An Overview on the Field of Micro- and Nanotechnologies for Synthetic Peptide-Based Vaccines

18 p.

Extended ageing time and temperature effects on quality of sub-primal cuts of boxed beef

[EN]Most of the information indicating ageing improves tenderness has been collected on the loin and rib-eye muscles over relatively short ageing times, assuming that all muscles will react similarly. In the present study, the effect of extended ageing times on instrumental texture (56 d) and sensory characteristics (42 d) of six different beef sub-primals [striploin (SL), inside round (IR), outside round (OR), eye of round (ER), blade eye (BE) and chuck tender (CT)] was studied. The effects of two ageing temperatures (1and 58C) were also compared. In general, ageing increased tenderness (P<0.05) of SL, BE, ER and CT sub-primals, although BE shear force increased after 42 d of ageing. On the other hand, ageing had no effect on IR tenderness (P<0.05) and resulted in a decrease in tenderness of OR (P<0.05) until day 35, with a later increase after 42 d of ageing. Increasing ageing temperature (58C) had limited effect on tenderness, but ageing time and temperature increases led to lower flavour and higher off-flavour intensity (P<0.05) of the studied sub-primals. These results suggest that cutspecific maximum ageing times and rigid adherence to temperature maximums would be of benefit to optimize postslaughter processes and meat quality

Recognition of Membrane-Bound Fusion-Peptide/MPER Complexes by the HIV-1 Neutralizing 2F5 Antibody : Implications for Anti-2F5 Immunogenicity

13 p.

1-42 beta-Amyloid peptide requires PDK1/nPKC/Rac 1 pathway to induce neuronal death

1-42 beta-Amyloid (A beta(1-42)) peptide is a key molecule involved in the development of Alzheimer's disease. Some of its effects are manifested at the neuronal morphological level. These morphological changes involve loss of neurites due to cytoskeleton alterations. However, the mechanism of A beta(1-42) peptide activation of the neurodegenerative program is still poorly understood. Here, A beta(1-42) peptide-induced transduction of cellular death signals through the phosphatidylinositol 3-kinase (PI3K)/phosphoinositol- dependent kinase (PDK)/novel protein kinase C (nPKC)/Rac 1 axis is described. Furthermore, pharmacological inhibition of PDK1 and nPKC activities blocks Rac 1 activation and neuronal cell death. Our results provide insights into an unsuspected connection between PDK1, nPKCs and Rac 1 in the same signal-transduction pathway and points out nPKCs and Rac 1 as potential therapeutic targets to block the toxic effects of A beta(1-42) peptide in neurons.

Role of G protein coupled inwardly rectifier K+ channels (GIRK) on the neurobiology depression

353 págs.