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 showed significantly higher values in group 3 as com

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

6 BOP was significantly higher among controls than WPs (P

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

8 BOP, PI, and GI showed significant clinical improvements

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

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

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

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

13 Peri-implant PI (P <0.01), BOP (P <0.01), PD (P <0.01), and CBL (P <0.01) were sign

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

15 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

16 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

17 The GI score (P = 0.039), BOP% (P = 0.023), serum CRP level (P < 0.001) and oral p

18 as more effective in reducing PI (P < 0.05), BOP (P < 0.05) and PD (P < 0.05) at 3-month follow-up.

19 Peri-implant PI (P <0.05), BOP (P <0.05), PD (P <0.05), and CBL (P <0.05) were sign

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

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

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

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

24 <0.01), PD (all time points: P <0.001), and BOP (3 months: P <0.05; 6 months: not statistically sign

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

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

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

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

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

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

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

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

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

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

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

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 ps resulted in significant changes in GI and BOP at Day 42 compared to control and un-flossed control

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

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

42 =50%; and 5) P3, >/=1 site with PD >3 mm and BOP >50%.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

57 showed positive correlation with GI, PI, and BOP in both groups.

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

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

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

61 wer relationship for single-site pockets and BOP.

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

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

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

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

66 provements in clinical outcomes (PD and CAL, BOP) from baseline to 12 months.

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

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

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

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

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

72 become edematous and more likely to develop BOP.

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

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

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

76 associated with blast overpressure exposure (BOP) in Warfighters and civilians, yet little is known a

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

78 lung injury was identified at 24 h following BOP by assessing the extent of surface hemorrhage/contus

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

80 and 2 continued having reduced levels of GI, BOP, and PI at Day 60 (P<0.05).

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

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

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

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

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

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

87 methylamino)phosphonium hexafluorophosphate (BOP).

88 : 95.00%, specificity: 100%) and defined HI: BOP <=0.25%; PIM: BOP >0.25%, PD <=4.5 mm; PIMP: BOP >0.

89 Children with CF had significantly higher BOP scores (P = 0.001) and calprotectin levels (P = 0.01

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

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

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

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

94 Peri-implant BOP was significantly higher among CS and NS with T2DM t

95 th plant defense, are essential cofactors in BOP-dependent regulation of development.

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

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

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

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

100 bo groups showed significant improvements in BOP, PD, and CAL after periodontal surgical procedures (

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

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

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

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

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

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

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

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

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

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

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

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

113 Our ML BOP models predict both the correct experimental melting

114 arned coarse-grained (CG) models (ML-BOP, ML-BOP(dih), and ML-mW) that accurately describe the struct

115 chine-learned coarse-grained (CG) models (ML-BOP, ML-BOP(dih), and ML-mW) that accurately describe th

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

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

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

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

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

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

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

123 2 mm) and one healthy site (PD </= 3 mm, no BOP) from each individual at baseline and 3 and 6 months

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

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

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

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

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

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

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

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

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

133 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

134 neral obesity was noted on the percentage of BOP.

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

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

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

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

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

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

141 iodontal parameters of VPI, GBI, PD, CAL, or BOP 2 years after completion of the periodontal therapy.

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

143 s and combinations (i.e. blast overpressure (BOP) intensity and exposure frequency) using an advanced

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

145 PD, BOP, API, and the number of sites with PD >=5 mm were si

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

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

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

149 ng depth >=4 mm with bleeding on probing (PD/BOP) or with clinical attachment level >=4 mm (CAL).

150 inks during pregnancy was associated with PD/BOP (MR = 1.34; 95% confidence interval (CI): 1.03 to 1.

151 associated with the number of teeth with PD/BOP in pregnant women, suggesting that beverage consumpt

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

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

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

155 Peri-implant PI, BOP, PD, and CBL were measured.

156 y significant difference in peri-implant PI, BOP, PD, and mesial and distal CBL among individuals in

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

158 significant difference in the scores of PI, BOP, PD, clinical AL and MBL when SRP was performed with

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

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

161 Periodontal parameters (PI, BOP, PD, clinical AL and mesial and distal MBL) were mea

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

163 ity: 100%) and defined HI: BOP <=0.25%; PIM: BOP >0.25%, PD <=4.5 mm; PIMP: BOP >0.25%, PD >4.5 mm an

164 %, PD >4.5 mm and RANKL <=19.9 pg/site; PIM: BOP >0.25%, PD >4.5 mm, and RANKL >19.9 pg/site.

165 <=0.25%; PIM: BOP >0.25%, PD <=4.5 mm; PIMP: BOP >0.25%, PD >4.5 mm and RANKL <=19.9 pg/site; PIM: BO

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

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

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

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

170 o probing depths > 5mm, bleeding on probing (BOP) <=25%, no pain and satisfactory function.

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

172 RP outcomes in terms of bleeding on probing (BOP) (OR = 1.02, P <0.05) and mean PD (P <0.05) reductio

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

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

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

176 attachment level (CAL), bleeding on probing (BOP) and microbiological assays (PCR) were evaluated bef

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

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

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

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

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

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

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

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

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

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

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

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

189 plaque score (VPS), and bleeding on probing (BOP) were assessed and compared.

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

191 Gingival index (GI) and bleeding on probing (BOP) were evaluated in addition to plaque index (PI), po

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 probing depth (PD), and bleeding on probing (BOP) were recorded as the clinical outcomes.

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

197 , plaque index, GI, and bleeding on probing (BOP) were recorded at baseline, 3 and 6 months.

198 plaque index (PI), and bleeding on probing (BOP) were recorded on fully erupted teeth and saliva sam

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

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

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

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

203 gival crevicular fluid, bleeding on probing (BOP), and interleukin-1beta were tested (ELISA) at basel

204 (PD), attachment level, bleeding on probing (BOP), and interproximal plaque index (API) were signific

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

206 lant plaque index (PI), bleeding on probing (BOP), and probing depth (PD) were evaluated and crestal

207 lant plaque index (PI), bleeding on probing (BOP), and probing depth (PD) were recorded and marginal

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

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

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

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

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

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

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

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

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

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

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

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

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

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

222 ingival recession (GR), bleeding on probing (BOP), plaque index (PI), and count of 40 subgingival mic

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

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

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

226 Bleeding on probing (BOP), plaque index, and probing depth (PD) were confirme

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

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

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

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

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

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

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

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

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

236 lant plaque index (PI), bleeding on probing (BOP), probing depth (PD), and mesial and distal CBL were

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

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

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

240 ingival index (GI), and bleeding on probing (BOP), were compared for M2 at baseline (T0) and 6-months

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

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

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

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

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

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

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

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

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

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

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

252 o 24.53%, P = 0.75) for bleeding on probing (BOP); a WMD of 0.36 mm (95% CI = 0.12 to 0.59 mm, P = 0.

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

254 outh plaque-index (PI), bleeding-on-probing (BOP), probing depth (PD), clinical attachment loss (AL),

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

256 plaque index [PI], and bleeding on probing [BOP] in shamma users and non-users [controls] with chron

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

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

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

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

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

262 rs (probing depth [PD], bleeding on probing [BOP], and clinical attachment loss (CAL); P < 0.05).

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

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

265 les (plaque index [PI], bleeding on probing [BOP], probing depth (PD) and crestal bone loss [CBL]) ar

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

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

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

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

270 ps showed significant improvements regarding BOP, PD, and CAL compared to baseline, with no significa

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

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

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

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

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

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

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

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

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

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

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

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

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

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

285 Male Sprague Dawley rats were exposed to BOP frontally and laterally at a pressure range of ~ 8.5

286 d blast simulator was used to expose rats to BOP and assessments were made to identify structural and

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

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

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

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

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

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

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

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

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

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

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

298 82.6% sensitive for at least two sites with BOP.

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

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

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