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1.
Surg Infect (Larchmt) ; 19(7): 696-703, 2018 Oct.
Article in English | MEDLINE | ID: mdl-30183520

ABSTRACT

BACKGROUND: Surgical site infection (SSI) surveillance has become increasingly important during the peri-operative period of esophagectomy with cervical anastomosis (McKeown esophagectomy). This study sought to clarify the risk factors for SSI and to develop a stratification scoring system to predict SSI after esophagectomy with cervical anastomosis. PATIENTS AND METHODS: All patients who underwent elective esophagectomy with cervical anastomosis were studied between January 2010 and December 2016 in the Chinese Academy of Medical Sciences Cancer Hospital (CAMS). Univariable analysis and multivariable logistic regression were used to screen the independent risk factors. A risk stratification scoring system was developed based on multivariable logistic regression parameters. The model derivation set involved 711 consecutive cases, and the validation set involved 168 consecutive cases. RESULTS: In the model derivation set, there were 711 patients, of whom 146 were found to have SSI and the incidence rate was 20.53%. Multivariable analysis found that SSI was associated independently with the following adverse risk factors: peripheral vascular disease, prior chest surgery, no pre-operative surgical antibiotic prophylaxis (SAP) administration within 120 minutes prior to incision, low serum albumin, and low pre-albumin at post-operative day zero to three, respectively. Each of these factors contributed one point to the risk score and a risk stratification scoring system was established. The SSI rates were increased gradually in the low, intermediate, high, and extremely high-risk groups (p < 0.001). The area under the receiver operating characteristic (AUROC) curve was 0.706 for the logistic regression model and 0.704 for the scoring system. In the validation set, the model performed equivalently (AUC = 0.824). CONCLUSIONS: The validated stratification scoring system could predict accurately the risk of SSI after esophagectomy with cervical anastomosis. This could be helpful in the selection of high-risk patients requiring frequent monitoring and more aggressive interventions to decrease the incidence of SSI.


Subject(s)
Anastomosis, Surgical/adverse effects , Esophageal Neoplasms/surgery , Esophagectomy/adverse effects , Surgical Wound Infection/etiology , Aged , Anastomosis, Surgical/methods , Antibiotic Prophylaxis , Esophagectomy/methods , Female , Humans , Male , Neck/surgery , Operative Time , Risk Factors , Surgical Wound Infection/prevention & control
2.
Innate Immun ; 24(5): 285-296, 2018 07.
Article in English | MEDLINE | ID: mdl-29969931

ABSTRACT

Previous studies have reported that lipoxin A4 (LXA4) and the angiotensin I-converting enzyme 2 (ACE2), angiotensin-(1-7) [Ang-(1-7)], and its receptor Mas [ACE2-Ang-(1-7)-Mas] axis play important protective roles in acute lung injury (ALI). However, there is still no direct evidence of LXA4-mediated protection via the ACE2-Ang-(1-7)-Mas axis during ALI. This work was performed using an LPS-induced ALI mouse model and the data indicated the following. First, the animal model was established successfully and LXA4 ameliorated LPS-induced ALI. Second, LXA4 could increase the concentration and activity of ACE2 and the levels of Ang-(1-7) and Mas markedly. Third, LXA4 decreased the levels of TNF-α, IL-1ß, and reactive oxygen species while increasing IL-10 levels. Fourth, LXA4 inhibited the activation of the NF-κB signal pathway and repressed the degradation of inhibitor of NF-κB, the phosphorylation of NF-κB, and the translocation of NF-κB. Finally, and more importantly, BOC-2 (LXA4 receptor inhibitor), MLN-4760 (ACE2 inhibitor), and A779 (Mas receptor antagonist) were found to reverse all of the effects of LXA4. Our data provide evidence that LXA4 protects the lung from ALI through regulation of the ACE2-Ang-(1-7)-Mas axis.


Subject(s)
Acute Lung Injury/metabolism , Imidazoles/metabolism , Leucine/analogs & derivatives , Lipoxins/metabolism , Peptidyl-Dipeptidase A/metabolism , Angiotensin I/metabolism , Angiotensin II/analogs & derivatives , Angiotensin II/metabolism , Angiotensin-Converting Enzyme 2 , Animals , Cell Line, Tumor , Disease Models, Animal , Humans , Imidazoles/antagonists & inhibitors , Leucine/antagonists & inhibitors , Leucine/metabolism , Lipopolysaccharides/immunology , Male , Mice , NF-kappa B/metabolism , Peptide Fragments/metabolism , Proto-Oncogene Mas , Proto-Oncogene Proteins/metabolism , Receptors, G-Protein-Coupled/metabolism , Signal Transduction
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