Anti-CTSH monoclonal antibody, clone BG25E8

Background: Recent preclinical studies demonstrated the potential antiepileptogenic effect of curcumin. Its molecular pathways in modulating epileptogenesis remain unclear. Objectives: This study investigated the epileptogenic processes induced by kainic acid (KA) and to investigate the antiepileptogenic pathways associated with curcumin therapy. Methods: A single dose of KA 10 mg/kg was used to induce a convulsive status epilepticus in female Wistar rats. After one week of curcumin treatment, gene expression profiling by using microarray was conducted on hippocampal tissues. A set of differential expression changes was determined based on criteria of dual fold change in either direction and p < 0.05, whereas gene annotation and pathway analysis had been performed using Database for Annotation, Visualization and Integrated Discovery software. Results: A number of genes significantly altered in expression during KA-induced epileptogenesis. Inflammation and immune response were the prominent overexpressed processes induced by KA. Genes of cell surface molecule (CD74), cytokines and immune response related genes (11.18, IFNGR1, C3, RT1-BA) were significantly up-regulated. Changes of genes related to cell death and gliosis (NCSTN, CTSH) were also observed in KA-induced epileptogenesis. This study revealed that curcumin modulated the epileptogenic process by up-regulating genes related to antiinflammatory cytokines (IL10RB, CXCL16, and CXCL17) and protecting against cell loss by up-regulating NCSTN. It was also likely to exert neuroprotective effects through the up-regulation of CX3CL1 and CXCL16. Conclusion: This study provides novel insights into the mechanisms of curcumin in epileptic brain, which form the basis for future studies looking into its molecular pathway as an antiepileptogenic agent.

Thyroglobulin autoantibody (TGAA) was measured in serum from dogs with hypothyroidism (n = 42), non-thyroidal illness (NTI) (n = 77) and clinically healthy dogs (n = 70) using a commercially available enzyme immunoassay kit. Precision studies were consistent with good intra-assay and inter-assay repeatability. TGAA positive results occurred in 15 of the 42 (36 per cent) hypothyroid and four healthy dogs of the remaining 147 animals resulting in a lower incidence of false positive results than obtained with previous TGAA assays. The presence of TGAA was not influenced by age, sex, neutering or pedigree status. Of the four apparently healthy TGAA-positive dogs, two had additional clinicopathological evidence of hypothyroidism. TGAA was positive in 43 per cent of hypothyroid dogs with unexpectedly normal serum CTSH concentrations and was particularly useful in the classification of these cases.