dbcAMP was injected i. p. into four U_(14) ascitic tumor bearing mice on 3,4,5,6 and 7 days after inoculation of tumor cells. The ascites was aspirated 0.5-1 hour after last injection. For scanning electron microscopy, the tumor cells, washed twice in Hanks solution, were fixed in glutaraldehyde and OsO_4, dehydrated with ethyl alcohol and dried with camphene. For flow microcytometric analysis, the treated tumor cells were fixed in 70% cold ethyl alcohol and stained with propidium iodide. Under SEM, the untreated tumor cells were large, spherical, and uniform in size with numerous long thin microvilli on the cell surface. A few barely visible minute protrusions were present on the microvilli and cell membrane. The great majority of treated tumor cells became smaller and variable in size, with shortened microvilli which reduced in number and even disappeared in some area. Many granular protrusions, larger than that of the control, were clearly observed on the cell membrane and microvilli. The result of flow microcytometric analysis showed that the DNA histogram and cell cycle profile from dbcAMP treated cells have no significant difference from the untreated controls, so it is evident that morphologic changes resulted from dbcAMP were not caused by cell cycle alteration. The morphogenesis of microvilli and cell membrane changes in dbcAMP treated cells is not clear. The relation of these configurations to differentiation of malignant tumor cells is discussed.

Murine ARS reticulum sarcoma cells, when incubated with 1.5, 2.0 and 2.5% DMSO in vitro, were induced to differentiate into macrophage like cells. They showed reduction of cellular and nuclear size and lowering of nucleo-cytoplasmic ratio with marked change in nuclear size. The most effective one was 2.5% DMSO which caused marked reduction of nucleolar size. Tumor cells with nucleo-cytoplasmic ratio less than 0.5 and with reduced nucleoli resembled macrophage. 2.5% DMSO induced the increase of non-specific esterase positive cells and the increase of polystyrene phagocytic percentage and phagocytic index. Under EM, 2.5% DMSO treated ARS cells with nucleocytoplasmic ratio less than 0.5 exhibited abundant cytoplasmic organelles, developed Golgi complex and secondary lysosomes. Scanning EM showed that many large cells with numerous dense slender microvilli were observed in the control. Under the action of 2.5% DMSO, large cells were reduced, small cells were increased and microvilli markedly decreased and shortened. These small cells appeared to be differentiated macrophage like cells and were similar to small cells seen under EM and light microscope. In 2.5% DMSO treated groups, the mitotic index of ARS cells were markedly lowered.

Objective To explore the clinical application of reconstructing silicone elastomer nose prosthesis by means of selected laser sintering and wax powder PCPI. Methods Laser scanning was used to get the 3-D data of a nose model. Surfacere 10.0 etc softwares was used to reconstruct the nose by mirroring the digitalized model of absent nose. Selective laser sintering and wax powder was chosen to fabricate a wax nose model and the nose prosthesis made by silicone clastomer. Results Perfect silicone clastomer nose prosthesis was made for 2 patients. Conclusion This study suggests that the wax nose model and the new wax powder can meet the requirement of clinical expectation for maxillofacial prosthesis.

Objective:To reconstruct a 3-D wax nose model and make a s ilicone elastomer nose prosthesis. Methods:Laser scanning was us ed to get the data of a nose model, selective laser sintering and wax powder wer e used to fabricate a wax nose model,the nose prosthesis was made by silicone el astomer. The differences in length(L),width(W),deepth(D),height(H) and tip-angl e(TA) among the nose models made with plaster, wax powder and silicone elastomer were compared. Results:L(mm) in plaster, wax and silicon e models was 36.61,36.60 and 36.60 respectively.W(mm),D(mm),H(mm) and TA(?) in the three kinds of models were the same:36.23,18.45,43.14 and 74.57 respectively .Conclusion:Nose model made of the wax powder is precise and can meet the requirements for maxillofacial prosthesis.

Our study demonstrated that ARS cells can be induced to differentiate into macrophage-like cells with changes in phenotype, nonspecific esterase activity and phagocytic function by adding ginsenosides in short-term cultures. Synthesis of DNA, mitosis and the growth of the culture cells transplanted in mouse are also inhibited in this condition. The size of cells, nuclei and nucleoli, as well as nuclear-cytoplasmic ratio of ginsenosides treated cells are diminished significantly. Microvilli of these cells are reduced in number with formation of. ruffles on the cell surface. Mitochondria are increased, their size and distribution become regular. The fact that numerous small cells, induced by ginsenosides exhibit the most conspicuous alteration mentioned above along with marked phagocytic activity indicates that they are highly differentiated macrophage-like cells. Whether the inhibition of cell growth and induction of differentiation by ginsenosides is caused through its action on the molecules regulating the gene expression of cell growth and differentiation needs further study.

Objective To observe the influence of selenocysteine synthase(SEPSECS) on injury of human umbilical vein endothelial cell line EVC-304 induced by hydrogen peroxide (H2O2). Methods Transfection was conducted to transfect EVC-304 which was maintained in vitro. The cells were divided into four groups: control group, SEPSECS over-expression group, empty vector group and SEPSECS silenced expression group, then Real-time PCR and Western blotting were performed to detected SEPSECS mRNA and protein expression , respectively. Flow cytometry(FCM) was performed to detect cell cycle. Different concentrations of H2O2, which including 0, 200, 400, 600, 800, 1 000 μmol/L, were used to treat EVC-304 . Then malonaldehyde (MDA), superoxide dismutase(SOD) secreted by the cells which were treated with H2O2 for 6 h, were checked by MDA or SOD kit. Results The SEPSECS mRNA expressions of control, SEPSECS silenced expression, empty vector and SEPSECS over-expression groups were 1.03 ± 0.24, 0.43 ± 0.11, 0.98 ± 0.27 and 1.61 ± 0.13, respectively. The protein expressions of control, SEPSECS silenced expression, empty vector and SEPSECS over-expression groups were 1.00 ± 0.26, 0.51 ± 0.10, 1.12 ± 0.38 and 1.51 ± 0.20, respectively. There was a significant difference between control and SEPSECS silenced expression groups (all P<0.05), at the same time , this phenomenon was also observed between empty vector and SEPSECS over-expression groups (all P<0.05). The level of MDA was increased along with the H2O2 concentration. Besides, cell cycle was also tested, however, significant difference was not observed(all P > 0.05). Meanwhile, MDA of SEPSECS silenced expression groups[(15.8 ± 0.5),(19.6 ± 1.5)μmol/L] were significantly higher than control groups[(12.4 ± 0.1),(17.1 ± 0.5)μmol/L, all P < 0.05], on the other hand, MDA of SEPSECS over-expression groups[(10.8 ± 0.4),(14.2 ± 1.1)μmol/L] were lower than empty vector groups [(12.7 ± 0.7),(16.2 ± 1.1)μmol/L, all P < 0.05], when the H2O2 concentration was 800 or 1 000μmol/L. The level of SOD was decreased along with the H2O2 concentration. SOD of SEPSECS silenced expression groups[(7.7 ± 0.4),(2.4 ± 0.3)μmol/L] were lower than control groups[(10.0 ± 1.0),(6.0 ± 0.6)μmol/L, all P < 0.05], on the contrary, SOD of SEPSECS over-expression groups[(11.3 ± 0.6),(12.7 ± 1.6)μmol/L] were higher than empty vector groups[(9.2 ± 0.6),(6.7 ± 0.2)μmol/L, all P < 0.05], when the H2O2 concentration was 800 or 1 000μmol/L. Conclusion Expression of SEPSECS has a significant protective role on damaged EVC-304 which was induced by H2O2.

Mesenchymal stem cells (MSCs) not only exhibit a marked tropism for tumors,but also exert antitumorigenic activity or as an emerging vectors to express foreign genes continuously and efficiently within the tumor microenvironment,suppress tumor's growth and metastasis.Conversely,MSCs can accelerate tumor development through promoting tumor stroma remodeling and tumor vascular formation,inhibiting tumor local immune and changing tumor phenotype.The reason for this discrepancy may be attributable to different sources of MSCs,the heterogeneity of MSCs,differences in tumor microenviroment,or another factor that is not yet appreciated.

Objective To examine the expression of potassium channel mRNA in myocardial tissue of mice with low selenium.Methods Forty C57BL/6 mice were randomly divided into four groups according to body weight(18-22 g),10 mice in each group,half male and half female.The low-selenium treatment groups were fed with low-selenium diet(selenium content was 0.004 mg/kg) for 4,12 and 24 weeks,respectively,and the control group was fed with normal diet(selenium content was 0.256 mg/kg).The mice were killed by cutting neck method,hearts were taken out and RNA was extracted by Trizol method.The expressions of potassium ion channel genes (KCNA4,KCND2,KCND3,KCNE1,KCNE2,KCNJ2,KCNJ12 and KCNQ1) at the mRNA level in heart were determined using real-time polymerase chain reaction.Results In low-selenium 4 weeks group,the mRNA expressions of KCNA4 gene(25.3 ± 0.09) and KCND2 gene(4.85 ± 0.05) were higher than that of the control group (1.00 ± 0.00,1.00 ± 0.00,all P ＜ 0.05); in low-selenium 24 weeks group,the mRNA expression of KCNJ12 gene (22.7 ± 0.10) was higher than that of the control group(1.00 ± 0.00,P ＜ 0.05); the mRNA expressions of KCND3,KCNE1,KCNE2,KCNJ2,KCNQ1 genes were compared with the corresponding control groups,the differences were not statistically significant(all P ＞ 0.05).Conclusions Low selenium can affect the mRNA expression of mouse cardiac potassium ion channel genes.