ライフサイエンスコーパス: PGA

1 PGA is produced by the Gram-negative periodontopathogen

2 PGA is user friendly software that can facilitate decisi

3 PGA levels were triphasic; they were nondetectable at 24

4 PGA mediates intercellular adhesion and attachment of ce

5 PGA mutase activity was dependent upon the presence of d

6 PGA overproduction appeared to be the result of an incre

7 PGA production was undetectable in an nhaR mutant strain

8 PGA-specific antibodies bound to encapsulated bacilli an

9 te, phosphate, and 2-phosphoglyceric acid (2-PGA).

10 The formation of pyruvate and 2-PGA suggests that the reaction catalyzed by KDO8-P synth

11 nduced structural perturbations in apo and 2-PGA-bound forms of TIM that are atypical of WT.

12 dered kinetic mechanism wherein binding of 2-PGA precedes binding of the second metal ion, and releas

13 n-intermediate analog, 2-phosphoglycolate (2-PGA).

14 3-PGA acts synergistically with both ATP and ADP-Glc in he

15 h are activated by 3-phosphoglyceric acid (3-PGA) and inhibited by phosphate.

16 classic regulators 3-phosphoglyceric acid (3-PGA) and inorganic phosphate (Pi) stabilize maize (Zea m

17 lly activated with 3-phosphoglyceric acid (3-PGA).

18 AGPase to the same extent as the activator 3-PGA, albeit with higher K(a) (activation constant) value

19 n both the small and large subunits--bound 3-PGA more weakly than the wild type (A(50) increased by 3

20 not always mimic the changes observed for 3-PGA.

21 In addition, extent of 3-PGA activation and extent of 3-PGA affinity were found t

22 , extent of 3-PGA activation and extent of 3-PGA affinity were found to be separate entities, mapping

23 In the presence of 3-PGA, ADP-Glc is a competitive inhibitor with respect to

24 In the presence of 3-PGA, enzyme properties of Mos(1-198)/SH2 are quite simil

25 In the absence of 3-PGA, however, the mosaic enzyme exhibits greater activit

26 Finally, in the absence of 3-PGA, inorganic phosphate, a classic inhibitor or antiact

27 In the absence of 3-PGA--with or without 5.0 mm inorganic phosphate--ADP-Glc

28 e, is a potent inhibitor in the absence of 3-PGA.

29 e-6-P and Glc-6-P is comparable to that of 3-PGA.

30 When 3-phosphoglycerate (3-PGA), the putative physiological activator, was present

31 norganic phosphate and 3-phosphoglycerate (3-PGA).

32 y enhanced catalytic activity and restored 3-PGA activation.

33 In fact, compared to 3-PGA, fructose-6-phosphate is a more efficient activator

34 equential mechanism was also followed when 3-PGA was absent, but product inhibition patterns changed

35 r the binding interactions associated with 3-PGA in which allosteric activators and inorganic phospha

36 on of the (32)P-labeled phosphoenzyme with 3-PGA resulted in the disappearance of radioactive phospha

37 rtensive use (OR, 7.05 [CI, 3.05 to 16.31]), PGA score greater than 1 (OR, 4.02 [CI, 1.84 to 8.82]),

38 The addition of 0.9% PGA caused 7S, 11S, daidzein and genistein to coacervate

39 raction (SPF) following incubation with 0.9% PGA for 1h.

40 the 7S and 11S proteins into the SPF by 0.9% PGA.

41 A PGA response was achieved by 155 (47.1%) of 329 patients

42 ) [corrected] in the 100 mg group achieved a PGA response, compared with 7 patients (4%) in the place

43 ) and the proportion of patients achieving a PGA score of "clear" or "almost clear" (PGA response), a

44 lycaprolactone sheet seeded with SMCs, and a PGA sheet seeded with fibroblast, were wrapped in turn o

45 A pipeline with an R package, assigned as a PGA utility, was developed that enables automated treatm

46 nt of wild-type biofilms with dispersin B, a PGA-degrading enzyme, rendered them sensitive to detachm

47 t week 40, the proportion of patients with a PGA score of 0 or 1 remained significantly higher in the

48 t week 16, the proportion of patients with a PGA score of 0 or 1 was significantly higher in each gus

49 sule mutant, and a poly-N-acetylglucosamine (PGA) mutant.

50 patients (58%) in the 100 mg group achieved PGA responses, compared with 11 patients (7%) in the pla

51 52, 79.2% of q4-wk-treated patients achieved PGA "clear/minimal" compared with 41.6% and 6.0% of q12-

52 s. 4.3% of placebo-treated patients achieved PGA "clear/minimal," and 80.7% vs. 4.5%, respectively, a

53 er imputation compared proportions achieving PGA "clear/minimal" (weeks 12 and 52) and >/=75% improve

54 thick fabricated from poly-l-glutamic acid (PGA) and poly-l-lysine (PLL) can be loaded, post-fabrica

55 hagocytic gamma-linked poly-d-glutamic acid (PGA) capsule and two binary toxins, complexes of protect

56 oly-l-lysine (PLL) and poly-l-glutamic acid (PGA) in their non-alpha-helical states.

57 rmidis secretes poly-gamma-DL-glutamic acid (PGA) to facilitate growth and survival in the human host

58 ugating capsular poly-gamma-d-glutamic acid (PGA) to protective antigen (PA), converting the weakly i

59 ently linked to poly(alpha)-L-glutamic acid (PGA) via reducible disulfide and acid-sensitive hydrazon

60 kin prick test for poly-gamma-glutamic acid (PGA) which is a component of jellyfish stings was negati

61 tide composed of poly-gamma-D-glutamic acid (PGA).

62 , covalently linked to poly-l-glutamic acid (PGA).

63 Our method simply uses photogenerated acid (PGA) in solution to trigger deprotection of the 5'-OH gr

64 P was first conjugated to polyglutamic acid (PGA) to form anionic PGA-CDDP which was electrostaticall

65 ain viability relative to polyglycolic acid (PGA) non-woven mesh controls.

66 A polyglycolic acid (PGA) sheet and a polycaprolactone sheet seeded with SMCs

67 iomerically pure D- and L-pyroglutamic acid (PGA) are capable of recurring self-actuation due to rapi

68 Poly(glycolic acid) (PGA) fiber scaffolds were wrapped around the hydrogels,

69 e further show that A. actinomycetemcomitans PGA cross-reacts with antiserum raised against polysacch

70 the synthesis of the polysaccharide adhesin PGA (poly-beta-1,6-N-acetyl-d-glucosamine) of Escherichi

71 d levels of platelet/granulocyte aggregates (PGAs) are found in patients suffering from many differen

72 investigated the propylene glycol alginate (PGA)-induced coacervation of beta-conglycinin (7S), glyc

73 d in a vehicle of propylene glycol alginate (PGA).

74 A pheromone trail-based genetic algorithm (PGA) was used to search globally for the optimal placeme

75 All PGAs increased MMP-1, -3, and -9.

76 All PGAs increased TIMP-3, but only unoprostone increased TI

77 h 85.0% of eyes in the prostaglandin analog (PGA) group (P < 0.001), and qualified success (IOP </=21

78 atients were receiving prostaglandin analog (PGA) monotherapy.

79 mized to either SLT or prostaglandin analog (PGA; travoprost, 0.004%).

80 ffectiveness of the prostaglandin analogues (PGAs) bimatoprost, latanoprost, and unoprostone.

81 he "Power for Genetic Association analyses" (PGA) package which comprises algorithms and graphical us

82 Because PGA(1) and PGA(2) have previously been shown to be peroxisome proli

83 of isopeptidase activity, whereas PGA(1) and PGA(2) with simple alpha,beta-unsaturated pentenones wer

84 The cyPG, PGA(1) and PGA(2), inhibited HIV-1 replication in acutely infected

85 eration was observed for PGA-TMC/rhBMP-2 and PGA-TMC control sites.

86 asurements indicate that PLL (at pH = 2) and PGA (at pH = 9) exist mainly in a mixture of polyproline

87 modified Facial SASI (0.40 [0.17-0.72]), and PGA scores (0.40 [0.18-0.70]).

88 proportion of patients achieving PASI 75 and PGA response (score of 0 or 1 with >/=2 grade score redu

89 CSAMI Activity scale (0.69 [0.51-0.87]) and PGA (0.66 [0.47-0.85]), weak for the CSAMI Damage scale

90 icient at increasing complement activity and PGA formation.

91 EMD (containing AMEL and PGA) or PGA alone eliminated recoverable CFUs of P. ging

92 ing units/ml was treated with EMD, AMEL, and PGA in Hank's balanced salt solution (HBSS) for 1, 3, an

93 atients with DM using the CDASI, CAT-BM, and PGA scales.

94 the horizontally acquired pgaABCD operon and PGA biosynthesis at multiple levels.

95 y higher levels of antibodies against PA and PGA than PA-PGA conjugate.

96 e report the characterization of LF, PA, and PGA levels during the course of inhalation anthrax in fi

97 In addition, we find that a PLL and PGA mixture at neutral pH is approximately 60% beta-shee

98 ctions in daily health assessment scores and PGA scores compared with baseline levels (P < 0.05).

99 here were no differences between the SLT and PGA groups in the absolute mean reduction of IOP (4.0 vs

100 symptoms, as measured by WOMAC subscales and PGA scores, was observed in all groups, with no treatmen

101 cells, whereas TGN-LVs containing the XG and PGA/RG-I epitopes fuse with the plasma membrane of both

102 d to polyglutamic acid (PGA) to form anionic PGA-CDDP which was electrostatically complexed with the

103 or in subgroups based on previous use of any PGA, any non-PGA, latanoprost, or travoprost monotherapi

104 Pediatric granulomatous arthritis (PGA) has been associated with 12 different substitutions

105 erity and the Physician's Global Assessment (PGA) as a reference instrument.

106 T-BM), with the Physician Global Assessment (PGA) as the "gold standard".

107 endpoints were Physician Global Assessment (PGA) at week 4 and change from baseline to 4 weeks in th

108 recalled using the Parent Global Assessment (PGA) measure.

109 ns in which the physician global assessment (PGA) of disease activity was the dependent variable, we

110 AS/WG and the physician's global assessment (PGA) of disease activity were high, even when patients i

111 higher and a Physician's Global Assessment (PGA) of moderate or severe, and had failed to respond to

112 lear or minimal physician global assessment (PGA) score at week 16, comparing adalimumab 0.8 mg/kg wi

113 tients with a Physician's Global Assessment (PGA) score of 0 (indicating cleared psoriasis) or 1 (ind

114 (WOMAC) index and patient global assessment (PGA) scores, and in slowing radiographic progression.

115 ssment forms, physician's global assessment (PGA), and measurement of inflammatory markers including

116 ints included physician's global assessment (PGA), time to response, response duration, and time to p

117 ated with the Physician's Global Assessment (PGA).

118 Index and the Physician's Global Assessment (PGA).

119 ement >/=10%, Physician's Global Assessment [PGA] score >/=3, and Psoriasis Area and Severity Index [

120 uboptimal (HS Physician's Global Assessment [PGA] score of moderate or worse) at weeks 28 or 31.

121 (score on the physician's global assessment [PGA]).

122 lly reduced, and it had less cell-associated PGA.

123 NOD2-associated PGA can be a multisystem disorder with significant visce

124 Because PGA(1) and PGA(2) have previously been shown to be perox

125 dditionally, interobserver agreement between PGA and PtGA scores was good (acne, kappa = 0.68; psoria

126 Specific binding between PGA and LPS was consistently detected by surface plasmon

127 acetylase catalytic activity of PgaB blocked PGA export and biofilm formation, implying that N-deacet

128 ion were similar between the two meshes, but PGA constructs had contracted significantly.

129 When activation by PGA is accounted for, the catalytic rate for the "active

130 s, polyglycolic acid-trimethylene carbonate (PGA-TMC) membrane combined with a rhBMP-2 construct in a

131 ic polyglycolic acid/trimethylene carbonate (PGA/TMC) barrier membrane with an increased absorption t

132 jection of debris or splintering, the chiral PGA crystals respond to internal strain with unprecedent

133 ng a PGA score of "clear" or "almost clear" (PGA response), analysed in the full analysis set (all pa

134 monoclonal antibody directed against E. coli PGA, we now demonstrate that PgaD is also needed for PGA

135 The cyPG, PGA(1) and PGA(2), inhibited HIV-1 replication in acutel

136 On the basis of a published dataset, PGA was employed to identify peptides, resulting in 636

137 hydrolase named dispersin B, which degrades PGA.

138 I alone is more immunogenic than PA, and DNI-PGA conjugate elicits significantly higher levels of ant

139 al nucleotide phosphoramidite monomers (i.e. PGA-gated deprotection), with the rest of the reactions

140 that the protein was a moderately effective PGA mutase that also exhibited low levels of phosphohydr

141 complement-mediated mechanisms that enhance PGA formation in human whole blood stimulated with throm

142 y, our data indicate that properdin enhances PGA formation via increased production of C5a, and that

143 nts important novel biological functions for PGA and indicates that PGA represents an excellent targe

144 ion of the pgs operon that encodes genes for PGA synthesis.

145 now demonstrate that PgaD is also needed for PGA formation.

146 mited cementum regeneration was observed for PGA-TMC/rhBMP-2 and PGA-TMC control sites.

147 ent glycosyltransferase that is required for PGA synthesis.

148 hat it forms the outer membrane secretin for PGA.

149 2) and PGD(2), or PGB(2), which differs from PGA(2) only in that its electrophilic carbon is rendered

150 Furthermore, PGA protected S. epidermidis from high salt concentratio

151 ed to purified Nod factor and to poly-GalUA (PGA) heptamers.

152 cation of gamma-poly-dl-glutamic acid (gamma-PGA) as an exopolymer that increases biofilm formation,

153 Poly-gamma-glutamic acid (gamma-PGA) is an important biochemical product with a variety

154 ponsible for poly-gamma-glutamic acid (gamma-PGA) synthesis), were intentionally knocked out in the B

155 ation of these regulators as affecting gamma-PGA production and biofilm formation suggests that these

156 omestic strain was sufficient to allow gamma-PGA production.

157 In addition to controlling gamma-PGA production, ComPA and DegSU were also shown to activ

158 he genes pgsB and pgsC responsible for gamma-PGA biosynthesis were increased by 8.21- and 5.26-fold,

159 ogenase), WX-zwf, produced the highest gamma-PGA concentration (9.13 g/L), 35% improvement compared t

160 rk reports a novel approach to improve gamma-PGA through over expression of key enzymes in cofactor N

161 Production of gamma-PGA by Bacillus subtilis was known to be dependent on th

162 estic strain of B. subtilis to produce gamma-PGA was mapped to two base pairs; a single base pair cha

163 generation were over-expressed in the gamma-PGA producing strain B. licheniformis WX-02.

164 s an effective strategy to improve the gamma-PGA production in B. licheniformis.

165 As predicted, if poly-beta-1,6-GlcNAc (PGA) mediates cohesion, metaperiodate caused biofilm dis

166 1,6-N-acetyl-D-glucosamine (beta-1,6-GlcNAc; PGA) serves as an adhesin for the maintenance of biofilm

167 dhesin poly-beta-1,6-N-acetyl-D-glucosamine (PGA) by binding to the pgaABCD mRNA leader, inhibiting p

168 dhesin poly-beta-1,6-N-acetyl-d-glucosamine (PGA).

169 ugating the capsular poly-gamma-d-glutamate (PGA) with PA to elicit the production of antibodies spec

170 extracellular polymer poly-gamma-glutamate (PGA) to confer a mucoid colony phenotype.

171 Hence, PGA can identify novel peptides and generate an HTML-bas

172 polygalacturonic acid/rhamnogalacturonan-I (PGA/RG-I) are detected in the trans-most cisternae and T

173 igen (PA), converting the weakly immunogenic PGA to a potent immunogen, and synergistically enhancing

174 Importantly, PGA efficiently sheltered S. epidermidis from key compon

175 Lupus flare was defined as an increase in PGA of > or = 1.0, M-SLEDAI > or = 3, M-LAI > or = 0.1,

176 auses an approximately threefold increase in PGA production and an approximately sevenfold increase i

177 tor prevents properdin-mediated increases in PGA formation.

178 All physiological properdin forms increase PGA formation, but properdin tetramers are the most effi

179 ation in diseases characterized by increased PGA formation.

180 ment alternative pathway activity, increases PGA formation when added to TRAP-stimulated blood.

181 part of the innate immune system, influences PGA formation, but the mechanisms for its effects are un

182 e cohorts of PGA patients, the International PGA Registry and a Spanish cohort.

183 several phylogenetically diverse bacteria is PGA, a linear polymer of N-acetylglucosamine residues in

184 nt of the Escherichia coli biofilm matrix is PGA, a linear polymer of N-acetyl-D-glucosamine residues

185 all other kinetic parameters (i.e., K(m), K(PGA), etc.) being nearly the same.

186 n ATM mutant MCL cell line, an ATM knockdown PGA CLL cell line, and 9 ATM-deficient primary CLLs indu

187 the concomitant appearance of (32)P-labeled PGA at rates comparable to those measured in steady-stat

188 Longitudinal PGA severity scores were collected for acne and psoriasi

189 Our findings suggest that the LT PGA/TMC barrier membrane, used in conjunction with an al

190 ter a GBR procedure using the long-term (LT) PGA/TMC membrane and an allograft in a thermoplastic car

191 In the presence of 20 micro M PGA(1), p53 accumulated preferentially in the cytosol.

192 bioabsorbable, space-providing, macroporous PGA-TMC membrane appears to be a compatible biomaterial

193 and became incorporated into the macroporous PGA-TMC membrane in sites receiving rhBMP-2.

194 Mean PGA score at week 4 was 0.6 (SD 1.0) in the placebo grou

195 locally by leukocytes, impairs TRAP-mediated PGA formation to the same level as specific inhibition o

196 methotrexate group achieved clear or minimal PGA (p=0.083).

197 on of patients who achieved clear or minimal PGA compared with methotrexate.

198 ASI75 and 16 (41%) achieved clear or minimal PGA.

199 an's global assessment "clear" or "minimal" (PGA "clear/minimal") at week 12 were then re-randomized

200 st, patients who continued taking brand name PGAs were 28% less likely to have improved adherence (od

201 ween persons who continued to use brand-name PGAs once generic latanoprost became available and other

202 ps based on previous use of any PGA, any non-PGA, latanoprost, or travoprost monotherapies.

203 Notably, PGA was synthesized by all tested strains of S. epidermi

204 synthesis of cyclic di-GMP, an activator of PGA production.

205 to those measured in steady-state assays of PGA mutase activity.

206 We report a case of PGA in a 6-year-old girl with the NOD2 E383K gene substi

207 on of PGA may explain the rapid clearance of PGA that is observed in vivo compared to the slow cleara

208 ed merged data from 2 prospective cohorts of PGA patients, the International PGA Registry and a Spani

209 d as a function of time and concentration of PGA(1).

210 ased with exposure time and concentration of PGA(1).

211 This degradation of PGA may explain the rapid clearance of PGA that is obser

212 plants with Nod factor alters the effect of PGA by limiting the maximum H(2)O(2) efflux rate to 125%

213 n about the uptake and intracellular fate of PGA.

214 d the primary amine content (glucosamine) of PGA.

215 also revealed a conditional localization of PGA at the cell poles, the initial attachment site for b

216 ellular uptake and organelle localization of PGA in the murine macrophage-like cell line J774.2.

217 pgs operon, suggesting a second mechanism of PGA control.

218 The pipeline of PGA, aimed at being platform-independent and easy-to-use

219 ion and expression of p53 in the presence of PGA(1) and celecoxib, a selective COX-2 inhibitor in hum

220 d 2.1 in the controls and in the presence of PGA(1) in HCT-116 cells but were 22 and 4, respectively,

221 rain that was deficient in the production of PGA (poly-N-acetyl-glucosamine), a biofilm matrix polysa

222 ith the reduced expression and production of PGA.

223 tions in known transcriptional regulators of PGA synthesis (Com and Deg two-component systems) as wel

224 The X-ray crystal structures of PGA bound to the H98Q and H98N variants were both determ

225 ne oxide inhibited the binding and uptake of PGA in these cells.

226 An extended version of PGA can predict additional candidate connections for eac

227 th significantly higher flare rates based on PGA (18 of 84, 21%; P = 0.0014), M-SLEDAI (27 of 89, 30%

228 demonstrate that the effects of properdin on PGA formation are tightly regulated by Factor H.

229 ponders (good, excellent, or clear rating on PGA), compared with two of 11 (18%) in the placebo group

230 EMD (containing AMEL and PGA) or PGA alone eliminated recoverable CFUs of P. gingivalis.

231 caused by A. actinomycetemcomitans and other PGA-producing bacteria.

232 ontinuation of use as generic forms of other PGA agents become available.

233 itory (DNI) mutant to replace PA in PA or PA-PGA vaccines.

234 els of antibodies against PA and PGA than PA-PGA conjugate.

235 New patient PGA outcomes showed considerable improvement over time.

236 osphoglycerate-independent phosphoglycerate (PGA) mutases [iPGMs].

237 d the competitive inhibitor phosphoglyolate (PGA) acts as an activator of this variant.

238 brane proteins PgaA and PgaB did not prevent PGA synthesis but did block its export, as shown by the

239 tion, implying that N-deacetylation promotes PGA export through the PgaA porin.

240 l for antigen clearance showed that purified PGA accumulates in the liver and spleen, most notably in

241 compromised regeneration in sites receiving PGA-TMC/rhBMP-2.

242 patients with psoriasis in clinic, recording PGA scores for each patient.

243 Residual PGA-TMC could not be observed at 24 weeks postsurgery.

244 le and renal clearance route of the selected PGA-doxy candidate, settling the adequacy of our conjuga

245 randomly assigned to receive the dome-shaped PGA-TMC (100 to 120 microm pores) membrane with rhBMP-2

246 ly maps all publicly available gene-specific PGA data onto LocusLink using dynamically generated cros

247 a DeltapgaC mutant, which cannot synthesize PGA.

248 e was sensitized to some allergen other than PGA via a route different from that of jellyfish sting.

249 We concluded that PGA protects A. actinomycetemcomitans cells from detachm

250 Our findings confirm that PGA functions as a biofilm matrix polysaccharide in phyl

251 Our results demonstrated that PGA is a potent coagulant for the coacervation of 7S, 11

252 resent genetic and biochemical evidence that PGA is also a major matrix component of biofilms produce

253 We found that PGA binds to and is internalized by J774.2 cells and acc

254 Finally, we found that PGA is degraded in J774.2 cells starting 4 h after uptak

255 logical functions for PGA and indicates that PGA represents an excellent target for therapeutic maneu

256 Therefore, we propose that PGA serves as an adhesin that stabilizes biofilms of E.

257 We also show that PGA is a substrate for dispersin B, a biofilm-releasing

258 g on simulated and real data sets shows that PGA significantly outperforms previous methods, especial

259 y diverse bacterial species and suggest that PGA may play a role in intercellular adhesion and cellul

260 The PGA can be readily incorporated into practice to track p

261 The PGA severity scores were analyzed over time, with the hy

262 The PGA severity scores were included on physicians' billing

263 The PGA-TMC biomaterial was occasionally associated with a l

264 trains, the biofilm of the O antigen and the PGA mutants was dramatically reduced, and it had less ce

265 tion coefficient between the BVAS/WG and the PGA was r = 0.81 (95% confidence interval 0.73-0.87).

266 = 0.93 for the BVAS/WG and r = 0.88 for the PGA in the first and r = 0.91 for the BVAS/WG and r = 0.

267 = 0.91 for the BVAS/WG and r = 0.88 for the PGA in the second.

268 Furthermore, the PGA-gated chemistry should be applicable to microarray s

269 1) and by 4.2 mm Hg (95% CI, 3.5-4.9) in the PGA group (P < .001).

270 LT group, compared with 84.0% of eyes in the PGA group (P = .008).

271 s in the SLT group compared with 8.0% in the PGA group (P = .05).

272 , 49 patients in the SLT group and 47 in the PGA group completed follow-up.

273 Two patients in the PGA group exited owing to drug-related complications (1

274 efined as a 1.0 (or greater) increase in the PGA, a 3-point increase in the M-SLEDAI, a 0.1 increase

275 he CAT-BM were significant predictors of the PGA scales.

276 ares occurred at 12% of visits, based on the PGA measure of disease activity.

277 lares occurred at 12% of visits based on the PGA, 19% based on the M-SLEDAI, 25% based on the M-LAI,

278 czema severity as recalled by parents on the PGA, estimated by the within-patient score change (4.27)

279 bioresorbable hyaluronan (Hy) carrier or the PGA-TMC membrane with Hy alone (control).

280 effect in the scoring of the BVAS/WG or the PGA.

281 y score with the highest R(2) to predict the PGA.

282 Jaw quadrants receiving the PGA-TMC membrane alone experienced exposures at various

283 gnificantly increased in sites receiving the PGA-TMC/rhBMP 2 combination compared to control (3.8 +/-

284 Jaw quadrants receiving the PGA-TMC/rhBMP-2 combination remained intact, although on

285 ing 20 to 30 min after exposure, whereas the PGA elicitor, at > 75 nM, caused a rapid increase in H(2

286 owed moderate correlations (95% CI) with the PGA (0.67 [0.57-0.75] and 0.57 [0.45-0.66], respectively

287 The highest R(2) with the PGA was obtained by scoring WG activity based on the fol

288 d soft tissue healing when combined with the PGA-TMC membrane.

289 e PDAI also correlated more closely with the PGA.

290 related significantly more strongly with the PGA.

291 ndomized to SLT and 50 patients (99 eyes) to PGA medical therapy.

292 t is genetically and structurally related to PGA.

293 adherence rates were calculated for topical PGA use during the 18 months before the introduction of

294 e employed; three anchor-based methods using PGA as the anchor: the within-patient score change, betw

295 inhibitor of isopeptidase activity, whereas PGA(1) and PGA(2) with simple alpha,beta-unsaturated pen

296 bset of clinics and dates were compared with PGA scores to assess within-clinic reliability, with the

297 rates and lower IOP reduction compared with PGA therapy in eyes with persistent appositional angle c

298 statistically significant correlations with PGA scores.

299 Forty-five patients with PGA (23 sporadic cases and 22 from familial pedigrees) a

300 ering effectiveness in clinical studies with PGAs.