Rabbit Anti-Mouse Serpinc1 (a.a. 33-465) Polyclonal antibody

Inherited antithrombin (AT) deficiency is a rare autosomal disease that could increase the risk of venous thromboembolism (VTE) and usually caused by mutations of SERPINC1. Although a number of mutations of SERPINC1 have been reported in Chinese Han population, the impact of different subtypes of these mutations on the thrombotic phenotype is still unknown. Here, we performed a retrospective cohort study including 169 AT patients from 63 families to compare the clinical features between null mutation carriers and missense mutation carriers. We found that patients carrying null mutations have a higher risk of VTE (HR 2.29, 95% CI 1.16-4.69, P = 0.02 adjusted for sex and VTE family history) and earlier median onset age of VTE (27 vs. 32 years, P = 0.045) as well as lower AT activities (47.6 +/- 1.0% vs. 59.1 +/- 2.3%, P < 0.001) than those with missense mutations. We also observed that thrombus location sites showed no difference between null mutation carriers and missense mutation carriers, gene locations of the mutations did not relate with the incidence rate of VTE. This study demonstrated that different types of SERPINC1 mutations may play different roles in the development of VTE and should be considered in the prevention of VTE. (C) 2016 Published by Elsevier Inc.

Echinococcosis is a worldwide anthropozoonosis which is highly endemic over large animal husbandry areas in northwestern China. The current clinical therapeutic medicine against echinococcosis is albendazole, although it caused serious side effects in patients. The component in traditional Chinese herb medicine, Sophora moorcroftiana alkaloids (SA), is thought to be a potential drug to treat echinococcosis. In order to explore the effect and mechanism of SA treatment against echinococcosis, we established animal echinococcosis model and treated rats with albendazole alone, alkaloids alone, and combined therapy. The combined treatment showed effective inhibition against parasite infection due to induction of host response and alleviated liver injury; meanwhile albendazole caused serious liver problem. The proteomics study revealed that the combined therapy might induce complement activation through C3, C4, C5, SERPINA1, and SERPINC1 proteins and cell adhesion by ANXA2, EZR, YWHAB, HSP90AN1, and PRKAR2A proteins, while albendazole treatment could induce liver injury through CRYAB, YWHAZ, SLC25A24, and HSPA1B proteins that were involved in cell death. In all, we consider that the combinational treatment displayed better therapeutic effects against liver echinococcosis as well as alleviated liver injury, which could be considered as an effective strategy to treat echinococcosis clinically.