Objective:To investigate the expression of cyclooxygenase-2 in primary hepatocellular carcinoma, in cancer surrounding tissues and normal liver tissue and its relationship with clinical pathological features.Methods:The expression of COX-2 was detected in 30 cases of hepatocellular carcinoma, 20 cases of cancer surrounding tissue and 10 normal liver tissue by flow cytometry (FCM) and immunohistochemistry (SP). The clinical data were analyzed retrospectively.Results:(1)The expression of COX-2 in the HCC tissue was significantly higher than in cancer surrounding tissues and normal liver tissue (P0.05).Conclusion:The hyperexpression of COX-2 in tissue can reflex the biological behavior of HCC,and have very important role in the development of HCC.The specificness of COX-2 protein expression make it to be new target of tumor diagnosis and treatment.These results provide a theoretical basis for the chemoprevention of hepatoma.

Objective:To study the expression of COX-2 and Survivin in HCC tissues and their relationship for supplying experimental evidence for gene diagnosis and treatment of HCC.Methods:The expression of COX-2 and Survivin was detected in 30 cases of hepatocellular carcinoma and 10 normal liver tissue by Flow cytometry (FCM) and immunohistochemistry (SP).Results:Two experimental methods showed that the positive expression of COX-2 and Survivin in HCC was significanly higher than that in normal liver tissue and there was significanly positive correlation between the expression of COX-2 and Survivin.Conclusion:The hyper-expression of COX-2 and Survivin in tissue can reflex the biological behavior of HCC and there are synergistic effect between them during the development of HCC.A possible mechanism is inhibition of tumor cell apoptosis through upregulating Survivin by COX-2,and promoting abnormal cell proliferation in development of hepatocellular carcinoma.

BACKGROUND: Prognosis is determined by degrees of outside force and time of spinal cord compression after spinal cord injury. The former factor cannot be changed, but the latter one can be changed through relieving spinal cord compression as early as possible to promote nervous function recovery.OBJECTIVE: To compare the effect of surgical intervention time on nervous function recovery within 72 hours and 10 to 14 days after cervical spinal cord injury.DESIGN: Randomized controlled and before-after controlled study.SETTING: Department of Spine Surgery of the Second Hospital affiliated to Harbin Medical University.PARTICIPANTS: A total of 32 patients with cervical spinal cord injury were selected from the Department of Spine Surgery of the Second Hospital affiliated to Harbin Medical University from April 1998 to August 2001.All patients were divided into two groups according to randomly alternative criteria. There were 16 cases including 10 males and 6 females in early surgical group (within 72 hours) and there were also 16 cases including 12males and 4 females in delayed surgical group (within 10-14 days).METHODS: Patients in early surgical group were undertaken operation at 72 hours after hospitalization, and patients in delayed surgical group were at 10-14 days after hospitalization. Frankel grade, sensory and motor scores were recorded according to criteria set by American Spinal Injury Association before operation and within 24 months after operation.MAIN OUTCOME MEASURES: ① Sensory and motor scores before and after operation; ② Frankel grade before and after operation.RESULTS: ① Improved level of sensory score (difference before and after operation) was higher in early surgical group than that in delayed surgical group (42.6±20.2, 19.2±19.1, P ＜ 0.01). ② Improved level of motor score (difference before and after operation) was higher in early surgical group than that in delayed surgical group (39.7±17.8, 17.3±18.6, P ＜ 0.01). ③Improved level of Frankel grade in early surgical group was superior to that in delayed surgical group (P ＜ 0.01).CONCLUSION: Nervous function recovery of patients with acute cervical spinal cord injury who were suffered from operation within 72 hours is superior to that of those within 10 to 14 days. Therefore, surgical intervention should be undertaken as early as possible in order to promote nervous function recovery after cervical spinal cord injury.

Objective To investigate the relationship between the expressions of P16 and proliferating cell nuclear antigen(PCNA) in osteosarcoma and clinicopathological features,and explore the effects of them in occurrence and development of osteosarcoma.Methods The expressions of P16 and PCNA were detected by immunohistochemistry(SP) in 71 osteosarcima tissues and 10 normal bone tissues.Results ①The positive rate of P16 expression in osteosarcoma tissues was lower than that in normal bone tissues(P0.05).The expression of PCNA had positive relationship with osteosarcoma's prognosis(P0.05).③There was negative correlation between P16 and PCNA expressions(rs=-0.58,P

Objective To study the influence of survivin targetedly inhibited with antisense oligonucleotide (ASODN)technique on the apoptosis of hepatoma carcinoma cells SMMC-7221,and to clarify the mechanism of promotion effect of survivin-ASODN on the apoptosis of SMMC-7721 cells.Methods The ASODN sequence of survivin marked by FAM fluorescein was designed and synthized. The SMMC-7721 cells were transfected by different concentrations (100,200,300,400,and 600 nmol· L-1 )of survivin-ASODN (ASODN transfection groups),at the same time blank control group and blank liposome control group and sense oligonucleotide (SODN) control group were set up.The apoptotic rates and the changes of cell cycle of the SMMC-7721 cells 24,48,and 72 h after transfected with different concentrations of survivin-ASODN were detected by FCM. The expression levels of survivin were measured by Western blotting method.Results Compared with each control group,24 h after transfection,the apoptotic rates of survivin-ASODN transfected SMMC-7221 cells were increased,the growth of cells was inhibited (P<0.05),and the effects had time-dose dependent tendency.48 h after transfection,the hypodiploid apoptotic peak appeared in ASODN transfection groups before G1 phase, the number of the cells at G0/G1 phase was decreased (P<0.05)and the number of the cells at G2/M phase wsa increased (P<0.05). Compared with each control group,the survivin expression levels in the SMMC-7721 cells in ASODN transfection groups were decreased (P<0.05 ), and the effects of survivin-ASODN was time-dose dependent (P<0.05 ). Conclusion Survivin-ASODN can block the expression of survivin in SMMC-7721 cells and inhibit the proliferation of SMMC-7721 cells by changing the cell cycle and increasing apoptosis in a time-dose dependent manner.

Objective To explore the potential mechanisms of non-small cell lung carcinoma cells to rsTRAIL protein-induced apoptosis by phosphatidylinositol 3′-kinase (PI3K/Akt)inhibitor LY294002,and to provide new ways to increase killing activities of rsTRAIL protein for non-small cell lung cancer.Methods The A549 cells at logarithmic growth phase were selected and randomly divided into rsTRAIL group and LY294002+rsTRAIL group. The inhibitory rate of growth of the A549 cells was tested by MTT assay.The cell cycle and apoptotic rate were detected by flow cytometry analysis. The expression levels of Ser473 phosphorylated form of Akt (p-Akt),c-FLIPL protein and Bcl-2 protein in the A549 cells in two groups were analyzed by Western blotting method. Results The inhibitory rate of growth of the A549 cells in LY294002+rsTRAIL group (74.6 %± 2.63%)was higher than that in rsTRAIL group (5.61% ± 0.32%) (P< 0.05 ). Compared with rsTRAIL group, the percentage of the cells at G0/G1 phase in LY294002+rsTRAIL group was increased(P<0.05)and the percentage of the cells at S phase was decreased(P<0.05).The apoptotic rate of the A549 cells in LY294002+rsTRAIL group (61.5%±3.02%)was higher than that in rsTRAIL group (3.21%±0.96%)(P<0.05). The Western blotting results showed that the expression levels of p-Akt, c-FLIPL and Bcl-2 proteins in the A549 cells in LY294002+rsTRAIL group were decreased (P<0.05 )and the ratio of Bax/Bcl-2 was increased (P<0.05 ) compared with rsTRAIL group.Conclusion LY294002 can increase the killing activity of rsTRAIL protein in A549 cells by inhibiting the activity of PI3K.

Objective:To investigate mechanism of TRAIL-resistance in A549 cells ( a cell line of non-small cell lung carcino-ma cells) due to Akt phosphorylation .Methods:A549 cells were treated with Akt inhibitor Perifosine and rsTRAIL protein individual-ly and in combination.The expressions of Akt phosphorylation(p-Akt),c-FLIPLL and caspase-8 were detected by Western blot.The apoptotic rate of the A549 cells treated was detected by flow cytometry and the cell proliferation was evaluated by MTT assay .Results:A549 cells showed the increased level of Akt phosphorylation mediated by rsTRAIL protein .Treatment with the Akt inhibitor Perifosine induced a suppression of Akt activation in A 549 cells and a concomitant decrease in the expression of c-FLIPLL .As a result, Perifosine significantly enhanced TRAIL-induced apoptosis rate of (76.5 ±3.02)%and cytotoxic rate of (83.2 ±2.54)%by promoting the activ-ity of caspase-8.Conclusion:Akt activity promotes A549cells survival against TRAIL-induced apoptosis and that the cytotoxic effect of rsTRAIL protein can be enhanced by modulating the Akt phosphorylation in human non -small cell lung carcinoma cells .

The aim of this study was to explore the effects of ZGXF decoction on amphetamine-induced rotation in PD rats with syndrome of liver-yang hyperactivity,and its mechanism involved.Rats received 6-OHDA administration via intra-substantia nigra injection and were intragastrically treated by Fu Zi decoction to establish the PD model with the syndrome of liver-yang hyperactivity.Three doses of ZGXF decoction or selegiline were given by a 28-day intragastric administration.The rats were tested for amphetamine-induced rotation asymmetry.In addition,real-time PCR were adopted to analyze the expressions of Nfe212 and Hmox1 mRNAs,while western blot to analyze the expression of Keap1 protein.As a result,it was found that ZGXF decoction dose-dependently attenuated amphetamine-induced rotation,up-regulated the expressions of Nfe212 and Hmox-1 mRNAs,and down-regulated the expression of Keap1 protein in the substantia nigra in PD rats with syndrome of liver-yang hyperactivity.It was suggested that anti-PD effects of ZGXF decoction be attributed to the up-regulation of Nfe212 and Hmox-1 mRNAs and the down-regulation of Keap1 protein,being associated with oxidative stress,in the substantia nigra of PD rats with syndrome of liver-yang hyperactivity.

OBJECTIVETo study the effect of vitamin C on preventing oxidative modification of low density lipoprotein cholesterol (LDL) in vitro.

METHODSDifferent levels of vitamin C were added to two different systems of lipid peroxidation of LDL induced by either Cu(2+) or macrophage. The level of VC in systems induced by Cu(2+) were 10, 50, 100 and 200 micromol/L respectively and by macrophage were 50, 100, 200 micromol/L respectively. Vitamin E (200 micromol/L) and VC(0) (0 micromol/L) were served as positive and negative control respectively. The content of TBARS, Ox-LDL, fluorescent compounds, electrophoretic mobility of LDL and the lag-phage of oxidation of LDL were measured.

RESULTSIn the oxidative systems induced by Cu(2+), the groups with higher levels of VC (100, 200 micromol/L) reduced the levels of TBARS, Ox-LDL at 3, 6, and 9 hour after adding Cu(2+), but low dose groups (10, 50 micromol/L) had no the effects. In the macrophage systems, higher levels of VC (100, 200 micromol/L) significantly reduced levels of fluorescent compounds and TBARS, and also lowered electrophoretic mobility of LDL and increased the lag-phage of oxidation of LDL.

CONCLUSIONVitamin C has dual effect on oxidation of LDL. Low dose treatment enhanced oxidation of LDL, but high doses has anti-oxidative effects on LDL.

Animals ; Antioxidants ; metabolism ; pharmacology ; Ascorbic Acid ; metabolism ; pharmacology ; Cells, Cultured ; Copper ; Electrophoresis, Agar Gel ; methods ; Fluorescent Dyes ; Lipofuscin ; analysis ; Lipoproteins, LDL ; biosynthesis ; metabolism ; Macrophages, Peritoneal ; cytology ; drug effects ; metabolism ; Male ; Oxidation-Reduction ; Rats ; Rats, Sprague-Dawley ; Thiobarbituric Acid Reactive Substances ; metabolism

Background:The occurrence of gastric cancer is a gradual process with multiple factors and multiple steps. In addition to cytological and structural abnormalities,there are abnormal molecular expressions,which involve the activation of many oncogenes and the inactivation of tumor suppressor genes. Aims:To explore the expressions and significance of Ki-67,p53 and P504s in normal gastric mucosa,atrophic gastritis with intestinal metaplasia,low-grade intraepithelial neoplasia,high-grade intraepithelial neoplasia and early gastric cancer. Methods:A total of 44 cases of normal gastric mucosa,44 cases of atrophic gastritis with intestinal metaplasia,41 cases of low-grade intraepithelial neoplasia,38 cases of high-grade intraepithelial neoplasia and 35 cases of early gastric cancer from Jan. 2015 to Dec. 2016 at the Affiliated Drum Tower Hospital of Nanjing University Medical School were collected. Expressions of Ki-67,p53 and P504s were detected by immunohistochemical staining. Results:Compared with normal gastric mucosal tissue,the positivity rates of expression of Ki-67,p53 and P504s in atrophic gastritis with intestinal metaplasia,low-grade intraepithelial neoplasia,high-grade intraepithelial neoplasia and early gastric cancer were obviously increased (P＜0.05). With the increasing of severity of the lesion,the positivity rate gradually increased. Conclusions:The expressions of Ki-67,p53 and P504s are closely related to the occurrence and development of gastric cancer,and are involved in the early process of gastric cancer. The detections of these molecular markers are helpful for determining the severity and trend of the lesion,and beneficial for improving the detection rates of gastric precancerous lesion and early gastric cancer.