Fast Min-Sum Algorithms for Decoding of LDPC over GF(q)

In this paper, we present a fast min-sum algorithm for decoding LDPC codes over GF(q). Our algorithm is different from the one presented by David Declercq and Marc Fossorier in ISIT 05 only at the way of speeding up the horizontal scan in the min-sum algorithm. The Declercq and Fossorier's algorithm speeds up the computation by reducing the number of configurations, while our algorithm uses the dynamic programming instead. Compared with the configuration reduction algorithm, the dynamic programming one is simpler at the design stage because it has less parameters to tune. Furthermore, it does not have the performance degradation problem caused by the configuration reduction because it searches the whole configuration space efficiently through dynamic programming. Both algorithms have the same level of complexity and use simple operations which are suitable for hardware implementations.Comment: Accepted by IEEE Information Theory Workshop, Chengdu, China, 200

Activation of the p38/MAPK pathway regulates autophagy in response to the CYPOR-dependent oxidative stress induced by zearalenone in porcine intestinal epithelial cells

Zearalenone (ZEA) can widely contaminate crops and agricultural products. The ingestion of ZEA-contaminated food or feed affects the integrity and functions of the intestines. In this study, we aimed to find the potential protective mechanism against ZEA ingestion. We found that ZEA induced cell death in IPEC-J2 cells. Meanwhile, the cytoprotective autophagy was activated in ZEA-treated cells. Further studies demonstrated that a p38/MAPK inhibitor down-regulated autophagy and increased cell death compared to those of the controls. Furthermore, ZEA could induce the accumulation of ROS, and eliminating ROS with NAC resulted in a decline in cell death, p38/MAPK phosphorylation, and the expression of LC3-II compared to those of ZEA-group. In addition, cytochrome P450 reductase (CYPOR) was significantly increased in ZEA-treated cells compared to that in the controls, and an inhibitor of CYPOR decreased ROS levels and mitigated cell death compared to those of the ZEA-group. More importantly, we found that blocking both p38/MAPK signalling and autophagy could enhance CYPOR expression and elevate ROS levels. Overall, our study indicated that the p38/MAPK pathway could activate protective autophagy in response to the CYPOR-dependent oxidative stress that was induced by ZEA in IPEC-J2 cells

Estrogen receptor 8 activation inhibits colitis by promoting NLRP6-mediated autophagy

Estrogen receptor 8 (ER8) and NOD-like receptor family pyrin domain containing 6 (NLRP6) are highly ex-pressed in intestinal tissues. Loss of ER8 and NLRP6 exacerbate colitis in mouse models; however, the un-derlying mechanisms are incompletely understood. Here, we report that ER8 directly activates the NLRP6 gene expression via binding to estrogen responsive element of Nlrp6 gene promoter. ER8 also physically in-teracts with the NLRP6 nucleotide-binding domain and promotes NLRP6 inflammasome assembly. The ER8-NLRP6 axis then interacts with multiple autophagy-related proteins, including ULK1, BECN1, ATG16L1, LC3B, and p62, and affects the autophagosome biogenesis and autophagic flux. Finally, NLRP6-mediated autophagy suppresses the inflammatory response by promoting the K48-linked poly-ubiquitination of ASC, Casp-1 p20, IL-18, TNF-o, and prohibitin-2. Thus, ER8-NLRP6 direct an anti-inflamma-tory response by promoting autophagy. Our work uncovers an ER8-NLRP6-autophagy pathway as a regula-tory mechanism that maintains intestinal epithelial cell homeostasis and facilitates tissue repair in colitis