Anti-F13A1 monoclonal antibody, clone MAAG4331

Highly polymorphic microsatellite markers provide useful genetic markers for detection of complete or mixed chimerism in patients after allogeneic BMT (allo-BMT). We report application of automated DNA sizing technology for detection of post-BMT chimerism using fresh peripheral blood, BM, or archival blood smears and various DNA isolation techniques. Donors' and recipients' DNA was amplified with fluorescent PCR primers specific for short tandem repeat (STR) marker loci: FGA, VWA, TH01, F13A1, D21S11. Chimerism was assessed in 14 recipients after allo-BMT. A complete chimerism was detected in 10 patients, in 3 patients we observed fluctuations of chimerism status, and mixed chimerism was assessed in 1 patient. We show that DNA from different types of biologic specimens (whole peripheral blood, BM suspension, archival blood smears), prepared according to the various isolation techniques (salting-out method, phenol chloroform extraction, Chelex procedure) and amplified with fluorescent PGR primers for microsatellite markers, enable identification of chimerism status following allo-BMT in children.

Factor XIIIA (FXIIIA) levels are independent predictors of early prognosis after acute myocardial infarction (AMI) and the Valine-to-Leucine (V34L) single nucleotide polymorphism (SNP) seems associated with lower AMI risk. Since the long-term AMI prognosis merits deeper investigation, we performed an observational study evaluating relationships between FXIIIA residual levels, cardiovascular risk-factors, and inherited genetic predispositions. FXIIIA V34L was genotyped in 333 AMI patients and a five-year follow-up was performed. FXIIIA levels assessed at day-zero (d0) and four days after AMI (d4), and conventional risk factors were analyzed, focusing on the development of major adverse cardiovascular events (MACE). FXIIIA assessed at d0 and d4 was also an independent MACE predictor in the long-term follow-up (FXIIIA(d0), Odds Ratio (OR) = 3.02, 1.79-5.1, p = 0.013; FXIIIA(d4), OR = 4.46, 2.33-8.55, p = 0.0001). FXIIIA(d4) showed the strongest MACE association, suggesting that the FXIIIA protective role is maximized when high levels are maintained for longer time. Conversely, FXIIIA levels stratified by V34L predicted MACE at a lesser extent among L34-carriers (Hazard Risk (HR)(VV34) = 3.89, 2.19-6.87, p = 0.000003; HRL34-carriers = 2.78, 1.39-5.57, p = 0.0039), and V34L did not predict all MACE, only multiple-MACE occurrence (p = 0.0087). Finally, in survival analysis, heart failure and death differed significantly from stroke and recurrent ischemia (p = 0.0013), with FXIIIA levels appreciably lower in the former (p = 0.05). Overall, genetically-determined FXIIIA levels have a significant long-term prognostic role, suggesting that a pharmacogenetics approach might help to select those AMI patients at risk of poor prognosis in the need of dedicated treatments.