0.05).The recurrence of pterygium was related to the age.If the age increased five years,the risk of recurrence decreased 18.1%. Conclusion The application of MMC(during) the operation could decrease the recurrence rate of pterygium.The recurrence rate of pterygium was not related to the time of application of 0.02% MMC,and detainment for 3 min was enough during the operation.

Objective To investigate the role of survivin and P53 in apoptosis of gastric adeno- carcinoma,as well as its relationship with the clinicopathologic features and the prognosis.Methods The gas- tric tissue microarrays were composed of those from 100 cases of gastric cancer and 30 controls.At these tissue microarrays,expressions of survivin and P53 were investigated immunohistochemically,and tumor cell apoptosis index was examined by TUNEL method.Of the 100 cases,47 cases were followed-up from 14 months to 13 years,in which the survival was analyzed.Results Two paraffin-embedded gastric carcinoma tissue micro- arrays were successfully constructed,including 114 and 116 tissue spots,respectively.Immunohistochemical analysis showed that survivin was expressed in 78 cases (78%).No expression of survivin was detected in control tissue (P0.05).In the 47 cases with followed-up data,univariant analysis revealed that the survival was correlated with invading of vessel and nerve,TNM stages,and expression of survivin.The histological grades and expression of P53 were not related to prognosis.However,Cox stepwise proportional hazards analysis showed that only TNM staging and survivin status retained significant independently in prospecting prognosis.Conclusions The expression of survivin was associated with the pathologic features,TNM stages and prognosis in gastric carcinoma,indicating that overex- pression of survivin may be a poor prognosis factor for gastric carcinoma.

Objective To explore the relationship between self-efficacy and health behavior among stroke survivors.Methods Self-efficacy for Managing Chronic Disease 6-item Scale and Health Promoting Lifestyle Profile II were used to measure 96 stroke survivors’ self-efficacy and health behaviors.Pearson correlation analysis was used for the analysis of correlation.Results The mean score of overall health behaviors was (2.41±0.33).Pearson’s correlation coefficient between self-efficacy and health behavior was 0.36 (P<0.05).Conclusions The health behaviors of stroke survivors were at the intermediate or lower level and their self-efficacy was at the intermediate level.In order to help stroke survivors to improve their health behaviors,self-efficacy should be enhanced by specific health education.

Objective To investigate the expression level of endogenetic nitric oxide(NO) in the reproduction process of human anterior cruciate ligament cells. Methods Anterior cruciate ligament cells were isolated and subcultured from the human anterior cruciate ligament. LPS was used to induce the anterior cruciate ligament cell to express the inducible nitric oxide synthase(iNOS ), and N-monomethyl -L-Arginine (L-NMMA) was used as the interdiction of nitric oxide. They were alone or together added in the culture medium of anterior cruciate ligament cells in different groups. The level of NO was indirectly measured in the medium of HACL. Results LPS promoted significantly anterior cruciate ligament cells to produce endogenetic nitric oxide, compared with the control group(P

Objective To explore the effect of interferon-?(IFN-?)on phenotypic transition of human Tenon’s conjunctival capsular fibroblast(HTCF). Methods Cultured HTCF derived from 4 operated human cataracts was induced for 48 hours in absence or presence of IFN-? and/or transforming growth factor-?1(TGF-?1). Then immunocytochemistry and Western blot technology were used to detect the ?-smooth muscle actin(?-SMA)expression and identificate the cell phenotype. Results In contrast to normal HTCF, IFN-?(10 ng/mL) inhibited the expression of ?-SMA(P

BACKGROUND: Intra-articular injection of hormone has been applied in the treatment of arthritis because it can alleviate arthralgia rapidly, which is accompanied commonly by progressive cartilage impairments. It is not clear if supplement of growth factor like insulin effect can play a protective role in articular chondrocytes.OBJECTIVE: To observe the effects of insulin or hydrocortisone alone and the combination on the proliferation of chondrocytes.DESIGN: Grouping comparative study, the effect of one medicine was analyzed by using one-factor analysis of variance, while the combined effect was analyzed with multi-factor analysis of variance.SETTING: Guangdong Institute of Trauma Sugery.MATERIALS: Articular cartilage from the knees of New Zealand white rabbits of 4 - 6 weeks old.METHODS: This study was carried out at Guangzhou Traumatic Research Institute from Feberary 2000 to May 2001. Chondrocytes were isolated from the knee joints of New Zealand white rabbits, digested with hyaluronidase,pancreatin and type Ⅱ collagenase and exposed to insulin, hydrocortisone or the combination of insulin and hydrocortisone of different dosage. They were divided into four groups:Control group ( without adding insulin and hydrocortisone), insulin group (0. 035,0. 35,3.5,35 mg/L subgroups), hydrocortisone group(1,5,10,50,100 mg/L subgroups) and insulin(0. 35 mg/L) combined with hydrocortisone(50 mg/L) group. Their influence on chondrocytes proliferation was observed with methyl thiazolyl tetrazolium(MTT) method.sulin.at the concentration of 0. 035 mg/L( P ＜ 0.01 ), reaching the maximum at could inhibit the proliferation of chondrocytes ( P ＜ 0.05 ), which became significant with increasing concentration and no viable chondrocytes could be exposed to 0 . 35 mg/L insulin combined with 50 mg/L hydrocortisone, the promoting effect of insulin was inhibited due to negative cooperation.CONCLUSION: Insulin at low concentration could enhance the proliferation of chondrocytes, but hydrocortisone displayed inhibiting effect on the growth of chondrocytes. The function of insulin was antagonized when combined with hydrocortisone.

BACKGROUND: Type Ⅱ collagen has been used as the carrier for chondrocyte transplantation in animal models, but whether type Ⅱ collagen may cause arthritis or mediate cytotoxicity remains unknown.OBJECTIVE: To detect the cellular immune functions of the New Zealand rabbits immunized by porcine type Ⅱ collagen.DESIGN: An exploratory comparative study based on the observations.SETTING: An institute of trauma surgery of a municipal hospital.MATERIALS: The study was conducted in the Institute of Trauma Surgery,Guangzhou Red Cross Hospital from August 1999 to February 2000. Six New Zealand rabbits, whose body mass ranged from 2.0 kg to 3.0 kg, were chosen of either gender.METHODS: The rabbits were immunized by porcine type Ⅱ collagen for 60days, during which the plasma was regularly taken for detection of type Ⅱ collagen antibody. On the 60th day, the peripheral blood as well as the spleens and lymph nodes were taken to separate the lymphocytes, which were subjected to secondary stimulation with type Ⅱ collagen in vitro to observe the reactive cell proliferation. The lymphocytes were randomly divided into two groups, and the first group was treated with phytohemagglutinin(PHA) of different concentrations to serve as the positive control, in which non-specific immunity was examined; The second group was treated with type Ⅱ collagen of different concentrations for examining specific immunity.peripheral blood lymphocytes of normal and immunized rabbits.RESULTS: On the 21st day, the titer of the antibody presented the first peak, and 40 days after the re-injection of the antigen the second peak appeared, which maintained for 20 days and then gradually descended. The lymphocytes of the normal rabbits proliferated in response to PHA stimulation but not to the first stimulation with the type Ⅱ collagen. The lymphocytes of the immunized rabbits exhibited significant proliferation upon stimulations with both PHA and type Ⅱ collagen. At the concentration of 25 mg/L, type Ⅱ collagen stimulation was sufficient to induce lymphocyte proliferation, the peak of which occurred when the collagen concentration reached 50 mg/L.CONCLUSION: Xenogenic type Ⅱ collagen at an adequate concentration may induce the increase of the type Ⅱ collagen antibody in immunized rabbits and proliferation of lymphocytes of the spleens and peripheral blood to cause cellular immune reaction and even immunological arthritis in relation to the transplantation.

Objective To study the characteristics of clustering of cardiovascular risk factors in patients less than 50 years-old of premature stable coronary heart disease(PSCHD)complicated with nonalcoholic fatty liver(NAFL).Methods One hundred and six patients with documented PSCHD were recruited into this study and their clinical data,including biochemical parameters,high-sensitivity C-reactive protein(hsCRP),white blood cell(WBC)count,ete.,were analyzed based on whether they had NAFL by B-type ultrasound scanning and their homeostasis model assessment ratio(Homa-IR)by the criteria for metabolic syndrome formulated by the International Diabetes Federation.Results Thirty-two (30.1percent)of 106 patients of PSCHD complicated with NAFL,and 74(69.9 percent)without NAFL. As compared to patients without NAFL,patients with NAFL had higher fasting blood glucose(FBS),serum level of insulin(INS),total cholesterol(TC),triglyceride(TG),serum activity of alanine aminotransferase(ALT),hsCRP,WBC count,body mass index(BMI),Homa-IR,and higher proportion of those with abnormal blood glucose,hypertension.metabolic syndrome(MS)and carotid atherosclerosis (CA)(P＜0.05),respectively.Bi-variate correlation analysis revealed that hsCRP positively correlated to BMI,TG,ALT and Homa IR(r=0.420,P=0.000;r=0.200,P=0.040;r=0.218,P=0.048:and r=0.546,P=0.000,respectively)and inversely correlated with serum level of high-density lipoprotein cholesterol(HDL-C)(r=-0.220,P=0.023).WBC count positively correlated with FBS(r=0.211,P=0.030).BMI,hsCRP,ALT,and proportions of hypertension,diabetes,MS,NAFL and CA in patients with Homa-IR above median were significantly higher than those in patients with that below median ( P＜0.05,respectively).Conclusions More risk faetors for chronic inflammatory reaction,cardiovascular disease and insulin resistance were clustered more obviously in patients of PSCHD complicated with NAFL.

Objective To observe hypoxia-induced pulmonary arterial endothelial-to-mesenchymal transition and investigate the role of transforming growth factor β1 (TGF-β1) in the process. Methods Pulmonary arterial cells improved by adherence method were cultured in normoxia (containing 21%O2,5%CO2 and 74%N2) or hypoxia (containing 1%O2,5%CO2 and 94%N2) for 1,4,or 7 days,respectively. Endothelial-to-mesenchymal transition was confirmed with morphological observation and expression of α-smooth muscle actin (α-SMA) by immunocytochemistry. Expression of TGF-β1 was evaluated by RT-PCR and Western blot,and α-SMA by Western blot. Results Hypoxia-induced paving-stone-like pulmonary arterial endothelial cells transdifferentiating to polygonal cells with high-expression of α-SMA. TGF-β1 expression was increased significantly after 7 days of hypoxia. TGF-β1 stimulating alone increasedα-SMA expression of pulmonary arterial en-dothelial cells;while,SD-208,inhibitor of TGF-β1,abolished the above effect. Conclusion Hypoxia can induce endothelial-to-mesenchymal transition. And TGF-β1 plays an important role in the process.

Objective The role of long non-coding RNA Linc00467 in human lung adenocarcinoma is not yet clear.This study was to investigate the expression of long non-coding RNA Linc00467 in human lung adenocarcinoma, its clinical significance, and the effects of Linc00467 on the functions of the tumor and endothelial cells in vitro.Methods Lung adenocarcinoma tissue and normal tissue surrounding the malignance were obtained from 60 patients with pathologically proved stage I-Ⅲa lung adenocarcinoma.Human umbilical vein endothelial cells (HUVECs) were transfected with the over-expressed plasmid pccl-Linc00467 (HUVEC experimental group) or the empty vector pccl (HUVEC control group), A549 cells with Linc00467-siRNA (A549 experimental group) or negative siRNA (A549 control group), and H1299 cells, too, with Linc00467-siRNA (H1299 experimental group) or negative siRNA (H1299 control group).The expression level of Linc00467 in the lung adenocarcinoma tissue was detected by qRT-PCR with an analysis of its correlation with the clinicopathological characteristics of the patients;the influence of Linc00467 on the proliferation of the A549, H1299 and HUVEC cells was assayed with CCK-8;and the role of Linc00467 in the angiogenesis of the HUVECs was assessed by fibrin bead sprouting assay.Results The expression of Linc00467 in the lung adenocarcinoma tissue was 2.72±1.31 times as high as that in the normal lung tissue (P<0.01), and those in the A549 and H1299 cells were 3.45±0.25 and 3.22±0.33 times as high as those in the human bronchial epithelial (HBE) cells (P<0.01).The expression level of Linc00467 was significantly correlated with the tumor size and vascular invasion (P<0.05).After transfection of Linc00467-siRNA, the expressions of Linc00467 in the A549 and H1299 experimental groups were down-regulated by 72% and 68% as compared with those in the A549 and H1299 control groups (P<0.01).The number of living cells was remarkably decreased in the A549 experimental group in comparison with the A549 control at 48 h (1.29±0.07 vs 1.51±0.09), 72 h (1.53±0.15 vs 2.13±0.11), and 96 h after culturing (1.98±0.18 vs 3.02±0.12), and so was it in the H1299 experimental versus the H1299 control group, but markedly increased in the HUVEC experimental versus the HUVEC control group (P<0.05).At 5 days, HUVEC experimental group, as compared with the HUVEC control, showed a significantly increased number of newly formed vascular branches (7.36 vs 4.25/superbead, P<0.01) and relative length of the blood vessels (3.12 vs 1, P<0.01).Conclusion Linc00467 promotes tumor cell proliferation and angiogenesis and is highly expressed in the lung adenocarcinoma tissue, which is correlated with the tumor size and vascular invasion and suggests that Linc00467 could be a potential biomarker and therapeutic target.