Association between maternal thallium exposure and risk of gestational diabetes mellitus: Evidence from a birth cohort study.

BACKGROUND: The adverse effects of TI exposure on pregnant women are still unclear, especially regarding the risk of gestational diabetes mellitus (GDM) Objective: We explored the association between maternal urinary Tl burden and the risk of GDM. METHODS: A subsample of 1789 pregnant women were enrolled who provided spot urine samples before the diagnostic 75-g oral glucose tolerance test. Urinary Tl concentration was measured using inductively coupled plasma mass spectrometry. Logistic regression and covariance analysis were carried out to estimate the association between Tl exposure and GDM risk. RESULTS: The median of urinary Tl concentration was 0.382 µg/L or 0.525 µg/g creatinine (CC-Tl). There were 437 (24.4%) participants who were diagnosed with GDM, and the urinary CC-Tl concentrations of pregnant women with GDM were higher than that of pregnant women without GDM [0.548 (0.402, 0.788) vs 0.518 (0.356, 0.724), p = 0.014]. After adjusting for the relevant covariates, an association between urinary Tl concentrations and GDM was found. In comparison to the pregnant women in the lowest quartile of urinary CC-Tl concentration, the pregnant women in the highest quartile had a higher risk of GDM [OR (95% CI) = 1.44 (1.03, 2.02), p-trend = 0.055]. If limited to the pregnant women without family history of diabetes, the results were still robust [OR (95% CI) = 1.59 (1.11, 2.30), p-trend = 0.012]. CONCLUSION: Urinary CC-Tl concentration was associated with GDM among Chinese pregnant women. Our findings provide evidence that moderately high Tl exposure may be a novel risk factor for pregnant women health.

microRNA-145-3p inhibits non-small cell lung cancer cell migration and invasion by targeting PDK1 via the mTOR signaling pathway.

The mammalian target of rapamycin (mTOR) pathway is dysregulated in more than 50% of all human malignancies and is a major target in cancer treatment. In this study, we explored the underlying mechanism involving microRNA-145-3p (miR-145-3p) in the development and progression of non-small cell lung cancer (NSCLC) by targeting PDK1 via the mTOR signaling pathway. NSCLC tissues and adjacent normal tissues were obtained from 83 NSCLC patients. miR-145-3p, PDK1, and mTOR levels were determined by quantitative real-time polymerase chain reaction (qRT-PCR) and immunohistochemistry. Human NSCLC cell lines A549 and H1299 were transfected with miR-145-3p and siPDK1 to confirm the effect of miR-145-3p and PDK1 on NSCLC cells in vitro. Cell growth was evaluated by a CCK8 assay. Cell motility and chemotaxis analysis were determined by the scratch test and chemotaxis assay, respectively. The protein levels of PDK1 and mTOR were measured using the western blotting. Results showed lower level of miR-145-3p and higher levels of PDK1 and mTOR in NSCLC tissues compared to the adjacent normal tissues. In vitro results showed that cell growth, cell motility, and chemotaxis were all inhibited in cells transfected with miR-145-3p and those transfected with siPDK. Additionally, dual luciferase reporter gene assay helped confirmed that PDK1 is a target of miR-145. Finally, levels of PDK1, mTOR, and phosphorylated-mTOR were lower in cells transfected with miR-145-3p as well as those with siPDK1. These findings indicate that miR-145-3p may inhibit cell growth, motility, and chemotaxis in NSCLC by targeting PDK1 through suppressing the mTOR pathway.