Rabbit Anti-Human CTSS Polyclonal Antibody

Networks of Timed Automata (NTA) and Time Petri Nets (TPNs) are well-established formalisms used to model, analyze and control industrial real-time systems. The underlying theories are usually developed in different scientific communities and both formalisms have distinct strong points: for instance, conciseness for TPNs and a more flexible notion of urgency for NTA. The objective of the paper is to introduce a new model allowing the joint use of both TPNs and NTA for the modeling of timed systems. We call it Clock Transition System (CTS). This new model incorporates the advantages of the structure of Petri nets, while introducing explicitly the concept of clocks. Transitions in the network can be guarded by an expression on the clocks and reset a subset of them as in timed automata. The urgency is introduced by a separate description of invariants. We show that CTS allow to express TPNs (even when unbounded) and NTA. For those two classical models, we identify subclasses of CTSs equivalent by isomorphism of their operational semantics and provide (syntactic) translations. The classical state-space computation developed for NTA and then adapted to TPNs can easily be defined for general CTSs. Armed with these merits, the CTS model seems a good candidate to serve as an intermediate theoretical and practical model to factor out the upcoming developments in the TPNs and the NTA scientific communities.

The analysis of gene expression patterns in cancers has improved the understanding of the mechanisms underlying the process of metastatic progression. However, the acquisition of invasive behavior in melanoma is poorly understood. In melanoma, components of the immune system can contribute to tumor progression, and inflammatory cells can influence almost all aspects of cancer progression, including metastasis. Recent studies have attributed an important role to B-1 cells, a subset of B lymphocytes, in melanoma progression. In vitro interactions between B16 melanoma cells and B-1 lymphocytes lead to increased B16 cell metastatic potential, but the molecular changes induced by B-1 lymphocytes on B16 cells have not yet been elucidated. In this study, we used a microarray approach to assess the gene expression profile of B16 melanoma cells following contact with B-1 lymphocytes (B16B1). The microarray analysis identified upregulation in genes involved with metastatic progression, such as ctss, ccl5, cxcl2 and stat3. RT-qPCR confirmed this increase in mRNA expression in B16B1 samples. As previous studies have indicated that the ERK1/2 MAPK cascade is activated in melanoma cells following contact with B-1 lymphocytes, RT-qPCR was performed with RNA from melanoma cells before and after contacting B-1 cells and untreated or treated with ERK phosphorylation inhibitors. The results showed that the expression of stat3, ctss and cxcl2 increased in B16B1 but decreased following ERK1/2 MAPK inhibition. Ccl5 gene expression increased after contacting B-1 cells and was maintained at the same level following inhibitor treatment. Stat3 was verified and validated at the protein level by Western blot analysis. STAT3 expression was also significantly increased in B16B1, suggesting that this pathway can also contribute to the increased metastatic phenotype observed in our model. These results indicated that B-1 cells induce important global gene expression changes in B16 melanoma cells. We also evaluated the relationship of some of the genes identified as differentially expressed and the ERK1/2 MAPK cascade. This work may have important implications for understanding the role of B-1 lymphocytes and the ERK/MAPK cascade in the metastatic process. (C) 2013 Elsevier GmbH. All rights reserved.