Long non-coding RNAs (lncRNAs) are an important class of pervasive genes involved in a variety of biological functions. They are aberrantly expressed in many types of diseases. In this study, we aimed to investigate the lncRNA profiles in preeclampsia. Preeclampsia has been observed in patients with molar pregnancy where a fetus is absent, which demonstrate that the placenta is sufficient to cause this condition. Thus, we analyzed the lncRNA profiles in preeclampsia placentas. In this study, we described the lncRNA profiles in six preeclampsia placentas (T) and five normal pregnancy placentas (N) using microarray. With abundant and varied probes accounting for 33,045 LncRNAs in our microarray, 28,443 lncRNAs that were expressed at a specific level were detected. From the data, we found 738 lncRNAs that were differentially expressed (≥1.5-fold-change) among preeclampsia placentas compared with controls. Coding-non-coding gene co-expression networks (CNC network) were constructed based on the correlation analysis between the differentially expressed lncRNAs and mRNAs. According to the CNC network and GO analysis of differentially expressed lncRNAs/mRNAs, we selected three lncRNAs to analyze the relationship between lncRNAs and preeclampsia. LOC391533, LOC284100, and CEACAMP8 were evaluated using qPCR in 40 preeclampsia placentas and 40 controls. These results revealed that three lncRNAs were aberrantly expressed in preeclampsia placentas compared with controls. Our study is the first study to determine the genome-wide lncRNAs expression patterns in preeclampsia placenta using microarray. These results revealed that clusters of lncRNAs were aberrantly expressed in preeclampsia placenta compared with controls, which indicated that lncRNAs differentially expressed in preeclampsia placenta might play a partial or key role in preeclampsia development. Misregulation of LOC391533, LOC284100, and CEACAMP8 might contribute to the mechanism underlying preeclampsia. Taken together, this study may provide potential targets for the future treatment of preeclampsia and novel insights into preeclampsia biology.

A rapid and sensitive method based on wooden-tip electrospray ionization mass spectrometry (WT-ESI-MS) has been established for the quantitative detection of neopterin and biopterin in urine with only little sample preparation required. The limits of detection (LODs) for the analyses of neopterin and biopterin were determined to be 30 ng mL⁻¹ and 50 ng mL⁻¹ (S/N ≥ 3), respectively. Acceptable relative standard deviation (RSD) values (6.3–9.5%) and recovery values (90–133.6%) were obtained for direct measurements of neopterin and biopterin in raw urine. Moreover, neopterin and biopterin were directly detected from 9 clinical urine samples by WT-ESI-MS. A single sample analysis was completed within a few minutes, indicating that the present WT-ESI-MS method is a promising strategy for the rapid analysis of clinical samples.

Wooden-tip electrospray ionization (wooden-tip ESI) is applied to the rapid, in situ, direct qualitative and quantitative trace analysis of toxic and hazardous compounds in food samples. To evaluate the potential of wooden-tip ESI mass spectrometry (MS) in food analysis, pesticides, toxicants, date-rape drugs, and illicit additives were detected in various food samples. Wooden-tip ESI-MS experiments were performed using wooden tip sampling and ionization, with examination using MS and tandem mass spectrometry (MS/MS). The results proved that wooden-tip ESI allows the detection and confirmation of traces of toxic and hazardous compounds in food. In addition, selected analytes in beverages were obtained at absolute levels as low as ∼10 pg. Quantitation of analytes in liquid and powder samples was also evaluated. Single sample analysis was completed within 2 min. The data obtained shows that the wooden-tip ESI-MS is a promising tool for rapid analysis of food samples.

Preeclampsia (PE) and fetal growth restriction (FGR) have abnormal placental implantation and endothelial dysfunction in common. However, their etiologies are not well understood. Both heat shock p...

Background: Intrahepatic cholestasis of pregnancy (ICP) can cause adverse pregnancy outcomes, such as spontaneous preterm delivery and stillbirth. It is a complex disease influenced by multiple factors, including genetics and the environment. Previous studies have reported that functioning nuclear receptor subfamily 1 group H member 4 (NR1H4) plays an essential role in bile acid (BA) homeostasis. However, some novel variants and their pathogenesis have not been fully elucidated. Therefore, this research aimed to investigate the genetic characteristics of theNR1H4gene in ICP.Methods: In this study, we sequenced the entire coding region ofNR1H4in 197 pregnant women with ICP disease. SIFT and PolyPhen2 were used to predict protein changes. Protein structure modelling and comparisons between NR1H4 reference and modified protein structures were performed by SWISS-MODEL and Chimera 1.14rc, respectively. T-tests were used to analyse the potential significant differences betweenNR1H4mutations and wild types for 29 clinical features. Fisher’s test was conducted to test the significance of differences in mutation frequencies between ICP and the three databases.Results: We identified four mutations: two novel missense mutations, p.S145F and p.M185L; rs180957965 (A230S); and rs147030757 (N275N). The two novel missense mutations were absent in 1029 controls and three databases, including the 1000 Genomes Project (1000G_ALL), Exome Aggregation Consortium (ExAC) and ChinaMAP. Two web-available tools, SIFT and PolyPhen2, predicted that these mutations are harmful to the function of the protein. Moreover, compared to the wild-type protein structure, theNR1H4p.S145F and p.M185L protein structure showed a slight change in the chemical bond in two zinc finger structures. Combined clinical data indicate that the mutation group had higher levels of total bile acid (TBA) than the wild-type group. Therefore, we hypothesized that these two mutations altered the protein structure ofNR1H4, which impaired the function ofNR1H4itself and its target gene and caused an increase in TBA.Conclusions: To our knowledge, this is the first study to identify the novel p.S145F and p.M185L mutations in 197 ICP patients. Our present study provides new insights into the genetic architecture of ICP involving the two novelNR1H4mutations.