PuSH - Publikationsserver des Helmholtz Zentrums München

Kong, B.* ; Bruns, P. ; Raulefs, S.* ; Rieder, S.* ; Paul, L.* ; da Costa, O.P.* ; Buch, T.* ; Theis, F.J. ; Michalski, C.W.* ; Kleeff, J.*

Metabolism gene signatures and surgical site infections in abdominal surgery.

Int. J. Surg. 14, 67-74 (2015)
DOI Verlagsversion bestellen
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
INTRODUCTION: Surgical site infections (SSI) represent a significant cause of morbidity in abdominal surgery. The objective of this study was to determine the gene expression signature in subcutaneous tissues in relation to SSI. METHODS: To determine differences in gene expression, microarray analysis were performed from bulk tissue mRNA of subcutaneous tissues prospectively collected in 92 patients during open abdominal surgery. 10 patients (11%) developed incisional (superficial and deep) SSI. RESULTS: Preoperative risk factors in patients with SSI were not significantly different from those in patients without wound infections. 1025 genes were differentially expressed between the groups, of which the AZGP1 and ALDH1A3 genes were the highest down- and upregulated ones. Hierarchical clustering demonstrated strong similarity within the respective groups (SSI vs. no-SSI) indicating inter-group distinctness. In a functional classification, genes controlling cell metabolism were mostly down-regulated in subcutaneous tissues of patients that subsequently developed SSI. CONCLUSION: Altered expression of metabolism genes in subcutaneous tissues might constitute a risk factor for postoperative abdominal SSI.
Weitere Metriken?
Zusatzinfos bearbeiten [➜Einloggen]
Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Aldh1a3 ; Azgp1 ; Cellular Metabolism ; Subcutaneous Tissue ; Surgical Site Infection; Hematopoietic Stem-cells; Wound-infection; Hair Follicle; Reactive Oxygen; Adipose-tissue; Risk; Mice; Homeostasis; Contribute; Cancer
ISSN (print) / ISBN 1743-9191
e-ISSN 1743-9159
Quellenangaben Band: 14, Heft: , Seiten: 67-74 Artikelnummer: , Supplement: ,
Verlag Oxford University Press
Verlagsort Oxford [u.a.]
Begutachtungsstatus Peer reviewed