AOA: artificial oocyte activation; AOD: oocyte activation deficiency; Ca: Calcium; CAMKII: Ca/calmodulin-dependent protein kinase II; CICR: calcium-induced calcium-release; DAG: diacylglycerol; GM-CSF: granulocyte-macrophage colony-stimulating factor; ICSI: intra-cytoplasmic sperm injection; InsPR: inositol-trisphosphate receptor; IP: inositol 1,4,5-trisphosphate; IVF: in vitro fertilization; MAP: mitogen-activated protein; MII: metaphase II; NADP: nicotinic acid adenine dinucleotide phosphate; NO: nitric oxide; PAWP: post-acrosomal WW-binding domain protein; PIP: phosphatidylinositol 4,5-bisphosphate; PLC: phospholipase C; PLCζ: phospholipase C-zeta; SOAFs: spermatozoon-released oocyte-activating factors; Sr: strontium; TFF: total fertilization failure.

Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in women of childbearing age. The criteria required for the diagnosis identify various phenotypes, with different reproductive, metabolic, and cardiovascular (CV) risk characteristics. Emerging evidence links adipocyte-secreted hormones as candidates in the pathogenesis of endothelial dysfunction in PCOS, independently of additional risk factors. The aim of this review was to collect, analyze, and qualitatively resynthesize evidence on biomarkers of endothelial dysfunction (visfatin, vascular endothelial growth factor [VEGF], matrix metalloproteinase 9 [MMP-9]) in women with PCOS. Women with PCOS exhibit (a) increased plasma visfatin concentrations compared with controls with a similar body mass index; (b) increased VEGF production along with chronic, mild inflammation; and (c) increased MMP-9 concentrations, which might be related to either excessive CV risk or abnormalities of ovarian extracellular matrix remodeling, multiple cyst formation, follicular atresia, and chronic anovulation. As PCOS has been associated with CV risk, early identification of endothelial dysfunction is clinically relevant.

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Our findings support the notion that the presence of innate immune SNPs, such as functional polymorphisms of TLRs along with MBL deficiency, might exert a protective effect on the COPD phenotype, similar with other immune-mediated disorders.

έγκριση διδακτορικής διατριβής από το τμήμα Νοσηλευτικής του Πανεπιστημίου Αθηνών δε σημαίνει και αποδοχή των γνωμών του συγγραφέα''. (Σχετικές οι διατάξεις του άρθρου 50 του νόμου 1268/82 σε συνδυασμό με τις διατάξεις του οργανισμού του πανεπιστημίου Αθηνών,άρθρο 202 παρ.2 του νόμου 5343). Η παρούσα Διδακτορική Διατριβή έγινε ομόφωνα δεκτή από το τμήμα Νοσηλευτικής του Πανεπιστημίου Αθηνών στη Συνεδρίαση της 12 ης Δεκεμβρίου 2006 με βαθμό ''ΑΡΙΣΤΑ''.