OBJECTIVETo examine the procoagulant effects of thrombolytic agent on hemostasis and study the role of hemostatic markers as predictors of clinical outcomes.

METHODSIn the present study, eighteen patients with acute myocardial infarction (AMI) received 1.5 or 2.0 million U nonspecific urokinase (UK), or 70 approximately 80 mg fibrin-specific recombinant tissue plasminogen activator (rt-PA) and did not use heparin until 8 hours after intravenous injection of the above agents. Eight patients with AMI and without thrombolytic therapy were enrolled as controls. Coagulant and thrombolytic activity markers included thrombin-antithrombin III complex (TAT), D-dimer, fibrinogen (Fg), FMPV/Amax. All markers were determined before, immediately, 1, 2, 4 and 8 hours after the administration of thrombolytic agents respectively.

RESULTSMolecular marker of thrombin generation--TAT showed an activated coagulant state immediately after thrombolytic therapy. Level of TAT showed no significant changes between every two observed phases in controls. However, level of TAT increased significantly from 4.95 +/- 1.75 microg/L ( 4.63 +/- 1.37 microg/L) to 14.71 +/- 3.31 microg/L (14.25 +/- 2.53 microg/L) before and immediately after administration of thrombolytic agents UK (or rt-PA). There was significant difference between level of serum TAT of patients with and without thrombolytic therapy (P < 0.05). Patients achieving clinical reperfusion had lower TAT level than those failing in thrombolytic therapy, and higher FMPV/Amax level than controls. D-dimer, a surrogate of thrombolytic activity increased markedly and Fg significantly declined after thrombolytic therapy (P < 0.05).

CONCLUSIONSThrombin generation occurred in plasma in response to excess fibrinolysis induced by thrombolytic therapy. Both urokinase and rt-PA had procoagulant action. This transient activation of the coagulant system might contribute to early reocclusion. These data provided the theoretical support for simultaneous administration of anticoagulant therapy with thrombolytic agents. These results also suggested that TAT might be useful in predicting clinical outcomes of patients treated with thrombolytic therapy for AMI.

Aged ; Antithrombin III ; Biomarkers ; blood ; Female ; Fibrin Fibrinogen Degradation Products ; metabolism ; Fibrinogen ; metabolism ; Fibrinolytic Agents ; therapeutic use ; Humans ; Male ; Middle Aged ; Myocardial Infarction ; blood ; drug therapy ; Peptide Hydrolases ; blood ; Recombinant Proteins ; therapeutic use ; Thrombolytic Therapy ; Tissue Plasminogen Activator ; therapeutic use ; Urokinase-Type Plasminogen Activator ; therapeutic use

We designed and constructed a fuse expression gene OAAT and staphylococcal enterotoxin A (SEA) on the basis of the OAAT designed and constructed which consists of the structural protein VP1 genes from serotypes A and O FMDV, 5 major VP1 immunodominant epitopes from two genotypes of Asia1 serotype, and 3 Th2 epitopes originating from the non-structural protein, 3ABC gene and structural protein VP4 gene. The recombinant plasmids pEA was constructed using SEA as a genetic adjuvant. Expressions of target gene from the pEA in Hela cell were verified by IFA and Western blotting. The experiment of BALB/c mice immunized with the DNA vaccines showed that pA and pEA could induce simultaneously specific antibodies against serotypes A, Asia1, and O FMDV, and the highest antibody titres were found in the pEA and inactivated vaccine groups compared to pA vaccinating mice. Compared with the control, the levels of IL-2, IFN-gamma, IL-4, and IL-10 expression by splenic lymphocytes from mice immunized with pA and pEA were significantly increased. In addition, we found that the levels of IL-2, IFN-gamma and IL-4 from the mice immunized with pEA was higher than mice immunized with pA did. The results of viral challenge in guinea pigs showed the pA, pEA and inactivated vaccine provided full protection in 2/4, 2/4, 3/4, 3/4 and 4/4, 4/4 guinea pigs from challenge with FMDV O/NY00 and Asial/YNBS/58, respectively. The results demonstrated fuse protein OAAT and SEA may be potential immunoge against FMDV, furthermore, SEA may be an effective genetic adjuvant for DNA vaccine.
Adjuvants, Immunologic ; genetics ; Animals ; Antigens, Viral ; immunology ; Capsid Proteins ; genetics ; immunology ; Enterotoxins ; genetics ; immunology ; Epitopes ; immunology ; Foot-and-Mouth Disease ; immunology ; prevention & control ; Foot-and-Mouth Disease Virus ; immunology ; Guinea Pigs ; HeLa Cells ; Humans ; Mice ; Mice, Inbred BALB C ; Peptide Fragments ; genetics ; immunology ; Vaccines, DNA ; immunology ; Viral Structural Proteins ; genetics ; immunology ; Viral Vaccines ; immunology

Objective:To study the risk factors of surgical therapy in neonates with necrotizing enterocolitis (NEC).Methods:From January 2016 to July 2020, neonates with a confirmed diagnosis of NEC (Bell's Stage Ⅱ and above) admitted to our hospital were retrospectively enrolled. They were assigned into surgical group and conservative group according to whether surgeries were performed. The conditions during perinatal period, clinical characteristics and laboratory examinations at the onset of NEC were compared between the two groups. Multivariate Logistic regression analysis was used to determine the risk factors of surgical therapy.Results:A total of 177 neonates with NEC were identified, including 62 cases (35.0%) in the surgical group and 115 cases (65.0%) in the conservative group. Multivariate Logistic regression analysis showed that male gender ( OR=3.178,95% CI 1.457~6.929, P=0.004), comorbidity with shock ( OR=3.434, 95% CI 1.112~10.607, P=0.032), mechanical ventilation>7 d before NEC onset ( OR=3.663, 95% CI 1.098~12.223, P=0.035) and lymphocytes <2.0×10 9/L ( OR=4.121, 95% CI 1.801~9.430, P=0.001) at the onset of NEC were independent risk factors for surgical therapy. Conclusions:Male gender, comorbidity with shock, mechanical ventilation >7 d before NEC and lymphocytopenia at the onset are independent risk factors for surgical therapy in neonates with NEC (Stage Ⅱ and above).

Ferroptosis is a non-apoptotic regulated cell death caused by iron accumulation and subsequent lipid peroxidation. Currently, the therapeutic role of ferroptosis on cancer is gaining increasing interest. Baicalin an active component in