Increased s(P)RR concentrations during the first trimester may predict the development of GDM later in pregnancy.

BackgroundAlthough an increased risk of preeclampsia in pregnancies conceived by in vitro fertilization (IVF) has been reported, it remains unknown whether IVF is associated with preeclampsia. In the present study, we sought to investigate whether IVF is associated with preeclampsia in pregnant women using propensity score matching analysis.MethodsThis study included 3,084 pregnant women who visited the National Center for Child Health and Development before 20 weeks of gestation without hypertension or renal disease and delivered a singleton after 22 weeks of gestation between 2009 and 2011. Of the 3084 patients, 474 (15.4%) conceived by IVF (IVF group) and 2,610 (84.6%) conceived without IVF (non-IVF group). The propensity score for receiving IVF was estimated using multiple logistic regression with 27 maternal and paternal variables. This model yielded a c-statistic of 0.852, indicating a strong ability to differentiate between those conceiving with and without IVF. The association between IVF and onset of preeclampsia was assessed by the propensity matched sample (pair of N = 474).ResultsThere were 46 preeclampsia cases (1.5%) in the total study population, with a higher proportion of cases in the IVF group (15 cases, 3.2%) than the non-IVF group (31 cases, 1.2%). Before propensity score matching, the IVF group was 2.72 (95% confidence intervals [CI]: 1.46-5.08) times more likely to have preeclampsia when unadjusted, and 2.32 (95% CI: 1.08-4.99) times more likely to have preeclampsia when adjusted for maternal and paternal variables by logistic regression. After propensity score matching, the IVF group did not show a significantly greater association with preeclampsia compared to the non-IVF group (odds ratio: 2.50, 95% CI: 0.49-12.89), although point estimates showed a positive direction.ConclusionsPropensity score matching analysis revealed that the association between IVF and preeclampsia became weaker than when conventional adjustments are made in multivariate logistic regression analysis, suggesting that the association between IVF and preeclampsia might be confounded by residual unmeasured factors.

Intracellular mRNA levels are not always proportional to their respective protein levels, especially in the placenta. This discrepancy may be attributed to various factors including post-transcriptional regulation, such as mRNA methylation (N6methyladenosine: m 6 A). Here, we conducted a comprehensive m 6 A analysis of human placental tissue from neonates with various birth weights to clarify the involvement of m 6 A in placental biology. The augmented m 6 A levels at the 5′-untranslated region (UTR) in mRNAs of small-for-date placenta samples were dominant compared to reduction of m 6 A levels, whereas a decrease in m 6 A in the vicinity of stop codons was common in heavy-for-date placenta samples. Notably, most of these genes showed similar expression levels between the different birth weight categories. In particular, preeclampsia placenta samples showed consistently upregulated SMPD1 protein levels and increased m 6 A at 5′-UTR but did not show increased mRNA levels. Mutagenesis of adenosines at 5′-UTR of SMPD1 mRNAs actually decreased protein levels in luciferase assay. Collectively, our findings suggest that m 6 A both at the 5′-UTR and in the vicinity of stop codon in placental mRNA may play important roles in fetal growth and disease.

Scale parameters are used to combine two or more models in different scales into one integrative model. One of the crucial issues in the research eld of biosimulation in hemodynamics is how to determine the scale parameters in comprehensive hemodynamic models comprising a cardiac cellular contraction model and a circulation model. In this report, we propose a method for determining the scale parameters using mathematical equations derived from the shape of the left ventricle (LV), which is assumed to be a hemisphere. In this method, we derived ve equations with seven unknown scale parameters. By using measured values of hemodynamic parameters such as the end-systolic and end-diastolic pressures and LV volume, we successfully determined seven scale parameters to reproduce pathological data of progressive hypertension in Dahl salt-sensitive rats. From the results, we found that accompanying the progression of hypertension, the active contraction force at end-diastole rst increase by 54%, followed by 93% increase of the passive elastic force. We also successfully reproduced normal human physiological hemodynamics.