Docking studies of few substituted 5-benzyl-2, 4-thiazolidinedione with PPAR-γ for antidiabetic activity

Docking studies of few substituted 5-benzyl-2, 4-thiazolidinedione moiety, which acts as peroxisome proliferator-activated receptor γ agonist was performed by using Glide v4.5. The docking studies reveal hydrogen bond formation to Thr241 with Gscore -7.22 and energy -62.2 kcal/mole. We found hydrogen bond formation of most of compounds with good Gscore and low energy as compared to the most active rosiglitazone.Colegio de Farmacéuticos de la Provincia de Buenos Aire

Quantitative structure activity relationship studies of some 5-aryl thiazolidine-2, 4-diones as antidiabetic agents

Quantitative Structure Activity Relationship (QSAR) studies were carried out for a series of 16 compounds which acts as ligands for PPAR-γ receptor. TSAR software was used to identify the essential structural and physicochemical features for their PPAR-γ agonistic activity by performing multiple regression analysis. Significant correlation coefficients (q² = 0.9178) was obtained. The predicted values are in good agreement with the observed activity, suggesting that the model could be useful in the design of novel, more potent PPAR-γ agonist.Colegio de Farmacéuticos de la Provincia de Buenos Aire

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field