[Clinical significance of monitoring coagulation- and fibrinolysis-related indexes during catheter-directed thrombolysis for acute lower-extremity deep venous thrombosis].

OBJECTIVE: To investigate the patterns of changes in serum levels of of D-dimer, fibrinogen (FIB) and fibrin degradation product (FDP) during catheter-directed thrombolysis (CDT) in patients with acute lower-extremity deep venous thrombosis (DVT) and explore their clinical significance. METHODS: From June, 2014 to June, 2015, 50 patients with acute lower-extremity DVT received CDT. The serum concentrations of D-dimer, FIB and FDP were measured before, during and after CDT in all the subjects, with 50 healthy subjects serving as the control group. RESULTS: Compared with the control group, the patients in DVT group showed significantly increased serum levels of D-dimer (29.17±38.67 vs 0.21 ±0.27 µg/mL), FIB (3.66±0.95 vs 3.32±0.65 g/L) and FDP (76.14±131.48 vs 1.08±0.73 µg/mL) before CDT (P<0.05). Based on the effect of CDT, the patients with DVT were divided into recanalization group (n=34) and failed recanalization group (n=16), and the patients with recanalization had significantly increased serum concentration of D-dimer and FDP (P<0.05) and decreased FIB level (P<0.05) compared with those with failed recanalization at 24 h of CDT. D-dimer, FDP, and FIB showed no significant changes in the patients with failed recanalization after the procedure (P>0.05). Correlation analysis showed that serum D-dimer (r=0.66, P<0.05) and FDP (r=0.50, P<0.05) at 24 h of the procedure were positively correlated with the outcomes of CDT. CONCLUSION: Serum levels of D-dimer, FIB and FDP are important indicators for evaluating and predicting the effectiveness of CDT in patients with acute DVT.

Thyroid hormone prevents cognitive deficit in a mouse model of Alzheimer's disease.

This study aimed to examine the feasibility of using thyroid hormone (TH) as a therapeutic agent for Alzheimer's disease (AD). Mice were injected intra-hippocampally aggregated amyloid beta-peptide (Abeta) to produce AD animal model. Intraperitoneal administration of l-thyroxine (L-T4) into Abeta-induced AD model mice prevented their cognitive impairment and improved their memory function. The mechanisms of L-T4 treating AD might be associated with regulating cholinergic function, protecting the brains of AD model mice against damage from free radicals, and rescuing hippocampal neurons from apoptosis. The results of the present study indicate that the use of TH has some therapeutic potential in AD.