BackgroundEnteral nutrition is increasingly advocated in the treatment of acute pancreatitis, but its timing is still controversial. The aim of this meta-analysis was to find out the feasibility of early enteral nutrition within 48 hours of admission and its possible advantages.Methods and FindingsWe searched PubMed, EMBASE Databases, Web of Science, the Cochrane library, and scholar.google.com for all the relevant articles about the effect of enteral nutrition initiated within 48 hours of admission on the clinical outcomes of acute pancreatitis from inception to December 2012. Eleven studies containing 775 patients with acute pancreatitis were analyzed. Results from a pooled analysis of all the studies demonstrated that early enteral nutrition was associated with significant reductions in all the infections as a whole (OR 0.38; 95%CI 0.21–0.68, P<0.05), in catheter-related septic complications (OR 0.26; 95%CI 0.11–0.58, P<0.05), in pancreatic infection (OR 0.49; 95%CI 0.31–0.78, P<0.05), in hyperglycemia (OR 0.24; 95%CI 0.11–0.52, P<0.05), in the length of hospitalization (mean difference −2.18; 95%CI −3.48−(−0.87); P<0.05), and in mortality (OR 0.31; 95%CI 0.14–0.71, P<0.05), but no difference was found in pulmonary complications (P>0.05). The stratified analysis based on the severity of disease revealed that, even in predicted severe or severe acute pancreatitis patients, early enteral nutrition still showed a protective power against all the infection complications as a whole, catheter-related septic complications, pancreatic infection complications, and organ failure that was only reported in the severe attack of the disease (all P<0.05).ConclusionEnteral nutrition within 48 hours of admission is feasible and improves the clinical outcomes in acute pancreatitis as well as in predicted severe or severe acute pancreatitis by reducing complications.

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BackgroundAlthough the chemopreventive effect of 5-aminosalicylates on patients with ulcerative colitis has been extensively studied, the results remain controversial. This updated review included more recent studies and evaluated the effectiveness of 5-aminosalicylates use on colorectal neoplasia prevention in patients with ulcerative colitis.MethodsUp to July 2013, we searched Medline, Embase, Web of Science, Cochrane CENTRAL, and SinoMed of China for all relevant observational studies (case-control and cohort) about the effect of 5-aminosalicylates on the risk of colorectal neoplasia among patients with ulcerative colitis. The Newcastle-Ottawa Scale was used to assess the quality of studies. Adjusted odds ratios (ORs) were extracted from each study. A random-effects model was used to generate pooled ORs and 95% confidence intervals (95%CI). Publication bias and heterogeneity were assessed.ResultsSeventeen studies containing 1,508 cases of colorectal neoplasia and a total of 20,193 subjects published from 1994 to 2012 were analyzed. 5-aminosalicylates use was associated with a reduced risk of colorectal neoplasia in patients with ulcerative colitis (OR 0.63; 95%CI 0.48–0.84). Pooled OR of a higher average daily dose of 5-aminosalicylates (sulfasalazine ≥ 2.0 g/d, mesalamine ≥ 1.2 g/d) was 0.51 [0.35–0.75]. Pooled OR of 5-aminosalicylates use in patients with extensive ulcerative colitis was 1.00 [0.53–1.89].ConclusionOur pooled results indicated that 5-aminosalicylates use was associated with a reduced risk of colorectal neoplasia in patients with ulcerative colitis, especially in the cases with a higher average daily dose of 5-aminosalicylates use. However, the chemopreventive benefit of 5-aminosalicylates use in patients with extensive ulcerative colitis was limited.

Mangrove soils have been recognized as sources of greenhouse gases, but the atmospheric fluxes are poorly characterized, and their adverse warming effect has rarely been considered with respect to the potential contribution of mangrove wetlands to climate change mitigation. The current study balanced the warming effect of soil greenhouse gas emissions with the plant carbon dioxide (CO 2 ) sequestration rate derived from the plants' net primary production in a productive mangrove wetland in South China to assess the role of mangrove wetlands in reducing the atmospheric warming effect. Soil characteristics were also studied in the summer to examine their relationships with gas fluxes. The soil to atmosphere fluxes of nitrous oxide (N 2 O), methane (CH 4 ) and CO 2 ranged from −1.6 to 50.0 μg m −2 h −1 , from −1.4 to 5360.1 μg m −2 h −1 and from −31 to 512 mg m −2 h −1 , respectively, which indicated that the mangrove soils act as sources of greenhouse gases in this area. The gas fluxes were higher in summer than in the cold seasons and were variable across mangrove sites. Gas fluxes in summer were positively correlated with the soil organic carbon, total nitrogen, and ammonia contents. The mangrove plants sequestered a considerable amount of atmospheric CO 2 at rates varying from 3652 to 7420 g CO 2 m −2 yr −1 . The ecosystem acted as a source of CH 4 and N 2 O gases but was a more intense CO 2 sink. However, the warming effect of soil gas emissions accounted for 9.3-32.7% of the plant CO 2 sequestration rate, partially reducing the benefit of mangrove plants, and the two trace gases comprised 9.7-33.2% of the total warming effect. We therefore propose that an assessment of the reduction of atmospheric warming effects by a mangrove ecosystem should consider both soil greenhouse gas emissions and plant CO 2 sequestration.

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Background/Aims: To investigate the biological roles and underlying molecular mechanisms of long non-coding RNA (lncRNA) PVT1 in Hepatocellular carcinoma (HCC). Methods: qRT-PCR was performed to measure the expression of miRNA and mRNA. Western blot was performed to measure the protein expression. CCK-8 assay was performed to determine cell proliferation. Flow cytometry was performed to detect cell apoptosis. Wounding-healing assay and Transwell assay was performed to detect cell migration and invasion. Dual luciferase reporter assay was performed to verify the target relationship. Quantichrom iron assay was performed to check uptake level of cellular iron. Results: PVT1 expression was up-regulated in HCC tissues and cell lines. Function studies revealed that PVT1 knockdown significantly suppressed cell proliferation, migration and invasion, and induced cell apoptosis in vitro. Furthermore, PVT1 could directly bind to microRNA (miR)-150 and down-regulate miR-150 expression. Hypoxia-inducible protein 2 (HIG2) was found to be one target gene of miR-150, and PVT1 knockdown could inhibit the expression of HIG2 through up-regulating miR-150 expression. In addition, the expression of miR-150 was down-regulated, while the expression of HIG2 was up-regulated in HCC tissues and cell lines. Moreover, inhibition of miR-150 could partly reverse the biological effects of PVT1 knockdown on proliferation, motility, apoptosis and iron metabolism in vitro, which might be associated with dysregulation of HIG2. In vivo results showed that PVT1 knockdown suppressed tumorigenesis and iron metabolism disorder by regulating the expression of miR-150 and HIG2. Conclusion: Taken together, the present study demonstrates that PVT1/miR-150/HIG2 axis may lead to a better understanding of HCC pathogenesis and provide potential therapeutic targets for HCC.

Proliferative change and intestinal barrier dysfunction in intestinal mucosa of diabetes have been described, but the differentiation characteristics of intestinal epithelial cells (IECs) and the mechanisms in the IECs development remain unclear. To explore the intestinal epithelial constitution patterns and barrier function, the diabetic mouse model was induced by streptozotocin. Tight junctions between IECs were significantly damaged and the serum level of D-lactate was raised in diabetic mice (P < 0.05). The expression of Zo1 and Ocln in the small intestine of diabetic mice were lower, while the markers for absorptive cell (SI) and Paneth cell (Lyz1) were significantly higher than in control mice (P < 0.05). The expression of Msi1, Notch1, and Dll1 in small intestine gradually increased throughout the course of hyperglycemia in diabetic mice (P < 0.05). However, the expression of NICD, RBP-jκ, Math1, and Hes1 had a reverse trend compared with Msi1 and Notch1. Intestinal absorptive cells and Paneth cells had a high proliferation rate in diabetic mice. However, the intestinal barrier dysfunction associated with the decreased expressions of Zo1 and Ocln was detected throughout hyperglycemia. In conclusion, downregulation of Notch/Hes1 signal pathway caused by depressed Notch/NICD transduction is associated with the abnormal differentiation of IECs and intestinal barrier dysfunction in diabetic mice.

Mangrove forests have the potential to export carbon to adjacent ecosystems but whether mangrove-derived organic carbon (OC) would enhance the soil OC storage in seagrass meadows adjacent to mangroves is unclear. In this study we examine the potential for the contribution of mangrove OC to seagrass soils on the coast of North Sulawesi, Indonesia. We found that seagrass meadows adjacent to mangroves had significantly higher soil OC concentrations, soil OC with lower δ 13C, and lower bulk density than those at the non-mangrove adjacent meadows. Soil OC storage to 30 cm depth ranged from 3.21 to 6.82 kg C m−2, and was also significantly higher at the mangrove adjacent meadows than those non-adjacent meadows. δ13C analyses revealed that mangrove OC contributed 34 to 83% to soil OC at the mangrove adjacent meadows. The δ13C value of seagrass plants was also different between the seagrasses adjacent to mangroves and those which were not, with lower values measured at the seagrasses adjacent to mangroves. Moreover, we found significant spatial variation in both soil OC concentration and storage, with values decreasing toward sea, and the contribution of mangrove-derived carbon also reduced with distance from the forest.