Objectives: This study examines the effects of sleep restricted to four hours for three consecutive nights on blood parameters, known to be associated with cardiovascular risk, in young healthy men. Material and methods: Eight young healthy men (age 24.5 ± 3.3 years) were studied in the sleep restricted group. Nine young healthy men (age 24 ± 2 years) were included in the control group and spent the days and nights in the sleep lab, while sleeping eight hours/night. One baseline night was followed by three nights of sleep restriction to four hours and by one recovery night of eight hours. Blood samplings were performed after the baseline night and after the third night of sleep restriction or without restriction for the control group. Results: A signifi cant increase in white blood cells (WBC) (5.79 ± 1.05 vs. 6.89 ± 1.31 10 3 cell/μl, p = 0.03), and neutrophils (3.17 ± 0.69 vs 4.24 ± 0.97 10 3 cell/μl, p = 0.01) was observed after the third night of sleep restriction. Other blood parameters were not affected. No signifi cant variation was observed in the control group. Conclusion: Sleep restriction affected WBC count, mainly neutrophils, considered as risk factor for cardiovascular disease. Stress induced by the short term sleep restriction could be involved in this observation.

Both ageing and vitamin C (VC) deficiency result in immune defect. Since low serum and tissue levels of VC are found in the elderly, we have in a placebo-controlled study, tested the effect of VC supplements (500 mg/day i.m. for 1 month) on various immune parameters. Indeed, VC enhances the proliferative response of T lymphocytes in vitro, and the tuberculin skin hypersensitivity in vivo. Neither the serum concentrations of IgA, IgG and IgM, nor the proportion of E-rosette-forming cells were modified. No significant change was observed in the placebo-treated group.

No abstract

In sepsis, desialylation under the influence of increased neuraminidase activity may contribute to the alterations in RBC rheology. Inhibition of neuraminidase may represent a new therapeutic option to ameliorate RBC rheology and perhaps oxygen delivery to the cells.

Background: Recent reports have identified the apnoea and hypopnoea index (AHI) as an additional independent risk factor for cardiovascular morbidity and mortality. However, several studies reported contradictory results about the association between the serum C-reactive protein (CRP) level and the severity of apnoea. Objective: The purpose of this work is to study this association in patients referred to the sleep laboratory for clinical suspicion of sleep apnoea and presenting a wide range of AHI. Methods: Forty-nine consecutive patients were included in the study. The SigmaStat^® software package (Jandle Scientific) was used. Multilinear regression analysis was tested using a stepwise backward selection of the explicative variables. The clinical characteristics (diabetes, hypertension, smoking habits, gender) were treated as dichotomous variables, while all other data (age, BMI, lipids, white blood cells) were continuous ones; high-sensitivity (hs)-CRP was the dependent variable. Results: In univariate analysis, AHI was correlated to hs-CRP: R = 0.43, p = 0.002. In multivariate analyses, we found an independent association between the AHI, adjusted for classical cardiovascular risk factors, and hs-CRP. Conclusion: In a sample of 49 patients, referred to the sleep laboratory for suspicion of sleep apnoea in routine practice, we observed an independent association between the AHI and hs-CRP.

BackgroundBlood fluidity is maintained by a delicate balance between coagulation and fibrinolysis. The endothelial cell surface is a key player in this equilibrium and cell surface disruptions can upset the balance. We investigated the role of pericellular myeloperoxidase oxidized LDLs (Mox-LDLs) in this balance.Methods and ResultsWe designed a technical device that enabled us to monitor fibrinolysis in real-time at the surface of an endothelial cell line (EA.hy926), and showed that Mox-LDL decreased pericellular fibrinolysis. There were no changes in fibrinolysis when EA.hy926 endothelial cells were exposed to native LDL (24 hours) at doses of 10, 50, 100 and up to 1250 µg/ml. However, treatment of EA.hy926 endothelial cells with 10 and 50 µg/ml of Mox-LDL (physiological serum concentrations) increased the lysis time by 15 and 13%, respectively (p<0.001), although this effect was not present at higher concentrations of 100 µg/ml. This effect was not correlated with any changes in PAI-1 or t-PA or PA Receptor (PAR) expression. No effect was observed at the surface of smooth muscle cells used as controls.ConclusionOur data link the current favorite hypothesis that modified LDL has a causal role in atheroma plaque formation with an old suggestion that fibrin may also play a causal role. Our data help complete the paradigm of atherosclerosis: Modified LDL locally enhances fibrin deposition (present work); fibrin deposits enhance endothelial permeability; this effect allows subendothelial accumulation of lipid and foam cells.

No abstract

Nine healthy volunteers received epinephrine and hydrocortisone intravenously in order to assess the typical acute response to a brief stress, of leukocyte and lymphocyte subsets, acute phase reactants and lymphocyte reactivity to T and B mitogens. At 10 min., all leukocyte subsets were increased, especially mononuclear cells. At 1 hour, moderate lymphopenia and monocytopenia occurred. At 6 hours, neutrophilia and eosinopenia were observed. During the lymphocytic early wave, all the lymphocyte subset counts increased, particularly T-suppressive/cytotoxic and natural killer cells. As a consequence, the percentage of T cells decreased and the CD4/CD8 ratio fell. No changes in acute phase reactants occurred over the 24 hours of the study. All leukocyte and lymphocyte subsets were normalized and mitogen reactivity was unchanged 24 hours after the stress. These typical shifts in leukocyte subsets could probe the adrenocortical and medullary response to an environmental stressor.