1.Clinical study of relationship between diameter of early gastric cancer as well as lymph node metastasis and expression of VEGF and MMP-7
Guangda XU ; Shaotong LAI ; Xiuqi BAO ; Zhaobin DENG
Chinese Journal of Postgraduates of Medicine 2006;0(11):-
Objective To investigate the relationship between diameter of early gastric cancer as well as lymph node metastasis and expression of vascular endothelial growth factor(VEGF) and Matrix metalloproteinases-7(MMP-7)in gastric cancer. Method VEGF and MMP-7 expressions of gastric cancer tissue in 55 cases were examined by immumohistochemical assay. The diagnosis was confirmed by mucous stain and pathology. Results The level of VEGF and MMP-7 expression in group of early gastric cancer with diameter ≤ 10 mm was significantly lower than that of diameter ≥ 10 mm and ≤ 20 mm (P0.05). Conclusion It is significant that relation of the diameter of early gastric cancer with VEGF and MMP-7 expression, the cases of strongly positive over-expression of both VEGF and MMP-7 in tissue of patients with early gastric cancer are accompanied by more likelihood of lymph node metastasis.
2.Toxoplasma gondii Induces Apoptosis via Endoplasmic Reticulum Stress-Derived Mitochondrial Pathway in Human Small Intestinal Epithelial Cell-Line
Hao WANG ; Chunchao LI ; Wei YE ; Zhaobin PAN ; Jinhui SUN ; Mingzhu DENG ; Weiqiang ZHAN ; Jiaqi CHU
The Korean Journal of Parasitology 2021;59(6):573-583
Toxoplasma gondii, an intracellular protozoan parasite that infects one-third of the world’s population, has been reported to hijack host cell apoptotic machinery and promote either an anti- or proapoptotic program depending on the parasite virulence and load and the host cell type. However, little is known about the regulation of human FHs 74 small intestinal epithelial cell viability in response to T. gondii infection. Here we show that T. gondii RH strain tachyzoite infection or ESP treatment of FHs 74 Int cells induced apoptosis, mitochondrial dysfunction and ER stress in host cells. Pretreatment with 4-PBA inhibited the expression or activation of key molecules involved in ER stress. In addition, both T. gondii and ESP challenge-induced mitochondrial dysfunction and cell death were dramatically suppressed in 4-PBA pretreated cells. Our study indicates that T. gondii infection induced ER stress in FHs 74 Int cells, which induced mitochondrial dysfunction followed by apoptosis. This may constitute a potential molecular mechanism responsible for the foodborne parasitic disease caused by T. gondii.