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1 cterial lipopeptide, and polymicrobial intra-abdominal sepsis.
2 outcome of experimental polymicrobial intra-abdominal sepsis.
3 is graft secondary to bowel injury and intra-abdominal sepsis.
4 Forty animals were randomized, and 1 died of abdominal sepsis.
5 e cecum was ligated and punctured to produce abdominal sepsis.
6 echanism underlying its protective effect in abdominal sepsis.
7 ional activities during the host response to abdominal sepsis.
8 mice underwent a cecal slurry model of intra-abdominal sepsis.
9 ion for an open abdomen (n = 398, 68.9%) was abdominal sepsis.
10 dults with abdominal injury (46.7%) or intra-abdominal sepsis (52.3%) were randomly allocated to the
11 , enteroatmospheric fistula (EAF), and intra-abdominal sepsis/abscess (IAS) are major challenges for
13 well-accepted model of murine polymicrobial abdominal sepsis and begin characterizing (in the parlan
14 -3, and CIS was transiently increased during abdominal sepsis and temporally associated with the deve
15 vival of mice subjected to various models of abdominal sepsis because of an overwhelming innate immun
18 al ligation and puncture (CLP) as a model of abdominal sepsis, followed 24 h later by intratracheal (
19 ncture (CLP), a well-accepted model of intra-abdominal sepsis, followed by daily subcutaneous injecti
23 riction for 3 weeks followed by induction of abdominal sepsis or endotoxemia by intraperitoneal injec
25 hematologic, and biochemical consequences of abdominal sepsis produced by intraperitoneal implantatio
27 severe (n = 21) or non-severe (n = 8) intra-abdominal sepsis; severe (n = 23) or non-severe (n = 21)
28 on of sophorolipids after induction of intra-abdominal sepsis significantly decreases mortality in th
31 iate abscess formation associated with intra-abdominal sepsis, the role of T-cell activation and the
32 e function aggravates the clinical course of abdominal sepsis via HIF-1alpha- and NF-kappaB-mediated
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