JMJ704 positively regulates rice defense response against Xanthomonas oryzae pv. oryzae infection via reducing H3K4me2/3 associated with negative disease resistance regulators

A schematic representation showing the genomic regions of the three genes for ChIP-PCR assay. White box indicates untranslated region, black box indicates coding sequence, line through the box indicates intron region of the genes, lines and numbers above the gene indicate the regions and positions used for ChIP-PCR assay. (TIF 2795 kb

Anomaly Detection and Explanation Discovery on Event Streams

International audienceAs enterprise information systems are collecting event streams from various sources, the ability of a system to automatically detect anomalous events and further provide human readable explanations is of paramount importance. In this position paper, we argue for the need of a new type of data stream analytics that can address anomaly detection and explanation discovery in a single, integrated system, which not only offers increased business intelligence, but also opens up opportunities for improved solutions. In particular , we propose a two-pass approach to building such a system, highlight the challenges, and offer initial directions for solutions

Vitamin D Supplementation Enhances the Fixation of Titanium Implants in Chronic Kidney Disease Mice

Vitamin D (Vit D) deficiency is a common condition in chronic kidney disease (CKD) patients that negatively affects bone regeneration and fracture healing. Previous study has shown that timely healing of titanium implants is impaired in CKD. This study aimed to investigate the effect of Vit D supplementation on implant osseointegration in CKD mice. Uremia was induced by 5/6 nephrectomy in C57BL mice. Eight weeks after the second renal surgery, animals were given 1,25(OH)2D3 three times a week intraperitoneally for four weeks. Experimental titanium implants were inserted into the distal end of femurs two weeks later. Serum measurements confirmed decreased 1,25(OH)2D levels in CKD mice, which could be successfully corrected by Vit D injections. Moreover, the hyperparathyroidism observed in CKD mice was also corrected. X-ray examination and histological sections showed successful osseointegration in these mice. Histomorphometrical analysis revealed that the bone-implant contact (BIC) ratio and bone volume (BV/TV) around the implant were significantly increased in the Vit D-supplementation group. In addition, resistance of the implant, as measured by a push-in method, was significantly improved compared to that in the vehicle group. These results demonstrate that Vit D supplementation is an effective approach to improve the fixation of titanium implants in CKD

Increased Expression and Altered Methylation of HERVWE1 in the Human Placentas of Smaller Fetuses from Monozygotic, Dichorionic, Discordant Twins

<div><h3>Background</h3><p>The human endogenous retroviral family W, Env(C7), member 1 gene (<em>HERVWE1</em>) is thought to participate in trophoblast cell fusion, and its expression is diminished in the placentas of singleton intrauterine growth-retarded pregnancies. However, there is limited information about the role of <em>HERVWE1</em> in discordant fetal growth in twins. This study was to compare <em>HERVWE1</em> gene expression between the placentas of discordant monozygotic twins and to identify its regulation by methylation.</p> <h3>Methodology/Principal Findings</h3><p>Fetuses from twenty-one pairs of monozygotic, dichorionic, discordant twins were marked as “smaller” or “larger” according to birth weight. Placental <em>HERVWE1</em> mRNA and protein expression profiles were analyzed using quantitative RT-PCR and immunohistochemistry (IHC) staining. Methylation profiles of the <em>HERVWE1</em> promoter region were analyzed using a pyrosequencing assay. DNA methyltransferase (<em>DNMT</em>) transcript levels were analyzed by RT-PCR. 5-methyl cytosine (5-MC) was stained using an immunohistochemical assay. There was a significant negative correlation between <em>HERVWE1</em> mRNA levels and birth weight in twins (<em>P</em><0.01). Whereas the mean methylation level of the <em>HERVWE1</em> promoter region was diminished in the smaller group in discordant twins(<em>P</em><0.01), increased mRNA and protein levels of <em>HERVWE1</em> were found in smaller fetuses compared with larger fetuses in discordant twins(<em>P</em><0.01). There was no significant difference in 5-MC staining intensity between discordant twins (<em>P</em>>0.05). The <em>DNMT3b3</em> mRNA levels in the smaller group were significantly downregulated compared with the larger group in discordant twins(<em>P</em><0.05), whereas the <em>DNMT3b7</em> mRNA levels in the smaller group were significantly upregulated compared with the larger group in discordant twins(<em>P</em><0.05).</p> <h3>Conclusions/Significance</h3><p>In discordant, monozygotic, dichorionic twins, <em>HERVWE1</em> expression was higher in smaller fetuses and lower in larger fetuses. Methylation of the <em>HERVWE1</em> gene promoter region may participate in the regulation of <em>HERVWE1</em> gene expression in discordant twin pregnancies.</p> </div

SIRT5 promotes IDH2 desuccinylation and G6PD deglutarylation to enhance cellular antioxidant defense

Abstract Excess in mitochondrial reactive oxygen species (ROS) is considered as a major cause of cellular oxidative stress. NADPH, the main intracellular reductant, has a key role in keeping glutathione in its reduced form GSH, which scavenges ROS and thus protects the cell from oxidative damage. Here, we report that SIRT5 desuccinylates and deglutarylates isocitrate dehydrogenase 2 (IDH2) and glucose‐6‐phosphate dehydrogenase (G6PD), respectively, and thus activates both NADPH‐producing enzymes. Moreover, we show that knockdown or knockout of SIRT5 leads to high levels of cellular ROS. SIRT5 inactivation leads to the inhibition of IDH2 and G6PD, thereby decreasing NADPH production, lowering GSH, impairing the ability to scavenge ROS, and increasing cellular susceptibility to oxidative stress. Our study uncovers a SIRT5‐dependent mechanism that regulates cellular NADPH homeostasis and redox potential by promoting IDH2 desuccinylation and G6PD deglutarylation