In order to investigate the role of antiapoptosis gene, survivin in the resistance to palcitaxel, the expression of survivin mRNA and protein in the process of paclitaxel treatment in breast cancer cell line MCF-7 was detected MCF-7 cells were incubated with paclitaxel at different concentrations. The growth inhibition rate of MCF-7 was investigated by tetrazolium bromide (MTT) colorimetry. The change of apoptosis was detected by Annexin-V/PI methods. The changes in the expression of survivin mRNA and protein were studied by reverse transcription polymerase chain reaction (RT-PCR) and Western-blot assay respectively. The growth inhibition rate of MCF-7 was increased in a concentration-and time-dependent manner. Paclitaxel of higher concentration could effectively induce apoptosis in MCF-7 cells after 48 h, while the expression of survivin was increased at early time (within 6 h) and decreased after 24 h regardless of treatment concentrations of paclitaxel. It suggested that tumor cells might evade the paclitaxel-induced cell cycle arrest and apoptosis by increasing the level of survivin at early treatment time.

To experimentally evaluate the ectopic osteogenetic capacity of synthesized BMP2-derived peptide P24 combined with poly lactic-co-glycolic acid (PLGA), Wistar rats were divided into two groups: group A, in which BMP2-derived peptide P24/PLGA complex was implanted, and group B which received simple PLGA implant. The complex was respectively implanted into the back muscles of rats. Samples were taken the 1st, 4th, 8th, and the 12th week after the implantation. Their bone formation was detected by X-ray examination, and tissue response was histologically observed. Western blotting was used for the detection of the expression of collagen I (Col-I) and osteopontin (OPN). There was acute inflammation in the tissue around both types of implants at early stage. The cartilage was found around implant areas 4 weeks after the implantation of BMP2-derived peptide p24/PLGA complex, 8 weeks after the implantation, osteoblasts were found, and 12 weeks after the implantation, typical trabecular bone structure was observed. In group B, after 12 weeks, no osteoblasts were found. It is concluded that PLGA is an ideal scaffold material for bone tissue engineering. BMP2-derived peptide can start endochondral ossification and is more effective in inducing ectopic osteogenesis.

Connexin-43 (Cx43) expression in prostate cancer (PCa) cells and the potency of gap junctional intercellular communication (GJIC) in the cells were investigated, with an attempt to elucidate the reason why the so-called “bystander effect” mediated by thymidine kinase (TK) suicide gene therapy on PCa cells is not of significance and to explore the role of GJIC in PCa carcinogenesis. mRNA and protein expression of Cx43 in a PCa cell line PC-3m was detected by reverse-transcription polymerase chain reaction (RT-PCR) and strapt-avidin-biotin-enzyme complex (SABC) immunohistochemical staining, and inherent GJIC of PC-3m cells was assayed by scrape-loading and dye transfer (SLDT) assay. The expression of Cx43 in human normal and malignant prostate tissues was determined by SABC immunohistochemistry as well. It was found that Cx43 mRNA and protein expression in PC-3m cells was slightly reduced as compared with positive controls and the location of Cx43 protein was aberrant in cytoplasm rather than on membrane. Assessment of paraffin sections demonstrated that the expression of Cx43 protein in PCa cells was abnormally located and markedly diminished as compared with normal prostatic epithelial ones, displaying a negative correlation to the pathological grade (χ²=4.025, P<0.05). Additionally, capacity of inherent GJIC in PC-3m cells was disrupted, which was semi-quantified as (+) or (−). It was indicated that both down-regulated expression of Cx43 mRNA and aberrant location of Cx43 protein participated in the mechanisms leading to deficient GJIC in PC-3m cells. Lack of efficient GJIC is a molecular event, which may contribute not only to limited extent of “bystander effect”, but also to initiation and progression of prostatic neoplasm.

The effects of oxygen partial pressure on cryopreservation of the cells with organ preservation solution were explored. Hypoxic UW solution was made by purging the UW solution with argon. The pig proximal tubule epithelial cells (LLC-PK1 cells) were cryopreserved in hypoxic UW solution (Ar-UW group) or standard UW solution (UW group) at 4°C for 48 h. Trypan blue staining and LDH detection were performed to evaluate the injury of the cells. The results showed that the oxygen partial pressure in Ar-UW group was significantly declined from 242±6 mmHg to 83±10 mmHg. After cryopreservation at 4°C for 48 h, LDH leakage rate and Trypan blue-stained rate in Ar-UW group were (11.3±3.4)% and (10.5±4.7)%, respectively, which were significantly lower than in UW group [(49.5±6.9)% and (47.6±9.3)% respectively, both P<0.01]. It was concluded that lower oxygen partial pressure of UW solution was more beneficial to the cryopreservation of LLC.

The suppressive effect of anti-KDR antibody against VEGF on proliferation of hemangioma-derived vascular endothelial cells (HVECs) was investigated. HVECs from one case of hemangioma in proliferative phase were cultured. Both primary culture and sub-culture were conducted in M199 medium. The HVECs of passage 3 were divided into 4 groups based on the concentrations of anti-KDR antibody. Cell count was performed and inhibitory rate of HVECs was measured before and 9 days after interference. The results showed that the number of HVECs in the anti-KDR antibody-treated groups was significantly decreased and the inhibitory rate of HVECs by anti-KDR antibody (50, 10 and 2 μg/mL) was 84%, 63% and 39% respectively at 9th day after interference, with the difference being significant. In the control group, the number of HVECs was increased significantly. In was concluded that the anti-KDR antibody could suppress the activity of VEGF through blocking the KDR, indicating the potential clinical applications of anti-KDR antibody in the treatment of hemangioma.

To assess the normal value of left ventricular twist (LVtw) and examine the changes with normal aging by 2-dimensional ultrasound speckle-tracking imaging (STI), 121 healthy volunteers were divided into three age groups: a youth group (19–45 y old), a middle-age group (46–64 y old) and an old-age group (≥65 y old). Basal and apical short-axis images of left ventricular were acquired to analyse LV rotation (LVrot) and LVrot velocity. LVtw and LVtw velocity was defined as apical LVrot and LVrot velocity relative to the base. Peak twist (Ptw), twist at aortic valve closure (AVCtw), twist at mitral valve opening (MVOtw), untwisting rate (UntwR), half time of untwisting (HTU), peak twist velocity (PTV), time to peak twist velocity (TPTV), peak untwisting velocity (PUV), time to peak untwisting velocity (TPUV) were separately measured. The results showed that the normal LV performs a wringing motion with a clockwise rotation at the base and a counterclock-wise rotation at the apex (as seen from the apex). The LVtw velocity showed a systolic counterclock-wise twist followed by a diastolic clockwise twist. Peak twist develops near the end of systole (96%±4.2% of systole). With aging, Ptw, AVCtw, MVOtw, HTU and PUV increased significantly (P<0.05) and UntwR decreased significantly (P<0.05). However, no significant differences in TPUV, PTV and TPTV were noted among the 3 groups (P>0.05). It is concluded that LV twist can be measured non-invasively by 2-dimensional ultrasound STI imaging. The age-related changes of LVtw should be fully taken into consideration in the assessment of LV function.