3D hydrosedimentary models of the Loire Estuary using TELEMAC-3D-TOMAWAC and GAIA

Hydrodynamic

Myocardial function at the early phase of traumatic brain injury: a prospective controlled study

The concept of brain-heart interaction has been described in several brain injuries. Traumatic brain injury (TBI) may also lead to cardiac dysfunction but evidences are mainly based upon experimental and clinical retrospective studies. Methods We conducted a prospective case-control study in a level I trauma center. Twenty consecutive adult patients with severe TBI were matched according to age and gender with 20 control patients. The control group included adult patients undergoing a general anesthesia for a peripheral trauma surgery. Conventional and Speckle Tracking Echocardiography (STE) was performed within the first 24 post- traumatic hours in the TBI group and PRE/PER-operative in the control group. The primary endpoint was the left ventricle ejection fraction (LVEF) measured by the Simpson’s method. Secondary endpoints included the diastolic function and the STE analysis. Results We found similar LVEF between the TBI group and the PER-operative control group (61 % [56–76]) vs. 62 % [52–70]). LV morphological parameters and the systolic function were also similar between the two groups. Regarding the diastolic function, the isovolumic relaxation time was significantly higher in the TBI cohort (125 s [84–178] versus 107 s [83–141], p = 0.04), suggesting a subclinical diastolic dysfunction. Using STE parameters, we observed a trend toward higher strains in the TBI group but only the apical circumferential strain and the basal rotation reached statistical significance. STE-derived parameters of the diastolic function tended to be lower in TBI patients. Discussion No systematic myocardial depression was found in a cohort of severe TBI patients. Conclusions STE revealed a correct adaptation of the left systolic function, while the diastolic function slightl

Vascular smooth muscle function in type 2 diabetes mellitus: a systematic review and meta-analysis

Aims/hypothesis In type 2 diabetes, in contrast to the well-documented endothelial dysfunction, studies assessing vascular smooth muscle (VSM) function have yielded discrepant results over the last two decades. We therefore sought to determine whether or not VSM function is impaired in individuals with type 2 diabetes. Methods We conducted a systematic search of MEDLINE, Cochrane, Scopus and Web of Science databases, from their respective inceptions until December 2012, for articles evaluating VSM function in individuals with type 2 diabetes. A meta-analysis was performed to compare the standardised mean difference (SMD) in VSM function between individuals with type 2 diabetes and age-matched controls. Subgroup analyses and meta-regression were used to identify sources of heterogeneity. Results Twenty-seven articles (1,042 individuals with type 2 diabetes and 601 control subjects) were included in this analysis. VSM function was significantly impaired in diabetic compared with control subjects (SMD −0.68, 95% CI −0.84, −0.52; p < 0.001). Although moderate heterogeneity among studies was found (I 2 = 52%), no significant publication bias was detected. Subgroup analyses showed a further decline in VSM function assessed in the microcirculation compared with the macrocirculation of individuals with type 2 diabetes (p = 0.009). In meta-regression, VSM function in the microcirculation was inversely associated with BMI and triacylglycerols and was positively associated with HDL-cholesterol. Conclusions/interpretation In addition to the endothelium, the VSM is a source of vascular dysfunction in type 2 diabetes. An exacerbation of VSM function in the microcirculation may be a distinctive feature in type 2 diabetes

Effects of a Lifestyle Program on Vascular Reactivity in Macro- and Microcirculation in Severely Obese Adolescents

Context and Objective: This study aimed to comprehensively assess the macro- and microcirculation of severely obese adolescents (SOA) and normal-weight counterparts and to determine the longitudinal effects of weight loss on vascular function in SOA. Design, Setting, Participants, and Outcome Measures: Seventeen SOA (body mass index z-score = 4.22 ± 0.73) and 19 puberty-matched normal-weight counterparts (body mass index z-score = −0.02 ± 1.04) were included. The SOA participated in a 4 month weight loss program. Brachial artery flow-mediated dilation and response to sublingual nitrate (nitrate-mediated dilation [NMD]) were assessed by high-resolution ultrasound. Microvascular reactivity was evaluated by laser Doppler flowmetry in response to NMD, iontophoresis of acetylcholine and sodium nitroprusside, and local hyperthermia. Plasma insulin, leptin, resistin, C-reactive protein, myeloperoxidase, and tissue plasminogen activator were measured. Results: At baseline, SOA had similar flow-mediated dilation and impaired NMD in the brachial artery compared to normal-weight adolescents. Similarly, peak responses to acetylcholine and sodium nitroprusside iontophoresis and to local hyperthermia were unaltered, whereas cutaneous blood flow after NMD was lower in the forearm microcirculation of SOA. All plasma measurements were significantly higher in SOA. After the 4-month program, SOA presented a weight reduction of 7.4 ± 3.1%, but neither brachial artery nor microvascular reactivity variables were improved. Significant decreases were detected in plasma leptin, myeloperoxidase, and tissue plasminogen activator. Conclusions: Macro- and microvascular endothelial function are preserved in adolescents with severe obesity. Conversely, weight loss does not improve their impaired smooth muscle response to exogenous organic nitrate in both vascular beds, despite reducing plasma markers adversely related to vascular homeostasis.This study was supported by grants from the French Society of Vascular Medicine 2010-2012 (to A.V. and A.P.M), and the Spanish Ministry of Health (CIBERobn CB12/03/30038) (to E.R.

Long-term effects of high intensity resistance and endurance exercise on plasma leptin and ghrelin in overweight individuals:the RESOLVE Study

International audienceThe objective of this study was to evaluate the effects of high-intensity resistance and endurance exercise on body composition and plasma leptin and ghrelin concentrations in overweight individuals. One hundred participants were randomly assigned to 3 exercise interventions: high-resistance–low-aerobic exercise (Re), low-resistance–high-aerobic exercise (rE), low-resistance–low-aerobic exercise (re). Interventions began with 3 weeks of residential supervision (phase 1) after which participants had to manage the physical activity programs individually (phase 2). Body composition and plasma variables were measured at baseline and after phase 1 as well as after 3, 6, and 12 months. Significant decreases in body weight and fat were observed after phase 1 (p < 0.001) and continued at a lower rate for up to 3 months and then remained stable for the rest of the protocol. Once a body weight plateau was reached, body fat loss after the Re and rE conditions exceeded the fat loss observed in the re condition by 1.5–2 kg (p < 0.05). Leptin was significantly decreased after day 21 and month 3 (p < 0.001) and remained stable for the rest of the study. Ghrelin was significantly increased after day 21 and month 3 (p < 0.001) and returned to a level comparable to baseline between month 6 and 12 when body weight and fat had reached a plateau. In conclusion, this study reinforces the idea that an increase in exercise intensity may accentuate body fat loss before the occurrence of a body weight plateau. Resistance to further fat loss was accompanied by a decrease in plasma leptin and an increase in plasma ghrelin

Generation of neutralizing antibodies and divergence of SIVmac239 in cynomolgus macaques following short-term early antiretroviral therapy.

Neutralizing antibodies (NAb) able to react to heterologous viruses are generated during natural HIV-1 infection in some individuals. Further knowledge is required in order to understand the factors contributing to induction of cross-reactive NAb responses. Here a well-established model of experimental pathogenic infection in cynomolgus macaques, which reproduces long-lasting HIV-1 infection, was used to study the NAb response as well as the viral evolution of the highly neutralization-resistant SIVmac239. Twelve animals were infected intravenously with SIVmac239. Antiretroviral therapy (ART) was initiated ten days post-inoculation and administered daily for four months. Viral load, CD4(+) T-cell counts, total IgG levels, and breadth as well as strength of NAb in plasma were compared simultaneously over 14 months. In addition, envs from plasma samples were sequenced at three time points in all animals in order to assess viral evolution. We report here that seven of the 12 animals controlled viremia to below 10(4) copies/ml of plasma after discontinuation of ART and that this control was associated with a low level of evolutionary divergence. Macaques that controlled viral load developed broader NAb responses early on. Furthermore, escape mutations, such as V67M and R751G, were identified in virus sequenced from all animals with uncontrolled viremia. Bayesian estimation of ancestral population genetic diversity (PGD) showed an increase in this value in non-controlling or transient-controlling animals during the first 5.5 months of infection, in contrast to virus-controlling animals. Similarly, non- or transient controllers displayed more positively-selected amino-acid substitutions. An early increase in PGD, resulting in the generation of positively-selected amino-acid substitutions, greater divergence and relative high viral load after ART withdrawal, may have contributed to the generation of potent NAb in several animals after SIVmac239 infection. However, early broad NAb responses correlated with relatively preserved CD4(+) T-cell numbers, low viral load and limited viral divergence