Objective: To investigate the effect of loss of function of lanosterol synthase( LSS) gene on intestinal function in a mouse model of non-alcoholic fatty liver disease( NAFLD) induced by a high-fat diet． Methods: LSS gene heterozygous knockout C57 mice ( LSS + / －) were established using the CRISRP / Cas9 system．After being fed a high-fat diet with 60% fat content for 6 months，the fat deposition in liver tissues was detected by HE and Oil red O staining，the morphological changes of small intestine tissue were detected by HE staining．The changes in total cholesterol content in intestinal tissue were detected by kits．The gastrointestinal motility function of mice was detected by phenol red paste．The intestinal permeability was detected by Evans blue staining，and the expression of LSS，tight junction protein ( Claudin) -1，Claudin-5，cluster of differentiation 36 ( CD36) ，and Niemann-Pick type C1-like 1 protein ( NPC1L1) proteins in small intestinal tissues were detected by Western blot． Results : The results of HE and Oil red O staining of liver tissues showed that liver fat deposition in LSS gene heterozygous knockout mice was lower than that in wild-type mice in the high-fat diet group．The total cholesterol content in intestinal tis- sue of LSS gene heterozygous knockout mice decreased ( P ＜0. 01) ，but no morphological differences were ob- served between the two groups of mice by HE staining of intestinal tissues．The gastrointestinal motility function of LSS gene heterozygous knockout mice did not show significant changes．The intestinal permeability of LSS gene het- erozygous knockout mice in the high-fat diet group decreased as detected by Evans blue ( P＜0. 05) ．The expres- sion levels of Claudin-5 protein in the intestinal tissue of LSS gene heterozygous knockout mice in the high-fat diet group increased ( P ＜0. 05 ) ，while the expression of LSS protein in the intestinal tissues of LSS heterozygous knockout mice decreased ( P ＜0. 05) ． Conclusion In the NAFLD model induced by a high-fat diet，LSS gene heterozygous knockout reduces liver fat deposition induced by a high-fat diet and improves intestinal barrier function by regulating cholesterol metabolism in intestinal tissues and up-regulating the expression of Claudin-5．

Objective To treat hematospermia by ureteroscopy and investigate its application value for the treatment of hematospermia.Methods Nineteen patients with persistent hematospermia, TRUS,seminal vesicle MRI or CT were examined to exclude seminal vesicle tumor, tuberculosis, prostatic occupancy and preoperative prostatic fluid and drug sensitivity.Transurethral 4.5 - 6 F ureteroscopy entered through the microscopic seminal vesicle, wash of the old blood, reserved perfusion with Quinolones, and the lithoclasty on the seminal stones by holmium laser, resection of small polypi.Results The ureteroscopy was successful in 18 (95%) cases for bilateral seminal vesicle, wash and drug reserved perfusion, and one case was also successful seminal vesicle microscopy on the affected side; five cases with the seminal stones by olmium laser, three cases with small polypi by resection.The averse duration of the procedure was 35 10 -75) min.There were no compliocations during or after the operation.In 18 cases at 6 - 12 months follow-up the hematospermia and symptoms of hematospermia disappeared fully after 90 d.There was recurrence in one case which improved with anti-inflammaotry treatment.Conclusions Ureteroscopic treatment for persistent hematospermia by 4.5 - 6 F ureteroscopy through the seminal vesicle is effective and safe method and results in a micro-wound.