Glycaemic Control in Patients Undergoing Percutaneous Coronary Intervention: What Is the Role for the Novel Antidiabetic Agents? A Comprehensive Review of Basic Science and Clinical Data

Coronary artery disease (CAD) remains one of the most important causes of morbidity and mortality worldwide, and revascularization through percutaneous coronary interventions (PCI) significantly improves survival. In this setting, poor glycaemic control, regardless of diabetes, has been associated with increased incidence of peri-procedural and long-term complications and worse prognosis. Novel antidiabetic agents have represented a paradigm shift in managing patients with diabetes and cardiovascular diseases. However, limited data are reported so far in patients undergoing coronary stenting. This review intends to provide an overview of the biological mechanisms underlying hyperglycaemia-induced vascular damage and the contrasting actions of new antidiabetic drugs. We summarize existing evidence on the effects of these drugs in the setting of PCI, addressing pre-clinical and clinical studies and drug-drug interactions with antiplatelet agents, thus highlighting new opportunities for optimal long-term management of these patients.     

What Molecular Recognition Systems Do Mesenchymal Stem Cells/Medicinal Signaling Cells (MSC) Use to Facilitate Cell-Cell and Cell Matrix Interactions? A Review of Evidence and Options

Mesenchymal stem cells, also called medicinal signaling cells (MSC), have been studied regarding their potential to facilitate tissue repair for >30 years. Such cells, derived from multiple tissues and species, are capable of differentiation to a number of lineages (chondrocytes, adipocytes, bone cells). However, MSC are believed to be quite heterogeneous with regard to several characteristics, and the large number of studies performed thus far have met with limited or restricted success. Thus, there is more to understand about these cells, including the molecular recognition systems that are used by these cells to perform their functions, to enhance the realization of their potential to effect tissue repair. This perspective article reviews what is known regarding the recognition systems available to MSC, the possible systems that could be looked for, and alternatives to enhance their localization to specific injury sites and increase their subsequent facilitation of tissue repair. MSC are reported to express recognition molecules of the integrin family. However, there are a number of other recognition molecules that also could be involved such as lectins, inducible lectins, or even a MSC-specific family of molecules unique to these cells. Finally, it may be possible to engineer expression of recognition molecules on the surface of MSC to enhance their function in vivo artificially. Thus, improved understanding of recognition molecules on MSC could further their success in fostering tissue repair.     

The Impact of Water on CO Oxidation with Au/TiO<Subscript>2</Subscript> Catalysts: Poison or Promotor? A Study with an Au–TiO<Subscript>2</Subscript>/MCM-48 Model Catalyst

Abstract  

CO oxidation was studied with a model catalyst containing Au and TiO _x nanoaggregates confined in a siliceous MCM-48 host. With this material, which has a particular small ratio between the TiO _x and Au components, activities well comparable to those of unconfined Au/TiO₂ catalysts were obtained in particular when a thermal activation in inert gas at temperatures between 523 and 673 K was applied. When the subsequent catalytic tests were performed in a feed containing ca. 20 ppm H₂O, strong deactivation phenomena were observed which could be reverted by repeated thermal treatment and are most likely caused by carbonate deposition. This deactivation was strongly attenuated when the water content of the feed was decreased to ca. 6 ppm, which suggests that water plays an important role in the formation of the poisoning species. With unconfined Au/TiO₂ catalysts, a promoting role of water on the formation of catalyst poison was observed as well, but to a much lower extent. The effect may therefore have escaped undetected so far as a contribution to the well-known catalyst deactivation by carbonate species.