Inflammation 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. Male 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. AUDA 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. Administration 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.

A 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. A PubMed database was searched through Feb 2016, and randomized controlled trials comparing omega-3 fatty acids with control were selected by two reviewers independently. Eleven 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. Omega-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.

Hair follicle regeneration has been successful in mice but failed in human being for years. Dermal papilla cells, a specialized mesenchymal stem cell derived from dermal papilla within hair follicles, is considered the key cells for hair follicle regeneration function as both regeneration initiator and regulator. Injectable platelet rich fibrin (i-PRF), a novel biomaterial rich in a variety of growth factors and three-dimensional scaffolds, has shown promising effects on tissue regeneration. In this study, we aimed to evaluate the application of i-PRF in human hair follicle regeneration by examining the biological effects of i-PRF on human dermal papilla cells (hDPCs). Biomaterial compatibility, cell viability, proliferation, migration, alkaline phosphatase activity and trichogenic inductivity were assessed after exposing hDPCs to different concentrations of i-PRF extracts. In addition, we investigated the ultrastructure of i-PRF with all cell components filtered. The results revealed that i-PRF possessing excellent biocompatibility and could significantly promote hDPCs proliferation, migration, and trichogenic inductivity. Furthermore, the concentration of i-PRF is able to remarkably influence hDPCs behavior in a dose-dependent pattern. Different concentrations exhibited differential effects on hDPCs behavior. In general, lower concentration promotes cell proliferation better than higher concentration, while higher concentration promotes cell function better reversely. Best concentration for hDPCs in vitro expending is 1% concentration. 20% concentration is optimal for hair follicle regeneration. In summary, our findings concluded that i-PRF facilitates hair follicle regeneration by promoting human dermal papilla cell proliferation, migration, and trichogenic inductivity.

Background: Angiotensin II plays a vital role in the pathogenesis of acute respiratory distress syndrome (ARDS). However, its mechanism is not well defined. Angiotensin II upregulates the expression of soluble epoxide hydrolase (sEH; Ephx2). sEH is suggested as a potential pharmacologic target for ARDS. The present study investigates whether the sEH is involved in the angiotensin II-triggered pulmonary inflammation and edema using an angiotensin II-induced lung injury animal model. Methods: Lung injury was induced by angiotensin II intratracheally instillation in wild-type or Ephx2 deficient mice. Results: sEH activities were markedly increased in wild-type mice treated with angiotensin II. Angiotensin II markedly increased the levels of tumor necrosis factor-α and interleukin-1β in bronchoalveolar lavage fluid, worsened alveolar capillary protein leak and lung histological alterations, and elevated activity of activator protein-1 and nuclear factor-κB. However, these changes were significantly improved in Ephx2 deficient mice. Moreover, Losartan, an angiotensin II receptor 1 antagonist, abolished the sEH induction and improved mortality. Conclusions: Angiotensin II-induced lung injury was improved in sEH gene deleted mice. The angiotensin II-triggered pulmonary inflammation is mediated, at least in part, through the sEH.

To evaluate the effect of glutamine supplement on patients with burns, we conducted a systematic review and meta-analysis via synthesizing up-to-date studies. Databases including PubMed, Cochrane Central Register, EMBASE, and Google scholar, Wanfang data, and ClinicalTrials.gov were searched up to Oct, 2023 to find randomized trials evaluating glutamine supplement on patients with burns. Main outcomes included hospital stay, in hospital mortality, infection, and wound healing. Twenty-two trials which randomized a total of 2,170 patients were included in this meta-analysis. Pooled the length of hospital stay was shortened by glutamine supplement (WMD = -7.95, 95%CI -10.53 to -5.36, I² = 67.9%, 16 trials)). Both pooled wound healing rates (WMD = 9.15, 95%CI 6.30 to 12.01, I² = 82.7%, six studies) and wound healing times (WMD = -5.84, 95%CI -7.42 to -4.27, I² = 45.7%, seven studies) were improved by glutamine supplement. Moreover, glutamine supplement reduced wound infection (RR = 0.38, 95%CI 0.21 to 0.69, I² = 0%, three trials), but not non-wound infection (RR = 0.88, 95%CI 0.73 to 1.05, I² = 39.6%, 9 trials). Neither in hospital mortality (RR = 0.95, 95%CI 0.74 to 1.22, I² = 36.0%, eight trials) nor the length of ICU stay (WMD = 1.85, 95%CI -7.24 to 10.93, I² = 78.2%, five studies) was improved by glutamine supplement. Subgroup analysis showed positive effects were either influenced by or based on small-scale, single center studies. Based on the current available data, we do not recommend routine use of glutamine supplement for burn patients in hospital. Future large-scale randomized trials are still needed to give a conclusion about the effect of glutamine supplement on burn patients.