[Combination therapy of azintamid and domperidone in functional dyspepsia: a randomised, double-blind, placebo-controlled trial].

OBJECTIVE: To study the efficacy and safety of combined therapy of compound azintamid and domperidone in functional dyspepsia. METHODS: A randomised, double-blind, placebo-controlled trial. Two hundred and eight patients with functional dyspepsia were randomly grouped into group A (experimental group, 102 cases) and group B (control group, 106 cases). The patients in the group A were given 2 tablets of compound azintamid 3 times a day in addition to domperidone 10 mg 3 times per day for four weeks. The patients in the group B were only given domperidone 10 mg 3 times per day for 4 weeks. The therapeutic efficacy was evaluated by modified Severity of Dyspepsia Assessment (mSODA) and Global Patient Assessment (GPA). RESULTS: Subscore in mSODA: the change of bloating/pain intensity score in group A is -12.35 ± 5.48 while group B is -10.52 ± 4.65 (P = 0.009), the change of non-bloating/pain symptoms score in group A is -5.75 ± 3.31 while group B is -4.86 ± 2.65 (P = 0.033), and the change of satisfaction score in group A is 7.09 ± 3.78 while group B is 5.62 ± 3.54 (P = 0.004). The response rate in group A is 89.2% which is significantly higher than 76.4% in group B (P = 0.015). Other symptoms for response assessment included loss of appetite, early satiety, fullness after meal, diarrhea. No severe side-effect was found in both groups. CONCLUSIONS: Combined therapy of compound azintamid and domperidone may lead to bigger improvement in overall efficacy and health related quality of life in patients with functional dyspepsia than use of motility medicine alone. Potential mechanisms that may account for the efficacy of compound azintamide in functional dyspepsia include modulation of visceral sensitivity and/or gastrointestinal motility.

[Effects of vascular endothelial growth factor on apoptosis of sinusoidal endothelial cells caused by ethanol: experiment with rats].

OBJECTIVE: To investigate the cell death pattern of sinusoidal endothelial cells (SECs) caused by ethanol and the effects of vascular endothelial growth factor (VEGF) on this cell death, as well as the underlying mechanism involving Ets-1 and Caspase-8. METHODS: SECs were isolated from male Wistar rats and cultured in medium containing ethanol (25 - 100 mmol/L). VEGF (20 - 30 ng/ml) was added into the medium to be co-incubated for up to 6 h. Apoptosis was detected by terminal deoxynucleotidyl transferase (TdT)-mediated d-uridine triphosphate (dUTP)-biotin nick end labeling (TUNEL) technique. The protein expression of Ets-1, prototype of anti-apoptotic Ets family, was determined by Western blotting and the Caspase-8 was measured by FLICE/caspase-8 colorimetric protease assay kit. RESULTS: Three days after culture, the SECs showed spindle-like shapes and nearly confluent, however, the cells tended to shrink and die during the time course of ethanol incubation under phase contrast microscope. The control SECs contained only a few percent of TUNEL-positive cells; however, the TUNEL-positive cells started to increase 2 hours after the addition of ethanol (100 mmol/L), and about 75% of the cells were TUNEL-positive 6 hours after ethanol incubation (P < 0.05) under fluorescent microscope. Again, TUNEL-positive cells increased 6 hours after ethanol (25 - 100 mmol/L) incubation in a dose dependent manner (P < 0.05). Six hours after VEGF (20 - 30 ng/ml) was added into the medium with ethanol (100 mmol/L) the percentage of TUNEL positive SECs decreased in a dose dependent manner (P < 0.05), the level of ethanol-induced apoptotic cells in the presence of VEGF (30 ng/ml) being around 71% 6 hours after ethanol incubation alone. The Ets-1 protein level of the SECs decreased 6 hours after ethanol (100 mmol/L) incubation, which was prevented almost completely by VEGF (30 ng/ml). The Caspase-8 activity level was significantly increased to 44.9 +/- 14.3 2 hours after ethanol (100 mmol/L) incubation, and decrease to 30.4 +/- 2.0 and 25.2 +/- 2.2 respectively after the addition of VEGF (20 - 30 ng/ml) (both P < 0.05). CONCLUSION: VEGF prevents the apoptosis of primary cultured SECs induced by ethanol, through at least in part, inhibition of ethanol-induced down-regulation of Ets-1 protein expression and ethanol-induced up-regulation of Casepase-8 activity in SECs.

[The detection and significance of human papilloma virus 11b virus like particles and its serum antibody in juvenile larynx papilloma].

OBJECTIVE: To study the relationship between human papilloma virus 11b virus like particles (HPV11bVLPS) serum antibody and the development and prognosis of juvenile larynx papilloma (JLP). METHODS: Enzyme linked immunosorbent assay (ELISA) was used to detect the serum HPV11bVLP antibody (Ab) of 46 JLP's samples in different stage and 20 controls using HPV11bVLPS which was produced by recombinant bacilovirus in insect cells. Grouping: A: control group (n = 20); B: the time of onset was 1 years (n = 15); C: the time of onset was 2 years (n = 15); the patients were followed-up 1 year without recurrence (n = 8); E: The patients were followed-up 2 years without recurrence (n = 8). RESULTS: A value of HPV11bVLP Ab among A, B, C, D, E. group were: (0.073 +/- 0.035); (0.120 +/- 0.049); (0.137 +/- 0.057); (0.518 +/- 0.122); (0.557 +/- 0.144). There was a significant difference between JLP patients and the control group (P < 0.05). The level of HPV11bVLP Ab in (D + E) group (0.534 +/- 0.132) was higher than (B + C) group (0.128 +/- 0.053) (t = 14.90, P < 0.001). CONCLUSION: The results suggested that HPV serum antibody was produced in JLP with HPV infection. There is close relationship between the development and prognosis of the disease and the level of HPV11Ab in serum. The assay of serum HPV11bVLPAb and HPV-VLP could be used as immunological study of HPV11-infection associated disease.