0.05); When the IAP level reached 20 cm H2O, there was significant elevation (P

Objective: To investigate the feasibility of magnetic anastomosis for uretero-ileal anastomosis using experimental rabbit models. Methods: Six experimental rabbits were used as the models.The lower part of the left ureter was cut with scissors，the daughter magnet (DM) was placed in the middle of the ureter，and the distal end of the ureter was ligated.After that，the ileum wall was opened，the parent magnet (PM) was inserted through it，the positions of the PM and DM were adjusted so that their ends were attracted to each other，and then ileum wall incision was sutured.The operation time，intraoperative blood loss，postoperative complications and magnet discharge time were recorded.Two weeks after operation，left ureterography was performed to obtain the specimens of the uretero-ileal anastomosis，and to observe the patency of the anastomosis.The formation of the anastomosis was observed with naked eyes and light microscope. Results: Uretero-ileal magnetic anastomosis was performed successfully in 6 experimental rabbits.The operation time was 28-39（32.50±3.94） min，and the intraoperative blood loss was less than 5 mL.The rabbits recovered well after operation，and no complications were observed.All animals survived to the end point of observation.The disconnection time of magnet after operation was 9-13(10.83±1.72) days.The gross specimen showed that the anastomosis was patent.The histological observation showed that the mucosa of the anastomosis was continuous and smooth，and the anastomosis was well formed. Conclusion: Magnetic anastomosis is feasible for uretero-ileal anastomosis with simple operation and good anastomosis formation.After further experimental verification，this technique is expected to be used in clinical practice.

【Objective】 To construct an acute toxoplasma encephalitis mouse model by observing the pathological changes in the hippocampus of mice infected with Toxoplasma gondii strain RH. 【Methods】 The quantitative RH Toxoplasma gondii (100, 500, and 1 000 trophozoites) were injected into the hippocampal CA1 region of mice by the stereotaxic surgery; the survival status of mice was observed. Giemsa staining was used to observe the changes of toxoplasma in mouse ascites and brain tissue homogenates. Nissl staining and HE staining were used to observe the pathological changes of hippocampal nerve tissue. The distribution of Toxoplasma gondii in brain tissue was observed by immunohistochemical ABC method. 【Results】 The RH Toxoplasma gondii infected mice showed obvious symptoms such as arched back, bristling hair, abdominal distension, subtle tremor and hemiplegia on the fourth day of infection. The survival of mice in 100 trophozoites group was longer, no trophozoites of Toxoplasma gondii were found in ascites, a few pseudocysts were found in brain tissue homogenates after infected for 96 hours, and more trophozoites were found after death. Nysl staining and HE staining showed more tissue necrosis foci and loss of nerve cells in CA1 area after infected 144 h. The injury aggravated with the prolongation of infection time. Toxoplasma trophozoites were found in ascites and brain homogenates of mice in 500 and 1000 trophozoites groups. Nissl staining revealed neuronal loss and massive necrosis in the hippocampus. HE staining showed necrosis and inflammatory cell infiltration. The brain tissue injury significantly aggravated compared with 100 trophozoites group. The distribution of Toxoplasma gondii in the necrotic foci was confirmed by immunohistochemistry. 【Conclusion】 The survival of 100 trophozoite mice infected with Toxoplasma gondii strain RH was longer, and the pathological changes of brain tissue gradually aggravated. The damage was relatively confined to the brain tissue, and the mice showed typical symptoms of toxoplasma encephalitis. Therefore, the mouse model of acute toxoplasma encephalitis can be constructed by localized infection of 100 toxoplasma trophozoites, which can lay a foundation for future research on the mechanism of toxoplasma injury to cranial nerves.