Assessment of Hardness Based on Phase Diagrams

This chapter summarizes the methodology and development of a general equation, in order to obtain a series of equations to assess the hardness of different Al-Cu-Zn alloys, based on their chemical composition. This methodology produces an assessment of hardness with a maximal deviation of 5%, in as-cast, homogenized and quenching alloys, for both alloys created in laboratories like commercials. This method entails the generation of linear equations by a linear regression method, obtained from a zone of the phase diagram, when the composition is changed from linear to planar form. Therefore, if the chemical composition of samples varies, the percentage of each phase will also vary, causing a change in mechanical properties in a linear manner. If the heat treatments are the same for all samples, then the changes in mechanical properties are proportional for each of them, maintaining the linear relationship in mechanical properties in accordance with chemical composition. This methodology is applicable for any ternary alloy along with its equilibrium diagram

Tyrphostin AG17 inhibits adipocyte differentiation in vivo and in vitro

Abstract Background Excessive subcutaneous adiposity in obesity is associated to positive white adipocyte tissue (WAT) differentiation (adipogenesis) and WAT expandability. Here, we hypothesized that supplementation with the insulin inhibitor and mitochondrial uncoupler, Tyrphostin (T-AG17), in vitro and in vivo inhibits adipogenesis and adipocyte hypertrophy. Methods We used a 3T3-L1 proadipocyte cell line to identify the potential effect of T-AG17 on adipocyte differentiation and fat accumulation in vitro. We evaluated the safety of T-AG17 and its effects on physiological and molecular metabolic parameters including hormonal profile, glucose levels, adipogenesis and adipocyte hypertrophy in a diet-induced obesity model using C57BL/6 mice. Results We found that T-AG17 is effective in preventing adipogenesis and lipid synthesis in the 3T3-L1 cell line, as evidenced by a significant decrease in oil red staining (p < 0.05). In obese C57BL/6 mice, oral administration of T-AG17 (0.175 mg/kg for 2 weeks) lead to decreased fat accumulation and WAT hypertrophy. Further, T-AG17 induced adipocyte apoptosis by activating caspase-3. In the hepatocytes of obese mice, T-AG17 promoted an increase in the size of lipid inclusions, which was accompanied by glycogen accumulation. T-AG17 did not alter serum biochemistry, including glucose, insulin, leptin, free fatty acids, creatinine, and aspartate aminotransferase. Conclusion T-AG17 promotes adipocyte apoptosis in vivo and is an effective modulator of adipocyte differentiation and WAT hypertrophy in vitro and in vivo. Therefore, T-AG17 may be useful as a pharmacological obesity treatment