Interconversion between Methoxylated and Hydroxylated Polychlorinated Biphenyls in Rice Plants: An Important but Overlooked Metabolic Pathway

To date, there is limited knowledge on the methoxylation of polychlorinated biphenyls (PCBs) and the relationship between hydroxylated polychlorinated biphenyls (OH-PCBs) and methoxylated polychlorinated biphenyls (MeO-PCBs) in organisms. In this study, rice (Oryza sativa L.) was chosen as the model organism to determine the metabolism of PCBs in plants. Limited para-substituted 4′-OH-CB-61 (major metabolite) and 4′-MeO-CB-61 (minor metabolite) were found after a 5-day exposure to CB-61, while ortho- and meta-substituted products were not detected. Interconversion between OH-PCBs and MeO-PCBs in organisms was observed for the first time. The demethylation ratio of 4′-MeO-CB-61 was 18 times higher than the methylation ratio of 4′-OH-CB-61, indicating that formation of OH-PCBs was easier than formation of MeO-PCBs. The transformation products were generated in the roots after 24 h of exposure. The results of in vivo and in vitro exposure studies show that the rice itself played a key role in the whole transformation processes, while endophytes were jointly responsible for hydroxylation of PCBs and demethylation of MeO-PCBs. Metabolic pathways of PCBs, OH-PCBs, and MeO-PCBs in intact rice plants are proposed. The findings are important in understanding the fate of PCBs and the source of OH-PCBs in the environment

microRNA-3129 promotes cell proliferation in gastric cancer cell line SGC7901 via positive regulation of pRb

<div><p>Several microRNAs (miRNAs) have been reported as oncogenes or tumor suppressors in many cancers, including gastric cancer (GC). However, the role and molecular mechanism of miR-3129 in GC is largely unknown. We aimed to explore the function and the underlying molecular mechanism of miR-3129 in GC. Cancer tissues and corresponding adjacent tissues were collected from 50 patients with GC, and the expression of miR-3129 was detected by RT-qPCR. The expression of miR-3129 and pRb in human GC cell line SCG7091 was altered by transient transfection. Thereafter, MTT and flow cytometry assays were used to analyze cell viability and cell cycle. The expression of cyclin E, CDK2, CDK2 inhibitors (p16 and 21), and pRb were detected by RT-qPCR and western blot. A significant up-regulation of miR-3129 was observed in GC tissues compared to adjacent tissues. Overexpression of miR-3129 significantly improved cell viability after 4 days of post-transfection. Flow cytometry assay results showed that the miR-3129 overexpression arrested more SGC7901 cells at S phase. Moreover, overexpression of miR-3129 down-regulated the expression of CDK2 inhibitors while it up-regulated the expression levels of cyclin E, CDK2, and pRb. Interestingly, we found that pRb inhibition reversed the effect of miR-3129 inhibitor on cell proliferation in SGC7901 cells, increased cell viability, reduced cells at G0/1 phase, and modulated the expression of proliferation-related factors. Our results revealed that miR-3129 functioned as an oncogene through positive regulation of pRb and may prove to be a promising option for molecular therapy of GC.</p></div

Estimating Emissions and Environmental Fate of Di-(2-ethylhexyl) Phthalate in Yangtze River Delta, China: Application of Inverse Modeling

A georeferenced multimedia model was developed for evaluating the emissions and environmental fate of di-2-ethylhexyl phthalate (DEHP) in the Yangtze River Delta (YRD), China. Due to the lack of emission inventories, the emission rates were estimated using the observed concentrations in soil as inputs for the multimedia model solved analytically in an inverse manner. The estimated emission rates were then used to evaluate the environmental fate of DEHP with the regular multimedia modeling approach. The predicted concentrations in air, surface water, and sediment were all consistent with the ranges and spatial variations of observed data. The total emission rate of DEHP in YRD was 13.9 thousand t/year (95% confidence interval: 9.4–23.6), of which urban and rural sources accounted for 47% and 53%, respectively. Soil in rural areas and sediment stored 79% and 13% of the total mass, respectively. The air received 61% of the total emissions of DEHP but was only associated with 0.2% of the total mass due to fast degradation and intensive deposition. We suggest the use of an inverse modeling approach under a tiered risk assessment framework to assist future development and refinement of DEHP emission inventories

Begg’s funnel plot for publication bias analysis.

<p>Each point represents a separate study, lnhr is natural logarithm of HR, and horizontal line represents the mean effect size.</p

Main results of meta-analysis.

a<p>Analysis of the association of miR-181a/b and OS in a variety of cancers;</p>b<p>Subgroup analysis of the association of miR-181a/b and OS in hematological malignancies;</p>c<p>Subgroup analysis of the association of miR-181a and OS in a variety of cancers;</p>d<p>The P value was calculated using the fixed-effects model (the Mantel-Haenszel method).</p

Sensitivity analysis.

<p>The middle vertical axis represents the pooled HR and the 2 vertical axes indicate the corresponding 95% CI. Each hollow circle represents the pooled HR when the left study was omitted in this meta-analysis, and the 2 ends of every broken line indicate the 95% CI.</p

Flow diagram of the studies identification and selection.

<p>Flow diagram of the studies identification and selection.</p

Angiotensin II (Ang II) increases cathepsin S (Cat S) expression in mouse heart.

<p>(<b>A</b>) Co-localization of Cat S with F4/80-positive macrophages and (<b>B</b>) α-smooth muscle actin (α-SMA) in WT and Cat S^−/− hearts. Bars, 25 µm. (<b>C)</b> Measurement of blood pressure in WT and Cat S^−/− mice. (<b>D</b>) Left ventricle ejection fraction (EF %) in WT and Cat S^−/− hearts. (<b>E</b>) Immunohistochemical staining of Ang II-induced Cat S expression in mice. Bars, 25 µm. Data are mean±SEM (n = 8 per group). **P<0.01 <i>vs</i>. saline control. ^§§P<0.01 <i>vs</i>. saline control.</p

Cat S deficiency enhances Ang II-induced cardiac fibrosis in mouse heart.

<p>(<b>A</b>) Representative Masson trichrome staining of WT and Cat S^−/− hearts with saline or Ang II infusion and quantitative analysis of fibrotic areas. Immunohistochemical staining and quantification of (<b>B</b>) collagen I, (<b>C</b>) transforming growth factor (TGF)- β1 (<b>D</b>) and (<b>E</b>) α-SMA in WT and Cat S^−/− hearts with saline or Ang II infusion. Bars, 50 µm. Data are mean±SEM (n = 4 per group). **P<0.01 <i>vs.</i> saline Cat S KO control; ^#P<0.05, ^##P<0.01 <i>vs.</i> Ang II-infused WT mice. ^§P<0.05 <i>vs.</i> saline WT control.</p

Cat S deficiency increases Ang II-induced infiltration and expression of proinflammatory cytokines in mouse heart.

<p>(<b>A</b>) Representative hematoxylin and eosin staining of WT and Cat S^−/− hearts. Bars, 50 µm. (<b>B</b>) Immunohistochemical staining and (<b>C</b>) quantification of Mac-2 positivity. Bars, 25 µm. (<b>D</b>) Immunohistochemical staining and (<b>E</b>) quantification of TNF-α and IL-1β expression. Bars, 50 µm. (<b>F</b>) Real-time PCR analysis of mRNA expression of TGF–β1, TNF-α and IL-1β in WT and Cat S KO mouse hearts. Bars, 50 µm. Data are mean±SEM (n = 4 per group). **P<0.01 <i>vs.</i> saline Cat S KO control; ^##P<0.01 <i>vs.</i> Ang II-infused WT mice.</p