Anti-CPB2 polyclonal antibody

Thrombin-activable fibrinolysis inhibitor (TAFI) is a plasma zymogen that acts as a molecular link between coagulation and fibrinolysis. Numerous single nucleotide polymorphisms (SNPs) have been identified in CPB2, the gene encoding TAFI, and are located in the 5'-flanking region, in the coding sequences, and in the 3'-untranslated region (UTR) of the CPB2 mRNA transcript. Associations between CPB2 SNPs and variation in plasma TAR antigen concentrations have been described, but the identity of SNPs that are causally linked to this variation is not known. In the current study, we investigated the effect of the SNPs in the 5'-flanking region on CPB2 promoter activity and SNPs in the 3'-UTR on CPB2 mRNA stability. Whereas the 5'-flanking region SNPs (with 2 exceptions) did not have a significant effect on promoter activity, either alone or in haplotypic combinations seen in the human population, all of the 3'-UTR SNPs substantially affected mRNA stability. We speculate that these SNPs, in part, contribute to variation in plasma TAFI concentrations via modulation of CPB2 gene expression through an effect on mRNA stability.

Cases of acute fatal myonecrosis in cattle, reportedly vaccinated with standard blackquarter vaccine were investigated for the etiology. The cultures originating from tissue samples were identified as Clostridium perfringens type A by toxin-antitoxin assay. In in-vitro antibiotic sensitivity test, isolates were sensitive to gentamicin, enrofloxacin, norfloxacin, ampicillin and amoxycillin but resistant to tetracycline, oxytetracycline and bacitracin. No difference in whole cell polypeptide profiles was observed among the isolates in SDS-PAGE. Two different plasmid patterns comprising 2 to 3 plasmids in the range of 2.4-23.1 kb size were found. In PCR, only primer specific for cpa amplified (324 bp) the template DNA out of 6 primers (cpa, cpb, etx, iA, cpe, and cpb2 genes of C. perfringens) used for all the isolates. However, only I isolate was also positive for cpb2 gene. The result thus indicated that the isolates were mostly C. perfringens Type A and rarely beta toxigenic C. perfringens type A. The noninvolvement of gastro-intestinal tract, acute malignant nature of the myonecrosis and presence of the alpha toxin gene in the isolates amply suggested that atypical blackleg was caused by C. perfringens Type A and not by the C. chauvoei.