Objective To detect the safe application of autoblood re-trasfusion of medical trioxyen. Methods 50 patients who received fundamental autohemotherapy with German DR.HANSLER OZONOSAN treating system were extracted 100ml venous blood,which was mixed with 100ml,10~20?g/m1 medical trioxyen and then retransfused into the patients.We observed the adverse effect during the course of treatment and measured the blood pressure and blood glucose of every patient accordingly. Results Among the 50 cases,4 (about 8%) had adverse effect after blood extracting. 5 cases (about 10%) had adverse effect after the trioxyen re-transfusion. The cardinal symptoms included:dizziness,nausea,emesia,cold sweat,blood pressure decrease,shock etc. Conclusion Before retransfusing the medical trioxyen,handling the indications,contraindications,making the patients have good sleep and diet and have necessary comunication with them can make the negative reaction lower at most.

Hypoxic cells that exist in nasopharyngeal cancer can not be killed easily and they are the underlying cause for recurrence and metastasis. In radiotherapy for nasopharyngeal cancer, the application of Qi-benefiting and blood-supplementing Chinese medicines can improve blood circulation, increase oxygenation of tumor body, and ameliorating the status of hypoxic cells. Besides medical ozone can promote oxygen-carrying ability of hemoglobin and releasing of oxygen capacity and improve oxygen supplying. If the method of radiotherapy combined with ozone and Chinese medicines can solve the problem of resistance of hypoxic cells to radiation and promote the oxygen effect in radiation and the interaction between organisms, then it will play an important role in the treatment of nasopharyngeal cancer.

AIM: To observe the regulation of octreotide (OCT) on the expression of somatostatin receptor 2 (SSTR2) in Bel7402 hepatocellular carcinoma (HCC) cells, and the inhibition effect of OCT on the growth of HCC. METHODS: The effect of OCT on proliferative ability of Bel7402 cells was observed by MTT assay. The cell form was observed by light invert microscope. The adhesive and invasive ability was detected by cell adhesion and migration experiments. The cell cycle, SSTR2 expression of 7402 cells were determined by immunofluorescence flow cytometry. Nude mice bearing xenografts in situ were treated with OCT or saline control for 7 weeks since tumor implantation. The immunohistochemistry for SSTR2 was performed. SSTR2 mRNA expression in cell line and xenografts was measured by semi-quantitative RT-PCR. RESULTS: After OCT treatment, the proliferative ability and cell form of 7402 cells didn't change significantly. The adhesive and invasive ability decreased significantly. The ratio of cells in resting state (G 0/G 1) increased, but no apoptosis peak was observed. The SSTR2 expression on 7402 cell membranes decreased significantly. SSTR2 expression in cell line of OCT group was higher than control group, but there was no significant difference between them. The mean tumor weight in mice given OCT was significantly lower than that in control group. SSTR2 immunostaining in tumor cells of treatment group showed stronger positivity, compared with control group. SSTR2 mRNA expression in xenografts after OCT treatment was significantly higher than that in control group. CONCLUSIONS: OCT inhibits the growth of HCC through SSTR2. SSTR2 is regulated by its ligand, the long-term OCT treatment increases the SSTR2 expression and enhances the effect of inhibiting HCC, however, short-term treatment may induce its desensitization and the decrease in anti-tumor effect. [

Objective To investigate the expressions of RGC-32 and E-cadherin in pancreatic cancer and analyze their clinicopathological significance and the correlation with each other.Methods SP immunohistochemistry was used to detect the expressions of RGC-32 and E-cadherin in 42 cases of pancreatic cancer tissues,12 cases of chronic pancreatitis tissues and 8 cases of normal pancreatic tissues.Results The positive staining for RGC-32 was predominantly observed in the cytoplasm of pancreatic acinar cells.The positive staining for E-cadherin was mainly observed in the cytomembrane of normal pancreatic and chronic pancreatitis acinar cells,but aberrant expression ( cytoplasm expression and ( or ) weaker expression) could be found in pancreatic cancer cells.The positive expression rate of RGC-32 and aberrant expression rate of E-cadherin were 78.6％ (33/42) and 54.8％ (23/42),respectively,in pancreatic cancer tissues,which were significantly higher than those in normal pancreatic tissues [37.5％ (3/8) and 0] and chronic pancreatitis [41.7％ (5/12)and 8.3％ (1/12) with statisticai significance,P ＜0.05].The expression of RG C-32 in pancreatic cancer was associated with lymph node metastasis and TNM staging (P =0.016,0.025,respectively),but not with age,gender and differentiation degree ( P =0.831,1.000,0.629,respectively).The aberrant expression of E-cadherin was associated with differentiation degree,lymph node metastasis and TNM staging ( P =0.024,0.004,0.004,respectively),but not with age and gender ( P =0.970,1.000,respectively).A significantly positive correlation was found between positive expression rate of RGC-32 and aberrant expression rate of E-cadherin (r =0.458,P ＜0.01 ).Conclusions Both positive expression rate of RGC-32 and aberrant expression rate of E-cadherin are up-regulated significantly in pancreatic cancer tissues and RGC-32 may be involved in the invasion and metastasis of pancreatic cancer by regulating epithelial mesenchymal transition.

ObjectiveTo observe the effect of donor liver pretreated by breviscapine on liver transplantation ischemia/reperfusion injury in rats. Methods SD rats served as liver donors and recipients (n =48 each).The recipients were divided into four groups by random number table.The donors in groups A and C were not pretreated with breviscapine,but those in groups B and D were pretreated with 20 mg/L Breviscapine.The cold ischemia time in donor livers of groups A and B was 30-40 min,and that in groups C and D was 12 h. Clotting function, liver function, serum thrombomodulin,caspase3,and relative activity of NF-kB after liver transplantation were assessed,and the pathological changes and TUNEL apoptosis staining were observed.ResultsThe mortality in groups C and D was 40.0％ (8/20) and 29.4％ (5/17),respectively (P＞0.05).There were no significant changes in coagulation function in all groups after operation. The liver function was improved,pathological lesions were alleviated,and apoptosis rate,serum TM,caspase3 expression and activity of NF-kB in the liver tissues of group D were significantly decreased as compared with group C at 3rd day after operation (P＜0.01),but all these parameters in group B had no significant change compared to group A.ConclusionPretreatment of donor livers with breviscapine can reduce the ischemia/reperfusion injury and apoptosis after liver transplantation in rats probably by inhibiting the apoptosis-related pathway and alleviating the damage to the endothelial cells of the liver microcirculation.

ObjectiveTo investigate the influence of cobalt chloride ( CoCl2 )-mimetic hypoxia on theproliferation,apoptosis and migration of human pancreatic cancer cell fine PANC1.MethodsPANC1 cells were treated with 0(control),100,200,400,800 μmol/L CoCl2 respectively for 24 h.Real-time RT-PCR and Western blot were used to determine hypoxia induced factor ( HIF)-1o mRNA and protein expression respectively,and cell counting kit-8(CCK-8) assays,flow cytometry and cell scratch test were used to examine the proliferation,apoptosis and migration of PANC1 cells,respectively.ResultsIn the control group and 100,200,400 and 800 μmol/L CoCl-2 groups,the expressions of HIF-1t mRNA were 1,1.08 ±0.12,1.12 ± 0.09,1.04±0.11,0.66 ±0.07,and the expressions of VEGF mRNA were 1,2.69±0.35,4.81 ±0.54,2.19 ± 0.21,0.79 ± 0.08,while the expressions of HIF-1 α protein were 0.23 ± 0.03,0.36 ± 0.04,1.15 ± 0.11,1.08 ± 0.09,0.44 ± 0.04; and the expressions of VEGF protein were 0.14 ± 0.02,0.12 ± 0.01,0.95 ±0.09,0.87 ±0.09,0.55 ±0.06; and cell viability rates were 100％,(98.43 ±2.88)％,(76.15 ± 0.70)％,(53.87 ±0.77)％,(35.23 ±0.67)％ ; while cell apoptotic rates were (5.2 ±1.12)％,(5.74 ± 1.07)％,(6.82 ± 1.85)％,(12.09 ±3.53)％,(31.88 ±6.95)％ ; the cell migration distance of PANC1 cells were (43.24 ±3.67)％,(59.46 ±5.39)％,(80.56 ±8.05)％,(63.89 ±5.96)％,(9.09 ± 1.59 ) ％.Compared with those of control group,the expressions of VEGF mRNA,VEGF and HIF-1 α protein,cell migration distance showed a two-way variation ( ascending first and descending later) (P ＜0.05 ),and the expression of HIF-1α mRNA and cell proliferation rate was decreased in a dose-dependent manner,while the cell apoptosis was increased in a dose-dependent manner.Conclusions CoCl2 significantly inhibits the proliferation and promotes apoptosis of PANC1 cells at certain level.CoCl2 has a two-way effect on the migration of PANC1 cells,and it may be related to the direct injury of high concentration of CoCl2 on cells.

BACKGROUND: The repair of articular cartilage defect is always a problem that is dedicatedly solved by doctors of orthopaedics. Autologous perichondrium, periosteum or allografting of cartilage have been used previously; however, the source of the donor is limited, the fixation is difficult as well as the occurrence of endochondrial ossification and delamination between the inferior cartilage and reparative cartilage, etc. Type Ⅱ collagen, the main component of cartilage matrix, has certain effects in the repair of articular cartilage defect.OBJECTIVE: To investigate the effects of type Ⅱ collagen sponge filling on the repair of articular cartilage defect.DESIGN: A randomized controlled trial.SETTING and MATERIALS: The study was conducted in the Guangzhou Institute of Traumatic Surgery. Materials were 24 adult male purebred New Zealand Rabbits(48 knees), ordinary grade, with a body mass of (2.29 ±0. 25) kg. Animals were fed with standard feeding in separate cage.INTERVENTIONS: A full-thickness defect in articular cartilage was made on the femoral trochlear surface by a drill of 5 mm in diameter and 3 mm in depth. Rabbits were allocated into filling group(type Ⅱ collagen sponge was grafted into left keen joint defect) and control group(right knee joint defect site was set as control) according to random number table.MAIN OUTCOME MEASURES: Gross morphological and histological observation of the defect repair in each dual week within 12 weeks after operation.RESULTS: During 10 - 12 weeks, in cuntrol group: The defect area was repaired by white and soft tissue that had no resistance to press. The repaired tissue was still lower than the surrounding articular surface with clear boundary. By histological observation, it was found that the defect was repaired by the mechanism similar to inflammatory reaction and the defect is ultimately filled by the hyperplasia of hyaline degenerative fibrous tissues. In filling group: the defect was repaired by semi-transparent, smooth, textured tissues with polish that had resistance to press as well as elasticity. The repaired tissue was almost similar to the shape of the surrounding cartilage,difficult to be distinguished. After histological observation, it was found that there was no inflammatory reaction, but active hyperplasia of inner bonetissue and cartilage tissues; a lot of osteoid tissues and trabeculation were found. Newlborn cartilage was fused with surrounding cartilage tissue and connected with surrounding tissues. Type Ⅱ collagen had significantly promoting effects in the repair of articular cartilage defect, and the repaired cartilage was close to normal cartilage. CONCLUSION: The self-made high purity type Ⅱ collagen sponge has favorable promoting effects in the repair of articular cartilage defect with good histocompatibility but without obvious toxic side effect.

Objective To investigate the effect and mechanism of oetreotide (OCT) on DENA related hepatoeareinogenesis in rats. Methods Fresh diethylnitrosamine (DENA) solution was given to induce the model of rat hepatoeellular carcinoma. The rats were divided randomly into two groups: OCT treatment group and control group. The survival rate and hepatoeareinogenesis rate were observed. SSTR2 mRNA and protein expression were measured. Results The survival rote of OCT treatment group (70.0%, 7/10) was significantly higher than that of control group (30.0%, 6/20) (X2 = 4.344, P<0.05). 16 weeks after DENA treatment, the difference of bepatoearcinogenesis rate between the two groups was not remarkable though the value of OCT treatment group (0%, 0/10) was lower than that of control groups (30.0%, 6/20)(X2 = 3.750, P＞0.05). However, 22 weeks after DENA treatment, hepatoeareinogenesis in control group (83.3%, 10/12) was markedly higher than that in OCT treatment group (22.2% , 2/9)(X2 =7.843, P<0.01). With liver cirrhosis progressing, the expressions of SSTR2 mRNA and protein increased, and reached the peak 16 weeks after DENA treatment, then began to decrease. The expressions of SSTR2 mRNA and protein in hepatocellular carcinoma were significantly lower than those in the liver 22 weeks after DENA treatment (F = 35.010 and 13. 386, P<0.01). The expression levels in OCT treatment group were similar to those in control group 8 and 16 weeks after DENA treatment. But the expression levels in OCT group 22 weeks after DENA treatment didn't lower markedly, and were higher significantly than those in control group (t = 2.806 and 4.498, P<0.05). Conclusion OCT can inhibit efficiently hepatocareinogenesis and reduce the mortality of rots treated with DENA possibly by a mechanism maintaining the expression levels of SSTR2.

Objective To observe the effect of somatostatin (SST) on the expression of metalloproteinase-2(MMP-2) and tissue inhibitor matrix metalloproteinase-2(TIMP-2) of implanted tumor in nude mice after partial hepatectomy.Method Nude mice were divided into group A(n=10) implanted by human hepatocellular carcinoma(HCC),group B(n=10, partial hepatectomy) and C(n=10,HCC implantation after liver resection). SST(250 ?g/kg,b.i.d) was given intraperitoneally in group C. Mice were sacrificed on 35th d, tumor was measured, the expression of MVD.MMP-2 and TIMP-2 was detected by immunochemical staining and quantitative image computer-analysis. Results In group B, the weight and volume and expression of MVD.MMP-2 of tumor tissue was markedly incressed than in group A(P

AIM: To study effects of urokinase-type plasminogen activator (uPA) signal transduction on expression of matrix metalloproteinase-2 (MMP-2) and tissue inhibitor of matrix metalloproteinase-3 (TIMP-3) in giant cell tumor of bone (GCT). METHODS: Expression of uPAR, MMP-2 and TIMP-3 in GCT tissue was detected by immunohistochemistry. Phosphorylation level of mitogen-activated protein kinase (p44) in uPA/uPAR signal pathway in cultured GCT cells was detected by immunoprecipitation. The expression of MMP-2 and TIMP-3 in cultured cells after treatment with uPA-ATF or anti-uPAR antibody was also detected by Western blotting. RESULTS: 1) Urokinase-type plasminogen activator receptor (uPAR) was positive on the cell membrane and in cytoplasm of some mononuclear stromal cells (MSCs) and multinucleated giant cells (MGCs); 2) MMP-2 was positive in the cytoplasm and on the cell membrane of almost all of MSCs and some of MGCs. The polar distribution of MMP-2 in the cytoplasm of MGCs was especially obvious; 3) The expression of TIMP-3 of some MSCs and MGCs in GCT was much lower than MMP-2. The positive signal also showed a prominent polarity; 4) After treatment with uPA-ATF, the phosphorylation level of p44 in GCT cultured cells was much higher than the control. Addition of anti-uPAR antibody in the cells remarkably down-regulated the phosphorylation level of p44 as compared with the control group, suggesting that uPA-ATF participates cell signal transduction and this reaction can be inhibited by anti-uPAR antibody; 5) uPA-ATF cell signal pathway up-regulated expression of MMP-2 and TIMP-3, while anti-uPAR antibody down-regulated the expression of MMP-2 and TIMP-3. CONCLUSION: These results demonstrate for the first time that uPA-ATF directly regulates the expression of MMP-2 and TIMP-3 by signal transduction pathway, and the over-expression of MMP-2 and TIMP-3 may play an important role in local osteolysis of GCT. [