ライフサイエンスコーパス: GTR

1 GTR is related to better prognosis.

2 GTR procedure was performed in furcation defect sites us

3 GTR provides clinicians with the opportunity to reverse

4 GTR therapy utilizing bioabsorbable membranes offers the

5 GTR therapy was associated with significantly lower CV f

6 GTR was observable as a 49-kDa band on sodium dodecyl su

7 GTR-based procedures with or without combined grafting t

8 GTR-based root coverage utilizing collagen membrane, wit

9 enerative therapy (seven DBM, 22 BRG, and 26 GTR) to OFD and meeting inclusion criteria provided mean

10 Purified His(6)-GTR was catalytically active in vitro when it was incuba

11 eases the regenerative potential of MPP as a GTR membrane and results in increased defect fill.

12 ccumulate in the leaf abaxial epidermis in a GTR-independent manner.

13 cid sequence has more than 55% identity to a GTR sequence of Arabidopsis thaliana, and significant si

14 to compare these 2 techniques, SCTG versus a GTR-based procedure (GTRC), for root coverage/recession

15 finity column chromatography to yield active GTR.

16 After GTR, CAL gains were 4.6 +/- 2 mm.

17 TFE membranes, recovered from patients after GTR; cells adherent to ePTFE augmentation membranes, rec

18 as greater than 96% more than 10 years after GTR.

19 DBM was discernible in all GTR+DBM defects with limited, if any, evidence of bone m

20 by use of the bioabsorbable membrane alone (GTR, or control group).

21 emineralized freeze-dried bone allograft and GTR and superior to open flap debridement procedures in

22 ignificantly augment the effects of BPBM and GTR in promoting the clinical resolution of intrabony de

23 The individual role played by PRP, BPBM, and GTR in this combined therapy is unclear and needs to be

24 Although differences between CTG and GTR in mean root coverage and prevalence of complete cov

25 Differences between GTR+DBM and GTR defects were evaluated using a paired t-test (N = 6)

26 n 2.0+/-1.3 and 1.6+/-1.7 mm for GTR+DBM and GTR defects, respectively.

27 ation were observed for both the GTR+DBM and GTR defects.

28 DBM and GTR therapy support more consistent improvements in clin

29 mbination technique including BPBM, EMP, and GTR results in better clinical resolution of intrabony d

30 VBF in MBA and GTR + MBA groups was significantly higher than that in t

31 /-0.9 mm, and 1.1+/-0.9 mm for OFD, MBA, and GTR+MBA groups, respectively.

32 bout 2-fold at 2 h into the light phase, and GTR protein levels also increased and peaked 2-fold at 4

33 g the use of combination techniques, such as GTR procedures with osseous grafts.

34 PRGF with GTR, as well as GTR alone, was effective in improving clinical and radio

35 ut further therapy, which supports attempted GTR of cerebral and cerebellar hemisphere low-grade astr

36 = 2 mm compared with the CAL observed before GTR treatment, and loss of > or = 2 mm compared with the

37 Differences between GTR+DBM and GTR defects were evaluated using a paired t-

38 FE) membranes were used to provide bilateral GTR.

39 tudy show that both combinations of PRP/BPBM/GTR and PRP/BPBM are effective in the treatment of intra

40 /- 0.83 mm on lingual sites for the PRP/BPBM/GTR group.

41 /- 0.92 mm on lingual sites for the PRP/BPBM/GTR group.

42 4.74 +/- 1.30 mm on lingual sites; PRP/BPBM/GTR group: 4.96 +/- 1.28 mm on buccal and 4.78 +/- 1.32

43 reated with either a combination of PRP/BPBM/GTR or PRP/BPBM.

44 defects in humans: a combination of PRP/BPBM/GTR versus a combination of PRP/BPBM.

45 BM/GTR/PRP (experimental group) or with BPBM/GTR (control group).

46 Defects were treated with BPBM/GTR/PRP (experimental group) or with BPBM/GTR (control g

47 e glutamyl-tRNA-dependent NADPH oxidation by GTR.

48 Each patient was treated by GTR using a bioabsorbable membrane.

49 ed by complementation of an Escherichia coli GTR-defective mutant for restoration of ALA prototrophy.

50 Log rank test confirmed GTR correlated with significantly better survival.

51 In a coupled enzyme assay containing GTR and wild-type GSAT, addition of inactive mutant GSAT

52 R had 60 to 70% less bound heme than control GTR, and it was inhibited by hemin in vitro.

53 mly assigned to test (PRGF+GTR) and control (GTR alone) treatment groups.

54 e anatomy of the resulting intrabony defect, GTR was considered the ideal treatment.

55 ridement followed by the placement of DFDBA (GTR+DFDBA, or test group) and a bioabsorbable barrier, w

56 ingival recession defects by means of either GTR or CTG results in clinically and statistically signi

57 is limited by ALA and that the hemA-encoded GTR reductase is a rate-limiting enzyme in the pathway.

58 The hemA-encoded GTR reductase was found to be regulated by ALA.

59 bean (Glycine max) root-nodule cDNA encoding GTR was isolated by complementation of an Escherichia co

60 ng expanded polytetrafluoroethylene (ePTFE), GTR using a bioabsorbable membrane with or without demin

61 t inhibit the activity of purified expressed GTR in vitro.

62 The expressed GTR contained 1 mol of tightly bound heme per mol of pep

63 etention and clinical improvements following GTR treatment of intrabony defects can be maintained lon

64 ive results from the utilization of DUIS for GTR and the advantage of its bioresorbability warrant fu

65 ived a collagen/polylactic acid membrane for GTR.

66 regeneration 2.0+/-1.3 and 1.6+/-1.7 mm for GTR+DBM and GTR defects, respectively.

67 ta-analysis revealed decreased mortality for GTR compared with STR at 1 year (RR, 0.62; 95% CI, 0.56-

68 ed by the expression levels of the mRNAs for GTR or GSAT, or by the cellular abundance of these enzym

69 t significantly enhanced space provision for GTR while alveolar bone formation appeared to be enhance

70 Variability in defect fill was similar for GTR and OFD.

71 Cells from GTR membranes which did not exhibit gains in clinical at

72 h cells from GBR procedures, most cells from GTR procedures also secreted lower amounts of TIMP-1.

73 T for binding to GTR and channeling GSA from GTR to GSAT.

74 However, GTR and GSAT were present at all phases of the cycle.

75 If GTR is not achieved, adjuvant therapy might delay tumour

76 In GTR/EMD with and without laser treatment, the WMD of CAL

77 defects, the use of PLA or ePTFE barriers in GTR procedures yielded comparable clinical results; howe

78 ked collagen membrane could be beneficial in GTR treatment of Class II mandibular furcation involveme

79 be used successfully as a barrier device in GTR-based root coverage procedures.

80 FD, 1.9+/-1.4 mm in MBA, and 0.7+/-0.9 mm in GTR+MBA groups.

81 to the efficacy of bone substitutes used in GTR procedures.

82 the defect left after the removal of an LPC, GTR, along with bone grafting, can be a very useful tool

83 Purified mature GTR was not inhibited by heme, but heme inhibition was r

84 The deduced C. reinhardtii mature GTR amino acid sequence has more than 55% identity to a

85 tly affects the outcome of collagen membrane GTR-based root coverage procedures.

86 the following therapies: collagen membrane (GTR), human demineralized freeze-dried bone (DFDB) graft

87 een the most commonly investigated modality, GTR, biologics, and combination therapies have also been

88 approximately 40 kDa, indicating that native GTR is a monomer.

89 gains > or = 4 mm were observed in 50.9% of GTR sites and 33.3% of control sites.

90 the CAL observed 1 year after completion of GTR.

91 have been conducted utilizing the concept of GTR to promote root coverage.

92 y published study of the clinical effects of GTR therapy without the use of bone or bone substitutes

93 earlier study which compared the effects of GTR utilizing an ePTFE or a PLA barrier in intrabony def

94 defects, as well as the general efficacy of GTR in different clinical settings.

95 and histologically evaluate the efficacy of GTR-based root coverage using collagen membrane (GTRC) a

96 r evidence supporting kinetic interaction of GTR and GSAT is the observation that both wild-type and

97 However, at present, the outcomes of GTR procedures have not been shown to be predictable.

98 files identified distinct sub-populations of GTR cells in which fibronectin expression was markedly u

99 tion was to assess the long-term survival of GTR treated sites in terms of clinical attachment level

100 ived GTR and the coral biomaterial (cGTR) or GTR alone.

101 ns, in regenerative studies comparing DBM or GTR to OFD therapy for the management of intrabony defec

102 0.001) reject the most general phylogenetic (GTR) models commonly in use.

103 hile loss of CAL compared to the 1-year post-GTR result was observed in 37.8% of cases.

104 defects were randomly assigned to test (PRGF+GTR) and control (GTR alone) treatment groups.

105 he web and through FTP (ftp.ncbi.nih.gov/pub/GTR/_README.html).

106 an inhibitor of heme synthesis, the purified GTR had 60 to 70% less bound heme than control GTR, and

107 hood trees for each combination using RAxML (GTR + Gamma), and compared their topologies to the corre

108 aw quadrants in consecutive animals received GTR and the coral biomaterial (cGTR) or GTR alone.

109 We have used purified recombinant GTR and GSAT from the unicellular alga Chlamydomonas rei

110 rifugation results indicate that recombinant GTR and GSAT enzymes specifically interact.

111 The enzyme glutamyl-tRNA reductase (GTR) catalyzes the first committed step in this pathway,

112 mialdehyde (GSA) by glutamyl-tRNA reductase (GTR) in an NADPH-dependent reaction.

113 sis is catalyzed by glutamyl-tRNA reductase (GTR) in plants.

114 The enzyme glutamyl-tRNA reductase (GTR), encoded by the hemA gene, catalyzes the first comm

115 mialdehyde (GSA) by glutamyl-tRNA reductase (GTR).

116 LPC treated with guided tissue regeneration (GTR) and bone allograft.

117 ble membrane for guided tissue regeneration (GTR) as regenerative therapy for intrabony defects in hu

118 igid membrane in guided tissue regeneration (GTR) for osseous defects.

119 bone grafts and guided tissue regeneration (GTR) for the correction of intrabony and furcation defec

120 /- 2.1 mm in the guided tissue regeneration (GTR) group and 2.6 +/- 1.8 mm in the control group (P =

121 The use of guided tissue regeneration (GTR) has become an effective procedure for the treatment

122 eral (BPBM), and guided tissue regeneration (GTR) has been shown to be effective in promoting reducti

123 ical benefits of guided tissue regeneration (GTR) has not been fully explored.

124 term efficacy of guided tissue regeneration (GTR) in Class II furcation defects and establish the fac

125 neral (BPBM) and guided tissue regeneration (GTR) in the treatment of intrabony defects in humans.

126 Guided tissue regeneration (GTR) is a clinical procedure used to restore the attachm

127 aterials used in guided tissue regeneration (GTR) is known to adversely affect treatment outcomes.

128 gen barrier as a guided tissue regeneration (GTR) material has shown particular promise in procedures

129 biomaterial and guided tissue regeneration (GTR) membranes, and were evaluated following a 4-week he

130 ximal defects by guided tissue regeneration (GTR) necessitates inclusion of healthy adjacent teeth to

131 widely used for guided tissue regeneration (GTR) of the human periodontal ligament (PL).

132 the effect of a guided tissue regeneration (GTR) procedure in comparison to connective tissue graft

133 The use of guided tissue regeneration (GTR) procedures in the treatment of gingival recession h

134 tudied following guided tissue regeneration (GTR) procedures using both nonresorbable and bioabsorbab

135 For guided tissue regeneration (GTR) procedures, collagen membranes have been shown to b

136 ation for use in guided tissue regeneration (GTR) procedures.

137 matrix (DBM) and guided tissue regeneration (GTR) support substantial gains in clinical attachment le

138 Clinicians using guided tissue regeneration (GTR) techniques are also enjoying significant success in

139 Guided tissue regeneration (GTR) techniques have been reported to enhance bone regen

140 tcomes following guided tissue regeneration (GTR) treating human Class II furcation defects with a ne

141 Guided tissue regeneration (GTR) uses expanded polytetrafluoroethylene (ePTFE) membr

142 wing treatments: guided tissue regeneration (GTR) using expanded polytetrafluoroethylene (ePTFE), GTR

143 associated with guided tissue regeneration (GTR) versus GTR only in the treatment of intrabony defec

144 ement grafts and guided tissue regeneration (GTR) were defined as state of the art for clinical perio

145 e the effects of guided tissue regeneration (GTR) with expanded polytetrafluoroethylene (ePTFE) non-r

146 Guided tissue regeneration (GTR) with resorbable (GTRr) and non-resorbable (GTRnr) m

147 Guided tissue regeneration (GTR)-based root coverage has been utilized to correct gi

148 en membranes for guided tissue regeneration (GTR)-based root coverage procedures have reported promis

149 rier membrane in guided tissue regeneration (GTR)-based root coverage procedures.

150 In addition, guided tissue regeneration (GTR)-based root coverage using collagen membrane (GTRC)

151 tcomes following guided tissue regeneration (GTR).

152 matrix (DBM) to guided tissue regeneration (GTR).

153 ugh resection is guided tissue regeneration (GTR).

154 ement grafts and guided tissue regeneration (GTR).

155 Similarly, in guided tissue regeneration (GTR)/enamel matrix derivative (EMD) with and without las

156 llagen membrane (guided tissue regeneration [GTR]+MBA) groups.

157 llular green alga Chlamydomonas reinhardtii, GTR and GSAT were found in the chloroplasts and were not

158 Gross total resection (GTR) was achieved in 16/27 (59.3%) patients, subtotal re

159 Gross total resection (GTR) was attempted for cerebellar and cerebral hemispher

160 ssess mortality after gross total resection (GTR), subtotal resection (STR), and biopsy.

161 cted transit peptide, the mature 480-residue GTR has a calculated molecular weight of 52,502.

162 spikes called the gap termination response (GTR).

163 The nonstationary general time reversible (GTR) model, used with AWP or EMC, accurately recovered t

164 ), symmetric (SYM), general time-reversible (GTR) and all rates different (ARD).

165 Compared with STR, GTR substantially improves overall and progression-free

166 The His-tagged GTR protein was purified using Ni affinity column chroma

167 cells contained significantly more GSAT than GTR on a molar basis.

168 rt the in vitro results and demonstrate that GTR and GSAT are components of a high molecular mass com

169 alga Chlamydomonas reinhardtii to show that GTR and GSAT form a physical and functional complex that

170 The results also suggest that GTR adds no clinical benefit to PRP/BPBM.

171 The GTR mRNA level increased in the light and peaked about 2

172 The GTR-based technique using PCG was effective in reducing

173 stically significant differences between the GTR+DBM versus the GTR condition for any histometric par

174 ntum regeneration were observed for both the GTR+DBM and GTR defects.

175 To characterize the GTR protein, the hemA gene from C. vibrioforme was clone

176 Mean CAL gain was 2.0 mm for the GTR group and 2.2 mm for the CTG group.

177 ce of complete root coverage was 58% for the GTR group and 83% for the CTG group.

178 mm) were obtained 1 year postsurgery for the GTR sites.

179 ever, it remains unknown whether and how the GTR plays a causal role in gap detection.

180 , the WMD of PD was negligible; however, the GTR/EMD group showed better outcomes (P = 0.005) than th

181 ed factors significant to the success of the GTR procedures, should enhance the consistency of the cl

182 2-fold greater in cGTR sites compared to the GTR control (3.3 +/- 1.8 versus 1.4 +/- 0.5 mm2), howeve

183 in this study, the addition of DFDBA to the GTR procedure did not significantly enhance the clinical

184 t differences between the GTR+DBM versus the GTR condition for any histometric parameter examined.

185 However, when the GTR was expressed in the presence of 3-amino-2,3- dihydr

186 hance the clinical results obtained with the GTR procedure alone.

187 bone (DFDB) grafting (BG), combined therapy (GTR + BG) and a DFDB-glycoprotein sponge matrix (MAT).

188 for non-contained defects, combined therapy (GTR + BG) demonstrated clinically significant (P < or =

189 ollowing guided tissue regeneration therapy (GTR) with a bioabsorbable barrier composed of polylactic

190 value of the coral implant as an adjunct to GTR.

191 een wild-type and mutant GSAT for binding to GTR and channeling GSA from GTR to GSAT.

192 e provision was enhanced in cGTR compared to GTR sites (6.1 +/- 1.6 versus 2.4 +/- 0.8 mm2; P<0.05).

193 significantly increased in cGTR compared to GTR sites averaging 1.9 +/- 0.6 and 1.2 +/- 0.6 mm, resp

194 needed to determine whether adding DFDBA to GTR-based procedures using collagen membranes is of any

195 freeze-dried DBM has no adjunctive effect to GTR in periodontal fenestration defects over a four-week

196 Clinical data related to GTR therapy for Class II furcations were analyzed from 7

197 psis thaliana, and significant similarity to GTR proteins of other plants and prokaryotes.

198 f rHb1.1 and the hemA-encoded glutamyl-tRNA (GTR) reductase increased intracellular levels of ALA and

199 se findings suggest that patients undergoing GTR procedures with synthetic absorbable devices for the

200 Generally, cells from unsuccessful GTR procedures produced low molecular weight gelatinases

201 one regeneration capacity of a commonly used GTR procedure (demineralized freeze-dried bone allograft

202 Studies were identified that used GTR approaches to treat gingival recession from January

203 with guided tissue regeneration (GTR) versus GTR only in the treatment of intrabony defects (IBDs) in

204 icant difference in PFS for patients in whom GTR was achieved versus those with incomplete resections

205 additive effect of PRGF when used along with GTR in the treatment of IBDs in patients with CP in term

206 f this study show that cells associated with GTR barrier membranes and with the underlying tissue app

207 re used to examine the cells associated with GTR compared with normal human PL and gingival cells.

208 ion of clinical failures was associated with GTR therapy.

209 um carbonate biomaterial in conjunction with GTR.

210 od of disease progression was decreased with GTR compared with STR at 6 months (RR, 0.72; 95% CI, 0.4

211 reased from 2.5 mm presurgery to 0.5 mm with GTR (81% root coverage), and from 2.5 mm to 0.1 mm with

212 PRGF with GTR, as well as GTR alone, was effective in improving cl

213 lar bone and to improve space provision with GTR devices.

214 All sites had been treated with GTR more than 2 years previously and had received full p