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Objective To study the impact of splenectomy and esophagogastric devascularization on the nutritional status of patients with cirrhosis and portal hypertension.Methods Sixty consecutive patients with cirrhosis and portal hypertension who underwent splenectomy and esophagogastric devascularization at the Beijing YouAn Hospital from April 5,2015 to January 23,2017 were included in this study.The body mass index (BMI),albumin (Alb),prealbumin (PA) and lymphocyte counts were prospectively collected at the end of 1-week,1-month,3-month,6-month and 1-year after surgery.The postoperative results were compared with the preoperative results in these patients.Results The BMI results obtained at 1-week and 1-month after surgery were significantly lower than the preoperative level [(22.14 ± 3.08)kg/m2 vs.(22.85 ± 3.14) kg/m2,(21.72 ± 3.05) kg/m2 vs.(22.86 ± 3.16) kg/m2,P ＜ 0.05].The BMI result at the end of 1-year after surgery was significantly elevated when compared with the preoperative level [(23.24 ± 3.64) kg/m2 vs.(22.68 ± 3.47) kg/m2,P ＜ 0.05].The ALB levels at 1-month and 3-month after surgery were significantly higher than the preoperative level [(39.87 ± 4.22)g/L vs.(35.35 ±5.15) g/L,(39.35 ± 4.75) g/L vs.(34.82 ± 5.50) g/L,P ＜ 0.05].The PA obtained at 1-week after surgery was significantly lower than the preoperative levels [(79.59 26.52)mg/L vs.(121.77 ±39.96)mg/L,P ＜ 0.05].The lymphocyte counts at all the points after surgery were significantly higher than the preoperative level (P ＜ 0.05).Conclusion Short term and long term nutritional status improved in patients with cirrhosis and portal hypertension after splenectomy and esophagogastric devascularization.
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Objective To investigate the role of cytokines combined with CLIF Consortium organ failure score (CLIF-COFs) in determining the prognosis of liver transplant in hepatitis B-related acute-on-chronic liver failure (HB-ACLF) patients.Methods Thirty-seven cases of HB-ACLF patients undergoing liver transplantation were divided into HB-ACLF patients with complications group (n =15) and those without complications (n =22).Plasma were prospectively collected immediately before LT and on the 1st,3rd,5th,7th day after LT in HB-ACLF patients.The serum levels of twenty-seven cytokines were determined by 200 LUMINEX liquid chip technology.Cytokines and CLIF-COFs were analyzed with logistic regression and the receiver operating characteristic to confirm the correlation with the total complications post-LT.Results The serum levels of post-transplant G-CSF and MCP-1 in HB-ACLF patients with complications were higher than those of without complications (P ＜ 0.05).The COX analysis indicated that MCP-1 and CLIF-COFs were predictors of post-LT complications [A UC:0.821,95％ CI:0.668-0.974;AUC:0.738,95％ CI:0.578-0.898].The discriminatory power of MCP-combined with CLIF-COFs [AUC:0.839,95％ CI:0.703-0.975] was better than that of either.Conclusions MCP-1 combined with CLIF organ failure score can better predict the short-term outcomes of liver transplantation in HB-ACLF patients.
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The Rictor/mTOR complex plays a pivotal role in a variety of cellular functions including cellular metabolism, cell proliferation and survival by phosphorylating Akt at Ser473 to fully activate the Akt kinase. However, its upstream regulatory pathways as well as whether it has additional function(s) remain largely unknown. We recently reported that Rictor contains a novel ubiquitin E3 ligase activity by forming a novel complex with Cullin-1, but not with other Cullin family members. Furthermore, we identified SGK1 as its downstream target. Interestingly, Rictor, but not Raptor or mTOR, promotes SGK1 ubiquitination. As a result, SGK1 expression is elevated in Rictor(-/-) MEFs. We further defined that as a feedback mechanism, Rictor can be phosphorylated by multiple AGC family kinases including Akt, S6K and SGK1. Phosphorylation of Rictor at the Thr1135 site did not affect its kinase activity towards phosphorylating its conventional substrates including Akt and SGK1. On the other hand, it disrupted the interaction between Rictor and Cullin-1. Consequently, T1135E Rictor was defective in promoting SGK1 ubiquitination and destruction. This finding further expands our knowledge of Rictor's function. Furthermore, our work also illustrates that Rictor E3 ligase activity could be governed by specific signaling kinase cascades, and that misregulation of this process might contribute to SGK overexpression which is frequently observed in various types of cancers.