ライフサイエンスコーパス: Helicobacter infection

1 ession were increased in MNU-treated mice by Helicobacter infection.

2 and accelerated development of dysplasia by Helicobacter infection.

3 development and progression to cancer during Helicobacter infection.

4 ynthase (iNOS) is upregulated in response to Helicobacter infection.

5 de (AlOH) was evaluated in a murine model of Helicobacter infection.

6 in orchestrating diverse growth responses to Helicobacter infection.

7 sed in vitro and in vivo as a consequence of Helicobacter infection.

8 influence the gastric epithelial response to Helicobacter infection.

9 esponse in disease outcome following gastric Helicobacter infection.

10 duced by interleukin-1beta (IL-1beta) and/or Helicobacter infection.

11 r development of drugs to specifically treat Helicobacter infections.

12 ocolitis similar to that observed with other helicobacter infections.

13 role in determining the clinical outcome of Helicobacter infections.

14 el to evaluate the role of host responses in Helicobacter infections.

15 Eradication of Helicobacter infection after 2 or 6 months of infection

16 tology, culture, and PCR for the presence of Helicobacter infection and by histology for the presence

17 hypergastrinemia in mice can synergize with Helicobacter infection and contribute to eventual pariet

18 and systemic antibody responses generated by Helicobacter infection and immunization.

19 igating the connection between acid balance, Helicobacter infection and mucin disruption in the progr

20 ies have demonstrated an association between Helicobacter infection and several risk factors for card

21 There was no association between Helicobacter infection and the presence or severity of g

22 rains in vivo should be useful in studies of Helicobacter infection and virulence mechanisms and stud

23 These data demonstrate that Helicobacter infection and/or immunization stimulate a p

24 e dual actions of sulforaphane in inhibiting Helicobacter infections and blocking gastric tumor forma

25 rom uninfected mice and mice with documented Helicobacter infections and by testing DNA from other ba

26 esis of chronic inflammation associated with Helicobacter infection, and how chronic inflammation con

27 ch the immune response can eradicate gastric Helicobacter infection are unknown.

28 Helicobacter infections are present in approximately 50%

29 e spontaneous and vaccine-induced control of Helicobacter infection, as well as the development of ga

30 tly in association with acid suppression and Helicobacter infection, but its role in the progression

31 an section-rederived IL-10(-/-) mice without helicobacter infection did not have histological evidenc

32 outlines the histologic progression of human Helicobacter infection from the early stages of inflamma

33 upregulated in the gastric mucosa by chronic Helicobacter infection; however, whether it plays a posi

34 on may help reducing tissue damage caused by Helicobacter infection in both humans and pigs, highligh

35 Gastric Helicobacter infection in healthy pet cats is not well c

36 prevent or cure an otherwise chronic gastric Helicobacter infection in several different animal model

37 These findings question a direct role for Helicobacter infection in the pathogenesis of gastritis

38 lutely required for the efficient control of Helicobacter infection in vaccinated mice.

39 A fecal PCR assay for detection of Helicobacter infections in laboratory rodents was develo

40 IL-1beta produced during Helicobacter infection inhibited gastric acid, intracell

41 oric stenosis have underlying ulcer disease, helicobacter infection is a relatively common finding.

42 Helicobacter infection is associated with gastric cell g

43 Helicobacter infection is characterized by induction of

44 Helicobacter infection is the leading cause of gastric c

45 Helicobacter infection is the primary risk factor for ga

46 In both human subjects and rodent models, Helicobacter infection leads to a decrease in Shh expres

47 ly (P <0.05) by LD but not slowed further by helicobacter infection (males, 9.4+/-0.5 (uninfected), 9

48 of the tumor can be reproduced by prolonged Helicobacter infection of BALB/c mice.

49 Helicobacter infection of wild-type mice elicited a mild

50 H1 and TH2 cell-mediated immune responses in Helicobacter infection: one associated with the pathogen

51 When we induce PC atrophy by Helicobacter infection or tamoxifen treatment, this CD44

52 in a down-regulated Th1 response to gastric helicobacter infection, possibly because of T-cell senes

53 Helicobacter infection reduced gastric acidity and inhib

54 hils in the local immune response to gastric Helicobacter infection remains unknown.

55 that the combination of hypergastrinemia and Helicobacter infection resulted in accelerated gastric c

56 issues from Smad3/Rag2-DKO mice 1 week after Helicobacter infection revealed an influx of macrophages

57 may vary in mouse models of unknown enteric helicobacter infection status and, importantly, variable

58 ere was a highly significant main effect for Helicobacter infection status for all fundic and antral

59 ole of IL-10 in the host response to gastric Helicobacter infection, stomachs of IL-10(-/-) and wild-

60 atory, and gastric hyperplastic responses to Helicobacter infection, suggesting the possibility of a

61 ew provides an update on the pathogenesis of Helicobacter infection, the malignancies associated with

62 present study was to use an animal model of Helicobacter infection to test, under controlled conditi

63 importance of humoral immunity in containing Helicobacter infections to the mucosal surface is illust

64 Helicobacter infection up-regulated gastric cell Fas ant

65 e aim of this study was to determine whether Helicobacter infection was associated with cholecystitis

66 on status, whereas lesions characteristic of helicobacter infection were present in ferrets infected

67 animal models to support the association of Helicobacter infection with gastric cancer.