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“Disadvantages of the regulatory pyrogen test to assure safety of the end-product Human Serum Albumin (HSA) for parenteral use call for the implementation of an alternative test. In the current study, 16 HSA batches were assayed for pyrogens in parallel with the Rabbit Pyrogen Test, conventional and endotoxin-specific LAL assay and monocyte activation test (MAT).\n\nIt was found that all HSA batches were contaminated with (1,3)-beta-glucans, which interfere with the conventional LAL. Endotoxin-specific

LAL was not suitable to test HSA due to unacceptable endotoxin recovery. Experiments combining polymyxin B and MAT demonstrated that pyrogenic batches were mainly contaminated with endotoxins. However, endotoxin-specific LAL failed to detect this website one of them. The contaminating (1,3)-beta-glucans enhanced the MAT/IL-6 response to endotoxin, but not that of MAT/IL-1 beta. The endotoxin equivalent concentrations obtained using the IL-6 readout were usually higher

than those using IL-1 beta, probably owing to the direct induction of IL-6 release from monocytes by (1,3)-beta-glucans.\n\nThe MAT correlates with the rabbit pyrogen test, providing a higher safety APR-246 mouse level for pyrogenicity testing of HSA and probably other therapeutic proteins.”
“Nucleophosmin (NPM) is a nucleolar protein involved in ribosome biogenesis. NPM1 gene is frequently mutated in acute myeloid leukaemia (AML), correlating with aberrant cytoplasmic localization of the protein. NPM attachment

to the nucleolus in physiological conditions probably depends on binding to nucleic acids, and this recognition could be altered in AML. NPM associates to guanine-rich DNA sequences, able to fold as “G-quadruplexes”. We have analyzed the interaction of pentameric, full length NPM with https://www.selleckchem.com/products/pnd-1186-vs-4718.html G-rich oligonucleotides, finding that the protein binds preferentially high-order G-quadruplexes. AML-associated mutation significantly hampers DNA binding, pointing to a possible mechanism contributing to pathological mislocalization of NPM. (C) 2013 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.”
“Alpha (alpha)-synuclein neuronal effects are continually being defined although its role in regulating glial phenotypes remains unclear. An ability to regulate microglial activation was investigated using primary cultures from wild type and alpha-synuclein deficient mice (Snca (-/-)).