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Experimental studies suggest that the FAS/APO-1/CD95 (cytokine receptor protein TNF-receptor superfamily, member 6) cell surface molecule is involved in the apoptotic effect of radiotherapy. In this study we investigated the role of amifostine in protecting the CD95+ (CD: cluster of differentiation) lymphocytic subpopulation in patients with head and neck cancer undergoing radiotherapy.Using flow-cytometry we examined the expression of FAS/CD95 antigen on CD4+ (helper/inducer T cells), CD8+ (suppressor/cytotoxic T cells) and CD56+ (NK, natural killer) T-lymphocytes of 28 patients with head and neck cancer undergoing radiotherapy (with and without amifostine).The numbers of peripheral blood lymphocytes were significantly reduced after treatment from (mean value +/- STD error) 1477 +/- 129 to 1015 +/- 77 for T lymphocytes, 700 +/- 70 to 454 +/- 38 for CD4, 449 +/- 46 to 296 +/- 34 for CD8 and, 140 +/- 18 to 118 +/- 13 for NK, before and after treatment, respectively. CD95 expressing lymphocytes showed a faster recovery rate in patients receiving amifostine. CD95 expressing CD56 lymphocytes increased during radiotherapy in patients receiving daily cytoprotection with amifostine to values higher than the pre-treatment levels (p = 0.004).It is suggested that amifostine enhances recovery of T- and NK-lymphocyte subpopulations expressing the CD95 antigen in head-neck cancer patients undergoing RT and may enhance the efficacy of the later by interfering FAS-related immunological pathways.

Background Central arterial stiffness represents a well-established predictor of cardiovascular disease. Decreased circulating endothelial progenitor cells (EPCs), increased asymmetric dimethyl-arginine (ADMA) levels, traditional cardiovascular risk factors and insulin resistance have all been associated with increased arterial stiffness. The correlations of novel and traditional cardiovascular risk factors with central arterial stiffness in prediabetic individuals were investigated in the present study. Methods The study population consisted of 53 prediabetic individuals. Individuals were divided into groups of isolated impaired fasting glucose (IFG), isolated impaired glucose tolerance (IGT) and combined IGT-IFG. Age, sex, family history of diabetes, smoking history, body mass index (BMI), waist to hip ratio (WHR), waist circumference (WC), blood pressure, lipid profile, levels of high sensitive C-reactive protein (hsCRP), glomerular filtration rate (GFR), and history of antihypertensive or statin therapy were obtained from all participants. Insulin resistance was evaluated using the Homeostatic Model Assessment (HOMA-IR). Carotid -femoral pulse wave velocity was used as an index of arterial stiffness. Circulating EPC count and ADMA serum levels were also determined. Results Among studied individuals 30 (56.6%) subjects were diagnosed with isolated IFG, 9 (17%) with isolated IGT (17%) and 14 with combined IFG-IGT (26.4%). In univariate analysis age, mean blood pressure, fasting glucose, total cholesterol, LDL cholesterol, and ADMA levels positively correlated with pulse-wave velocity while exercise and GFR correlated negatively. EPC count did not correlate with PWV. In multivariate stepwise regression analysis PWV correlated independently and positively with LDL-Cholesterol (low density lipoprotein) and ADMA levels and negatively with exercise. Conclusions Elevated ADMA and LDL-C levels are strongly associated with increased arterial stiffness among pre-diabetic subjects. In contrast exercise inversely correlated with arterial stiffness.

OBJECTIVE: Endothelial progenitor cells (EPCs) have recently been considered as a potential novel marker of vascular integrity, atherosclerosis and cardiovascular risk. This study was performed to investigate the main determinants of EPC levels in individuals with prediabetes. DESIGN: Thirty-nine participants with newly diagnosed prediabetes were enrolled. Flow cytometric analysis was used to quantify EPCs (CD34 + CD133 + VEGFR-2+). Traditional risk factors, high-sensitivity C-reactive protein (hs-CRP), homeostasis model assessment of insulin resistance (HOMA-IR) and anthropometric parameters, including ultrasonographic-determined visceral and subcutaneous fat, were recorded. RESULTS: In univariate analysis, EPC levels significantly correlated with waist circumference (p = 0.017), mean arterial pressure (p = 0.009), total cholesterol (p = 0.003), hs-CRP (p = 0.006), HOMA-IR (p = 0.031) and visceral fat (p = 0.040). However, in stepwise multivariate ordinal logistic regression analysis, only visceral fat retained its statistical significance (OR=0.79, 95%Cl:0.64–0.98, p = 0.032). CONCLUSIONS: Visceral fat seems to be the main determinant of EPC levels in individuals with prediabetes and to form a plausible link between mild metabolic abnormalities, cardiovascular risk and vascular homeostasis process.