Comparison of Scoring Systems in Predicting Severity and Prognosis of Hypertriglyceridemia-Induced Acute Pancreatitis.

BACKGROUND: In China, hyperlipidemia is the second major reason of acute pancreatitis. AIMS: Comparison of Scoring Systems in identification patients at risk for severe acute pancreatitis (SAP), pancreatic necrosis (PNec), and infected pancreatic necrosis (IPN) early in the course of hypertriglyceridemia-induced acute pancreatitis (HTG-AP). METHODS: Predictive accuracy of scoring systems was measured by the area under the receiver operating characteristic curve (AUC) in a retrospective study. Pairwise AUC comparisons were performed to calculate the difference between scoring systems. RESULTS: A total of 238 patients diagnosed with HTG-AP were included. Sixty patients (25.2%) were classified as SAP. Twenty-nine patients (12.2%) had evidence of PNec. Nine patients (3.8%) were diagnosed with IPN. One patient (0.4%) died during hospitalization. In predicting SAP in HTG-AP, the AUCs of APACHE-II, SOFA, SIRS, Ranson's, BISAP, and MMS were 0.77, 0.83, 0.73, 0.88, 0.83, and 0.85, respectively; in predicting PNec, were 0.75, 0.77, 0.75, 0.86, 0.80, and 0.75, respectively; and in predicting IPN, were 0.92, 0.86, 0.76, 0.85, 0.84, and 0.87, respectively. Pairwise AUC comparisons revealed that Ranson's, MMS, BISAP, and SOFA had higher accuracy than SIRS, Ranson's and MMS had higher accuracy than APACHE-II in predicting SAP; Ranson's had the same accuracy with BISAP, but higher than other four criteria in predicting PNec; APACHE-II had higher accuracy than SIRS in predicting IPN. CONCLUSIONS: APACHE-II had high performance in predicting IPN, and all other score systems had medium performance in predicting SAP, PNec, and IPN in HTG-AP. Each score has its merit and weakness; BISAP may be the best criterion in predicting severity and prognosis of HTG-AP.

Inhibition of hepatitis C virus replication by single and dual small interfering RNA using an HCV-infected cell model.

Dual siRNA against different regions of gene in hepatitis C virus (HCV) synergistically inhibited replication of HCV RNA. An HCV-infected cell model was established, and HCV RNA and core protein were detected by RT-PCR and Western blot, respectively. Four HCV-specific siRNAs (siCore, siNS3, siNS4B, siNS5B) were designed and transfected into HCV-infected Huh7.5.1 cells. The antiviral efficacies of the siRNAs were compared using real time PCR and agarose gel electrophoresis. HCV replication in infected cells was inhibited by IFNα-2b in a dose-dependent manner. Synergistic inhibition effects were achieved with combination treatment of any two of the siRNAs (siCore, siNS3 and siNS5B) at low doses (0.1 and 10 nM), as compared to single siRNA treatment (P < 0.05). Furthermore, CCK-8 assay showed no toxicity of the siRNAs to Huh7.5.1 cells. These findings indicate a promising new therapeutic approach for treatment of HCV.

[Inhibition of hepatitis C virus replication by small interfering RNA in cells infected by HCV].

OBJECTIVE: To investigate the inhibitive effects of small interfering RNA (siRNA) on hepatitis C virus (HCV) replication in cells infected by HCV in vitro. METHODS: The HCV RNA transcripts prepared by pFL-JC1 were transfected into Huh-7.5.1 cells. Na ve Huh-7.5.1 cells were incubated with the supernatants of transfected cells and the expression of HCV core protein in infected cells was detected by indirect immunofluorescence. The infected cells were transfected with 4, 40 and 200 nmol/L of NS5B siRNA for 24 h, 48 h and 72 h, respectively. The normal Huh-7.5.1 cells were transfected with 4, 40 and 200 nmol/L of NS5B siRNA. Group of blank, lipofectamine 2000, unrelated siRNA and IFNα-2b (1000 IU/ml) served as controls. The HCV RNA and PKR mRNA levels were examined by quantitative RT-PCR. RESULTS: The HCV core protein in HCV infected cells was detected. Compared with control groups, the HCV RNA levels in infected cells significantly decreased when transfected with 40 and 200 nmol/L of siRNA for 24 h; 4, 40 and 200 nmol/L of siRNA for 48 h and 72 h (P<0.05). The HCV RNA levels in infected cells treated with IFNα-2b (1000 IU/ml) for 24 h, 48 h and 72 h were significantly lower than those in control groups (P<0.05 or P<0.01). The PKR mRNA levels in Huh-7.5.1 cells transfected with siRNA of three concentrations did not have significant difference, as compared with control groups (P>0.05). CONCLUSION: siRNA against HCV NS5B region can effectively inhibit HCV replication in HCV infected cells, but can not activate the dsRNA-dependent protein kinase (PKR).

[Alteration of mi-RNA expression profile after interferon treatment in HCV-infected Huh7.5.1 cells].

OBJECTIVE: To screen the mi-RNA expression profile after interferon treatment in cells infected with hepatitis C virus (HCV). METHODS: Huh-7.5.1 cells was infected with HCV by in vitro transcription and cultured with interferon. The mi-RNA microarray was used to measure the mi-RNA expression in the control group, HCV transcription group and interference group. Intra-group differences were analyzed by the 2 ((-delt delt CT)) method. RESULTS: With mi-RNA expressed in normal Huh-7.5.1 cells as a benchmark, expressions of 13 kinds of mi-RNAs were up-regulated after HCV infection and then down-regulated following interferon treatment; 7 were down-regulated after HCV infection and then up-regulated following interferon treatment. CONCLUSION: mi-RNA10a, mi-RNA21, mi-RNA149, mi-RNA152 and mi-RNA210 may be related to hepatitis C virus replication and transcription.