The clinical manifestation,endoscopic findings and histopathological characteristics of 162 patients with gastrointestinal schistosomiasis were retrospectively analyzed.Among 162 patients,there were 29 cases of gastric schistosomiasis and 133 cases of intestinal schistosomiasis.The main clinical manifestations included stomachache,diarrhea and mucous bloody stool.Endoscopic findings:in 29 cases of gastric schistosoniasis,18 were ulcerative type,5 inflammatory type,6 proliferative type and 7 cases combined with gastric cancer.In 133 cases of intestinal schistosomiasis,17 were acute inflammatory type,81 chronic inflammatory type,33 mixture inflammatory type and 32 combined with colorectal cancer.Forty nine cases (30.25％) were misdiagnosed for various reasons; commonly misdiagnosed as ulcerative colitis,intestinal tuberculosis,chronic gastritis,and gastrointestinal tumors.There are no specific clinical manifestations or endoscopic findings of gastrointestinal schistosomiasis; epidemiological data,endoscopy combined with multi-site multi-block biopsy may improve the diagnosis.

Objective:To explore the mechanism of Golgi phosphoprotein 3 (GOLPH3) regulating the proliferation and apoptosis of endometrial cancer (EC) cells through PI3K/AKT/GSK3β signal.Methods:Human endometrial adenocarcinoma HEC-1-B cells were divided into control group, GOLPH3 group and GOLPH3 + GDC-0941 group. GOLPH3 was over-expressed by transfection of the GOLPH3 pcDNA. The PI3K inhibitor GDC-0941 was used to block the PI3K/AKT/GSK3β pathway. Cell viability, cell proliferation and apoptosis were measured by CCK-8 method, clone formation experiment and flow cytometry, respectively. The protein phosphorylation level in PI3K/AKT/GSK3β pathway was detected by Western blotting.Results:Transfection experiments were successful, and the PI3K inhibitor GDC-0941 did not affect GOLPH3 mRNA and protein expression. The relative cell viability of the control group, the GOLPH3 group and the GOLPH3 + GDC-0941 group were (100.00±4.63)%, (131.56±7.85)% and (97.85±7.36)%, and the difference among the three groups were significant ( F=7.437, P<0.001). The cell viability of the GOLPH3 group was higher than that of the control group ( P<0.001). The cell viability of the GOLPH3 + GDC-0941 group was lower than that of the GOLPH3 group ( P<0.001). The numbers of cell clones in the three groups were 46.86±3.56, 89.32±4.78 and 46.48±4.05, and the difference was significant ( F=20.437, P<0.001). GOLPH3 group had more clones than control group ( P<0.001). The number of clones formed in the GOLPH3 + GDC-0941 group was less than that in the GOLPH3 group ( P<0.001). The apoptosis rates of the three groups were (5.17±0.61)%, (2.34±0.56)% and (6.85±0.53)%, and the difference was significant ( F=11.643, P<0.001). The apoptosis rate of the GOLPH3 group was lower than that of the control group ( P<0.001), and the apoptosis rate of the GOLPH3 + GDC-0941 group was higher than that of the GOLPH3 group ( P<0.001). The phosphorylated PI3K/PI3K levels of the three groups were 1.00±0.09, 3.32±0.19 and 0.93±0.06, respectively; phosphorylated AKT/AKT levels were 1.00±0.11, 4.63±0.63 and 1.15±0.16, respectively; phosphorylated GSK3β/GSK3β levels were 1.00±0.08, 4.06±0.57 and 1.04±0.14, respectively. The differences were statistically significant ( F=12.532, P<0.001; F=16.792, P<0.001; F=15.311, P<0.001). The phosphorylation levels of each protein in the GOLPH3 group were higher than those in the control group (all P<0.001), and the GOLPH3 + GDC-0941 group were lower than the GOLPH3 group (all P<0.001). Conclusion:In EC cells, over-expression of GOLPH3 can promote cell proliferation and inhibit apoptosis by activating the PI3K/AKT/GSK3β pathway, suggesting that GOLPH3 is involved in the occurrence and development of EC.