LncRNA NEAT1 regulates proliferation, apoptosis and invasion of liver cancer.

OBJECTIVE: The occurrence and progression of hepatocellular carcinoma (HCC) is a multi-step complex process and the exact molecular mechanisms remain to be elucidated. LncRNA NEAT1 is involved in tumorigenesis and progression. However, the role of LncRNA NEAT1 in HCC remains unclear. PATIENTS AND METHODS: The tumor tissues and adjacent tissues of HCC patients were collected and LncRNA NEAT1 expression was detected by Real time PCR. The hepatoma cell line HepG2 was cultured and transfected with lnc RNA NEAT1 siRNA or lnc RNA NEAT1 plasmid followed by analysis of LncRNA NEAT1 expression, cell proliferation by MTT assay, as well as Caspase 3 activity. In addition, cell apoptosis and cell cycle were assessed by flow cytometry and cell invasion was measured by transwell chambers. The expression of EGFR, Bax and Bcl-2 was detected by Western blot. RESULTS: LncRNA NEAT1 expression was significantly increased in HCC tissues compared with adjacent tissues (p < 0.05). Compared with the siRNA group, transfection of lncRNA NEAT1 siRNA into HepG2 cells significantly inhibited cell proliferation, increased Caspase 3 activity and apoptosis, reduced cell invasion, as well as arrested cell cycle (p < 0.05). Meanwhile, lncRNA NEAT1 siRNA also significantly decreased Bcl-2 and EGFR expression and increased Bax expression (p < 0.05). Transfection of lncRNA NEAT1 plasmid in hepatoma cells HepG2 reversed the above changes, compared with vector group, the differences were statistically significant (p < 0.05). CONCLUSIONS: LncRNA NEAT1 expression is increased in liver cancer tissues. Down-regulation of LncRNA NEAT1 can inhibit EGFR expression and promote hepatoma cell apoptosis, inhibit cell cycle, thus inhibiting tumor proliferation and invasion.

[The clinical characteristics and surgical treatment strategy of acute gangrenous cholecystitis after biliary tract stenting].

Objective: To analysis of the possible cause and surgical diagnosis and treatment strategies of acute gangrenous cholecystitis (AGC) after biliary stent drainage. Methods: The clinical data of 273 patients who received biliary stent drainage in Beijing Chaoyang Hospital from January 2015 to March 2016 were analyzed retrospectively. Among them, 22 patients who underwent surgical treatment were divided into two groups: 9 cases of AGC group and 13 cases of non-AGC group. The risk factors of AGC and surgical approach were analyzed. Result: All 22 patients underwent laparoscopic surgery. In AGC group, 1 patient with toxic shock died of multiple organ viscera function failure caused by infection, and 1 patient with gallbladder triangle inflammatory adhesion suffered from biliary leakage. The postoperative pathology of 2 patients was acute gangrenous cholecystitis. Non-AGC group had no death, bile duct injury and bleeding, with postoperative pathology of chronic cholecystitis. Patients were followed up for 2 month to restore well, without biliary calculi residual. Operation time, intraoperative blood loss, hospitalization days and hospitalization expenses of AGC group were higher than those of non-AGC group. Conclusion: The advocated AGC after biliary stent drainage should actively surgery after early diagnosis and endoscopic therapy should not be repeated. Laparoscopic surgery is a safe and effective treatment for AGC after carotid stenting.

Sirolimus-based immunosuppressive therapy in liver transplant recipient with tacrolimus-related chronic renal insufficiency.

BACKGROUND: While providing potent immunosuppression for liver transplant recipients, calcineurin inhibitors (CNI) exhibit nephrotoxicity as a major side effect. The purpose of this study was to evaluate the safety and efficacy of conversion from CNI to sirolimus (SRL) among liver transplant recipients with CNI-induced chronic nephrotoxicity. METHODS: Between January 2004 and June 2005, we performed conversion in 16 recipients after a median period of 8.5 months after liver transplantation. The indication for conversion was CNI-related nephrotoxicity with a serum creatinine (sCr) value >132.6 umol/L. Renal function was measured before and after conversion to SRL. Clinical and laboratory data related to the clinical course of the patients were recorded to investigate the safety and efficacy of conversion. RESULTS: Sixteen patients were converted to SRL after developing nephrotoxicity. Their renal function improved gradually after conversion. The levels of sCr decreased significantly within the first 30 days (164.1 +/- 12.48 micromol/L to 130.1 +/- 5.573 micromol/L), and over the next 60 days after conversion (97.86 +/- 11.69 micromol/L to 90.7 +/- 8.95 micromol/L) (P < .01). Similarly, the mean glomerular filtration rate (GFR) increased significantly during the same period. Four recipients experienced hypercholesterolemia, 1 with ankle edema, and 1 with acute rejection. The median follow-up was 2.4 years. No patient discontinued SRL due to side effects. No patient needed dialysis or kidney transplantation during the study period. CONCLUSIONS: SRL is a safe, effective replacement agent as primary immunosuppressive therapy following withdrawal of CNIs in liver transplant recipients with CNI-induced chronic nephrotoxicity.