ライフサイエンスコーパス: gastric inflammation

1 pepsinogen (PG) I and II levels (measures of gastric inflammation).

2 s expression correlates with the severity of gastric inflammation.

3 Coro1A(-/-) mice, resulting in an attenuated gastric inflammation.

4 on of host defense against the bacterium and gastric inflammation.

5 ls is important to regulatory suppression of gastric inflammation.

6 to H. felis-induced gastritis, with enhanced gastric inflammation.

7 t in individuals with non-H. pylori -induced gastric inflammation.

8 f the -511T/T genotype was related to severe gastric inflammation.

9 ction of IL-8, and induction of neutrophilic gastric inflammation.

10 uction and, at the same time, contributes to gastric inflammation.

11 igate the impact of sex on the regulation of gastric inflammation.

12 rogens exert overlapping effects to regulate gastric inflammation.

13 lation and contributes to the development of gastric inflammation.

14 test the effects of androgens on regulating gastric inflammation.

15 igated whether BMP signaling pathways affect gastric inflammation after bacterial infection of mice.

16 s, H. pylori colonization of gerbils induced gastric inflammation and a systemic antibody response to

17 ich a high-salt diet leads to high levels of gastric inflammation and associated oxidative stress in

18 mucosal IL-1beta levels and were related to gastric inflammation and atrophy, factors thought to be

19 tments and correlated with the occurrence of gastric inflammation and carcinogenesis.

20 lammatory signaling pathways contributing to gastric inflammation and carcinogenesis.

21 genicity island is associated with increased gastric inflammation and decreased epithelial repair.

22 ith the cagA mutant strain had low levels of gastric inflammation and did not develop hypochlorhydria

23 es that Th1-independent mechanisms can cause gastric inflammation and disease due to H. pylori.

24 7BL/10J and BALB/c mice also did not develop gastric inflammation and displayed a mixed Th1/Th2 splen

25 ins by Helicobacter pylori may contribute to gastric inflammation and epithelial damage.

26 se chain reaction and colony hybridization), gastric inflammation and epithelial injury (assessed his

27 n of inflammatory cytokines promoted chronic gastric inflammation and expansion and transformation of

28 .01), whereas IFN-gamma-/- mice exhibited no gastric inflammation and higher levels of IL-4 productio

29 e histopathology of HP group showed moderate gastric inflammation and many HP colonization.

30 pylori infection elevates IFN-gamma-mediated gastric inflammation and may suppress IFN-gamma signalin

31 ng within the stomach to prevent spontaneous gastric inflammation and metaplasia, and suggest that gl

32 eroid hormones that are required to suppress gastric inflammation and metaplasia.

33 critical role for sex hormones in regulating gastric inflammation and metaplasia.

34 NLRC5 is a negative regulator of gastric inflammation and mucosal lymphoid formation in r

35 l mucous gland cells to protect animals from gastric inflammation and resulting hyperplasia.

36 nalectomized female mice develop spontaneous gastric inflammation and spasmolytic polypeptide-express

37 Treatment of female mice with DHT prevented gastric inflammation and SPEM development when administe

38 effects and triggered spontaneous pathogenic gastric inflammation and SPEM.

39 The intensity of gastric inflammation and the extent of Helicobacter colo

40 serum pepsinogens levels (PGs) as markers of gastric inflammation and the immune response to single-d

41 n was fully recapitulated in mouse models of gastric inflammation and tumorigenesis.

42 h factors influence mucosal IL-1beta levels, gastric inflammation, and atrophy, multiple regression a

43 e were evaluated for cellular proliferation, gastric inflammation, and cytokine and Ab production at

44 iated with bacterial virulence determinants, gastric inflammation, and duodenal ulceration, suggestin

45 itis, as indicated by anti-parietal cell Ab, gastric inflammation, and the presence of cells capable

46 licobacter pylori infection not only induces gastric inflammation but also increases the risk of gast

47 Helicobacter pylori infection induces gastric inflammation but the host fails to generate prot

48 oidal anti-inflammatory drug (NSAID) induces gastric inflammation, causing degradation of the extrace

49 GAS mice exhibited a significant increase in gastric inflammation compared with either uninfected or

50 L/6 mice exhibited a significant increase in gastric inflammation compared with uninfected or infecte

51 sa were well correlated with the severity of gastric inflammation, confirming that H. pylori-induced

52 Infected C57BL/6J SCID mice did not develop gastric inflammation despite colonization by many bacter

53 gastrin release could be related to chronic gastric inflammation, elevated luminal ammonia level, or

54 a significant reduction in morphine-induced gastric inflammation, gastric delaying, and improved mor

55 Helicobacter pylori causes gastric inflammation, gland hyperplasia and is linked to

56 e protein oipA to promote IL-8 secretion and gastric inflammation have also been explored.

57 , those fed a high-salt diet had more severe gastric inflammation, higher gastric pH, increased parie

58 The mice were scored for severity of gastric inflammation, hyperplasia, glandular atrophy, an

59 roliferation correlated with the severity of gastric inflammation in both immunized/challenged (prote

60 1 cytokine IFN-gamma in H. pylori-associated gastric inflammation in C57BL/6J mice.

61 gamma resulted in a significant reduction of gastric inflammation in H. felis-infected, as well as im

62 ked whether Muc1 might also counter-regulate gastric inflammation in response to H. pylori infection.

63 lori in piglets but does induce neutrophilic gastric inflammation in some infected piglets.

64 at 18 weeks postinoculation revealed minimal gastric inflammation in the animals that received the mu

65 ase reactions can occur during IgE-dependent gastric inflammation in the mouse and that the infiltrat

66 eutrophils during immunoglobulin E-dependent gastric inflammation in the mouse.

67 as well as TH1 or TH2 cell lines exacerbated gastric inflammation in the recipients.

68 of IL-8 in vitro and significantly decreased gastric inflammation in vivo.

69 The gastric inflammation in wt and IL-10(-/-) mice contained

70 gated the role of IL-17 signaling in chronic gastric inflammation induced by Helicobacter pylori, a G

71 Immunoglobulin E-dependent gastric inflammation is characterized by neutrophil infi

72 of epithelial injury, and we have shown that gastric inflammation is increased in H. pylori-infected

73 diated injury, our experiments now show that gastric inflammation is increased within the context of

74 H. pylori infection and gastric inflammation may enhance humoral immunity to ora

75 D/+);gp130(F/F) mice promoted more extensive gastric inflammation, metaplastic transformation, and tu

76 onization density was higher and mononuclear gastric inflammation more severe in infected IL-17RA(-/-

77 ld-type mice did not affect the intensity of gastric inflammation or the extent of Helicobacter colon

78 acterial colonization density, the degree of gastric inflammation, or the presence of lymphoid follic

79 y resulted in the rapid onset of spontaneous gastric inflammation, oxyntic atrophy, and spasmolytic p

80 ction which can result in various degrees of gastric inflammation, peptic ulcer disease, and a predis

81 d with these pathogenic bacteria can develop gastric inflammation, termed gastritis.

82 elicobacter pylori infection induces chronic gastric inflammation that can progress to cancer.

83 known to be responsible for inducing chronic gastric inflammation that progresses to atrophy, metapla

84 A8/S100A9 are critical in the progression of gastric inflammation to cancer.

85 nd interferon gamma signaling that sustained gastric inflammation to induce VGPC transformation and g

86 ing was shown to aggravate H. pylori-induced gastric inflammation via activation of the lymphotoxin b

87 IgE-dependent gastric inflammation was elicited in genetically mast ce

88 Gastric inflammation was induced by infection of mice wi

89 Gastric inflammation was mild or was absent for all cats

90 Severe gastric inflammation was only observed in d3Tx mice.

91 on, two rodent models of chronic lymphocytic gastric inflammation were examined.

92 rences in bacterial colonization density and gastric inflammation were not apparent at 1 mo postinfec

93 Two rat models of mild gastric inflammation were studied.

94 Colonization induces chronic gastric inflammation which can progress to a variety of

95 gree of association of chronic intestinal or gastric inflammation with the development of cancer, has

96 ck a gastric microbiota, C. albicans induced gastric inflammation within 1 week of inoculation.