No abstract

BackgroundIt is unknown whether sedative per se contributes to the postoperative sleep disturbance. Diagnostic upper gastrointestinal endoscopy (UGE) is a minimally invasive procedure which is not likely to cause tissue trauma and pain. The purpose of this study was to evaluate the sleep quality of patients undergoing routine (without sedative) diagnostic UGE or UGE with sedative, before, 1 week, and 1 month after the procedure.MethodsOne thousand and thirty-three patients undergoing UGE were enrolled. Patients chose sedative or without sedative. Propofol and sufentanil were administered to the sedative group, not allowed for the routine group. The Pittsburgh Sleep Quality Index (PSQI) was measured before, 1 week and 1 month after the procedure.ResultsFive hundred and ten patients were enrolled in the sedative group and 523 in the routine group. One week after the procedure, patients in the sedative group showed significantly higher PSQI scores (worse sleep quality) than the baseline PSQI scores (p < 0.001), but there was no significant change for the routine group in the same period (p = 0.096). One month after the procedure, there was no significant difference in PSQI scores between the two groups compared with the baseline values (p = 0.358 for sedative group, p = 0.161 for routine group). There were also no significant difference in the PSQI scores between the two groups in the entire 1 month follow-up period (p = 0.885).ConclusionsThe sedative group showed impaired sleep quality 1 week after diagnostic UGE. Propofol and sufentanil may independently affect the sleep quality of patients after sedative of diagnostic UGE for only one week.Trial registrationThis study is registered on Chinese Clinical Trial Registry (IDChiCTR-OCH-13003128). Registered 2 April 2013.Electronic supplementary materialThe online version of this article (doi:10.1186/s12871-017-0341-3) contains supplementary material, which is available to authorized users.

Progranulin (PGRN), which plays an anti-inflammatory role in acute lung injury (ALI), is promising as a potential drug. Studies have shown that regulatory T cells (Tregs) and interleukin- (IL-) 10 can repress inflammation and alleviate tissue damage during ALI. In this study, we built a lipopolysaccharide- (LPS-) induced ALI mouse model to illustrate the effect of PGRN on regulation of Treg differentiation and modulation of IL-10 promoting macrophage polarization. We found that the proportion of Tregs in splenic mononuclear cells and peripheral blood mononuclear cells was higher after treatment with PGRN. The increased proportion of Tregs after PGRN intratracheal instillation was consistent with the decreased severity of lung injury, the reduction of proinflammatory cytokines, and the increase of anti-inflammatory cytokines. In vitro, the percentages of CD4+CD25+FOXP3+ Tregs from splenic naïve CD4+ T cells increased after PGRN treatment. In further research, it was found that PGRN can regulate the anti-inflammatory factor IL-10 and affect the polarization of M1/M2 macrophages by upregulating IL-10. These findings show that PGRN likely plays a protective role in ALI by promoting Treg differentiation and activating IL-10 immunomodulation.