Animal dietary exposure : overview of current approaches used at EFSA

At EFSA, animal dietary exposure estimates are undertaken by several Panels/Units to assess the risk of feed contaminants, pesticide residues, genetically modified feed and feed additives. Guidance documents describing methodologies for animal dietary exposure assessment are available both at EFSA and international levels. Although appropriate within pertinent regulatory frameworks, the methodologies used to assess animal dietary exposure vary across risk assessment areas. There are different approaches ranging from quick worst-case estimations to more refined methods assessing actual exposure, resulting from the use of a heterogeneous selection of animal populations and default values to estimate feed intake. Furthermore, current feed classification systems in place at international and national levels contain a large and heterogeneous number of feed materials, which may benefit from further harmonisation efforts. This technical report presents an overview of the current approaches in place at EFSA to assess the exposure to chemicals in feed. The possibility for a greater harmonisation of feed classification and terminology is also addressed by comparing the structure of the EU catalogue of feed materials and the Harmonised OECD tables of feedstuffs derived from field crops with the EFSA FoodEx2 system

Tumor protein D52 (TPD52): A novel B-cell/plasma-cell molecule with unique expression pattern and Ca2+-dependent association with annexin VI

We generated a murine monoclonal antibody (B28p) detecting an antigenic determinant shared by the immunoglobulin superfamily receptor translocation-associated 1 (IRTA1) receptor (the immunogen used to raise B28p) and an unrelated 28-kDa protein that was subsequently subjected to extensive characterization. The expression of the 28-kDa protein in normal lymphohematopoietic tissues was restricted to B cells and plasma cells and clearly differed from that expected for IRTA1 (selectively expressed by mucosa-associated lymphoid tissue [MALT] marginal zone B cells). Two-dimensional polyacrylamide gel electrophoresis (2D-PAGE)/mass-spectrometry analysis identified the 28-kDa protein as human tumor protein D52 (TPD52), whose expression had been previously described only in normal and neoplastic epithelia. Specific B28p reactivity with TPD52 was confirmed by immunostaining/immunoblotting of TPD52-transfected cells. TPD52 expression pattern in normal and neoplastic B cells was unique. In fact, unlike other B-cell molecules (paired box 5 [PAX5], CD19, CD79a, CD20, CD22), which are down-regulated during differentiation from B cells to plasma cells, TPD52 expression reached its maximum levels at the plasma cell stage. In the Thiel myeloma cell line, TPD52 bound to annexin VI in a Ca2+-dependent manner, suggesting that these molecules may act in concert to regulate secretory processes in plasma cells, similarly to what was observed in pancreatic acinar cells. Finally, the anti-TPD52 monoclonal antibody served as a valuable tool for the diagnosis of B-cell malignancies

The anti-inflammatory activity of estrogen in glial cells is regulated by the PKC-anchoring protein RACK-1

It has recently been suggested that estrogen inhibits glial activation and the release of neurotoxic mediators. The mechanisms involved in this anti-inflammatory effect are unclear. We found that an nM concentration of 17-\u3b2 estradiol inhibits protein kinaseC-\u3b2II translocation induced by lipopolysaccharide in primary astrocytes. Estradiol treatment did not change the total content of kinaseC-\u3b2II or of lipopolysaccharide receptor, but dose-dependently reduced the levels of receptors for activated C kinases-1 (RACK-1), the anchoring protein involved in protein kinase C (PKC) shuttling. This decrease could thus account for the defective protein kinaseC-\u3b2II activation. Pre-treatment with 1 nM \u3b2-estradiol, which reduced by 3c35% the expression of RACK-1, prevented the lipopolysaccharide-induced expression of tumour necrosis factor-\u3b1 mRNA and of the inducible form of nitric oxide (NO) synthase. As a consequence, the production of tumour necrosis factor-\u3b1 and NO were decreased. An antisense oligonucleotide for RACK-1 also reduced tumour necrosis factor-\u3b1 and nitric oxide production on lipopolysaccharide stimulation. These results demonstrate that estrogen reduction of the RACK-1 expression, leading to a defective protein kinase-C activation counteracts the inflammatory response in astrocytes