Objective:To explore the role of Pim-1 in the pathology of inflammatory bowel disease and the potential effect of Pim-1 inhibitor on treating such disease.Methods:Forty-five BALB/c mice were randomly divided into 5 groups (n=9):A normal control group,a inflammatory bowel disease group,two different dose of Pim-1 inhibitor treatment groups,and steroidhormone treatment group.The model of inflammatory bowel disease was induced by intracolonic administration of 2,4,6-trinitrobenzenestdfonic acid (TNBS) and ethanol mixture.Mice were treated with Pim-1 inhibitor [intraperitoneal inject,5 or 10 mg/(kg.d)] for 5 days and prednisone (intragastric administration,0.1 mg/d) for 5 days.The DAI,colon length,gross score and pathological grade were evaluated.The expressions ofT cell master transcription factors T-box expressed in T cells (T-bet),GATA binding protein 3 (GATA-3),RA orphan receptorγ (RORyt)and forkhead box P3 (Foxp3) were measured by Real-time PCR and Western blot,respectively.Results:Pim-1 inhibitor and prednisone showed therapeutic effect on acute TNBS colitis in vivo.GATA3 and RORγt were significantly up-regulated in acute TNBS colitis (P＜0.05).In contrast,the expression of Foxp3 was suppressed in the inflammatory bowel disease group,whereas it did not cause any significant change in T-bet expression (P＞0.05).Administration of Pim-1 inhibitor and prednisone resulted in suppression of GATA3,RORγt expression,and the increase of Foxp3 expression (P＜0.05).Administration of Pim-1 inhibitor and prednisone resulted in inhibition of T-bet mRNA expression (P＜0.05),but only prednisone could inhibit T-bet protein expression (P＞0.05).Conclusion:Pim-1 inhibitor significantly suppresses Th2-and Th17-type immune responses.Furthermore,Pim-1 inhibitor could induce T-cell differentiation towards a Treg phenotype.Pim-1 inhibitor has therapeutic effect on acute TNBS colitis.

Objective:To explore a multimodal perioperative analgesia plan for patients undergoing microvascular decompression surgery for trigeminal neuralgia.Methods:Eighty patients who underwent microvascular decompression surgery for trigeminal neuralgia admitted to the Xiangya Hospital, Central South University from April 2017 to April 2019 were randomly divided into a nerve block group (group A) and a control group (group C) using a random number table method, with 40 patients in each group. The group A underwent surgical block of the lateral occipital and auricular nerves under ultrasound guidance before induction, with 3 ml of 0.5% ropivacaine used at each site. The group C did not undergo nerve block. Both groups received intravenous injections of midazolam, sufentanil, cisatracurium, etomidate, and lidocaine for anesthesia induction, followed by tracheal intubation and maintenance of anesthesia with propofol and remifentanil. After surgery, an analgesic pump was connected. The total amount of intraoperative use of sufentanil and remifentanil in both groups was recorded, as well as the pain Visual Analogue Scale (VAS) and postoperative anesthesia related complications at 2, 6, 24, and 48 hours after surgery.Resultsl:The total amount of sufentanil and remifentanil used during surgery in the group A was less than that in the group C (all P<0.05). The incidence of postoperative nausea and vomiting in the group A patients was lower than that in the group C ( P<0.05), and the nausea and vomiting score was also lower than that in the group C ( P<0.05). There was no statistically significant difference in the incidence of other postoperative complications (all P>0.05). There was a statistically significant difference in VAS scores between the two groups at 6 hours after surgery ( P<0.05). Conclusions:Occipital and auricular nerve blockade can reduce the amount of opioid drugs used during microvascular decompression surgery in patients with trigeminal neuralgia, thereby reducing the incidence of nausea and vomiting. The postoperative analgesic effect is good.