ライフサイエンスコーパス: diseased site

1 nize targets expressed preferentially at the diseased site.

2 romycin levels to be higher in periodontally diseased sites.

3 le for the delivery of therapeutic agents to diseased sites.

4 nce in tissues and fluids near periodontally diseased sites.

5 of inflammation were selected and designated diseased sites.

6 ered via local delivery routes directly into diseased sites, affirming improvement in periodontal sta

7 nd MI models, CRPPR liposomes accumulated in diseased sites, although less than in surrounding health

8 ch also circulate freely but accumulate at a diseased site and amplify their own accumulation at that

9 release of the encapsulated drug only at the diseased site and at controllable rates.

10 d in 247 individual tissue samples (183 from diseased sites and 64 from healthy sites) using a standa

11 e JP2 sequence was identified in 75% of LAgP diseased sites and in 56.67% of healthy sites.

12 ive objective measure distinguishing between diseased sites and non-diseased sites in patients and co

13 Increased GCF levels of sTREM-1 at diseased sites and their positive correlation with clini

14 Finally, we demonstrated that cultures from diseased sites are composed of cells with higher levels

15 Nine mediators were elevated in LAP diseased sites as compared with healthy sites (TNFalpha,

16 enhance the distribution of ciprofloxacin to diseased sites, but it is not a major determinant of GF

17 vealed that PG1334 was expressed in 88.0% of diseased sites, compared with 42.1% of healthy sites, ev

18 he hypothesis that gingival fibroblasts from diseased sites contribute to pathogenesis by possessing

19 The organisms identified only from diseased sites deserve further study as potential pathog

20 samples and demonstrate that healthy but not diseased sites display a wide variation in TLR4 agonist

21 as observed in the percentage of periodontal diseased sites, gingival index, plaque index, and clinic

22 Since GF flow was significantly higher at diseased sites, however, more ciprofloxacin was distribu

23 01) and anaerobes (P <0.001) were present in diseased sites in DM-periodontitis subjects compared to

24 istinguishing between diseased sites and non-diseased sites in patients and control subjects when eva

25 nflammation were selected and designated non-diseased sites in patients.

26 y Capnocytophaga spp. present in healthy and diseased sites in periodontitis patients with and withou

27 e which is known to vary between healthy and diseased sites in the periodontium.

28 tes of the children with AgP relative to non-diseased sites in the same children (P = 0.002), as well

29 ingival plaque samples from both healthy and diseased sites in the same individual were obtained from

30 l plaque bacteria from clinically healthy or diseased sites in the same individuals.

31 s were elevated in AgP sites relative to non-diseased sites in the same subjects, in siblings, and in

32 The MMP levels from diseased sites in the subjects with AgP were statistical

33 The accumulation in the diseased sites increased with time post-injury: the rati

34 riodontitis is that pathogenic bacteria from diseased sites infect healthy sites.

35 mulation of nanotherapeutics specifically at diseased sites, limiting efficacious responses in diseas

36 that selective chemoattraction of Tregs into diseased sites may offer a novel approach to the modulat

37 ediators in gingiva obtained from normal and diseased sites of periodontal disease.

38 MMP-8 was significantly elevated in the diseased sites of the children with AgP relative to non-

39 to 17.5%, 6.45%, and 3.23%, respectively, in diseased sites (P <0.001) and to 2.5%, 3.23%, and 0%, re

40 ith placebo, achieved a 10-fold reduction of diseased sites (P = 0.007).

41 e was collected from three healthy and three diseased sites per subject.

42 that predict extinction, populations in long-diseased sites persist.

43 ny advantages including direct access to the diseased site, potent knockdown of disease symptoms, and

44 GCF was collected from one diseased site (probing depth [PD] >4 mm, bleeding on pro

45 uman gingival fibroblasts (HGF) derived from diseased sites produce greater amounts of interleukin (I

46 at baseline could differentiate healthy from diseased sites (sensitivity and specificity >/=77%).

47 Subgingival plaque from diseased sites strongly activated TLR4, whereas matched

48 delivery, the nanoparticles passively target diseased sites, such as solid tumors or blood clots, whe

49 is shown to be elevated in the periodontally diseased site, the possible interaction between caffeine

50 At diseased sites, the external elastic membrane may actual

51 rsus non-DM-periodontitis (P = 0.025) and at diseased sites versus healthy sites (P <0.001).

52 The archaeal community at diseased sites was dominated by a Methanobrevibacter ora

53 ration of caspase-3 in female gingiva at all diseased sites was significantly greater than in gingiva

54 , IL-18, and IFN-gamma adjacent to 4 to 6 mm diseased sites were greater than adjacent to < or =3 mm

55 The maximally and minimally diseased sites were selected in each segment as defined