ライフサイエンスコーパス: pustule

1 at involve the appearance of neutrophil-rich pustules.

2 subcorneal, intraepidermal, and subepidermal pustules.

3 m blood of infected volunteers who developed pustules.

4 ocalized with IL-36gamma around neutrophilic pustules.

5 viduals fail to clear the infection and form pustules.

6 ulatory T (T(reg)) cells in the formation of pustules.

7 ents (63%), commonly in those with cutaneous pustules.

8 , based on whether they formed 0, 1, 2, or 3 pustules.

9 aris lesions such as comedones, papules, and pustules.

10 ining pustules and in the dermis of 10 of 16 pustules.

11 eous nodules, several of which had overlying pustules.

12 , and 2 of the 3 cases demonstrated multiple pustules/abscesses in the region of the lacrimal gland t

13 phonuclear leukocytes and macrophages in the pustule and at its base, but was not associated with T c

14 study, Haemophilus ducreyi was found in the pustule and dermis of samples obtained at the clinical e

15 , by 48 h, bacteria were readily seen in the pustule and dermis.

16 reyi was recovered from biopsies of 12 of 15 pustules and 1 of 7 papules, suggesting that H. ducreyi

17 ed a dramatic decrease in the development of pustules and a partial decrease in acanthosis.

18 ed a significantly higher number of lesions, pustules and erupted pustules than leaves of non-transge

19 hilic infiltrates of all positively staining pustules and in the dermis of 10 of 16 pustules.

20 d perilesional epithelium - in particular in pustules - and a less marked upregulation of defensin-1

21 lved, 69% (95% CI, 47.1%-86.6%) evolved into pustules, and 4% remained at the papular stage.

22 culated with the mutant produced papules and pustules at rates similar to the rates observed at sites

23 eriments, the neuA mutant formed papules and pustules at rates that were no different than those of i

24 We identified H. ducreyi in 16 of 18 pustules but did not detect bacteria in the one papule e

25 FOXP3(+) T cells were found throughout pustules but were most abundant at their base.

26 disease entity manifested with blisters and pustules clinically and lower epidermal blister, acantho

27 In addition to the formation of pustules, common adverse events included the formation o

28 less than its parent and was unable to form pustules compared to the parent.

29 Papules and pustules contained a predominant T cell infiltrate that

30 Both papules and pustules contained mixed or T helper 1 type cytokine mRN

31 n papule counts (-4.2 vs -2.2; P =.08), mean pustule counts (0 vs -1.0; P =.12), or mean comedone cou

32 nd closed comedones to inflammatory papules, pustules, cysts, and nodules, and scarring may result.

33 th similar doses of 35000HP and 35000HPwecA, pustules developed at 46.7% (95% confidence interval [CI

34 Pustules developed at 7 of 10 sites inoculated with 3500

35 ived similar doses of the parent and mutant, pustules developed at 7 of 15 sites (46.7%; 95% confiden

36 Pustules developed at a similar rate at sites inoculated

37 Subjects with pustules developed local symptoms that required withdraw

38 eveloped in immune-competent animals in that pustules did not form and surface epithelia remained int

39 g-phase bacteria), H. ducreyi harvested from pustules differentially expressed approximately 93 genes

40 Characterized by sterile pustules, erosions, and crusts, EPD is difficult to trea

41 or genes, pthA*, pthB, and pthC, also direct pustule formation and expression of CsLOB1.

42 ion, but not the CsSWEET1 promoter, promoted pustule formation and higher bacterial leaf populations.

43 (TAL) effector genes for the characteristic pustule formation at the site of infection.

44 that of hemolysin, nor both are required for pustule formation by H. ducreyi in humans.

45 ptose trisaccharide core is not required for pustule formation by H. ducreyi in humans.

46 globoside nor sialylated LOS is required for pustule formation by H. ducreyi in humans.

47 that expression of MOMP is not required for pustule formation by H. ducreyi in the human model of in

48 the csrA mutant was partially attenuated for pustule formation compared to its parent.

49 showed it was also partially attenuated for pustule formation in human volunteers.

50 e double mutant was partially attenuated for pustule formation in human volunteers.

51 Compared to 35000HP, FX517 does not cause pustule formation in human volunteers.

52 creyi to initiate disease and to progress to pustule formation in humans.

53 expressed in vivo, FtpA is not required for pustule formation in the human challenge model.

54 The outcome (either pustule formation or resolution) of infected sites for a

55 caused papules to form at similar rates, the pustule formation rate at sites inoculated with 35000HPs

56 The pustule formation rate in 5 volunteers was 33% (95% conf

57 The pustule formation rate was 55.6% (95% confidence interva

58 The pustule formation rate was 58% (95% confidence interval

59 The pustule formation rate was 72% (95% confidence interval

60 Overall, the papule and pustule formation rates for 35000HP and FX533 were simil

61 For EDDs of >/=25 CFU, the pustule formation rates were 30% for both 35000HP and 35

62 The pustule formation rates were 40% (95% confidence interva

63 The pustule formation rates were 44% (95% CI, 5.8 to 77.6%)

64 The pustule formation rates were 75% (95% confidence interva

65 ted delivered doses (EDDs) of >/=25 CFU, the pustule formation rates were 80% for 35000HP and 58% for

66 The pustule formation rates were similar at both parent and

67 The pustule formation rates were similar for the parent and

68 The papule and pustule formation rates were similar to those observed i

69 st effects on the possible clinical outcomes-pustule formation versus spontaneous resolution of infec

70 ependent; the most important determinants of pustule formation were sex and host effects.

71 test whether sialylated LOS was required for pustule formation, a second trial comparing an isogenic

72 ragloboside-like structures was required for pustule formation, an isogenic mutant (35000HP-RSM2) was

73 To test whether CDT was required for pustule formation, six human subjects were inoculated wi

74 ous resolution of infection or progresses to pustule formation, which is associated with the failure

75 dicate the hemolysin does not play a role in pustule formation.

76 35000HP-sodC-cat and observed for papule and pustule formation.

77 35000 and FX517 and observed for papule and pustule formation.

78 r gene products did not play a major role in pustule formation.

79 ng association of the TLR9 TA haplotype with pustule formation; logistic regression showed a trend to

80 The pustule-formation rate in 5 volunteers was 93.3% (95% co

81 The pustule-formation rate was 55% (95% confidence interval

82 The overall pustule-formation rate was 61.1% at parent sites and 22.

83 inoculated with the mutant and parent, while pustules formed at 36.4% of parent sites and at 0% of mu

84 Pustules formed at five of nine parent sites and one of

85 In a reinfection trial, 2 of 11 previous pustule formers and 6 of 10 previous resolvers resolved

86 ired in its ability to form both papules and pustules in humans.

87 ibutes to the ability of H. ducreyi to cause pustules in humans.

88 nts of 35000HP and FX527 were recovered from pustules in semiquantitative culture.

89 95% CI, 36.8%-90.9%) of papules evolved into pustules in the reinfection group, compared with 41% (95

90 Pustules in various sizes could be found in 18 patients

91 stopathology of biopsy samples obtained from pustules inoculated with 35000HP or 35000HP-SMS1 were si

92 racterized by the presence of intraepidermal pustules, keratinocyte cytopathology, and epidermal and

93 acteria present in a mutant inoculation site pustule lacked a PAL-specific epitope.

94 nts, 14 with purpuric drug eruptions without pustules (mean [SD] age, 60 [11] years; 12 female and 2

95 le) and 18 with purpuric drug eruptions with pustules (mean [SD] age, 64 [11] years; 12 female and 6

96 erized by the formation of sterile cutaneous pustules, neutrophilia, fever and features of systemic i

97 ps contains intracorneal and intraepithelial pustules, nucleated corneocytes, and dilated superficial

98 surface markers in skin biopsy specimens of pustules obtained from experimentally infected volunteer

99 In pustules obtained from infected human volunteers, there

100 Biopsies of pustules obtained from volunteers infected with H. ducre

101 Pustules only developed at mutant-injected sites at dose

102 th H. ducreyi until they developed a painful pustule or for 14 days.

103 skin of a predisposed patient may elicit the pustules or ulcerations associated with pathergy.

104 developed papular lesions that evolved into pustules resembling natural disease.

105 ubsequently, there were numerous papules and pustules--similar to the rash seen in patients receiving

106 tes, defined by the presence of a vesicle or pustule ("take") at the inoculation site 6-11 days after

107 gher number of lesions, pustules and erupted pustules than leaves of non-transgenic plants containing

108 In pustules, there was a significant enrichment of CD4(+)FO

109 35000HPwecA caused pustules to form at 3 sites inoculated with a dose 2.5-f

110 enged twice, some subjects form at least one pustule twice (PP group), while others have all inoculat

111 Grouped pustules were present under the right breast.

112 He noticed a small pustule with surrounding erythema developing on the skin

113 n isogenic hemolysin-deficient mutant caused pustules with a rate similar to that of its parent.