Objective To explore the influencing factors of lymph node metastasis of Siewert Ⅱ/Ⅲ gastroesophageal junction adenocarcinoma (AEG) and its influence on prognosis of this kind of patients. Methods The clinical and pathological data of 49 patients with Siewert Ⅱ/Ⅲ AEG who admitted to Shiyan Hospital of Traditional Chinese from January 2010 to January 2013 were retrospectively analyzed. Univariate and multivariate analyses of factors affecting lymph node metastasis of AEG were performed by using a chi-square test and an unconditional logistic regression model; the effect of lymph node metastasis on the prognosis of patients with Siewert Ⅱ/Ⅲ AEG was performed by log-rank test. Results Multivariate unconditional logistic regression analysis showed that, tumor diameter (P=0.008), depth of invasion (P=0.019), vascular tumor thrombus (P=0.020), and degree of differentiation (P=0.017) were all influencing factors of lymph node metastasis. Patients with Siewert Ⅱ/Ⅲ AGE without lymph node metastasis had better survival than those with lymph node metastasis (P=0.005). Conclusion Tumor diameter, depth of invasion, degree of differentiation, and vascular tumor thrombus are independent risk factors for lymph node metastasis in patients with Siewert Ⅱ/Ⅲ AEG, and lymph node metastasis is associated with poor prognosis.
ObjectiveTo investigate the effects of smoking combined with intermittent hypoxia on the pathophysiology of lung tissue and thoracic aorta, and the endothelial injury.MethodsTwenty-four rats (SPF, female, six weeks old) were divided randomly into 4 groups (n=6). The control group was given false smoking and normal oxygen exposure, the smoking-exposed group was exposed in smoking, the intermittent hypoxia group was exposed in intermittent hypoxia environment, and the overlap group was exposed to smoking and intermittent hypoxia. After 8 weeks, body weight, right ventricular hypertrophy index (RVHI), the pathological changes of lung tissue and thoracic aorta were measured, and the level of endothelin-1 (ET-1), endothelial nitric oxide synthase (eNOS), vascular endothelial growth factor (VEGF) and stromal cell-derived factor-1α (SDF-1α) in serum of rats were evaluated.ResultsRVHI of rats in the smoking-exposed group, intermittent hypoxia group, overlap group were higher than that in the control group. In addition, RVHI in the overlap group was higher than that in the smoking-exposed group, intermittent hypoxia group (all P<0.05). The levels of ET-1, VEGF and SDF-1α in the serum of the smoking-exposed group, intermittent hypoxia group and overlap group were higher than those in the control group, while the level of eNOS was lower than that in the control group, (all P<0.05), the most significant difference was between control group and the overlap group. Pathological observation of lung tissue and thoracic aorta showed obvious emphysema in the smoking-exposed group and overlap group, which was more obvious in the overlap group than that in the smoking-exposed group (all P<0.05). Lung interstitial inflammatory infiltration, bronchial wall lymphocyte hyperplasia and pulmonary fibrosis were shown in different degrees in the smoking-exposed group, intermittent hypoxia group and overlap group, and the pulmonary arteriole wall showed thickening, fibrosis and peripheral inflammatory infiltration also were found in these groups. Thoracic aorta in the smoking-exposed group, intermittent hypoxia group and overlap group showed different degrees of endothelial cell injury, middle membrane thickening, and collagen fiber hyperplasia. The pathological features of the overlap group were most obvious compared to the other two groups.ConclusionsSmoking and intermittent hypoxia exposure can lead to different degrees of lung tissue and vascular endothelial injury and decrease of vascular endothelial protective factors in rats, resulting in dysfunction of vascular endothelial cells, which leads to the structural remodeling of pulmonary arterioles and aorta, such as thickening, fibrosis, etc. Combined smoking and intermittent hypoxia exposure can lead to more serious pathological damage.