According to inclusion and exclusion standards, from October 2017 to June 2018, 30 consecutive patients of aneurysmal subarachnoid hemorrhage admitted to Intensive Care Unit, Department of Neurosurgery at Xuanwu Hospital, were given remote ischemic conditioning 5 times intervention to each patient within 7 days, and blood coagulation function testing, including prothrombin activity (PTA), prothrombin time (PT), activated partial prothrombin time (APTT), fibrinogen (Fib), D-dimer, and thromboelastogram (TEG, including R, K, Angle, MA, EPL, LY30, A, CI, G, and A30) were performed for each patient before and after the RIC intervention, as well as venous ultrasound monitoring before and after the RIC intervention for detection of deep vein thrombosis (DVT).
It has been recently reported that a G-->A transition at nucleotide position 20210 in the 3'-untranslated region of the prothrombin gene is associated with elevated plasma prothrombin levels and an increased risk of deep venous thrombosis.
Comparison of activated partial thromboplastin time, antithrombin III, D-dimer, lupus anticoagulant, free S protein (PS), C protein, and antiphospholipid and PS antibodies was performed on children with acute VZV and DVT (group I), acute uncomplicated VZV (group II), and 30 healthy controls of both sexes (15 boys and 15 girls, mean age 7.5 ± 2.6 years, group III).
Our findings thus indicate that regulation of TF by NF-kappaB transcription factor p50 is essential for the pathogenesis of deep vein thrombosis and suggest that specific inhibitors of p50, such as Andro, may be therapeutically valuable for preventing and perhaps treating venous thrombosis.
The proband suffered from recurrent deep vein thrombosis and showed reduced PS anticoagulant activity (31%), and total, free PS antigen and C4bBP levels in the normal range.
Taken together, this suggested that E(2) might repress PROS1 transcription depending upon ERalpha-Sp1 recruiting transcriptional repressors in HepG2-ERalpha cells and, consequently, that high levels of E(2) leading to reduced levels of plasma PS would be a risk for deep venous thrombosis in pregnant women.
We aimed to study whether the association between F9 Malmö and deep vein thrombosis is explained by linkage disequilibrium with nearby single-nucleotide polymorphisms, and whether the association is explained biologically by F9 Malmö affecting factor IX antigen levels or activation of factor IX.
Higher levels and activity of FSAP have been reported in patients with deep vein thrombosis, but there are no data on plasma FSAP in ischemic stroke (IS).
Importantly, small pulmonary emboli could be detected along with a mild phenotype of PA endothelial dysfunction and oxidative stress in the absence of PA-pressure elevation. mRNA expression of plasminogen activator inhibitor-1 was increased in PAs of mice with recurrent PE after repetitive thrombin injections and to a lesser extent in DVT mice.
Therefore, PAI-1 gene promoter was screened for possibly new polymorphisms and to investigate the contribution of these sequence variations to PAI-1 levels in patients with deep vein thrombosis (DVT).
In postmenopausal women who are estrogen-progestin HRT users, the presence of the factor V Leiden mutation or an elevated factor VIII level appears to have a multiplicative effect on their overall risk of DVT, increasing it 17-fold compared to women without these blood abnormalities who are HRT nonusers.
This is a rare case of concomitant CVT and DVT induced by high factor VIII activity due to hyperthyroidism under the presence of meningitis, an additional risk factor for thrombosis.
MMP-1, MMP-2 and inflammatory factors play an important role in the occurrence and development of DVT, of which the levels of IL-6, IL-8 and TNF-α are positively correlated with the levels of MMP-1 and MMP-2, respectively.
The concentrations of free and total tissue factor pathway inhibitor, C-reactive protein, von Willebrand factor and D-Dimer were significantly higher in patients with deep venous thrombosis than in patients without deep venous thrombosis (P < 0.001 for all quantities).
Basal plasma levels of von Willebrand factor and recruitment of platelets to the inferior vena cava wall after DVT induction were reduced in MC-deficient mice.