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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 ine Streptococcus spp. were found, including S. mitis (25 strains, 50.0% of 50); currently unnamed St
9 ion mutant showed that the capsule protected S. mitis against phagocytosis by RAW 264.7 macrophages.
11 pneumococci and the closely related species S. mitis and S. oralis, showing up to 10.4% nucleotide d
12 e than to most CSPs previously reported from S. mitis and S. oralis, suggesting that these particular
13 oniae, isolates phenotypically identified as S. mitis and S. oralis, which included isolates previous
15 s genetic exchange is known to occur between S. mitis and Streptococcus pneumoniae, this finding may
16 rains of S. gordonii, S. sanguis, S. mutans, S. mitis, and S. oralis but only weakly by S. salivarius
19 and genetically are most closely related to S. mitis but which harbor genes encoding the virulence d
20 s, we hypothesize that P. gingivalis induces S. mitis cell death by an unknown mechanism, shaping the
22 lts demonstrating that P. gingivalis induces S. mitis death and DNA fragmentation in an in vitro biof
24 ked the toxic effect of E. corrodens extract S. mitis extracts contained a single, strongly reactive
29 olates did fall into a well-separated group, S. mitis isolates did not cluster into a well-separated
30 We show that while the polysaccharide from S. mitis J22 is flexible, requiring multiple conformatio
31 the oral streptococci, including isolates of S. mitis known to possess pneumolysin and autolysin.
32 neutralization assay results, one isolate of S. mitis may produce a further hemolytic toxin in additi
41 be SSA-3 hybridized to DNA from S. gordonii, S. mitis, S. oralis, S. parasanguinis, and S. vestibular
42 The LLY gene was identified in strains of S. mitis, S. pneumoniae, and Streptococcus pseudopneumon
44 ened a Tn916deltaE-derived mutant library of S. mitis strain SF100 for reduced binding to human plate
46 n (MIC, 4 to 12 mug/ml) was noted only among S. mitis strains (28.0%, 7/25) and not non-S. mitis stra
49 Significantly more S. mitis strains than non-S. mitis strains were resistant to fluoroquinolones and
53 ge life cycle, lysin mediates the binding of S. mitis to human platelets via its interaction with fib
55 GR4 showed higher rates of survival than the S. mitis type strain or the capsule-switching mutant, ex
57 to platelets and play a significant role in S. mitis virulence in the endocardium, but have never pr
59 le cells in chambers from mice infected with S. mitis were PI positive (apoptotic) or negative (live)
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