ライフサイエンスコーパス: DSA

1 DSA allows investigators to manage large collections of

2 DSA developed within 4 weeks of all sensitizing grafts a

3 DSA MFI greater than 10 000 versus MFI 1000 to 10 000 at

4 DSA prior to treatment decisions is helpful for characte

5 DSA requires the control of interfacial properties on bo

6 included 95 patients with high peak or day 0 DSA levels (mean fluorescence intensity [MFI] > 3000) wi

7 r with increasing DSA (8.2% -DSA/-XM, 17.0% +DSA/-XM, 30.6% +DSA/low +XM, and 51.2% +DSA/high +XM, P

8 n (HR, 2.18; 95% CI, 1.38-3.43; P = 0.0008), DSA greater than 500 MFI at transplant (HR, 1.64; 95% CI

9 imilar in groups without baseline DSA (8.1% -DSA/-XM vs 15.4% -DSA/+XM, P = 0.19).

10 posttransplant (DSA negative: 613(300-1090); DSA positive 106(34-235) pmol/L [p = 0.004]).

11 d treatment, DSA decreased, in 4 (36%) of 11 DSA were below 500 mean fluorescence intensity after tre

12 .0% +DSA/-XM, 30.6% +DSA/low +XM, and 51.2% +DSA/high +XM, P < 0.01), but similar in groups without b

13 biopsy was higher with increasing DSA (8.2% -DSA/-XM, 17.0% +DSA/-XM, 30.6% +DSA/low +XM, and 51.2% +

14 based on glomerular miRNAs identified 18/20 DSA+ and 8/10 controls correctly.

15 ithout baseline DSA (8.1% -DSA/-XM vs 15.4% -DSA/+XM, P = 0.19).

16 at 229 adult kidney transplant centers in 58 DSAs.

17 g DSA (8.2% -DSA/-XM, 17.0% +DSA/-XM, 30.6% +DSA/low +XM, and 51.2% +DSA/high +XM, P < 0.01), but sim

18 Our study included 86 DSA+ kidney transplant recipients subjected to protocol

19 -transplant screening identified 186 (21.9%) DSA-positive patients.

20 ulopathy (AV) after aorta transplantation, a DSA-mediated process.

21 port distances that were more uniform across DSAs, saved about 20 additional lives, and reduced DSA-a

22 notype associated with complement-activating DSA was characterized by complement deposition and accum

23 rate in patients with complement-activating DSAs (56%; 95% confidence interval [95% CI], 38% to 74%

24 kidney recipients for complement-activating DSAs and used histopathology, immunostaining, and allogr

25 t not in those with noncomplement-activating DSAs (9%; 95% CI, 2% to 25% versus 13%; 95% CI, 2% to 40

26 ith the obliteration of PAVM during or after DSA are poorly understood.

27 patients with donor-specific alloantibodies (DSA) mean florescence intensity (MFI) greater than 10 00

28 r de novo HLA donor-specific alloantibodies (DSA).

29 e presence of donor-specific alloantibodies (DSAs) at the time of transplantation leads to acute and

30 Although DSA number or HLA class specificity were not different,

31 Among DSA+ study patients, 44 recipients (51%) had AMR, 24 of

32 nds as well as descriptive sensory analysis (DSA).

33 ular capillaritis Banff score (P=0.002), and DSA mean fluorescence intensity (P<0.001) after treatmen

34 on (calculated reaction frequency [cRF]) and DSA was determined.

35 and BIVV009 profoundly inhibited overall and DSA-triggered CP activation in serum.

36 iated routine post-transplant BK viremia and DSA screening at our center; 785 kidney or kidney-pancre

37 +DSA/-XM, +DSA/low +XM, +DSA/high +XM, and -DSA/+XM and followed up for a mean of 4.1 +/- 1.9 years

38 erated shortly after diagnostic angiography (DSA).

39 t follow-up digital subtraction angiography (DSA) after initial DSA with results negative for aneurys

40 mpared with digital subtraction angiography (DSA) as the reference standard.

41 Digital subtraction angiography (DSA) of cerebral vessels with rotational scanning was pe

42 g (MRI) and digital subtraction angiography (DSA) revealed a dissection beginning at the cervical seg

43 roduction is the dimensionally stable anode (DSA), Ti coated by a mixed oxide of RuO2 and TiO2.

44 ed early donor specific anti-HLA antibodies (DSA) after lung transplantation were preemptively treate

45 reduction of donor-specific HLA antibodies (DSA) below 500 mean fluorescence intensity.

46 th donor-specific anti-human HLA antibodies (DSA) detected in the first year post-transplant.

47 ning for donor-specific anti-HLA antibodies (DSA) using bead-based multiplex assays to determine tran

48 de novo donor-specific anti-HLA antibodies (DSA).

49 en), and donor-specific anti-HLA antibodies (DSA).

50 Development of donor-specific antibodies (DSA) after lung transplantation is associated with antib

51 tatus (P = 0.02), donor-specific antibodies (DSA) against HLA class II (P = 0.03), donor age (P = 0.0

52 AABMR), with C4d, donor-specific antibodies (DSA) and other lesions of chronic tissue injury.

53 accepted that HLA donor-specific antibodies (DSA) are associated with antibody-mediated rejection and

54 Circulating donor-specific antibodies (DSA) detected on bead arrays may not inevitably indicate

55 with preexisting donor-specific antibodies (DSA) is very challenging.

56 existing anti-HLA donor-specific antibodies (DSA) or in patients who develop de novo DSA.

57 ansplant, de novo donor-specific antibodies (DSA), antibody-mediated rejection (AMR), acute cellular

58 complement-fixing donor-specific antibodies (DSA).

59 of patients with donor-specific antibodies (DSA).

60 rance of donor-specific anti-HLA antibodies (DSAs) did not accelerate the rate of islet graft attriti

61 tivating anti-HLA donor-specific antibodies (DSAs) are associated with impaired kidney transplant out

62 Preexisting, donor-specific antibodies (DSAs) are culprits of hyperacute rejection.

63 he development of donor-specific antibodies (DSAs) make it an interesting agent in hand transplantati

64 ding activity for donor-specific antibodies (DSAs) were determined.

65 esized that de novo donor-specific antibody (DSA) causes complement-dependent endothelial cell injury

66 Avoiding donor-specific antibody (DSA) is difficult for sensitized patients.

67 stigate the role of donor-specific antibody (DSA) on intestinal graft outcomes.

68 progression of late donor-specific antibody (DSA)-positive ABMR.

69 mismatch to induce donor-specific antibody (DSA).

70 icle, we describe the Digital Slide Archive (DSA), an open-source web-based platform for digital path

71 tes varies greatly by donation service area (DSA) due to geographic differences in availability of or

72 borhood-a collection of donor service areas (DSA) surrounding the OPO that acts as the OPO's region i

73 unevenly throughout 58 donor service areas (DSAs) in the United States.

74 Directed self-assembly (DSA) of block copolymers (BCPs) has been a recently demo

75 Directed self-assembly (DSA) of block copolymers is an emergent technique for na

76 Directed self-assembly (DSA) of the domain structure in block copolymer (BCP) th

77 We assessed DSA characteristics and performed systematic allograft b

78 We assessed DSA characteristics, including specificity, HLA class sp

79 EMS correlated with the risk of HLA-A and -B DSA development.

80 urvival in patients who underwent IVIG-based DSA treatment (group A, n = 57) versus contemporary pati

81 transplanted with varied levels of baseline DSA detected by single antigen beads and B flow cytometr

82 .01), but similar in groups without baseline DSA (8.1% -DSA/-XM vs 15.4% -DSA/+XM, P = 0.19).

83 ric LTx and assess the impact of C1q-binding DSA on allograft outcomes.

84 type was associated with DSA and C1q-binding DSA, with odds ratios of 13 (P = 0.015) and 8.6 (P = 0.0

85 rmation set of 20 human transplant biopsies (DSA+) compared to 10 matched controls without evidence f

86 had DSA class I, 9% class II, and 2.4% both DSA classes 1 and 2.

87 lective perfusion deficits were confirmed by DSA and MRI in all monkeys.

88 Outcomes varied greatly by DSA; for candidates with allocation MELD 25-29, the 25th

89 he persistence of antibodies is predicted by DSA strength and specificity.

90 acteristics and annual kidney transplants by DSA.

91 lt to assess damage inflicted exclusively by DSAs when alloreactive T cell and B cell responses coinc

92 howed significantly higher IgG, C1q, and C3d DSA MFI than nonrejecting or C4d-negative patients, resp

93 h isolated TG, TG suspicious for CAABMR (C4+/DSA- or C4d-/DSA+) and TG with definite CAABMR (C4d+/DSA

94 C4d-/DSA+) and TG with definite CAABMR (C4d+/DSA+) were 63%, 20%, and 17%, respectively.

95 , TG suspicious for CAABMR (C4+/DSA- or C4d-/DSA+) and TG with definite CAABMR (C4d+/DSA+) were 63%,

96 eted a cross-sectional study to characterize DSA in long-term survivors of pediatric LTx and assess t

97 ogic parameters, histopathology, circulating DSA, and allograft gene expression for all patients with

98 96%; P=0.12), urinary protein concentration, DSA levels, or morphologic or molecular rejection phenot

99 lotransplantation model were used to confirm DSAs' specificity for allo-major histocompatibility comp

100 that likely preceded the use of the current DSA technique.

101 s transplanted with isolated preformed Cw/DP DSA (Cw/DP DSA group) with (i) 104 matched HLA-sensitize

102 itive flow cytometry crossmatch in the Cw/DP DSA group was more frequent than in the No DSA group and

103 ted with isolated preformed Cw/DP DSA (Cw/DP DSA group) with (i) 104 matched HLA-sensitized kidney tr

104 We analyzed the clinical impact of Cw/DP DSA through a retrospective study, comparing 48 patients

105 t that preformed anti-HLA-Cw and anti-HLA-DP DSA are as deleterious as anti-HLA A/B/DR/DQ DSA.

106 grams, preformed anti-HLA-Cw and anti-HLA-DP DSA are not considered in organ allocation policies beca

107 transplantation, with the majority being DQ DSA.

108 nt recipients with preformed A, -B, -DR, -DQ DSA (A/B/DR/DQ DSA group).

109 ith preformed A, -B, -DR, -DQ DSA (A/B/DR/DQ DSA group).

110 urvival was worse in the Cw/DP and A/B/DR/DQ DSA groups than in the No DSA group (65%, 84%, 93%, P =

111 val was lower in the Cw/DP and the A/B/DR/DQ DSA groups than in the No DSA group (87%, 89%, 95%, P =

112 DSA are as deleterious as anti-HLA A/B/DR/DQ DSA.

113 ed with the development of HLA-DR and HLA-DQ DSA, but only EMS correlated with the risk of HLA-A and

114 -six percent of recipients with dnDSA had DQ-DSA.

115 e sum of mean fluorescence intensity of DSA (DSA MFI-Sum) of 6,000 or higher (OR, 18; 95% CI, 7.0-47;

116 Patients with new early DSA but without graft dysfunction that are treated with

117 ary lung transplant recipients without early DSA.

118 The open-source model enables DSA to be extended to provide additional capabilities.

119 A (group C, n = 180), as well as to evaluate DSA clearance in IVIG-treated patients versus historic p

120 Three subjects never exhibited DSA.

121 t cytotoxicity mediated by complement-fixing DSAs and phagocytic cells.

122 Patients were grouped as follows: -DSA/-XM, +DSA/-XM, +DSA/low +XM, +DSA/high +XM, and -DSA

123 nd 2010 who were systematically screened for DSA at transplant, 1 and 2 years post-transplant, and th

124 Patients were screened for DSA pretransplant, monitored regularly posttransplant an

125 l cells were the only accessible targets for DSAs, which induced the development of typical microvasc

126 Forty-four DSA-positive kidney transplant recipients with character

127 ntation from January 2000 to April 2009, had DSA (MFI >/=1000) in serum 10 to 14 months postliver tra

128 Nine percent of the subjects had DSA class I, 9% class II, and 2.4% both DSA classes 1 an

129 At transplant, 110 (12.9%) patients had DSAs; post-transplant screening identified 186 (21.9%) D

130 binding antibodies had worse eGFR and higher DSA mean fluorescence intensity.

131 f donor-specific anti-HLA antibody (anti-HLA DSA) characterization.

132 toantibodies and the interaction between HLA DSA and non-HLA autoantibodies remains uncharacterized.

133 s from 1 of 2000 to 4 of 2009 with known HLA DSA status for angiotensin II type-1 receptor and endoth

134 A autoantibody combined with a preformed HLA DSA is associated with an increased mortality risk.

135 [HR], 1.66; P = 0.02) especially if the HLA DSA was of the IgG3 subclass (HR, 2.28; P = 0.01).

136 C4d staining pattern when compared with HLA DSA (71% vs 3%; P < 0.001).

137 , circulating complement-activating anti-HLA DSAs are associated with a specific histomolecular kidne

138 of preformed non-HLA autoantibodies and HLA-DSA were associated with an increased risk for death (ha

139 entrations in the presence or absence of HLA-DSA (P = 0.007 and 0.03 for g scores; p = 0.005 and 0.03

140 subjects showed intermittent de novo class I DSA, 4 subjects showed persistent de novo class II DSA,

141 miRNA signature associated with HLA class I-DSA could improve our understanding of ABMR and be usefu

142 Class II DSA was predominantly against donor DQ antigens, often o

143 subjects showed persistent de novo class II DSA, and 5 subjects showed persistent preexisting class

144 jects showed persistent preexisting class II DSA.

145 dian MFI of the immunodominant class I or II DSA in the peak or day 0 serum was 9421 (interquartile r

146 The MFI of the immunodominant DSA (iDSA, the DSA with the highest MFI level) was 6724+

147 better evaluated through the immunodominant DSA MFI than through the sum of DSA MFI.

148 a cAMR score greater than 13 (P = 0.004) in DSA+ patients with MFI 1000 to 10 000.

149 d 2 downregulated (miR29b-3p, miR-885-5p) in DSA+ vs. CONTROLS: A random forest analysis based on glo

150 e estimate a 50% prevalence of silent AMR in DSA+ long-term recipients and conclude that assessment o

151 sed to risk-stratify putative chronic AMR in DSA+ patients with MFI from 1000 to 10 000.

152 eath-censored long-term allograft failure in DSA+ patients regardless of MFI, and higher MFI at 1 yea

153 The IVIG yielded increased DSA clearance compared with historic tPE-based treatment

154 rveillance biopsy was higher with increasing DSA (8.2% -DSA/-XM, 17.0% +DSA/-XM, 30.6% +DSA/low +XM,

155 costimulation-deficient" cells should induce DSA synthesis but not naive cytotoxic T lymphocyte (CTL)

156 subtraction angiography (DSA) after initial DSA with results negative for aneurysms in subjects with

157 eurysmal subarachnoid hemorrhage and initial DSA negative for aneurysms, the yield of follow-up DSA f

158 substituted at the interaction surface (INT/DSA/3 H) to impart a pH-sensitive response.

159 The INT/DSA/3 H exhibits stronger affinity to iMVP (K Dapp = 24

160 mpared with DSA mean fluorescence intensity, DSA IgG3 positivity and C1q binding capacity adequately

161 eatment end (92% vs 64%; P = 0.002) and last DSA control (90% vs 75%; P = 0.04).

162 roved understanding of the risk of low level DSA is needed.

163 Kidney transplantation with low-level DSA with or without a low positive XM is a reasonable op

164 to the following metrics: total mortalities, DSA-average model for end-stage liver disease (MELD) at

165 ith PM hemorrhage who had undergone multiple DSA examinations.

166 Murine DSAs bound to allogeneic targets expressed by islet cell

167 treatment, yet spontaneous clearance of new DSA also remains common.

168 transplant recipients with No DSA at D0 (No DSA group) and (ii) 47 kidney transplant recipients with

169 % or greater are at risk for CAMR even if no DSA is detected.

170 w/DP and A/B/DR/DQ DSA groups than in the No DSA group (65%, 84%, 93%, P = 0.001 and P = 0.05, respec

171 and the A/B/DR/DQ DSA groups than in the No DSA group (87%, 89%, 95%, P = 0.02 and P = 0.1, respecti

172 P DSA group was more frequent than in the No DSA group and as frequent as in the A/B/DR/DQDSA group.

173 sitized kidney transplant recipients with No DSA at D0 (No DSA group) and (ii) 47 kidney transplant r

174 The risk for CAMR is low in patients with no DSA even if the XM is positive.

175 The incidence of weak de novo DSA or non-DSA at a mean fluorescence intensity of 500 or higher wa

176 e impact of circulating HLA and noncytotoxic DSA detected before transplant on development of Chronic

177 , neither the presence of HLA antibodies nor DSA translated to an increased risk of allograft dysfunc

178 1) and for patients with C1q-binding de novo DSA (P=0.002) than for patients without de novo DSA.

179 lower for patients with C1q-binding de novo DSA (P=0.003).

180 ior graft survival compared with the de novo DSA ABMR (63% versus 34% at 8 years after rejection, res

181 ristics and treatment, we identified de novo DSA ABMR (hazard ratio [HR], 1.82 compared with preexist

182 preexisting DSA ABMR, patients with de novo DSA ABMR displayed increased proteinuria, more transplan

183 De novo DSA ABMR was characterized by increased expression of IF

184 rs for the appearance of C1q-binding de novo DSA and their long-term impact.

185 between patients with C1q-nonbinding de novo DSA and those without de novo DSA, but was lower for pat

186 In conclusion, C1q-binding de novo DSA are associated with graft loss occurring quickly aft

187 ents experiencing AR had circulating de novo DSA at the time of AR.

188 g-term persistence of C1q-nonbinding de novo DSA could lead to lower graft survival.

189 wer for patients with C1q-nonbinding de novo DSA detected at both 2 and 5 years (P<0.001) and for pat

190 De novo DSA directed against most recent islet transplant were a

191 tch is a significant risk factor for de novo DSA emergence, whereas the persistence of antibodies is

192 ly graft failure, whereas those with de novo DSA experienced accelerated graft loss once DSA was dete

193 De novo DSA formation, particularly early in the posttransplant

194 De novo DSA mean fluorescence intensity >6237 and >10,000 at 2 a

195 Impact of de novo DSA on graft function over 12 months following first isl

196 The incidence of weak de novo DSA or non-DSA at a mean fluorescence intensity of 500 o

197 the freedom from the development of de novo DSA was observed (HR, 2.26 for HLA antibodies and ETAR;

198 ower freedom from the development of de novo DSA was observed for recipients with antibodies detected

199 When de novo DSA were analyzed at 2 and 5 years, the 10-year death-ce

200 When de novo DSA were analyzed at 2 years, the 5-year death-censored

201 s associated with increased risk for de novo DSA, although the exact mechanism is unclear.

202 ditional 24 (25%) patients developed de novo DSA, and of these, 71% had persistent antibodies.

203 inding de novo DSA and those without de novo DSA, but was lower for patients with C1q-binding de novo

204 nd 5 years after transplantation for de novo DSA, which was followed when positive by a C1q Luminex a

205 diagnosed in 5 of 36 recipients with de novo DSA.

206 rage efforts to monitor patients for de novo DSA.

207 d with increased risk of C1q-binding de novo DSA.

208 (P=0.002) than for patients without de novo DSA.

209 ients, respectively, had C1q-binding de novo DSA.

210 numerically higher in patients with de novo DSA.

211 ve (19%) grafts were associated with de novo DSA.

212 ies (DSA) or in patients who develop de novo DSA.

213 ad preexisting DSA and 102 (50%) had de novo DSA.

214 Addition of DSA IgG3 positivity or C1q binding capacity increased di

215 y suggests that DSA MFI-Sum and HLA class of DSA are characteristics predictive of AMR and graft fail

216 The MFI distribution of DSA+ recipients were as follows: 66% had MFI 1000 to 499

217 We performed a retrospective evaluation of DSA in sera from 43 children who had received transplant

218 ure in those with the identified features of DSA is attributable to increased risk of AMR.

219 The sum of mean fluorescence intensity of DSA (DSA MFI-Sum) of 6,000 or higher (OR, 18; 95% CI, 7.

220 nvestigated whether systematic monitoring of DSA with extensive characterization increases performanc

221 nce interval, 0.50-1.54) nor the presence of DSA (adjusted hazard ratio, 1.56; 95% confidence interva

222 % CI, 7.0-47; P < 0.001) and the presence of DSA against both HLA class I and II (OR, 39; 95% CI, 14-

223 The presence of DSA is associated with inferior graft outcomes among int

224 munodominant DSA MFI than through the sum of DSA MFI.

225 Overall, the predictive value of DSA characteristics was moderate, whereby the highest ac

226 In contrast, the vasculature of DSA-exposed allogeneic islet grafts was devoid of lesion

227 A fourth patient had significant levels of DSAs at time of conversion and progressed to a severe ne

228 rism combined with vascular sequestration of DSAs protects islet grafts from humoral rejection.

229 gh the selectivity for chlorine evolution on DSA is high, the fundamental reasons for this high selec

230 ined the effect of CTLA4-Ig and rapamycin on DSA-mediated cytolysis.

231 DSA experienced accelerated graft loss once DSA was detected, reaching a 28% failure rate within 2 y

232 much work remains to understand and optimize DSA methods in order to move this field forward.

233 tion inflammation, gene expression patterns, DSA levels, or kidney function.

234 function in patients with chronic persistent DSA based on our pilot a priori significance threshold.

235 ct was lost among recipients with persistent DSA.

236 We initiated a routine posttransplant DSA monitoring and surveillance biopsy program for dnDSA

237 quartile range]) at 3 months posttransplant (DSA negative: 613(300-1090); DSA positive 106(34-235) pm

238 ss of MFI, and higher MFI at 1 year predicts DSA persistence at 5 years.

239 Overall, 103 (50%) patients had preexisting DSA and 102 (50%) had de novo DSA.

240 The preexisting DSA ABMR had superior graft survival compared with the d

241 Compared with patients with preexisting DSA ABMR, patients with de novo DSA ABMR displayed incre

242 of AKI transcripts compared with preexisting DSA ABMR.

243 d ratio [HR], 1.82 compared with preexisting DSA ABMR; 95% confidence interval [95% CI], 1.07 to 3.08

244 Recipients with preformed DSA demonstrated elevated risks of early graft failure,

245 Pretransplant DSA was detected in 12 (11%) recipients with 50% continu

246 han 1 year, and (3) absence of pretransplant DSA.

247 ted rejection in patients with pretransplant DSA, neither the presence of HLA antibodies nor DSA tran

248 e after transplant, 5.0 years; pretransplant DSA documented in 19 recipients), who were identified on

249 testing of future immunotherapies to prevent DSA-induced pathology.

250 Outcomes are reported by transplant program, DSA, region, and the nation for comparison, and can be s

251 immunosuppression intensity, and prospective DSA surveillance.

252 we have developed a novel model to quantify DSA-mediated cytotoxicity in vivo.

253 saved about 20 additional lives, and reduced DSA-average MELD standard deviation by an additional 17%

254 ic or molecular disease features, or reduces DSA, despite significant toxicity.

255 vitro; however, passive transfer of the same DSAs did not affect islet graft survival in murine model

256 Serum DSA levels and the deposition of IgG and C4d in the allo

257 A subsequent DSA depicted a medium-sized nidus, receiving blood suppl

258 ummary aneurysm detection rate at subsequent DSA was 1.6% (95% confidence interval: 0.7%, 3.8%; range

259 ry rate of aneurysm detection for subsequent DSA was calculated by using a fixed-effects model.

260 These results suggest that DSA-sensitized patients with high MFI levels can receive

261 Our study suggests that DSA MFI-Sum and HLA class of DSA are characteristics pre

262 Live imaging revealed that DSAs were sequestrated in the circulation of the recipie

263 The DSA clearance was better in group A than group B at trea

264 reatic enzymes was noticed shortly after the DSA procedure.

265 The MFI of the immunodominant DSA (iDSA, the DSA with the highest MFI level) was 6724+/-464, and 41.6

266 results showed that neighborhoods reduce the DSA-average MELD standard deviation by 29% and save abou

267 We design 58 neighborhoods for the DSAs with several attractive properties and optimize the

268 rvival was similar in all groups except the +DSA/high +XM group, which was lower at 79.1% versus 96.2

269 hich was lower at 79.1% versus 96.2% in the -DSA/-XM group (P < 0.01).

270 f reporting diffuse ptc, which may relate to DSA binding strength and potentially to chronic graft in

271 re and leukocytic composition in relation to DSA binding strength (mean fluorescence intensity [MFI]_

272 Here we expand on traditional DSA chemical patterning.

273 Thus, pre- and post-transplant DSA monitoring and characterization may improve individu

274 Post-transplant DSA monitoring improved the prediction of allograft loss

275 nd-stage liver disease (MELD) at transplant, DSA-average MELD standard deviation, and average organ t

276 4%) of 11 patients, who completed treatment, DSA decreased, in 4 (36%) of 11 DSA were below 500 mean

277 morrhage at computed tomography (CT) and two DSA examinations negative for aneurysm within 10 days we

278 aphic results negative for aneurysm, and two DSA examinations within 10 days.

279 It is found that these two DSA methods do synergistically enhance long-range order

280 This is in contrast to the typical DSA, wherein assembly of a single-component block copoly

281 s with cPRA of 80% or greater and undetected DSA and negative XM at baseline.

282 f the procedure was confirmed on a follow-up DSA after 8.0+/-4.1 months from the initial treatment.

283 gative for aneurysms, the yield of follow-up DSA for detection of causative aneurysms is very low.

284 No aneurysms were seen at follow-up DSA in the single-center study (0.0%).

285 Three aneurysms were detected at follow-up DSA in three of six studies from the literature (one of

286 On a follow-up DSA, complete embolization was present in 25 aneurysms (

287 5.0 degrees C and atmospheric pressure using DSA-5000 M.

288 CAMR (hazard ratio, 5.2; P = 0.03) even when DSA was undetected at baseline.

289 However, it is unclear whether DSA monitoring is necessary and could predict graft outc

290 ced understanding of the mechanisms by which DSA causes allograft injury, and effective strategies ta

291 he nontolerant phenotype was associated with DSA and C1q-binding DSA, with odds ratios of 13 (P = 0.0

292 Compared with DSA mean fluorescence intensity, DSA IgG3 positivity and

293 ing techniques, should not be evaluated with DSA due to the potential risk of severe complications, s

294 Combining the urinary CXCL10:Cr ratio with DSA monitoring significantly improves the noninvasive di

295 rticipants (five control, 10 treatment) with DSA and deteriorating renal function were enrolled.

296 on in 116 independent kidney recipients with DSAs at transplant receiving rejection prophylaxis with

297 between April 2013 and January 2015 without DSA (group C, n = 180), as well as to evaluate DSA clear

298 identified 154 patients with and 389 without DSA.

299 Patients were grouped as follows: -DSA/-XM, +DSA/-XM, +DSA/low +XM, +DSA/high +XM, and -DSA/+XM and f

300 ere grouped as follows: -DSA/-XM, +DSA/-XM, +DSA/low +XM, +DSA/high +XM, and -DSA/+XM and followed up

301 follows: -DSA/-XM, +DSA/-XM, +DSA/low +XM, +DSA/high +XM, and -DSA/+XM and followed up for a mean of