resistance to azole antifungals and their ability to form biofilms. Objectives: The first objective of this study was to quantify biofilm biomass in the most virulent C. glabrata isolates detected in a Lebanese hospital. In addition, other pathogenicity attributes were evaluated. The second objective was to identify the mechanisms of azole resistance in those isolates. Methods: A mouse model of disseminated systemic infection was developed to evaluate the degree of virulence of 41 azole-resistant C. glabrata collected from a Lebanese hospital. The most virulent isolates were further evaluated alongside an isolate having attenuated virulence and a reference strain for comparative purposes. A DNA sequencing approach was adopted to detect single nucleotide polymorphisms (SNPs) leading to amino acid changes in proteins involved in azole resistance and biofilm formation. This genomic approach was supported by several phenotypic assays. Results: All chosen virulent isolates exhibited increased adhesion and biofilm biomass compared to the isolate having attenuated virulence. The amino acid substitutions D679E and I739N detected in the subtelomeric silencer Sir3 are potentially involved— in increased adhesion. In all isolates, amino acid substitutions were detected in the ATP-binding cassette transporters Cdr1 and Pdh1 and their transcriptional regulator Pdr1. Conclusions: In summary, increased adhesion led to stable biofilm formation since mutated Sir3 could de-repress adhesins, while decreased azole susceptibility could result from mutations in Cdr1, Pdh1 and Pdr1.
In the Prayer to ask of God the proper use of sickness, Pascal distances himself from a profane and worldly use of health and illness, to appropriate them according to a theological, christo-soteriological, pharmacological and anthropological use. Pascalian illness is then a religious épochè according to the “reason of the effects”. The Pascalian pharmakon is twofold: on the one hand, poison is a remedy, because illness can be the occasion of spiritual health and salvation; and on the other hand, the remedy is poison, because health is an open door to illness. This inversion occurs through grace in the heart, according to an anthropology of disproportion. The heart is the place of conflict where health and illness are both worldly indices of finitude and divine indices of infinity. Despite the rhetorical trap of guilt and moralization, and despite the lack of distancing from the Christian God, Pascal invites to a disposition of openness of the heart that heals the heart itself.
In the Prayer to ask of God the proper use of sickness, Pascal distances himself from a profane and worldly use of health and illness, to appropriate them according to a theological, christo-soteriological, pharmacological and anthropological use. Pascalian illness is then a religious épochè according to the “reason of the effects”. The Pascalian pharmakon is twofold: on the one hand, poison is a remedy, because illness can be the occasion of spiritual health and salvation; and on the other hand, the remedy is poison, because health is an open door to illness. This inversion occurs through grace in the heart, according to an anthropology of disproportion. The heart is the place of conflict where health and illness are both worldly indices of finitude and divine indices of infinity. Despite the rhetorical trap of guilt and moralization, and despite the lack of distancing from the Christian God, Pascal invites to a disposition of openness of the heart that heals the heart itself.
Quality assurance framework for the design and delivery of virtual, real-time courses.
Background: The prevalence of Candida glabrata healthcare-associated infections is on the rise worldwide and in Lebanon, Candida glabrata infections are difficult to treat as a result of their resistance to azole antifungals and their ability to form biofilms. Objectives: The first objective of this study was to quantify biofilm biomass in the most virulent C. glabrata isolates detected in a Lebanese hospital. In addition, other pathogenicity attributes were evaluated. The second objective was to identify the mechanisms of azole resistance in those isolates. <br /> Methods: A mouse model of disseminated systemic infection was developed to evaluate the degree of virulence of 41 azole-resistant C. glabrata collected from a Lebanese hospital. The most virulent isolates were further evaluated alongside an isolate having attenuated virulence and a reference strain for comparative purposes. A DNA sequencing approach was adopted to detect single nucleotide polymorphisms (SNPs) leading to amino acid changes in proteins involved in azole resistance and biofilm formation. This genomic approach was supported by several phenotypic assays. <br /> Results: All chosen virulent isolates exhibited increased adhesion and biofilm biomass compared to the isolate having attenuated virulence. The amino acid substitutions D679E and I739N detected in the subtelomeric silencer Sir3 are potentially involved— in increased adhesion. In all isolates, amino acid substitutions were detected in the ATP-binding cassette transporters Cdr1 and Pdh1 and their transcriptional regulator Pdr1. <br /> Conclusions: In summary, increased adhesion led to stable biofilm formation since mutated Sir3 could de-repress adhesins, while decreased azole susceptibility could result from mutations in Cdr1, Pdh1 and Pdr1.<br /> <div> </div>
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