Furthermore, hyperexpression of miR-514a-5p exacerbated the morphological characteristics of lung and right ventricular tissues, and caused increased RVHI and lung index values, as well as increased BNP and NT-pro-BNP levels in the PTE model rats, possibly by downregulating Chordin-like 1 (CHRDL1) expression.
Overall, our studies provide conclusive evidence on the thrombo-protective role of plasma gelsolin in mice model of pulmonary thromboembolism and thrombosis.
The activated tissue factor pathway with amniotic fluid produced soft and fragile clots due to its influence on platelets, which may be associated with, at least partly, the high incidence of PTE in early puerperium, particularly after cesarean section.
The combination of PMPs, platelet distribution width, P-selectin and D-dimer exhibited high sensitivity (88.24%), specificity (91.18%) and accuracy (89.71%) in the diagnosis of PTE.
The incidence of PTE in AECOPD patients was 22.9% (96/419), which increased with COPD severity degree ranging from 3.5% (2/57) in mild, 13.6% (19/140) in moderate and 33.8% (75/222) in severe subgroups (P < .05).
Hypodysfibrinogenemia with a Heterozygous Mutation of γCys326Ser by the Novel Transversion of TGT to TCT in a Patient with Pulmonary Thromboembolism and Right Ventricular Thrombus.
Hypodysfibrinogenemia with a Heterozygous Mutation of γCys326Ser by the Novel Transversion of TGT to TCT in a Patient with Pulmonary Thromboembolism and Right Ventricular Thrombus.
Our study suggests that FABP4 could be a potential biomarker and intervention point for the inflammation-related disease in HPAECs such as pulmonary thromboembolism.
Purpose To evaluate potential diagnostic performance of TRO CT with restricted volume coverage for detection of pulmonary thromboembolism (PTE) and aortic dissection (AD).
The variance difference at rs778026543 between pedigree members and healthy controls was significant (P < 0.001), supporting its potential heredity.The PEAR1 polymorphism, rs778026543, but not rs1952294 and rs822442, may be a susceptibility SNP for PTE.
As a result, plasminogen activator inhibitor-1 gene polymorphism or its concomitant presence with mentioned mutations was not found to be associated with increased risk for pulmonary thromboembolism or recurrent disease in this study.
As a direct consequence, Orai1 deficiency in mice results in resistance to pulmonary thromboembolism, arterial thrombosis, and ischemic brain infarction, but only mild bleeding time prolongation.
The effects of TAFI deficiency were also investigated in thrombin-induced pulmonary thromboembolism, Factor X coagulant protein-induced thrombosis and endotoxin-induced disseminated intravascular coagulation models.
Elevated expression of urokinase-like plasminogen activator and plasminogen activator inhibitor type 1 during the vascular remodeling associated with pulmonary thromboembolism.
A poor anticoagulant response to activated protein C based on a single point mutation of the factor V gene (Arg506Gln) was found to be a pathogenetic factor for venous thrombosis and PTE in North America and Europe.
We investigated the sensitivity to APC in 180 Japanese controls and in 96 Japanese patients with venous and arterial thrombosis (28 with deep vein thrombosis; 13 with pulmonary thromboembolism; 41 with cerebral infarction; and 14 with coronary artery disease).
The aim of this study was to investigate the association of plasminogen activator inhibitor-1 gene polymorphism and its coexistence with factor-V-Leiden and prothrombin-20210 mutations in pulmonary thromboembolism.
In addition, the presence of heterozygous prothrombin and methylene tetrahydrofolate reductase mutations might serve as synergistic cofactors triggering pulmonary thromboembolism.
Factor V gene G1691A mutation, prothrombin gene G20210A mutation, and MTHFR gene C677T mutation are not risk factors for pulmonary thromboembolism in Chinese population.
However, there is no significant difference of factor V Leiden or 20210 A prothrombin mutation in patients with DVT than in patients with combined DVT/PTE, therefore patients with DVT, carriers of the mutations, do not appear to be at lower risk for pulmonary embolism.
Fatal pulmonary thromboembolism. A retrospective autopsy study: searching for genetic thrombophilias (Factor V Leiden (G1691A) and FII (G20210A) gene variants) and dating the thrombus.