Objective We aimed to examine prospective associations between circulating fatty acids in early pregnancy and incident gestational diabetes mellitus (GDM) among Chinese pregnant women. Methods Analyses were based on two prospective nested case-control studies conducted in western China (336 GDM cases and 672 matched controls) and central China (305 cases and 305 matched controls). Fasting plasma fatty acids in early pregnancy (gestational age at enrollment: 10.4 weeks [standard deviation, 2.0]) and 13.2 weeks [1.0], respectively) were determined by gas chromatography-mass spectrometry, and GDM was diagnosed based on the International Association of Diabetes in Pregnancy Study Groups criteria during 24-28 weeks of gestation. Multiple metabolic biomarkers (HOMA-IR [homeostatic model assessment for insulin resistance], HbA1c, c-peptide, high-sensitivity C-reactive protein, adiponectin, leptin, and blood lipids) were additionally measured among 672 non-GDM controls at enrollment. Results Higher levels of saturated fatty acids (SFAs) 14:0 (pooled odds ratio, 1.41 for each 1-standard deviation increase; 95% confidence interval, 1.25, 1.59) and 16:0 (1.19; 1.05, 1.35) were associated with higher odds of GDM. Higher levels of n-6 polyunsaturated fatty acid (PUFA) 18:2n-6 was strongly associated with lower odds of GDM (0.69; 0.60, 0.80). In non-GDM pregnant women, higher SFAs 14:0 and 16:0 but lower n-6 PUFA 18:2n-6 were generally correlated with unfavorable metabolic profiles. Conclusions We documented adverse associations of 14:0 and 16:0 but a protective association of 18:2n-6 with GDM among Chinese pregnant women. Our findings highlight the distinct roles of specific fatty acids in the onset of GDM.

Long non-coding RNAs (lncRNAs) have emerged as important regulators in cancer, including breast cancer. The precise expression pattern of long noncoding RNA 00899 (LINC00899) in breast cancer and its mechanisms of action have not been reported. Here, we found that LINC00899 is downregulated in breast cancer tissues and cell lines. Kaplan-Meier analysis showed that elevated LINC00899 expression is closely associated with better relapse-free survival (RFS) in breast cancer, including the basal, luminal A or luminal B breast cancer subtypes. Gene Ontology terms and Kyoto Encyclopedia of Genes and Genomes pathway analysis suggested that LINC00899 is closely related to several cancer associated processes, including tight junction- and metabolism-associated pathways. Functional assays indicated that LINC00899 overexpression suppresses proliferation, migration and invasion of breast cancer cells in vitro. Moreover, LINC00899 was found to competitively bind miR-425, thereby functioning as a tumor suppressor by enhancing DICER1. Overexpression of miR-425 attenuated the LINC00899-induced inhibition of breast cancer cell proliferation and invasion. These findings highlight the important role of the LINC00899-miR-425-DICER1 axis in breast cancer cell proliferation and invasion, and could potentially lead to new lncRNA-based diagnostics or therapeutics for breast cancer.

The lower uterine segment scar becomes stable at 3 years after cesarean delivery, and by 9 years, the scar is mature.

The molecular mechanism that leads to pregnancy-induced hypertension (PIH), a pregnancy-specific syndrome, remains poorly understood. It has been suggested that microRNAs (miRNAs) may be potentially useful biomarkers for severe preeclampsia (PE), which is an important condition associated with PIH. The aim of the present study was to identify miR-204 by verifying differentially expressed serum miRNAs in patients with PIH during pregnancy compared with normal controls. Subsequently, the effects of miR-204 on proliferation and apoptosis of human choriocarcinoma (JAR) cells in hypoxic microenvironment were investigated. Previous studies indicated a number of miRNA candidates and the present study validated the expression of eight miRNAs in serum samples using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). A higher expression of miR-204 was identified in patients with PIH. To assess the impact of miR-204 inhibition on hypoxic JAR cells function in vitro, cell proliferation was detected using a Cell Counting Kit-8 assay. The rate of apoptosis and cell cycle progression was then examined by flow cytometry. RT-qPCR confirmed that serum miR-204-5p is more highly expressed in patients with PIH. Further statistical analysis indicated that the survival ratio of JAR cells in hypoxic microenvironments was increased in the miR-204-5p inhibitor group. However, the miR-204-5p inhibitor protected hypoxic JAR cells from apoptosis. The analysis of cell-cycle status demonstrated that the percentage of cells in the G2/G1 phase was larger compared with the control group. The results of the present study suggest that low levels of miR-204-5p may increase cell proliferation and reduce cell apoptosis with cell cycle changes in vitro. Therefore, serum miR-204-5p may be used as a notable biomarker for the diagnosis, prevention and treatment of PIH.

To explain gastrodin improved cell apoptosis induced by preeclampsia in vivo and in vitro study. The PE and normal rats were injected with normal saline (Model), low‐dose gastrodin (Gas‐L), medium‐dose gastrodin (Gas‐M), and high‐dose gastrodin (Gas‐H) groups at 50, 100, or 200 mg/kg per day. The rat blood pressure and 24‐hr urine protein level were measured at pregnant days 10, 16, and 20. Evaluating pathology by H&E staining, the cell apoptosis by TUNEL, and MyD88 and NF‐κB (p65) proteins by IHC assay using H/R to simulate PE cell model. Measuring cell proliferation, apoptosis, and MyD88 and NF‐κB (p65) protein expression by MTT, flow cytometry, and WB assay. The SBP, DBP, and 24‐hr urine protein levels were significantly different in PE rats (p < .05). The SBP, DBP, and 24‐hr urine protein levels were significantly improved (p < .05) in vivo and in vitro. The positive apoptosis cells and apoptosis rate were significantly increased with MyD88 and NF‐κB (p65) proteins upregulation (p < .05). The positive apoptosis cells and apoptosis rate were significantly decreased with MyD88 and NF‐κB (p65) proteins depressing in gastrodin‐treated groups with dose‐dependent (p < .05). Gastrodin improves PE‐induced cell apoptosis and pathology changed via MyD88/NF‐κB pathway in vitro and in vivo study.