ライフサイエンスコーパス: LAgP

1 LAgP is used as an example of a severe periodontal disea

2 LAgP patients' whole saliva had higher LF levels than co

3 LAgP PMNs also had significantly higher levels of Fe(3+)

4 LAgP PMNs are primed to express higher levels of CP, lea

5 Neutrophils from 10 normal subjects and 10 LAgP patients were isolated from peripheral venous blood

6 Neutrophils from 12 normal subjects and 12 LAgP patients were isolated from peripheral venous blood

7 Peripheral blood was collected from 30 LAgP, 10 healthy unrelated, and 10 healthy sibling parti

8 Whole blood or saliva was obtained from 48 LAgP and 67 periodontally-healthy African-American subje

9 as follows: NP, 0.65919 (0.4901 to 0.8869); LAgP, 1.10138 (0.8265 to 1.468); and GAgP, 2.05318 (1.53

10 ings demonstrate hyper-responsive trait in a LAgP cohort, along with an attenuated hyper-responsivene

11 (GAgP), from 97 patients with localized AgP (LAgP), and from 91 healthy controls (non-periodontitis [

12 however, about the relationship of CD38 and LAgP patients.

13 s of the periodontium was observed in CP and LAgP.

14 LTB4 concentration compared to both GAgP and LAgP groups (P<0.005).

15 differences for any species between GAgP and LAgP.

16 tical difference between normal subjects and LAgP patients in resting CD38 expression (basal level).

17 evant to human inflammatory diseases such as LAgP.

18 A recent study has associated LAgP with 2 polymorphisms in the FPR: 110Phe-->Ser and 1

19 used on the level of CD38 expression between LAgP and normal subjects and examined the involvement of

20 CRP levels in both LAgP and GAgP subjects were significantly greater than t

21 imary versus permanent dentition affected by LAgP.

22 type appeared at greater risk for developing LAgP (odds ratio 2.271, 95% confidence interval: 1.005 t

23 ences in these two proximal dental diseases (LAgP and proximal decay) in LAgP could be due to the eff

24 Based on the recent findings, LAgP neutrophils are not "hypofunctional" or "deficient.

25 t it could be used as an early biomarker for LAgP.

26 y with systemic antibiotics is effective for LAgP in both primary and permanent dentitions.

27 oth loss per patient-year, respectively, for LAgP, GAgP, and un-specified AgP.

28 ut the differences were only significant for LAgP and CP groups (P<0.005).

29 d, and subgingival plaque was collected from LAgP diseased and healthy sites for each participant.

30 Whole and parotid saliva was collected from LAgP patients and matched controls.

31 These data suggest that LF from LAgP patients has a reduced capacity to bind iron and th

32 ts, and secretory products of monocytes from LAgP patients enhance IgG2 responses of lymphocytes from

33 Neutrophils from LAgP patients have been shown to exhibit diminished chem

34 tly different from LCP and GCP, but not from LAgP.

35 ontal disease, crevicular fluid samples from LAgP patients were found to contain prostaglandin E2 (PG

36 GAgP, LAgP, and CP groups had higher GT PAF levels than those

37 GAgP, LAgP, and CP groups had significantly higher GCF PAF lev

38 GAgP, LAgP, and CP groups had similar amounts of GCF and GT PA

39 GAgP, LAgP, and CP groups had similar GCF PAF levels (P>0.005)

40 GAgP, LAgP, and G groups had similar amounts of GCF and GT LTB

41 GAgP, LAgP, and G groups had similar LTB4 concentration compar

42 gnificant difference was found between GAgP, LAgP, and G groups (P>0.005).

43 data were expressed as concentration, GAgP, LAgP, and CP groups were found to have higher concentrat

44 assess DGKalpha spliced transcripts in human LAgP neutrophils.

45 In this study, we focused on NOS activity in LAgP neutrophils and examined the involvement of NOS in

46 S-NOS activity in LAgP neutrophils was higher than that in normal neutroph

47 lated and FMLP-stimulated MA-NOS activity in LAgP neutrophils was statistically significantly higher

48 sentation of the Fc gammaRIIIb-NA2 allele in LAgP patients compared to controls (P = 0.024).

49 A greater reduction in CAL in LAgP of primary dentition may suggest that younger child

50 dental diseases (LAgP and proximal decay) in LAgP could be due to the effect of saliva on the growth

51 a significant decrease of CD38 expression in LAgP subjects compared to normal subjects.

52 be related to altered neutrophil function in LAgP.

53 ociated with elevated neutrophil function in LAgP.

54 2)(-) generation was significantly higher in LAgP PMNs before and after stimulation with formyl-methi

55 NOS activity is increased in LAgP and is negatively correlated to chemotaxis response

56 ess and neutrophil-mediated tissue injury in LAgP.

57 sis that the chemotactic defects observed in LAgP patients are due at least in part to molecular alte

58 a suggest that the elevated PGE2 observed in LAgP patients may contribute to increased IFN-gamma prod

59 termined that the autoreactivity observed in LAgP was more severe and diverse than that observed in C

60 bound iron in LF is significantly reduced in LAgP patients compared to controls.

61 responses in GAgP are comparable to those in LAgP, but higher than in GCP or LCP for several species.

62 AgP were significantly greater than those in LAgP.

63 otein was identified as being upregulated in LAgP neutrophils.

64 els may play an important role in Aa-induced LAgP.

65 aggressive periodontal disease in juveniles (LAgP).

66 viduals and from 53 patients with localized (LAgP) and 49 patients with generalized (GAgP) aggressive

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

68 Neutrophils from peripheral blood of LAgP patients, but not from healthy volunteers, also gen

69 nomycetemcomitans (Aa), the reputed cause of LAgP.

70 of CD38 in abnormal neutrophil chemotaxis of LAgP patients.

71 Moreover, PBL cultures from a group of LAgP patients with high IgG2 levels had elevated levels

72 uccessful in reducing clinical parameters of LAgP and subgingival presence of JP2 in diseased and hea

73 uperoxide anion replicating the phenotype of LAgP PMNs.

74 study was to determine whether the saliva of LAgP patients and subjects with Aa had higher levels of

75 relationship of LF iron levels in saliva of LAgP patients as compared to their age-, gender-, and ra

76 organisms have been made through studies of LAgP.

77 ate MMP levels in the GCF after treatment of LAgP and to correlate these levels with clinical respons

78 Treatment of LAgP with SRP and systemic antibiotics was effective in

79 gents in localized aggressive periodontitis (LAgP) and weak responses in generalized aggressive perio

80 nts with localized aggressive periodontitis (LAgP) had minimal proximal decay.

81 ren with localized aggressive periodontitis (LAgP) have been reported previously by the present autho

82 ility to localized aggressive periodontitis (LAgP) in an African-American population.

83 Localized aggressive periodontitis (LAgP) is a disease characterized by rapid loss of alveol

84 Localized aggressive periodontitis (LAgP) is associated with neutrophil dysfunction includin

85 Localized aggressive periodontitis (LAgP) is associated with neutrophil dysfunction includin

86 Localized aggressive periodontitis (LAgP) is associated with various functional abnormalitie

87 (NP) and localized aggressive periodontitis (LAgP) patients (6.8% and 3.2%).

88 vated in localized aggressive periodontitis (LAgP) patients, and secretory products of monocytes from

89 cts with localized aggressive periodontitis (LAgP) present multiple functional abnormalities associat

90 nts with localized aggressive periodontitis (LAgP) produce elevated levels of IgG2 both in vivo and i

91 tible to localized aggressive periodontitis (LAgP) was conducted to evaluate chemokines/cytokines fou

92 nts with localized aggressive periodontitis (LAgP), 10 patients with chronic periodontitis (CP), 6 wi

93 nts with localized aggressive periodontitis (LAgP), 6 patients with gingivitis (G), and 6 periodontal

94 rum from localized aggressive periodontitis (LAgP), chronic periodontitis (CP), and periodontally hea

95 nts with localized aggressive periodontitis (LAgP), suggesting a genetic basis.

96 ort diagnosed with aggressive periodontitis (LAgP).

97 pe, with localized aggressive periodontitis (LAgP).

98 in E. coli and P. gingivalis LPS-stimulated LAgP cultures when compared with those of healthy unrela

99 es nor their allelic frequencies between the LAgP patients and controls.

100 ammaRIIIb NA2/NA2 genotype was higher in the LAgP group relative to the control population.

101 When iron was added to parotid saliva, the LAgP saliva bound 20 to 30 times less iron than controls

102 eneration and iron ion conversion similar to LAgP PMNs.

103 represent risk markers for susceptibility to LAgP in African-Americans.

104 ocalized aggressive periodontitis treatment (LAgP) affecting primary and permanent dentition is unkno

105 nd 59 females, aged 11 to 76 years), 18 with LAgP, 37 with GAgP, 37 with LCP, and 27 with GCP.

106 ermanent dentitions affected) diagnosed with LAgP were included.

107 African-American individuals diagnosed with LAgP.

108 evaluate presence of JP2 in individuals with LAgP after periodontal treatment.

109 In an expression library of a patient with LAgP, PMNs were screened for different DGKalpha transcri

110 Sixty African-American patients with LAgP, aged 5 to 25 years, were examined.

111 phils from normal subjects and patients with LAgP.

112 PMNs from healthy subjects and patients with LAgP.

113 Eleven Aa-positive subjects (seven with LAgP) were matched with 11 Aa-negative controls.

114 m were significantly higher in subjects with LAgP compared to the PMNs and serum samples from matched

115 igher concentrations in sera from those with LAgP (7.6 +/- 2.2 pg/mL) and GAgP (17.1 +/- 2.3 pg/mL).

116 solated from healthy subjects and those with LAgP (N = 36).