Augustin (saint)

Saint Augustin appartient à la culture universelle, et les diverses composantes de son expérience d’homme, de pasteur, d’écrivain, de théologien, de mystique sont naturellement indissociables les unes des autres. Mais, pour cette présentation d’un grand Africain dans le cadre de cette « Encyclopédie berbère », on a, tout naturellement aussi, privilégié les aspects proprement africains de cette vie, de cette « carrière », de cette action. « Berbère », c’est-à-dire de sang « indigène », pour l’..

Circoncellions

Le mot « circoncellions » est en soi une définition, limitée au seul aspect de la réalité sociale de la catégorie visée, si l’on en croit l’étymologie qu’en a donnée saint Augustin, dans l’une de ses œuvres de polémique antidonatiste : « ... victus sui causa cellas circumiens rusticanas, unde et circumcellionum nomen accepit » (Aug., Contra Gaudentium, I, XXVIII, 32). Les circoncellions seraient donc des « rôdeurs de celliers », assurant ainsi leur subsistance. Mais cette définition apparaît ..

Christianisme

Des origines à la « paix de l’Église » Le premier document authentique relatif au christianisme africain ne remonte pas plus haut que l’année 180 de notre ère : ce sont les Actes des martyrs scillitains. Mais le sentiment commun que les origines chrétiennes en Afrique étaient bien plus anciennes a fait naître sur l’introduction du christianisme en ces contrées toute une série de légendes. L’Église de Rome une fois fondée, saint Pierre serait venu prêcher à Carthage et y aurait laissé comme év..

Carthage

La Carthage punique (S. Lancel) Si, pour dater la fondation de Carthage par des Phéniciens venus de Tyr en passant par Chypre, on ne prend pas en considération une tradition haute -représentée en particulier par la Chronique de saint Jérôme – qui fixait en 1215 avant notre ère cet événement, on s’accorde en général sur une tradition « basse » qui retient pour cette fondation une date située à la fin du ixe siècle, plus précisément en 814 avant J.-C. Cette date, mentionnée aussi par Cicéron da..

Targeting late diagnosis of HIV in Kent, Medway and Picardy: evaluation of interventions in the Anglo-French IMPRESS Health 2 (Interreg IVA Channel Programme) project 4282

This report outlines the results and final stakeholder evaluations for the intervention phase (phase 3) of the Interreg IVA Channel Programme 4282 IMPRESSHealth 2 study. It describes how recommendations from the phase 1 report were implemented in Kent, Medway and Picardy in Northern France, the impact which these had on the uptake and timeliness of HIV testing in these areas; and analysis of the reasons for variance between the two countries (UK and France). The report contains examples of some of the public health and social media materials developed to increase the uptake and timeliness of HIV testing, and the results of the stakeholder assessment of its success. Overall, the impact of the interventions have been successful, with widespread increases in both the number and timeliness of HIV testing in the UK though less so in France. Reasons for these differences are discussed in the report. The report also highlights the huge contribution which social and broadcasting media can make to public health campaigns of this nature, and the value of multi-sector and inter-organisational team working

Rev-erb-alpha modulates skeletal muscle oxidative capacity by regulating mitochondrial biogenesis and autophagy

The nuclear receptor Rev-erb-α modulates hepatic lipid and glucose metabolism, adipogenesis and the inflammatory response in macrophages. We show here that Rev-erb-α is highly expressed in oxidative skeletal muscle and plays a role in mitochondrial biogenesis and oxidative function, in gain- and loss-of function studies. Rev-erb-α-deficiency in skeletal muscle leads to reduced mitochondrial content and oxidative function, resulting in compromised exercise capacity. This phenotype was recapitulated in isolated fibers and in muscle cells upon Rev-erbα knock-down, while Rev-erb-α over-expression increased the number of mitochondria with improved respiratory capacity. Rev-erb-α-deficiency resulted in deactivation of the Stk11–Ampk–Sirt1–Ppargc1-α signaling pathway, whereas autophagy was up-regulated, resulting in both impaired mitochondrial biogenesis and increased clearance. Muscle over-expression or pharmacological activation of Rev-erb-α increased respiration and exercise capacity. This study identifies Rev-erb-α as a pharmacological target which improves muscle oxidative function by modulating gene networks controlling mitochondrial number and function

Gender-Sensitive Violence Risk Assessment:Predictive Validity of Six Tools in Female Forensic Psychiatric Patients

Most violence risk assessment tools have been validated predominantly in males. In this multicenter study, the Historical, Clinical, Risk Management-20 (HCR-20), Historical, Clinical, Risk Management-20 Version 3 (HCR-20(V3)), Female Additional Manual (FAM), Short-Term Assessment of Risk and Treatability (START), Structured Assessment of Protective Factors for violence risk (SAPROF), and Psychopathy Checklist-Revised (PCL-R) were coded on file information of 78 female forensic psychiatric patients discharged between 1993 and 2012 with a mean follow-up period of 11.8 years from one of four Dutch forensic psychiatric hospitals. Notable was the high rate of mortality (17.9%) and readmission to psychiatric settings (11.5%) after discharge. Official reconviction data could be retrieved from the Ministry of Justice and Security for 71 women. Twenty-four women (33.8%) were reconvicted after discharge, including 13 for violent offenses (18.3%). Overall, predictive validity was moderate for all types of recidivism, but low for violence. The START Vulnerability scores, HCR-20(V3), and FAM showed the highest predictive accuracy for all recidivism. With respect to violent recidivism, only the START Vulnerability scores and the Clinical scale of the HCR-20(V3) demonstrated significant predictive accuracy

Relative contribution of three main virulence factors in Pseudomonas aeruginosa pneumonia:

Objective: The pathogenesis and the outcome of Pseudomonas aeruginosa ventilator-acquired pneumonia depend on the virulence factors displayed by the bacteria as well as the host response. Thus, quorum sensing, lipopolysaccharide, and type 3 secretion system have each individually been shown to be important virulence systems in laboratory reference strains. However, the relative contribution of these three factors to the in vivo pathogenicity of clinically relevant strains has never been studied. We analyzed the virulence of 56 nonclonal Pseudomonas aeruginosa strains isolated from critically ill patients with ventilator-acquired pneumonia. To avoid the variation of human immune response, we used a murine model of pneumonia. The aim was to determine which virulence factor was the most important.Setting: Research laboratory of a university. Subjects: Male adult BALB/c mice. Interventions: In vitro, the phenotype of each strain was established as to the expression of quorum sensing-regulated factors (elastase and pyocyanin), type 3 secretion system exotoxin secretion (Exotoxin U, S and/or T, or “nonsecreting”), and lipopolysaccharide O-antigen serotype. Strain pathogenicity was evaluated in vivo in a mouse model of acute pneumonia through lung injury assessment by measuring alveolar–capillary barrier permeability to proteins, lung wet/dry weight ratio, and bacterial dissemination. Associations were then sought between virulence system phenotypes and levels of lung injury. Measurements and Main Results: In univariate analysis, elastase production, O11 serotype, and type 3 secretion system exotoxin secretion were associated with increased lung injury and exotoxin U was linked to an increase risk of bacteremia. In multivariate analysis, we observed that type 3 secretion system exotoxin secretion and to a lesser degree elastase production were associated with increased lung injury. Conclusion: In a murine model of pneumonia, our data suggest that type 3 secretion system and elastase are the most important virulence factors in clinically relevant P. aeruginosa strains

Metabolic and Innate Immune Cues Merge into a Specific Inflammatory Response via the UPR

Erratum in : Metabolic and Innate Immune Cues Merge into a Specific Inflammatory Response via the UPR. [Cell. 2019]International audienceInnate immune responses are intricately linked with intracellular metabolism of myeloid cells. Toll-likereceptor (TLR) stimulation shifts intracellular metabolism toward glycolysis, while anti-inflammatorysignals depend on enhanced mitochondrial respiration. How exogenous metabolic signals affect theimmune response is unknown. We demonstrate that TLR-dependent responses of dendritic cells (DC)are exacerbated by a high fatty acid (FA) metabolic environment. FA suppress the TLR-inducedhexokinase activity and perturb tricarboxylic acid cycle metabolism. These metabolic changesenhance mitochondrial reactive oxygen species (mtROS) production and, in turn, the unfolded proteinresponse (UPR) leading to a distinct transcriptomic signature, with IL-23 as hallmark. Interestingly,chemical or genetic suppression of glycolysis was sufficient to induce this specific immune response.Conversely, reducing mtROS production or DC-specific deficiency in XBP1 attenuated IL-23expression and skin inflammation in an IL-23-dependent model of psoriasis. Thus, fine-tuning of innateimmunity depends on optimization of metabolic demands and minimization of mtROS-induced UPR

AMP-activated protein kinase deficiency reduces ozone-induced lung injury and oxidative stress in mice

<p>Abstract</p> <p>Background</p> <p>Acute ozone exposure causes lung oxidative stress and inflammation leading to lung injury. At least one mechanism underlying the lung toxicity of ozone involves excessive production of reactive oxygen and nitrogen intermediates such as peroxynitrite. In addition and beyond its major prooxidant properties, peroxynitrite may nitrate tyrosine residues altering phosphorylation of many protein kinases involved in cell signalling. It was recently proposed that peroxynitrite activates 5'-AMP-activated kinase (AMPK), which regulates metabolic pathways and the response to cell stress. AMPK activation as a consequence of ozone exposure has not been previously evaluated. First, we tested whether acute ozone exposure in mice would impair alveolar fluid clearance, increase lung tissue peroxynitrite production and activate AMPK. Second, we tested whether loss of AMP-activated protein kinase alpha1 subunit in mouse would prevent enhanced oxidative stress and lung injury induced by ozone exposure.</p> <p>Methods</p> <p>Control and AMPKα1 deficient mice were exposed to ozone at a concentration of 2.0 ppm for 3 h in glass cages. Evaluation was performed 24 h after ozone exposure. Alveolar fluid clearance (AFC) was evaluated using fluorescein isothiocyanate tagged albumin. Differential cell counts, total protein levels, cytokine concentrations, myeloperoxidase activity and markers of oxidative stress, i.e. malondialdehyde and peroxynitrite, were determined in bronchoalveolar lavage (BAL) and lung homogenates (LH). Levels of AMPK-Thr¹⁷²phosphorylation and basolateral membrane Na(+)-K(+)-ATPase abundance were determined by Western blot.</p> <p>Results</p> <p>In control mice, ozone exposure induced lung inflammation as evidence by increased leukocyte count, protein concentration in BAL and myeloperoxidase activity, pro-inflammatory cytokine levels in LH. Increases in peroxynitrite levels (3 vs 4.4 nM, p = 0.02) and malondialdehyde concentrations (110 vs 230 μmole/g wet tissue) were detected in LH obtained from ozone-exposed control mice. Ozone exposure consistently increased phosphorylated AMPK-Thr¹⁷²to total AMPK ratio by 80% in control mice. Ozone exposure causes increases in AFC and basolateral membrane Na(+)-K(+)-ATPase abundance in control mice which did not occur in AMPKα1 deficient mice.</p> <p>Conclusions</p> <p>Our results collectively suggest that AMPK activation participates in ozone-induced increases in AFC, inflammation and oxidative stress. Further studies are needed to understand how the AMPK pathway may provide a novel approach for the prevention of ozone-induced lung injury.</p