EVALUACIÓN DE FIREWALLS BASADOS EN SOFTWARE LIBRE (FIREWALL EVALUATION BASED ON OPEN SOURCE SOFTWARE)

En este trabajo se propone la evaluación de firewalls basado en software libre GNU/LINUX con las características que les permitan integrarse a una cama de pruebas en la cual se estudiaron, evaluaron y analizaron diversos entornos de red y escenarios de ataque. Los firewalls de software libre son una buena alternativa cuando se trata de brindar seguridad en una red, en este trabajo fueron evaluados cuatro distribuciones Linux que han sido especialmente diseñadas para brindar este servicio. Las herramientas de software libre empleadas demostraron ser las adecuadas para las pruebas realizadas a los diferentes firewalls, de este modo se logró obtener resultados que muestran la factibilidad de ClearOS para ser implementado en la cama de pruebas. También se probó su efectividad al mostrar una buena respuesta en la defensa de los ataques, con y sin la inyección del tráfico de fondo generado por la herramienta iperf.In this work we propose the evaluation of firewalls based on free software GNU / LINUX with the characteristics that allow them to be integrated into a test bed in which various network environments and attack scenarios were studied, evaluated and analyzed. Free software firewalls are a good alternative when it comes to providing security in a network, in this work were evaluated four Linux distributions that have been specially designed to provide this service. The free software tools used, proved to be adequate for the tests carried out on the different firewalls, in this way it was possible to obtain results that show the feasibility of ClearOS to be implemented in the test bed. Its effectiveness was also proven by showing a good response in the defense of attacks, with and without the injection of background traffic generated by the iperf tool

Formation à la communication scientifique et interpersonnelle en anglais pour la santé : quelle prise en charge en formation initiale et en formation continue ? Vers une harmonisation de l’enseignement en France métropolitaine

Contexte : L’enseignement de l’anglais dans les facultés de médecine est obligatoire depuis 1992 mais cette disposition est diversement respectée. Buts : Bilan et perspectives ouvertes par le partenariat entre l’Association nationale des étudiants en médecine de France (ANEMF) et le Groupe d’étude et de recherche en anglais de Spécialité (GERAS) membre de la Société des anglicistes de l’enseignement supérieur (SAES). Matériel : Exploitation de différents travaux publiés (articles, DEA, manuels), enquêtes, réunions GERAS-ANEMF. Résultats : Les enseignants de médecine, d’abord confrontés à la difficulté d’introduire un nouvel enseignement, avec une diminution du volume horaire des matières médicales et la nécessité de déployer des ressources matérielles et humaines, participent à présent à l’enseignement de l’anglais. Les difficultés initiales rencontrées par les enseignants d’anglais sont compensées par des succès visibles dans certaines facultés. L’enseignement de l’anglais, loin d’être au mieux une remédiation, au pire une perte de temps, vise une compétence effective en communication écrite, orale et interpersonnelle des professionnels de la santé du XXIe siècle. Les étudiants, longtemps hostiles à la réforme, montrent désormais leur intérêt et souhaitent une harmonisation nationale des contenus, conscients de la nécessité pour eux de pouvoir travailler en anglais. Conclusions : La mise en œuvre et le succès de la Charte d’enseignement de l’anglais élaborée par l’ANEMF et le GERAS dépendront étroitement du soutien apporté par les autorités compétentes de chaque faculté à ce projet, dont la visée est une aide au déroulement de la carrière et de l’activité clinique aussi bien qu’au développement personnel des futursprofessionnels de la santé

4-Hydroxynonenal Contributes to Fibroblast Senescence in Skin Photoaging Evoked by UV-A Radiation

International audienceSolar ultraviolet A (UV-A) radiation promotes a huge variety of damages on connective tissues and dermal fibroblasts, including cellular senescence, a major contributor of skin photoaging. The mechanisms of skin photoaging evoked by UV-A partly involve the generation of reactive oxygen species and lipid peroxidation. We previously reported that 4-hydroxynonenal (HNE), a lipid peroxidation-derived aldehyde, forms adducts on elastin in the skins of UV-A irradiated hairless mice, possibly contributing to actinic elastosis. In the present study, we investigated whether and how HNE promotes fibroblast senescence in skin photoaging. Dermal fibroblasts of skins from UV-A-exposed hairless mice exhibited an increased number of γH2AX foci characteristic of cell senescence, together with an accumulation of HNE adducts partly colocalizing with the cytoskeletal protein vimentin. Murine fibroblasts exposed to UV-A radiation (two cycles of 15 J/cm2), or HNE (30 µM, 4 h), exhibited senescence patterns characterized by an increased γH2AX foci expression, an accumulation of acetylated proteins, and a decreased expression of the sirtuin SIRT1. HNE adducts were detected on vimentin in cultured fibroblasts irradiated by UV-A or incubated with HNE. The HNE scavenger carnosine prevented both vimentin modification and fibroblast senescence evoked by HNE in vitro and in the skins of UV-A-exposed mice. Altogether, these data emphasize the role of HNE and lipid peroxidation-derived aldehydes in fibroblast senescence, and confirm the protective effect of carnosine in skin photoaging

Synthesis, antioxidant and cytoprotective evaluation of potential antiatherogenic phenolic hydrazones. A structure–activity relationship insight

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Synthesis and evaluation of antioxidant phenolic diaryl hydrazones as potent antiangiogenic agents in atherosclerosis

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4-Hydroxynonenal Contributes to Angiogenesis through a Redox-Dependent Sphingolipid Pathway: Prevention by Hydralazine Derivatives

The neovascularization of atherosclerotic lesions is involved in plaque development and may contribute to intraplaque hemorrhage and plaque fragilization and rupture. Among the various proangiogenic agents involved in the neovascularization process, proatherogenic oxidized LDLs (oxLDLs) contribute to the formation of tubes via the generation of sphingosine 1-phosphate (S1P), a major mitogenic and proangiogenic sphingolipid mediator. In this study, we investigated whether 4-hydroxynonenal (4-HNE), an aldehydic lipid oxidation product abundantly present in oxLDLs, contributes to their proangiogenic properties. Immunofluorescence analysis of human atherosclerotic lesions from carotid endarterectomy showed the colocalization of HNE-adducts with CD31, a marker of endothelial cells, suggesting a close relationship between 4-HNE and neovessel formation. In vitro, low 4-HNE concentration (0.5–1 µM) elicited the formation of tubes by human microvascular endothelial cells (HMEC-1), whereas higher concentrations were not angiogenic. The formation of tubes by 4-HNE involved the generation of reactive oxygen species and the activation of the sphingolipid pathway, namely, the neutral type 2 sphingomyelinase and sphingosine kinase-1 (nSMase2/SK-1) pathway, indicating a role for S1P in the angiogenic signaling of 4-HNE. Carbonyl scavengers hydralazine and bisvanillyl-hydralazone inhibited the nSMase2/SK1 pathway activation and the formation of tubes on Matrigel® evoked by 4-HNE. Altogether, these results emphasize the role of 4-HNE in the angiogenic effect of oxLDLs and point out the potential interest of pharmacological carbonyl scavengers to prevent the neovascularization process

Protein disulfide isomerase modification and inhibition contribute to ER stress and apoptosis induced by oxidized low density lipoproteins.

International audienceAIMS: Protein disulfide isomerase (PDI) is an abundant endoplasmic reticulum (ER)-resident chaperone and oxidoreductase that catalyzes formation and rearrangement (isomerization) of disulfide bonds, thereby participating in protein folding. PDI modification by nitrosative stress is known to increase protein misfolding, ER stress, and neuronal apoptosis. As LDL oxidation and ER stress may play a role in atherogenesis, this work was designed to investigate whether PDI was inactivated by oxLDLs, thereby participating in oxLDL-induced ER stress and apoptosis. RESULTS: Preincubation of human endothelial HMEC-1 and of macrophagic U937 cells with toxic concentration of oxLDLs induced PDI inhibition and modification, as assessed by 4-HNE-PDI adducts formation. PDI inhibition by bacitracin potentiated ER stress (increased mRNA expression of CHOP and sXBP1) and apoptosis induced by oxLDLs. In contrast, increased PDI activity by overexpression of an active wild-type PDI was associated with reduced oxLDL-induced ER stress and toxicity, whereas the overexpression of a mutant inactive form was not protective. These effects on PDI were mimicked by exogenous 4-HNE and prevented by the carbonyl-scavengers N-acetylcysteine and pyridoxamine, which reduced CHOP expression and toxicity by oxLDLs. Interestingly, 4-HNE-modified PDI was detected in the lipid-rich areas of human advanced atherosclerotic lesions. Innovation and CONCLUSIONS: PDI modification by oxLDLs or by reactive carbonyls inhibits its enzymatic activity and potentiates both ER stress and apoptosis by oxLDLs. PDI modification by lipid peroxidation products in atherosclerotic lesions suggests that a loss of function of PDI may occur in vivo, and may contribute to local ER stress, apoptosis, and plaque progression