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Under the strategic background of the "Healthy China" and the "coordinated development of Beijing-Tianjin-Hebei",based on the perspective of cross-boundary integration,taking the Beijing-Tianjin-Hebei health industry as the study case,it analyzed the basic condition of the health industry cross-boundary integration of the Beijing-Tianjin-Hebei region and considered that the Beijing-Tianjin-Hebei healthcare industry marketplace was immerse,which had good industrial foundation conditions and a certain degree of dislocation,provided with foundation for cross-border integration development.Therefore,it put forward further development path of the horizontal industry crossover and vertical industry chain integration in Beijing-Tianjin-Hebei healthcare industry,building and perfecting industrial chain,extending industrial development space,and promoting the cultivation and development of healthcare industry in three places.
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<p><b>OBJECTIVE</b>To elucidate the pathogenic role of leukotriene B4 (LTB4) in increased pulmonary microvascular endothelial cell permeability induced by one lung ventilation (OLV) in rabbits.</p><p><b>METHODS</b>Forty-eight healthy Japanese white rabbits were randomly divided into control group (group C), saline pretreatment group (group S), bestatin (a leukotriene A4 hydrolase (LTA4H) inhibitor) plus saline pretreatment group (group B), OLV group (group O), saline pretreatment plus OLV group (group SO) and bestatin plus saline pretreatment with OLV group (group BO). ELISA was used to detect LTB4 content in the lung tissues, and LTA4H and phospholipase Cεl (PLCEl) expressions were examined by Western blotting and quantitative PCR. The wet/dry weight (W/D) ratio of the lung, lung permeability index and the expressions of myosin light chain kinase (MLCK) protein and mRNA in the lung tissues were determined to evaluate the permeability of the pulmonary microvascular endothelial cells (PMVECs). The severities of lung injury were evaluated by lung histomorphological scores.</p><p><b>RESULTS</b>No significant differences were found among groups C, S and B except that LTA4H expressions was significantly lower in group B than in groups C and S (P<0.05). OLV significantly increased the expressions of LTA4H (P<0.05) and resulted in LTB4 overproduction in the lungs (P<0.05) accompanied by significantly enhanced PLCE1 expression and PMVEC permeability (P<0.05). Pretreatment with bestatin, significantly reduced the expression of LTA4H and LTB4 production (P<0.05) and down-regulated the expression of PLCE1 in the lungs of the rabbits receiving OLV (P<0.05).</p><p><b>CONCLUSION</b>Bestatin plays a protective role in OLV-induced rabbit lung injury by downregulating LTA4H to reduce the production of LTB4 in the lungs. LTB4 can increase PMVEC permeability by up-regulating PLCE1 expression in rabbits with OLV-induced lung injury.</p>
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Objective: To investigate the expressions of actin filament-associated protein 1 antisense RNA 1 (AFAP1-AS1), a long non-coding RNA (IncRNA) in four common human digestive system cancers including esophageal cancer, gastric cancer, liver cancer and colorectal cancer, and their clinical significance. Methods: The expression of AFAP1-AS1 was preliminarily detected in several digestive system tumor tissues and their corresponding adjacent normal tissues from 82 cases by multi-tumor tissue microarrays. These 82 patients included 11 with esophageal cancer, 11 with gastric cancer, 26 with liver cancer, and 34 with colorectal cancer. The expression of AFAP1-AS1 which had significant difference in liver tumor tissues was further tested by in situ hybridization (additional 70 cases) and real-time fluorescence quantitative PCR (additional 30 cases). The relationship between the expression of AFAP1-AS1 and the clinicopathological features was analyzed. The role of AFAP1-AS1 in tumor lymph node metastasis was assessed. Results: The expression of AFAP1-AS1 in liver cancer was significantly lower than that in its corresponding adjacent normal liver tissue (P 0.05). Further test also revealed that the expression of AFAP1-AS1 was significantly down-regulated in liver cancer, and this effect was associated with clinical stage and lymph node metastasis (P < 0.05). The sensitivity, specificity, coincidence rate, positive predictive value and negative predictive value of AFAP1-AS1 serving as a molecular marker of metastasis were 68.75%, 65.00%, 65.63%, 28.21% and 91.23%, respectively. Conclusion: The expression of AFAP1-AS1 may play a role in the pathogenesis and progression of liver cancer and esophageal cancer, but this effect is different between these two cancer types. It is suggested that AFAP1-AS1 may become a noval molecular marker for clinical diagnosis of liver cancer. Copyright© 2014 by TUMOR.
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<p><b>OBJECTIVE</b>To investigate the role of nicotine on the proliferation and cell apoptosis in SCC15 oral squamous cell carcinoma cells.</p><p><b>METHODS</b>The growth, apoptosis, reactive oxygen species (ROS) level and nuclear factor kappalight-chain-enhancer of activated B cell (NF-κB) DNA binding activity were detected in SCC15 oral cancer cell using methly thiazolyl tetrazolium assay, flow cytometry, enzyme linked immunosorbent assay.</p><p><b>RESULTS</b>In SCC15 cells treated with nicotine for 48 h at different concentrations (0.1, 1, 10 µmol/L) ROS level was (98.24 ± 0.04)%, (98.50 ± 0.06)%, (98.61 ± 0.07)%, respectively, which were significantly higher than in control groups [(96.01 ± 0.58)%, P = 0.000] and the A value for cell growth was 2.19 ± 0.08, 2.20 ± 0.11 and 2.38 ± 0.08, respectively, which were significantly higher than in control groups (1.93 ± 0.13) (P < 0.05). Only 1 µmol/L nicotine induced significantly higher cell apoptosis than in other groups (P = 0.000). Cell growth was inhibited in SCC15 cells treated with 1 µmol/L nicotine for 72 h, which had statistically significant difference compared with control (P = 0.022). Cell apoptosis rate in 1 µmol/L nicotine treated groups for 24 h was significantly higher than 48 h and 72 h (P = 0.000). NF-κB expression in the nucleus were increased in SCC15 cells treated with 1 µmol/L nicotine for 24, 48 and 72 h and the A value for NF-κB DNA binding activity was 1.509, 1.093 and 0.746, respectively, which were higher than in control group (0.544).</p><p><b>CONCLUSIONS</b>Nicotine induced SCC15 cell growth and apoptosis, which maybe by NF-κB signal pathway activated in oral cancer cells.</p>
Subject(s)
Humans , Apoptosis , Carcinoma, Squamous Cell , Metabolism , Pathology , Cell Line, Tumor , Cell Proliferation , Mouth Neoplasms , Metabolism , Pathology , NF-kappa B , Metabolism , Nicotine , Pharmacology , Reactive Oxygen Species , MetabolismABSTRACT
<p><b>OBJECTIVE</b>To study the indoor environmental factors associated with the prevalence of asthma and related allergies among school children.</p><p><b>METHODS</b>A cluster sampling method was used and the ISAAC questionnaire was conducted. A total of 4612 elementary students under Grade Five of 7 schools were enrolled in the survey for the impact of indoor environmental factors on the prevalence of asthma and related allergies in several urban and suburban schools of Beijing.</p><p><b>RESULTS</b>A total of 4060 sample were finally analyzed including 1992 urban and 2068 suburban. The prevalence of wheeze, allergic rhinoconjunctivitis and atopic eczema in the past 12 months was 3.1% (61/1992), 5.3% (106/1992), 1.1% (22/1992) among urban children while 1.3% (27/2068), 3.1% (65/2068), 1.0% (22/2068) among suburban children respectively. The prevalence of wheeze and allergic rhinoconjunctivitis of the past 12 months in urban were both significantly higher than that in suburban (χ(2) = 14.77, 11.93, P < 0.01). The incidences of having asthma and eczema ever among urban children (5.3% (105/1992), 29.4% (586/1992)) were significantly (χ(2) = 39.03, 147.22, P < 0.01) higher than that among suburban (1.7% (35/2068), 13.8% (285/2068)). Although the distributions of indoor environmental factors were similar in both areas, passive smoking and interior decoration had different influence on the prevalence of asthma and related allergies among school children in the two areas. The significant impact of passive smoking on having asthma ever among suburban children was observed (OR = 2.70, 95%CI = 1.17 - 6.23) while no significant result in urban (OR = 1.06, 95%CI = 0.71 - 1.58); the percentage of interior decoration was 84.0% (1673/1992) among urban children and 80.0% (1655/2068) among suburban children, there was significant impact of interior decoration on the prevalence of having eczema ever among urban children (OR = 1.57, 95%CI = 1.17 - 2.10) but no significant results were found in suburban sample (OR = 1.06, 95%CI = 0.76 - 1.48).</p><p><b>CONCLUSION</b>The prevalence of asthma and related allergies among school children is much higher in urban areas than that in suburban areas and the indoor environmental factors such as passive smoking and interior decoration may differently explain the prevalence of asthma and related allergies in the two areas.</p>