Associations between insulin and heart rate variability in police officers.

OBJECTIVE: Low heart rate variability (HRV) has been linked to cardiovascular disease. Our objective was to examine the cross-sectional association between insulin and HRV. METHODS: Insulin levels were measured in 355 nondiabetic officers from the BCOPS study, following a 12 h fast. HRV was performed according to methods published by the task force of the European Society of Cardiology and the North American Society of Pacing Electrophysiology for measurement and analysis of HRV. Mean values of high (HF) and low frequency (LF) HRV were compared across tertiles of insulin using ANOVA and ANCOVA; p-values were obtained from linear regression models. RESULTS: Higher mean levels of insulin were significantly associated with lower (i.e., worse) mean levels of HRV before and after risk-factor adjustment. The results for HF HRV (ms(2)) were as follows: 1st insulin (µU/ml) tertile (156.3; 95% confidence interval (CI) = 128.6-189.9); 2nd tertile (154.3; 95% CI = 124.3-191.5); 3rd tertile (127.9; 95% CI = 105.0-155.8), p for trend = 0.017. Results with LF HRV were similar to HF HRV. Insulin was also inversely and significantly associated with HRV among officers with BMI ≥ 25 kg/m(2), with ≥ 25.5% body fat, and among those who reported low (

Adiposity, muscle, and physical activity: predictors of perturbations in heart rate variability.

OBJECTIVES: This study examines cross-sectional associations of indices of adiposity, lean body mass, and physical activity, with heart rate variability (HRV), a marker for parasympathetic cardiac vagal control. METHODS: The study population consists of 360 officers from the Buffalo New York Police Department. Indices of adiposity include body mass index, waist circumference, and a fat-mass index taken from dual-energy X-ray absorptiometry (DEXA) measurements. Lean body mass indices were derived from DEXA measurements of trunk mass and extremity lean mass. Physical activity was measured using a 7-day self-report questionnaire. HRV was obtained from 5-min electrocardiogram measurements by means of parametric spectral analysis resulting in estimates for high-frequency (HF) and low-frequency (LF) HRV. RESULTS: Both HF and LF HRV were significantly associated with markers for adiposity, two components of lean mass and physical activity with all associations being in the expected direction except that for trunk lean mass. This unexpected result is explained by the possibility that trunk mass is a marker for visceral adiposity rather than lean mass. Body mass index did not explain any additional variance in HRV above and beyond waist circumference and the DEXA indices. CONCLUSIONS: Higher levels of physical activity, lower levels of markers for central adiposity and higher lean mass in the extremities predict higher levels of HRV in this population of police officers. This association between modifiable risk factors and markers for autonomic function suggest possible interventions that may improve health and performance.

Late CD8+ T cell-dependent xenoantibody production in innate tolerant nude rats after hamster islet grafting but not after hamster heart grafting.

BACKGROUND: Xenograft rejection can be provoked by both the innate and adaptive immune compartments and close reciprocal interactions exist between these two systems. We investigated the interdependent roles of T and B lymphocytes in vascularized (heart) and cellular (islet) xenograft rejection in a model with established xeno-nonreactivity of the innate immune system. METHODS: Specific innate xenotolerance was induced in nude rats bearing either a hamster heart or a hamster pancreatic islet graft by a tolerizing regimen consisting of donor antigen infusion, temporary natural killer cell depletion and a 4-week administration of leflunomide. One month after transplantation, syngeneic CD4 and CD8 T cells were adoptively transferred. RESULTS: Both vascular and cellular xenografts were rejected after CD4 T cell reconstitution, corresponding with production of high IgM and IgG xenoantibody titers. Deposition of xenoantibodies and complement was seen in the heart but not in the islet xenografts. After infusion of CD8 T cells, xenohearts underwent a delayed type of rejection without xenoantibody production and xenoislets were not rejected. In xenoislet recipients, CD8 dependent B cells were not tolerized, resulting in the production of IgG xenoantibodies belonging to Th2-dependent isotypes, known not to cause graft rejection, and deposited at the graft implantation site. CONCLUSIONS: We conclude that distinct mechanisms of immune activation underlie xenogeneic reactions against vascular and cellular grafts.

CD4+ T lymphocytes expressing CD40 ligand help the IgM antibody response to soluble pneumococcal polysaccharides via an intermediate cell type.

Streptococcus pneumoniae causes serious infections in children, the elderly, and immunocompromised patients. Protection against infections with S. pneumoniae is mediated through Abs against the capsular polysaccharides (caps-PS). We previously showed that the murine Ab response to caps-PS is dependent on CD40-CD40L interaction. In the present paper, we addressed the question of whether the CD40-CD40L-mediated modulation of the anti-caps-PS immune reaction is the result of a direct interaction between B lymphocytes and T lymphocytes or of an indirect interaction. SCID/SCID mice reconstituted with B lymphocytes from wild-type mice did not mount anti-caps-PS Abs. SCID/SCID mice reconstituted with B lymphocytes from wild-type mice and CD4+ T lymphocytes from wild-type mice but not CD4+ T lymphocytes from CD40L knockout mice stimulated the anti-caps-PS Ab response. This indicated that CD4+ T lymphocytes stimulated the anti-caps-PS Ab response in a CD40L-dependent manner. SCID/SCID mice reconstituted with B lymphocytes from CD40 knockout mice and CD4+ T lymphocytes from wild-type mice generated an anti-caps-PS Ab response that could be inhibited by MR1, a blocking anti-CD40L Ab. These data indicated that CD4+ T lymphocytes stimulated the anti-caps-PS Ab response in an indirect way. Finally, lethally irradiated CD40 knockout mice reconstituted with bone marrow from wild-type mice mounted an anti-caps-PS Ab response that was comparable to the Ab response in wild-type mice, revealing that the required CD40 was on hemopoietic cells. In conclusion, we provide evidence that CD4+ T lymphocytes expressing CD40L stimulate the Ab response to soluble caps-PS by interacting with CD40-expressing non-B cells.