Differential Biological Effects of Dietary Lipids and Irradiation on the Aorta, Aortic Valve, and the Mitral Valve

peer reviewedAimsDietary cholesterol and palmitic acid are risk factors for cardiovascular diseases (CVDs) affecting the arteries and the heart valves. The ionizing radiation that is frequently used as an anticancer treatment promotes CVD. The specific pathophysiology of these distinct disease manifestations is poorly understood. We, therefore, studied the biological effects of these dietary lipids and their cardiac irradiation on the arteries and the heart valves in the rabbit models of CVD.Methods and ResultsCholesterol-enriched diet led to the thickening of the aortic wall and the aortic valve leaflets, immune cell infiltration in the aorta, mitral and aortic valves, as well as aortic valve calcification. Numerous cells expressing α-smooth muscle actin were detected in both the mitral and aortic valves. Lard-enriched diet induced massive aorta and aortic valve calcification, with no detectable immune cell infiltration. The addition of cardiac irradiation to the cholesterol diet yielded more calcification and more immune cell infiltrates in the atheroma and the aortic valve than cholesterol alone. RNA sequencing (RNAseq) analyses of aorta and heart valves revealed that a cholesterol-enriched diet mainly triggered inflammation-related biological processes in the aorta, aortic and mitral valves, which was further enhanced by cardiac irradiation. Lard-enriched diet rather affected calcification- and muscle-related processes in the aorta and aortic valve, respectively. Neutrophil count and systemic levels of platelet factor 4 and ent-8-iso-15(S)-PGF2α were identified as early biomarkers of cholesterol-induced tissue alterations, while cardiac irradiation resulted in elevated levels of circulating nucleosomes.ConclusionDietary cholesterol, palmitic acid, and cardiac irradiation combined with a cholesterol-rich diet led to the development of distinct vascular and valvular lesions and changes in the circulating biomarkers. Hence, our study highlights unprecedented specificities related to common risk factors that underlie CVD

Anomalie du gène TCF2/HNF-1b (première cause de reins hyperéchogènes bilatéraux dépistés in utéro)

Notre étude rétrospective sur 10 ans porte sur 57 fœtus présentant des reins hyperéchogènes bilatéraux isolés. Un tiers des grossesses a été médicalement interrompu. 60 % des enfants ont une IRC. Seuls 10 % des patients n'ont pas développé de pathologies, les autres présentent des étiologies habituelles de la littérature : PKAR, PKAD, dysplasie rénale.... Une cause émergente essentielle est identifiée : l'anomalie du gène TCF2, codant pour le facteur de transcription HNF-1b, impliqué dans le développement embryonnaire du rein. Ceci ouvre de nouvelles perspectives pour le conseil prénatal et le devenir à long terme. Une conduite à tenir pratique est proposée devant la découverte anténatale de reins hyperéchogènes, en tenant compte des difficultés quant à l'évaluation du pronostic et quant à l'orientation du diagnostic étiologique.TOULOUSE3-BU Santé-Centrale (315552105) / SudocPARIS-BIUM (751062103) / SudocSudocFranceF

Tourniquet syndrome: Interest of a systematic analysis of families’ social conditions to detect neglect situations

International audienc

Severe Global Inflammatory Involvement of Ocular Segments and Optic Disc Swelling in a 12-Year-Old Girl with Kawasaki Disease

International audienc

Bioactive surface coating for preventing mechanical heart valve thrombosis.

peer reviewedBACKGROUND: Prosthetic heart valves are the only treatment for most patients with severe valvular heart disease. Mechanical valves, made of metallic components, are the most long-lasting type of replacement valves. However, they are prone to thrombosis and require permanent anticoagulation and monitoring, which leads to higher risk of bleeding and impacts the patient's quality of life. OBJECTIVES: To develop a bioactive coating for mechanical valves with the aim to prevent thrombosis and improve patient outcomes. METHODS: We used a catechol-based approach to produce a drug-releasing multilayer coating adherent to mechanical valves. The hemodynamic performance of coated Open Pivot valves was verified in a heart model tester, and coating durability in the long term was assessed in a durability tester producing accelerated cardiac cycles. Coating antithrombotic activity was evaluated in vitro with human plasma or whole blood under static and flow conditions and in vivo after surgical valve implantation in a pig's thoracic aorta. RESULTS: We developed an antithrombotic coating consisting of ticagrelor- and minocycline-releasing cross-linked nanogels covalently linked to polyethylene glycol. We demonstrated the hydrodynamic performance, durability, and hemocompatibility of coated valves. The coating did not increase the contact phase activation of coagulation, and it prevented plasma protein adsorption, platelet adhesion, and thrombus formation. Implantation of coated valves in nonanticoagulated pigs for 1 month efficiently reduced valve thrombosis compared with noncoated valves. CONCLUSION: Our coating efficiently inhibited mechanical valve thrombosis, which might solve the issues of anticoagulant use in patients and the number of revision surgeries due to valve thrombosis despite anticoagulation

Schistosomiasis Haematobium, Corsica, France

International audienceIn Europe, urinary schistosomiasis has previously been detected only in Portugal, where this focus disappeared during the 1950s . However, freshwater snails of the species Bulinus contortus, B. truncatus, and Planorbarius metidjensis, which are recognized intermediate hosts for Schistosoma haematobium trematodes, have been found in Portugal , Spain , and Corsica . This finding suggested that autochthonous schistosomiasis could re-emerge in southern Europe if these mollusks become infected. We report a probable focus for transmission of schistosomiasis haematobium in Corsica, France

Protective Effect of Ticagrelor Against Infective Endocarditis Induced by Virulent Staphylococcus aureus in Mice

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