T lymphocytes and monocytes/macrophages are the most abundant cells found in the atherosclerotic plaque. These cells can migrate towards the activated endothelium through the local release of chemotactic cytokines, or chemokines. Given the important role of leukocyte migration in atherosclerosis and the role of stress in mediating leukocyte trafficking, the present study examined the effects of an acute stressor on the redistribution of T cells (CD3+) and monocytes that express the chemokine receptors CCR5, CCR6, CXCR1, CXCR2, CXCR3, and CXCR4. Forty-four undergraduate students underwent a public speaking task. The acute stressor induced sympathetic cardiac activation, parasympathetic cardiac withdrawal, lymphocytosis, and monocytosis (all p<.001). Although the total number of T lymphocytes did not change, there was a selective increase in the number of circulating T cells expressing CXCR2, CXCR3, and CCR5. The ligands of these receptors are chemokines known to be secreted by activated endothelial cells. Analyses of individual differences in stress-induced responses demonstrated a positive relationship between sympathetic cardiac reactivity and mobilization of the various T cell subsets (.35

Objective and Methods: 
Two functionally distinct natural killer (NK) subsets can be identified according to surface CD56 expression: CD56lo cells compose the majority of NK cells and function as cytotoxic cells, whereas CD56hi cells have an immunomodulatory function through the secretion of cytokines. These NK subsets also differ in the expression levels of adhesion molecules such as CD62L and CD11a, indicating distinct potentials to migrate to lymphoid and nonlymphoid tissues. We investigated whether NK cell mobilization during acute stress varies according to these functional and phenotypic distinctions.
Methods and Results: 
Fifty-three undergraduate students performed a public-speaking task and 21 students participated in a control session. The task increased heart rate and catecholamines. No change was observed for the immunoregulatory CD56hi NK subset, whereas the number of cytotoxic CD56lo NK cells tripled. In line with the observation that NK mobilization is related to cytotoxic function, we found larger increases in NK cells that express higher levels of CD16 (a receptor that mediates antibody-dependent cytotoxicity). Consistent with known subset differences in adhesion molecule expression, we also found larger stress-induced increases for NK cells that were CD62L-negative and CD11ahi. Plasma levels of soluble CD62L remained unaltered, suggesting that the increase in CD62L-negative NK cells did not result from CD62L shedding. Regression analyses demonstrated independent contributions of epinephrine and norepinephrine to NK subset mobilization.
Conclusion: 
The marked specificity and robustness of these effects support the idea that NK cell mobilization is a functionally relevant response that is aimed at protecting the organism during acutely stressful situations.
ANOVA = analysis of variance;
CD = cluster of differentiation;
ECG = electrocardiogram;
ELISA = enzyme-linked immunosorbent assay;
Hb = hemoglobin;
HPLC = high-pressure liquid chromatography;
Htc = hematocrit;
NK = natural killer;
POMS = Profile of Mood States;
sCD62L = soluble CD62L;
SEM = standard error of mean.

Introduction
Stroke volume (SV) and cardiac output are important measures in the clinical evaluation of cardiac patients and are also frequently used in research applications. This study was aimed to improve SV scoring derived from spot-electrode based impedance cardiography (ICG) in a pediatric population of healthy volunteers and patients with a corrected congenital heart defect.
Methods
128 healthy volunteers and 66 patients participated. First, scoring methods for ambiguous ICG signals were optimized to improve agreement of B- and X-points with aortic valve opening/closure in simultaneously recorded transthoracic echocardiography (TTE). Building on the improved scoring of B- and X-points, the Kubicek equation for SV estimation was optimized by testing the agreement with the simultaneously recorded SV by TTE. Both steps were initially done in a subset of the sample of healthy children and then validated in the remaining subset of healthy children and in a sample of patients.
Results
SV assessment by ICG in healthy children strongly improved (intra class correlation increased from 0.26 to 0.72) after replacing baseline thorax impedance (Z0) in the Kubicek equation by an equation (7.337–6.208∗dZ/dtmax), where dZ/dtmax is the amplitude of the ICG signal at the C-point. Reliable SV assessment remained more difficult in patients compared to healthy controls.
Conclusions
After proper adjustment of the Kubicek equation, SV assessed by the use of spot-electrode based ICG is comparable to that obtained from TTE. This approach is highly feasible in a pediatric population and can be used in an ambulatory setting.

Metrics of heart period variability are widely used in the behavioral and biomedical sciences, although somewhat confusingly labeled as heart rate variability (HRV). Despite their wide use, HRV metrics are usually analyzed and interpreted without reference to prevailing levels of cardiac chronotropic state (i.e., mean heart rate or mean heart period). This isolated treatment of HRV metrics is nontrivial. All HRV metrics routinely used in the literature exhibit a known and positive relationship with the mean duration of the interval between two beats (heart period): as the heart period increases, so does its variability. This raises the question of whether HRV metrics should be “corrected” for the mean heart period (or its inverse, the heart rate). Here, we outline biological, quantitative, and interpretive issues engendered by this question. We provide arguments that HRV is neither uniformly nor simply a surrogate for heart period. We also identify knowledge gaps that remain to be satisfactorily addressed with respect to assumptions underlying existing HRV correction approaches. In doing so, we aim to stimulate further progress toward the rigorous use and disciplined interpretation of HRV. We close with provisional guidance on HRV reporting that acknowledges the complex interplay between the mean and variability of the heart period.