Objective To understand the antagonism of puerarin flavonoids (P) to octylphenol (OP) in the sperm damage. Methods Sixty male SD rats were randomly divided into three experimental groups (treated with octylphenol at doses of 80,160,320 mg/kg)and two intervention groups (0.5 g/kg P+320 mg/kg OP,5 g/kg P+320 mg/kg OP)and one control group. The administration was conducted by gavage,2 h after treated with octylphenol followed by puerarin flavonoids,three times a week for 60 consecutive days. Testicular morphological examination and sperm mobility were conducted. Results Compared with the control group,spermcount and mobility in the exposed groups and intervention groups were lower,malformation rate was highe(rP

20 cup-years) were found to have increased risk for pancreatic cancer (OR 3.681; 95%CI 1.604～8.443). Daily diet with high meat intake was also linked to pancreatic cancer. About 18.49% of the pancreatic cancer patients had diabetes mellitus compared to the control group of 5.77% (P=0.0003). Typical symptoms of pancreatic cancer were anorexia, upper abdominal pain, bloating, jaundice and weight loss. The high risk score of the two groups were 80.6 (95% CI 74.9～86.3) and 7.4(95% CI 6.0～8.7) (P

Objective To explore the expression of angiopoietin-1 (Ang-1) and lung development in neonatal rat with hy-peroxia-induced bronchopulmonary dysplasia (BPD). Methods A total of forty-eight 1-to 3-day-old neonatal rats were random-ly divided into hyperoxia group and control group with 24 rats in each group, fed in high concentration oxygen (≥95%) or in air respectively. At 1st, 3rd and 7th day after high oxygen exposure, the histological changes in lung tissue were observed by HE stai-ning under a light microscope and the expressions of Ang-1 mRNA and its protein in lung tissue were detected by RT-PCR and Western blot. Results With extended exposure to high concentrations of oxygen, rats in hyperoxia group presented such patho-logic change of lung tissue dysplasia as alveolar simplification, reduction in alveolar number and arrested pulmonary microvas-cular development. At 7th day after high oxygen exposure, Ang-1 mRNA and protein expressions in hyperoxia group were (0.33± 0.18) and (0.20±0.07), significantly lower than those [(0.83±0.46) and (0.57±0.44)] in control group (P<0.05). Conclusions Ang-1 plays an important regulatory role in the pulmonary vascular development and participates in the pathogenesis of BPD.

Objective:This study has two objectives. One is to detect the methylation status of reversion-inducing cysteine-rich protein with Kazal motifs (RECK, a new tumor suppressor gene) gene promoter in primary laryngeal squamous cell carcinoma and nor-mal laryngeal mucosa. The other is to analyze the correlation between RECK gene methylation status and radiosensitivity in laryngeal squamous cell carcinoma. Methods:Methylation-specific polymerase chain reaction was used to detect the RECK gene methylation of 70 specimens of laryngeal squamous cell carcinoma and 15 normal tissues of laryngeal mucosa. The patients underwent six cycles of ra-diotherapy and were followed-up for 5 years. The correlation between RECK gene methylation status and radiosensitivity in laryngeal squamous cell carcinoma was analyzed. Results: After six cycles of radiotherapy, 47 patients (67.14%) showed sensitivity and 23 (32.86%) showed tolerance to radiotherapy. The methylation level of the RECK gene was lower in the radiation-sensitive group than in the nonradiation-sensitive group (P<0.05). The methylation level of the RECK gene was lower in the remission group than in the non-remission group. RECK gene methylation could increase the risk of cancer by approximately 5.010 times (OR=5.010, 95%CI:1.616-15.533). Conclusion:RECK gene promoter methylation in human laryngeal squamous cell carcinoma is an early event that is correlated with the patient's sensitivity to radiotherapy. Thus, the patient's sensitivity to radiation can be predicted by detecting the meth-ylation status of the RECK gene promoter.

Burns ; complications ; therapy ; Cicatrix, Hypertrophic ; therapy ; Humans ; Keloid ; therapy

The study of subjects with different serum levels (mmol/L) of glucose, including NC (FPG6.1 mmol/L,

Chemokine CXCL9/Mig (monokine induced by IFN-?) belongs to the subfamily of chemotactic cytokines known as CXC-chemokines. In vivo CXCL9 is mainly induced by IFN-? in macrophages and primary glial cells. In vitro, CXCL9 can be secreted by cells such as macrophages, microvascular endothelial cells and neutrophils, in response to the synergy of IFN-? and TLR(toll-like receptor) ligands. CXCL9 is a chemoattractant for activated T lymphocytes, tumor-infiltrating T-lymphocytes, but not for neutrophils or monocytes. The receptor specific for CXCL9 is CXCR3, a G protein-coupled protein which has seven transmembrane domain. The structure and the chemical characterization of CXCL9, as well as its effects on autoimmune deseases, allograft rejection, cancer therapy were reviewed.

Objective To investigate the inhibitory effects and mechanism of ginsenoside Rg3 on vasculogenic mimicry of human breast cancer MCF-7 cell line. Methods The MCF-7 cells at logarithmic growth phase were obtained, and were cultured with different concentrations (0, 20, 50, 100, 150 and 300 mg/L) of ginsenoside Rg3. Cells cultured without Rg3 were served as controls. The IC50 were determined by CCK8 assay and anti-angiogenic effects were performed for testing the potential of tube-like structure (TLSs) formation. The expression levels of VEGF-A, MMP 9 and HIF-1αwere detected by Western blotting and real-time PCR. The secreted contents of VEGF-A and MMP9 were detected by enzyme linked immunosorbent assay (ELISA). Results The ginsenoside Rg3 suppressed the proliferation of MCF-7 cells in a dose-dependent manner, in which IC50 was (115.34±8.50) mg/L. The formation numbers of TLSs in MCF-7 cells were significantly inhibited by Rg3 in concentration dependent manner in 50 mg/L, 100 mg/L and 150 mg/L for (19.0 ± 1.0), (15.0 ± 1.5), and (10.0±1.7) vs. controls (22.0±1.8, F=150.805, P<0.05). The mRNA and protein expression levels of VEGF-A, MMP9 and HIF-1αprotein were inhibited by 50 mg/L,100 mg/L and 150 mg/L Rg3 vs. controls (P<0.05). Meanwhile, the contents of VEGF-A in MCF-7 cell supernatant was down-regulated by 50 mg/L,100 mg/L and 150 mg/L Rg3 vs. controls (P<0.05). The contents of MMP-9 in MCF-7 cell supernatant was down-regulated by 100 mg/L and 150 mg/L Rg3 vs. controls (P<0.05). There was no significant difference in MMP-9 expression between 50 mg/L group and control group. Conclusion The ginsenoside Rg3 is able to inhibit the vasculogenic mimicry of MCF-7 cells, which may be related with the down-
regulation of VEGF-A, MMP9 and HIF-1α.

Objective To investigate the role of antisense RNA of plasminogen activator inhibitor 1 (PAI 1) in regulating the expression of PAI 1 and vascular endothelial growth factor (VEGF) in aorta endothelial cells (EC) cultured in vitro. Methods The second extron of PAI 1 was amplified by polymerase chain reaction(PCR) and the product was inserted into eukaryotic cell expression vector pcDNA3.1(-) to construct PAI 1 antisence RNA recombinant plasmid. The recombinant plasmid was transfected into EC and the PAI 1 expression was detected by immunohistochemistry, Westernblot and ELISA. The effects of PAI 1 variation on VEGF were examined by immunofluorescence method. Results PAI 1 antigen was the lowest (0 017 ng/ml) in cells and the immunofluorescence representing the expression of VEGF in the cytoplasm showed the weakest at the third day after transfection. At the fifth day, PAI 1 antigen increased to 0 093 ng/ml with VEGF expression increased correspondingly. At the seventh day, PAI 1 antigen(0 143 ng/ml) and VEGF increased closed to normal level. Conclusions PAI 1 antisense RNA blocked the translation of PAI 1 proteins effectively and inhibited the expression of VEGF in aorta endothelial cells.

Objective To analyze the results of distal tibial pilon fractures treated with delayed open reduction and internal fixation. Methods From September 1997 to May 2001, 26 pilon fractures were stabilized temporarily by application of plaster splint, bandage, calcaneal traction (closed fracture) or unilateral external fixations (open fracture) immediately after injury. There were 19 males and 7 females with an average age of 37.6 years ( 15 to 58 years). Of 26 cases, 6 were open fractures and 20 close fractures, 18 of which were associated with fibular fracture. According to Ruedi-Allgower classification, the fractures were classified as typeⅠin 2, typeⅡin 15, and typeⅢ in 9. The conditions of soft tissue were divided into mild close injury without tension vesicle in 8, and severe injury with tension vesicle or open wound in 18. The definitive internal fixations were performed on an average of 10.2 days (range, 7 to 15 days) after injury as soon as the soft tissue recovered. The final outcomes of treatment were evaluated based on clinical rating and radiographic results. Results All patients were available for follow-up at an average of 3.8 years (range, 2 to 5.5 years) after surgery. All fractures healed at an average of 12.7 weeks (range, 8 to 29 weeks) postoperatively. There were 9 excellent(34.6%), 12 good (46.2%), 3 fair (11.5%), and 2 poor (7.7%) results according the ankle score of Teeny and Wiss. The results were significantly affected by the type of fracture and the severity of soft tissue injury, the excellent and good rate was 88.2% in typeⅠandⅡ, and 66.7% in typeⅢ; the total excellent and good rate was 100% in the patients with mild soft tissue injury, and 72.2% in the patients with severe soft tissue injury. The complications including 2 wound superficial infection and 1 skin necrosis, occurred in 3 patients(11.5%), which were successfully treated by local dressing changes. The incidence of osteoarthritis were found in 16 patients (61.5%) showed by X-ray films, but the radiographic manifestations did not correspond well with the clinical score. Conclusion This two-stage treatment protocol for pilon fracture has some advantages of fewer complications and good function.