In a parallel composition of timed automata, some transitions are independent to others. Generally the basic method generates one successors for each of the legal permutations of the transitions. These successors may be combined into one bigger symbolic state. In other words, the basic algorithm slices one big symbolic state into pieces. The number of these pieces can be up to n!, where n is the number of independent transitions. In this paper, we introduce a concept, 'partial order path', to avoid treating the permutations one by one. A partial order path includes a set of transitions and a partial order on this set. Our algorithm generates one symbolic successor w.r.t. each partial order path. This big symbolic successor is just the combination of the successors w.r.t. all the global paths which are consistent to this partial order path. It is shown by some case studies that this method may result in significant space reduction.

The purpose of this research was to evaluate HSYA' effects and mechanisms to improve Scars Induced by Anticoagulant Injection by vivo and vitro study. New Zealand rabbits were divided into Normal control (NC), Anticoagulant, Anticoagulant+HSYA-Low, Anticoagulant+HSYA-Middle and Anticoagulant+HSYA-High. Measuring TGF-β1 and IL-1β concentration by Elisa assay; evaluating pathology and fibrosis level by HE and Masson staining, measuring collage I, collage III, TLR4 and NF-κB(p65) protein expression by IHC assay. Relative gene expression (Collage I, Collage III, TLR4 and NF-κB(p65)) were evaluated by RT-qPCR assay. Relative proteins expression (Collage I, Collage III, TLR4 and NF-κB(p65)) were evaluated by WB assay. And using TGF-β1 to stimulate cell to make cell model. Compared with NC group, TGF-β1 and IL-1β concentration were significantly increased (P < 0.001); The pathology and fibrosis level were significantly deteriorated, meanwhile, Collage I, Collage III, TLR4 and NF-κB(p65) proteins and gene expression were significantly up-regulation in Anticoagulant group (P < 0.001). With HSYA supplement, TGF-β1 and IL-1β concentration were significantly depressed, Pathology and fibrosis levels were significantly improved, Collage I, Collage III, TLR4 and NF-κB(p65) proteins and gene expressions were significantly improved with dosedependent (P < 0.05). HSYA could improve anticoagulant injury induced subcutaneous scar via regulation TLR4/NF-κB(p65).

Histone deacetylases (HDACs) inhibitors are promising therapeutic agents against proteinuric kidney diseases, here, we investigated the effect of MC1568, a selective inhibitor of HDAC class IIa, on the development and progression of nephrotic syndrome in a murine model induced by Adriamycin (ADR). In kidney tissues of FSGS patients, all four members of HDAC IIa were significantly upregulated in podocytes. In ADR-treated cultured human podocyte, expression of HDAC IIa were induced, meanwhile inhibition of HDAC IIa with MC1568 restored cytoskeleton structure and suppressed expression of desmin and α-SMA. In mice, administration of MC1568 at 14 days after ADR ameliorated proteinuria and podocyte injury, also decreased expression of Fibronectin and α-SMA. Mechanistically, MC1568 inhibited ADR induced β-catenin activation in vitro and in vivo. Together, these finding demonstrate that HDAC IIa inhibition ameliorates podocyte injury and proteinuria, which provide a possibility that MC1568 may be used in nephrotic syndrome.

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