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The cells were washed twice and analyzed by ow cytometry and the mean uorescent intensity of the different cell populations were recorded.However, this does not affect all other comparisons, where cells were labeled using both FITC and phycoerythrin stains.Monocyte DNA damage could not be measured in any subject because of the loss of CD expression on monocytes following the xation process.These relationships were also all nonsignicant for the monocyte and lymphocyte subgroups. The diabetic group members were in reasonab leglycem ic <a href="http://www.molbioglobal.com/archives/296"></a> control years.There was no signicant difference between groups in median hsCRP. MESF by owuorescent in situ hybridization and DNA damage by ow cytometry of oxoguanine as described in text.This re lationsh ip was notapparentin the monocyte or lymphocyte subgroups.One strength of this study is that the diabetic group was selected to limit confounding by variables that inuence telomere length such as age, sex, ethnicity, drug therapy, smoking, and inammatory processes such as established vascular disease or hypertension, which make clinical studies on telomere length less easy to in te rp ret, and in other studies we have shown that monocytes from type diabetic subjects demonstrate increased adhes ion mo lecu le expression during glycemic excursions and increased expression of the LDL scavengerreceptor, CD also appear to have signicantly shortened telomeres.This suggests that the peripheral venous monocyte population adhering to the vascular endothelium in type diabetes, are a population with shorter telomeres.Telomere shortening indicates a cell population at increased risk of replicative senescence and apoptosis at cell division, and active monocyte and macrophage proliferation occurs within developing vascular plaque. In some studies, macrophages have been the dominant proliferating cell type, and proliferative activity and macrophage density are directly related to areas of plaque degeneration and instability. The data in the present study would support the original hypothesis that increased oxidative DNA damage in type diabetes is associated DIABETES CARE, VOLUME, NUMBER, FEBRUARY with telomere attrition and shortening, at least in monocytes.It would also imply that transformed macrophages in type diabetes would be at increased risk of further telomere attrition, senescence, and apoptosis, leading to enhanced atherogenesis and plaque instability in type diabetes that telomere length in the peripheral blood of adult males and females without diabetes is strongly associated with coronary death. Vascu lar endo thelialcells, smoo thcells, and monocytemacrophage cells within vascular plaque have all been described as demonstrating senescent and apoptotic phenotypes. A weakness of the present study is that the mechanism for monocyte telomere shortening in type diabetes is unclear.Increased susceptibility to oxidative DNA damage in type diabetes is wellrecognized, andmonocytic endothelial cell precursors from diabetic and nondiabetic animal models are susceptible to oxidative damage in vitro. Therefore, it is probable that monocyte telomere shortening reects increased oxidative damage to monocytic marrow precursors, a suggestion supported by the inverse relationships between telomere length and oxidative DNA damage in PBMC.The increased susceptibility of   the GGG sequence in telomeres to oxidative damage compared with the rest of the chromosomal DNA could account for the trend toward higher levels of oxidative DNA damage in the diabetic group but very much more signicantly shorter monocyte telomere lengths than control subjects.

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