Basic study on reaction products in ASR with Raman spectroscopy

Alkali-silica reaction (ASR) can be considered to be a serious durability concern for concrete structures. At this point, to avoid ASR, the use of non-reactive aggregate is advised, or the use of low alkali cement or blended cement, or cement of limited alkali content is recommended. However, complete avoidance of ASR over long time periods is difficult and the precise mechanism of ASR remains unclear. So far, our research group have studied the properties of reactive aggregate and ASR products with Raman spectroscopy. As a result, formation of a large amount of CaCO3, in addition to Na2O-SiO2 was observed around aggregates in accelerated test specimens. Initial results in this study showed a difference in the reaction products formed between accelerated tests and real-life samples, when examined using Raman spectroscopy. Subsequently, in order to consider the reasons for this difference, a series of samples were prepared by reacting calcium ions with sodium silicate solutions of varying Na2O/SiO2 ratios. The results clearly showed that the difference in behaviour between artificial and real samples was due to changes in the sodium contents of the products

Activation of peroxisome proliferator-activated receptor δ induces fatty acid β-oxidation in skeletal muscle and attenuates metabolic syndrome

In this study, we defined the role of peroxisome proliferator-activated receptor β/δ (PPARδ) in metabolic homeostasis by using subtype selective agonists. Analysis of rat L6 myotubes treated with the PPARδ subtype-selective agonist, GW501516, by the Affymetrix oligonucleotide microarrays revealed that PPARδ controls fatty acid oxidation by regulating genes involved in fatty acid transport, β-oxidation, and mitochondrial respiration. Similar PPARδ-mediated gene activation was observed in the skeletal muscle of GW501516-treated mice. Accordingly, GW501516 treatment induced fatty acid β-oxidation in L6 myotubes as well as in mouse skeletal muscles. Administration of GW501516 to mice fed a high-fat diet ameliorated diet-induced obesity and insulin resistance, an effect accompanied by enhanced metabolic rate and fatty acid β-oxidation, proliferation of mitochondria, and a marked reduction of lipid droplets in skeletal muscles. Despite a modest body weight change relative to vehicle-treated mice, GW501516 treatment also markedly improved diabetes as revealed by the decrease in plasma glucose and blood insulin levels in genetically obese ob/ob mice. These data suggest that PPARδ is pivotal to control the program for fatty acid oxidation in the skeletal muscle, thereby ameliorating obesity and insulin resistance through its activation in obese animals