ライフサイエンスコーパス: DLI

1 DLI administration resulted in a decrease in host-derive

2 DLI administration to mixed chimeras produced dramatical

3 DLI also converted mixed chimeras to full chimeras witho

4 DLI amplified allografts to full donor engraftment long-

5 DLI analysis highlighted the divergent responses of EOM

6 DLI caused no sustained graft-versus-kidney effects in t

7 DLI consisted of 3 x 10(7) CD4(+) donor T cells per kilo

8 DLI neither facilitated conversion to full donor chimeri

9 DLI produced a further response in three of 15 recipient

10 DLI-1, like its vertebrate homologs, contains a putative

11 DLI-induced GVHD was prevented in lymphopenic recipients

12 DLI-treated mice either maintained long-term tolerance o

13 K), were recognized by sera from three of 19 DLI responders.

14 and September 2001, 73 patients received 94 DLI treatments.

15 iological requirements to quickly generate a DLI product ex vivo using a negligible fraction of a cor

16 Furthermore, upon adoptive transfer in a DLI model, ex vivo sFasL-treated T cells were able to re

17 Activated DLI was dose escalated from 1 x 10(6) to 1 x 10(8) CD3+

18 rformed a phase 1 trial of ex vivo-activated DLI (aDLI) for 18 patients with relapse after SCT.

19 DLI-mediated alloresponses, we administered DLI alone or after topical application of the TLR7 ligan

20 After DLI, 50% of patients developed acute (> or = II) or exte

21 an those with donor BM-derived T cells after DLI, even though both groups had comparable levels of to

22 patients with myeloma who achieved CR after DLI and 1 patient who was in CR before DLI.

23 in mixed chimeras, as late as 20 days after DLI, also provoked severe GVHD.

24 proliferation was elevated at 14 days after DLI.

25 was at 35 days (range, 11 to 406 days) after DLI.

26 Liver GVHD developed after DLI in 22 (30%) patients whose median age was 43 years (

27 DLI and expanded approximately 10-fold after DLI.

28 lted in significantly more severe GVHD after DLI.

29 had no impact on the severity of GVHD after DLI.

30 e graft-versus-leukemia response (GVL) after DLI, we used CML post-DLI responder sera to screen a CML

31 Significant GVM responses were noted after DLI in 10 patients with persistent disease, resulting in

32 ociated with GVHD are expanded de novo after DLI.

33 However, GVHD sometimes occurs after DLI in established mixed chimeric patients.

34 rvations suggest that GVHD that occurs after DLI may have distinct clinical features.

35 de that delayed administration of RAPA after DLI does not interfere with their LH-GVH reactivity but

36 patients who developed GVL reactivity after DLI in the absence or presence of GVHD.

37 date have achieved molecular remission after DLI.

38 atients who achieve complete remission after DLI.

39 t the majority of molecular remissions after DLI are durable, and thus the majority of responding pat

40 tients who achieved durable remissions after DLI developed a significant B-cell lymphocytosis after t

41 ody response and time of best response after DLI.

42 parent graft-versus-leukemia responses after DLI.

43 irst 6 months after BMT and for 1 year after DLI.

44 However, perforin-deficient alloreactive DLI induced significantly less apoptosis of vaccine-resp

45 inical cell processing of BMT allografts and DLI infusions.

46 However, the therapeutic utility of BMT and DLI is reduced by the high incidence of graft-versus-hos

47 remission following further chemotherapy and DLI.

48 Both RLI and DLI significantly delayed tumor mortality.

49 aNK-DLI demonstrated potent killing capacity and displayed h

50 aNK-DLI were CD3(+)-depleted, CD56(+)-selected lymphocytes,

51 derived IL-15/4-1BBL-activated NK cells (aNK-DLI) following HLA-matched, T-cell-depleted (1-2 x 10(4)

52 aft-versus-host disease (GVHD) following aNK-DLI, with grade 4 GVHD observed in 3 subjects.

53 r GVHD in this setting, we conclude that aNK-DLI contributed to the acute GVHD observed, likely by au

54 spite significant advances in applicability, DLI has not been available for single-unit recipients of

55 When given as DLI together with wild-type spleen cells, marked expansi

56 c allogeneic engraftment was achieved before DLI only in the presence of both anti-CD40L mAb and CTLA

57 CR at a low level in peripheral blood before DLI and expanded approximately 10-fold after DLI.

58 Salvage treatment with chemotherapy before DLI can help some patients with advanced myeloid relapse

59 after DLI and 1 patient who was in CR before DLI.

60 ociated with GVHD were not detectable before DLI or before the development of clinical GVHD.

61 sive conditioning therapy immediately before DLI.

62 was not observed with plasma obtained before DLI and from DLI nonresponders and imatinib-treated pati

63 eloma specificity that may be present before DLI.

64 A strong association was found between DLI and whether or not a surgeon accepts an offered live

65 ymphoblastic leukemia was also eradicated by DLI in major histocompatibility complex (MHC)-mismatched

66 Immune modulation by DLI strategies or second HSCT is advised if relapse occu

67 specific immunity that can be transferred by DLI was unknown and was investigated in these experiment

68 CD4(+) DLI was also associated with increased numbers of TRECs

69 ic BMT was combined with prophylactic CD4(+) DLI administered 6 to 9 months after BMT in an effort to

70 oth groups, but patients who received CD4(+) DLI developed increased numbers of CD20(+) B cells.

71 nic myelogenous leukemia who received CD4(+) DLI in the pre-tyrosine kinase inhibitor era.

72 analysis of CDR3 Vbeta repertoire after CD4+ DLI demonstrated previously that the development of GVM

73 ate that GVHD after HLA-DPB1-mismatched CD4+ DLI can be mediated by allo-reactive HLA-DPB1-directed C

74 At the time of CD4+ DLI, both patients contained residual patient-derived T

75 ed severe acute GVHD after prophylactic CD4+ DLI after 10/10-HLA-matched, but HLA-DPB1-mismatched TCD

76 s that received high-dose (30 x 10(6) cells) DLI.

77 In conclusion, DLI is a potential treatment strategy, with acceptable t

78 rapy, and all patients received conventional DLI (median, 1.5 x 10(8) mononuclear cells/kg) followed

79 le remissions in diseases where conventional DLI has been disappointing.

80 In summary, immunologic targets of curative DLI responses include multiple antigens on CML progenito

81 sing Fas ligand-deficient or TRAIL-deficient DLI had no impact on apoptosis of HY-specific T cells.

82 ction of mixed chimerism followed by delayed DLI provides an approach to inhibiting GVHD that optimiz

83 HC class II-negative tumor following delayed DLI require CD4(+) T-cell help and are reduced significa

84 eras showed increased GVHD following delayed DLI.

85 ameliorating GVHD in the setting of delayed DLI in established mixed chimeras.

86 for GVHD in mixed chimeras receiving delayed DLI.

87 ing GVHD in mixed chimeras receiving delayed DLI.

88 ke leukemia, combined treatment with delayed DLI and the kinase inhibitor imatinib eradicates leukemi

89 After early DLI, CML-like leukemia cannot be transferred into immuno

90 ibodies later after transplant to facilitate DLI-mediated GVL without GVHD complications.

91 Only the patients receiving Cy/Flu/DLI became lymphopenic at the time of DLI.

92 with controls, patients who received Cy/Flu/DLI developed significantly more grades II to IV (60% vs

93 In Cy/Flu/DLI patients, T-cell proliferation was elevated at 14 da

94 relapsed non-CML disease who received Cy/Flu/DLI were compared with 63 controls who received DLI with

95 n independent risk factor for GVHD following DLI in the absence of known inflammatory stimuli.

96 t graft-versus-host disease (GVHD) following DLI, whereas RLI led to loss of chimerism.

97 dicating this is not an essential domain for DLI-1 function.

98 Indications for DLI were unsatisfactory response/disease progression in

99 lear count, and performance of prior LVL for DLI collection.

100 lay relapse and postpone the requirement for DLI in 22 patients with chronic myeloid leukemia (CML) a

101 ved with plasma obtained before DLI and from DLI nonresponders and imatinib-treated patients.

102 suggest that depletion of CD8(+) cells from DLI could impair GvL against CML, while increased MHC di

103 lymphocyte infusion (DLI) (median time from DLI to imatinib mesylate therapy, 4 months [range, 2-39

104 s, compared with 1 of 5 mixed chimeras given DLI by vaccination from sensitized donors.

105 In addition, 10 (77%) of 13 patients given DLI for relapse after transplantation experienced remiss

106 e the role of residual host LCs in governing DLI-mediated alloresponses, we administered DLI alone or

107 The 9 h DLI group, when both tumor and plasma concentrations of

108 permitted withholding of potentially harmful DLI in those with PET-negative masses on CT scans.

109 bone marrow abrogates GVHD, allowing higher DLI doses to be tolerated, but improves vaccine response

110 However, DLI donors sensitized by kidney transplantation converte

111 d chimeras that the remaining hyporesponsive DLI-derived CD4+ T cells secrete large amounts of IL-10,

112 at circulating antibody-antigen complexes in DLI-responsive patients carry nucleic acids that can eng

113 considered in the differential diagnosis in DLI recipients with unexplained hepatitis.

114 We found discordance in DLI-mediated LH-GVH reactivity depending on the timing o

115 No GVHD occurred in DLI recipients.

116 The donor liver index (DLI) was based on factors shown to affect graft survival

117 ified using an aggregate disease load index (DLI) to measure stage-dependent transcriptional impact i

118 Donor leukocyte infusion (DLI) can induce graft-versus-leukemia (GvL) reactions in

119 In mice, donor leukocyte infusion (DLI) given to established mixed allogeneic chimeras can

120 volving delayed B6 donor leukocyte infusion (DLI) to established mixed allogeneic (B6-->BALB/c) chime

121 isease response to donor leukocyte infusion (DLI) was seen in 10 of 14 patients.

122 or chimerism after donor leukocyte infusion (DLI).

123 T) can be cured by donor leukocyte infusion (DLI); however, the cellular mechanisms and strategies to

124 undergone salvage donor lymphocyte infusion (DLI) (median time from DLI to imatinib mesylate therapy,

125 r GVHD induced by donor lymphocyte infusion (DLI) affects the persistence, proliferation, and surviva

126 ll-depleted (TCD) donor lymphocyte infusion (DLI) after TCD allogeneic hematopoietic stem cell transp

127 calating doses of donor lymphocyte infusion (DLI) alone or with pentostatin to convert to complete do

128 t lymphocytes for donor lymphocyte infusion (DLI) and other therapies was performed before G-CSF admi

129 patients received donor lymphocyte infusion (DLI) as interventional therapy for MRD, and the 2-year C

130 owed by postponed donor lymphocyte infusion (DLI) can experience graft-versus-leukemia (GVL) reactivi

131 Donor lymphocyte infusion (DLI) can restore durable molecular remission in a high p

132 examined whether donor lymphocyte infusion (DLI) could be used as adoptive immunotherapy to convert

133 therapies such as donor lymphocyte infusion (DLI) for chronic myelogenous leukemia (CML) may result f

134 d remission after donor lymphocyte infusion (DLI) for progression, was 65% for LG-NHL, 50% for MCL, a

135 effectiveness of donor-lymphocyte infusion (DLI) for treatment of relapsed chronic myelogenous leuke

136 Donor lymphocyte infusion (DLI) has been used in postnatal circumstances of mixed c

137 Donor lymphocyte infusion (DLI) has been used to enhance graft-versus-leukemia acti

138 logeneic SCT with donor lymphocyte infusion (DLI) in patients with lymphoid malignancy after failure

139 In two delayed lymphocyte infusion (DLI) models, T cells lacking B7-H3 are capable of provid

140 7 days following donor lymphocyte infusion (DLI) or RLI on day 35.

141 ntation (BMT) and donor lymphocyte infusion (DLI) provide valuable treatments for a range of diseases

142 Donor lymphocyte infusion (DLI) re-establishes failing grafts and treats malignant

143 Donor lymphocyte infusion (DLI) reliably induces durable remission in 75-80% of pat

144 Prophylactic donor lymphocyte infusion (DLI) strategies are recommended in patients at high risk

145 administration of donor lymphocyte infusion (DLI) to established mixed chimeras has been shown to ach

146 Donor lymphocyte infusion (DLI) was administered in 26 episodes of relapse and was

147 patients received donor lymphocyte infusion (DLI) with a median CD3 dose of 1 x 10(7) cells/kg.

148 Donor lymphocyte infusion (DLI), a standard relapse treatment after allogeneic stem

149 le in response to donor lymphocyte infusion (DLI), an established and potentially curative immune the

150 mission following donor lymphocyte infusion (DLI), showing the potency of donor-derived immunity in e

151 Donor lymphocyte infusion (DLI), whereby donor mononuclear cells are infused into p

152 role in governing donor lymphocyte infusion (DLI)-mediated alloresponses.

153 ceived concurrent donor lymphocyte infusion (DLI).

154 ion of GVHD after donor lymphocyte infusion (DLI).

155 rvival benefit of donor lymphocyte infusion (DLI).

156 ism by the use of donor lymphocyte infusion (DLI; P = .03).

157 The use of donor lymphocytes infusion (DLI) continues to treat relapsed chronic myeloid leukemi

158 y and toxicity of donor leukocyte infusions (DLI) after unrelated donor bone marrow transplantation (

159 rent disease with donor leukocyte infusions (DLI) has been proven to be effective salvage therapy for

160 Donor leukocyte infusions (DLI) in the allogeneic hematopoietic transplant setting

161 mmunotherapy with donor leukocyte infusions (DLI) results in complete remission for 60-80% of patient

162 o treatment with donor lymphocyte infusions (DLI) and the survival in 66 consecutive patients who rel

163 Donor lymphocyte infusions (DLI) provide effective therapy for patients with multipl

164 dministration of donor lymphocyte infusions (DLI) to established mixed chimeras.

165 d the ability of donor lymphocyte infusions (DLI) to mediate GVL effects without GVHD in mixed chimer

166 in vivo fate of donor lymphocyte infusions (DLI)-derived T cells, their function, and their antitumo

167 or efficacy in terms of drug-light interval (DLI), and to investigate the impact of rapid PDT effects

168 Infusions of donor lymphocytes (DLI) sensitized against hematopoietic cells converted mi

169 eptor (TLR) ligands was required to maximize DLI-mediated LH-GVH and GVL reactivities in chimeras wit

170 Most DLI-treated mice converted to full allogeneic chimerism

171 teins were recognized by more than 1 myeloma DLI responder.

172 nistered 7 days later (100% mortality in non-DLI controls; P<0.001).

173 nodeficient hosts could not be cured by NST, DLI, and vaccine administration.

174 are responsible for the impaired ability of DLI to induce GVHD.

175 ated with markedly increased accumulation of DLI-derived alloreactive T cells in parenchymal GVHD tar

176 Accumulation of DLI-derived effector T cells and host hematopoietic cell

177 ixed chimerism followed by administration of DLI can mediate powerful GVL effects.

178 es, often allowing earlier administration of DLI in patients with recurrent lymphoma, and permitted w

179 Administration of DLI on day 35 post-BMT led to conversion from mixed to f

180 -free survival compared to administration of DLI to full donor chimeras.

181 VHD enabled the subsequent administration of DLI to improve further clinical responses in this poor-r

182 w-up is required to determine the benefit of DLI and the graft-versus-lymphoma effect.

183 on-specific genes in pretreatment T cells of DLI responders and significant downregulation of gene co

184 In contrast, coadministration of DLI with antigen-presenting cell (APC) activators was in

185 The major drawback of DLI remains graft-versus-host disease, but novel regimen

186 of GVHD and the frequency and durability of DLI responses make this an extremely encouraging strateg

187 the mechanisms of the antileukemic effect of DLI are unknown, and the procedure is complicated by gra

188 meras in B6 mice and evaluated the effect of DLI on EL4 T-cell lymphoma.

189 d surprisingly powerful antitumor effects of DLI in patients achieving mixed chimerism after nonmyelo

190 kemia activity after BMT, but the effects of DLI on immune reconstitution have not been established.

191 se same mechanisms may limit the efficacy of DLI in cancer therapy under some conditions.

192 tion, jeopardizing the potential efficacy of DLI.

193 role of host-derived LCs in the induction of DLI-mediated graft-vs-host alloresponses.

194 edian interval from relapse to initiation of DLI was 9.4 months (range 1-70).

195 use of novel anti-PD1/PDL1 agents in lieu of DLI.

196 The late loss of DLI-mediated GVL effects may reflect the eventual loss o

197 ation mouse model to study the mechanisms of DLI in MHC-matched, minor histocompatibility antigen-mis

198 ed mixed chimerism influences the potency of DLI-mediated alloreactivity only in the MHC-mismatched b

199 tion of RAPA preserved the GVL reactivity of DLI.

200 -Thy1 allelic mAb increased the GVHD risk of DLI, indicating that a Thy1(+) host T cell regulated DLI

201 T-cell exhaustion as a therapeutic target of DLI and support the potential use of novel anti-PD1/PDL1

202 s is a feature common to antibody targets of DLI.

203 ethal total body irradiation, at the time of DLI, contribute to DLI-GVHD resistance.

204 Cy/Flu/DLI became lymphopenic at the time of DLI.

205 tigen-presenting cells (APCs) at the time of DLI.

206 low, resulting in lymphopenia at the time of DLI.

207 rable levels of total T cells at the time of DLI.

208 to determine the efficacy and optimum use of DLI for patients with each disease treated by nonmyeloab

209 The use of DLI to treat certain solid tumors is under investigation

210 l influence of donor-host incompatibility on DLI-mediated GVH responses and suggest that in MHC-match

211 which host T cells are required for optimal DLI resistance were determined.

212 Three illumination time points (DLI = 0.5, 9, or 48 h) were selected for the treatment b

213 Post-DLI depletion of donor BM-derived T cells in mixed chime

214 Post-DLI patient serum was able to induce complement-mediated

215 ked decline in their numbers by week 10 post-DLI.

216 a response (GVL) after DLI, we used CML post-DLI responder sera to screen a CML cDNA expression libra

217 tigens elicited greater reactivity from post-DLI versus pre-DLI plasma.

218 expression signature was detectable in post-DLI but not pre-DLI blood, consistent with an active cir

219 BCMA antibodies were only found in post-DLI responders and not in other allogeneic transplant pa

220 gh-titer antibody reactivity greater in post-DLI than in pre-DLI plasma.

221 nsistent with this, we report here that post-DLI plasma from 5 CML patients that responded to DLI tre

222 panel of 13 gene products reactive with post-DLI serum but negative with pre-DLI and pre-BMT serum.

223 a myeloma cDNA expression library with post-DLI serum from 4 patients with myeloma who achieved CR a

224 led to do so (95% versus 53% at 3 years post-DLI, P = .0001).

225 ed approach of IUHSCTx followed by postnatal DLI can convert low-level, mixed hematopoietic chimerism

226 y reactivity greater in post-DLI than in pre-DLI plasma.

227 ature was detectable in post-DLI but not pre-DLI blood, consistent with an active circulating TLR8/9-

228 greater reactivity from post-DLI versus pre-DLI plasma.

229 ve with post-DLI serum but negative with pre-DLI and pre-BMT serum.

230 ng CD8(+) (but not CD4(+)) T cells predicted DLI response, even in the setting of high leukemia burde

231 transplantation, (2) the toxicity of primary DLI, and (3) whether a graft-versus-tumor (GVT) reaction

232 IFN-gamma promotes DLI-mediated conversion from mixed to full donor chimeri

233 though this study suggests that prophylactic DLI induces significant GVM responses after allogeneic B

234 ed 6 months with no GVHD and did not receive DLI (41%) (P =.13).

235 w a higher proportion of patients to receive DLI and the benefit from the GVM effect after transplant

236 T, only 58% of patients were able to receive DLI despite T-cell--depleted BMT.

237 5 of whom subsequently relapsed and received DLI.

238 Fifteen of 35 assessable patients received DLI after SCT.

239 Patients received DLI for persistent disease (n = 8), disease relapse (n =

240 Patients received DLI from their original transplant donors on a bulk-dose

241 All relapsed patients received DLI to reinduce remission.

242 Fourteen patients received DLI, 3 in complete response and 11 with persistent disea

243 proved more rapidly in patients who received DLI (P =.01).

244 Six of 16 patients who received DLI for chimerism had increases in donor chimerism leadi

245 were compared with 63 controls who received DLI without chemotherapy.

246 GVHD occurred in seven patients who received DLI.

247 Of 48 patients receiving DLI for treatment of disease, 7 achieved CR and 5 PR, wi

248 The 14 patients receiving DLI had an improved 2-year current PFS (65%) when compar

249 icating that a Thy1(+) host T cell regulated DLI-GVHD lethality.

250 However, the overall impact of salvage DLI therapy on the survival of CP CML patients initially

251 ut promotes the emergence of IL-10-secreting DLI-derived CD4+ T cells that might contribute to the dr

252 Twenty-eight days after sensitization, DLI were administered to the mixed-hematopoietic chimera

253 All 8 recipients of mHA-sensitized DLI had conversion to greater than 98% donor chimerism w

254 Complications from mHA-sensitized DLI included graft-versus-host disease in 2 dogs and mar

255 blishes immune tolerance, and mHA-sensitized DLI is required to break tolerance, thereby converting m

256 ZYG-12 is able to bind the dynein subunit DLI-1 in a two-hybrid assay and is required for dynein l

257 Rechallenging the surviving DLI recipients, which had converted to full chimerism, w

258 Long-term DLI recipients had anti-host proliferative responses, bu

259 The DLI is an index of liver quality which enables analysis

260 ients (35%) at a median of 48 days after the DLI; partial responses occurred in 6 patients (total res

261 he PTX prodrug was greatly influenced by the DLI.

262 radiation, at the time of DLI, contribute to DLI-GVHD resistance.

263 dicating that CD28 and 4-1BB are critical to DLI-GVHD resistance.

264 Philadelphia(+) B-lymphoblastic leukemia to DLI.

265 ell recovery from the thymus occurs prior to DLI administration, human T cell reconstitution followin

266 nors, CML-like disease was more resistant to DLI.

267 To determine whether patients who respond to DLI also develop B-cell immunity to CML-associated antig

268 lts demonstrate that patients who respond to DLI generate potent antibody responses to CML-associated

269 nity in patients with myeloma who respond to DLI.

270 plasma from 5 CML patients that responded to DLI treatment induced massive upregulation of MIP-1alpha

271 a patient with relapsed CML who responded to DLI.

272 Our data demonstrate that response to DLI is associated with quantity of preexisting marrow CD

273 The response to DLI was dose dependent, with conversion to complete dono

274 e temporally associated with the response to DLI.

275 received and were assessable for response to DLI.

276 express CD28 or 4-1BB were as susceptible to DLI-GVHD as anti-Thy1 allelic mAb-treated recipients, in

277 t produce IFN-gamma were more susceptible to DLI-GVHD, whereas those deficient in IL-12 or p55 TNFRI

278 not individually were highly susceptible to DLI-GVHD.

279 t occur in patients who were unresponsive to DLI.

280 plasma antibody responses developing in two DLI-treated patients who achieved long-term remission wi

281 sistent disease or relapse, and 15 underwent DLI for mixed hematopoietic chimerism.

282 Twenty-one patients underwent DLI for matched related donor (MD)-persistent disease or

283 irst, 8 mixed chimeras were given unmodified DLI between day 36 and day 414 after stem-cell transplan

284 We identified 58 recipients of unrelated DLI (UDLI) for the treatment of relapsed disease from th

285 ell help was bypassed almost completely when DLI was administered to freshly irradiated recipients, i

286 xacerbated graft-vs-host disease (GVHD) when DLI was administered at 21 days after BMT.

287 ic chimeras with CML-like leukemia, in which DLI can be administered at the time of transplantation (

288 sed this question in a murine model in which DLI is given to stable mixed chimeras resulting in lymph

289 sus-leukemia (GvL) responses associated with DLI for the treatment of CLL by analyzing the specificit

290 d anti-PDC-E2 antibodies in association with DLI response; 2 of 12 (17%) patients in the MGUS pretrea

291 When combined with DLI, a synergistic effect was observed in recipients of

292 owed by targeted adoptive immunotherapy with DLI for those patients with evidence of recurrent diseas

293 owed by targeted adoptive immunotherapy with DLI in 25 CP CML patients undergoing allogeneic BMT from

294 al host chimerism correlated negatively with DLI-mediated alloreactivity irrespective of the timing o

295 ogeneic versus syngeneic BMT recipients with DLI doses below the threshold for clinical GVHD, especia

296 ogenous leukemia (CML) patients treated with DLI develop high-titer plasma antibodies specific for CM

297 for CML, did not benefit from treatment with DLI, and then was administered STI571 at a dose of 400 m

298 atients who underwent allogeneic BMT without DLI and 5 patients with acute graft-versus-host disease

299 ar myeloablative therapy and BMT but without DLI.

300 ear CIR and LFS for patients with or without DLI was 24% vs 87% (P5.001) and 64%vs 0%(P < .001), resp