戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (１語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 ized a macrolide toxin, mycolactone, from M. ulcerans.
2 on of subcutaneous tissue with Mycobacterium ulcerans.
3  Mycobacterium tuberculosis or Mycobacterium ulcerans.
4 ess and did not confer protection against M. ulcerans.
5 litating disease, is caused by Mycobacterium ulcerans.
6 disease caused by the pathogen Mycobacterium ulcerans.
7 a C. diphtheriae infection and one due to C. ulcerans.
8 fections caused by toxigenic Corynebacterium ulcerans.
9 rme, Fusobacterium russii, and Fusobacterium ulcerans.
10 lecule appears so far to be restricted to M. ulcerans.
11 had 87.7% sequence homology to Mycobacterium ulcerans, 87.6% homology to Mycobacterium tuberculosis,
12 rom diphtheria, is caused by Corynebacterium ulcerans, a zoonotic bacterium that can also produce dip
13 inguishable from diphtheria, is caused by C. ulcerans, a zoonotic bacterium that can also produce dip
14 evealed a significant association between M. ulcerans and Aedes notoscriptus.
15                  Mycolactone is unique to M. ulcerans and an immunological Ag capture assay would rep
16  detailed field data in space and time on M. ulcerans and Buruli ulcer available today, we assess the
17 htheriae from the closely related species C. ulcerans and C. pseudotuberculosis Analytical sensitivit
18 iae strains and occasionally by toxigenic C. ulcerans and C. pseudotuberculosis strains.
19                            In contrast to M. ulcerans and conventional M. marinum, mycolactone F-prod
20 onship between possum excreta shedding of M. ulcerans and humans developing BU.
21  We summarise the current understanding of M ulcerans and its relations with human beings.
22  in some mycobacteria, such as Mycobacterium ulcerans and Mycobacterium kansasii.
23                                Mycobacterium ulcerans and Mycobacterium marinum are closely related p
24 acterium liflandii, is closely related to M. ulcerans and Mycobacterium marinum, and as further evide
25 ynebacterium diphtheriae and Corynebacterium ulcerans and show that the C. ulcerans hmuO mutation res
26 stralian native possums are reservoirs of M. ulcerans and that they shed the bacteria in their fecal
27 de in understanding the immune response to M ulcerans and there have been major advances in managemen
28 ossums are a local wildlife reservoir for M. ulcerans and, although mosquitoes have been implicated i
29 , C. striatum, C. tuberculostearicum, and C. ulcerans) and was detected in 50 of 157 (31.8%) isolates
30 Additionally, strains of beta-susceptible C. ulcerans, and C. glutamicum, a species non-permissive fo
31 rculosis, Mycobacterium bovis, Mycobacterium ulcerans, and Mycobacterium marinum.
32 caused by Corynebacterium diphtheriae and C. ulcerans, and use of diphtheria anti-toxin in the United
33                                Mycobacterium ulcerans cases from an observational cohort at Barwon He
34 ynebacterium diphtheriae and Corynebacterium ulcerans cause invasive disease in humans and animals.
35                                Mycobacterium ulcerans causes Buruli ulcer disease (BUD), an ulcerativ
36                                           M. ulcerans causes Buruli ulcer, a severe human skin lesion
37                                Mycobacterium ulcerans causes Buruli ulcer, the third most frequent my
38                  One member of the genus, M. ulcerans, causes a necrotizing skin disease called Burul
39 ngle-nucleotide-polymorphism profiles for M. ulcerans detected in mosquitoes, possum excreta and huma
40 n the occurrence of Buruli ulcer cases and M ulcerans detection from studies of any type for the evid
41 or records of Buruli ulcer and Mycobacterium ulcerans detection, with no limits on study type, public
42 ronic necrotizing pathology of Mycobacterium ulcerans disease (Buruli ulcer).
43 d histopathology in making a diagnosis of M. ulcerans disease in a field setting.
44    Punch biopsy specimens from Mycobacterium ulcerans disease lesions were used to compare the sensit
45      For 70 clinically diagnosed cases of M. ulcerans disease, the modified PCR was 98% sensitive and
46 ive, simple, cheap and safe treatment for M. ulcerans disease.
47 terval, 68 to 82%) showed the presence of M. ulcerans DNA by PCR.
48 ture-positive samples were able to detect M. ulcerans DNA in all 21 culture-confirmed patients.
49  evaluated the IS2404-based PCR to detect M. ulcerans DNA in tissue specimens from 143 BUD patients d
50 mmalian Sec61 inhibited by the Mycobacterium ulcerans exotoxin mycolactone via electron cryo-microsco
51 s of both Corynebacterium diphtheriae and C. ulcerans fail to use heme as an iron source.
52                                       The M. ulcerans genome strain has a deletion in RD1 and lacks t
53                In many European countries, C ulcerans has become the organism commonly associated wit
54                                        As C. ulcerans has never previously been isolated from cats, t
55                     The genome sequence of M ulcerans has now been published and it transpires that t
56 nd hmuD genes complemented a Corynebacterium ulcerans heme oxygenase mutant in trans for utilization
57  utilization deficiency of a Corynebacterium ulcerans heme oxygenase mutant, demonstrating in vivo ac
58 orynebacterium ulcerans and show that the C. ulcerans hmuO mutation results in a significant reductio
59     We also show that expression from the C. ulcerans hmuO promoter exhibits minimal regulation by ir
60 teomyelitis in boys; systematic search for M ulcerans in osteomyelitis cases of non-specific aspect i
61 dicate Ae. notoscriptus probably transmit M. ulcerans in southeastern Australia and highlight mosquit
62 mRNA expression in biopsies of Mycobacterium ulcerans-infected human tissue was investigated using re
63  drivers of tissue necrosis in Mycobacterium ulcerans infection (Buruli ulcer disease) have historica
64 ar necrosis and apoptosis upon Mycobacterium ulcerans infection and treatment with mycobacterial exud
65     Together, these data demonstrate that M. ulcerans infection causes systemic perturbations in the
66 n drug to rifampicin (RIF) for Mycobacterium ulcerans infection in the intervention arm of a WHO drug
67 t membranes were disrupted in vivo during M. ulcerans infection in the mouse model.
68 rial species isolated from areas in which M. ulcerans infection is endemic.
69                     This in vivo model of M. ulcerans infection now paves the way for new avenues of
70 ted tropical disease caused by Mycobacterium ulcerans infection that damages the skin and subcutis.
71 the treatment of Buruli ulcer (Mycobacterium ulcerans infection), the evolution of lesions of patient
72 r understanding of the pathophysiology of M. ulcerans infection, and the development of new therapeut
73 s all other mouse strains with respect to M. ulcerans infection, presented a spontaneous healing afte
74 stating skin disease caused by Mycobacterium ulcerans infection, yet it is one of the most neglected
75 nce of innate immune responses to control M. ulcerans infection.
76 acle to understand the pathophysiology of M. ulcerans infection.
77                                  However, M. ulcerans infections are not limited to skin, and osteomy
78 adiological features in all patients with M. ulcerans infections with bone involvement, identified fr
79 nts with polymerase chain reaction-proved M. ulcerans infections.
80 actone, a lipid-like exotoxin secreted by M. ulcerans, inhibits the Sec61 translocon, driving tissue
81                                Mycobacterium ulcerans is an environmental organism which is responsib
82                                           M. ulcerans is an opportunistic environmental pathogen; how
83  immunosuppressive activity of Mycobacterium ulcerans is attributed to mycolactone, a macrolide toxin
84                   At the molecular level, M. ulcerans is distinguished from M. marinum by the presenc
85                                Mycobacterium ulcerans is known to cause Buruli ulcer (BU), a necrotiz
86 suggest that the human immune response to M. ulcerans is similar to that seen with some other mycobac
87                                Mycobacterium ulcerans is the causative agent of Buruli ulcer, a sever
88                                Mycobacterium ulcerans is the causative agent of Buruli ulcer, a tropi
89 bcutaneous infection caused by Mycobacterium ulcerans, is increasing in prevalence in southeastern Au
90        The causative organism, Mycobacterium ulcerans, is sensitive to temperatures above 37 degrees
91 pressive macrolide produced by Mycobacterium ulcerans, is the central virulent factor in the skin dis
92  human clinical isolates, suggesting that C. ulcerans isolated from cats could be a potential reservo
93                        For selected small M. ulcerans lesions, 6 weeks may be as effective as 8 weeks
94 are highly effective in curing Mycobacterium ulcerans lesions, but are associated with significant to
95  combination antibiotic therapy for small M. ulcerans lesions.
96 soils were Mycobacterium tuberculosis and M. ulcerans, M. tuberculosis (macrolide-lincosamide-strepto
97 r data suggest that additional factors in M. ulcerans may be involved in Buruli ulcer pathogenesis.
98 rge environmental data sets on Mycobacterium ulcerans (MU), an environmentally persistent microorgani
99 asmid library complemented several of the C. ulcerans mutants and three of the C. diphtheriae mutants
100                        C. diphtheriae and C. ulcerans mutants defective in haemin iron utilization we
101                  The relationship between M. ulcerans, mycolactone, and Ae. aegypti further suggests
102 tion of responses such as effects between M. ulcerans, mycolactone, and S. aureus virulence that will
103  of mycolactone F is identical to that of M. ulcerans mycolactones, but a unique side chain structure
104 on cultured cells but is less potent than M. ulcerans mycolactones.
105 ed occasionally by toxigenic Corynebacterium ulcerans or, rarely, Corynebacterium pseudotuberculosis
106 logical diagnosis, a positive culture for M. ulcerans, or a smear positive for acid-fast bacilli (AFB
107 difficulties associated with diagnosis of M. ulcerans osteomyelitis, with one-fourth of patients havi
108 ys show that locales where possums harbor M. ulcerans overlap with human cases of BU, raising the pos
109                                           M. ulcerans pathogenesis may not only be an individual act
110 -random, co-correlated clustering of both M. ulcerans positive possum excreta and human BU cases.
111 tics revealed overlap between clusters of M. ulcerans-positive Ae. notoscriptus, M. ulcerans-positive
112 of M. ulcerans-positive Ae. notoscriptus, M. ulcerans-positive possum excreta and Buruli ulcer cases,
113 ducted extensive field survey analyses of M. ulcerans prevalence among mosquitoes in the Mornington P
114                                           M. ulcerans produces the polyketide-derived macrolide mycol
115  disease of the skin caused by Mycobacterium ulcerans, recognized by WHO as a neglected tropical dise
116  Diseases Surveillance System (NNDSS) and C. ulcerans-related diphtheria-like illness identified thro
117              Incidental identification of C. ulcerans-related diphtheria-like illness suggests survei
118                            Infection with M. ulcerans results in persistent severe necrosis without a
119 cimens of which 11% were PCR positive for M. ulcerans-specific DNA.
120 e report that some toxigenic Corynebacterium ulcerans strains show atypical results in a real-time PC
121 the relationship between M. liflandii and M. ulcerans, strains were analyzed for the presence of the
122 s to assess using statistical modeling if M. ulcerans surveillance of possum excreta provided useful
123 utants of C. diphtheriae and Corynebacterium ulcerans that are defective in acquiring iron from heme
124 sion, using the human pathogen Mycobacterium ulcerans that is responsible for Buruli ulcer.
125   Infection of human skin with Mycobacterium ulcerans, the causative agent of Buruli ulcer, is associ
126                                Mycobacterium ulcerans, the causative agent of Buruli ulcer, produces
127 ex macrolide toxin produced by Mycobacterium ulcerans, the causative agent of skin lesions called Bur
128                                Mycobacterium ulcerans, the causative agent of the neglected tropical
129 lactone congeners from the human pathogen M. ulcerans, the frog pathogen Mycobacterium liflandii, and
130 but the specific route of transmission of M. ulcerans to humans remains unclear.
131 r, resulted in greatly reduced ability of C. ulcerans to use hemin or hemoglobin as an iron source.
132                                       The M. ulcerans toxin does not cause cell death but instead arr
133 ynebacterium diphtheriae and Corynebacterium ulcerans use haemin and haemoglobin as essential sources
134                                           M. ulcerans was s.c. inoculated in three consanguine mouse
135        Buruli ulcer, caused by Mycobacterium ulcerans, was identified as a neglected emerging infecti
136 released by the human pathogen Mycobacterium ulcerans, was previously shown to impair Sec61-dependent
137 veral primer sequences, the MLST genes in C. ulcerans were also amplified, thereby providing the basi
138  hemin iron utilization from Corynebacterium ulcerans were cloned and characterized.
139 phtheria-like illness caused by toxigenic C. ulcerans were identified.
140 a; 12 (60.0%) were caused by Corynebacterium ulcerans, where animal contact was the predominant risk
141  of a toxin in the culture supernatant of M. ulcerans which causes a cytopathic effect on the mouse f
142 pid toxin from the culture supernatant of M. ulcerans which is capable of causing the cytopathic effe
143 secreted by the human pathogen Mycobacterium ulcerans, which induces the formation of open skin lesio
144 sease caused by infection with Mycobacterium ulcerans, which produces a potent toxin known as mycolac
145 phtheria caused by toxigenic Corynebacterium ulcerans who developed a right hand flexor sheath infect
146 by the environmental pathogen, Mycobacterium ulcerans whose major virulence factor is mycolactone, a
147 mportant to understand the interaction of M. ulcerans with other bacteria encountered during skin inf
148 n of the folate stress-sensing Fusobacterium ulcerans ZTP riboswitch, we apply a single-molecule vect

 
Page Top