ライフサイエンスコーパス: pustule

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

2 es for ascorbic acid uptake, is increased in pustules.

3 eous nodules, several of which had overlying pustules.

4 nd 10 had palmoplantar plaque psoriasis with pustules.

5 berries and, 18 directly from colonized rust pustules.

6 lly in these diseases to induce palmoplantar pustules.

7 racterized by eruptions of neutrophil-filled pustules.

8 subcorneal, intraepidermal, and subepidermal pustules.

9 m blood of infected volunteers who developed pustules.

10 viduals fail to clear the infection and form pustules.

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

12 at involve the appearance of neutrophil-rich pustules.

13 ocalized with IL-36gamma around neutrophilic pustules.

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

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

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

17 ients) or palmoplantar plaque psoriasis with pustules (10 patients) treated at 1 of 7 tertiary dermat

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

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

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

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

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

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

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

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

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

27 Stability was achieved for papule, pustule, and abscess.

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

29 rash, with papules that evolve to vesicles, pustules, and crusts in the genital, anal, or oral regio

30 ting PPP, palmoplantar plaque psoriasis with pustules, and SAPHO syndrome.

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

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

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

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

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

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

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

38 Papules and pustules contained a predominant T cell infiltrate that

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

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

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

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

43 Pustules developed at 7 of 10 sites inoculated with 3500

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

45 Pustules developed at a similar rate at sites inoculated

46 Subjects with pustules developed local symptoms that required withdraw

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

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

49 sion, skin trauma, thoracic edema, malignant pustule edema, lymphadenopathy, and evidence of coagulop

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

67 e >=2-fold higher than those of 35000HP, the pustule formation rate was 25% for 35000HP versus 11.7%

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

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

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

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

72 ion mutant at multiple sites; the papule and pustule formation rates of the mutant and parent strains

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

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

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

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

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

78 The pustule formation rates were similar at both parent and

79 The pustule formation rates were similar for the parent and

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

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

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

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

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

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

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

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

88 35000HP-sodC-cat and observed for papule and pustule formation.

89 35000 and FX517 and observed for papule and pustule formation.

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

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

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

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

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

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

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

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

98 Skin histology of papules and pustules from 5 men having sex with men with mpox infect

99 /tenderness in 118 of 481 (25%), and papules/pustules in 117 of 481 (24%).

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

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

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

103 95% CI, 36.8%-90.9%) of papules evolved into pustules in the reinfection group, compared with 41% (95

104 Pustules in various sizes could be found in 18 patients

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

106 erythema and macroscopically visible sterile pustules." It can occur with or without systemic symptom

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

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

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

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

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

112 Eight HS primary lesions, including papule, pustule, nodule, plaque, ulcer, abscess, comedo, and tun

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

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

115 In pustules obtained from infected human volunteers, there

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

117 h wounded skin, ascorbic acid is enriched in pustules of humans experimentally infected with Haemophi

118 terion was, "Macroscopically visible sterile pustules on erythematous base and not restricted to the

119 sing eruptions of neutrophil-filled, sterile pustules on the palms and soles that can be clinically d

120 d by eruptions of painful, neutrophil-filled pustules on the palms and soles.

121 Pustules only developed at mutant-injected sites at dose

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

123 ay manifest as an acute form with widespread pustules or a subacute variant with an annular phenotype

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

125 ined stages (macules, papules, vesicles, and pustules) over 2 to 4 weeks.

126 (PPP) and palmoplantar plaque psoriasis with pustules remain challenging to treat.

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

128 addition, the formation of intra-epithelial pustules resulting in ulceration and hypodermal necrosis

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

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

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

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

133 35000HPwecA caused pustules to form at 3 sites inoculated with a dose 2.5-f

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

135 Grouped pustules were present under the right breast.

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

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