ライフサイエンスコーパス: intestinal injury

1 rotected mice from ethanol-induced liver and intestinal injury.

2 and iNOS play different roles in PAF-induced intestinal injury.

3 ce of matrix metalloproteinase (MMP)8 during intestinal injury.

4 prevention or treatment of radiation-induced intestinal injury.

5 responses to proliferative signals following intestinal injury.

6 ne diseases, as well as a model of transient intestinal injury.

7 ed inflammation in Nod2(-/-) mice upon small-intestinal injury.

8 reduced inflammatory response and attenuated intestinal injury.

9 ining neutrophil mobilization in response to intestinal injury.

10 but also developed significant AKI and small intestinal injury.

11 ainst and enhances recovery from DSS-induced intestinal injury.

12 hepatic IR-induced acute liver, kidney, and intestinal injury.

13 ream pathways known to be protective against intestinal injury.

14 and to maintain intestinal homeostasis after intestinal injury.

15 he gut inflammatory responses in the face of intestinal injury.

16 omeostasis in dextran sodium sulfate-induced intestinal injury.

17 glutamine, have been beneficial in models of intestinal injury.

18 terin precursor) also attenuated PAF-induced intestinal injury.

19 ic colitis and delay the recovery from acute intestinal injury.

20 (I-FABP), is detectable in serum only after intestinal injury.

21 itro and in vivo), BAL fluid LPS levels, and intestinal injury.

22 ciency predisposes mice to DSS-induced small intestinal injury, a segment never reported as affected

23 ne response and the downstream mechanisms of intestinal injury, alongside their potential role in ope

24 n shown to protect against radiation-induced intestinal injury, although the underlying mechanisms re

25 inst both ischemic and reperfusion phases of intestinal injury, an effect abolished in MOR(IEC-/-) mi

26 thereby preventing and treating DSS-induced intestinal injury and acute colitis.

27 G (LGG)-derived soluble protein, ameliorates intestinal injury and colitis, reduces apoptosis, and pr

28 with dextran sulphate sodium (DSS) to induce intestinal injury and colitis.

29 asc(-/-) and casp-1(-/-) mice also had less intestinal injury and decreased IL-1beta and IL-18 produ

30 of AREG-expressing ILC2s increases following intestinal injury and genetic disruption of the endogeno

31 ane post-conditioning protects against small intestinal injury and hepatic and renal dysfunction afte

32 gulating neutrophil mobilization after acute intestinal injury and highlights C3aR agonism as a poten

33 stinal mucosa against bile salt (BS)-induced intestinal injury and how this property may be blocked b

34 A murine model of IR-induced intestinal injury and in vitro and in vivo models of hum

35 We developed a mouse model in which intestinal injury and increased permeability were induce

36 Intestinal injury and inflammation (myeloperoxidase cont

37 ii (Sb), a probiotic yeast, protects against intestinal injury and inflammation caused by a wide vari

38 lipid binding domain V of beta2-GPI blocked intestinal injury and inflammation, including cellular i

39 he impact of oxymatrine in an acute model of intestinal injury and inflammation.

40 t of treatment with antibiotics in models of intestinal injury and pathogenic bacterial infection.

41 ents with immune dysfunction can have severe intestinal injury and prolonged diarrhea.

42 ling may represent a novel mean to alleviate intestinal injury and promote the wound-healing response

43 cts of NOD2 on enterocyte TLR4 signaling and intestinal injury and repair were assessed in enterocyte

44 G1B) protein, which is a putative measure of intestinal injury and repair, was tested as a noninvasiv

45 es interleukin-1beta (IL-1beta) release upon intestinal injury and that this is mediated via the NLRP

46 udying NEC, including mathematical models of intestinal injury and the use of humanized mice.

47 attenuated DSS-induced histologic and gross intestinal injury and weight loss; diminished Ifng, Tnf,

48 leads to enhanced proinflammatory response, intestinal injury, and colorectal cancer.

49 essure, hematocrit, white blood cell counts, intestinal injury, and intestinal cNOS and iNOS activiti

50 eep hypothermic circulatory arrest, and that intestinal injury, and local and systemic inflammatory r

51 ibute to epithelial barrier repair following intestinal injury, and may offer a therapeutic avenue in

52 The stages of T cell activation, intestinal injury, and subsequent T tolerance are depend

53 by Klebsiella pneumoniae infection to induce intestinal injury; and iii) in bacterially infected IEC-

54 sed sensitivity to doxorubicin-induced acute intestinal injury, as evidenced by decreased villus heig

55 After intestinal injury, both the number and type of intestina

56 f CD73 significantly enhanced not only local intestinal injury, but also secondary organ injury, foll

57 njury (necrosis) plays a crucial role in the intestinal injury, cardiovascular failure, and multiple

58 n failed to protect GF mice from I/R-induced intestinal injury compared with control, a phenomenon co

59 CDC88B protein increases in the colon during intestinal injury, concomitant with an influx of CCDC88B

60 nd cathepsin B-deficient mice suffer limited intestinal injury during the ischemic phase.

61 pecies in feces, and enhanced sensitivity to intestinal injury following administration of dextran so

62 ch localized to the areas of the most severe intestinal injury, i.e., the necrotic epithelial cells a

63 We have demonstrated that after acute intestinal injury, IL-23R(+) gammadelta T cells in the c

64 rally administered fluorophores can identify intestinal injury in a rat model.

65 amin D deficiency predisposes to more-severe intestinal injury in an infectious model of colitis.

66 nhanced susceptibility to Salmonella-induced intestinal injury in coinfected mice was found to be ass

67 Herein, we report that I/R-induced intestinal injury in germ-free (GF) C57BL/6 wild-type (W

68 rmacological inhibition of MMP8 would reduce intestinal injury in mice subjected to intestinal ischem

69 (CDK4/6), prevents radiation-induced lethal intestinal injury in mice.

70 disruption precedes or is the consequence of intestinal injury in necrotizing enterocolitis (NEC) rem

71 ement activation, neutrophil recruitment and intestinal injury in otherwise IR-resistant Rag1(-/-) mi

72 F on intestinal microvascular blood flow and intestinal injury in rat pups subjected to experimental

73 We hypothesize that the intestinal injury in this disease is a consequence of sy

74 ulating genotoxic chemotherapy-induced small intestinal injury in vitro and in vivo.

75 ress, a common endpoint of numerous types of intestinal injury including ischemia and immune-mediated

76 nase-activated receptor-2 (PAR(2)) modulates intestinal injuries induced by ischemia/reperfusion.

77 s and PAR activation could also modulate the intestinal injury induced by ischemia-reperfusion (I-R).

78 ion was downregulated, which correlated with intestinal injury, interrupted enterocyte migration, and

79 nt modality for gastrointestinal tumors, but intestinal injury is a common side effect.

80 iota-mediated protection against I/R-induced intestinal injury is abrogated in conventionally derived

81 the platelet-activating factor (PAF)-induced intestinal injury is attenuated by peptido-leukotriene a

82 examining the effect of PDL on T/HS-induced intestinal injury, lung injury, and RBC deformability.

83 onstrate for the first time that significant intestinal injury occurs during ischemia prior to reperf

84 Intestinal injury or chronic inflammation induce cytokin

85 educed XO activity and ameliorated liver and intestinal injury (p < 0.05).

86 Tetrahydrobiopterin prevents PAF-induced intestinal injury, probably by stabilizing nNOS and main

87 dose (1.5 micrograms/kg) below that causing intestinal injury rapidly up-regulated intestinal PLA2-I

88 role of this cytokine/receptor pair in acute intestinal injury/repair pathways.

89 gulation of mucosal homeostasis during acute intestinal injury/repair, which contrasts with its known

90 ng toward ischemia/reperfusion (I/R)-induced intestinal injury response is unknown.

91 and adiponectin, known to directly influence intestinal injury responses.

92 nd non-activated MSC-CM on radiation-induced intestinal injury (RIII).

93 Thus, upon intestinal injury, selective members of the microbiota s

94 of intestinal goblet cells protects against intestinal injury, suggesting that this epithelial cell

95 hat Cr2(-/-) mice did not demonstrate severe intestinal injury that was readily observed in control C

96 However, crucially we find that after intestinal injury they are capable of extensive prolifer

97 erial infection and promote bacteria-induced intestinal injury through a mechanism that involves the

98 D34(+)gp38(+) cells are rapidly activated by intestinal injury, up-regulating niche factors Gremlin1

99 abilis promoted intestinal inflammation upon intestinal injury via the production of hemolysin, which

100 Newborn intestinal injury was associated with decreased intestin

101 Intestinal injury was determined by histologic analysis

102 Intestinal injury was determined by histologic analysis

103 Intestinal injury was graded using a standard histologic

104 NEC-like intestinal injury was induced in newborn rats by hypoxia

105 C3aR deficiency worsened intestinal injury, which corresponded with increased num

106 erocolitis (NEC), a devastating condition of intestinal injury with extensive inflammation in prematu

107 We hypothesized that intestinal injury with increased intestinal permeability