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1 events it from forming protein aggregates in Streptococcus mutans.
2 mensal Streptococcus gordonii and pathogenic Streptococcus mutans.
3 conditions to inhibit competing species like Streptococcus mutans.
4 were assayed by 74 DNA probes and by PCR to Streptococcus mutans.
5 commensal S. gordonii and the oral pathogen Streptococcus mutans.
6 ression of important virulence attributes of Streptococcus mutans.
7 r the production of the alarmone (p)ppGpp in Streptococcus mutans.
8 e of repressing mutacin I gene expression in Streptococcus mutans.
9 y Actinobacillus actinomycetemcomitans), and Streptococcus mutans.
10 nii, Streptococcus sanguinis, and cariogenic Streptococcus mutans.
11 d functional maturation of the adhesin P1 of Streptococcus mutans.
12 in Gram-positive bacteria does not apply to Streptococcus mutans.
13 bstrata of Streptococcus gordonii but not on Streptococcus mutans.
14 siologic functions and virulence factors for Streptococcus mutans.
15 peratively on the expression of virulence of Streptococcus mutans.
16 ce development for genetic transformation in Streptococcus mutans.
17 sensing is involved in biofilm formation of Streptococcus mutans.
18 ding for a PDE promoted biofilm formation in Streptococcus mutans.
19 eptococcal species Streptococcus sanguis and Streptococcus mutans.
20 d is produced by the Gram-positive bacterium Streptococcus mutans.
21 strong antigenic relationship with GBPs from Streptococcus mutans.
22 rmus thermophilus, Synechocystis PCC6803 and Streptococcus mutans.
23 is closely associated with the virulence of Streptococcus mutans.
24 e, mediated by the cariogenic oral bacterium Streptococcus mutans.
25 t of genetic competence in the oral pathogen Streptococcus mutans.
26 ence factors of the cavity-causing bacterium Streptococcus mutans.
27 P1 is an adhesin on the surface of Streptococcus mutans.
28 l for biofilm formation by the oral pathogen Streptococcus mutans.
29 Composites were inoculated with Streptococcus mutans.
32 ells versus 8.0 x 10(5) cells; P <0.05), and Streptococcus mutans (6.2 x 10(5) cells versus 2.0 x 10(
33 significant antibiofilm bioactivity against Streptococcus mutans, a causative agent of human dental
34 timated timing of a demographic expansion in Streptococcus mutans, a causative agent of human dental
41 There are suggestions that the phylogeny of Streptococcus mutans, a member of the human indigenous b
43 prevalent infectious disease associated with Streptococcus mutans, a pathogen also linked to endocard
47 at inhibits the glucosyltransferase (GTF) of Streptococcus mutans, a virulence enzyme involved in ora
49 inked properties of oral pathogens including Streptococcus mutans, Actinomyces naeslundii and Prevote
50 ecies-specific adherence/aggregation between Streptococcus mutans AgI/II and Streptococcus gordonii S
51 e with the surface adhesin protein AgI/II of Streptococcus mutans alone or in combination with LT-IIa
52 e with the surface adhesin protein AgI/II of Streptococcus mutans alone or in combination with LT-IIa
53 y by gastric intubation or intranasally with Streptococcus mutans alone or S. mutans complexed with a
54 e with the surface protein adhesin AgI/II of Streptococcus mutans alone or supplemented with an adjuv
58 the LraI family gene (designated sloC) from Streptococcus mutans, an agent of dental caries and endo
59 ar mass component of human saliva that binds Streptococcus mutans, an oral bacterium implicated in de
60 showed a significant microbicidal effect for Streptococcus mutans and an unencapsulated strain of Por
61 ractions of the response regulator ComE from Streptococcus mutans and DNA binding sites through DNase
62 ocalized on the surface of the oral pathogen Streptococcus mutans and facilitates an interaction with
64 tro wear, and antibacterial activity against Streptococcus mutans and Lactobacillus casei (in both pl
65 firmed the association of the acid producers Streptococcus mutans and Lactobacillus spp. with childho
66 e complexes (IC) of the cariogenic bacterium Streptococcus mutans and mAbs against its surface adhesi
68 evaluated the ability of the oral pathogens Streptococcus mutans and Porphyromonas endodontalis to i
73 hen tested against the gram-positive species Streptococcus mutans and Streptococcus mitis, however, l
76 s study, we used two oral bacterial species, Streptococcus mutans and Streptococcus sanguinis (former
80 zing glucosyltransferase enzyme (GTF-I) from Streptococcus mutans and thioredoxin from Escherichia co
81 oxidase is involved in both competition with Streptococcus mutans and virulence for infective endocar
82 , adjusted for age, sex, and the presence of Streptococcus mutans) and SM surfaces (1,004 participant
83 terococcus faecalis, Actinomyces naeslundii, Streptococcus mutans, and Aggregatibacter actinomycetemc
84 cterium nucleatum, Porphyromonas gingivalis, Streptococcus mutans, and Campylobacter rectus are also
85 , including oral streptococci, lactobacilli, Streptococcus mutans, and Candida, in saliva than did HI
87 ive group were Actinomyces sp. strain B19SC, Streptococcus mutans, and Lactobacillus spp., which exhi
88 treptococcus oralis, the late oral colonizer Streptococcus mutans, and the pioneer enteric bacterium
89 s including those of Salmonella typhimurium, Streptococcus mutans, and Thermus aquaticus encode a ded
93 ssing the saliva-binding region (SBR) of the Streptococcus mutans antigen I/II adhesin, either alone
94 encoding the saliva-binding region (SBR) of Streptococcus mutans antigen I/II adhesin, either alone
95 cidal effect was observed against cariogenic Streptococcus mutans at pH 7.4, even when using NO-relea
96 ppear to synthesize it and others, including Streptococcus mutans ATCC 33402, import it from their gr
100 oups (N-G, N-H, A-G and A-H) were exposed to Streptococcus mutans biofilm for 4, 8, 15, 20 or 25 days
104 lood mononuclear cells (PBMC) after engaging Streptococcus mutans, but monocytes in developing endoca
105 Carbohydrate catabolite repression (CCR) in Streptococcus mutans can be independent of catabolite co
107 Actinomyces israelii, Streptococcus sanguis, Streptococcus mutans, Candida tropicalis, Candida paraps
108 Addition of tears to late-exponential-phase Streptococcus mutans cells resulted in time- and dose-de
111 that the underlying mechanisms by which the Streptococcus mutans ClpXP protease affects virulence tr
112 ously that mucosal immunization of mice with Streptococcus mutans coated with the monoclonal antibody
114 that examines whether HIV infection affects Streptococcus mutans colonization in the oral cavity.
115 ns, all Caucasians had significantly greater Streptococcus mutans colonization, but only Db-negative
117 en salivary agglutinin and the adhesin P1 of Streptococcus mutans contribute to bacterial aggregation
118 with a bacterial protein antigen (AgI/II of Streptococcus mutans) coupled to the B subunit of choler
119 d with 50 to 100 microg of free or liposomal Streptococcus mutans crude glucosyltransferase (C-GTF) w
121 eractions between sucrose- (and starch-) and Streptococcus mutans-derived exoenzymes present in the p
123 mRNA (irvA) from the dental caries pathogen Streptococcus mutans directly modulates target mRNA (gbp
126 An insertionally inactivated fabM strain of Streptococcus mutans does not produce unsaturated membra
132 s in humans, and the primary caries pathogen Streptococcus mutans encodes multiple enzymes involved i
134 ce TLR2 was associated with poor response to Streptococcus mutans, Enterococcus faecalis, and Lactoba
136 (for Streptococcus GTP-binding protein) is a Streptococcus mutans essential GTPase which has signific
144 which are derived from functional domains of Streptococcus mutans glucosyltransferases (GTF) have bee
148 inding region (SBR) of the adhesin AgI/II of Streptococcus mutans has been shown to induce a mixed Th
153 y partially characterized the dnaK operon of Streptococcus mutans (hrcA-grpE-dnaK) and demonstrated t
156 ndida albicans cells are often detected with Streptococcus mutans in plaque biofilms from children af
157 frequently detected with heavy infection of Streptococcus mutans in plaque-biofilms from children af
159 efore investigated the roles of cnm-positive Streptococcus mutans in this single hospital-based, obse
160 or age, education group, and the presence of Streptococcus mutans) in self-reported whites (ages 14 t
164 expression of the fructanase gene (fruA) of Streptococcus mutans: induction by levan, inulin, or suc
177 environmental stress, especially low pH, by Streptococcus mutans is central to the virulence of this
181 urface Cnm protein expressed on cnm-positive Streptococcus mutans is involved in the development of C
197 3 bp region (igr66) between grpE and dnaK of Streptococcus mutans lacks a promoter but is required fo
199 ith special emphasis on the immunobiology of Streptococcus mutans, leading to active and passive vacc
201 omologous with transcriptional regulators of Streptococcus mutans (MetR), Streptococcus iniae (CpsY),
202 ed a previously constructed stress-sensitive Streptococcus mutans mutant Tn-1 strain resulting from d
203 jor cell-surface adhesion protein SA I/II of Streptococcus mutans, one of the major causative agents
204 essential for in vitro biofilm formation by Streptococcus mutans or Streptococcus gordonii grown in
205 causative agent of dental caries in humans, Streptococcus mutans, outcompetes other bacterial specie
207 bacterium Cluster 1 (p = 0.11), and by qPCR, Streptococcus mutans (p = 0.008) and Scardovia wiggsiae
212 cal enterotoxin B, splenocytes cultured with Streptococcus mutans produced significantly greater amou
216 ed evidence that the oral cariogenic species Streptococcus mutans remains viable but physiologically
217 n of the agmatine deiminase system (AgDS) of Streptococcus mutans requires agmatine and is optimal at
218 ormerly designated salivary agglutinin) with Streptococcus mutans requires an alanine-rich repetitive
219 demonstrated that competence development in Streptococcus mutans requires the type II ComRS quorum-s
221 secretion and acid tolerance (sat) operon of Streptococcus mutans resulted in an acid-sensitive pheno
223 t shows homology to the N-terminal domain of Streptococcus mutans SagA protein (42% similarity), prev
224 ll-known acidogenic/aciduric species such as Streptococcus mutans, Scardovia wiggsiae, Parascardovia
225 species associated with severe ECC included Streptococcus mutans, Scardovia wiggsiae, Veillonella pa
226 source of CO(2), buffers acid production by Streptococcus mutans (Sm), a key organism associated wit
227 ated, infected with Actinomyces viscosus and Streptococcus mutans (sobrinus) 6715, and fed a cariogen
228 ported identification of two Spx proteins in Streptococcus mutans - SpxA1 was the primary activator o
229 eptococcus pyogenes, Streptococcus gordonii, Streptococcus mutans, Staphylococcus aureus, and Enteroc
230 tococcus pyogenes, Streptococcus pneumoniae, Streptococcus mutans, Staphylococcus aureus, and Lactoco
236 colonizing species of the human oral flora (Streptococcus mutans, Streptococcus gordonii and Strepto
237 Antibacterial material was synthesized, and Streptococcus mutans, Streptococcus gordonii, and Strept
238 The salivary bacterial levels evaluated were Streptococcus mutans, Streptococcus sobrinus, Streptococ
240 ecombinant DNA methods were used to make the Streptococcus mutans supercolonizing strain, JH1140, lac
241 clonal antibody (MAb) 6-11A directed against Streptococcus mutans surface adhesin P1 was shown previo
242 an N-terminal saliva-binding region (SBR) on Streptococcus mutans surface antigen I/II (AgI/II) and s
243 Allelic replacement of the C terminus of a Streptococcus mutans surface protein affects murein hydr
244 lly modified lantibiotic peptide secreted by Streptococcus mutans T8, which inhibits the energy metab
245 ne segments were identified from a strain of Streptococcus mutans that was isolated from a patient wi
247 ccus gordonii, Streptococcus intermedius and Streptococcus mutans, the genes were cloned and expresse
249 d the metabolism of lactose and galactose by Streptococcus mutans, the major etiological agent of hum
250 he facultative anaerobic human oral pathogen Streptococcus mutans, the mechanisms used to protect aga
251 hment to the dental surfaces was studied for Streptococcus mutans, the most abundant cariogenic bacte
252 However, the function of this molecule in Streptococcus mutans, the primary aetiological agent of
257 trigger factor homologue, was identified in Streptococcus mutans, the primary etiological agent of h
258 h-coverage genome sequence of 57 isolates of Streptococcus mutans, the primary etiological agent of h
261 sives and the DOX-containing eluates against Streptococcus mutans through agar diffusion assays.
262 films by an important opportunistic pathogen Streptococcus mutans through the action of a family of 3
263 licated in the ability of certain strains of Streptococcus mutans to bind to collagen and to invade h
264 ugh substantial epidemiologic evidence links Streptococcus mutans to caries, the pathobiology of cari
269 -containing enzyme used by the oral pathogen Streptococcus mutans to reduce diatomic oxygen to water
270 hibited binding of a cell surface adhesin of Streptococcus mutans to salivary receptors in vitro, as
272 elocity water microdrop on the detachment of Streptococcus mutans UA159 biofilms from the interproxim
274 o remove biofilms of the cariogenic pathogen Streptococcus mutans UA159, as well as Actinomyces naesl
277 t was found to fail to inhibit the growth of Streptococcus mutans under microaerobic conditions.
280 caries (ECC), while strongly associated with Streptococcus mutans using selective detection (culture,
281 e human oral cavity plays a putative role in Streptococcus mutans virulence gene expression and in ap
283 ), which is an important virulence factor of Streptococcus mutans, was recombinantly expressed in the
287 implicated in the acid tolerance response of Streptococcus mutans when a mutation in its gene resulte
288 lular polysaccharide (IPS) is accumulated by Streptococcus mutans when the bacteria are grown in exce
289 reptococcus mitis, Streptococcus oralis, and Streptococcus mutans, whereas dentate individuals had hi
291 sis that cytokines elicited by antigens from Streptococcus mutans, which frequently dominates shallow
292 the basis of these findings, we propose that Streptococcus mutans, which resides in a multispecies or
294 ified enolase as a cell surface component of Streptococcus mutans, which was confirmed by enzyme-link
295 en I/II) is a sucrose-independent adhesin of Streptococcus mutans whose functional architecture on th
296 (p < 0.001), Scardovia wiggsiae (p = 0.003), Streptococcus mutans with bifidobacteria (p < 0.001), an
297 able to selectively kill cariogenic pathogen Streptococcus mutans with high efficacy within a human s
298 h for noninvasive treatment based on killing Streptococcus mutans with high-frequency microwave energ
300 r the function of the Escherichia coli YidC, Streptococcus mutans YidC2, and the chloroplast Arabidop
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