https://www.selleckchem.com/products/Adriamycin.html Building on an improved theoretical understanding, we analysed the robustness of 489 E. coli, Shigella, Salmonella, and fungal genome-scale metabolic models (GSMMs). In contrast to the popular "congruence theory", which explains the origin of genetic robustness as a byproduct of selection for environmental flexibility, we found no correlation between network robustness and the diversity of growth-supporting environments. On the contrary, our analysis indicates that amino acid synthesis rather than carbon metabolism dominates metabolic robustness.Biofilm growth is a widespread mechanism that protects bacteria against harsh environments, antimicrobials, and immune responses. These types of conditions challenge chronic colonizers such as Helicobacter pylori but it is not fully understood how H. pylori biofilm growth is defined and its impact on H. pylori survival. To provide insights into H. pylori biofilm growth properties, we characterized biofilm formation on abiotic and biotic surfaces, identified genes required for biofilm formation, and defined the biofilm-associated gene expression of the laboratory model H. pylori strain G27. We report that H. pylori G27 forms biofilms with a high biomass and complex flagella-filled 3D structures on both plastic and gastric epithelial cells. Using a screen for biofilm-defective mutants and transcriptomics, we discovered that biofilm cells demonstrated lower transcripts for TCA cycle enzymes but higher ones for flagellar formation, two type four secretion systems, hydrogenase, and acetone metabolism. We confirmed that biofilm formation requires flagella, hydrogenase, and acetone metabolism on both abiotic and biotic surfaces. Altogether, these data suggest that H. pylori is capable of adjusting its phenotype when grown as biofilm, changing its metabolism, and re-shaping flagella, typically locomotion organelles, into adhesive structures. Canine mammary carcinoma (CMC) has been