ライフサイエンスコーパス: giardiasis

1 rate of quinacrine in those with persistent giardiasis.

2 tribute to diarrheal disease associated with giardiasis.

3 ns with giardiasis and 19663 persons without giardiasis.

4 nts pathological CD8(+) T cell activation in giardiasis.

5 moebiasis equals or exceeds the incidence of giardiasis.

6 s and immune responses in the mouse model of giardiasis.

7 affected disaccharidase levels during murine giardiasis.

8 ith perceived food intolerance 3 years after giardiasis.

9 ates, and their efficacy in a mouse model of giardiasis.

10 ineffectiveness in drug resistance cases of giardiasis.

11 atic; all 3 were subsequently diagnosed with giardiasis.

12 n a fast food restaurant, was diagnosed with giardiasis.

13 the absence of fever and was diagnosed with giardiasis.

14 all, 1262 patients had laboratory confirmed giardiasis.

15 ding of the clinical variation seen in human giardiasis.

16 targets for developing new therapies against giardiasis.

17 ta-giardins, that are also detected in human giardiasis.

18 reatment of cryptosporidiosis and refractory giardiasis.

19 proach to the epidemiologic investigation of giardiasis.

20 tigue has previously been reported following giardiasis after a large waterborne outbreak in Bergen,

21 dence regarding the management of refractory giardiasis after treatment with nitroimidazoles.

22 d natural course of fatigue five years after giardiasis among patients who reported chronic fatigue t

23 he matched cohort included 3935 persons with giardiasis and 19663 persons without giardiasis.

24 Cryptosporidiosis, giardiasis and microsporidiosis are serious human diseas

25 ghlight recent work focused on the impact of giardiasis and the mechanisms that contribute to the var

26 Dengue, giardiasis, and insect bites had high proportionate morb

27 oridiosis and the diagnosis of amebiasis and giardiasis, and some new leads on the treatment of crypt

28 Cryptosporidiosis and giardiasis are major public health concerns.

29 eton is a promising drug target for treating giardiasis, as we predict drugs that interfere with the

30 In refractory giardiasis, assemblage A and B were found responsible in

31 Almost 20% of patients presented persistent giardiasis, belonging to both assemblages A and B, after

32 icrobiota may explain observed variations in giardiasis between hosts with respect to host pathology,

33 Giardiasis care infrequently follows all aspects of clin

34 vage pathway, is a potential target for anti-giardiasis chemotherapy.

35 Giardiasis could be an ecological disease, and the obser

36 We examined the relationship between giardiasis diagnosis and irritable bowel syndrome (IBS)

37 Persons with at least 1 giardiasis diagnosis were individually matched on age gr

38 ment length in months to 5 persons without a giardiasis diagnosis.

39 We investigated sequences of giardiasis diagnostic and treatment events using MarketS

40 ng all patients who had laboratory confirmed giardiasis during the Bergen outbreak (n=1252) were invi

41 After giardiasis enteritis at least 5% developed clinical char

42 ducation after a large community outbreak of giardiasis enteritis in the city of Bergen, Norway were

43 study estimates the proportion of persistent giardiasis in 3 hospitals in Barcelona, describes associ

44 nflicting results, placing endemic pediatric giardiasis in a state of equipoise.

45 udinal cohort of 2995 persons diagnosed with giardiasis (International Classification of Diseases, Ni

46 incidence of IBS was higher in persons with giardiasis (IR = 37.7/1000 person-years vs 4.4/1000 pers

47 Giardia lamblia, the causative agent of giardiasis, lacks de novo purine biosynthesis and relies

48 malnutrition to demonstrate that persistent giardiasis leads to epithelial cell apoptosis and crypt

49 and were more effective than Mz in a murine giardiasis model.

50 an effectiveness rate of 100% in refractory giardiasis (n = 13; 95% confidence interval = 75-100).

51 inal complaints has been reported after some giardiasis outbreaks.

52 .007) and anorexia (P = .02), with previous giardiasis (P = .03), and with previous antibiotic (P =

53 uture research on risk factors for IBS among giardiasis patients and the pathophysiology of postinfec

54 e mechanisms of pathogenesis associated with giardiasis remain unclear, as the parasite neither produ

55 blia, the protozoan parasite responsible for giardiasis, requires purine salvage from its host for RN

56 protozoa (amebiasis, cryptosporidiosis, and giardiasis), rotavirus, astrovirus, and enterotoxigenic

57 ng 724 individuals with laboratory confirmed giardiasis six years earlier, and 847 controls matched b

58 Here we show in murine models of giardiasis that small-intestinal hypermotility occurs in

59 Giardiasis, the most common enteric parasitic infection

60 lude that CD8(+) T cells become activated in giardiasis through an antibiotic-sensitive process and c

61 ational study was conducted in patients with giardiasis treated with nitroimidazoles.

62 Refractory giardiasis was associated with malaise (P = .007) and an

63 in the period from three to five years after giardiasis was found.

64 Concomitant giardiasis was neither a risk factor nor protective.

65 Using a mouse model of giardiasis, we examined the role of host immunity and pa

66 lates from a previously reported epidemic of giardiasis were accurately classified by this technique,

67 nfectious fatigue after laboratory confirmed giardiasis were diagnosed with CFS.

68 surance database, individuals diagnosed with giardiasis were more likely to have a subsequent IBS dia

69 Those with persistent giardiasis were provided quinacrine.

70 e (30.8%) in the exposed group 6 years after giardiasis were significantly elevated compared with con

71 12 with symptoms consistent with intestinal giardiasis) were determined to be positive for G. lambli

72 The patient was diagnosed with giardiasis, which led to examination of her mother, fath

73 eople are estimated to have acute or chronic giardiasis, with infection rates approaching 90% in area