ABSTRACT
Objective To explore the shielding effects of 1-4 layers of lead aprons (LPs) and body shielding devices (BSDs) against stray radiation (SR) outside the electron beam field of 6-15 MeV.Methods JR-115B LiF TLDs were used to measure the stray radiation doses (SRDs) to the patient undergoing treatment,before and after being shielding,for different distances,different energies,different applicators,variable layers of LPs,and different thickness of body shielding devices (BSDs),respectively,along long calculating and comparing the shielding ratios of LPs and BSDs against SR.Results When the applicator (10 cm × 10 cm) is unchanged,the shielding ratio increased with the increased distance from measuring point (r =0.717,P ＜ 0.05) and decreased with the increased electron energy (r =-0.678,P ＜ 0.05);when the energy was constant,there was no correlation between the shielding ratio and the size of applicator (P ＞ 0.05);For lower energy electron beam of 6 and 9 MeV,the shielding ratio for 1 mm Pb-BSD was slightly higher than that for 2 layers of LA (t =2.519,2 662,P ＜ 0.05),ranging from 81.5％ to 95.3％ and 55.4％ to 84.6％,respectively.For 12 and 15 MeV higher energy electron beam,the shielding ratio for 2 mm Pb-BSD was slightly higher than that for 4 layers of LA (t=3.768,7.934,P＜0.05),ranging from 64.6％ to 93.4％ and 51.1％ to 92.4％,respectively.Conclusions LAs or BSDs are availavle for effectively reducing the doses from stray radiation,and may help reduce the secondary risks from stray radiation.BSDs have more obvious advantages than LPs with regard to shielding effect.
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Objective To observe the level of hypoxia-inducible factor-1 alpha (HIF-1α) and its downstream target gene cyclooxygenase-2 (COX-2) in LPS-treated intestinal epithelial cells,and to explore the possible intervention targets of Rheum emodin.Methods Human intestinal epithelial cells were cultured in vitro treated with LPS to establish the experimental model.The protein level trends of HIF-1α and COX-2 were measured by Western blot in LPS dose-dependent and time-dependent manners.The protein level trends of HIF-1α,COX-2,Phospho-IκB-α and Phospho-NF-κB p65 were measured in LPS plus various concentrations of Rheum emodin treated groups.The expression of HIF-1α mRNA were detected by PCR after cells treated with LPS or LPS plus Rheum emodin,respectively.The effect of Rheum emodin on the proliferation of intestinal epithelial cells was measured by MTT assay in each group.Data were analyzed with ANOVA,and P ＜0.05 was considered significant.Results LPS induced the protein level of HIF-1α in a dose-dependent and a time-dependent manners.With increasing concentrations of LPS,the protein level of HIF-1α increased to the peak when cells were treated with LPS at 10-30mg/mL,and then gradually decreased (P ＜0.05).Firstly the protein level of HIF-1α reached the peak at 0.5 h after treatment,and then decreased to the lowest level at 4 h,and finally returned to a high level (P＜0.05).The protein level trend of COX-2 went a similar way to that of HIF-1α (P ＜0.05).Rheum emodin inhibited the protein levels of LPS-induced HIF-1α,COX-2,Phospho-IκB-α and Phospho-NF-κB p65 with a significant dose-effect relationship (P ＜ 0.05).The PCR showed Rheum emodin inhibited LPS-induced increasing expression of HIF-1α mRNA.MTT assay showed different concentrations of Rheum emodin (0 μmol/L,20 μmol/L,40 μmol/L,60 μmol/L,80 μmol/L) had no significant effect on cell proliferation (0.95 ± 0.02,0.89 ± 0.03,0.88 ± 0.04,0.91 ± 0.03,0.83 ± 0.03,P ＞ 0.05).Although Rheum emodin produced biological effect at this concentration range,and it had no toxicity to intestinal cells.Conclusions LPS induces HIF-1α/COX-2 signaling pathway in a time-dependent and a dose-dependent manners in intestinal epithelial cells.Rheum emodin blocks the hypoxia pathway of LPS/HIF-1α/COX-2 and the inflammatory pathway of LPS/IκB-α/NF-κB/COX-2,which may play a protective effect on intestinal epithelial cells.
ABSTRACT
To investigate the expressions and changes of serum soluble intercellular adhesion molecule-1 (sICAM-1) in lung cancer patients before and after operation and the roles of sICAM-1 in differential diagnosis, metastatic potential, and prognosis. Methods From 2002 to 2003, a total of 17 samples of lung carcinoma tissues and sera were studied. The other 11 non-cancer patients were employed as the controls. Cell surface sICAM-1 levels were analyzed by immunohistochemistry method and ELISA. Results The serum sICAM-1 concentration in the cancer patients was (432.0?124.4) ng/ml. In the controls, however, the serum concentration of sICAM-1 was (262.3?77.7) ng/ml. In patients with lung cancer, the serum concentration of sICAM-1 was significantly higher than that of the controls (P0.05). Conclusion The serum sICAM-1 concentrations in lung cancer patients may play an important role in staging and may also serve as a useful indicator of advanced disease.