RESUMEN
Foamed styrene-in-water emulsions can serve as templates for solid polystyrene foams as the pore size dpore in the solid polystyrene foam matches the bubble size dbubble of the liquid foam template. By producing monodisperse foamed emulsions with a microfluidic device it is possible to adjust the pore size, the connectivity of the pores, as well as the density of the solid polystyrene foams. The pore size can be tuned either by varying the gas pressure used to form the emulsion or by varying the chip dimension. Using three different chip dimensions we are able to produce monodisperse polystyrene foams with pore sizes ranging from 115 µm up to 588 µm. The relative density can be varied easily in a range from 0.10 to 0.30. Increasing the liquid fraction leads initially to smaller interconnections and ultimately to a mainly closed cell foam. It is practically impossible to produce a fully closed cell foam since, even at high liquid fractions, two adjacent bubbles eventually touch and form a film that will rupture during polymerization. By closely investigating the structure of the polystyrene foams we noticed an additional porosity in the pore walls which matches the water content of the styrene-in-water emulsion. During polymerization, the styrene droplets in the aqueous matrix fuse and build up a continuous but porous structure which makes up the pore walls of the macropores. This additionally porosity also leads to lower Young's and shear moduli than expected, as predicted by Gibson and Ashby's model. The relationship between relative density and moduli is in good agreement with the model.
RESUMEN
Obesity and type 2 diabetes mellitus are multifactorial health threats caused by a complex interplay between genetic predisposition and the environment with dramatically increasing worldwide prevalence. The role of heritability in their etiology is well recognized, however, the numerous attempts made in order certain genetic variants determining individual susceptibility to be identified have had limited success, until recently. At present the advancements in human genetics and the utilization of the genome-wide association approach have led to the identification of over 20 genetic loci associated with, respectively obesity and type 2 diabetes. Most of the genes identified to date, however, have modest effect on disease risk suggesting that both diseases are unlikely to develop without the individual being exposed to obesity- and/or type 2 diabetes-promoting environment. Indeed, unhealthy lifestyle, characterized by physical inactivity and food overconsumption is an unequivocally established risk factor for obesity and type 2 diabetes. Numerous epidemiological studies and randomized controlled trials, on the other hand, have demonstrated that lifestyle modification is effective in obesity and type 2 diabetes prevention. Furthermore, gene-lifestyle interaction studies suggest that genetic susceptibility to obesity and type 2 diabetes may be partially or totally kept under control by healthy lifestyle or lifestyle modification and that lifestyle determines whether an individual is likely to develop the disease. Inherited factors, however, seem to influence individual response to a lifestyle intervention program and even the motivation for lifestyle change. Personalized interventions according to genotype may be, therefore, considered in the future. By then lifestyle modification targeting dietary change and increased physical activity may be recommended for successful obesity and type 2 diabetes prevention irrespectively of genetic susceptibility.