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1 d to detect 2/3 clinical blood cultures with Streptococcus agalactiae.
2 function was conserved in Gap homologs from Streptococcus agalactiae.
3 hologous mutants of Streptococcus mutans and Streptococcus agalactiae.
4 rot broth culture alone for the detection of Streptococcus agalactiae.
5 mmonly has been used to distinguish GAS from Streptococcus agalactiae.
7 atus (1), the Streptococcus bovis group (5), Streptococcus agalactiae (9), the Streptococcus anginosu
8 streptococcal enzymes, from S.pneumoniae and Streptococcus agalactiae, allowed for insights into this
10 cus pneumoniae, vancomycin, and ceftriaxone, Streptococcus agalactiae, ampicillin, and cefotaxime, Es
11 s multiplexed detection of Candida albicans, Streptococcus agalactiae and Chlamydia trachomatis with
13 GacI homologs perform a similar function in Streptococcus agalactiae and Enterococcus faecalis In co
14 monstrated the presence of a supragenome for Streptococcus agalactiae and Haemophilus influenzae, it
16 coccus pyogenes), group B streptococci (GBS; Streptococcus agalactiae), and Streptococcus pneumoniae
17 illus plantarum, Neisseria meningitidis, and Streptococcus agalactiae, and 3% of the residues in its
18 terococcus faecalis, Streptococcus pyogenes, Streptococcus agalactiae, and viridans streptococci.
23 ens, such as the group B streptococcus (GBS) Streptococcus agalactiae, are an important cause of syst
28 esent report, we show that crude extracts of Streptococcus agalactiae catalyze the gamma-GCS and GS r
32 model of Saccharomyces cerevisiae and one of Streptococcus agalactiae constructed using the KEGG data
33 eria meningitidis, Streptococcus pneumoniae, Streptococcus agalactiae, cytomegalovirus, enterovirus,
34 tococcus pneumoniae, Streptococcus pyogenes, Streptococcus agalactiae, Escherichia coli, Klebsiella p
35 Enterococcus faecalis, Enterococcus faecium, Streptococcus agalactiae, Escherichia coli, Klebsiella p
37 ine and human macrophages induced by group B Streptococcus agalactiae (GBS) is likely an important vi
39 A streptococci), and recombinant SCPB, from Streptococcus agalactiae (group B streptococci), were co
40 ave previously shown that the human pathogen Streptococcus agalactiae (Group B Streptococci, GBS) enc
53 on of phoZ in Escherichia coli, E. faecalis, Streptococcus agalactiae (group B streptococcus [GBS]),
65 e is presented by the Gram-positive bacteria Streptococcus agalactiae (Group B Streptococcus; GBS) ty
71 cated in gastritis and peptic ulcer disease, Streptococcus agalactiae, implicated in neonatal meningi
72 perinatal treatment of women colonized with Streptococcus agalactiae include vancomycin prophylaxis
76 apsulated, intact Neisseria meningitidis nor Streptococcus agalactiae inhibited the OVA-specific IgG
82 Streptococcus pyogenes (</=0.12 microg/mL), Streptococcus agalactiae (</=0.12 microg/mL), Streptococ
83 tans (MetR), Streptococcus iniae (CpsY), and Streptococcus agalactiae (MtaR) that regulate methionine
88 ntly described the crystal structures of the Streptococcus agalactiae SAG2603 V/R sortase SrtC1 in tw
90 he whole-genome shotgun draft sequence for a Streptococcus agalactiae strain representing multilocus
92 ts, Staphylococcus aureus in 8 patients, and Streptococcus agalactiae, Streptococcus pyogenes, and St
94 the five major disease-causing serotypes of Streptococcus agalactiae, the main cause of neonatal inf
96 ed a mutant strain of group B Streptococcus (Streptococcus agalactiae) type III (GBS-III) that expres
97 nce and transmission of antibiotic-resistant Streptococcus agalactiae, we compared phenotypic and gen
99 corresponding region of a GspB homologue of Streptococcus agalactiae, which is acidic rather than ba
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