The identification of genes that were up- and down-regulated during oocyte maturation greatly improves our understanding of oocyte biology and will provide new markers that signal viable and competent oocytes. Furthermore, genes found expressed in cumulus cells are potential markers of granulosa cell tumours.

BACKGROUND Cigarette smoking is associated with lower fecundity rates, adverse reproductive outcomes and a higher risk of IVF failures. Over the last few decades, prevalence of smoking among women of reproductive age has increased. This review focuses on current knowledge of the potential effects of smoke toxicants on all reproductive stages and the consequences of smoke exposure on reproductive functions. METHODS We conducted a systematic review of the scientific literature on the impact of cigarette smoking and smoke constituents on the different stages of reproductive function, including epidemiological, clinical and experimental studies. We attempted to create hypotheses and find explanations for the deleterious effects of cigarette smoke observed in experimental studies. RESULTS Cigarette smoke contains several thousand components (e.g. nicotine, polycyclic aromatic hydrocarbons and cadmium) with diverse effects. Each stage of reproductive function, folliculogenesis, steroidogenesis, embryo transport, endometrial receptivity, endometrial angiogenesis, uterine blood flow and uterine myometrium is a target for cigarette smoke components. The effects of cigarette smoke are dose-dependent and are influenced by the presence of other toxic substances and hormonal status. Individual sensitivity, dose, time and type of exposure also play a role in the impact of smoke constituents on human fertility. CONCLUSIONS All stages of reproductive functions are targets of cigarette smoke toxicants. Further studies are necessary to better understand the deleterious effects of cigarette smoke compounds on the reproductive system in order to improve health care, help to reduce cigarette smoking and provide a better knowledge of the molecular mechanisms involved in reproductive toxicology.

Identification of new criteria for embryo quality is required to improve the clinical outcome of in vitro fertilization. The aim of this study was to determine the gene expression profile of cumulus cells (CC) surrounding the oocyte as biomarkers for embryo potential and to identify genes to be used as prognostic indicators of successful pregnancy. CC from single oocytes were analysed using DNA microarrays. Gene expression profiles of CC surrounding the oocyte associated with good embryonic quality and pregnancy outcome were computed. We observed that CC issued from oocytes that developed into embryos with a good morphology had differing gene expression profile according to the pregnancy outcome of the embryo. We demonstrated that the expression of BCL2L11, PCK1 and NFIB in CC is significantly correlated with embryo potential and successful pregnancy. These results were confirmed by quantitative RT-PCR. The gene expression profiling of human CC correlates with embryo potential and pregnancy outcome. BCL2L11, PCK1 and NFIB genes are proposed as biomarkers for predicting pregnancy. Our findings suggest a non-invasive approach, offering a new potential strategy for competent embryo selection. This approach should be validated in single-embryo transfer programmes.

No abstract

Five genes have been identified for the first time as being up-regulated during the implantation window and are proposed as new biomarkers for exploration of endometrial receptiveness. As the endometrial biopsy procedure can be performed during a natural cycle, it would be worth testing this approach as a novel strategy in patients with poor implantation after IVF or ICSI.

The protein Z-protein Z-dependent inhibitor complex is a factor Xa inhibitor. Protein Z deficiencies have recently been described in patients with ischemic stroke. As placenta infarction leads to poor pregnancy outcome, we studied protein Z plasma concentrations in nonthrombotic, nonthrombophilic consecutive patients with unexplained pregnancy wastage. A significant amount of protein Z deficiencies was only found in the early fetal loss group (< 1 mg/L; 44 of 200, P < 10 ؊4 ) and mainly in the case of fetal demise between the beginning of the 10th and the end of the 15th week of gestation (odds ratio, 6.7 [3.1-14.8], P < 10 ؊3 ). These deficiencies were not due to partial vitamin K1 deficiency, and at least some of them were constitutional ones. In women, protein Z deficiency may induce an enhanced risk of severe placental insufficiency soon after the connection of maternal and fetal circulations. IntroductionProtein Z is a vitamin K-dependent plasma protein that serves as a cofactor for the control of the coagulation factor Xa by the protein Z-dependent protease inhibitor. 1,2 Protein Z null mice have an apparently normal phenotype, but protein Z deficiency dramatically increases the thrombotic phenotype in mice carrying the factor V Leiden genotype. 3 Studies to determine the role of protein Z in human thrombosis have, to date, led to the description of an association between prior ischemic stroke and protein Z deficiency. 4 Ultrasonographic data indicate that the placenta replaces the yolk sac as the source of blood supply to the embryo from the beginning of the 8th to the end of the 9th week of gestation. 5 From this crucial step, pregnancy outcome is dependent on sustained placental development; thrombosis in the maternal placenta may lead to fetal demise.Here we describe the incidence of protein Z deficiency in women with unexplained pregnancy loss. Study design PatientsAll the women we studied had given their informed consent for participation to our Abnormal Pregnancy Study Program, based on the recruitment of a vast cohort of patients from the South of France with at least one miscarriage/fetal loss, and of healthy parity-and age-matched control subjects (NOHA studies 6-9 ). In this program, they were all investigated for classical prothrombotic factors as described (essential thrombocythemia; antiphospholipid/anticofactor antibodies; dysfibrinogenemia; deficiency in antithrombin, protein C, or protein S; factor V Leiden mutation; 20210A allele in the prothrombin gene; high plasminogen activator inhibitor 1 plasma levels; or hyperhomocysteinemia).We studied 4 groups of consecutive women with negative thrombotic antecedents and prothrombotic factors: 200 patients with unexplained primary recurrent miscarriages before the 8th week of gestation (3 episodes; median age, 26.2 years), 200 patients with one unexplained primary episode of early fetal death from the 10th to the end of the 19th week (median age, 23.1 years), 50 patients with one unexplained primary episode of late fetal death from the beginning ...

Not applicable.

No abstract