ライフサイエンスコーパス: PRA

1 PRA and PRB have distinct roles in gene expression and i

2 PRA is normally synthesized by phosphoribosyl pyrophosph

3 PRA is safe, avoids intra-abdominal adjacent organ mobil

4 PRA may be the preferred technique for removing benign a

5 PRA represses the PRB activity.

6 PRA screening is used to determine the presence of pre-f

7 PRA was equivalent between nonresponders and responders

8 A total of 135 PRA, 126 primary anastomoses with defunctioning stoma (P

9 R,1.21 [95% CI,1.12 to 1.31]) in PRA 1%-19%, PRA 20%-79%, and PRA 80%-100% categories compared with P

10 neous vaccination with recombinant antigen 2/PRA (rAg2/PRA) protected BALB/c mice against intranasal

11 xty-five patients were included, of whom 61 (PRA 30, LTLA 31) completed the 5-year follow-up.

12 Twelve percent of the cohort was PRT-75+/PRA-, and only 5% of the patients were PRA+/PRT-75+, ind

13 A PRA value of >/=10% was used to define clinically meanin

14 ional data), with 9 (7.4%) patients having a PRA more than 90%.

15 reas only one of seven (14%) patients with a PRA greater than 15% had AR.

16 Ly markedly raised plasma renin activity (PRA) and aldosterone, and exerted more effective anti-al

17 uced water intake and plasma renin activity (PRA) and found that weight loss decreased water intake a

18 hod was developed for plasma renin activity (PRA) and was evaluated on fifty-three clinical samples.

19 longed suppression of plasma renin activity (PRA) is observed after aliskiren withdrawal.

20 t sensitivity and low plasma renin activity (PRA).

21 serum aldosterone and plasma renin activity (PRA).

22 Plasma renin activity (PRA; >4 ng/mL/hour) was used as a surrogate of effective

23 osterior retroperitoneoscopic adrenalectomy (PRA) is a minimally invasive approach to removal of the

24 rategy only when risk of complications after PRA and PADS reached 50% and 44%, respectively.

25 Complications after PRA reduced patients QALYs to a baseline of 2.713.

26 ith 9.44 QALYs after HP and 9.02 QALYs after PRA.

27 ) DNA (lacking the signal sequence), and Ag2/PRA(1-194) DNA (full length) were inserted in the pVR101

28 of a proline-rich coccidioidal antigen (Ag2/PRA) of Coccidioides immitis were analyzed by comparison

29 Expression plasmids for Ag2/PRA(1-18) DNA (signal sequence), Ag2/PRA(19-194) DNA (la

30 f gamma interferon when splenocytes from Ag2/PRA(1-18)-immunized mice were stimulated with recombinan

31 d in mice immunized with the full-length Ag2/PRA(1-194) DNA.

32 for Ag2/PRA(1-18) DNA (signal sequence), Ag2/PRA(19-194) DNA (lacking the signal sequence), and Ag2/P

33 ifference with IRD transplantation were age, PRA, previous transplant, and the expected time until th

34 All PRA procedures were performed using a 3-trocar technique

35 Phosphoribosyl amine (PRA) is an intermediate in purine biosynthesis and also

36 Phosphoribosyl amine (PRA) is the first intermediate in the common portion of

37 rst common metabolite, phosphoribosyl amine (PRA), can be generated in the absence of the first enzym

38 d States by PCR restriction enzyme analysis (PRA) of the 441-bp Telenti fragment of the hsp-65 gene a

39 ad the same PCR restriction enzyme analysis (PRA) profile as the hsp65 gene of M. porcinum (ATCC 3377

40 PCR restriction analysis (PRA) of the hsp65 gene has been proposed as a rapid and

41 this process "pattern recognition analysis" (PRA).

42 12 to 1.31]) in PRA 1%-19%, PRA 20%-79%, and PRA 80%-100% categories compared with PRA 0%, respective

43 essure reduction and blunted aldosterone and PRA responses to the DASH diet.

44 n age, end-stage renal disease etiology, and PRA matched group of patients remaining on dialysis duri

45 A periodontal examination and PRA were performed after active periodontal therapy and

46 8.3, 95% CI 2.5-27.9), followed by HCV+ and PRA > 20%.

47 erforated diverticulitis lies between HP and PRA.

48 less than 20%, group 2: 16 retransplants and PRA more than 20% who were FC crossmatch-negative, and g

49 -negative, and group 3: 20 retransplants and PRA more than 20% who were FC crossmatch-positive.

50 addition, endpoint titers, MESF units, and % PRA of 26 sera were established.

51 on (AVR) than panel reactive HLA antibodies (PRA).

52 ve; D, 0-B,Dr-MM; panel reactive antibodies (PRA) <40%; E, 0-B,Dr payback; F, local use.

53 aphics, cytotoxic panel reactive antibodies (PRA) against T-cell targets and flow cytometric crossmat

54 detected by FLOW panel reactive antibodies (PRA) and donor-specific cellular sensitization was detec

55 ree of anti-human panel reactive antibodies (PRA) and xenoreactivity against either standard or GalT-

56 of pretransplant panel reactive antibodies (PRA) are known to be associated with detrimental effects

57 Panel reactive antibodies (PRA) were determined using Flowbeads and concentration c

58 her percentage of panel-reactive antibodies (PRA), were more likely to receive a cadaveric transplant

59 the assessment of panel reactive antibodies (PRA).

60 didates with high panel-reactive antibodies (PRA).

61 nd had lower peak panel-reactive antibodies (PRA; 5.1% vs. 15.6%, P=0.07) when compared with their bi

62 transplants, high panel reactive antibodies (PRAs) (>20%), and prolonged cold ischemic times (>24 hou

63 dies, measured as panel reactive antibodies (PRAs), are related to mortality in ESRD.

64 sitized patients (panel reactive antibodies [PRA] <20%) receiving a primary transplant in 1999 or lat

65 rval [CI] 1.1-7.9), panel reactive antibody (PRA) > 20% (HR 2.8, 95% CI 1.1-7.2) and female donor gen

66 Panel reactive antibody (PRA) analysis was performed on posttransplant sera (2 we

67 Cytotoxic panel-reactive antibody (PRA) and SAB assays were analyzed in HTX recipients unde

68 patients with a low panel reactive antibody (PRA) before transplantation and follow-up PRA testing at

69 t and pretransplant panel reactive antibody (PRA) data.

70 tcome was change in panel reactive antibody (PRA) from prior to recipient's initial transplant to the

71 otype mismatch, and panel reactive antibody (PRA) greater than 30%.

72 ry transplants with panel-reactive antibody (PRA) less than 20%, group 2: 16 retransplants and PRA mo

73 ed sensitization as panel reactive antibody (PRA) more than 10% or a positive T-cell crossmatch (TXM)

74 re in-patients with panel reactive antibody (PRA) more than or equal to 80%.

75 four an increase in panel reactive antibody (PRA) of at least 20% (P=0.002).

76 ed by FLXM and flow panel reactive antibody (PRA) screening beads.

77 Pretransplantation panel reactive antibody (PRA) testing assesses posttransplantation risk for antib

78 Panel-reactive antibody (PRA) testing provides assessment of the breadth of sensi

79 ansplant and having panel reactive antibody (PRA) values greater than 85% and 50 randomly selected no

80 Mean peak panel-reactive antibody (PRA) was 47+/-32.

81 s (Ab), reported as panel-reactive antibody (PRA), prolong patient waiting time for kidney transplant

82 of 35 pretransplant panel reactive antibody (PRA)-negative patients with failed allografts were exami

83 HLA, and recipient panel-reactive antibody (PRA).

84 unction of race and panel reactive antibody (PRA).

85 odies or to percent panel-reactive antibody (PRA; by complement-dependent cytotoxicity) and anti-MICA

86 tion of percentage panel reactive antibody ("PRA screen") with limited antibody identification testin

87 ed to HLA antigens (panel reactive antibody [PRA] > or =50% monthly for 3 mo) enrolled onto an NIH-sp

88 highly sensitized (panel reactive antibody [PRA] of 52%) recipient.

89 sensitized patient (panel reactive antibody [PRA]>80%; HS).

90 We applied PRA to 278 MAC isolates, including 126 from blood of hum

91 ysis patients who differ from those that are PRA+.

92 Because PRB, as well as PRA, coimmunoprecipitated with FAK, both isoforms can in

93 n 30 isolates and by plaque-reduction assay (PRA) in 18 isolates.

94 ociation of the periodontal risk assessment (PRA) model with the recurrence of periodontitis and toot

95 e performed a probabilistic risk assessment (PRA) of the donor-recipient matching processes for thora

96 of early-onset progressive retinal atrophy (PRA) was supported by reduced direct and consensual pupi

97 cessive form of progressive retinal atrophy (PRA), is phenotypically similar to early-onset forms of

98 photographs based on the pupil ruff atrophy (PRA) grading system.

99 Among 2484 CLK recipients with available PRA or TXM information, 30% had positive TXM or PRA more

100 f AKI in this setting are prerenal azotemia (PRA), acute tubular necrosis (ATN), and hepatorenal synd

101 lative contributions of PR isoforms A and B (PRA and PRB, respectively) in cancer cell migration rema

102 or isoforms, progesterone receptors A and B (PRA and PRB, respectively), each with unique cellular ef

103 Baseline PRA levels were similar in both groups.

104 Associations between PRA and the study outcomes were accentuated in competing

105 ing parental T47-Dco cells that express both PRA and PRB and clonal derivatives that express either P

106 Specific binding of both PRA and PRB to the BCRP promoter through the identified

107 By PRA, 5 isolates had an IC(50) >400 microM and genotypic

108 By PRA, 78 of 81 clinical isolates (96%) from the United St

109 ore accurately defined by sequencing than by PRA or commercial probe.

110 The evolution of calculated PRA (cPRA) reflects the commitment of the transplant com

111 tion rates according to recipient calculated PRAs; however, RATG was associated with an increased ris

112 a sixfold greater chance of having a T-cell PRA >10% at the time of transplant (p < 0.05), and a fou

113 Sixteen of 18 isolates had concordant PRA and DHA phenotypes.

114 %) group (n = 15) was compared to a control (PRA < 20%) group (n = 27) to evaluate the efficacy of VX

115 ation after LVAD is common despite cytotoxic PRA being negative.

116 TrpD-dependent PRA formation in vitro was inhibited by S. enterica YjgF

117 ession was discontinued invariably developed PRA+.

118 A total of 15 different PRA patterns were observed.

119 Thirteen subjects displayed PRA+ at follow-up, eight of whom were de novo.

120 matching, non-white recipient, female donor, PRA as a continuous variable, and cold ischemia time.

121 Sixty-eight PRAs were performed in 62 patients; there were 6 convers

122 cells by adenoviral vectors encoding either PRA or PRB.

123 B and clonal derivatives that express either PRA (YA cells) or PRB (YB cells) or lack PR (Y cells).

124 so correlated well with a conventional ELISA PRA assay, with a coefficient of determination of 0.98.

125 ced by progesterone only in cells expressing PRA.

126 DA-MB-231 breast cancer cell line expressing PRA and/or PRB, we analyzed the effect of conditional PR

127 f a recessively inherited early-onset feline PRA.

128 Flow PRA determined HLA antibody, donor-specific flow cytomet

129 including 2 patients who expressed>80% Flow PRA.

130 patients had donor-specific antibody by flow PRA (two anti-DR4 and one anti-A2).

131 with donor antigen specific antibodies, flow-PRA specificity analysis demonstrated eight were specifi

132 ytometry based panel reactive antibody (flow-PRA) provides a highly sensitive means to identify the d

133 the presence of anti-HLA antibodies by flow-PRA.

134 ntain anti-HLA antibodies detectable by flow-PRA.

135 as defined by a negative pretransplant flow-PRA were analyzed posttransplant for the presence of ant

136 2 months and annually thereafter) using Flow-PRA.

137 morbidity and mortality was 55% and 30% for PRA, 40% and 25% for PADS, and 35% and 20% for HP, respe

138 When adjusted for PRA >20%, HLA mismatch > or =5, and multiple transplant

139 AHR but lost significance when adjusted for PRA >20%.

140 TrpE proteins, was shown to be essential for PRA formation in strains lacking both yjgF and purF.

141 urified with AphA and was also necessary for PRA formation.

142 Patients positive for PRA and sCD30 tests were at significantly higher risk fo

143 erone receptor (PR) negative or positive for PRA, PRB, or both.

144 Quantitative estimates from PRA can be used to assess risks in healthcare and to gau

145 of M. porcinum presently requires hsp65 gene PRA or 16S rRNA or hsp65 gene sequencing.

146 striction analysis targeting the hsp65 gene (PRA-hsp65) and sequencing of the rpoB gene, and suscepti

147 owed that the mutant AS was able to generate PRA from ammonia and phosphoribosyl pyrophosphate.

148 d that wild-type AS-PRT was able to generate PRA in vivo and that the P362L mutant of TrpD facilitate

149 midotransferase mechanisms exist to generate PRA sufficient for thiamine but not purine synthesis.

150 The activity generating PRA in a yjgF mutant background has features that distin

151 llograft loss included HCV, cadaveric graft, PRA >20%, HLA mismatch > or =5, retransplantation, DGF,

152 r incomplete conditioning; the other two had PRA greater than 20%.

153 Here, PRA synthesis was reconstituted in vitro with anthranila

154 resented with BK infection/CMV disease, high PRA greater than 80% seemed to be protective.

155 American race, also contributed to a higher PRA at relisting.

156 kg +/- 7.9 mg/kg, had a significantly higher PRA, and received more plasmapheresis and IVIG at the ti

157 antation prior to kidney transplants, higher PRA, and to receive cadaveric transplants.

158 tients were highly sensitized (class I or II PRA >/=80%).

159 to the manual method and an automated iMALDI PRA assay, but was 4-times faster than the manual approa

160 Of importance, PRA coexpression potentiated PRB-mediated migration, whe

161 t rejection rate increased after month 12 in PRA+MICA- group and was higher early after transplantati

162 1.18]; and HR,1.21 [95% CI,1.12 to 1.31]) in PRA 1%-19%, PRA 20%-79%, and PRA 80%-100% categories com

163 There was no appreciable change in PRA for patients receiving a first 0 HLA-A, -B, -DR, or

164 transplant were associated with a change in PRA from first to second transplant.

165 Absolute change in PRA levels were examined in general linear models and th

166 subjects, there was no appreciable change in PRA.

167 other seven patients, one had a decrease in PRA from 87% to 51% with a concurrent decrease in fluore

168 ed sera history showing a marked decrease in PRA level before transplantation and a negative pretrans

169 ; and one patient had a fourfold decrease in PRA titer from 1:64 to 1:16 at 6 months after treatment.

170 =0.042) mostly due to pronounced decrease in PRA+MICA+ group early after transplantation.

171 ever, there was no statistical difference in PRA values among these sera (95%-100%).

172 are significant racial/ethnic differences in PRA among adults awaiting HT is poorly characterized.

173 tus, but at 3 months rejection was higher in PRA+MICA+ versus PRA-MICA- patients (14% vs. 2%; P=0.009

174 ariwise, there was a significant increase in PRA by increasing HLA mismatch of the first transplant.

175 For the primary endpoint of increase in PRA greater than or equal to 20%, African Americans (AA)

176 scriptional activity of the BCRP promoter in PRA-transfected cells; however, cotransfection of PRA an

177 ntracellular localization of Cx43 protein in PRA versus PRB expressing myocytes.

178 arisons, rejection incidence was superior in PRA+MICA- versus PRA-MICA- patients (17% vs. 7%; P=0.007

179 nd was higher early after transplantation in PRA+MICA+ group (P=0.033).

180 quent in patients with ascites and increased PRA than patients without ascites or with ascites but no

181 ASH diet lowers blood pressure and increases PRA and aldosterone concentrations.

182 decreasing regraft survival with increasing PRA reflects undetected sensitization to class II, and p

183 progressively in association with increasing PRA.

184 ull mutation in yjgF allows PurF-independent PRA formation by an unknown mechanism.

185 duct singly responsible for PurF-independent PRA formation.

186 However, PurF-independent PRA synthesis has been observed in strains having differ

187 PurF-independent PRA synthesis is dependent on both strain background and

188 n of the progesterone receptor (PR) isoforms PRA and PRB resulted in a similarly increased expression

189 Two functional PR isoforms, PRA and PRB, are expressed in progestin-responsive cells

190 terone receptor (PR) exists in two isoforms, PRA and PRB, and both contain activation functions AF-1

191 on immunosuppressive therapy to 68% by late PRA after weaning (P<0.001).

192 By late PRA testing, 56% of patients were highly sensitized (cla

193 esting at 6 to 24 months after failure (late PRA).

194 yte cell surface markers and HLA Ab levels (%PRA and titers) were tested using flow cytometry.

195 tients did not differ from patients with low PRA transplanted during the same period.

196 ed with an increased risk of BK virus in low-PRA patients.

197 t 6 months after transplantation and maximum PRA but not with the randomization group.

198 Six patients with a mean PRA of 72+/-22% were included in a four-level (L) protoc

199 that distinguish it from the TrpDE-mediated PRA formation shown previously for this enzyme in strain

200 UNOS mandatory 0-mm payback; C, 0 - B,Dr-MM; PRA> or = 40%; ROP tray negative; D, 0-B,Dr-MM; panel re

201 Mostly, PRA remained negative under adequate immunosuppression.

202 Among negative PRA patients risk for AR was significantly elevated if t

203 osyl anthranilate can result in nonenzymatic PRA formation sufficient for thiamine synthesis.

204 s without ascites or with ascites but normal PRA.

205 Moreover, unliganded PRB but not PRA enhanced FAK Tyr397 phosphorylation and colocalized

206 Surprisingly, unliganded PRB but not PRA strongly enhanced cell migration as compared with PR

207 CRP expression in BeWo cells via PRB but not PRA.

208 dysfunction occurred also in the absence of PRA+.

209 We performed a retrospective analysis of PRA status in 66 patients with type 1 diabetes mellitus

210 A negative association of PRA+ with allogeneic solid organ graft survival has been

211 ransfected cells; however, cotransfection of PRA and PRB significantly decreased the progesterone-res

212 We report the largest experience to date of PRA in the United States.

213 The distribution of PRA types and, by implication, phylogenetic lineages amo

214 ection and enhance the deleterious effect of PRA+ status early after transplantation.

215 ng the widely reported deleterious effect of PRA+ status, but at 3 months rejection was higher in PRA

216 ulted in a similarly increased expression of PRA and PRB, respectively.

217 wing differences were identified in favor of PRA vs LTLA: shorter duration of surgery (50.8 vs 77.3 m

218 hat express an equivalent or higher level of PRA than PRB.

219 Monitoring of PRA under immunosuppression may have little clinical val

220 However, outcomes of PRA operations were superior to LTLA in terms of shorter

221 ly challenged by an increasing popularity of PRA, which is believed by many surgeons (not evidence-ba

222 ct was associated with strong stimulation of PRA and aldosterone.

223 his work describes the in vitro synthesis of PRA in the presence of the purified components of the AS

224 ptophan, can play a role in the synthesis of PRA.

225 paper we continued to build on the theme of PRA as a potential resource in retrosynthetic blueprints

226 was coupled to R5020-dependent turnovers of PRA and PRB.

227 It is likely that the future value of PRA will be associated with its utility in leading the w

228 water intake after Iso, but had no effect on PRA.

229 or TXM information, 30% had positive TXM or PRA more than 10%.

230 her rate of incident hypertension than other PRA phenotypes (incidence rates per 1000 person-years of

231 Overall, PRA+ did not correlate with islet graft outcome: long-te

232 I trial of RTX in chronic dialysis patients (PRA >50%).

233 ts, of which 15 (12.3%) sensitized patients (PRA>or=80%) received transplants (P=0.004 compared with

234 Compared to recipients with 0% peak PRA level, recipients with peak PRA levels greater than

235 HR, 0.47; 95% CI, 0.24-0.91; P = 0.02), peak PRA greater than 80% (HR, 0.48; 95% CI, 0.27-0.84; P = 0

236 2.50; 95% CI, 1.02-6.13; P = 0.04), and peak PRA greater than 80% (HR, 0.45; 95% CI, 0.23-0.86; P = 0

237 Blacks had a higher peak PRA than did all other groups and were more likely to be

238 dney transplant recipients with varying peak PRA levels.

239 tized kidney transplant recipients with peak PRA greater than 80% had a greater risk of rejection, gr

240 with 0% peak PRA level, recipients with peak PRA levels greater than 80% were at increased risk of ac

241 (4.5%), and 318 (4.5%) recipients with peak PRA levels of 0%, 1% to 50%, 51% to 80%, and greater tha

242 erved in the presence of basal or persistent PRA+ and graft dysfunction occurred also in the absence

243 Phosphoribosylamine (PRA) is the first intermediate in the common pathway to

244 the thiamine precursor phosphoribosylamine (PRA) by a TrpD-dependent mechanism that is not present i

245 oncentrations, in the context of physiologic PRA phenotypes (suppressed, </=0.50 microg/L per hour; i

246 In contrast, a positive PRA was significantly associated with female gender but

247 patients (donor-specific antibody positive, PRA>80%) were desensitized using IVIG and rituximab.

248 Such an effect of PRB/PRA expression on FAK signaling might thus affect adhesi

249 ity (E/e' ratio), cardiopulmonary pressures, PRA, and natriuretic peptide levels.

250 Pretransplant PRA+ was observed in 10 subjects in the old trials and a

251 s, but the association between pretransplant PRA levels and long-term patient outcomes is unclear.

252 transplant regardless of their pretransplant PRA.

253 ination with recombinant antigen 2/PRA (rAg2/PRA) protected BALB/c mice against intranasal infection

254 contractility acting through its receptors (PRA/B).

255 d ABO and HLA types of donor and recipient, %PRA and specificity of recipient alloantibody, donor/rec

256 pothesized that rituximab (RTX) could reduce PRA via B-cell depletion.

257 However, IVIG significantly reduced PRA levels in study subjects compared with placebo.

258 A mutation that was able to restore PRA synthesis in a purF gnd mutant strain was identified

259 Mean (+/-SEM) PRA was significantly higher in participants in the DASH

260 A sensitized (PRA >/= 20%) group (n = 15) was compared to a control (P

261 d graft survival, albeit only in sensitized (PRA>5%) patients (hazard ratio 3.98, P=0.014).

262 t failure preserves nonsensitization status (PRA 0%) better than early immunosuppression withdrawal.

263 Thus in P4 stimulated PRA cells Cx43 protein forms GJs, whereas in PRB cells t

264 Aliskiren suppresses PRA when given either as monotherapy or in combination w

265 li and Salmonella enterica) that synthesizes PRA from ribose 5-phosphate and glutamine/asparagine.

266 The panel reactive antibody test (PRA) is an established method for assessing posttranspla

267 niation occurring more often after LTLA than PRA (16.1% vs 0%, P=0.022) and need for hernia repair (1

268 We propose that PRA is a master regulator of Cx43 expression, GJ formati

269 Our findings suggest that PRA is an independent predictor of mortality in wait-lis

270 ls and 3-7-fold in YB cells, suggesting that PRA inhibits PRB-dependent induction of VEGF.

271 The PRA model can be useful in particularizing the risk of p

272 The PRA model indicates that changes that followed the March

273 The PRA model indicates that the likelihood of such an event

274 luated the effect of these allografts on the PRA against HLA class I and II antigens in 11 ESRD patie

275 riants that segregated concordantly with the PRA phenotype.

276 a from 115 patients were evaluated for their PRA and sCD30 concentrations.

277 Four of six candidates improved their PRAs (from a mean of 66.2% to 25.5%; P=0.01) and were su

278 Thus, PRA and PRB differentially regulate BCRP expression in B

279 pothesis that multiple enzymes contribute to PRA synthesis, possibly as the result of side products f

280 Participants were assigned randomly to PRA or LTLA and followed for 5 years after surgery.

281 s used to capture all patients who underwent PRA between October 2005 and February 2008.

282 In contrast, unliganded PRA paradoxically activates Cx43 transcription by intera

283 y (PRA) before transplantation and follow-up PRA testing at 6 to 24 months after failure (late PRA).

284 Relationships between time-varying PRAs and all-cause or cardiovascular mortality were asse

285 ths rejection was higher in PRA+MICA+ versus PRA-MICA- patients (14% vs. 2%; P=0.009).

286 n incidence was superior in PRA+MICA- versus PRA-MICA- patients (17% vs. 7%; P=0.007) at 24 months, c

287 We found that P4, via PRA/B, differentially regulates Cx43 translation to gene

288 t of patients were PRT-75+, whereas 32% were PRA+.

289 T-75+/PRA-, and only 5% of the patients were PRA+/PRT-75+, indicating that T cell alloreactivity did

290 potentiated PRB-mediated migration, whereas PRA alone was ineffective.

291 The mechanisms by which PRA confers an incremental mortality risk in sensitized

292 ients were diagnosed with ATN, 19 (26%) with PRA, and 16 (22%) with HRS.

293 Loss of graft function was associated with PRA+ after lowering of immunosuppression or after infect

294 %, and PRA 80%-100% categories compared with PRA 0%, respectively.

295 baseline within 48 hours were diagnosed with PRA.

296 lant and no patients after LVAD implant with PRA more than 10%.

297 ated with improved survival in patients with PRA greater than 50% (HR, 0.57; 95% CI, 0.34-0.97) and c

298 andomly selected nonsensitized patients with PRA values less than 3%.

299 n pediatric heart transplant recipients with PRA greater than 50% or congenital heart disease, induct

300 0.10%, but did not differ between those with PRA, 0.27%, or ATN, 0.31%, P = 0.54.