BackgroundA previous systematic review and meta-analysis reported that omega-3 fatty acids nutrition may reduce mortality in septic patients. As new randomized controlled trials began to accumulate, we conducted an update.MethodsA PubMed database was searched through Feb 2016, and randomized controlled trials comparing omega-3 fatty acids with control were selected by two reviewers independently.ResultsEleven trials randomly assigning 808 patients were included in the present study. Using a fixed effects model, we found no significant effect of omega-3 fatty acids on overall mortality (risk ratio 0.84; 95 % confidence interval (CI): 0.67 to 1.05, P = 0.12), or infectious complications (risk ratio 0.95; 95 % CI: 0.72 to 1.25, P = 0.70). However, the duration of mechanical ventilation was markedly reduced by omega-3 fatty acids (weighted mean differences (WMD) = −3.82; 95 % CI: −4.61 to −3.04; P < 0.00001). A significant heterogeneity was found when the duration of hospital (I 2 = 93 %; WMD = −2.82; 95 % CI: −9.88 to 4.23, P = 0.43), or intensive care stay (I 2 = 87 %; WMD = −2.70; 95 % CI: −6.40 to 1.00, P = 0.15) were investigated.ConclusionsOmega-3 fatty acids confer no mortality benefit but are associated with a reduction in mechanical ventilation duration in septic patients. However, low sample size and heterogeneity of the cohorts included in this analysis limits the generalizability of our findings.Electronic supplementary materialThe online version of this article (doi:10.1186/s12871-016-0200-7) contains supplementary material, which is available to authorized users.

ObjectivesInflammation plays a key role in the pathogenesis of acute lung injury (ALI). Soluble epoxide hydrolase (sEH) is suggested as a vital pharmacologic target for inflammation. In this study, we determined whether a sEH inhibitor, AUDA, exerts lung protection in lipopolysaccharide (LPS)-induced ALI in mice.MethodsMale BALB/c mice were randomized to receive AUDA or vehicle intraperitoneal injection 4 h after LPS or phosphate buffered saline (PBS) intratracheal instillation. Samples were harvested 24 h post LPS or PBS administration.ResultsAUDA administration decreased the pulmonary levels of monocyte chemoattractant protein (MCP)-1 and tumor necrosis factor (TNF)-α. Improvement of oxygenation and lung edema were observed in AUDA treated group. AUDA significantly inhibited sEH activity, and elevated epoxyeicosatrienoic acids (EETs) levels in lung tissues. Moreover, LPS induced the activation of nuclear factor (NF)-κB was markedly dampened in AUDA treated group.ConclusionAdministration of AUDA after the onset of LPS-induced ALI increased pulmonary levels of EETs, and ameliorated lung injury. sEH is a potential pharmacologic target for ALI.

Melanoma is derived from melanocytes and accounts for ~80% of skin cancer-associated fatalities worldwide. The dysregulation of microRNAs (miRNAs/miRs) is involved in the development and progression of melanoma. Therefore, miRNAs may be novel diagnostic or prognostic biomarkers and promising therapeutic targets in the treatment of patients with melanoma. miR‑675 is differentially expressed in several types of human cancer and has important roles in the pathogenesis of several diseases. However, the expression levels and the biological roles of miR‑675 in melanoma remain unclear. Therefore, the present study aimed to assess the expression of miR‑675 in melanoma, explore the effects of miR‑675 on melanoma cells and investigate the underlying molecular mechanisms that may be involved in the actions of miR‑675. The present study indicated that miR‑675 expression was downregulated in melanoma tissues and cell lines. Functional assays demonstrated that the upregulation of miR‑675 impaired cell proliferation and invasion in melanoma. Bioinformatics analysis, luciferase reporter assay, reverse transcription‑quantitative polymerase chain reaction and western blot analysis demonstrated that metadherin (MTDH) was a direct target of miR‑675 in melanoma. The MTDH levels were upregulated in melanoma tissues and inversely correlated with the miR‑675 expression. Furthermore, restored MTDH expression rescued the inhibition effects in melanoma cells caused by miR‑675 overexpression. Thus, miR‑675 may be a potential therapeutic target for melanoma.

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