Objective To investigate the expression of hypoxia inducible factor-1?and VEGF in lung of mice during hypoxia and its relationship with angiogenesis.Methods The mice were divided into two group(hypoxia group and control group).The hypoxia group mice were placed in a hypoxia chamber with 10%,7%,or 5%O2 respectively for 3,6,9 days.Immuno- histochemical staining technique was used to examine HIF-1?,VEGF and MVD.The p rotein expression of HIF-1? and VEGF were observed by Western blot.Results HIF-1?proteins didn't express and VEGF proteins expressed weakly in control group mice;Compared with the controls,the expression of HIF-1?and VEGF increased dramadically.There were significant differences between the hypoxia groups and the control group;Positive relationships were found between the expression of HIF-1?,VEGF and MVD.Conclusion HIF-1?/VEGF pathway may play an important role in angiogenesis of hypoxia in the lung of mice.

Objective To investigate the setup errors of super chest segment of esophageal cancer patients before radiotherapy delivery by KV cone beam CT,and evaluate the margin from CTV to PTV.Methods From 2010 to 2012,13 patients with super chest segment of esophageal cancer whose IMRT planning CT images were included in this study.Delineate target on the CT images of treatment planning and enlarge the margin of CTV to form ITV,then enlarge the margin of ITV gradually 10 times by 1 mm each time to form varied PTV,and create the plan according to the size of the PTV,simulate setup errors in the new plan to obtain the simulation of the actual exposure curve and find a suitable PTV to assure 95％ ITV volume as ever to approach the prescription dose,obtained the outside enlarge distance of CTV → PTV.Results The maximum setup errors in the direction of the anterior and posterior positioning was (3.42 ±2.19) mm.The margin of ITV→PTV is 5 mm which was figured out by PTN enlarging method.Compared to the original plan that under the condition of draw up the radiotherapy plan that based on the method of PTV enlarging obtained the CTV→PTV and simulate the actual dose distribution according to the setup errors:total lung V5,spinal cord D1cm3,increased by about 0.87％,4.95 Gy,heart V40,PTV D95,PTV V100,ITV D95,ITV V100 were reduced about 0.62％,4.95 Gy,8.38％,1.84 Gy,1.87％,all of them have statistically difference.Conclusions Range of external expansion of the left to right,superior to inferior and anterior to posterior is 7 mm,8 mm and 7 mm respectively,according to the method of PTV enlarging obtained the margin of CTV→PTV of super chest segment of esophageal cancer patients.

BACKGROUNDIt has been proved that hypoxia is closely related to oncogenesis and development of tumor. The aim of this study is to observe the effect of dexamethasone on expression of hypoxia inducible factor 1α (HIF-1α) and vascular endothelial growth factor (VEGF) in lung tissues of hypoxic mice, and to investigate the relationship between hypoxia and angiogenesis and mechanism of dexamethasone.

METHODSThe Kunming mice were randomly divided into control group and three experimental groups (3-day hypoxia group, 6-day hypoxia group, and hypoxia+dexamethasone group). HIF-1α and VEGF protein expression was detected in lung tissues of mice by immunohistochemistry.

RESULTSExpression of HIF-1α and VEGF significantly increased in hypoxia group compared with control group (P < 0.05). Compared with hypoxia group, expression of HIF-1α and VEGF decreased dramatically in hypoxia+dexamethasone group (P < 0.05). A positive correlation was found between the expression of HIF-1α and VEGF (r=0.730, P=0.007).

CONCLUSIONSHypoxia can increase the expression of VEGF and HIF-1α in lung tissues of mice. Dexamethasone can inhibit the expression of VEGF and HIF-1α of hypoxic mice and it may have anti-angiogenetic effect.

OBJECTIVETo investigate the anti-tumor mechanisms of emodin on human lung adenocarcinoma cell line Anip973 (LACC).

METHODSThe influence of emodin of different concentration at different time on LACC proliferation were determined and compared using MTT colorimeric assay and cell growth curve assay. And the cell apoptotic rate was determined by flow cytometry and analyzed with electronic microscope.

RESULTSIn a certain range, the higher concentration and longer acting time of emodin could induce the stronger inhibitory effect on tumor cell growth and the higher apoptotic rate. The proliferation inhibitory rate reached 90% after LACC being treated with emodin 60 micromol/L for 72h.

CONCLUSIONEmodin can significantly inhibit proliferation of human LACC, showing dose-effect and time-effect relationship.

Adenocarcinoma ; pathology ; Antineoplastic Agents, Phytogenic ; pharmacology ; Apoptosis ; drug effects ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Dose-Response Relationship, Drug ; Emodin ; pharmacology ; Humans ; Lung Neoplasms ; pathology