Objective: Epithelial dysplasia of the esophagus and gastric cardia is precancerous lesion, including mild, moderate and severe levels. In 2000 year, WHO recommended to replace dysplasia with intraepithelial neoplasia. Mild and moderate dysplasia were classified as low-grade intraepithelial neoplasia (LIN). Cardia adenocarcinoma was suggested to be called esophageal-gastric junction adenocarcinoma. The risk of cancer development and the rule of time evolution were detected in esophagus and esophageal-gastdc junction LIN in high incidence area of esophageal cancer in Northern China, in an effort to provide scientific data for the prevention of esophageal cancer. Methods: Between October 2001 and October 2002, two townships of Cixian were chosen to carry out endoscopic iodine staining screening cohort study. The total population aged 0-85 was 22,016, of which 6,596 aged 40-69 (3257 males and 3339 females). Except for thoese with contraindications and those who refused to join the study, 3,506 cases were finally recruited in the study, and the screening rate was 53.2%. According to WHO criteria of the pathological diagnosis, the esophageal squamous epithelium with mild and moderate dysplasia and esophageal-gastric junction with mild dysplasia were classified into LIN groups (including 616 cases). The control group contained a total of 2,478 cases without precancerous lesions and free of cancer in endoscopic screening. Results: From June to September in 2008, the cohort was followed up and 174 cases were lost, with a follow-up rate of 95.0%. Follow-up was 3,970.7 person- years in the LIN group and 16,120.0 person-years in the control group.Carcinomous conversion rates were 251.7 and 68.2/per 100,000 person- years respectively in the LIN group and the control group. The median time in the two groups was 38 and 47 months, respectively. Compared with that of the normal population, the relative risk (RR) of LIN was 3.69 (95% CI=1.57-8.69, P=0.001). Conclusion: Population with LIN are at high-risk for esophageal cancer and endoscopic examination every year is absolutely necessary.

Aim To investigate the effects of isoliquiri-tigenin ( ISL) on anti-angiogenesis both in vitro and in vivo and its mechanisms. Methods We assessed the antiangiogenic activities of ISL on proliferation viabili-ty, migration and tube formation of human microvascu-lar endothelial cell line-1 (HMEC-1) in vitro. The cell proliferation viability was assessed using the Sulforho-damine B ( SRB ) assay. Modified Boyden Transwell chamber assay was done to study the effect of ISL on HMEC-1 cells migration. 2′, 7′-dichlorofluorescein di-acetate ( DCFH-DA) was used to measure the levels of intracellular reactive oxygen species ( ROS ) , which was induced by VEGF. Metalloproteinase-2 ( MMP-2 ) and metalloproteinase-9 ( MMP-9 ) expressions by HMEC-1 cells were assessed through gelatin zymogra-phy assay. HMEC-1 cells cycle was detected by flow cytometry. Moreover, we investigated the in vivo anti-angiogenic activity of ISL on chicken embryos nap al-lantoic membrane model ( CAM ) . Results ISL con-centration-dependently inhibited the growth of HMEC-1 cells as well as SW620 and A549 cells. ISL signifi-cantly and concentration-dependently suppressed the migration activity of HMEC-1 cells. Tube sample struc-ture formation further confirmed the effect of ISL on an-ti-angiogenesis. Moreover, ISL also inhibited intracel-lular ROS level, MMP-2 and MMP-9 expression by HMEC-1 cells. ISL induced endothelial cell apoptosis at a low concentration ( ISL 12 . 5 μmol · L-1 ) and blocked the cells in S phase of mitosis at higher con-centrations ( ISL 25~100 μmol·L-1 ) . Furthermore, ISL distinctly inhibited the angiogenesis of chick em-bryos in vivo. Conclusions ISL has anti-tumor and angiogenesis effects on HMEC-1 cells. The mechanism may be related to intracellular ROS scavenging and ap-optosis induction of HMEC-1 cells.

Catecholaminergic polymorphic ventricular tachycardia(CPVT)is a highly fatal inherited arrhythmia induced by emotional stress or exercise.It can be triggered by rapid polymorphism of ventricular tachycardia and ventricular fibrillation, and may lead to syncope or sudden death, with a poor prognosis.Genetic testing is one way to diagnose the disease.It has been found that the disease is related to abnormalities of RyR2, CASQ2, TECRL and other genes, whose mutations affect calcium homeostasis and lead to abnormal electrophysiological activity of the heart, leading to delayed depolar(DADs), and subsequently to malignant arrhythmia.This paper reviewes the mutation of the new pathogenic gene TECRL gene in catecholamine sensitive ventricular tachycardia, through the understanding and learning of the mutation gene reported in the previous literature, in order to further explore the pathogenesis of the disease, learn to deal with the occurrence of malignant arrhythmia, and promote the clinical precise treatment of the disease.