Université Nantes Angers Le Mans

About: Université Nantes Angers Le Mans is a education organization based out in Nantes, France. It is known for research contribution in the topics: Geology & Finite element method. The organization has 434 authors who have published 249 publications receiving 7208 citations. The organization is also known as: PRES Universite Nantes Angers Le Mans.

Incidence and Risk Factors for Thoracic Spine Pain in the Working Population: The French Pays de la Loire Study

Abstract: Objective To examine the incidence and risk factors for incident thoracic spine pain (TSP) in workers representative of a French region's working population. Methods In this prospective study, 3,710 workers were assessed in 2002–2005, and 2,332 (62.9%) of them were reassessed in 2007–2010. TSP was assessed by a self-administered Nordic questionnaire at baseline and at followup. At baseline, all participants completed a self-administered questionnaire on personal factors and work exposure. A total of 1,886 subjects (1,124 men and 762 women) without TSP at baseline were eligible for analysis. Associations between incident TSP and risk factors at baseline were analyzed by multivariate logistic regression. Results The incidence rate of TSP was 5.2 (95% confidence interval [95% CI] 3.9–6.6) per 100 men and 10.0 (95% CI 7.8–12.1) per 100 women. TSP was often associated with low back pain and neck pain. TSP in men was associated with age (odds ratios [ORs] ranging from 2.6 [95% CI 0.95–7.1] at 30–39 years to 6.0 [95% CI 2.1–17.3] at ≥50 years), being tall (OR 2.2 [95% CI 1.2–3.9]), frequent/sustained trunk bending (OR 3.0 [95% CI 1.5–6.1]), lack of recovery period or change in the task (OR 2.0 [95% CI 1.2–3.6]), and driving vehicles (OR 2.8 [95% CI 1.4–5.5]). Being overweight or obese was associated with lower risk (OR 0.5 [95% CI 0.3–0.96]). TSP in women was associated with high perceived physical workload (OR 1.9 [95% CI 1.1–3.3]), after adjustment for confounding variables. Conclusion The risk model of TSP combined personal and work-related organizational and physical factors. Trunk bending appeared to be a strong independent predictor of TSP in this working population.

Circulating microparticles from patients with obstructive sleep apnea enhance vascular contraction: mandatory role of the endothelium

Abstract: Obstructive sleep apnea (OSA) is characterized by repetitive apnea-hypopnea cycles during sleep associated with oxygen desaturation and sleep disruption. We evaluated the role of circulating microparticles (MPs) from patients with OSA in the regulation of vascular function. MPs from whole blood from patients with OSA or control subjects were injected i.v. into mice. Injection of MPs from patients with OSA induced ex vivo vascular hyperreactivity in aortas with functional endothelium but, in contrast, hyporeactivity in vessels without functional endothelium. Vascular hyperreactivity was blunted in the presence of a nitric oxide synthase inhibitor alone or combined with the cyclooxygenase inhibitor indomethacin. MPs from patients with OSA reduced endothelial nitric oxide synthase activity and nitric oxide production, increased aortic cyclooxygenase-1 and cyclooxygenase-2 expression, and increased thromboxane A(2) and prostacyclin production. Blockade of thromboxane A(2) receptor did not affect the serotonin response in arteries from OSA MP-treated mice. A superoxide dismutase mimetic reduced the vascular hyperreactivity induced by MPs from patients with OSA but had no effect on contraction in vessels from control and non-OSA MP-treated mice. These data provide evidence that circulating MPs from patients with OSA induce ex vivo vascular hyperreactivity with the obligatory role of the endothelium and subtle interactions between the nitric oxide and cyclooxygenase pathways and metabolites. These results highlight the participation of MPs in vascular dysfunction associated with OSA.

Polychlorinated biphenyl (PCB) decontamination kinetics in lactating goats (Capra hircus) following a contaminated corn silage exposure.

Abstract: This study aimed to determine the kinetics of contamination and decontamination of PCBs and PCDD/Fs in milk of lactating goats. Four goats were fed during 39 days with corn silage collected in an area accidentally contaminated and then with uncontaminated silage during 20 days. Concentrations of DL-PCBs + PCDD/Fs in milk exceeded rapidly (<15 days) the European limit value and approached steady state after 5 weeks. The decontamination kinetics in milk included first a rapid elimination phase (<10 days) followed by a slower elimination phase of 33, 51, and 59 days for DL-PCBs, NDL-PCBs, and PCDD/Fs, respectively. Therefore, in lactating goats, PCBs and PCDD/Fs contaminated forage raises concerns in terms of food safety. The study also indicates that a decontamination process of lactating animals remains feasible; 20 days was considered to be sufficient to obtain a DL-PCBs + PCDD/Fs level in milk below the regulatory value.

The synthetic pentasaccharide fondaparinux attenuates myocardial ischemia-reperfusion injury in rats via STAT-3.

Abstract: Acute myocardial infarction is a leading cause of mortality and morbidity worldwide. Although essential for successful recovery, myocardium reperfusion is associated with reperfusion injury. Two major cell survival signaling cascades are known to be protective against ischemia-reperfusion (I/R) injury: the reperfusion injury salvage kinase, including Akt, extracellular signal-regulated kinase 1/2, and the downstream target GSK-3β, and the survivor activating factor enhancement, which involves STAT-3. Pharmacologic inhibition of factor Xa has been shown to attenuate I/R injury, but the cellular mechanism is poorly understood. Our aim was to determine the role of whole blood in fondaparinux (FDX)-induced cardioprotection and the involvement of reperfusion injury salvage kinase and survivor activating factor enhancement pathways. We investigated FDX ability to prevent in vivo I/R injury using a transient coronary ligation rat model and ex vivo using a model of crystalloid-perfused isolated rat heart. In both models, infarct size was assessed after 120 min of reperfusion. Myocardial tissues were collected after 15 and 30 min of reperfusion for Western blot analysis. In vivo, FDX decreased infarct size by 29% and induced significant STAT-3 and GSK-3β phosphorylation in comparison to controls. Adding AG490, an inhibitor of JAK/STAT pathway, before I/R, prevented STAT-3 phosphorylation and abolished FDX-induced cardioprotection. On the contrary, FDX did not have an effect on infarct size or hemodynamic parameters in the isolated-heart model. Fondaparinux decreased I/R injury in vivo, but not in a crystalloid-perfused isolated heart. Under our experimental conditions, FDX required whole blood to be protective, and this beneficial effect was mediated through STAT-3 phosphorylation.