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1 C. botulinum A(B) strains were identified in California
2 C. botulinum C3 exoenzyme, a pharmacologic agent that sp
3 C. botulinum type B PFGE patterns from the infant and fr
4 C. botulinum was present up to 15000 MPN per gram dried
6 s Spo0A response regulator domain fused to a C. botulinum DNA-binding domain was capable of restoring
10 forming microorganisms such as B. anthracis, C. botulinum, and B. cereus, which can to be used for me
11 to neutralize the toxicity of known bivalent C. botulinum strains Ab, Ba, Af, and Bf also failed to n
13 for the isolation and identification of both C. botulinum and C. tetani demonstrates a sensitivity an
16 relative to Bacillus subtilis but the cloned C. botulinum Spo0A was unable to complement a spo0A muta
19 unction with previously described assays for C. botulinum neurotoxin types A, B, and E (BoNTA, -B, an
20 icate that Cladophora provides a habitat for C. botulinum, warranting additional studies to better un
21 s previously described in the literature for C. botulinum Group I type A1 into a population dynamics
22 n orphan nine-gene cluster was identified in C. botulinum and the related foodborne pathogen Clostrid
23 cheme for modelling neurotoxin production in C. botulinum Group I type A1, based on the integration o
24 med using a variety of techniques, including C. botulinum culture phenotypic properties, neurotoxin c
25 infant botulism identified the fourth known C. botulinum strain that produces both type B and type F
27 es seven antigenically distinct neurotoxins [C. botulinum neurotoxins (BoNTs) A-G] sharing a signific
30 warnings to the industry about the danger of C. botulinum and the importance of compliance with canne
31 t of Cladophora containing high densities of C. botulinum (>1000 MPN/g dried algae) showed that Clado
32 novel insights into the genetic diversity of C. botulinum and the clinical spectrum, occurrence, and
33 firm that the function of the H(C) domain of C. botulinum neurotoxin type A is limited to binding to
34 crystal structure of the catalytic domain of C. botulinum neurotoxin type E has been determined to 2.
39 is was lethal, suggesting phosphorylation of C. botulinum Spo0A repressed essential growth genes as a
40 h conservation of the amino acid sequence of C. botulinum Spo0A, some of these interactions have been
45 botulinum appeared to normally phosphorylate C. botulinum Spo0A and expression of this kinase in comb
48 une response with neutralizing antibodies to C. botulinum at week 19 was positive; these antibodies r
51 xpression of this kinase in combination with C. botulinum Spo0A in B. subtilis was lethal, suggesting
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