ライフサイエンスコーパス: intestinal injury

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

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

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

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

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

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

7 served in nod2-deficient zebrafish models of intestinal injury.

8 2A (PP2A) and genes regarding Cr(VI)-induced intestinal injury.

9 estinal epithelial cells and protection from intestinal injury.

10 patients continue to experience symptoms and intestinal injury.

11 at high risk for gut microbial dysbiosis and intestinal injury.

12 than dysbiosis to determine alcohol-induced intestinal injury.

13 d mice with susceptibility to Cr(VI)-induced intestinal injury.

14 nd LTalpha all contribute to TNF-independent intestinal injury.

15 ntial of EGF administration for treatment of intestinal injury.

16 e of Bacteroides uniformis and reductions in intestinal injury.

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

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

19 prevention or treatment of radiation-induced intestinal injury.

20 responses to proliferative signals following intestinal injury.

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

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

23 reduced inflammatory response and attenuated intestinal injury.

24 ferating cell nuclear antigen, indicative of intestinal injury.

25 ining neutrophil mobilization in response to intestinal injury.

26 but also developed significant AKI and small intestinal injury.

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

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

29 ream pathways known to be protective against intestinal injury.

30 and to maintain intestinal homeostasis after intestinal injury.

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

32 omeostasis in dextran sodium sulfate-induced intestinal injury.

33 ce PNAC, male C57BL/6 mice were subjected to intestinal injury (2% dextran sulfate sodium [DSS] for 4

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

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

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

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

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

39 ithelial function and protected mice against intestinal injury and bacterial infection.

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

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

42 Recipient IRX4204 treatment reduced intestinal injury and decreased IFN-y and TNF-a serum le

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

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

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

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

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

48 C, phytosterol containing PN synergizes with intestinal injury and IL-1B derived from activated hepat

49 C, phytosterol containing PN synergizes with intestinal injury and IL-1beta derived from activated he

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

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

52 Intestinal injury and inflammation (myeloperoxidase cont

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

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

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

56 results indicate that PEDV infection induces intestinal injury and inhibits the expression of genes e

57 dylserine at 40 mg/kg significantly improved intestinal injury and modulated oxidative, inflammatory,

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

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

60 rly stages of disease progression, decreases intestinal injury and prolongs survival.

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

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

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

64 ry, oxidative and nitrosative stress promote intestinal injury and sepsis-mediated lethality in Cebpd

65 a dual mechanism in preventing sugar-induced intestinal injury and supporting metabolic health: direc

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

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

68 pathways participated in Cr(VI)-caused small intestinal injury and urolithin A could potentially prot

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

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

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

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

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

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

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

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

77 d novel insight into potential mechanisms of intestinal injury associated with CHD.

78 odulatory pathway monitored clinically as an intestinal injury biomarker, regulates intrinsic epithel

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

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

81 utophagy might contribute to the severity of intestinal injury by compromising the integrity of the m

82 Paneth cells and enhanced susceptibility to intestinal injury by inhibiting the secretion of API5 fr

83 increased injury when mice were subjected to intestinal injury by other methods.

84 C/EBPdelta in protection against IR-induced intestinal injury by suppressing inflammation and nitros

85 ic and phenotypic features of EED-associated intestinal injury can be reconstituted in a human intest

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

87 as chronic heavy drinking (CHD), results in intestinal injury characterized by increased permeabilit

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

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

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

91 whole small intestine from radiation-induced intestinal injury during the radiotherapy of abdominal o

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

93 atelet activation and depletion occur during intestinal injury following exposure to bacterial produc

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

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

96 reported that RIC significantly reduces the intestinal injury in a rat model of NEC.

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

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

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

100 previously found that NF-kappaB mediates the intestinal injury in experimental NEC.

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

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

103 rce of the WNT agonist R-spondin 1 following intestinal injury in mice.

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

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

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

107 o determine whether puerarin could alleviate intestinal injury in piglets infected with PEDV.

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

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

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

111 a guarded role in the detection of continued intestinal injury, in particular as to sensitivity, as n

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

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

114 ice also showed high susceptibility to small intestinal injury induced by indomethacin, a nonsteroida

115 ice also showed high susceptibility to small intestinal injury induced by indomethacin, a nonsteroida

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

117 Intestinal injury induces the outgrowth of adrenergic ne

118 n exacerbates disease conditions, leading to intestinal injury, inflammation, and colorectal cancer.

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

120 hort study in Uganda, we measured markers of intestinal injury (intestinal fatty-acid binding protein

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

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

123 nocytes and conversion to macrophages during intestinal injury is also dependent upon CCR2, Nr4a1 and

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

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

126 The organ-chip model of EED-associated intestinal injury may facilitate the analysis of the mol

127 d healing in Caco-2 monolayers and two mouse intestinal injury models.

128 nergy, there is increasing hematopoietic and intestinal injury, necessitating dose reduction to achie

129 Intestinal injury occurs commonly in children hospitaliz

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

131 Intestinal injury or chronic inflammation induce cytokin

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

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

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

135 the therapeutic importance of mesenchyme for intestinal injury repair.

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

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

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

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

140 uration impaired weight recovery after acute intestinal injury, resulting in reduced survival.

141 Radiation-induced intestinal injury (RIII) constitutes a crucial clinical

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

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

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

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

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

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

148 ife-threatening condition that causes severe intestinal injury through oxidative stress, inflammation

149 dextran sulfate sodium (DSS) model of acute intestinal injury to study the contributions of type I a

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

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

152 Newborn intestinal injury was associated with decreased intestin

153 Intestinal injury was determined by histologic analysis

154 Intestinal injury was determined by histologic analysis

155 Intestinal injury was graded using a standard histologic

156 Intestinal injury was induced by serosally applying 75%

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

158 n in IL-17A production and concomitant overt intestinal injury was not evident.

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

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

161 We hypothesized that intestinal injury with increased intestinal permeability

162 jury, acidosis, impaired perfusion, coma and intestinal injury with increases in the abundance of Gra

163 then given RBC transfusions develop NEC-like intestinal injury with prominent necrosis, inflammation,

164 Intestinal injury worsens with increasing severity and t