Results 1 - 10 of 2574
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[en] Successful development of radiopharmaceuticals from monoclonal antibodies will require the control of several immunochemical aspects of the antibody molecules. A proposed set of methods is presented here for evaluating these immunochemical parameters. This approach consists of monitoring each monoclonal antibody harvest by selective affinity chromatography to determine the presence of detectable alterations in molecular homogeneity. The products are then evaluated by radioimmunoassay technique standardized for total immunoglobulin immunoreactivity. These assays are utilized to detect variation in the immunoreactivity secondary to changes in the hybridoma cell lines, and to measure any detectable denaturation secondary to purification, fragment production and radiolabeling. HPLC molecular sieving chromatography is presented as a practical and informative monitor of molecular stability of these radiopharmaceuticals in vitro and in vivo. (author)
[en] Infection with pathogens activates the endothelial cell and its sustained activation may result in impaired endothelial function. Endothelial dysfunction contributes to the pathologic angiogenesis that is characteristic of infection-induced inflammatory pathway activation. Nucleotide-binding oligomerization domain-containing protein 1 (NOD1) is a protein receptor which recognizes bacterial molecules and stimulates an immune reaction in various cells; however, the underlying molecular mechanisms in the regulation of inflammation-triggered angiogenesis are not fully understood. Here we report that peroxisome proliferator-activated receptor gamma (PPARγ)-mediated miR-125a serves as an important regulator of NOD1 agonist-mediated angiogenesis in endothelial cells by directly targeting NOD1. Treatment of human umbilical vein endothelial cells with natural PPARγ ligand, 15-Deoxy-Delta12,14-prostaglandin J2, led to inhibition of NOD1 expression; contrarily, protein levels of NOD1 were significantly increased by PPARγ knockdown. We report that PPARγ regulation of NOD1 expression is a novel microRNA-mediated regulation in endothelial cells. MiR-125a expression was markedly decreased in human umbilical vein endothelial cells subjected to PPARγ knockdown while 15-Deoxy-Delta12,14-prostaglandin J2 treatment increased the level of miR-125a. In addition, NOD1 is closely regulated by miR-125a, which directly targets the 3′ untranslated region of NOD1. Moreover, both overexpression of miR-125a and PPARγ activation led to inhibition of NOD1 agonist-induced tube formation in endothelial cells. Finally, NOD1 agonist increased the formation of cranial and subintestinal vessel plexus in zebrafish, and this effect was abrogated by concurrent PPARγ activation. Overall, these findings identify a PPARγ-miR-125a-NOD1 signaling axis in endothelial cells that is critical in the regulation of inflammation-mediated angiogenesis. - Highlights: • Expression of NOD1 is regulated by PPARγ signaling in HUVECs. • PPARγ-regulated NOD1 expression is mediated at least in part by of miR-125a. • NOD1 is a novel target gene of miR-125. • miR-125a inhibits inflammation induced angiogenesis in HUVECs. • PPARγ activation inhibits inflammation mediated angiogenesis in vitro and in vivo.
[en] The clinical evaluation of a meningococcal polysaccharide vaccine containing groups A, C, Y, and W135 antigens was described. The vaccine was found to be clinically acceptable and a significant antibody response was detected by both a bactericidal assay and a solid-phase radioimmune assay
[en] Lymphocytes were isolated from mouse spleen. Expression of MBLA-antigen (mouse bone marrow lymphocyte antigen) and theta(Thy-1)-antigen increased under UVC (254 nm, 450 J.m-2) or UVA (365 nm, 40 kJ.m-2) radiation. Antioxidants (AO) α-tocopherol or butylated hydroxytoluene (BHT) decreased the effects of UVA and UVC. Antioxidants exert their effects almost equally when added to lymphocyte suspension before and after irradiation. The increase in expression of lymphocyte surface antigens may be caused directly by the dark process of lipid peroxidation, which develops in plasma lymphocyte membranes after irradiation. (orig.)
[en] Macrophage activation syndrome (MAS) is a rare disorder characterised by benign, reactive, excessive, well-differentiated macrophage proliferation, secondary to an immune dysregulation in response to some triggering agents such as viral infection. We report a 3-year-old girl with MAS and pulmonary involvement. This is the first radiographic description of MAS on high-resolution CT. (orig.)