CD4+CD25+ regulatory T cells inhibit natural killer cell functions in a transforming growth factor–β–dependent manner

Tumor growth promotes the expansion of CD4+CD25+ regulatory T (T reg) cells that counteract T cell–mediated immune responses. An inverse correlation between natural killer (NK) cell activation and T reg cell expansion in tumor-bearing patients, shown here, prompted us to address the role of T reg cells in controlling innate antitumor immunity. Our experiments indicate that human T reg cells expressed membrane-bound transforming growth factor (TGF)–β, which directly inhibited NK cell effector functions and down-regulated NKG2D receptors on the NK cell surface. Adoptive transfer of wild-type T reg cells but not TGF-β−/− T reg cells into nude mice suppressed NK cell–mediated cytotoxicity, reduced NKG2D receptor expression, and accelerated the growth of tumors that are normally controlled by NK cells. Conversely, the depletion of mouse T reg cells exacerbated NK cell proliferation and cytotoxicity in vivo. Human NK cell–mediated tumor recognition could also be restored by depletion of T reg cells from tumor-infiltrating lymphocytes. These findings support a role for T reg cells in blunting the NK cell arm of the innate immune system

Optical 3D-storage in sol-gel materials with a reading by Optical Coherence Tomography-technique

We report on the recording of 3D optical memories in sol-gel materials by using a non-linear absorption effect. This effect induces a local change of the optical properties of the material which is read and quantified with a high resolution full-field Optical Coherence Tomography setup. It is the first time that this technique is used for this purpose. Data recording was performed by focused picosecond (ps) single-pulse irradiation at 1064 nm with energy densities of 10 and 33 J/cm2 per pulse.Comment: 19 pages, 7 figure

Seven to eight hours of sleep a night is associated with a lower prevalence of the metabolic syndrome and reduced overall cardiometabolic risk in adults.

Previous studies looking at the relationship between sleep duration and the metabolic syndrome have only used a dichotomous approach (presence/absence) and failed to adjust for important confounding factors. The objective of the present study was to examine the association between self-reported sleep duration and features of the metabolic syndrome in adults.A cross-sectional analysis from the Quebec Family Study (Canada) was conducted on 810 participants aged 18 to 65 years. Participants were categorized as short (≤6 h), adequate (7-8 h) or long (≥9 h) sleepers. The metabolic syndrome was defined according to the American Heart Association/National Heart, Lung, and Blood Institute's criteria.Overall, 24.6% of the sample had the metabolic syndrome. A U-shaped relationship between sleep duration and the prevalence of metabolic syndrome (33.3%, 22.0% and 28.8% in short, adequate and long sleepers, respectively) was observed (P<0.01). Only short sleepers had a significant increase in the odds of having the metabolic syndrome (OR = 1.76, 95% CI = 1.08-2.84) compared to adequate sleepers after adjustment for age, sex, smoking habits, highest education level, total annual family income, alcohol consumption, coffee intake, menopausal status, daily caloric intake, and moderate-to-vigorous physical activity. Likewise, the clustered cardiometabolic risk score (i.e. continuous risk score based on the metabolic syndrome components) was significantly higher in short sleepers compared to adequate sleepers after adjustment for covariates (P<0.05).Sleeping ≤6 h per night is associated with an elevated cardiometabolic risk score and an increase in the odds of having the metabolic syndrome after adjusting for possible confounders. These results strongly suggest that short sleep duration is a risk factor for the metabolic syndrome

Sedentary behaviour, visceral fat accumulation and cardiometabolic risk in adults: a 6-year longitudinal study from the Quebec Family Study.

Sedentary behaviour has recently emerged as a unique risk factor for chronic disease morbidity and mortality. One factor that may explain this relationship is visceral adiposity, which is prospectively associated with increased cardiometabolic risk and mortality. The objective of the present study was to determine whether sedentary behaviour was associated with increased accumulation of visceral fat or other deleterious changes in cardiometabolic risk over a 6-year follow-up period among adult participants in the Quebec Family Study.The current study included 123 men and 153 women between the ages of 18 and 65. Total sedentary time and physical activity were assessed by self-report questionnaire. Cross-sectional areas of visceral and subcutaneous abdominal adipose tissue were assessed using computed tomography. Cardiometabolic biomarkers including fasting insulin, glucose, blood lipids, HOMA-Insulin Resistance, and oral glucose tolerance were also measured. All variables of interest were collected at both baseline and follow-up.After adjustment for age, sex, baseline BMI, physical activity, energy intake, smoking, education, income and menopausal status, baseline sedentary behaviour was not associated with changes in visceral adiposity or any other marker of cardiometabolic risk. In the longitudinal model which adjusted for all studied covariates, every 15-minute increase in sedentary behaviour from baseline to follow-up was associated with a 0.13 cm increase in waist circumference (95% CI = 0.02, 0.25). However, there was no association between changes in sedentary behaviour and changes in visceral adiposity or other markers of cardiometabolic risk.These results suggest that neither baseline sedentary behaviour nor changes in sedentary behaviour are associated with longitudinal changes in visceral adiposity in adult men and women. With the exception of waist circumference, the present study did not find evidence of a relationship between sedentary behaviour and any marker of cardiometabolic risk in this population