ライフサイエンスコーパス: diseased site

1 nize targets expressed preferentially at the diseased site.

2 livery improving drug bioavailability at the diseased site.

3 romycin levels to be higher in periodontally diseased sites.

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

5 nce in tissues and fluids near periodontally diseased sites.

6 of inflammation were selected and designated diseased sites.

7 o therapeutic cells for targeted delivery at diseased sites.

8 res enhanced control over content release at diseased sites.

9 monocytes and are released upon reaching the diseased sites.

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

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

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

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

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

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

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

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

18 ttern from HNP 1-3: LL-37 was upregulated in diseased sites, and HNP 1-3 was increased in periodontal

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

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

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

22 imaging may distinguish between healthy and diseased sites by evaluating marginal periodontal morpho

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

24 a was enriched in both primary and permanent diseased sites, confirming that this microorganism is im

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

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

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

28 r the delivery and/or activation of drugs at diseased sites for a variety of indications.

29 ngival biopsy was obtained from one selected diseased site from each patient and prepared for immunoh

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

31 Diseased sites had significantly (P <0.05) higher levels

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

47 vels of LL-37 and HNP 1-3 when compared with diseased sites of non-smokers.

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

49 Diseased sites of smokers presented significantly lower

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

51 val Il1b and increased osteoclast numbers at diseased sites (P < 0.05).

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

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

54 eduction of 0.73 +/- 0.11 mm and decrease of diseased sites (PD >3 mm) were measured at 6 months illu

55 D) reduction of 0.73 0.11 mm and decrease of diseased sites (PD >3 mm) were measured at 6 months illu

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

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

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

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

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

61 cimens taken at each patient's most proximal diseased site relative to healthy controls.

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

63 in present in the inflammatory process) from diseased sites significantly decreased in both groups.

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

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

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

67 At diseased sites, the external elastic membrane may actual

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

69 The number of residual diseased sites was also significantly reduced, without d

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

71 gnificant decrease in the pocket size of the diseased sites was only observed at 6 months in the grou

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

73 lity of monocytes to actively penetrate into diseased sites, we designed aptamer-based lipid nanovect

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

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

76 improvement in topical delivery of drugs at diseased sites, when compared to prevalent spray techniq

77 ful delivery of nucleic acid therapeutics to diseased sites would present a pivotal advancement in ca