Stop-signal reaction time calculation.

<p>The figure illustrates the relation between stop signal delay, the stop signal reaction time and the distribution of go reaction times. The distribution of go reaction is integrated from the time of go signal presentation. For each stop signal delay, a probability of responding is obtained. If the stop signal delay of 50 ms resulted in an error rate = .20, this means that the end of the stop process should be at a point equal to 20% of the go RT distribution. If the point of 20% of the go RT distribution was 250 ms, so the observed SSRT would be 252–50 ms. The rest of the SSRT were calculated with the same procedure. A summary SSRT was acquired by averaging the observed three SSRTs that corresponded to 0.15[28].</p

Group means (±SD) of the characteristics of the tennis players, swimmers, and sedentary controls.

<p>Note: *** denotes significantly different from controls at <i>p</i><.001; – denotes no training experience.</p

Results of hierarchical stepwise regression analysis (<i>n</i> = 60).

<p>Note: **<i>p</i><.01;</p>***<p><i>p</i><.001; Entries represent standardized regression coefficients (β).</p

The procedures for the experimental sessions.

<p>Tennis players, swimmers and sedentary controls were firstly provided with informed consent, 7.-day physical activity recall questionnaire, and fitness questionnaire. Secondly, all eligible subjects took part in a stop-signal task consisted of three stages: get Go session, critical SSD session, and test session.</p

Inhibitory control performance across tennis players, swimmers and controls.

<p>(a) Mean stop-signal reaction times (b) Noncancelled rates (c) Inhibitory functions for each SSD. Each error bar shows the standard error of the mean. Note: **<i>p</i><.01; ***<i>p</i><.001.</p

Mean Go RTs (in milliseconds) for each condition across tennis players, swimmers, and controls.

<p>(a) No stop-signal condition. (b) Correct Go RTs in stop-signal condition. (c) Noncancelled Go RTs in stop-signal condition. Each error bar shows the standard error of the mean.</p

Correlation analysis for BMI, training experiences, estimated physical activity, estimated VO2max, group factors, and stop-signal reaction time.

<p>Note: ***denotes <i>p</i><.001;</p>**<p>denotes <i>p</i><.01;</p>*<p>denotes <i>p</i><.05.</p

Stop-signal task procedure.

<p>The stop-signal task consisted of go and stop trials. All trials began central fixation. Following offset of the central fixation, a white peripheral dot was presented to the left or right of the fixation. On 25% of the trials (stop trials), the central fixation dot reappeared as an instruction to withhold responses.</p

The NADPH oxidase-related pathway contribute to decreased tube formation in EPCs under high concentrated oxLDL.

<p>(A) EPCs were pretreated with DPI or APO for 1 hour prior to treatment with 5 or 50 μg/mL oxLDL for 24 hours. <i>In vitro</i> angiogenesis was assayed using ECMatrix gel. Data were expressed as the mean ± SEM of three experiments performed in triplicate. *<i>p</i> < 0.05 was considered significant. (B) EPCs were transfected with gp91^phox siRNA, the total gp91^phox protein were analyzed using western blotting. (C) EPCs were pretreated with DPI, LOX-1 blocking antibody for 1 hour or transfected with gp91^phox siRNA prior to 50 μg/mL of oxLDL treatment, subsequently eNOS and Akt activation (phosphorylation) were analyzed by Western blot. Total eNOS, Akt, and β-actin protein levels were used as loading controls. The graph showed the quantitative activation of eNOS (phospho-eNOS/total-eNOS ratio) and Akt (phospho-Akt/total-Akt ratio) density in oxLDL-treated EPCs. (D) EPCs were pretreated with 20 μM Rac1 inhibitor for 1 hour or transfected with gp91^phox siRNA prior to 50 μg/mL oxLDL treatment for 12 hours, subsequently membrane LOX-1 expression was analyzed by Western blot. β-actin protein levels were used as a loading control.</p

Statins, HMG-CoA Reductase Inhibitors, Improve Neovascularization by Increasing the Expression Density of CXCR4 in Endothelial Progenitor Cells

<div><p>Statins, inhibitors of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, are used to reduce cholesterol biosynthesis in the liver. Accordingly, statins regulate nitric oxide (NO) and glutamate metabolism, inflammation, angiogenesis, immunity and endothelial progenitor cells (EPCs) functions. The function of EPCs are regulated by stromal cell-derived factor 1 (SDF-1), vascular endothelial growth factor (VEGF), and transforming growth factor β (TGF-β), etc. Even though the pharmacologic mechanisms by which statins affect the neovasculogenesis of circulating EPCs, it is still unknown whether statins affect the EPCs function through the regulation of CXCR4, a SDF-1 receptor expression. Therefore, we desired to explore the effects of statins on CXCR4 expression in EPC-mediated neovascularization by <i>in vitro</i> and <i>in vivo</i> analyses. In animal studies, we analyzed the effects of atorvastatin or rosuvastatin treatments in recovery of capillary density and blood flow, the expression of vWF and CXCR4 at ischemia sites in hindlimb ischemia ICR mice. Additionally, we analyzed whether the atorvastatin or rosuvastatin treatments increased the mobilization, homing, and CXCR4 expression of EPCs in hindlimb ischemia ICR mice that underwent bone marrow transplantation. The results indicated that statins treatment led to significantly more CXCR4-positive endothelial progenitor cells incorporated into ischemic sites and in the blood compared with control mice. <i>In vivo</i>, we isolated human EPCs and analyzed the effect of statins treatment on the vasculogenic ability of EPCs and the expression of CXCR4. Compared with the control groups, the neovascularization ability of EPCs was significantly improved in the atorvastatin or rosuvastatin group; this improvement was dependent on CXCR4 up-regulation. The efficacy of statins on improving EPC neovascularization was related to the SDF-1α/CXCR4 axis and might be regulated by the NO. In conclusion, atorvastatin and rosuvastatin improved neovascularization in hindlimb ischemia mice; this effect may have been mediated by increased CXCR4 expression in EPCs.</p></div