ライフサイエンスコーパス: BOP

1 BOP (percentage) was significantly lower in the B group

2 BOP and AL were significantly higher in pregnant women w

3 BOP expression domains are differentially enlarged in bp

4 BOP was assessed with the ball-ended tip of the probe, a

5 BOP was significantly higher among controls than WPs (P

6 BOP was significantly higher in group 3 than in groups 1

7 n of severe CAL with tooth loss (P = 0.000), BOP (P = 0.004), and heavy smokers (P = 0.001).

8 eduction in ligature-induced GI (P <0.0001), BOP (P <0.0015), PD (P <0.0016), and CAL (P <0.0038).

9 levels in the GCF (r = 0.4672, P = 0.0002), BOP (r = 0.7491, P = 0.0001), and GI (r = 0.5420, P = 0.

10 PI (P <0.01), BOP (P <0.01), PD >3 mm (P <0.01), and clinical AL (P <0

11 was correlated with PI (r = 0.464, P <0.01), BOP (r = 0.401, P <0.05), and tooth loss (r = 0.245, P <

12 nth period (CAL, P = 0.0002; PD, P = 0.0156; BOP, P = 0.0079).

13 CAL (3 months: P <0.01; 6 months: P <0.02), BOP (3 months: P <0.01; 6 months: P >0.05), and GI (3 mo

14 CAL (3 months: P <0.01; 6 months: P <0.03), BOP (3 months: P <0.02; 6 months: P <0.05), and GI (3 mo

15 probing in a population that had > or = 20% BOP sites.

16 LEAVES2 (AS2) and LOB are upregulated in 35S:BOP and downregulated in bop mutant plants.

17 We determined a BOP of 145 kPa as upper mild TBI threshold (5% PMR).

18 had blood collected from sites with adequate BOP to obtain a sample without touching the tooth or gin

19 Clinical periodontal measures (PD, AL, BOP) and measures of glycemic control (HbA1c, random glu

20 ate model adjusting for age, gender, PD, AL, BOP, and PI, HbA1c and random glucose were independent p

21 e carcinogen N-nitrosobis(2-oxopropyl)amine (BOP) s.c. in five weekly injections (the first, 70 mg/kg

22 c carcinogen N-nitrosobis(2-oxopropyl)amine (BOP).

23 <0.01), PD (all time points: P <0.001), and BOP (3 months: P <0.05; 6 months: not statistically sign

24 s ratio [OR] = 2.9), smoking (OR = 3.7), and BOP in >30% of sites (OR = 4.1); and 2) for tooth loss,

25 ealed an effect of general obesity on AL and BOP in different teeth (RR: 1.44).

26 f abdominal obesity increased risk of AL and BOP in different teeth (RR: 1.47), AL and BOP in the sam

27 l outcomes (rate ratio [RR]: 1.45 for AL and BOP in different teeth; RR: 1.84 for AL and BOP in the s

28 nal obesity presented greater risk of AL and BOP in the same tooth (RR: 2.16) and percentage of BOP (

29 nd BOP in different teeth (RR: 1.47), AL and BOP in the same tooth (RR: 2.77), and percentage of BOP

30 BOP in different teeth; RR: 1.84 for AL and BOP in the same tooth).

31 The BOB and BOP maps have important points of convergence, but also

32 ht) and 57% (obesity) higher risk of CAL and BOP.

33 ing PD, clinical attachment level (CAL), and BOP, and GCF IL-1beta levels were measured immediately b

34 008) and periodontal parameters PD, CAL, and BOP was identified.

35 Significant improvements in PD, CAL, and BOP were observed at 1, 3, and 6 months in all sites (P<

36 PD, CAL, and BOP were significantly improved in all groups after 12 m

37 th groups showed improved plaque control and BOP scores.

38 Control and BOP-treated hamsters were fed a NO-ASA 3,000 ppm or conv

39 four sites per tooth, and probing depth and BOP were evaluated at six sites per tooth using an autom

40 plaque index, periodontal probing depth, and BOP using an automated pressure-sensitive probe.

41 r failure-free survival rates for BEP/EP and BOP/VIP-B were 60% (95% confidence interval [CI], 53% to

42 bserved between groups regarding PI, GI, and BOP.

43 g the myocyte enhancer factor 2C (MEF2C) and BOP transcription factors, suggesting that these cardiog

44 = 800 microIU, AST > or = 1,200 microIU, and BOP in the PS was significantly (P<0.02) lower at 6 and

45 (BOP) <10%; 2) gingivitis, all PD <3 mm and BOP >/=10%; 3) periodontitis (P)1, >/=1 site with PD >3

46 P </=10%; 4) P2, >/=1 site with PD >3 mm and BOP >10% but </=50%; and 5) P3, >/=1 site with PD >3 mm

47 =50%; and 5) P3, >/=1 site with PD >3 mm and BOP >50%.

48 and 53 healthy controls (PDs < or =4 mm and BOP < or =15%).

49 iodontitis (P)1, >/=1 site with PD >3 mm and BOP </=10%; 4) P2, >/=1 site with PD >3 mm and BOP >10%

50 r for persistence of sites with PD >4 mm and BOP at 12 months post-treatment.

51 reased the number of sites with PD >4 mm and BOP per patient significantly more than without (group A

52 y fewer sites with a persisting PD >4 mm and BOP than control patients (P <0.01).

53 reduction of implant sites with PD >4 mm and BOP was significantly higher in patients with AM than in

54 eduction of implant sites with PD > 4 mm and BOP was significantly higher in patients with AM than in

55 D (1.4 +/- 0.7 mm), CAL (1.3 +/- 0.8 mm) and BOP (33.4 +/- 17.2%).

56 attachment level (CAL) (1.3 +/- 0.8 mm), and BOP (33.4% +/- 17.2%).

57 atistically significant reductions in PD and BOP and gains in CAL.

58 inear correlations were noted between PD and BOP, PD and TC, PD and TG, and CAL and TG in each group

59 group analysis showed that VPI, GBI, PD, and BOP presented statistically significant improvements com

60 therapy significantly improved CAL, PD, and BOP relative to the placebo group during the 6- to 12-mo

61 ignificant reduction in mean PI, GI, PD, and BOP were found after treatment in all groups (P <0.001).

62 thout MMs, improves CALs, along with PDs and BOP over a 1-year period.

63 al horizontal/vertical defect depth, PI, and BOP), and background factors (endodontic status, smoking

64 outcome), probing depths (PDs), plaque, and BOP also were recorded at baseline and 6 and 12 months.

65 GI-DL/SB subjects, more severe pocketing and BOP were associated with higher levels of GCF IL-1beta,

66 wer relationship for single-site pockets and BOP.

67 at the observed greater reduction in PPD and BOP in persons using interdental brushing than in those

68 single dose of a small molecule antagonist (BOP (N-(benzenesulfonyl)-L-prolyl-L-O-(1-pyrrolidinylcar

69 ere similar for both groups in terms of API, BOP, PD in deep pockets, and CAL.

70 tatistically significant association between BOP and GI and CAD in patients with Al; and facial/lingu

71 ant positive correlations were found between BOP, PI scores, and biofluid parameters also in systemic

72 wledge, the first functionally characterized BOP gene in monocots, Cul4 suggests the partial conserva

73 schedule (bleomycin, vincristine, cisplatin [BOP])/etoposide, ifosfamide, cisplatin, and bleomycin [V

74 All periodontal conditions (BOP, PD, and CAL) were significantly worse in patients w

75 analysis after controlling for confounders, BOP and CAL correlated positively and significantly with

76 quitin ligases (SCF(EBF1/2), CUL3(LRB), CUL3(BOP), and CUL4(COP1-SPA)) that regulate PIF abundance bo

77 though placebo-treated beagles demonstrated %BOP scores of 43% at week 8, GED- and MEG-treated beagle

78 become edematous and more likely to develop BOP.

79 ally pure P-chiral dihydrobenzooxaphosphole (BOP) core 1 is developed that is amenable to large scale

80 f novel chiral biphenol-based diphosphinite (BOP) ligands was designed and created.

81 k 8, GED- and MEG-treated beagles exhibited %BOP scores of 21% and 26%, respectively.

82 r = 4 mm, the percentage of sites exhibiting BOP, smoking status, total cholesterol, LDL-cholesterol,

83 owed that the percentage of sites exhibiting BOP, the number of sites with PD > or = 4, the number of

84 va adjacent to a 4- to 6-mm sulcus featuring BOP was classified as "diseased, moderate" (DM); and gin

85 oderate/severe periodontitis, and 14.7%, for BOP and CAL.

86 Mixed anhydrides from BOP-Cl and Fmoc-alphaalphaAA-OH are used for anchoring a

87 erences in intergroup comparisons of PI, GI, BOP, and PD were found to be significant (P <0.05) in fa

88 e infected sites had a significantly greater BOP (67+/-14% versus 25+/-8% for uninfected sites at 12

89 In the hyperlipidemic group, BOP was significantly correlated with total cholesterol,

90 In both participant groups, BOP scores correlated significantly with VPI scores (r =

91 The odds of having BOP decreased 90% (down to 38% of patients) and 95% (26%

92 methylamino)phosphonium hexafluorophosphate (BOP) and DBU in CH(2)Cl(2), THF, or DMF.

93 methylamino)phosphonium hexafluorophosphate (BOP), base, and nitrogen nucleophiles leads to the forma

94 methylamino)phosphonium hexafluorophosphate (BOP).

95 ts with CP demonstrated significantly higher BOP, PI, GI, and percentage of sites with clinical AL >5

96 Furthermore, supernatants from I-BOP-treated A549-TPalpha cells enhanced MCP-1-dependent

97 ied that transcription factor SP1 mediates I-BOP-induced MCP-1 expression.

98 Here we show that TXA(2) mimetic, I-BOP, induced monocyte chemoattractant protein -1(MCP-1)/

99 RP correlated significantly with decrease in BOP (P <0.001).

100 A statistically significant difference in BOP was found in patients with > or = 20% of bleeding si

101 (GI) (P </=0.002) and a significant drop in BOP, PI, and GI post-treatment (P </=0.001).

102 BOP at baseline but also less improvement in BOP through direct effects.

103 one and CRP, together with an improvement in BOP, PD, and CAL in the absence of periodontal treatment

104 te yet statistically significant increase in BOP (12.4%) compared to the placebo group (there was no

105 sults demonstrated a significant increase in BOP when aspirin, 325 mg was compared to placebo (P <0.0

106 groups were not statistically significant in BOP, PD, relative GR, or CAL after 2 years.

107 l PD ranged from 4.8 to 8.8 mm, with initial BOP ranging from 19.7% to 100%.

108 The intensive BOP/VIP-B therapy was associated with more toxicity, but

109 trol group (P <0.001): lower PI and GI, less BOP, less increase in GCF volume, and lower IL-1beta tot

110 In contrast, smokers showed less BOP at baseline but also less improvement in BOP through

111 amination using novel diphosphonite ligands (BOPs) to provide 1-vinyltetrahydroisoquinoline key inter

112 mm [deep lesion (DL)] were divided into low BOP (18.0%), moderate BOP (BGI-DL/MB, 39.7%), and severe

113 use of fluoxetine was associated with lower BOP percentages and reduced AL.

114 amino acid epsilonNH2-Bodipy576/589-lysine (BOP-Lys) into a model protein.

115 R = 0.903; P < .001), the molecular marker (BOP; R = 0.908; P < .001), and regional atrophy (R = 0.6

116 After delivery mean BOP was 13.25%, mean PD 2.39 mm, and mean CAL 1.14 mm.

117 gnificant differences between groups on mean BOP and ICTP levels during the course of the study were

118 During pregnancy mean BOP was 21.03%, mean PD 2.62 mm, and mean CAL 1.20 mm.

119 n CAL, percentage of sites with CAL >/=5 mm, BOP, and GI in the atorvastatin group compared with the

120 ion of sites with PD 4 to 5 mm and >/= 6 mm, BOP, and ABL, except Aggregatibacter actinomycetemcomita

121 were divided into low BOP (18.0%), moderate BOP (BGI-DL/MB, 39.7%), and severe BOP (BGI-DL/SB, 12.9%

122 re evaluated, E2-deficient subjects had more BOP (43.8% versus 24.4%, P<0.04) and a trend toward a hi

123 AI patients exhibited significantly more BOP than H and RA+ (46.45% +/- 17.08%, 30.08% +/- 16.86%

124 : full-mouth plaque index (FMPI), full-mouth BOP score (FMBS), gingival recession, PD, and clinical a

125 , those subjects with 20% to 30% whole mouth BOP were randomly assigned to one of three arms: placebo

126 cause boric acid was superior in whole-mouth BOP as well as PD and CAL reduction for moderate pockets

127 mm) and a healthy papilla, if available (no BOP, PD < or =4 mm, and AL < or =2 mm).

128 2 mm) and one healthy site (PD </= 3 mm, no BOP) from each individual at baseline and 3 and 6 months

129 Using a related fluorescent analogue of BOP (R-BC154), we show that this class of antagonists pr

130 as the potential to affect the appearance of BOP.

131 bleeding on probing (BOP) and combination of BOP and attachment loss (AL).

132 s, Cul4 suggests the partial conservation of BOP gene function between dicots and monocots, while phy

133 While the delivery of BOP-Lys-tRNA(Lys) to the ribosome is limited by its poor

134 The extent of BOP exhibited a significant positive correlation with IL

135 e mortality rate as a non-linear function of BOP.

136 e associated with the increased incidence of BOP observed in the subjects who received aspirin therap

137 the same tooth (RR: 2.16) and percentage of BOP (RR: 1.37).

138 the same tooth (RR: 2.77), and percentage of BOP (RR: 1.49).

139 AL was 0.44 mm versus 0.30 mm, percentage of BOP sites was 16% versus 15%, and GI was 1.03 versus 0.5

140 neral obesity was noted on the percentage of BOP.

141 ontal health or disease, but the presence of BOP is not an accurate predictor of disease progression.

142 th (CAL gain, PD reduction, and reduction of BOP).

143 The mean score of BOP (P <0.05) was statistically significantly higher in

144 de is additionally controlled at the step of BOP-Lys-tRNA release from EF-Tu into the ribosome.

145 yielded significant improvements in terms of BOP and PD decrease and CAL gain compared to baseline va

146 sting for confounders, the risk variables of BOP (P = 0.047), smoking (P = 0.003), and diabetes (P =

147 Aspirin can have an affect on BOP in naturally occurring gingivitis patients.

148 ailure to consider the effects of aspirin on BOP could impair proper diagnosis and treatment planning

149 ry (bTBI) increases with blast overpressure (BOP) and impulse in dose-dependent manner.

150 aspirin ingestion on the clinical parameter BOP.

151 wing determination of a burden of pathology (BOP) score.

152 ted in a significant improvement in CAL, PD, BOP, and GI.

153 MM + SRP also improved PD, BOP, and CAL to a greater extent than SRP alone independ

154 A significant improvement of PD, BOP, and sites with plaque was observed 3 months after t

155 ease from baseline, respectively, in percent BOP.

156 present evidence that the BLADE-ON-PETIOLE (BOP) genes, which have previously been shown to control

157 omologs of the Arabidopsis BLADE-ON-PETIOLE (BOP) transcriptional cofactors, defined by the conserved

158 Peri-implant PI, BOP, and PD >/=4 mm were recorded, and mesial and distal

159 -smokers did not differ significantly in PI, BOP, CAL, radiographic, or biochemical parameters at any

160 statistically significant difference in PI, BOP, PD >/=4 mm, and total CBL among smokers with IL and

161 ificant reductions were observed in mean PI, BOP, and PD (P<0.05).

162 Periodontal inflammatory parameters (PI, BOP, and PD) were significantly higher in individuals wi

163 Periodontal parameters (PI, BOP, PD, and AL) (P <0.01) and MBL (P <0.01) were worse

164 In addition, PD, PI, BOP, MR, and SUP varied significantly according to PIMT

165 chemistry, use of polymer-supported BOP (Pol-BOP) did not lead to efficient nucleoside loading.

166 hort) with a similar "balance of pressures" (BOP) map proposed by MacCoun (2012).

167 pressures measured at the blowout preventer (BOP) over the 86-day period following the Deepwater Hori

168 ng depth (PD) <3 mm and bleeding on probing (BOP) <10%; 2) gingivitis, all PD <3 mm and BOP >/=10%; 3

169 months: P = 0.001), and bleeding on probing (BOP) (3 months: P <0.01; 6 months: P <0.02; 9 months: P

170 ercentage of sites with bleeding on probing (BOP) and clinical AL >/=5 mm.

171 and the combination of bleeding on probing (BOP) and clinical attachment loss (CAL) was estimated us

172 ercentage of teeth with bleeding on probing (BOP) and combination of BOP and attachment loss (AL).

173 evaluated for calculus, bleeding on probing (BOP) and loss of gingival attachment (LOA).

174 (PD) and assessments of bleeding on probing (BOP) and radiographic alveolar bone loss (ABL).

175 e supragingival plaque, bleeding on probing (BOP) and relative clinical attachment level (RCAL).

176 hment levels (CAL), and bleeding on probing (BOP) as well as gingival crevicular fluid bone marker as

177 ng depth (PD) >4 mm and bleeding on probing (BOP) at 12 months post-therapy.

178 ng depth (PD) >4 mm and bleeding on probing (BOP) at the 3-month reevaluation.

179 sed on probing depth or bleeding on probing (BOP) at the site of collection of the GCB sample.

180 plaque index (VPI) and bleeding on probing (BOP) from six sites per tooth.

181 Participants with bleeding on probing (BOP) in <10% of sites were classified as healthy, wherea

182 CI), gingival (GI), and bleeding on probing (BOP) indices were used to assess gingival health.

183 absence or presence of bleeding on probing (BOP) is a sign of periodontal health or disease, but the

184 Bleeding on probing (BOP) is widely interpreted as a sign of disease activity

185 D), plaque indices, and bleeding on probing (BOP) measured at baseline, intermediate, and final exami

186 ng depth (PD) >4 mm and bleeding on probing (BOP) per patient was the primary outcome.

187 lower odds of increased bleeding on probing (BOP) percentage values (OR = 0.62, 95% CI = 0.34 to 0.97

188 attachment level gain, bleeding on probing (BOP) reduction, radiographic bone fill (RBF), and mucosa

189 robing depths (PDs) and bleeding on probing (BOP) scores.

190 evel (CAL), and reduced bleeding on probing (BOP) to a greater extent than SRP alone (P <0.05).

191 patients with adequate bleeding on probing (BOP) were collected on special blood collection cards an

192 probing depth (PD), and bleeding on probing (BOP) were measured in implants and were evaluated at bas

193 probing depth (PD), and bleeding on probing (BOP) were measured, and gingival crevicular fluid (GCF)

194 chment level (CAL), and bleeding on probing (BOP) were observed both short and long term.

195 (PD) of > or =5 mm with bleeding on probing (BOP) were randomized into the test or control groups.

196 ingival index (GI), and bleeding on probing (BOP) were recorded at baseline and 1, 2, and 3 months af

197 chment level (CAL), and bleeding on probing (BOP) were recorded.

198 probing depth (PD) and bleeding on probing (BOP) were recorded.

199 and percentage of sites bleeding on probing (BOP) were significantly higher in the HLp group than the

200 attachment level (CAL), bleeding on probing (BOP), and gingival index (GI) at baseline and at 3 and 6

201 ), gingival index (GI), bleeding on probing (BOP), and horizontal and vertical bone sounding) and rad

202 attachment level (CAL), bleeding on probing (BOP), and plaque index were measured at four sites of ea

203 furcation involvement, bleeding on probing (BOP), and suppuration.

204 ), probing depths (PD), bleeding on probing (BOP), and the full-mouth plaque score (FMP).

205 ng depth (PD), gingival bleeding on probing (BOP), clinical attachment level (CAL), and surfaces with

206 attachment level (CAL), bleeding on probing (BOP), gingival index (GI), and periodontal inflamed surf

207 attachment level (CAL), bleeding on probing (BOP), gingival index (GI), and plaque index were measure

208 attachment level (CAL), bleeding on probing (BOP), gingival index (GI), plaque index (PI), RA disease

209 attachment level (CAL), bleeding on probing (BOP), gingival index (GI), plaque index, and wound heali

210 tal parameters included bleeding on probing (BOP), mean probing depth (PD), and mean clinical attachm

211 PD), plaque index (PI), bleeding on probing (BOP), mucosal redness (MR), suppuration (SUP), keratiniz

212 ), probing depths (PD), bleeding on probing (BOP), or relative clinical attachment levels (CAL) were

213 l-flow immunoassay with bleeding on probing (BOP), oral hygiene, and periodontal probing depth.

214 Plaque index (PI), GI, bleeding on probing (BOP), PD, and attachment gain were measured.

215 ), gingival index (GI), bleeding on probing (BOP), PD, gingival crevicular fluid (GCF) volume, and to

216 l parameters, including bleeding on probing (BOP), periodontal probing depths (PDs), and plaque index

217 ions were found between bleeding on probing (BOP), plaque index (PI) scores, and GCF APRIL, serum sRA

218 ed significantly higher bleeding on probing (BOP), plaque index (PI), and gingival index (GI) (P </=0

219 inical attachment loss, bleeding on probing (BOP), plaque index (PI), and tooth loss.

220 > or =2 mm, changes in bleeding on probing (BOP), plaque index, and mobility.

221 outh plaque index (PI), bleeding on probing (BOP), probing depth (PD) >/=4 mm, and clinical attachmen

222 ding plaque index (PI), bleeding on probing (BOP), probing depth (PD) >3 mm, clinical attachment loss

223 Plaque index (PI), bleeding on probing (BOP), probing depth (PD), and attachment level (AL) were

224 phic and biologic data, bleeding on probing (BOP), probing depth (PD), and clinical attachment level

225 index, gingival index, bleeding on probing (BOP), probing depth (PD), and clinical attachment level

226 mal plaque index (API), bleeding on probing (BOP), probing depth (PD), and clinical attachment level

227 nation with a record of bleeding on probing (BOP), probing depth (PD), and clinical attachment level

228 odontal examinations of bleeding on probing (BOP), probing depth (PD), and clinical attachment level

229 examination, including bleeding on probing (BOP), probing depth (PD), and clinical attachment level,

230 Plaque index (PI), bleeding on probing (BOP), probing depth (PD), and clinical attachment loss (

231 ), gingival index (GI), bleeding on probing (BOP), probing depth (PD), clinical attachment level (CAL

232 Bleeding on probing (BOP), probing depth (PD), relative GR, clinical attachme

233 ad increased sites with bleeding on probing (BOP), probing depth, clinical attachment level (CAL), wa

234 th, gingival recession, bleeding on probing (BOP), visible plaque, supragingival calculus, and mean t

235 chment level (CAL), and bleeding on probing (BOP), were performed, and subgingival plaque samples wer

236 depth (PD) >/=5 mm with bleeding on probing (BOP).

237 tachment loss (AL), and bleeding on probing (BOP).

238 acent probing depth and bleeding on probing (BOP).

239 probing depth (PD), and bleeding on probing (BOP).

240 chment level (CAL), and bleeding on probing (BOP).

241 AL), probing depth, and bleeding on probing (BOP).

242 chment level (CAL), and bleeding on probing (BOP).

243 depth (PD) >/=5 mm with bleeding on probing (BOP).

244 g PMT with a history of bleeding on probing (BOP).

245 chment level (CAL), and bleeding on probing (BOP).

246 epth (PD) >/= 5 mm with bleeding on probing (BOP).

247 ) plaque index (PI); 2) bleeding on probing (BOP); 3) probing depth (PD); and 4) clinical attachment

248 ; 2) gingival index; 3) bleeding on probing (BOP); 4) probing depth; and 5) attachment loss (AL).

249 probing depth (PD); 2) bleeding on probing (BOP); and 3) attachment loss (AL).

250 h (PD) > or =5 mm and bleeding upon probing (BOP) in need of access flap surgery (AFS).

251 GI), and percentage of bleeding on probing (%BOP) were observed in placebo-treated beagles.

252 plaque index [PI], and bleeding on probing [BOP]) and defect (vertical and horizontal defect depths)

253 achment loss [CAL], and bleeding on probing [BOP]) were performed.

254 depth [PD] >/=5 mm and bleeding on probing [BOP]) were selected and randomly allocated to a control

255 depth [PD] >/=5 mm with bleeding on probing [BOP]).

256 obing depth [PD] >4 mm, bleeding on probing [BOP], and clinical attachment level >/= 2 mm) and one he

257 ], gingival index [GI], bleeding on probing [BOP], and clinical attachment level) and photographs fro

258 depth [PD] > or =5 mm, bleeding on probing [BOP], and clinical attachment or radiographic bone loss)

259 ers (plaque index [PI], bleeding on probing [BOP], and probing depth [PD] >/=4 mm) and crestal bone l

260 proximal papillae (with bleeding on probing [BOP], probing depth [PD] > or =4 mm, and attachment loss

261 ers (plaque index [PI], bleeding on probing [BOP], probing depth [PD], clinical attachment loss [AL],

262 ers (plaque index [PI], bleeding on probing [BOP], probing depth [PD], clinical attachment loss [AL],

263 ons (plaque index [PI], bleeding on probing [BOP], probing depth [PD], marginal bone loss [MBL]) and

264 moderate BOP (BGI-DL/MB, 39.7%), and severe BOP (BGI-DL/SB, 12.9%).

265 reen for diabetes in persons with sufficient BOP to obtain a sample without touching the tooth or gin

266 solution chemistry, use of polymer-supported BOP (Pol-BOP) did not lead to efficient nucleoside loadi

267 throughout the study (P <0.05), except that BOP was not reduced in the PS protocol (P >0.05).

268 Moreover, we found that BOP proteins physically interact with both PIF4 and CULL

269 ate linear regression analysis revealed that BOP and CAL (dependent variable) (P = 0.009/R(2) = 0.05

270 This shows that BOP proteins act as substrate adaptors in a CUL3(BOP1/BO

271 ignificantly lower GI score was seen but the BOP score was unchanged.

272 on of the leaf, demonstrating a role for the BOP proteins as proximal-distal as well as adaxial-abaxi

273 attempt to gain mechanistic insight into the BOP-mediated reaction has been made using (31)P{(1)H} NM

274 clude that mild bTBI occurs in rats when the BOP is in the range of 85-145 kPa.

275 Compared with the BOP/vehicle group, NO-ASA reduced the incidence (88.9%,

276 essures indicate that any erosion within the BOP had little affect on cumulative discharge.

277 These BOP ligands were applied to a Pd-catalyzed intermolecula

278 TMF and three tomato BOPs (SlBOPs) interact with themselves and each other, a

279 The enhanced mobilization observed using BOP and AMD3100 is recapitulated in a humanized NODSCIDI

280 e healing response were also performed using BOP, gingival index (GI), and plaque index (Pl) at basel

281 Crack users had greater VPI, BOP, PD >/=3 mm, and CAL >/=4 mm than crack non-users.

282 The primary measure of interest was BOP in patients clinically demonstrating naturally occur

283 ic engraftment augmentation is observed when BOP is co-administered with AMD3100.

284 ificantly greater for older patients whereas BOP and calculus levels were relatively constant across

285 sed on 35%, and 70% PMR, respectively, while BOP above 290 kPa is lethal.

286 s (57%) with BEP/EP and 72 of 186 (54%) with BOP/VIP-B (P = 0.687).

287 h PD >/=4 mm and CAL >/=3 mm associated with BOP.

288 EP/EP, and there were more toxic deaths with BOP/VIP-B than BEP/EP (18 [9%] v nine [5%]).

289 1 was conjugated to 4-hydroxypiperidine with BOP and N-methylmorpholine, and the resulting 5-(N-pipyr

290 to screen for diabetes in most persons with BOP at the GCB collection site.

291 a, and weight loss were more pronounced with BOP/VIP-B than with BEP/EP, and there were more toxic de

292 e AI group had significantly more sites with BOP (27.8 versus 16.7; P = 0.02), higher worst-site AL (

293 sia, with increased percentage of sites with BOP and greater AL.

294 high sensitivity for at least two sites with BOP and two sites with periodontal pockets but a lower r

295 Mean number and percentage of sites with BOP decreased from 10.7 +/- 11.6 (mean +/- SD) and 6.5%

296 82.6% sensitive for at least two sites with BOP.

297 (N); gingiva adjacent to a 3-mm sulcus with BOP was classified as "diseased, slight" (DS); gingiva a

298 re classified as healthy, whereas those with BOP in >or=10% of sites were defined as having biofilm-g

299 l carcinoma from hamster islets treated with BOP in vitro.

300 ingiva adjacent to a <or=3-mm sulcus without BOP was classified as "normal" (N); gingiva adjacent to