ライフサイエンスコーパス: abdominal sepsis

1 eumonia, and 7.1% vs 20.0%, p = 3.4 x 10 for abdominal sepsis).

2 mice underwent a cecal slurry model of intra-abdominal sepsis.

3 ion for an open abdomen (n = 398, 68.9%) was abdominal sepsis.

4 outcome of experimental polymicrobial intra-abdominal sepsis.

5 is graft secondary to bowel injury and intra-abdominal sepsis.

6 Forty animals were randomized, and 1 died of abdominal sepsis.

7 gh potential for adjunctive therapy in intra-abdominal sepsis.

8 e cecum was ligated and punctured to produce abdominal sepsis.

9 echanism underlying its protective effect in abdominal sepsis.

10 ional activities during the host response to abdominal sepsis.

11 em to cecal ligature and puncture, to induce abdominal sepsis.

12 cterial lipopeptide, and polymicrobial intra-abdominal sepsis.

13 dults with abdominal injury (46.7%) or intra-abdominal sepsis (52.3%) were randomly allocated to the

14 , enteroatmospheric fistula (EAF), and intra-abdominal sepsis/abscess (IAS) are major challenges for

15 led among a multitude of problems, including abdominal sepsis and battlefield surgery.

16 well-accepted model of murine polymicrobial abdominal sepsis and begin characterizing (in the parlan

17 ere compared in vitro and in mouse models of abdominal sepsis and burn wound infection.

18 ailed to affect the inflammatory response to abdominal sepsis and pneumonia.

19 ned in mice subjected to polymicrobial intra-abdominal sepsis and secondary lung bacterial infections

20 -3, and CIS was transiently increased during abdominal sepsis and temporally associated with the deve

21 Complications of diverticulitis, such as abdominal sepsis, are less likely to occur with subseque

22 vival of mice subjected to various models of abdominal sepsis because of an overwhelming innate immun

23 Induction of polymicrobial, abdominal sepsis by cecal ligation and puncture.

24 Abscess formation associated with intra-abdominal sepsis causes severe morbidity and can be fata

25 al ligation and puncture (CLP) as a model of abdominal sepsis, followed 24 h later by intratracheal (

26 ncture (CLP), a well-accepted model of intra-abdominal sepsis, followed by daily subcutaneous injecti

27 formation of abscesses associated with intra-abdominal sepsis in humans.

28 inflammation after abdominal injury or intra-abdominal sepsis is associated with poor outcomes.

29 In a mouse model of abdominal sepsis, local effects of bacterial ATP were an

30 e by modifying a widely adopted murine intra-abdominal sepsis model to engender a phenotype that conf

31 Using the rat intra-abdominal sepsis model, we found that administration of

32 riction for 3 weeks followed by induction of abdominal sepsis or endotoxemia by intraperitoneal injec

33 is an option following laparotomy for severe abdominal sepsis or trauma.

34 hematologic, and biochemical consequences of abdominal sepsis produced by intraperitoneal implantatio

35 In murine intra-abdominal sepsis, pulmonary injury cannot be considered

36 severe (n = 21) or non-severe (n = 8) intra-abdominal sepsis; severe (n = 23) or non-severe (n = 21)

37 on of sophorolipids after induction of intra-abdominal sepsis significantly decreases mortality in th

38 These observations suggest that abdominal sepsis syndrome results in significant impairm

39 ponses in the context of pneumonia and intra-abdominal sepsis than wild-type animals.

40 iate abscess formation associated with intra-abdominal sepsis, the role of T-cell activation and the

41 e function aggravates the clinical course of abdominal sepsis via HIF-1alpha- and NF-kappaB-mediated

42 Intra-abdominal sepsis was induced in vivo in 166 rats via cec

43 Abdominal sepsis was produced in rats by cecal ligation

44 Using a mouse model of abdominal sepsis, we showed that innate response activat

45 r tissue sections from mice with and without abdominal sepsis were analyzed using multimodal nonlinea