Pregnancy complications including pre-eclampsia, gestational-diabetes mellitus, preterm birth and intrauterine growth restriction can cause acute and chronic health problems for the mother and lead to fetal loss or dysregulation of infant physiology. The human placenta is susceptible to oxidative stress and oxidative damage in early gestation contributes to the onset of these conditions later in pregnancy. Current methods of predicting pregnancy complications are limited and although a large number of factors are associated with disease progression, few biomarkers have been used to aid in disease diagnosis early in gestation. This review discusses the detection of oxidative stress markers in biological fluids and highlights the need for further studies to validate their use in the prediction or diagnosis of pregnancy disorders.

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We report a child with persistently low oxygen saturations (SpO 2 90%-92%) [normal SpO 2 > 98%], with delayed diagnosis due to the co-existing congenital pulmonary airway malformation with possible arterio-venous malformation. The diagnosis was only achieved after low oxygen saturations incidentally discovered from the child's father. The eventual cause was Hemoglobin I-Toulouse, making both patients the first reported cases with low oxygen saturations.

Aims: The aim of this study was to examine the effects of sericin on diabetic cognitive impairment (DCI) in rats based on neuroinflammation. Methods: SD rats were firstly fed with high sugar and high fat diet for 4 weeks, and then injected with 50 mg/kg streptozotocin intraperitoneally to establish a diabetic model. The diabetic rats were randomly divided into 3 groups and treated with distilled water (n=10), 500 mg/kg (n =10) and 1000 mg/kg (n=20) sericin, respectively, by gavage once a day for 8 weeks. Before the end of the trail, 10 rats in the 1000 mg/kg sericin group were injected with 10 μg EX527 (a SIRT1 inhibitor) into the lateral ventricles once every other day for 5 times. Results: Treated with sericin significantly reduced the fasting blood glucose, improved DCI in rats. Sericin significantly inhibited of neuroinflammation, reduced the expression of NLRP3, TXNIP proteins and reduced cell apoptosis, while increased the expression of SIRT1 protein in the hippocampus of diabetic rats. After inhibiting SIRT1 with EX527, the above effect of sericin on DCI rats was weakened. Conclusions: These results indicated that sericin may block DCI progression in rats by inhibiting TXNIP/NLRP3 neuroinflammation and neuronal apoptosis though SIRT1.