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Montravers P.,University Paris Diderot | Ichai C.,University of Nice Sophia Antipolis | Dupont H.,Center hospitalier University dAmiens | Payen J.F.,Joseph Fourier University | And 11 more authors.
Annales Francaises d'Anesthesie et de Reanimation | Year: 2013

Objectifs: Type d'étude: Méthodes: Résultats: Conclusion: Objectives: To clarify the procedures related to mechanical ventilation in the intensive care unit setting: allocation of ventilators, team education, maintenance and reference documents. Study design: Declarative survey. Methods: Between September and December 2010, we assessed the assignment and types of ventilators (ICU ventilators, temporary repair ventilators, non-invasive ventilators [NIV], and transportation ventilators), medical and nurse education, maintenance of the ventilators, presence of reference documents. Results are expressed in median/range and proportions. Results: Among the 62 participating ICUs, a median of 15 ventilators/ICU (range 1-50) was reported with more than one trademark in 47 (76%) units. Specific ventilators were used for NIV in 22 (35%) units, temporary repair in 49 (79%) and transportation in all the units. Nurse education courses were given by ICU physicians in 54 (87%) units or by a company in 29 (47%) units. Medical education courses were made by ICU senior physicians in 55 (89%) units or by a company in 21 (34%) units. These courses were organized occasionally in 24 (39%) ICU and bi-annually in 16 (26%) units. Maintenance procedures were made by the ICU staff in 39 (63%) units, dedicated staff (17 [27%]) or bioengineering technicians (14 [23%] ICU). Reference documents were written for maintenance procedures in 48 (77%) units, ventilator setup in 22 (35%) units and ventilator dysfunction in 20 (32%) ICU. Conclusions: This first survey shows disparate distribution of ventilators and practices among French ICU. Education and understanding of the proper use of ventilators are key issues for security improvement. © 2013 Société française d'anesthésie et de réanimation (Sfar). Source

Vassallo P.F.,Aix - Marseille University | Vassallo P.F.,Federal University of Espirito Santo | Simoncini S.,Aix - Marseille University | Ligi I.,Aix - Marseille University | And 18 more authors.
Blood | Year: 2014

Epidemiological and experimental studies indicate that early vascular dysfunction occurs in low-birth-weight subjects, especially preterm (PT) infants. We recently reported impaired angiogenic activity of endothelial colony-forming cells (ECFCs) in this condition. We hypothesized that ECFC dysfunction in PT might result from premature senescence and investigated the underlying mechanisms. Compared with ECFCs from term neonates (n = 18), ECFCs isolated from PT (n = 29) display an accelerated senescence sustained by growth arrest and increased senescence-associated β-galactosidase activity. Increased p16INK4a expression, in the absence of telomere shortening, indicates that premature PT-ECFC aging results from stress-induced senescence. SIRT1 level, a nicotinamide adenine dinucleotide-dependent deacetylase with anti-aging activities, is dramatically decreased in PT-ECFCs and correlated with gestational age. SIRT1 deficiency is subsequent to epigenetic silencing of its promoter. Transient SIRT1 overexpression or chemical induction by resveratrol treatment reverses senescence phenotype, and rescues in vitro PT-ECFC angiogenic defect in a SIRT1-dependent manner. SIRT1 overexpression also restores PT-ECFC capacity for neovessel formation in vivo. We thus demonstrate that decreased expression of SIRT1 drives accelerated senescence of PT-ECFCs, and acts as a critical determinant of the PT-ECFC angiogenic defect. These findings lay new grounds for understanding the increased cardiovascular risk in individuals born prematurely and open perspectives for therapeutic strategy. © 2014 by The American Society of Hematology. Source

Bonello L.,Aix - Marseille University | Harhouri K.,Aix - Marseille University | Baumstarck K.,University of Monastir | Arnaud L.,Aix - Marseille University | And 7 more authors.
Journal of Thrombosis and Haemostasis | Year: 2012

Background: Endothelial lesion and regeneration are critical events in the process leading to in-stent restenosis (ISR) after bare metal stent (BMS) percutaneous coronary intervention (PCI). Objectives: To prospectively investigate the relationship between biomarkers reflecting endothelial turnover and the occurrence of ISR. Methods: We performed a multicenter prospective observational study that included 156 patients undergoing elective PCI with BMS. Endothelial lesion was assessed by the enumeration of circulating endothelial cells (CECs). Endothelial regeneration was evaluated by enumeration of circulating CD34+ progenitor cells (CD34+ PCs) and CD34+KDR+ endothelial progenitor cells (EPCs). Measurements were performed before PCI, and 6 and 24h after PCI. Dynamic changes were evaluated by calculating the delta value of each marker. The primary and secondary endpoints of the study were clinical target lesion revascularizations (TLRs) and major adverse cardiovascular events (MACEs) after 6 months of follow-up. Results: During follow-up, 28 MACEs were recorded, including 27 TLRs. PCI induced a significant rise in the numbers of CECs, CD34+ PCs, and CD34+KDR+ EPCs. Baseline, 6-h and 24-h levels of these markers did not differ between patients with and without TLR. The delta percentage of CD34+KDR+ EPCs was significantly reduced in patients with TLR as compared with patients without TLR (-0.56±8.1 vs. 2.91±6.2; P=0.015). In multivariate analysis, the delta percentage of CD34+KDR+ EPCs independently predicted the occurrence of TLR and MACEs (P=0.02 and P=0.014, respectively). Conclusion: The endothelial regenerative response to injury induced by PCI, assessed by CD34+KDR+ EPCs mobilized among progenitor cells, determines the risk of TLR and MACEs in stable coronary artery disease patients. © 2012 International Society on Thrombosis and Haemostasis. Source

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