ライフサイエンスコーパス: GPA

1 GPA gives rise to soft communities that provide a differ

2 GPA implants showed massive destruction of the co-implan

3 GPA infestation of Arabidopsis resulted in a transient i

4 GPA spends more time actively feeding from the sieve ele

5 GPA treatment produced a significant increase in mtDNA i

6 GPA-16 function has been analyzed in vivo owing notably

7 GPA-modifying sulfotransferases are promising tools for

8 n- defective let-99(-) mutant zygotes, GOA-1/GPA-16 and NMY-2 act abnormally to oppose centration.

9 In GOA-1/GPA-16-depleted zygotes, NMY-2 aggregate displacement is

10 yosin II NMY-2 and the Galpha proteins GOA-1/GPA-16.

11 75-kDa erythrocyte-binding antigen (EBA-175)/GPA pathway was used by a minority of the parasite isola

12 ptors relative to the well-described EBA-175/GPA invasion pathway, we used an ex vivo erythrocyte cul

13 A GPA of 4.0 correlates with the best prognosis, whereas a

14 c cells induced a Th17 response, revealing a GPA-specific mechanism of immune polarization.

15 orrelates with the best prognosis, whereas a GPA of 0.0 corresponds with the worst prognosis.

16 The EBA-175/glycophorin A (GPA) and Rh5/basigin ligand-receptor interactions, refer

17 We chose glycophorin A (GPA) as a model integral protein to begin investigating

18 ivocal estimate of the use of glycophorin A (GPA) as a receptor, we found that the 175-kDa erythrocyt

19 Human red cell glycophorin A (GPA) enhances the expression of band 3 anion transport a

20 lays a key role by binding to glycophorin A (GPA) on the red cell surface, although the function of t

21 Ter-119) that binds to mouse glycophorin A (GPA) with a variant human single-chain low molecular wei

22 , including GYPA that encodes glycophorin A (GPA), and the up-regulation of members of the HSP70 fami

23 C3 cleavage, onto erythrocyte glycophorin A (GPA).

24 Furthermore, AMPK inactivation abrogated GPA-induced increases in the expression of peroxisome pr

25 Homodimeric StaL can accommodate GPA substrate in only one of the two active sites becaus

26 reatine analog beta guanidinopropionic acid (GPA) reduced ATP and PCr levels and increased AMPK mRNA

27 e treated with beta-guanidinopropionic acid (GPA), a creatine analog, which led to similar reductions

28 bolic stressor beta-guanidinopropionic acid (GPA), a creatine analogue that reduces ATP levels, activ

29 Activated GPA-12 has the same effect as activated RHO-1, inducing

30 ly blocks increased ACh release by activated GPA-12.

31 as steric constraints that suggest activated GPA-16(it143) is destabilized relative to wild type.

32 Biopsy specimens from patients with active GPA (n = 10) or sinusitis (controls, n = 6) were s.c. co

33 has an important role in antibiosis against GPA.

34 an essential function in antibiosis against GPA.

35 r reveal that PAD4-modulated defense against GPA does not involve EDS1.

36 PAD4-controlled defense against GPA requires neither EDS1 nor SA.

37 sability of EDS1 and SID2 in defense against GPA.

38 mutant plant and attenuated defense against GPA.

39 plays a role in Arabidopsis defense against GPA.

40 which is a key modulator of defenses against GPA.

41 onditioned antibiosis and deterrence against GPA feeding, but S118 was dispensable for deterring GPA

42 tes a phloem-based defense mechanism against GPA.

43 s accompanied by enhanced resistance against GPA in the Arabidopsis constitutive expresser of PR gene

44 Resistance against GPA was also higher in the trehalose hyper-accumulating

45 In contrast, resistance against GPA was compromised in the phytoalexin deficient4 (pad4)

46 b monotherapy and/or gastroprotective agent (GPA) cotherapy, and 1,207 (65.8%) received coxibs.

47 gy (PH) domain, followed by two Gly/Pro/Ala (GPA)-rich regions separated by a Src homology 3 (SH3) do

48 access to the Glaucoma Progression Analysis (GPA) printout.

49 Guided progression analysis (GPA) was also compared.

50 A) with HRT and Guided Progression Analysis (GPA) with Cirrus HD-OCT, respectively.

51 ormed using the Guided Progression Analysis (GPA; Carl-Zeiss Meditec, Inc., Dublin, CA).

52 ated perimetry guided progression analysis, [GPA]) and 21 healthy eyes from the University of Califor

53 2), function together with Galpha (GOA-1 and GPA-16) to generate asymmetric spindle pole elongation d

54 Caenorhabditis elegans G proteins ODR-3 and GPA-13.

55 kyrin were present in a complex with C3b and GPA in complement-treated cells.

56 e membranes of complement-treated cells, and GPA was physically associated with the membrane skeleton

57 eement between majority expert consensus and GPA was fair (kappa = 0.52, 95% confidence interval [CI]

58 eement between majority expert consensus and GPA, both before and after access to GPA data, was asses

59 enzyme) to roots restored water content and GPA population size in lox5 plants, thus confirming that

60 5) as progressing compared with VFI, MD, and GPA in suspects (3.8%, 2.7%, 5.6%, and 2.9%, respectivel

61 bditis elegans zygote, GOA-1 (Galpha(o)) and GPA-16 (Galpha(i)) are involved in generating forces tha

62 ed gene expression upon fruit production and GPA, and a drop in chlorophyll levels, suggestive of alt

63 etermination of visual field progression and GPA is fair.

64 RA and GPA may arise from a similar genetic predisposition.

65 The green peach aphid (GPA) (Myzus persicae Sulzer) is an important sap-sucking

66 Green peach aphid (GPA) Myzus persicae (Sulzer) is a phloem-feeding insect

67 er, commonly known as the green peach aphid (GPA), which is an important phloem sap-consuming pest of

68 r), commonly known as the green peach aphid (GPA).

69 Arabidopsis thaliana) and green peach aphid (GPA; Myzus persicae Sulzer), we found that GPA feeding i

70 ntial for defense against green peach aphid (GPA; Myzus persicae) and the pathogens Pseudomonas syrin

71 Extract of the green peach aphid (GPA; Myzus persicae) triggers responses characteristic o

72 the phloem sap-consuming green peach aphid (GPA; Myzus persicae), an agronomically important insect

73 rescences, i.e. global proliferative arrest (GPA) during which all maternal growth ceases upon the pr

74 nts with GM-positive invasive aspergillosis (GPA).

75 published the Graded Prognostic Assessment (GPA), a prognostic index for patients with brain metasta

76 icrobeads that contained covalently attached GPA analogues.

77 mechanism geometric preferential attachment (GPA), and validate it against the Internet.

78 Over 2 years, the grade point average (GPA) of African Americans was, on average, raised by 0.2

79 ised African Americans' grade-point average (GPA) relative to multiple control groups and halved the

80 isolated fibroblasts was comparable between GPA and controls, GPA samples showed a significant delay

81 The connections between GPA and cosmological models, including inflation, are al

82 breast graded prognostic assessment (breast-GPA), comprising age, tumor subtype, and Karnofsky perfo

83 We sought to validate the existing breast-GPA in an independent larger cohort and refine it integr

84 The modified breast-GPA incorporates four simple clinical parameters of high

85 We therefore developed the modified breast-GPA integrating a fourth clinical parameter.

86 mances of the breast-GPA and modified breast-GPA were compared using the concordance index.

87 0.85) for the breast-GPA and modified breast-GPA, respectively (P < .001).

88 ed to the development of the modified breast-GPA.

89 The performances of the breast-GPA and modified breast-GPA were compared using the conc

90 d 0.84 (95% CI, 0.83 to 0.85) for the breast-GPA and modified breast-GPA, respectively (P < .001).

91 In multivariable analysis of the breast-GPA and number of brain metastases (> three v </= three)

92 In our cohort of 1,552 patients, the breast-GPA was validated as a prognostic tool for OS (P < .001)

93 After validating the breast-GPA, multivariable Cox regression and recursive partitio

94 ected only 31% of locations deteriorating by GPA.

95 d progression by Bayesian slopes, but not by GPA.

96 The median survival times by GPA score and diagnosis were determined.

97 We then determined that DAF, C3b, GPA, and band 3 molecules were laterally immobilized in

98 mation of a membrane skeleton-linked DAF-C3b-GPA-band 3 complex on the erythrocyte surface.

99 d of haematopoietic progenitor cells (CD36(+)GPA(-/low)).

100 This study was designed to compare GPA with other causes of orbital inflammation and to ide

101 the inability of the tps11 mutant to control GPA infestation.

102 sts was comparable between GPA and controls, GPA samples showed a significant delay of apoptosis.

103 ding, but S118 was dispensable for deterring GPA settling and promoting senescence in GPA-infested pl

104 iagnosis, a robust separation into different GPA scores was discerned, implying considerable heteroge

105 is-Specific Graded Prognostic Assessment (DS-GPA) for patients with non-small-cell lung cancer (NSCLC

106 The original DS-GPA was based on 4 factors found in 1833 patients with N

107 patients studied for the creation of the DS-GPA had a median survival of 7 months from the time of i

108 cluded the original 4 factors used in the DS-GPA index plus 2 new factors: EGFR and ALK alterations i

109 corporating gene alteration data into the DS-GPA is a user-friendly tool that may facilitate clinical

110 The DS-GPA is based on data from patients diagnosed between 198

111 Forty-eight GPA patients and 38 age-matched healthy donors were incl

112 Two separate eliciting GPA-derived fractions trigger induced resistance to GPA

113 ines Agency (EMA) system with categories for GPA and MPA; and 3) classification based on ANCA with sp

114 ransmembrane domain of GPA are important for GPA dimer formation.

115 index of suspicion should be maintained for GPA when a patient presents with an orbital mass and sin

116 The median age at presentation for GPA patients was 30 years (mean +/- standard deviation,

117 BAK1 is required for GPA elicitor-mediated induction of reactive oxygen speci

118 fibers and reversal of blunted response for GPA in HD mice.

119 Notably, NK cells from GPA patients expressed markers of recent in vivo activat

120 Accordingly, circulating CD4+ T cells from GPA patients had a skewed distribution of Th9/Th2/Th17.

121 presence of CMV in renal biopsy tissue from GPA patients was investigated by immunohistochemistry an

122 releasing motor neurons depends on Galpha12 (GPA-12), which acts via the single C. elegans RGS RhoGEF

123 In addition, graph-GPA also promotes better understanding of genetic mechan

124 propose a novel statistical framework, graph-GPA, to integrate a large number of GWAS datasets for mu

125 Application of graph-GPA to a joint analysis of GWAS datasets for 12 phenotyp

126 datasets for 12 phenotypes shows that graph-GPA improves statistical power to identify risk variants

127 ar components of tissue destruction of human GPA tissue transplanted into immunodeficient mice.

128 and to proteinase 3, a major autoantigen in GPA, and analyzed the effects on NK cell activation.

129 The destruction of nasal cartilage in GPA is mainly mediated by fibroblasts that can be blocke

130 riving the expansion of CD4+CD28- T cells in GPA patients and how this might relate to clinical featu

131 The expansion of CD4+CD28- T cells in GPA patients is associated with CMV infection and leads

132 uggest that, upon inflammatory conditions in GPA, renal MECs may contribute to the recruitment and ac

133 These defects in GPA performance in the lox5 mutant were accompanied by r

134 11 function abolished trehalose increases in GPA-infested leaves of the tps11 mutant plant and attenu

135 ression was rapidly induced to high level in GPA-infested plants.

136 ing reactions on the terminal NRPS module in GPA biosynthesis.

137 ing GPA settling and promoting senescence in GPA-infested plants as well as for pathogen resistance.

138 Patients were divided into GPA and non-GPA groups on the basis of their final clini

139 elices, we incubated fluorescent dye-labeled GPA analogues in sodium dodecyl sulfate solution with mi

140 ain metastases, confirming the original Lung-GPA.

141 In WT mice, GPA treatment resulted in activation of muscle AMPK and

142 opomyosin, ICAM-4, GLUT4, Na/K-ATPase, NHE1, GPA, CD47, Duffy, and Kell were reduced.

143 Patients were divided into GPA and non-GPA groups on the basis of their final clinical diagnosi

144 analyzed and compared with those of the non-GPA group.

145 ny destruction (P = 0.048) compared with non-GPA patients.

146 r GPB mutants, including naturally occurring GPA/GPB hybrid molecules and insertion, deletion, and su

147 With reference to the HRT TCA and OCT GPA, ONH surface depression occurred before RNFL thinnin

148 emission in localized and generalized ocular GPA.

149 By ANCA specificity, categories of GPA, MPA, and kidney-limited disease did not distinguish

150 east in part, from increased connectivity of GPA with the spectrin-based skeleton.

151 from presentation to definitive diagnosis of GPA ranged from 3 to 20 months (mean, 12.1 months; media

152 olvement, of whom 7 had a final diagnosis of GPA.

153 regions outside the transmembrane domain of GPA are important for GPA dimer formation.

154 This effect of GPA could occur in two ways, enhancement of band 3 anion

155 yte culture system to decrease expression of GPA, GPB, or GPC via lentiviral short hairpin RNA transd

156 this hypothesis, we quantified the extent of GPA association to the cytoskeleton in erythroblasts, yo

157 ncreased in roots and in petiole exudates of GPA-colonized plants.

158 agnosis may not show the classic features of GPA.

159 ortant for restricting GPA growth; growth of GPA on the camalexin-biosynthesis mutant, pad3, and the

160 within granulomatous lesions in the lungs of GPA patients.

161 ition, examination of the oligomerization of GPA mutants showed that single amino acid substitutions

162 re compared to determine those predictive of GPA, and patients with GPA also had long-term evaluation

163 mutation (G202D) in the switch II region of GPA-16.

164 rafficking) to identify candidate regions of GPA for study.

165 Access to the results of GPA did not significantly change the level of agreement

166 We compared the sequences of GPA and its homolog glycophorin B (GPB; which does not f

167 perature despite defects in the structure of GPA-16(it143).

168 changes on imaging are highly suggestive of GPA and should prompt a full diagnostic workup.

169 Features highly suggestive of GPA were sinonasal symptoms, sinonasal changes, or paran

170 find that the C-terminal cytoplasmic tail of GPA enhances trafficking of band 3 to the cell surface,

171 ing progressing (by stereophotography and/or GPA) and healthy eyes were 0.778/0.809, 0.639/0.857, and

172 sion (nonprogressed) by stereophotography or GPA.

173 Orbital GPA can be associated with a high morbidity from potenti

174 A diagnosis of orbital GPA and development of systemic GPA were the main outcom

175 However, early diagnosis of orbital GPA may be difficult because anti-neutrophil cytoplasmic

176 Diagnosis of orbital GPA, especially in patients with lacrimal involvement as

177 nd no patient presenting with solely orbital GPA developed later systemic disease over a median follo

178 No patient with solely orbital GPA involvement at presentation developed systemic disea

179 ed systemic disease, suggesting that orbital GPA can remain localized in the long-term.

180 In comparison to the wild-type plant, GPA feeding-induced chlorophyll loss, cell death, and SA

181 rapy, 347 (18.9%) prescribed dual coxib plus GPA cotherapy, 173 (9.4%) prescribed a nonselective NSAI

182 scribed a nonselective NSAID (NS-NSAID) plus GPA cotherapy, and 453 (24.7%) prescribed an NS-NSAID wi

183 gories for granulomatosis with polyangiitis (GPA) (Wegener's), microscopic polyangiitis (MPA), and ki

184 lvement in granulomatosis with polyangiitis (GPA) commonly accompanies orbital disease, but occasiona

185 Granulomatosis with polyangiitis (GPA) is a systemic necrotizing vasculitis that is associ

186 Granulomatosis with polyangiitis (GPA), previously Wegener's granulomatosis, requires prom

187 s, such as granulomatosis with polyangiitis (GPA).

188 s found in granulomatosis with polyangiitis (GPA, formerly Wegener's) or the development of vasculiti

189 culitides, granulomatosis with polyangiitis (GPA, formerly Wegener's), microscopic polyangiitis (MPA)

190 ulitis and granulomatosis with polyangiitis (GPA, Wegener's granulomatosis).

191 feature of granulomatosis with polyangiitis (GPA; or Wegener's granulomatosis) is the granulomatous i

192 and imaging features most likely to predict GPA and its systemic spread.

193 loring enzymes, which can be used to produce GPA analogues that could overcome antibiotic resistance.

194 into how PR3 and PR3-targeting ANCAs promote GPA pathophysiology.

195 d 5-HT signaling requires the Galpha protein GPA-11.

196 at the spn-1 gene encodes the Galpha protein GPA-16, which appears to be required for centrosomal ass

197 tients with chronically relapsing refractory GPA.

198 Fifty-three patients with refractory GPA (median age 46 years [interquartile range (IQR) 30-6

199 sing on RTX use for patients with refractory GPA and MPA have been reported.

200 study of all patients with chronic relapsing GPA treated with at least 2 courses of RTX between Janua

201 remission in patients with chronic relapsing GPA.

202 signaling are not important for restricting GPA growth; growth of GPA on the camalexin-biosynthesis

203 gion (BR) (23 kDa) and two Gly/Pro/Ala-rich (GPA) regions, GPA1 (6 kDa) and GPA2 (15 kDa), flanking a

204 ranulomatosis with polyangiitis (Wegener's) (GPA).

205 ranulomatosis with polyangiitis (Wegener's) (GPA).

206 ranulomatosis with polyangiitis (Wegener's) (GPA).

207 granulomatosis with polyangiitis (Wegener's; GPA), microscopic polyangiitis (MPA), and eosinophilic g

208 However, the same GPA treatment in DN-AMPK mice had no effect on AMPK acti

209 cells were only expanded in CMV-seropositive GPA patients and controls.

210 In CMV-seropositive GPA patients we observed negative correlations between t

211 We constructed several GPA or GPB mutants, including naturally occurring GPA/GP

212 e (CYC) for induction of remission in severe GPA and MPA.

213 ive to CYC for remission induction in severe GPA and MPA.

214 is to present the updated diagnosis-specific GPA indices in a single, unified, user-friendly report t

215 s were used to define the diagnosis-specific GPA prognostic indices.

216 ansmembrane domain greatly reduce SDS-stable GPA dimer formation, implying that regions outside the t

217 s of orbital GPA and development of systemic GPA were the main outcome measures.

218 and 2.9%, respectively), and more eyes than GPA (P = 0.01) in glaucoma (16.0%, 15.3%, 12.0%, and 7.3

219 and 7.3%, respectively), and more eyes than GPA (P = 0.05) in PGON eyes (26.3%, 23.7%, 27.6%, and 14

220 Micrografting experiments demonstrated that GPA performance on foliage is influenced by the LOX5 gen

221 We discovered that GPA was more connected to the membrane cytoskeleton, eit

222 (GPA; Myzus persicae Sulzer), we found that GPA feeding induced premature chlorosis and cell death,

223 icroscopy and Western blotting we found that GPA sorted predominantly to reticulocytes.

224 ed microdeformation (FIMD) and observed that GPA underwent dramatic reorganization during terminal di

225 This suggests that GPA represents a form of bud dormancy, and that dominanc

226 zing function of ADF3 in defense against the GPA, we show that resistance in adf3 was restored by ove

227 important regulator of defenses against the GPA.

228 has an important role in defense against the GPA.

229 e.g., the BR has a membrane affinity and the GPA components bind F-actin in an ATP-independent manner

230 he BR binds to acidic phospholipids, and the GPA region binds to F-actin.

231 f agreement between expert consensus and the GPA result; however, expert consensus did change in 11 o

232 important for enzymatic modifications by the GPA-tailoring enzymes.

233 ion, once they found the sieve elements, the GPA fed for a more prolonged period from sieve elements

234 We have examined the GPA effect using GPA mutants.

235 el was built to incorporate results from the GPA in the prior distribution for the VFI slopes, allowi

236 Furthermore, the GPA population was larger on the mpl1 mutant than the wi

237 , progression criteria currently used in the GPA have high specificity, but some patients are more li

238 el in response to GPA feeding, modulates the GPA feeding-induced leaf senescence.

239 On average, the specificity of the GPA "likely progression" alert was high-for the entire s

240 ease in fecundity and population size of the GPA and a parallel reduction in callose deposition in th

241 Electrical monitoring of the GPA feeding behavior indicates that the GPA stylets foun

242 35S gene promoter curtailed the size of the GPA population.

243 nsferases modify distinct side chains on the GPA scaffold.

244 The collective data suggest that the GPA and GPB receptors are of greater importance than the

245 the GPA feeding behavior indicates that the GPA stylets found sieve elements faster when feeding on

246 eview and on reevaluation with access to the GPA printout, the level of agreement between majority ex

247 However, it must be considered when the GPA is used in clinical practice where specificity needs

248 likely progression" were determined with the GPA.

249 Their GPA improved, on average, 0.41 points, and their rate of

250 sus and GPA, both before and after access to GPA data, was assessed using kappa statistics.

251 to the time of VF deterioration according to GPA or until the last follow-up visit in stable eyes.

252 Seventy eyes (25.5%) worsened according to GPA.

253 erythrocyte, we show that EBA175 binding to GPA leads to an increase in the cytoskeletal tension of

254 A infestation, is required for resistance to GPA in the Arabidopsis accession Columbia.

255 Here, we show that resistance to GPA is unaltered in an eds1 salicylic acid induction def

256 ived fractions trigger induced resistance to GPA that is dependent on the leucine-rich repeat recepto

257 3 is also required for induced resistance to GPA, independently of BAK1 and reactive oxygen species p

258 utant, which exhibits enhanced resistance to GPA.

259 es, which contributes to basal resistance to GPA.

260 s expressed at elevated level in response to GPA feeding, modulates the GPA feeding-induced leaf sene

261 expressed at elevated levels in response to GPA infestation, is required for resistance to GPA in th

262 ere that the role of PAD4 in the response to GPA is conserved in Arabidopsis accessions Wassilewskija

263 onsumption, PGC-1alpha, NRF1 and response to GPA were significantly reduced in myoblasts from HD pati

264 with lacrimal gland involvement secondary to GPA and to compare them with those of other orbital infl

265 The adf3-conferred susceptibility to GPA was overcome by expression of the ADF3 coding sequen

266 jor Arabidopsis phytoalexin that is toxic to GPA.

267 received at least 2 courses of RTX to treat GPA relapses or to maintain remission.

268 structural information in generating unique GPA derivatives.

269 en species, however, strongly decreased upon GPA, a phenomenon that is associated with bud dormancy i

270 , and low mitotic activity in meristems upon GPA, but found that meristems retain their identity and

271 Thus, the upstream GPA-12/RHGF-1 pathway stimulates only a subset of RHO-1

272 We have examined the GPA effect using GPA mutants.

273 es of fields as showing progression than was GPA (P </= 0.002).

274 Twenty-two percent of patients (8/37) with GPA had evidence of systemic involvement at presentation

275 o identify only 32 of the 64 eyes (50%) with GPA progression.

276 PLR criteria led to improved agreement with GPA at the expense of higher false detection rate.

277 teria for PLR led to improved agreement with GPA at the expense of higher false detection rate.

278 The agreement with GPA was significantly better for the Bayesian compared w

279 es (kappa = 0.32 vs. 0.37 for agreement with GPA).

280 of global and pointwise trend analyses with GPA were explored.

281 ty markers was significantly associated with GPA (OR 1.05 per 1-unit increase in genetic risk score,

282 in CTLA4 were significantly associated with GPA in the single-marker meta-analysis (odds ratio [OR]

283 statistically significantly associated with GPA in this study.

284 In cases of disagreement with GPA, the expert consensus classification was usually pro

285 at the RGS domain of CeRhoGEF interacts with GPA-12 in an AIF4- activation-dependent manner and confi

286 dition, nasal fibroblasts from patients with GPA (n = 8) and control healthy nasal fibroblasts (n = 5

287 e those predictive of GPA, and patients with GPA also had long-term evaluation for systemic involveme

288 ascertained in a total of 880 patients with GPA and 1,969 control subjects of European descent.

289 A higher proportion of patients with GPA demonstrated sinonasal involvement (P = 0.011) and b

290 risk of malignancy observed in patients with GPA treated with cytotoxic agents and should be avoided

291 inical and imaging features of patients with GPA were analyzed and compared with those of the non-GPA

292 tive of all-cause mortality in patients with GPA, independent of other traditional risk factors for m

293 es were demonstrated in 29% of patients with GPA.

294 time, 64 (9%) had confirmed progression with GPA.

295 Associations of multiple SNPs with GPA were assessed using genetic risk scores based on sus

296 The HD mice treated with GPA had impaired activation of liver PGC-1alpha and deve

297 Treatment with GPA resulted in increased expression of AMPK, PGC-1alpha

298 Treatment with GPA significantly increased expression of PGC-1alpha, NR

299 es, which were exacerbated by treatment with GPA.

300 d 453 (24.7%) prescribed an NS-NSAID without GPA cotherapy.