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 for both platelet binding and aggregation by S. mitis.
2 wed a protective function for the capsule in S. mitis.
3 ed the mitilysin gene from seven isolates of S. mitis.
4 levels of bacteremia caused predominantly by S. mitis.
5 owever, hybridized to DNA from S. oralis and S. mitis.
6 ern China was caused by a toxigenic clone of S. mitis.
7 ic regions contribute to platelet binding by S. mitis.
8 to understanding the population structure of S. mitis.
9 ine Streptococcus spp. were found, including S. mitis (25 strains, 50.0% of 50); currently unnamed St
10 ion mutant showed that the capsule protected S. mitis against phagocytosis by RAW 264.7 macrophages.
11 lar typing and strain clustering schemes for S. mitis allow for the integration of new strain data, a
12  probe not only to image the permeability of S. mitis and C. matruchotii membranes to tetraethylammon
13 groups demonstrated increased proportions of S. mitis and S. oralis by day 1.
14  pneumococci and the closely related species S. mitis and S. oralis, showing up to 10.4% nucleotide d
15 e than to most CSPs previously reported from S. mitis and S. oralis, suggesting that these particular
16 oniae, isolates phenotypically identified as S. mitis and S. oralis, which included isolates previous
17 ovel CSPs from disease-associated strains of S. mitis and S. oralis.
18 s genetic exchange is known to occur between S. mitis and Streptococcus pneumoniae, this finding may
19 rains of S. gordonii, S. sanguis, S. mutans, S. mitis, and S. oralis but only weakly by S. salivarius
20 sly characterized isolates of S. pneumoniae, S. mitis, and S. oralis.
21                                              S. mitis appear to release mitilysin extracellularly.
22 ersity and biology, but schemes specific for S. mitis are not currently available.
23 le of the competence regulon QS circuitry in S. mitis are yet to be explored.
24 te the effects temporal QS modulation has on S. mitis as it inhabits its natural niche.
25   Here we use whole genome sequencing of 129 S. mitis bloodstream infection (BSI) isolates collected
26  and genetically are most closely related to S. mitis but which harbor genes encoding the virulence d
27 s, we hypothesize that P. gingivalis induces S. mitis cell death by an unknown mechanism, shaping the
28 enable new insights into the epidemiology of S. mitis colonization, disease and transmission.
29 both the pneumococcus ComD receptors and the S. mitis ComD-2 receptor with high potencies.
30       In a multivariate analysis, S. aureus, S. mitis, Corynebacterium accolens, and bacilli were sig
31 rmore, our analysis revealed that the native S. mitis CSP signal can modulate QS response in S. pneum
32 lts demonstrating that P. gingivalis induces S. mitis death and DNA fragmentation in an in vitro biof
33 high concordance (100%), capturing extensive S. mitis diversity with strains assigned to multiple uni
34  common among the strains of S. gordonii and S. mitis examined.
35 ked the toxic effect of E. corrodens extract S. mitis extracts contained a single, strongly reactive
36 dentified extensive within- and between-host S. mitis genetic diversity among isolates sampled from a
37 treptococcus pneumoniae from nonpneumococcal S. mitis group species.
38                    Our findings suggest that S. mitis in patients with clinically diagnosed IE is not
39 lighting the accidental pathogenic nature of S. mitis in patients with clinically diagnosed IE.
40 neate the competence regulon QS circuitry in S. mitis, including confirming the identity of the nativ
41 oval from the chamber compared to cells from S. mitis-infected chambers.
42 demiology and pathogenicity of IE-associated S. mitis is hampered by low IE incidence.
43                   These results suggest that S. mitis is the most common cause of viridans streptococ
44  but one other mitis group streptococci (one S. mitis isolate generated an OD-value above 2.1).
45 olates did fall into a well-separated group, S. mitis isolates did not cluster into a well-separated
46   We show that while the polysaccharide from S. mitis J22 is flexible, requiring multiple conformatio
47 the oral streptococci, including isolates of S. mitis known to possess pneumolysin and autolysin.
48 neutralization assay results, one isolate of S. mitis may produce a further hemolytic toxin in additi
49                                              S. mitis/oralis endophthalmitis is a devastating complic
50 lecular testing confirmed a common strain of S. mitis/oralis.
51 the affected patients also were positive for S. mitis/oralis.
52 tients, and 13 of those cases were caused by S. mitis (P = 0.007).
53 e regulon QS circuitry in initiating various S. mitis phenotypes.
54                                              S. mitis possesses a typical comABCDE competence regulon
55                       Under such conditions, S. mitis resistance to clearance could be enhanced by ca
56 d against challenge by the oral streptococci S. mitis, S. mutans, and S. salivarius.
57 cation observed for other species, including S. mitis, S. oralis, and S. pseudopneumoniae.
58                                We found that S. mitis, S. oralis, and S. sanguis, as well as oral act
59 be SSA-3 hybridized to DNA from S. gordonii, S. mitis, S. oralis, S. parasanguinis, and S. vestibular
60    The LLY gene was identified in strains of S. mitis, S. pneumoniae, and Streptococcus pseudopneumon
61 efine the MLST scheme and derived the global S. mitis sequence clusters using the PopPUNK clustering
62                           The oral commensal S. mitis spp associates with preserved lung function and
63 eudopneumoniae strains but misidentified one S. mitis strain as S. pseudopneumoniae, and fastANI diff
64 e lactate concentration produced by a single S. mitis strain at a rate of 2.7 x 10(-4) cm/s, and (3)
65              This effect was enhanced in the S. mitis strain expressing the S. pneumoniae capsule, wh
66 ened a Tn916deltaE-derived mutant library of S. mitis strain SF100 for reduced binding to human plate
67 g S. mitis strains (28.0%, 7/25) and not non-S. mitis strains (0/25) (P = 0.004).
68 n (MIC, 4 to 12 mug/ml) was noted only among S. mitis strains (28.0%, 7/25) and not non-S. mitis stra
69 ng the antigenic profile, we found that some S. mitis strains (P066 and P107) reacted with both serot
70                   When the direct binding of S. mitis strains SF100 and PS344 to immobilized ganglios
71                           Significantly more S. mitis strains than non-S. mitis strains were resistan
72 Significantly more S. mitis strains than non-S. mitis strains were resistant to fluoroquinolones and
73 moniae strains, 59 S. pneumoniae strains, 22 S. mitis strains, 24 S. oralis strains, 6 S. infantis st
74                                              S. mitis survival in horse blood or in a mouse model of
75           Since SM1 is the first prophage of S. mitis that has been identified and because of the pos
76 -198) also inhibited the binding in vitro of S. mitis to human fibrinogen and platelets.
77 ge life cycle, lysin mediates the binding of S. mitis to human platelets via its interaction with fib
78      pblA and pblB mediate the attachment of S. mitis to platelets and play a significant role in S.
79 GR4 showed higher rates of survival than the S. mitis type strain or the capsule-switching mutant, ex
80                           In this study, the S. mitis type strain switched capsule by acquisition of
81 and defined sequence clusters or lineages of S. mitis using a comprehensive global data set of 322 ge
82  to platelets and play a significant role in S. mitis virulence in the endocardium, but have never pr
83 c to HL60 cells, whereas similar extracts of S. mitis were nontoxic.
84 le cells in chambers from mice infected with S. mitis were PI positive (apoptotic) or negative (live)
85 show high genetic diversity of IE-associated S. mitis with virtually all isolates belonging to distin