Balthazar computed tomography severity index is superior to Ranson criteria and APACHE Ⅱ scoring system in predicting acute pancreatitis outcome

AIM: Acute pancreatitis (AP) is a process with variable involvement of regional tissues or organ systems.Multifactorial scales included the Ranson, Acute Physiology and Chronic Health Evaluation (APACHE Ⅱ) systems and Balthazar computed tomography severity index (CTSI).The purpose of this review study was to assess the accuracy of CTSI, Ranson score, and APACHE Ⅱ score in course and outcome prediction of AP.METHODS: We reviewed 121 patients who underwent helical CT within 48 h after onset of symptoms of a first episode of AP between 1999 and 2003. Fourteen inappropriate subjects were excluded; we reviewed the 107 contrastenhanced CT images to calculate the CTSI. We also reviewed their Ranson and APACHE Ⅱ score. In addition, complications,duration of hospitalization, mortality rate, and other pathology history also were our comparison parameters.RESULTS: We classified 85 patients (79%) as having mild AP (CTSI ＜5) and 22 patients (21%) as having severe AP (CTSI ≥5). In mild group, the mean APACHE Ⅱ score and Ranson score was 8.6±1.9 and 2.4±1.2, and those of severe group was 10.2±2.1 and 3.1±0.8, respectively. The most common complication was pseudocyst and abscess and it presented in 21 (20%) patients and their CTSI was 5.9±1.4. A CTSI ≥5 significantly correlated with death,complication present, and prolonged length of stay.Patients with a CTSI ≥5 were 15 times to die than those CTSI ＜5, and the prolonged length of stay and complications present were 17 times and 8 times than that in CTSI ＜5,respectively.CONCLUSION: CTSI is a useful tool in assessing the severity and outcome of AP and the CTSI ≥5 is an index in our study. Although Ranson score and APACHE Ⅱ score also are choices to be the predictors for complications,mortality and the length of stay of AP, the sensitivity of them are lower than CTSI.

Involvement of fatty acid-CoA ligase 4 in hepatocellular carcinoma growth: Roles of cyclic AMP and p38 mitogen-activated protein kinase

AIM: Fatty acid-CoA ligase 4 (FACL4) is an arachidonatepreferring enzyme which has been shown to be up-regulated in human colon cancer tissues and implicated in the colon tumorigenesis. The purpose of this study was to investigatethe role of FACL4 in the human hepatocellular carcinoma (HCC) tumorigenesis and the specific signal pathways involved in this process.METHODS: We investigated the expression and regulation of FACL4 in HCC, adjacent non-tumorous liver tissues, and cell lines.RESULTS: In HCC patients, we demonstrated that FACL4 gene expression was markedly elevated in the cancerous tissues than in the adjacent non-cancerous liver tissues.In addition, several human hepatoma cell lines, including Hep3B and HepG2, expressed high levels of FACL4. Stable overex-pression of FACL4 knockdown plasmids (small interfering RNA, siRNA) to Hep3B cells significantly decreased FACL4 expression and subsequently limited the cell proliferation. Treatment of Hep3B cells with 8bromo-cAMP and SB203508 (p38 MAPK inhibitor) significantly suppressed the FACL4 expression. CONCLUSION: FACL4 is involved in the HCC tumorigenesis and both cAMP and p38 MAPK pathways are associated with the regulation of FACL4 in HCC.

Molecular mechanisms of denbinobin-induced anti-tumorigenesis effect in colon cancer cells

AIM: To explore both the in vitro and in vivo effects of denbinobin against colon cancer cells and clarify its underlying signal pathways.METHODS: We used COLO 205 cancer cell lines and nude mice xenograft model to study the in vitro and in vivo anti-cancer effects of denbinobin. RESULTS: Denbinobin at concentration of 10-20 μmol/Ldose-dependently suppressed COLO 205 cell proliferation by NTT test. Flow cytometry analysis and DNA fragmentation assay revealed that 10-20 μmol/L denbinobin treatment induced COLO 205 cells apoptosis. Western blot analysis showed that caspases 3, 8, 9 and Bid protein were activated by denbinobin treatment to COLO 205 cells accompanied with cytochrome c and apoptosis-inducing factor (AIF) translocation. Pretreatment of MEK 1 inhibitor (U10126), but not p38 inhibitor (SB203580) and JNK inhibitor (SP600125), reversed denbinobin-induced caspase 8, 9 and Bid activation in COLO 205 cells suggesting that extracellular signal-regulated kinase were involved in the denbinobin-induced apoptosis in COLO 205 cells. Significant regression of tumor up to 68% was further demonstrated in vivo by treating nude mice bearing COLO 205 tumor xenografts with denbinobin 50 mg/kg intraperitoneally. CONCLUSION: Our findings suggest that denbinobin couldinhibit colon cancer growth both in vitro and in vivo. Activation of extrinsic and intrinsic apoptotic pathways and AIF were involved in the denbinobin-induced COLO205 cell apoptosis.

Influence of iron on the severity of hepatic fibrosis in patients with chronic hepatitis C

瞄准：与长期的丙肝(CHC ) 在病人在肝的纤维变性，浆液铁索引，和肝的铁店之中评估协会。方法：32 个 CHC 病人在我们的学习被包括。纤维变性和发炎活动的组织学的度根据 Metavir 系统被估计。包括含铁锡，铁和转铁蛋白浸透的浆液铁索引被测量。肝的铁免职被 Perl 的污点分级。结果：有严重肝的纤维变性的 CHC 病人(n = 16 ) 是比有温和纤维变性的 CHC 病人显著地旧的(n = 16 )(P = 0.024 ) 。浆液铁索引，增加的浆液铁店和积极的肝的铁污点不在二个组之间是显著地不同的。在里面多变量逻辑回归分析，在活体检视的年龄是严重肝的纤维变性的一个独立预言者(机会比率 = 1.312；P = 0.035 ) 。积极的肝的铁污点显著地与丙氨酸 aminotransferase (中高音) 的价值被联系(P = 0.017 ) ，含铁锡(P = 0.008 ) ，浆液铁(P = 0.019 ) 并且转铁蛋白浸透(P = 0.003 ) 。含铁听水平与中高音的价值显示出重要关联(r = 0.531；P = 0.003 ) ，铁(r = 0.467；P = 0.011 ) 并且转铁蛋白浸透(r = 0.556；P = 0.002 ) 。结论：我们的调查结果建议丙肝病毒(HCV ) 的严厉联系了肝损伤在活体检视与耐心的年龄被联系。有浆液的两个浆液铁索引和肝的铁免职表演关联长期的肝疾病索引，但是不与肝组织学的等级和舞台有关。