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Background: A retrospective analysis was carried out from patients and controls during the past 5 years from a series of studies investigating endothelial microparticles (MP). Methods: In total, 319 samples from 207 individuals were included in this analysis, from patients with type 2 diabetes (T2D, n?=?105), women with polycystic ovary syndrome (PCOS, n?=?145) and healthy volunteers (n?=?69). All data were generated via the same flow cytometry protocol with the same antibody clones. Endothelial markers CD105 (Endoglin) and CD106 (Vascular cell adhesion molecule-1) were used to enumerate MP in venous blood. Results: The ratio of CD105MP:CD106MP was significantly different between groups (F?=?63.43, p?<?0.0001). Women with PCOS were found to have a median CD105MP:CD106MP ratio of 0.40 (IQR 0.24–0.57), suggesting approximately two CD106MP were found per CD105MP. The T2D group showed a median ratio of 2.32 (1.51–3.69) whereas in healthy volunteers the ratio was 2.21 (1.63–3.55). Serum intercellular adhesion molecule-1 was also shown to be significantly increased in PCOS when compared with control or T2D groups (F?=?14.5, p?<?0.001). Conclusion: These data suggest that women with PCOS have an altered endothelial MP release in favour of CD106. Thus a potential activated endothelial state exists in women with PCOS with a shift towards a predominantly CD106MP profile.

Introduction: Decompression sickness is caused by gas bubbles released upon decompression. These bubbles have the potential to occlude blood vessels and damage the vascular endothelium. The aim of this study was to quantify damage to the vascular endothelium resulting from decompression by measuring endothelial microparticles (MP) and endothelial function. Methods: Five healthy male volunteers undertook a simulated (hyperbaric chamber) air dive and 1 wk later a second dive breathing 100"/ oxygen at 283 kPa (18 msw) for 60 mm bottom time, decompressed with 5-mm stops at 161 kPa (6 msw) and 131 kPa (3 msw). Endothelial function was tested pre- and postdive by reactive hyperemia peripheral artery tonometry (RH-PAT) and CD1O5 (Endoglin) positive MP were quantified by flow cytometry. Plasma E- and P-selectin, interleukin-6, and serum cortisol were also quantified. Results: RH-PAT showed a significantly decreased endothelial function post-decompression after breathing air when compared to oxygen (-0.33 ± 0.27 vs. +0.18 ± 0.14). CD1O5 MP pre- and postdive showed no change on the oxygen dive (460 ± 370 to 360 ± 163), however, they increased after breathing air (440 ± 70 to 1306 ± 359). There was no change in expression of CD1O5 on MP. Furthermore no changes were observed in plasma E- or P-selectin, IL-6, or serum cortisol. Conclusion: From the data, at least in the time frame involved, there appears to be no detectable physiological/stress response to decompression, rather decompression from breathing air probably caused mechanical damage to the endothelium, resulting in both MP release and a reduction in endothelial function. [ABSTRACT FROM AUTHOR]