To investigate the relationship between the ATP content in human oocytes and the developmental potential of human oocytes, unfertilized oocytes from clinical IVF and immature oocytes unsuitable for ICSI were collected. The ATP content of these unfertilized andin vitro matured eggs were determined quantitatively by measuring the luminescence using an ATP-dependent bioluminescence assay. The result showed that the ATP content of unfertilized oocytes was higher thanin vitro matured ones (2.20±0.67 pmol vs 1.72±0.49 pmol,P<0.05). In unfertilized oocytes, the ATP content of those whose fertilization rates (FR) was higher than 50% was 2.43±0.60 pmol, which was significantly different from those whose FR was less than 50% (1.72±0.56 pmol), while inin vitro matured oocytes, the ATP content of those whose FR more than 50% was 1.8±0.44 pmol, slightly higher than those less than 50% (1.55±0.40 pmol), without statistical significance. There was a tendency that the ATP content of oocytes of pregnant patients was higher than those of controls, but the sample number was too small to show any significance in statistics. Briefly, there was positive correlation between the ATP content in oocytes and developmental potential of oocytes.

In order to study the effect of tanshinone II_A on growth and apoptosis in human hepatoma cell line BEL-7402in vitro, the human hepatoma cell line BEL-7402 was treated with tanshione I_A at various concentrations for 72 h. Growth suppression was evaluated by MTT assay; apoptosis-related alterations in morphology and biochemistry were ascertained under cytochemical staining (Hoechst 33258), transmission electron microscopy (TEM), and DNA agarose gel electrophoresis. Apoptotic rate was quantified by flow cytometry (FCM). The results showed that Tanshinone II_A could inhibit the growth of hepatoma cells in a dose-dependent manner, with IC₅₀ value being 6.28 μg/ml. After treatment with 1–10 μg/ml tanshione II_A for 72 h, BEL-7402 cells apoptosis with nuclear chromatin condensation and fragmentation as well as cell shrinkage and the formation of apoptotic bodies were observed. DNA ladder could be demonstrated on DNA electrophoresis. FCM analysis showed hypodiploid peaks on histogram, and the apoptotic rates at 5 μg/ml concentration for 12 h, 24 h, 36 h, 48 h and 72 h were (2.32±0.16)%, (3.01±0.35)%, (3.87±0.43)%, (6.73±0.58)% and (20.85±1.74)% respectively, which were all significantly higher than those in the control group (1.07±0.13)%. It is concluded that Tanshione II_A could induce human hepatoma cell line BEL-7402 apoptosis, which may be related to the mechanism of growth inhibition.

In order to investigate the changes of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) expression in residual hepatocellular carcinoma (HCC) after transcatheter arterial chemoembolization (TACE), the expression levels of VEGF and bFGF expression in specimens surgically removed from 48 HCC patients were detected by immunohistochemical methods, and staining intensity of VEGF and bFGF was assessed by a computer-assisted image-analyzer. Among the 48 patients, 25 underwent partial hepatectomy alone (single operating group), and 23 were subjected to second stage surgical resection after TACE (TACE group). The results showed that the average absorbance value (A) of VEGF was higher in TACE group than that in single operating group (0.152±0.021 vs 0.131±0.012,P<0.01). The Average A of bFGF in TACE group was 0.127±0.023, higher than in single operating group (0.111±0.016,P<0.05). These results suggested that TACE of HCC can up-regulate the expression of VEGF and bFGF in HCC tissues possibly due to anoxia and ischemia.

To observe the protective effect of heparin-coated circuits (HCC) on the platelet function during cardiopulmonary bypass (CPB). 23 patients with heart valve replacement were studied. The system heparin dose was 3 mg/kg in the control group (n=15) and heparin-coated circuits in the HCC group (n=8). Platelet count, α-granule membrane protein-140 (GMP-140) concentrations were determined before CPB, at 60 min of CPB, 30 and 60 min after protamine administration, first 12 h after CPB, respectively. At end of CPB the arterial filters in the circuits were observed by electron microscopy. The amount of first 12-h postoperative blood loss was measured. There was significant reduction in platelet loss during and after CPB in the HCC group in contrast to the control group during CPB (P<0.05). During the first 12 h, postoperative blood loss was reduced in the HCC group as compared with that in the control group (218±61 ml, vs. 332±118 ml,P<0.05). Electron microscopy showed that in the HCC group the filter meshes and their fringes were clear and fragments of floccules were occasionally seen, without adherent cells or only few adherent cells on their surfaces, whereas several cellular and fibrous components were found to adhere to the surfaces of the filter meshes in the control group. This study indicates that heparin-coated circuits might reduce the platelet loss and activation during CPB and improve hemocompatibility of cardiopulmonary bypass equipment.