Background: Remifentanil protects against intestinal ischemia/reperfusion (I/R) injury; however, its exact mechanism remains to be elucidated. The objective of this study was to investigate the underlying molecular mechanism of remifentanil in intestinal I/R injury in mice.Methods: We evaluated the intestine-protective effect of remifentanil in adult male mice with 45 min superior mesenteric artery occlusion followed by 4 h reperfusion by determining the following: intestinal Chiu’s scores, diamine oxidase, and intestinal fatty acid binding protein in serum; the apoptotic index, lipid peroxidation product malondialdehyde (MDA), and superoxide dismutase (SOD) activity in the intestinal mucosa; and the intestinal mRNA and protein expressions of Bip, CHOP, caspase-12, and cleaved caspase-3, reflecting endoplasmic reticulum (ER) stress. Furthermore, conditional knockout mice, in which the protein disulfide isomerase A3 (PDIA3) gene was deleted from the intestinal epithelium, and SB203580 (a selective p38MAPK inhibitor) were used to determine the role of PDIA3 and p38MAPK in I/R progression and intestinal protection by remifentanil.Results: Our data showed that intestinal I/R induced obvious oxidative stress and endoplasmic reticulum stress–related cell apoptosis, as evidenced by an increase in the intestinal mucosal malondialdehyde, a decrease in the intestinal mucosal SOD, and an increase in the apoptotic index and the mRNA and protein expression of Bip, CHOP, caspase-12, and cleaved caspase-3. Remifentanil significantly improved these changes. Moreover, the deletion of intestinal epithelium PDIA3 blocked the protective effects of remifentanil. SB203580 also abolished the intestinal protection of remifentanil and downregulated the mRNA and protein expression of PDIA3.Conclusion: Remifentanil appears to act via p38MAPK to protect the small intestine from intestinal I/R injury by its PDIA3-mediated antioxidant and anti-ER stress properties.

Nucleosome positioning plays an important role in crucial biological processes such as replication, transcription, and gene regulation. It has been widely used to predict the genome’s function and chromatin organisation. So far, the studies of patterns in nucleosome positioning have been limited to transcription start sites, CTCFs binding sites, and some promoter and loci regions. The genome-wide organisational pattern remains unknown. We have developed a theoretical model to coarse-grain nucleosome positioning data in order to obtain patterns in their distribution. Using hierarchical clustering on the auto-correlation function of this coarse-grained nucleosome positioning data, a genome-wide clustering is obtained for Candida albicans. The clustering shows the existence beyond hetero- and eu-chromatin inside the chromosomes. These non-trivial clusterings correspond to different nucleosome distributions and gene densities governing differential gene expression patterns. Moreover, these distribution patterns inside the chromosome appeared to be conserved throughout the genome and within species. The pipeline of the coarse grain nucleosome positioning sequence to identify underlying genomic organisation used in our study is novel, and the classifications obtained are unique and consistent.

A fast recognition algorithm of weed is achieved and improved on the DSP of DM6437 with C64+ core in this paper. The algorithm is able to identify weeds between the crop rows with information of the locations and areas. Meanwhile, it is optimized based on the C64+ core. And it takes about 10.9ms to handle a weed image with 320*240 pixels, which meets the requirement of real-time application.

We calculated the patterns for the CCCTC transcription factor (CTCF) binding sites across many genomes on a first principle approach. The validation of the first principle method was done on the human as well as on the mouse genome. The predicted human CTCF binding sites are consistent with the consensus sequence, ChIP-seq data for the K562 cell, nucleosome positions for IMR90 cell as well as the CTCF binding sites in the mouse HOXA gene. The analysis of Homo sapiens, Mus musculus, Sus scrofa, Capra hircus and Drosophila melanogaster whole genomes shows: binding sites are organized in cluster-like groups, where two consecutive sites obey a power-law with coefficient ranging from to 0.3292 0.0068 to 0.5409 0.0064; the distance between these groups varies from 18.08 0.52kbp to 42.1 2.0kbp. The genome of Aedes aegypti does not show a power law, but 19.9% of binding sites are 144 4 and 287 5bp distant of each other. We run negative tests, confirming the under-representation of CTCF binding sites in Caenorhabditis elegans, Plasmodium falciparum and Arabidopsis thaliana complete genomes.