ライフサイエンスコーパス: ulcerans

1 litating disease, is caused by Mycobacterium ulcerans.

2 disease caused by the pathogen Mycobacterium ulcerans.

3 a C. diphtheriae infection and one due to C. ulcerans.

4 ess and did not confer protection against M. ulcerans.

5 fections caused by toxigenic Corynebacterium ulcerans.

6 rme, Fusobacterium russii, and Fusobacterium ulcerans.

7 lecule appears so far to be restricted to M. ulcerans.

8 ized a macrolide toxin, mycolactone, from M. ulcerans.

9 had 87.7% sequence homology to Mycobacterium ulcerans, 87.6% homology to Mycobacterium tuberculosis,

10 detailed field data in space and time on M. ulcerans and Buruli ulcer available today, we assess the

11 In contrast to M. ulcerans and conventional M. marinum, mycolactone F-prod

12 We summarise the current understanding of M ulcerans and its relations with human beings.

13 in some mycobacteria, such as Mycobacterium ulcerans and Mycobacterium kansasii.

14 Mycobacterium ulcerans and Mycobacterium marinum are closely related p

15 acterium liflandii, is closely related to M. ulcerans and Mycobacterium marinum, and as further evide

16 ynebacterium diphtheriae and Corynebacterium ulcerans and show that the C. ulcerans hmuO mutation res

17 de in understanding the immune response to M ulcerans and there have been major advances in managemen

18 Additionally, strains of beta-susceptible C. ulcerans, and C. glutamicum, a species non-permissive fo

19 ynebacterium diphtheriae and Corynebacterium ulcerans cause invasive disease in humans and animals.

20 Mycobacterium ulcerans causes Buruli ulcer disease (BUD), an ulcerativ

21 M. ulcerans causes Buruli ulcer, a severe human skin lesion

22 One member of the genus, M. ulcerans, causes a necrotizing skin disease called Burul

23 d histopathology in making a diagnosis of M. ulcerans disease in a field setting.

24 Punch biopsy specimens from Mycobacterium ulcerans disease lesions were used to compare the sensit

25 For 70 clinically diagnosed cases of M. ulcerans disease, the modified PCR was 98% sensitive and

26 ive, simple, cheap and safe treatment for M. ulcerans disease.

27 terval, 68 to 82%) showed the presence of M. ulcerans DNA by PCR.

28 ture-positive samples were able to detect M. ulcerans DNA in all 21 culture-confirmed patients.

29 evaluated the IS2404-based PCR to detect M. ulcerans DNA in tissue specimens from 143 BUD patients d

30 s of both Corynebacterium diphtheriae and C. ulcerans fail to use heme as an iron source.

31 The M. ulcerans genome strain has a deletion in RD1 and lacks t

32 In many European countries, C ulcerans has become the organism commonly associated wit

33 As C. ulcerans has never previously been isolated from cats, t

34 The genome sequence of M ulcerans has now been published and it transpires that t

35 nd hmuD genes complemented a Corynebacterium ulcerans heme oxygenase mutant in trans for utilization

36 utilization deficiency of a Corynebacterium ulcerans heme oxygenase mutant, demonstrating in vivo ac

37 orynebacterium ulcerans and show that the C. ulcerans hmuO mutation results in a significant reductio

38 We also show that expression from the C. ulcerans hmuO promoter exhibits minimal regulation by ir

39 teomyelitis in boys; systematic search for M ulcerans in osteomyelitis cases of non-specific aspect i

40 mRNA expression in biopsies of Mycobacterium ulcerans-infected human tissue was investigated using re

41 ar necrosis and apoptosis upon Mycobacterium ulcerans infection and treatment with mycobacterial exud

42 Together, these data demonstrate that M. ulcerans infection causes systemic perturbations in the

43 rial species isolated from areas in which M. ulcerans infection is endemic.

44 This in vivo model of M. ulcerans infection now paves the way for new avenues of

45 the treatment of Buruli ulcer (Mycobacterium ulcerans infection), the evolution of lesions of patient

46 r understanding of the pathophysiology of M. ulcerans infection, and the development of new therapeut

47 s all other mouse strains with respect to M. ulcerans infection, presented a spontaneous healing afte

48 stating skin disease caused by Mycobacterium ulcerans infection, yet it is one of the most neglected

49 nce of innate immune responses to control M. ulcerans infection.

50 acle to understand the pathophysiology of M. ulcerans infection.

51 However, M. ulcerans infections are not limited to skin, and osteomy

52 adiological features in all patients with M. ulcerans infections with bone involvement, identified fr

53 nts with polymerase chain reaction-proved M. ulcerans infections.

54 Mycobacterium ulcerans is an environmental organism which is responsib

55 immunosuppressive activity of Mycobacterium ulcerans is attributed to mycolactone, a macrolide toxin

56 At the molecular level, M. ulcerans is distinguished from M. marinum by the presenc

57 Mycobacterium ulcerans is known to cause Buruli ulcer (BU), a necrotiz

58 suggest that the human immune response to M. ulcerans is similar to that seen with some other mycobac

59 Mycobacterium ulcerans is the causative agent of Buruli ulcer, a sever

60 Mycobacterium ulcerans is the causative agent of Buruli ulcer, a tropi

61 The causative organism, Mycobacterium ulcerans, is sensitive to temperatures above 37 degrees

62 human clinical isolates, suggesting that C. ulcerans isolated from cats could be a potential reservo

63 soils were Mycobacterium tuberculosis and M. ulcerans, M. tuberculosis (macrolide-lincosamide-strepto

64 r data suggest that additional factors in M. ulcerans may be involved in Buruli ulcer pathogenesis.

65 rge environmental data sets on Mycobacterium ulcerans (MU), an environmentally persistent microorgani

66 asmid library complemented several of the C. ulcerans mutants and three of the C. diphtheriae mutants

67 C. diphtheriae and C. ulcerans mutants defective in haemin iron utilization we

68 The relationship between M. ulcerans, mycolactone, and Ae. aegypti further suggests

69 of mycolactone F is identical to that of M. ulcerans mycolactones, but a unique side chain structure

70 on cultured cells but is less potent than M. ulcerans mycolactones.

71 logical diagnosis, a positive culture for M. ulcerans, or a smear positive for acid-fast bacilli (AFB

72 difficulties associated with diagnosis of M. ulcerans osteomyelitis, with one-fourth of patients havi

73 M. ulcerans produces the polyketide-derived macrolide mycol

74 Infection with M. ulcerans results in persistent severe necrosis without a

75 e report that some toxigenic Corynebacterium ulcerans strains show atypical results in a real-time PC

76 the relationship between M. liflandii and M. ulcerans, strains were analyzed for the presence of the

77 utants of C. diphtheriae and Corynebacterium ulcerans that are defective in acquiring iron from heme

78 Infection of human skin with Mycobacterium ulcerans, the causative agent of Buruli ulcer, is associ

79 Mycobacterium ulcerans, the causative agent of Buruli ulcer, produces

80 ex macrolide toxin produced by Mycobacterium ulcerans, the causative agent of skin lesions called Bur

81 Mycobacterium ulcerans, the causative agent of the neglected tropical

82 lactone congeners from the human pathogen M. ulcerans, the frog pathogen Mycobacterium liflandii, and

83 but the specific route of transmission of M. ulcerans to humans remains unclear.

84 r, resulted in greatly reduced ability of C. ulcerans to use hemin or hemoglobin as an iron source.

85 The M. ulcerans toxin does not cause cell death but instead arr

86 ynebacterium diphtheriae and Corynebacterium ulcerans use haemin and haemoglobin as essential sources

87 M. ulcerans was s.c. inoculated in three consanguine mouse

88 Buruli ulcer, caused by Mycobacterium ulcerans, was identified as a neglected emerging infecti

89 released by the human pathogen Mycobacterium ulcerans, was previously shown to impair Sec61-dependent

90 veral primer sequences, the MLST genes in C. ulcerans were also amplified, thereby providing the basi

91 hemin iron utilization from Corynebacterium ulcerans were cloned and characterized.

92 a; 12 (60.0%) were caused by Corynebacterium ulcerans, where animal contact was the predominant risk

93 of a toxin in the culture supernatant of M. ulcerans which causes a cytopathic effect on the mouse f

94 pid toxin from the culture supernatant of M. ulcerans which is capable of causing the cytopathic effe

95 secreted by the human pathogen Mycobacterium ulcerans, which induces the formation of open skin lesio

96 sease caused by infection with Mycobacterium ulcerans, which produces a potent toxin known as mycolac

97 phtheria caused by toxigenic Corynebacterium ulcerans who developed a right hand flexor sheath infect