Glutamine Supplementation on Burn Patients: A Systematic Review and Meta-analysis.

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, Google scholar, Wanfang data, and ClinicalTrials.gov were searched up to October 2023 to find randomized trials evaluating glutamine supplement on patients with burns. The main outcomes included hospital stay, in-hospital mortality, infection, and wound healing. Twenty-two trials that randomized a total of 2170 patients were included in this meta-analysis. Pooled the length of hospital stay was shortened by glutamine supplement (weighted mean differences [WMD] = -7.95, 95% confidence interval [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%, 6 studies) and wound healing times (WMD = -5.84, 95% CI -7.42 to -4.27, I2 = 45.7%, 7 studies) were improved by glutamine supplement. Moreover, glutamine supplement reduced wound infection (risk ratios [RR] = 0.38, 95% CI 0.21 to 0.69, I2 = 0%, 3 trials), but not nonwound 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%, 8 trials) nor the length of intensive care unit stay (WMD = 1.85, 95% CI -7.24 to 10.93, I2 = 78.2%, 5 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 the 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.

Inhibitors of soluble epoxide hydrolase on acute lung injury: a meta-analysis of preclinical studies.

INTRODUCTION: This study investigated the effects of soluble epoxide hydrolase (sEH) inhibitors on acute lung injury (ALI) using the measure of meta-analysis. METHODS: Relative publications were systematic reviewed and retrieved by searching electronic databases including the Cochrane Library, PubMed, China National Knowledge Infrastructure, Wanfang Data, and Google Scholar. RESULTS: Seven animal studies were included in this meta-analysis. Our result showed that the lung injury scores (SMD = - 2.31, 95% CI - 3.50 to - 1.12) and lung wet to dry weight ratios (WMD-1.44, 95% CI - 1.69 to - 1.18) were reduced in sEH inhibitors-treated animals compared with control. The mortality was improved by sEH inhibitors at 48 h (RR = 0.62, 95% CI 0.42 to 0.92), 72 h, and 120 h, but not at 24 h (RR = 0.59, 95% CI 0.35 to 1.01) and 96 h, after induction of ALI model. CONCLUSIONS: The sEH inhibitor is a potent candidate of pharmacological agents for ALI/acute respiratory distress syndrome, as its effects on improvement of lung injury and mortality in preclinical researches.

Effect of Soluble Epoxide Hydrolase in Hyperoxic Acute Lung Injury in Mice.

Hyperoxic acute lung injury is a serious complication of oxygen therapy that causes high mortality. Inhibition of soluble epoxide hydrolase (sEH) has been reported to have protective effect on lipopolysaccharide-induced acute lung injury (ALI). This study investigates whether sEH plays any role in the pathogenesis of hyperoxic ALI. Wild-type and sEH gene knockout (sEH-/-) mice were exposed to 100% O2 for 72 h to induce hyperoxic ALI. Hyperoxia caused infiltration of inflammatory cells, elevation of interleukin-1ß and interleukin-6 levels, and deterioration of alveolar capillary protein leak as well as wet/dry weight ratio in the lung. The hyperoxia-induced pulmonary inflammation and edema were markedly improved in sEH-/- mice. Survival rate was significantly improved in sEH-/- mice compared with that in wild-type mice. Moreover, the levels of epoxyeicosatrienoic acids and heme oxygenase-1 activity were notably elevated in sEH-/- mice compared with those in wild-type mice after exposure to 100% O2 for 72 h. The nucleotide-binding domains and leucine-rich repeat pyrin domains containing 3 (NLRP3) inflammasome activation and caspase-1 activity induced by hyperoxia were inhibited in sEH-/- mice compared with those in wild-type mice. Inhibition of sEH by an inhibitor, AUDA, dampened hyperoxia-induced ALI. sEH plays a vital role in hyperoxic ALI and is a potential therapeutic target for ALI.

Soluble Epoxide Hydrolase Plays a Vital Role in Angiotensin II-Induced Lung Injury in Mice.

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-1ß 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.

Effects of a Soluble Epoxide Hydrolase Inhibitor on Lipopolysaccharide-Induced Acute Lung Injury in Mice.

OBJECTIVES: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.

Effects of omega-3 fatty acid nutrition on mortality in septic patients: a meta-analysis of randomized controlled trials.

BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.

[The thoracodorsal artery musculocutaneous perforator flap: anatomic study and clinical significance].

OBJECTIVE: To investigate the feasibility of clinical application of the thoracodorsal artery musculocutaneous perforator flap (TAMPF). METHODS: (1) The morphosis and blood supply of TAP flap on 15 formalized adult cadavers(30 sides) were examined by microsurgery anatomy. (2) An imitative operation of the TAMP flap and latissimus dorsi flap on 1 formalized adult cadavers (2 sides) was conducted. RESULTS: (1) A total of 102 musculocutaneous perforators larger than 0.5 mm were found in 16 specimens(32 sides). 56 perforators (55%) were originated from the medial branch and 46 (45%) originated from the lateral branch. The biggest perforator is (0.82 +/- 0.11) mm (0.68 - 1.08 mm). There was an average of 1.9 perforators (range, 1 - 3 perforators) of the medial branch and an average of 1.8 perforators (range, 1 - 3 perforators) of the lateral branch. Additionally, there were 24 perforators samller than 0.5 mm, and 76 perforators originated from intercostal artery and lumbar artery. (2) Musculocutaneous perforators over 0.5 mm were found only in proximity of the medial and lateral branches within a distance of 8.5 cm (6.4 cm - 9.2 cm) distal to the neurovascular hilus. CONCLUSIONS: With the characteristics of constant position, large caliber, long pedicle, the thoracodorsal artery musculocutaneous perforator was suitable to be musclocutaneous perforator flaps and "fan-shaped" flaps.