Recombinant Human BSG (a.a.138-323) [hFc]

The aim of this study was to investigate the possibility of application of brewer's spent grain (BSG), sugar beet pulp (SBP) and apple pomace (AP) in production of corn snack products. Additionally, in the case of BSG and SBP the pectin (0.5% and 1% d. m.) was added in an attempt to resolve the problems of poor expansion and textural properties. Samples were extruded in the laboratory single screw extruder, and physical and sensory properties of obtained extrudates were determined. By-products addition decreased expansion ratio and fracturability, whereas bulk density and hardness increased. Pectin addition at level of 1% resolved the problem of poor expansion in the extrudates with BSG and SBP, which resulted in successful incorporation of all three by-products in the production of acceptable expanded corn snack products. By-products addition and extrusion process had a significant effect on color change, water absorption and water solubility indexes. Industrial relevance: The production of nutritionally fortified snack products, with the acceptable physical and sensory properties is challenging. The addition of high-fibre and high-protein ingredients to starch based raw materials significantly affects the texture, expansion and overall acceptability of extruded snacks. This study provided a novel and effective way to resolve these problems in production of corn extrudates enriched with food industry by-products, by pectin addition. Furthermore, this investigation could partially help in the disposal of waste from the food industries in which the investigated by-products (brewer's spent grain, sugar beet pulp and apple pomace) are formed in large quantities.

Podocytes, which are susceptible to injury by various stimuli and stress, are critical regulators of proteinuric kidney diseases, regardless of the primary disease and pathogenesis. We further confirmed a significant correlation between urinary CD147/basigin (Bsg) levels and proteinuria in patients with focal segmental glomerulosclerosis. However, the molecular mechanism of podocyte injury involving Bsg is not fully understood. Here, the involvement of Bsg in the pathogenesis of podocyte injury was elucidated. Healthy podocytes rarely express Bsg protein. In two independent mouse models, including adriamycin-induced nephropathy and N-omega-nitro-t-arginine methyl ester (L-name)-induced endothelial dysfunction, Bsg induction in injured podocytes caused podocyte effacement, which led to development of proteinuria. Bsg silencing in cultured podocytes exposed to transforming growth factor-beta suppressed focal adhesion rearrangement and cellular motility via the activation of beta(1) integrin-focal adhesion kinase-matrix metallopeptidase signaling. In addition, induction of vascular endothelial growth factor and endothelin-1, which are implicated in podocyte-to-endothelial cross-communication, was lower in the supernatants of cultured Bsg-silenced podocytes stimulated with transforming growth factor-beta. In this setting, Bsg may be involved in a physiological positive feedback loop that accelerates podocyte cell motility and depolarization. The current study thus suggests that Bsg silencing via suppression of beta(1) integrin-focal adhesion kinase matrix metallopeptidase signaling may be an attractive therapeutic strategy for the maintenance of podocytes in patients with proteinuric kidney diseases.