Rabbit Anti-Human Tie2 (a.a. 401-550) Polyclonal antibody

In 2013, the European Union (EU) allowed the inclusion of non-ruminant processed animal proteins (PAP) in fish feeds. Plans also exist to allow non-ruminant PAP in poultry and pig feeds but to keep intraspecies recycling forbidden (e.g. poultry to poultry or pig to pig). However, due to the fear of transmissible spongiform encephalopathy (TSE), PAP from ruminant species remains illegal to use in feeds. To ensure feed safety, nations across Europe need to safeguard that commercial fish feeds do not contain PAP from ruminant species. In this work we report a multi-laboratory study on the detection of ruminant PAP in commercial PAP feed ingredients. A total of 19 non-ruminant PAP, provided by the European Fat Processors and Renderers Association (EFPRA), were analyzed for ruminant content with the European Union Reference Laboratory (EURL)-validated PCR assay by three labs and compared to the result obtained with an. immunoassay-based method (MELISA-TEK). Ruminant PAP was detected in five of the 19 non-ruminant PAP samples with both methods, but there were methodological and multi laboratory differences for the PCR method. Compared to the results with the EU-reference laboratory, 3 false-negatives were found by the two other laboratories. We speculate that the discrepancies seen for some of the samples determined with the PCR method rely on the homogenization and grinding step, which is not described in detail in the EURL Standard Operating Procedure (SOP), shift in the normal distribution of Ct-values near the cut-off of the PCR method, or PCR inhibition. In conclusion, this study demonstrates the presence of ruminant DNA in commercially available non-ruminant PAP by use of two methods for the detection of PAP in commercial feed ingredients, and highlights the importance of thorough homogenization prior to DNA extraction and assessment of normal distribution of Ct-values for successful PCR detection at low ruminant DNA contamination levels. (C) 2016 Elsevier Ltd. All rights reserved.

Purpose: A leading cause of blindness worldwide, glaucoma is often caused by elevated intraocular pressure (IOP) due to impaired aqueous humor outflow from the anterior chamber through Schlemm's canal (SC) and the trabecular meshwork. Despite the large clinical burden, glaucoma research and drug development are hindered by a limited selection of preclinical models that accurately recapitulate human disease. Here, we propose that Angpt1 conditional knockout mice may provide one such model. Angiopoietin/TEK (ANGPT/TEK) signaling is crucial for SC formation and integrity in mice and humans, and mice lacking TEK or its ligand ANGPT1 develop a hypomorphic SC insufficient for normal aqueous humor outflow. Methods: We used a comprehensive histology and physiology approach to characterize the glaucoma phenotype of Angpt1 inducible knockout mice, especially focusing on retina morphology and function. Results: Angpt1 deletion resulted in persistent ocular hypertension beginning in the first month after birth and leading to decreased visual acuity with age due to glaucomatous neuropathy. In the neural retina, we identified marked and specific loss of the retinal ganglion cells, whereas other retinal neurons exhibited largely normal morphology and patterning. Electroretinogram recordings demonstrated reduced scotopic threshold response, further indicating loss of retinal ganglion cell function. Conclusions: These findings highlight the potential of Angpt1 conditional knockout mice as a valuable new glaucoma model. Translational Relevance: Currently, few reliable, rapid-onset genetic glaucoma models are available, and Angpt1 knockout mice will provide an additional tool for studies of IOP-induced neural damage, mechanisms of disease progression, and novel treatment strategies.