Objective To investigate the effects of Notch signaling pathway on proliferation of insulin-induced endometrial carcinoma cells and apoptosis related protein expression levels.Methods The endometrial carcinoma Ishikawa 3-H-12 cell line was primarily cultured and subcultured in vitro.Then,the cultured cells were divided into five groups:the control group (3 mL PBS was added into the group),the insulin group (cells were stimulated by 1 × 106 mol/L insulin) and MW167 groups (different doses of γ-secretase inhibitor MW167 pretreated with insulin stimulation).After 48 h culturation,inhibition of endometrial carcinoma cell growth of each group was measured by MTT-colorimetric method,the apoptosis-related proteins (Caspase-3,Caspase-8) and Notch1 protein expression levels of each group were determined by Western blot.Results Insulin can promote Notch1 protein expression in endometrial carcinoma cells,after 48 h insulin stimulation,the Notch1 protein expression level was significantly higher than that in the control group (P＜0.05).MW167 can inhibit insulin-induced Notch1 protein expression in a concentration-dependent inhibition manner.The absorbance at 570 nm (A570) of endometrial carcinoma cells cultured for 24,48 and 72 h in different groups were significantly different (P＜0.05).The A570 values in the insulin group at each time point were higher than those in the control group (P＜0.05),and the insulin-induced endometrial carcinoma cell proliferation reached its highest level at 48 h.MW167 inhibited insulin-induced endometrial carcinoma cells proliferation in a concentration-and time-dependent manner,and 20 μmol/L MW167 persistently inhibited insulin-induced proliferation of endometrial carcinoma cells at 48 h.Western blot analysis showed that expression levels of Caspase-3 and Caspase-8 protein in the insulin group at each time point were lower than those in the control group (P＜0.05),and MW167 promoted the expressions of Caspase-3 and Caspase-8 in a concentration-and time-dependent manner.Conclusion MW167 can suppress the insulin-induced endometrial carcinoma cells proliferation and promote the expression of related apoptotic proteins by inhibiting Notch signaling pathway,and induce apoptosis of endometrial carcinoma ceils.

Objective: To explore the clinical value of echocardiography in differential diagnosis of segmental wall motion abnormalities in coronary heart disease(CHD), and to provide help for clinical treatment. Methods: From January 2017 to November 2018, 56 patients with segmental abnormal wall motion of CHD in Yuyao People's Hospital of Zhejiang Province were selected in the study.All patients were diagnosed by echocardiography and coronary angiography.The diagnostic coincidence rate, specificity, sensitivity, false negative rate, false positive rate and accuracy of echocardiography were evaluated. Results: Coronary angiography showed abnormal segmental wall motion in 56 patients, with 100.00% anastomosis rate.Echocardiography revealed abnormal segmental wall motion in 54 patients with CHD, 2 patients showed normal segmental wall motion, anastomosis rate was 96.43%.There was no statistically significant difference between the two diagnostic methods(χ²=0.635, P=0.152), but the specificity of ultrasound diagnosis(80.36%), sensitivity(78.57%) and accuracy(80.36%) were lower than those of coronary angiography(100.00%, 98.21%, 100.00%), there were statistically significant differences (χ²=4.173, P=0.034; χ²=5.154, P=0.024; χ²=4.173, P=0.034). Conclusion Cardiac echocardiography has a high diagnostic value in differential diagnosis of segmental wall motion abnormalities in CHD.It can guide the clinical treatment of these patients to formulate a reasonable treatment plan.Moreover, it is easy to operate, with low cost and more acceptable to patients.

Programmed death-1 and programmed death-ligand 1(PD-1/PD-L1)are regulatory immune checkpoint molecules that inhibit T cell activation and,therefore,play an important role in tumor immunotherapy.In recent years,increasing numbers of targeted therapeutic agents have been developed,but single immune checkpoint blockers cannot completely inhibit tumor occurrence,and tumor escape sporadically occurs.Consequently,combination therapy of targeted drugs is considered a useful method to inhibit tumorigenesis and tumor development.T cell immunoglobulin and immunoreceptor tyrosine-based inhibition motif(ITIM)domain(TIGIT)is an inhibitory type 1 poliovirus receptor that has recently been a hotspot of targeted drug therapy research.It has been shown that the combination therapy of TIGIT plus PD-1/PD-L1 can reduce tumor escape and inhibit tumorigenesis more effectively.Therefore,this review summarizes and discusses the progress on the dual blockade of TIGIT and PD-1/PD-L1 pathways in tumor immunotherapy to provide a theoretical basis for tumor im-munotherapy.