The Balanced Insulating Performance and Mechanical Property of PP by Introducing PP‑<i>g</i>‑PS Graft Copolymer and SEBS Elastomer

The PP/PP-<i>g</i>-PS/SEBS blends are prepared by melt extrusion in order to improve both insulating properties and toughness of PP. SEBS is used to reduce the rigidity of PP, while the insulating properties are improved by adding PP-<i>g</i>-PS without decreasing mechanical properties. The microstructure of PP blends is carefully investigated by SEM, DMA, XRD, and DSC. It is interesting to find that a core–shell dispersion phase formed in the blend with the adding of PP-<i>g</i>-PS, and the size of core is decreased while the thickness of shell is increased with further increasing volume of PP-<i>g</i>-PS. Due to this special structure, the nucleation ability of SEBS is decreased. Meanwhile, the rigid segments and compatibilization effect of PP-<i>g</i>-PS not only increased the glass transition temperature of both PP and SEBS, but also enhanced their adhesion. Therefore, the electrical properties were increased without decreasing the mechanical properties of the blends. Consequently, an insulation material with excellent mechanical properties was obtained

Genome-Wide Mapping of 5mC and 5hmC Identified Differentially Modified Genomic Regions in Late-Onset Severe Preeclampsia: A Pilot Study

<div><p>Preeclampsia (PE) is a leading cause of perinatal morbidity and mortality. However, as a common form of PE, the etiology of late-onset PE is elusive. We analyzed 5-methylcytosine (5mC) and 5-hydroxymethylcytosine (5hmC) levels in the placentas of late-onset severe PE patients (n = 4) and normal controls (n = 4) using a (hydroxy)methylated DNA immunoprecipitation approach combined with deep sequencing ([h]MeDIP-seq), and the results were verified by (h)MeDIP-qPCR. The most significant differentially methylated regions (DMRs) were verified by MassARRAY EppiTYPER in an enlarged sample size (n = 20). Bioinformatics analysis identified 714 peaks of 5mC that were associated with 403 genes and 119 peaks of 5hmC that were associated with 61 genes, thus showing significant differences between the PE patients and the controls (>2-fold, <i>p</i><0.05). Further, only one gene, <i>PTPRN2</i>, had both 5mC and 5hmC changes in patients. The ErbB signaling pathway was enriched in those 403 genes that had significantly different5mC level between the groups. This genome-wide mapping of 5mC and 5hmC in late-onset severe PE and normal controls demonstrates that both 5mC and 5hmC play epigenetic roles in the regulation of the disease, but work independently. We reveal the genome-wide mapping of DNA methylation and DNA hydroxymethylation in late-onset PE placentas for the first time, and the identified ErbB signaling pathway and the gene <i>PTPRN2</i> may be relevant to the epigenetic pathogenesis of late-onset PE.</p></div

Genome-wide mapping of 5mC and 5hmC in placentas of late-onset severe PE and normal pregnant women.

<p>(A and C) Normalized DMR (A) and DHMR(C) tag density distribution across the gene body. Each gene body was normalized to 0%-100%. Normalized Tag density is plotted from 20% of upstream of TSSs to 20% downstream of TSSs(Transcription Start Sites). (B and D) Normalized DMR (B) and DHMR (D) tag density distribution at gene promoters. -5 kb to +5 kb relative to TSSs is shown.</p

The effect of pre-eclampsia-like syndrome induced by L-NAME on learning and memory and hippocampal glucocorticoid receptor expression: A rat model

<p><i>Objective</i>: We aimed to study the impacts of pre-eclampsia on the cognitive and learning capabilities of adolescent rat offspring and to explore the possible underlying mechanisms at the molecular level. <i>Methods</i>: Pregnant rats were subcutaneously injected with saline solution (control) (<i>n</i> = 16) or NG-nitro-L-arginine methyl ester (L-NAME) (<i>n</i> = 16) from the 13th day of gestation until parturition. The brain tissues from fetal rats delivered by cesarean section were examined in both groups with hematoxylin and eosin (H&E) staining. Rats born vaginally in both groups were subjected to the Morris water maze test when 8-week-old and their hippocampi were analyzed for glucocorticoid receptor (GR) expression. <i>Results</i>: A pre-eclampsia-like model was successfully built in pregnant rats by infusion of the NO synthase inhibitor L-NAME, including phenotypes as maternal hypertension and proteinuria, high stillbirth rate, and fetal growth retardation. Neuroepithelial cell proliferation was found in the hippocampus of fetal rats in the L-NAME group. Grown to 8-week-old, the L-NAME group showed significantly longer escape latency than the control group in the beginning as well as in the end of navigation trials. At the same time, the swimming distance achieved by the L-NAME group was significantly longer than that of the control group. Such differences in cognitive and learning capabilities between the two groups were not gender dependent. Besides, the 8-week-old rats in the L-NAME group had increased GR expression in the hippocampus than the control group. <i>Conclusion</i>: Pre-eclampsia would impair cognitive and learning capabilities in adolescent offspring, and the upregulated expression of hippocampal GR may be involved in the underlying mechanisms.</p

Validation of the methylation status of <i>PTPRN2</i> in the two groups by MassARRAY EpiTYPER.

<p>(A)The overall methylation levels are displayed within amplicon A and amplicon B. (B,C) The average methylation of the CpG units of amplicon A and amplicon B are presented for late-onset severe PE and normal patients. Data are presented as means±SEM, n = 20 per group, *<i>p</i><0.05,**<i>p</i><0.01.A: Amplicon A, <i>p</i> = 0.0033;Amplicon B, <i>p</i> = 0.0017.B: Amplicon A: CpG_1, <i>p</i> = 0.0420; CpG_3, <i>p</i> = 0.4820; CpG_4, <i>p</i> = 0.1296; CpG_6, <i>p</i> = 0.2957; CpG_7, <i>p</i> = 0.6410; CpG_9, <i>p</i> = 0.0475, CpG_11, <i>p</i> = 0.0177; CpG_12.13, <i>p</i> = 0.0003. C: Amplicon B: CpG_1.2, <i>p</i> = 0.0134, CpG_3, <i>p</i> = 0.0210, CpG_4.5, <i>p</i> = 0.0185; CpG_6, <i>p</i> = 0.0163; CpG_7, <i>p</i> = 0.0019; CpG_8, <i>p</i> = 0.0001; CpG_9, <i>p</i> = 0.1268; CpG_10, <i>p</i> = 0.0192; CpG_11, <i>p</i> = 0.0583.</p

MeDIP-qPCR (A) and hMeDIP-qPCR (B) validations (mean values±SEM, n = 4 per group, <i>p</i><0.05) of representative DMRs and DHMRs.

<p>(A) MeDIP-qPCR validation of <i>ACAP2</i>, <i>CLIC6</i>, <i>GATA4</i>, <i>PCDH9</i> and <i>PTPRN2</i>-A. (B)hMeDIP-qPCR validation of <i>CCDC149</i>, <i>PTPRN2</i>-B and <i>RBFOX1</i>. <i>ACAP2</i>:<i>p</i> = 0.0032; <i>CLIC6</i>: <i>p</i> = 0.0235; <i>GATA4</i>: <i>p</i> = 0.0429;<i>PCDH9</i>: <i>p</i> = 0.0081; <i>PTPRN2-A</i>: <i>p</i> = 0.0216; <i>CCDC149</i>: <i>p</i> = 0.0068; <i>PTPRN2-B</i>: <i>p</i> = 0.0018; <i>RBFOX1</i>: <i>p</i> = 0.0250.</p

Pooled peak statistics for the hMeDIP and MeDIP data among 4 case samples (7,14,15,40) and 4 control samples(9, 10, 27, 28).

<p>Macs1.4, FDR%< = 5</p><p>Pooled peak statistics for the hMeDIP and MeDIP data among 4 case samples (7,14,15,40) and 4 control samples(9, 10, 27, 28).</p

MA plot of Case-Control contrast of (A) 5mC peaks and (B) 5hmC peaks normalized with tag density.

<p>The X axis indicates the normalized mean and the Y axis indicates the log2-fold change. Red is used to indicate significantly differently expressed observations (at least 2-fold density changes and <i>p</i>-value<0.05). The blue dots show no differential expression between the two groups.</p

Validation of the methylation status of candidate DMRs between the late-onset severe PE group and the normal group by MassARRAY EpiTYPER.

<p>(A) The methylation level of the CpG sites within <i>GATA4</i> amplicon. (B) The CpG methylation level sites within the <i>PCDH9</i> amplicon. (C) The methylation level of the CpG sites within <i>ACAP2</i> amplicon. (D) The CpG methylation sites within <i>CLIC6</i> amplicon. Data are shown as the means±SEM, n = 20 per group, *<i>p</i><0.05, **<i>p</i><0.01. <i>GATA4</i> amplicon: CpG_1, <i>p</i> = 0.0093; CpG_2, <i>p</i> = 0.0150; CpG_3, <i>p</i> = 0.5993; CpG_4, <i>p</i> = 0.0015; CpG_5, <i>p</i> = 0.9738; CpG_6, <i>p</i> = 0.0481; CpG_7.8, <i>p</i> = 0.0377; CpG_9, <i>p</i> = 0.0661.<i>PCDH9</i> amplicon: CpG_2, <i>p</i> = 0.6177; CpG_3, <i>p</i> = 0.1831; CpG_4, <i>p</i> = 0.0294; CpG_6, <i>p</i> = 0.0265; CpG_8, <i>p</i> = 0.0529; CpG_10, <i>p</i> = 0.8818; CpG_13, <i>p</i> = 0.0158. <i>ACAP2</i> amplicon: CpG_1, <i>p</i> = 0.0316; CpG_4, <i>p</i> = 0.0349; CpG_7.8, <i>p</i> = 0.3524. <i>CLIC6</i> amplicon: CpG_99, <i>p</i> = 0.0446; CpG_100, <i>p</i> = 0.0424; CpG_101.102, <i>p</i> = 0.5504; CpG_103, <i>p</i> = 0.7697; CpG_105.106, <i>p</i> = 0.0310; CpG_108.109, <i>p</i> = 1.0000; CpG_110.111, <i>p</i> = 0.0084.</p

Gene ontology groups displaying the significant GO-terms of DMRs and DHMRs (p<0.05).

<p>(A)The significant GO-terms of DMRs between the groups. (B)The significant GO-terms of DHMRs between the groups.</p