ライフサイエンスコーパス: AMR

1 AMR bacteria in the environment, including sites relevan

2 AMR bacteria were detected at exposure-relevant sites (3

3 AMR bacteria were detected in the contamination sources

4 AMR is caused by donor-specific antibodies to HLA, which

5 AMR is highly associated with graft loss, but unfortunat

6 AMR showed a distinct pattern of injury characterized by

7 AMR was associated with subclinical thrombotic microangi

8 AMR-positive patients had more dnDSA with a significant

9 AMR-positive patients were also tested 6 to 12 months be

10 cetic acid-plasma samples of 64 patients (18 AMR, 8 cell-mediated rejection [CMR], 38 no rejection in

11 risk score (HR, 0.975 [95% CI, 0.972-0.977]; AMR/100, -0.18 [95% CI, -0.21 to -0.16]), sex and socioe

12 of a unique Model Ontology and accompanying AMR detection models to power sequence analysis, new vis

13 ansplant model of transfusion-elicited acute AMR.

14 on cyclophosphamide-based treatment of acute AMR based on modern diagnostics.

15 A noninvasive biomarker of acute AMR could lead to early diagnosis and treatment of this

16 onsecutive patients with biopsy-proven acute AMR with intravenous cyclophosphamide pulses (15 mg/kg a

17 Nine patients with acute AMR that received treatment showed a mean 72% decrease (

18 gh incidence of CLAD and poor survival after AMR.

19 lasma exosomes significantly increased among AMR compared with CMR and/or control patients.

20 An AMR occurred during the first posttransplant year in 31

21 n of 41 K, which cannot be obtained using an AMR with fewer layers.

22 d Banff criteria for AMR; n = 65) yielded an AMR score of 0.19 +/- 0.15, intermediate between scores

23 The MAR met criteria for both ACR and AMR.

24 between TTV load in the peripheral blood and AMR, 715 kidney transplant recipients (median, 6.3 years

25 stics for antimicrobial drug development and AMR detection.

26 evaluates histologic components in assessing AMR therapeutic responses.

27 pidemiology of N. gonorrhoeae and associated AMR in the Australian population.

28 independent predictors for allograft loss at AMR diagnosis.

29 We hypothesized that because AMR is associated with allograft endothelial injury and

30 ed overlapping metabolite signatures between AMR and TCMR, suggesting similar pathophysiology of tiss

31 ic antibodies and underwent protocol biopsy, AMR-positive patients (n = 46) showed only 25% of the TT

32 ion aHUS recurrence, yet may not fully block AMR pathogenesis.

33 computed for peak IgG MFI (AMR, 0.73; C4d + AMR, 0.71).

34 re not different, patients with AMR or C4d + AMR showed significantly higher IgG, C1q, and C3d DSA MF

35 Death-censored AMR-free and allograft survivals were significantly lowe

36 32.6%), and at one year, the rate of chronic AMR was 39.5%.

37 mplement is an important mediator of chronic AMR, a major cause of late graft loss.

38 The previously proposed chronic AMR (cAMR) score was used to risk-stratify putative chro

39 e was used to risk-stratify putative chronic AMR in DSA+ patients with MFI from 1000 to 10 000.

40 interferon-gamma effects accurately classify AMR and correlate with degree of injury and disease acti

41 Clinical AMR was diagnosed by simultaneous occurrence of pAMR on

42 One patient demonstrated clinical AMR at postoperative day 7 and one at 6 months (1-year i

43 PV) of C4d-CD68 and pAMR grades for clinical AMR as a function of time.

44 ay provide a potential endpoint for clinical AMR trials.

45 hologic markers) was predictive for clinical AMR, particularly after the initial postoperative period

46 a potential adjunctive treatment in clinical AMR.

47 ccurrence (pAMR2) was predictive of clinical AMR.

48 d its relevance to the diagnosis of clinical AMR.

49 pAMR) grades may be associated with clinical AMR, and because humoral responses may be affected by th

50 pread, and by which individuals can contract AMR infections, is through contaminated water.

51 Currently, AMR diagnosis relies on biopsy which is an invasive proc

52 l correlations and are used here to describe AMR resistance relationships.

53 No C1-INH patient developed AMR during the study.

54 Two patients developed AMR after the study.

55 Thirty-seven of 59 dnDSA patients developed AMR during 5.9 +/- 3.1 years follow-up.

56 Three placebo patients developed AMR, one during the study.

57 eristic of microvascular inflammation during AMR.

58 ndothelial cell-monocyte interactions during AMR.

59 Early AMR demonstrated histologic improvement in mean scores f

60 Early AMR was defined as occurring within 6 months after trans

61 hen assigned to 1 of the 6 categories--early AMR, early ACR, early MAR, late AMR, late ACR, and late

62 y, and interstitial fibrosis scores in early AMR patients and tubulitis, interstitial inflammation, g

63 Although the incidence of severe early AMR is declining, accumulating evidence strongly suggest

64 graft loss was higher with late versus early AMR (P = 0.01) and late versus early ACR (P = 0.03), but

65 pansion of the RGI for detection of emergent AMR threats.

66 Endocytic AMR controls TPO expression through Janus kinase 2 (JAK2

67 nciple, reduce its ability to rapidly evolve AMR.

68 Fifty-five AMR patients were analyzed.

69 The flexible AMR sensor is used to read a magnetic pattern with a thi

70 enters (January 1, 2006-January 1, 2011) for AMR.

71 er with gene set discrimination capacity for AMR identified in the discovery set, were reproduced in

72 (n = 278) were analyzed and a classifier for AMR was identified (area under receiver operating charac

73 gs identify a urine metabolic classifier for AMR.

74 e classified according to Banff criteria for AMR and partial least squares discriminant analysis was

75 als, 69 fulfilled the diagnosis criteria for AMR and were enrolled.

76 that partially fulfilled Banff criteria for AMR; n = 65) yielded an AMR score of 0.19 +/- 0.15, inte

77 b in patients receiving PE, IVIg, and CS for AMR.

78 C1q-dnDSA was an independent risk factor for AMR.

79 MFI levels comparable to those observed for AMR+/C1q + sera.

80 significant advantages over targeted PCR for AMR detection, particularly for species where mutations

81 ls were associated with a decreased risk for AMR after adjustment for potential confounders (risk rat

82 d the possibility of predicting the risk for AMR by measuring mRNA transcripts of AMR-associated gene

83 tool to stratify the immunological risk for AMR.

84 information to the classification schema for AMR diagnosis but it remains to be determined whether si

85 19 +/- 0.15, intermediate between scores for AMR and No AMR (0.28 +/- 0.14 and 0.10 +/- 0.13 respecti

86 imated to be the leading cause of death from AMR.

87 a comparable MFI level as the C1q - DSA from AMR- patients, and some C1q - antibodies converted to C1

88 Freedom from AMR significantly decreased for those recipients with st

89 used to estimate sparse Markov networks from AMR surveillance data.

90 Fifty-three percent (10/19) of sera from AMR+ patients had C1q + DSA, whereas only 13% (2/15) of

91 + DSA, whereas only 13% (2/15) of sera from AMR- patients contained C1q + DSA.

92 values regardless of whether they were from AMR+ or AMR- patients (16,118 +/- 6698 vs 6429 +/- 4003;

93 DSA+ study patients, 44 recipients (51%) had AMR, 24 of them showing C4d-positive rejection.

94 tive transcripts would be expressed in human AMR biopsies and would offer evidence for CD16a triggeri

95 dy-dependent cellular cytotoxicity, to human AMR in allotransplantation and xenotransplantation and i

96 obing (Raman-DIP), was developed to identify AMR bacteria in the River Thames.

97 be used to predict on-going and/or imminent AMR.

98 stics in multivariate models did not improve AMR prediction.

99 des evidence for NK cell CD16a activation in AMR.

100 were likely to be selective for NK cells in AMR.

101 , 0.975 [95% CI, 0.973-0.978]; difference in AMR/100, -0.24 [95% CI, -0.27 to -0.21]), comorbidities

102 , 0.973 [95% CI, 0.970-0.976]; difference in AMR/100, -0.44 [95% CI, -0.49 to -0.39]), and pharmacolo

103 , 0.972 [95% CI, 0.964-0.980]; difference in AMR/100, -0.53 [95% CI, -0.70 to -0.36]).

104 (HR, 1.02 [95% CI, 1.01-1.03]; difference in AMR/100, 0.59 [95% CI, 0.33-0.86]), which was associated

105 wever, we found no systematic differences in AMR rates between TCHs and SCHs in the United States.

106 1 genes previously identified as elevated in AMR.

107 Results: The increase in AMR has been driven by a diverse set of factors, includi

108 ell transcripts (eg, GNLY) were increased in AMR but not CD16a-inducible, their presence in AMR proba

109 +/AVB+) microvesicles were also increased in AMR patients compared with no AMR and healthy subjects.

110 igher grade of tubulitis and inflammation in AMR are negative predictors for responsiveness to rituxi

111 he genes, proteins and mutations involved in AMR.

112 R but not CD16a-inducible, their presence in AMR probably reflecting NK cell localization.

113 sults confirm a pivotal role for thrombin in AMR in vivo.

114 tive for responsiveness to this treatment in AMR patients, are required.

115 ect evidence for NK cell CD16a triggering in AMR is lacking.

116 System between 2004 and 2012 which included AMR results for 16 drugs from 14418 isolates.

117 graft after several complications, including AMR.

118 inimization strategy with ixazomib inhibited AMR and allograft injury as evidenced by reduced C4d sta

119 Late AMR (median posttransplant day 323) was diagnosed in 5 o

120 Late AMR showed improved mean scores for acute Banff componen

121 (2) Early and late AMR demonstrate differences in acute and chronic Banff c

122 on 23 consecutive patients treated for late AMR.

123 titial inflammation, g, ptc, and C4d in late AMR.

124 ories--early AMR, early ACR, early MAR, late AMR, late ACR, and late MAR.

125 investigated, evidence on treatment of late AMR manifesting after 6 months is sparse.

126 The results show that the 16-layer AMR system can operate up to 84% of Carnot cycle COP at

127 The performance of the 16-layer AMR system in different frequencies and utilizations has

128 The DoE results indicate that for a 16-layer AMR system, the uniform distribution is very close to th

129 sult, the computation speed of a multi-layer AMR case was very close to the single-layer configuratio

130 rate the simulation speed of the multi-layer AMR system.

131 gle AMR bacteria for the first time, linking AMR phenotype (reistance to antibiotics) and genotype (D

132 estigation of anisotropic magnetoresistance (AMR) and anomalous Hall resistance (AHR) of Rh and Pt th

133 ferromagnetic anisotropic magnetoresistance (AMR) with a harmonic angular dependence on the writing m

134 hest accuracy was computed for peak IgG MFI (AMR, 0.73; C4d + AMR, 0.71).

135 acological strategies to eliminate or modify AMR bacteria.

136 improve our ability to diagnose and monitor AMR, and they will also help guide the use of complement

137 Monitoring AMR bacteria in the environment currently requires that

138 , intermediate between scores for AMR and No AMR (0.28 +/- 0.14 and 0.10 +/- 0.13 respectively, P </=

139 2) higher than transplant recipients with no AMR and 24-fold (P = 0.008) than healthy volunteers.

140 o increased in AMR patients compared with no AMR and healthy subjects.

141 verify its utility for accurate, noninvasive AMR detection.

142 The abundance of AMR bacteria at exposure-relevant sites suggests risk fo

143 Analysis of AMR surveillance data has focused on resistance to indiv

144 ce and detection of mutations in an array of AMR-relevant genes, were used to predict resistance to 4

145 ues has become an indispensible biomarker of AMR, and several assays have recently been developed to

146 red, model centric, and spans the breadth of AMR drug classes and resistance mechanisms, including in

147 Edmonton, AB, Canada, including 27 cases of AMR and 71 controls.

148 We identified 73 cases of AMR: 28 (38%) were C4d-positive and 45 (62%) were C4d-ne

149 We believe that the challenge of AMR will give microfluidics a much-needed opportunity to

150 Histopathologic criteria of AMR occurred on 10.3% EMB with no particular time patter

151 ized according to the 2013 Banff criteria of AMR: T cell-mediated rejection with intimal arteritis (v

152 abolomics for early noninvasive detection of AMR in pediatric kidney transplant recipients.

153 species where mutations are major drivers of AMR.

154 ocusing on epidemiology, clinical effects of AMR, discovery of novel agents to treat AMR bacterial in

155 se sources could therefore limit emission of AMR bacteria to the environment.

156 he home, likely augments spillover events of AMR into the community on a scale that is currently unre

157 as shown to be an independent risk factor of AMR and graft loss and may be a useful tool to stratify

158 ups showed improved histological features of AMR and Banff scores at 1 and 6 months, with no signific

159 pendent approach for rapid identification of AMR bacteria at the single cell level in their natural c

160 ture-independent and rapid identification of AMR bacteria in-situ in complex environments is importan

161 tion of graft failure was not independent of AMR.

162 clinical and histological manifestations of AMR, and discusses the immunopathological mechanisms con

163 Mtb, is a previously unreported mechanism of AMR.

164 g able to identify the genetic mechanisms of AMR and predict the resistance phenotypes of bacterial p

165 y-mediated rejection (AMR) in a rat model of AMR in sensitized recipients.

166 Further, in a mouse model of AMR, in which C57BL/6.

167 p remains in terms of the pathophysiology of AMR and how detection of immune activity, injury degree,

168 ore should be initiated in an early phase of AMR.

169 ity (MFI), allows for improved prediction of AMR.

170 ass of DSA are characteristics predictive of AMR and graft failure.

171 on between C1q-binding activity, presence of AMR, DSA mean fluorescence intensity (MFI) values, and i

172 icles provides information about presence of AMR, its severity and response to treatment in transplan

173 and C1-INH may prove useful in prevention of AMR.

174 enal transplant recipients for prevention of AMR.

175 of DSA is attributable to increased risk of AMR.

176 e C3d-binding capacity of DSA at the time of AMR diagnosis allows for identification of patients at r

177 accurate risk stratification at the time of AMR diagnosis.

178 SA detection, and 1-year later or at time of AMR.

179 isk for AMR by measuring mRNA transcripts of AMR-associated genes in plasma exosomes from kidney tran

180 a valuable alternative for the treatment of AMR.

181 hibitors for the prevention and treatment of AMR.

182 and have shown efficacy for the treatment of AMR.

183 regardless of whether they were from AMR+ or AMR- patients (16,118 +/- 6698 vs 6429 +/- 4003; P < 0.0

184 Per the World Health Organization, AMR has an estimated annual cost of USD 34 billion in th

185 Because some pathologic AMR (pAMR) grades may be associated with clinical AMR, a

186 ased expression with increasing pathological AMR (pAMR) International Society for Heart and Lung Tran

187 in absolute mortality rate per 100 patients [AMR/100], -1.81 [95% CI, -1.95 to -1.67]).

188 Genotypic data were combined with phenotypic AMR information to define strain types.

189 re these to cases of definite (C4d-positive) AMR.

190 tudinal assessment of TTV load might predict AMR risk and help guide the type and intensity of immuno

191 tive predictive values for WGS in predicting AMR were 0.87, 0.98, 0.97, and 0.91, respectively.

192 including ixazomib are effective to prevent AMR including in sensitized kidney allograft recipients.

193 characterize cases of C4d-negative probable AMR and to compare these to cases of definite (C4d-posit

194 andomly assigned patients with biopsy-proven AMR to receive rituximab (375 mg/m) or placebo at day 5.

195 The hepatic Ashwell-Morell receptor (AMR) can bind and remove desialylated platelets.

196 arance through the Ashwell-Morrell receptor (AMR).

197 parallel plates active magnetic regenerator (AMR).

198 h biopsy-proven antibody-mediated rejection (AMR) + and 15 who were AMR-, were assayed in C1q-binding

199 f patients with antibody-mediated rejection (AMR) after kidney transplantation by rituximab and plasm

200 l dnDSA causing antibody-mediated rejection (AMR) and graft loss.

201 ocirculation in antibody-mediated rejection (AMR) and have been postulated to be activated by donor-s

202 nsplantation is antibody-mediated rejection (AMR) caused by anti-donor HLA antibodies.

203 Antibody-mediated rejection (AMR) contributes to heart allograft loss.

204 cornerstone for antibody-mediated rejection (AMR) diagnosis.

205 Antibody-mediated rejection (AMR) has been identified among the most important factor

206 could suppress antibody-mediated rejection (AMR) in a rat model of AMR in sensitized recipients.

207 treating early antibody-mediated rejection (AMR) in kidney transplants have been investigated, evide

208 Antibody-mediated rejection (AMR) is a major cause of kidney allograft loss.

209 Antibody-mediated rejection (AMR) is a major cause of kidney graft loss, yet assessme

210 Antibody-mediated rejection (AMR) is a major risk for renal allograft survival.

211 Antibody-mediated rejection (AMR) is a severe form of rejection, mediated primarily b

212 responsible for antibody-mediated rejection (AMR) is an important goal.

213 Antibody-mediated rejection (AMR) is an increasingly recognized form of lung rejectio

214 atment of acute antibody-mediated rejection (AMR) is based on a combination of plasma exchange (PE),

215 ransplantation, antibody-mediated rejection (AMR) is diagnosed and graded on the basis of immunopatho

216 Antibody-mediated rejection (AMR) of most solid organs is characterized by evidence o

217 ed genes during antibody-mediated rejection (AMR) of the renal allograft.

218 jury in patients with Ab-mediated rejection (AMR) of transplanted organs.

219 Antibody-mediated rejection (AMR) represents one of the cardinal causes of late allog

220 Antibody-mediated rejection (AMR) resulting in transplant allograft vasculopathy (TAV

221 roposed chronic antibody-mediated rejection (AMR) score has recently predicted 50%10-year death-censo

222 n early or late antibody-mediated rejection (AMR), acute cellular rejection (ACR) or mixed AR (MAR).

223 tibodies (DSA), antibody-mediated rejection (AMR), acute cellular rejection, and graft status.

224 in accelerated antibody-mediated rejection (AMR), complement activation, and graft thrombosis.

225 ute and chronic antibody-mediated rejection (AMR).

226 vely preventing antibody-mediated rejection (AMR).

227 s treatment for antibody-mediated rejection (AMR).

228 y patients with antibody-mediated rejection (AMR).

229 ute and chronic antibody-mediated rejection (AMR).

230 ndicate ongoing antibody-mediated rejection (AMR).

231 rimarily due to antibody-mediated rejection (AMR, 13% vs. 1.8%, P < 0.001) and not T cell-mediated re

232 t in the transmission of clinically relevant AMR bacteria to humans, a literature review was conducte

233 Antimicrobial resistance (AMR) by Neisseria gonorrhoeae is considered a serious gl

234 -growing threat of antimicrobial resistance (AMR) demands immediate countermeasures.

235 abundances of the antimicrobial resistance (AMR) gene families and enables accurate characterization

236 ls themselves fuel antimicrobial resistance (AMR) in the wider environment is largely unknown.

237 Surveillance of antimicrobial resistance (AMR) is an important component of public health.

238 Antimicrobial resistance (AMR) is becoming a major global-health concern prompting

239 ising incidence of antimicrobial resistance (AMR) makes it imperative to understand the underlying me

240 ence and spread of antimicrobial resistance (AMR) mechanisms in bacterial pathogens, coupled with the

241 ght to have higher antimicrobial resistance (AMR) rates when compared to small community hospitals (S

242 the development of antimicrobial resistance (AMR) that can potentially spread to humans.

243 However, antimicrobial resistance (AMR) threatens this progress and presents significant ri

244 Antimicrobial resistance (AMR) threats are typically represented by bacteria capab

245 Antimicrobial resistance (AMR), the ability of a bacterial species to resist the a

246 ding to escalating antimicrobial resistance (AMR), the US Department of Defense implemented an enterp

247 molecular basis of antimicrobial resistance (AMR), with an emphasis on the genes, proteins and mutati

248 methods to detect antimicrobial resistance (AMR), with targeted polymerase chain reaction (PCR) appr

249 ead distribution of antimicrobial resistant (AMR) bacteria has led to an increasing concern with resp

250 The development of antimicrobial-resistant (AMR) bacteria poses a serious worldwide health concern.

251 efficacious therapies to prevent and reverse AMR.

252 subjected to a systematical cross-sectional AMR screening and, in parallel, TTV quantification.

253 The molecular architecture and selective AMR transcripts, together with gene set discrimination c

254 We estimate a 50% prevalence of silent AMR in DSA+ long-term recipients and conclude that asses

255 jection (RACE) was applied to isolate single AMR bacteria for the first time, linking AMR phenotype (

256 A range of specific AMR concerns, including carbapenem- and colistin-resista

257 de an initial framework for species-specific AMR phenotype and genomic feature prediction in the RAST

258 urvival with ACR better than MAR better than AMR, which persisted for both early and late AR.

259 We conclude that AMR may cause allograft failure, but that the diagnosis

260 The AMR score was associated with the presence of donor-spec

261 The AMR was defined as 3 of 4 criteria: renal dysfunction, d

262 The AMR-selective gene sets accurately discriminated patient

263 Alternative approaches to address the AMR threat include new methods of antibacterial drug ide

264 ha, and CCL4 was significantly higher in the AMR than the CMR (P < 0.0001) and no rejection control g

265 chronic Banff components at the time of the AMR diagnostic biopsy, as well as differential responses

266 f alpha2-3Neu-VWF even in the absence of the AMR.

267 Binding of desialylated platelets to the AMR induces hepatic expression of thrombopoietin (TPO) m

268 ant organisms, and possible solutions to the AMR problem.

269 e access to genomes that are binned by their AMR phenotypes, as well as metadata including minimum in

270 echanism underlies the pathogenesis of these AMR.

271 recent findings indicate that in addition to AMR-triggered activation of the classical complement pat

272 searched for articles and entries related to AMR, focusing on epidemiology, clinical effects of AMR,

273 dentification of genomic regions relating to AMR, we have updated the PATRIC FTP server to enable acc

274 ovides insights into histologic responses to AMR therapy and may provide a potential endpoint for cli

275 biopsy, as well as differential responses to AMR therapy.

276 s of AMR, discovery of novel agents to treat AMR bacterial infections, and nonpharmacological strateg

277 The continuously varying AMR provides means for the electrical read-out of multip

278 One way AMR bacteria can spread, and by which individuals can co

279 y-mediated rejection (AMR) + and 15 who were AMR-, were assayed in C1q-binding assays (C1q Screen; On

280 76 +/- 2%) were metabolically active, whilst AMR bacteria to carbenicillin, kanamycin and both two an

281 ible transcripts were highly associated with AMR (P < 5 x 10): CCL4, CD160, CCL3, XCL1, CRTAM, FCRL3,

282 etry cross-match result were associated with AMR by bivariate analysis but neither was an independent

283 ssion levels, proposed to be associated with AMR, can be detected by established quantitative real-ti

284 jective: To identify factors associated with AMR, the current epidemiology of important resistant org

285 ion in human kidney transplant biopsies with AMR and in an extended human cell panel to determine the

286 ranscripts CD160 and XCL1 with biopsies with AMR provides evidence for NK cell CD16a activation in AM

287 C4d+/AVB+ microvesicles correlated with AMR biopsy severity.

288 have been collecting bacterial genomes with AMR metadata for several years.

289 We compared patients with AMR (n=55) with a matched control group of 55 patients w

290 in an independent cohort of 39 patients with AMR (P=0.04).

291 sets accurately discriminated patients with AMR from those without and included NK transcripts (area

292 ing activity by de novo DSA in patients with AMR largely reflects differences in antibody strength.

293 pecificity were not different, patients with AMR or C4d + AMR showed significantly higher IgG, C1q, a

294 munoglobulins is an option for patients with AMR.

295 In the 28 subjects with AMR, the density of C4d+/CD144+ microvesicles was on ave

296 amples of patients with (n = 40) and without AMR (n = 278) were analyzed and a classifier for AMR was

297 the TTV levels measured in patients without AMR (P = 0.003).

298 matched control group of 55 patients without AMR.

299 95% CI, 14-106; P < 0.0001) predicted 1-year AMR, independent of other covariates.

300 In the first posttransplantation year, AMR immunopathologic and histopathologic markers were re