ライフサイエンスコーパス: intestinal ischemia

1 other hemodynamic imbalances (heart failure, intestinal ischemia).

2 blood flow may result in clinically relevant intestinal ischemia.

3 (n = 24) and then subjected to 30 minutes of intestinal ischemia.

4 olved in the generation of activators during intestinal ischemia.

5 our after a 15-minute period of normothermic intestinal ischemia.

6 of recipients following SITx after prolonged intestinal ischemia (6 hours).

7 Intestinal ischemia after hemorrhagic shock results in g

8 te adhesion, and maintained blood flow after intestinal ischemia and may therefore be of value in red

9 le of T lymphocytes and neutrophils (PMN) in intestinal ischemia and reperfusion injury (IRI) using e

10 emote (lung) complement activation following intestinal ischemia and reperfusion injury and that CR2-

11 otal role in the burn- and endotoxin-induced intestinal ischemia and reperfusion injury, with subsequ

12 ce in sterile inflammatory injury induced by intestinal ischemia and reperfusion, as well as in a mod

13 talloproteinase-8 as a mediator of injury in intestinal ischemia and reperfusion.

14 nificantly increased in C3aR(-/-) mice after intestinal ischemia, and C3aR(-/-) mice also mobilized m

15 ed on patients who were diagnosed with acute intestinal ischemia between May 1993 and July 2000.

16 Intestinal ischemia followed by reperfusion leads to loc

17 C57Bl/6 mice were subjected to 90 minutes of intestinal ischemia followed or not by reperfusion.

18 Intestinal ischemia has a wide variety of causes, includ

19 restore adequate intestinal blood flow, and intestinal ischemia has been implicated in the activatio

20 of mucosal injury, yet the reasons for which intestinal ischemia in NEC occurs in the first place rem

21 Acute intestinal ischemia is reported to have a poor prognosis

22 e that the prognosis for patients with acute intestinal ischemia is substantially better than previou

23 Etiologies were intestinal ischemia (n = 30; 59%) and hemorrhage (n = 21

24 , 2 OR-TAA(A)] developed fatal postoperative intestinal ischemia on day 2 or 3.

25 to determine whether isoflurane, given after intestinal ischemia, protects against intestinal IRI and

26 ; 95% confidence interval [CI], 1.7 to 2.3), intestinal ischemia (relative risk, 6.0; 95% CI, 4.5 to

27 educe intestinal injury in mice subjected to intestinal ischemia-reperfusion (I/R) injury.

28 ti-inflammatory pathway in a murine model of intestinal ischemia-reperfusion (I/R) injury.

29 nt-rich preservation solution in alleviating intestinal ischemia-reperfusion (IR) injury in a large a

30 Intestinal ischemia-reperfusion (IR) injury is initiated

31 Intestinal ischemia-reperfusion (IR) injury is initiated

32 e used a neutrophil-dependent mouse model of intestinal ischemia-reperfusion (IR) injury to explore t

33 endent adenosine production in modulation of intestinal ischemia-reperfusion (IR) injury.

34 Intestinal ischemia-reperfusion (IR)-induced damage requ

35 Intestinal ischemia-reperfusion after severe shock state

36 he role of neutrophil-derived MMP-9 in acute intestinal ischemia-reperfusion and its interaction with

37 urane anesthesia, the mice were subjected to intestinal ischemia-reperfusion by occlusion (clamping)

38 Intestinal ischemia-reperfusion caused bacterial translo

39 Intestinal ischemia-reperfusion injury (IRI) can occur i

40 atile anesthetic-mediated protection against intestinal ischemia-reperfusion injury (IRI).

41 Intestinal ischemia-reperfusion injury was induced by te

42 growth factor significantly protects against intestinal ischemia-reperfusion injury.

43 There was up to 3-fold more tissue MDA after intestinal ischemia-reperfusion than after sham laparoto

44 iNOS mediates bacterial translocation after intestinal ischemia-reperfusion, using iNOS knockout mic

45 iNOS knockout mice were more resistant to intestinal ischemia-reperfusion-induced bacterial transl

46 e, suggesting that iNOS might play a role in intestinal ischemia-reperfusion-induced loss of gut barr

47 ng an in vivo isolated jejunal loop model of intestinal ischemia-reperfusion.

48 ion generally has a milder course than small intestinal ischemia-reperfusion.

49 Intestinal ischemia/reperfusion (I/R) injury is a relati

50 As beta2-GPI is critical for intestinal ischemia/reperfusion (IR)-induced tissue dama

51 at PAR(2) modulates GIT and tissue damage in intestinal ischemia/reperfusion by a mechanism dependent

52 ndence for local and remote injury following intestinal ischemia/reperfusion in a clinically relevant

53 lmonary vascular resistance in both sham and intestinal ischemia/reperfusion injured animals compared

54 Pathophysiological states that produce intestinal ischemia/reperfusion injury (I/R) initiate an

55 re, we report on the use of a mouse model of intestinal ischemia/reperfusion injury to investigate th

56 Following intestinal ischemia/reperfusion injury, PLV H-130 treate

57 when administered in a therapeutic manner in intestinal ischemia/reperfusion injury.

58 Our data provide primary evidence that intestinal ischemia/reperfusion is a leading pathophysio

59 re activated in a microenvironment shaped by intestinal ischemia/reperfusion, and investigated local

60 Using a mouse model of intestinal ischemia/reperfusion, we administered peptide

61 (Rv)D5n-3 DPA protected against colitis and intestinal ischemia/reperfusion-induced inflammation in

62 PLV PP-5 and a significantly lower (p <.05) intestinal ischemia/reperfusion-mediated increase in mic

63 g system in the neuroimmune communication in intestinal ischemia/reperfusion.

64 Acute intestinal ischemia was diagnosed in 170 patients.

65 Intestinal ischemia was induced in vivo for 60 min, foll

66 Mesenteric encasement with intestinal ischemia was successfully relieved in 10 of 1

67 PVG rats were subjected to 30-min intestinal ischemia with a subgroup of animals receiving

68 as opposed to IP microdialysis detects small intestinal ischemia with higher sensitivity and specific

69 Adult rats were subjected to intestinal ischemia, with histologic and biochemical dam