ライフサイエンスコーパス: mutans streptococci

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1 o a significant delay in the colonization of mutans streptococci.

2 their saliva than do children colonized with mutans streptococci.

3 ents, including subsequent colonization with mutans streptococci.

4 have lactoferrin in their saliva that kills mutans streptococci and have reduced proximal decay.

5 en the two groups were observed in levels of mutans streptococci and lactobacilli at all time-points.

6 Salivary levels of mutans streptococci and lactobacilli were enumerated at

7 ltured on modified Mitis Salivarius agar for mutans streptococci and on blood agar for total culturab

8 s that may protect against colonization with mutans streptococci and the development of dental caries

9 may influence the subsequent colonization of mutans streptococci, and this in turn may suggest severa

10 Glucosyltransferase (GTF) enzymes of mutans streptococci are considered virulence factors due

11 Mutans streptococci are major etiological agents of dent

12 Mutans streptococci are strongly implicated in caries in

13 lected Lactobacillus species, in addition to mutans streptococci, are risk markers for early childhoo

14 Hence, the role of mutans streptococci as a primary caries pathogen appears

15 n 11-mer peptide designed for this SNP kills mutans streptococci associated with caries by >1 log.

16 tal micro-organisms, total streptococci, and mutans streptococci by an order of magnitude.

17 s streptococci is the observation that after mutans streptococci colonize the infant, the levels of S

18 The metabolic acids produced by mutans streptococci demineralize the tooth surface and l

19 GLU) domains of glucosyltransferase (GTF) of mutans streptococci has resulted in enhanced levels of a

20 ldren who do not harbor detectable levels of mutans streptococci have significantly higher levels of

21 a significant effect on the incorporation of mutans streptococci in dental biofilm.

22 This study determined the dose-response of mutans streptococci in plaque and unstimulated saliva to

23 ylitol at 6.44 g/day and 10.32 g/day reduces mutans streptococci in plaque at 5 wks, and in plaque an

24 At 6 mos, mutans streptococci in plaque for G3 and G4 remained 10x

25 enzyme glucosyltransferase (GTF) produced by mutans streptococci is the key factor in this process.

26 apparent antagonism between S. sanguinis and mutans streptococci is the observation that after mutans

27 caries is not fully understood, and although mutans streptococci, lactobacilli, and A. naeslundii hav

28 Salivary levels of Bifidobacteria, mutans streptococci, lactobacilli, and yeasts were corre

29 after sucrose, and had significantly higher mutans streptococci levels in plaque than did the caries

30 At 5 wks, mutans streptococci levels in plaque were 10x lower than

31 Individual mediators, salivary log10 mutans streptococci, log10 lactobacilli, and fluoride le

32 Mutans streptococci (MS) are key organisms associated wi

33 nd and ws sites) from all subjects were: (1) mutans streptococci (MS) on mitis-salivarius-bacitracin

34 ey included all strains of Lactobacillus and mutans streptococci (MS), most Bifidobacterium strains a

35 acitracin and mitis-salivarius agar; (2) non-mutans streptococci (non-MS) on mitis-salivarius agar; (

36 i (MS), most Bifidobacterium strains and non-mutans streptococci (non-MS), and about 20% of the Actin

37 cts from the CAT or GLU region of the GTF of mutans streptococci or coimmunized with a combination of

38 Bactericidal effects on other mutans streptococci, S. salivarius, and Actinomyces visc

39 en if heat-killed, sensitively co-aggregates mutans streptococci specifically.

40 Mutans streptococci were not among the aciduric isolates

41 uences of the glucosyltransferases (GTFs) of mutans streptococci with those from the alpha-amylase fa

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