PurposeOur objective was to compare the diagnostic performance of glycated hemoglobin (HbA1c), GA, and fasting plasma glucose (FPG) for the diagnosis of GDM.MethodsWomen at their late second or early third trimesters seen from October 2011 to April 2012 were studied. GDM was diagnosed based on oral glucose tolerance test results, and GA and HbA1c were measured at the same time. Patients were divided into two groups (with and without GDM), and areas under the receiver-operating characteristic curves (AUCs) were calculated to determine the diagnostic value of FPG, GA, and HbA1c.ResultsA total of 698 women were included, of which 232 (33.2%) had GDM. Overall, FPG had the highest AUC for the detection of GDM, and was significantly higher than that of GA (0.692 vs. 0.568, p < 0.001) and HbA1c (0.692 vs. 0.619, p = 0.014). The AUC of FPG was significantly greater than that of GA and HbA1c. At 24–28 weeks’ gestation, the AUCs of FPG were significantly greater than those of GA and HbA1c.ConclusionsThese results do not support the use of GA as a screening tool for GDM.Electronic supplementary materialThe online version of this article (doi:10.1007/s40618-016-0605-7) contains supplementary material, which is available to authorized users.

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Epithelial ovarian cancer (EOC) is one of the leading causes of cancer-associated mortality in women. At present, the overall 5-year survival rate of patients with EOC remains poor despite advancements in diagnosis and treatment. Long non-coding RNAs (lncRNAs) have attracted increasing attention

Aim: To determine if activation of the NF-ĸB-VCAM-1 pathway is mediated by protein kinase C-α (PKC-α). Methods: PKC inhibitor polymyxin B was added to cultured human umbilical vein endothelial cells (HUVECs) from normal pregnancies. Sera from women with uncomplicated pregnancies and with preeclampsia (PE) were added to the control and intervention groups of the HUVECs. Cytoplasmic and membrane PKC, cytoplasmic NF-ĸB inhibitory factor (I-ĸB), and NF-ĸBp65 were measured. Cell viability, cell apoptosis, and VCAM-1 expression were determined. Results: Cytoplasmic PKC and I-ĸB in HUVECs incubated with sera from women with PE were significantly lower than in the control group, and the PKC content of the cell membrane, NF-ĸBp65, the expression of VCAM-1, and cell apoptosis were higher than in the normal pregnancy group. Cell viability was lower in the intervention than the control group. When HUVECs were pretreated with PKC inhibitor polymyxin B, the cytoplasmic PKC and I-ĸB content of the HUVECs increased in the PE group; the PKC content of the cell membrane, NF-ĸBp65, the expression of VCAM-1 and cell apoptosis decreased. Cell viability increased. Conclusions: Activation of the PKC-NF-ĸB signaling pathway may play an important role in the injury of HUVECs in women with PE.