RESULTS: No differences in patient characteristics or endoscopic procedures were observed between the two groups. The incidence of PEP was 4.2% (1/24) and 29.0% (9/31) in the Stent and no-stent groups, respectively, with the no-stent group having a significantly higher incidence (P = 0.031). The PEP severity was mild for all the patients in the stent group. In contrast, 8 had mild PEP and 1 had moderate PEP in the no-stent

group. The mean serum amylase levels (means +/- SD) 3 h after ERCP (183.1 +/- 136.7 vs 463.6 +/- 510.4 IU/L, P = 0.006) and on the day after selleck screening library ERCP (209.5 +/- 208.7 vs 684.4 +/- 759.3 IU/L, P = 0.002) were significantly higher in the no-stent group. A multivariate analysis identified the absence of pancreatic stenting (P = 0.045; odds ratio, 9.7; 95%CI: 1.1-90) as a significant risk factor for PEP. CONCLUSION: In patients with difficult cannulation in whom the bile duct is cannulated using P-GW, a pancreatic stent should be placed even if EST has been performed. (C) 2014 Baishideng Publishing Group Inc. All rights reserved.”
“Sarcoidosis is

a multisystem granulomatous disorder characterized by marked T-cell Bafilomycin A1 expansion of T helper 1 (Th1) cells. The cause of T-cell overactivity is unknown. We hypothesized that interleukin-10 (IL-10) production by a yet undefined cell type might be defective, resulting in loss of regulation of T-cell activity. Focusing on IL-10-producing monocytes, we first showed that monocytes isolated from the peripheral blood of corticosteroid-naive sarcoidosis patients (n

= 51) produced less IL-10 compared to controls, and were less able to suppress T-cell proliferation. In addition, monocytic IL-10 production correlated negatively with disease activity score. As invariant natural killer selleck chemicals T (iNKT) cells are known to both interact with monocytes and be reduced in sarcoidosis patients, we then asked whether iNKT-specific defects might be responsible for this reduced IL-10 production. We found that greater numbers of circulating iNKT cells was associated with higher IL-10 production. Moreover, iNKT cells enhanced monocytic IL-10 production in vitro. Defective IL-10 production and T-cell suppression by sarcoidosis monocytes could be restored following their coculture with iNKT cells, in a CD1d- and cell contact-dependent process. We suggest that reduced iNKT-cell numbers in sarcoidosis may lead to impaired monocytic IL-10 production and unchecked T-cell expansion in sarcoidosis. These findings provide fresh insight into the mechanism of sarcoidosis disease, and interaction between iNKT cells and monocytes.”
“In this report, we elaborate on a letter that Spallanzani wrote to Bonnet reporting his findings on regeneration in worms, snails, tadpoles, and salamanders. The letter (original in French and translated in English; see Supplementary Material, which is available online) was written to discuss whether or not regeneration in these animals supports Bonnet’s theory on germs.