12 research outputs found

    Step Count is Associated With Lower Nighttime Systolic Blood Pressure and Increased Dipping

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    BACKGROUND Higher nighttime blood pressure (BP) and the loss of nocturnal dipping of BP are associated with an increased risk for cardiovascular events. However, the determinants of the loss of nocturnal BP dipping are only beginning to be understood. We investigated whether different indicators of physical activity were associated with the loss of nocturnal dipping of BP. METHODS We conducted a cross-sectional study of 103 patients referred for 24-hour ambulatory monitoring of BP. We measured these patients' step count (SC), active energy expenditure (AEE), and total energy expenditure simultaneously, using actigraphs. RESULTS In our study population of 103 patients, most of whom were hypertensive, SC and AEE were associated with nighttime systolic BP in univariate (SC, r = -0.28, P < 0.01; AEE, r = -0.20, P = 0.046) and multivariate linear regression analyses (SC, coefficient beta = -5.37, P < 0.001; AEE, coefficient beta = -0.24, P < 0.01). Step count was associated with both systolic (r = 0.23, P = 0.018) and diastolic (r = 0.20, P = 0.045) BP dipping. Nighttime systolic BP decreased progressively across the categories of sedentary, moderately active, and active participants (125mm Hg, 116mm Hg, 112mm Hg, respectively; P = 0.002). The degree of BP dipping of BP increased progressively across the same three categories of activity (respectively 8.9%, 14.6%, and 18.6%, P = 0.002, for systolic BP and respectively 12.8%, 18.1%, and 22.2%, P = 0.006, for diastolic BP). CONCLUSIONS Step count is continuously associated with nighttime systolic BP and with the degree of BP dipping independently of 24-hour mean BP. The combined use of an actigraph for measuring indicators of physical activity and a device for 24-hour measurement of ambulatory BP may help identify patients at increased risk for cardiovascular events in whom increased physical activity toward higher target levels may be recommende

    The Swiss Kidney Stone Cohort (SKSC), a longitudinal, multi-centric, observational cohort to study course and causes of kidney stone disease in Switzerland

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    Kidney stone disease has a high prevalence worldwide of approximately 10 % of the population and is characterized by a high recurrence rate Kidney stone disease results from a combination of genetic, environmental, and life-style risk factors, and the dissection of these factors is complex. The Swiss Kidney Stone Cohort (SKSC) is an investigator-initiated prospective, multi-centric longitudinal, observational study in patients with kidney stones followed with regular visits over a period of 3 years after inclusion. Ongoing follow-ups by biannual telephone interviews will provide long-term outcome data up to 10 years. SKSC comprises 782 adult patients (age &gt; 18 yrs) with either recurrent stones or a single stone event with at least one risk factor for recurrence. In addition, a control cohort of 207 individuals without kidney stone history and absence of kidney stones on a low-dose CT-scan at enrolment has also been recruited. SKSC includes extensive collections of clinical data, biochemical data in blood and 24 hr urine samples, and genetic data. Biosamples are stored at a dedicated biobank. Information on diet and dietary habits were collected through food frequency questionnaires and standardized recall interviews by trained dieticians with the Globodiet software. SKSC provides an unique opportunity and resource to further study cause and course of kidney disease in a large population with data and samples collected of a homogenous collective of patients throughout the whole Swiss population

    Root structure - function relationships: evidence of a root economics spectrum?

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    Root structure - function relationships: evidence of a root economics spectrum?. Joint 2014 Annual Meeting Bristish Ecological Society and Société Française d'Ecologi

    Immune Dysfunction After Cardiac Surgery with Cardiopulmonary Bypass: Beneficial Effects of Maintaining Mechanical Ventilation

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    International audienceUnlabelled - Cardiac surgery with cardiopulmonary bypass (CPB) induces postoperative immunosuppression and impaired pulmonary function. Maintaining mechanical ventilation (MV) during CPB improves pulmonary function and diminishes postoperative systemic inflammation. However, there are no data about the influence of maintaining MV during CPB on postoperative immune dysfunction. Methods - Fifty patients were prospectively divided into two groups: without MV during bypass (n = 25) and dead space MV with positive end-expiratory pressure (n = 25). PaO2 (arterial oxygen tension)/FIO2 (inspired oxygen fraction) ratio, CXCL10 (C-X-C motif chemokine 10), CCL2 (chemokine ligand 2), tumor necrosis factor α (TNF-α), interleukin 10 (IL-10), human leukocyte antigen-DR antigen (HLA-DR), monocytic myeloid-derived suppressor cells (Mo-MDSCs, CD14HLA-DR monocytes), and blood cell count were collected before and after surgery. Results - Cardiopulmonary bypass induced a marked immunosuppression with a significant increase in plasmatic levels of TNF-α and IL-10 and a significant decrease in HLA-DR monocytic expression. The postoperative proportion of Mo-MDSCs was subsequently significantly increased. Maintaining MV during CPB significantly improved PaO2/FIO2 ratio and decreased postoperative plasmatic levels of TNF-α and IL-10 compared with patients without MV during CPB. Furthermore, nonventilated patients had a lower lymphocyte count after surgery compared with patients with MV during CPB. Conclusion - Our study suggests that maintaining MV during CPB for cardiac surgery decreases postoperative immune dysfunction and could be an interesting strategy to diminish the occurrence of postoperative nosocomial infection without hampering the surgical procedure. However, these findings have to be confirmed in a clinical trial using the incidence of nosocomial infection as an endpoint

    MONOCYTIC MYELOID-DERIVED SUPPRESSOR CELL EXPANSION AFTER CARDIAC SURGERY WITH CARDIOPULMONARY BYPASS INDUCES LYMPHOCYTE DYSFUNCTION

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    Cardiac surgery with cardiopulmonary bypass (CPB) is associated with an immune paresis that predisposes to the development of postoperative infections and sepsis. Among factors responsible for CPB-induced immunosuppression, circulating myeloid-derived suppressor cells (MDSCs) have been found to induce early lymphocyte apoptosis and lymphocyte proliferation inhibition. However, the mechanisms involved are not fully understood. In this study, we found that the main lymphocyte subsets decreased significantly 24 h after cardiac surgery with CBP. As expected, cardiac surgery with CPB induced a monocytic MDSC expansion associated with an increased T-cell apoptosis and decreased proliferation capacity. Noteworthy, granulocytic MDSCs remain stable. Myeloid-derived suppressor cell depletion restored the ability of T-cell to proliferate ex vivo. After CPB, indoleamine 2,3-dioxygenase activity and IL-10 plasma level were increased such as programmed death-ligand 1 monocytic expression, whereas plasma level of arginine significantly decreased. Neither the inhibition of indoleamine 2,3-dioxygenase activity nor the use of anti-programmed death-ligand 1 or anti-IL-10 blocking antibody restored the ability of T-cell to proliferate ex vivo. Only arginine supplementation restored partially the ability of T-cell to proliferate

    Neutrophil function and bactericidal activity against Staphylococcus aureus after cardiac surgery with cardiopulmonary bypass

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    International audienceStaphylococcus aureus is the main bacterial pathogen encountered in mediastinitis after cardiac surgical procedures; it remains a devastating complication with a high mortality rate. As neutrophils have a primordial role in the defense against staphylococcus infection and cardiopulmonary bypass (CPB) is known to induce immunosuppression, the aim of this study was to investigate CPB impact on neutrophil functions. Patients without known immunosuppression scheduled for cardiac surgery with CPB were included. Bone marrow and blood samples were harvested before, during, and after surgery. Neutrophil phenotypic maturation and functions (migration, adhesion, neutrophil extracellular trap [NET] release, reactive oxygen species (ROS) production, phagocytosis, and bacteria killing) were investigated. Two types of Staphylococcus aureus strains (one from asymptomatic nasal carriage and another from mediastinitis infected tissues) were used to assess in vitro bacterial direct impact on neutrophils. We found that CPB induced a systemic inflammation with an increase in circulating mature neutrophils after surgery. Bone marrow sample analysis did not reveal any modification of neutrophil maturation during CPB. Neutrophil lifespan was significantly increased and functions such as NET release and ROS production were enhanced after CPB whereas bacteria killing and phagocytosis were not impacted. Results were similar with the two different isolates of Staphylococcus aureus. These data suggest that CPB induces a recruitment of mature neutrophils via a demargination process rather than impacting their maturation in the bone marrow. In addition, neutrophils are fully efficient after CPB and do not contribute to postoperative immunosuppression

    Impaired efferocytosis and neutrophil extracellular traps clearance by macrophages in ARDS

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    International audienceExaggerated release of neutrophil extracellular traps (NETs) along with decreased NET clearance and inability to remove apoptotic cells (efferocytosis) may contribute to sustained inflammation in acute respiratory distress syndrome (ARDS). Recent studies in experimental models of ARDS have revealed the crosstalk between AMP-activated protein kinase (AMPK) and high-mobility group box 1 (HMGB1), which may contribute to effectiveness of efferocytosis, thereby reducing inflammation and ARDS severity.We investigated neutrophil and NET clearance by macrophages from control and ARDS patients and examined how bronchoalveolar lavage (BAL) fluid from control and ARDS patients could affect NET formation and efferocytosis. Metformin (an AMPK activator) and neutralising antibody against HMGB1 were applied to improve efferocytosis and NET clearance.Neutrophils from ARDS patients showed significantly reduced apoptosis. Conversely, NET formation was significantly enhanced in ARDS patients. Exposure of neutrophils to ARDS BAL fluid promoted NET production, while control BAL fluid had no effect. Macrophage engulfment of NETs and apoptotic neutrophils was diminished in ARDS patients. Notably, activation of AMPK in macrophages or neutralisation of HMGB1 in BAL fluid improved efferocytosis and NET clearance.In conclusion, restoration of AMPK activity with metformin or specific neutralisation of HMGB1 in BAL fluid represent promising therapeutic strategies to decrease sustained lung inflammation during ARDS
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