In the in vitro model of thrombolysis designed by ourselves, urokinase (500 000~ 5 000 000IU ? L-1) reduced the weight of artificial thrombi in a way of dose-dependence. At the level of 2 000 000 IU ? L-1, the action reached the peak. On the contrary, defibrase (6. 25~25 IU ? L-1) dose-relatedly increased the thrombus weight. After defibrinogenation in platelet-poor plasma by addition of porcine thrombin (100 000 IU ? L-1) , defibrase no longer increased the thrombus weight, whereas in comparison with saline, defibrase still showed no apprciable reduction in thrombus weight. The findings hinted that defibrase may have no direct thrombolytic property.

AIM: To observe the effects of cimetidine(Cim) on platelet function and thrombosis. METHODS: After incubated with Cim in vitro , rat platelets were activated with ADP or thrombin. The platelet aggregation, platelet malondialdehyde(MDA) formation, platelet intracellular free calcium([Ca 2+ ] i), and thromboxane B 2 (TXB 2) were measured. The effects of Cim on electric-induced thrombosis in rat carotid artery were examined. RESULTS: Cim potentiated ADP induced platelet aggregation , increased the thrombin induced [Ca 2+ ] i and MDA formation, decreased TXB 2. Also, Cim shortened the duration of electric-stimulated occlution time in rat carotid artery. CONCLUSION: Cim increased platelet function and accelerated thrombosis.

Objective: To analyze the characteristics of immunoglobulin heavy chain complementarity-determining region (IgH-CDR3) repertoire of peripheral B cells in a patient with primary biliary cholangitis (PBC) and to investigate the diversity of the immune system. Methods: Arm-PCR was used to amplify the IgH-CDR3 region of circulating B cells isolated from a PBC patient, and high-throughput sequencing was used to analyze the amplified product. The characteristics of immune repertoire were analyzed by bioinformatics. Results: In total, 329219 sequence reads were generated from the sample, with 325540 total CDR3 sequences and 72774 distinct CDR3 sequences, and the D50 of IGH-CDR3 was 7.7. The dominant CDR3 length of the sample was 45 nt (9.6%); the N addition with the highest frequency ranged from 13 to 14 nt (5.25%); the J trimming with the highest frequency was 0 nt (12.7%); the three most frequent V alleles were V4-59 (9.5%), V3-23 (8.1%), and V1-69 (6.4%). Conclusion The diversity of IgH-CDR3 repertoire is relatively low in this patient with PBC, with several B-cell clonal expansions. The specificity needs to be further verified after increasing the sample size.