Mapping Fuzzy Petri Net to Fuzzy Extended Markup Language

Use of model gives the knowledge and information about the phenomenon also eradicates the cost, the effort and the hazard of using the real phenomenon. Characteristics and concepts of Petri nets are in a way that makes it simple and strong to describe and study the information processing system; especially it is shown in those which are dealing with discrete, concurrent, distributed, parallel and indecisive events. Yet, due to Petri nets inability to face with systems working on obscure data and continues events, the interest to develop fundamental concept of Petri nets has been raised which is led to new style of presented model named "fuzzy Petri nets". The difference in Petri nets is in the elements that have been fuzzed. Transitions, places, signs and arcs can be fuzzed. PMNL, on the other hand as a markup language has been engaged in uttering Petri nets in previous researches. Fuzzy markup nets can model the uncertainty of concurrent scenarios different from a dynamic system by a board of parameters and use of fuzzy membership dependencies. Therefore, in order to define these uncertain data, it is vital to use a formal language to describe fuzzy Petri nets. To support this version in this thesis, a markup language will be presented stating the structure and grammar of markup language and covering fuzzy concepts in Petri nets as well. Presenting the suggested grammar accommodates the support of fuzzy develope.DOI:http://dx.doi.org/10.11591/ijece.v3i5.403

Small in size, but large in action: Micrornas as potential modulators of pten in breast and lung cancers

10.3390/biom11020304Biomolecules112Jan-3

The involvement of epithelial-to-mesenchymal transition in doxorubicin resistance: possible molecular targets

Considering the fact that cancer cells can switch among various molecular pathways and mechanisms to ensure their progression, chemotherapy is no longer effective enough in cancer therapy. As an anti-tumor agent, doxorubicin (DOX) is derived from Streptomyces peucetius and can induce cytotoxicity by binding to topoisomerase enzymes to suppress DNA replication, leading to apoptosis and cell cycle arrest. However, efficacy of DOX in suppressing cancer progression is restricted by development of drug resistance. Cancer cells elevate their metastasis in triggering DOX resistance. The epithelial-to-mesenchymal transition (EMT) mechanism participates in transforming epithelial cells into mesenchymal cells that have fibroblast-like features. The EMT diminishes intercellular adhesion and enhances migration of cells that are necessary for carcinogenesis. Various oncogenic molecular pathways stimulate EMT in cancer. EMT can induce DOX resistance, and in this way, upstream mediators such as ZEB proteins, microRNAs, Twist1 and TGF-β play a significant role. Identification of molecular pathways involved in EMT regulation and DOX resistance has resulted in using gene therapy such as microRNA transfection and siRNA in overcoming chemoresistance. Furthermore, curcumin and formononetin, owing to their cytotoxicity against cancer cells, can suppress EMT in mediating DOX sensitivity. For promoting efficacy in DOX sensitivity, nanoparticles have been developed for boosting ability in EMT inhibition

The role of SOX family transcription factors in gastric cancer

Gastric cancer (GC) is a leading cause of death worldwide. GC is the third-most common cause of cancer-related death after lung and colorectal cancer. It is also the fifth-most commonly diagnosed cancer. Accumulating evidence has revealed the role of signaling networks in GC progression. Identification of these molecular pathways can provide new insight into therapeutic approaches for GC. Several molecular factors involved in GC can play both onco-suppressor and oncogene roles. Sex-determining region Y (Sry)-box-containing (SOX) family members are transcription factors with a well-known role in cancer. SOX proteins can bind to DNA to regulate cellular pathways via a highly conserved domain known as high mobility group (HMG). In the present review, the roles of SOX proteins in the progression and/or inhibition of GC are discussed. The dual role of SOX proteins as tumor-promoting and tumor-suppressing factors is highlighted. SOX members can affect upstream mediators (microRNAs, long non-coding RNAs and NF-κB) and down-stream mediators (FAK, HIF-1α, CDX2 and PTEN) in GC. The possible role of anti-tumor compounds to target SOX pathway members in GC therapy is described. Moreover, SOX proteins may be used as diagnostic or prognostic biomarkers in GC