ライフサイエンスコーパス: AMR

1 AMR gene detection positively correlated with phenotypic

2 AMR profiles were assessed by the disc diffusion method,

3 AMR was tested in vitro and isolate genomes were sequenc

4 hotgun metagenomic sequencing identified 144 AMR genes in total, with higher AMR gene diversity prese

5 tantly, hypermutator alleles that accelerate AMR development did not arise without Mfd, at least duri

6 of arteriolar C4d staining in chronic-active AMR (c-aAMR).

7 erapy is safe and effective for early active AMR after kidney transplant or abrupt increases in donor

8 of eculizumab as primary therapy for active AMR early posttransplant.

9 o treat six consecutive patients with active AMR with B/B.

10 We hypothesized that the reversal of acute AMR requires rapid elimination of antibody-secreting pla

11 standard of care for the treatment of acute AMR.

12 d efficacy of eculizumab in preventing acute AMR in recipients of deceased-donor kidney transplants w

13 izumab compared with SOC in preventing acute AMR in recipients sensitized to their living-donor kidne

14 st patient who developed early, severe acute AMR that did not respond to steroids, plasmapheresis, an

15 ional patients who also resolved their acute AMR episode and had sustained disappearance of circulati

16 m plasmid-mediated acquisition of additional AMR genes, including an IncHI2 plasmid.

17 ty and potential functional efficacy against AMR bacteria.

18 To fight against AMR bacteria, new antimicrobial agents are continually n

19 play an important role in the fight against AMR.

20 Although AMR against S. Paratyphi was low across the three countr

21 e present an updated version of AmrPlusPlus (AMR ++ version 2.0), which improves accuracy of classifi

22 ough only 15 recipients (13.8%) developed an AMR episode, 2 of these were associated with a graft los

23 ens compared to DSA-negative (P < .0001) and AMR patients with DSA and PRA > 10% were identified as t

24 ed risk of allograft failure (P = .0025) and AMR (P = .02) compared with the DSA+ != TSA+ patients.

25 ll amount to total variation in RMR (2%) and AMR (0.2%) data.

26 ol to characterize the serovar diversity and AMR profiles in NTS.

27 ent assays positivity, presence of gDSA, and AMR occurrence.

28 ent assays positivity, presence of gDSA, and AMR occurrence.

29 gh correlation between transposase genes and AMR genes, as well as plasmid replicons, highlights the

30 etic lineages (strains), AMR mechanisms, and AMR vehicles underlying the expansion of specific resist

31 bacterial infection including meningitis and AMR among neonates in sub-Saharan Africa and assessed th

32 Microbiology and AMR patterns are likely to reflect institutional ecology

33 both RMR (maximum bias = 0.07 kcal/min) and AMR assessment (maximum bias = 0.53 kcal/min).

34 ates was performed to infer transmission and AMR events.

35 n limiting unnecessary antimicrobial use and AMR.

36 Among a selection of nine virulence and AMR genes, CC151, CC479 and CC133 carried more virulence

37 that enabled the classification of cases as AMR or non-AMR, morphometry was performed on biopsies fr

38 -HLA antibodies has become more prominent as AMR can be diagnosed in the absence of circulating DSA.

39 actions with livestock, acquiring associated AMR bacteria and genes, and wildlife's subsequent disper

40 The findings indicate that LQAS-based AMR survey is a feasible, sensitive, and affordable stra

41 ity, and affordability of a population-based AMR survey using lot quality assurance sampling (LQAS),

42 and affordable strategy for population-based AMR surveys, providing essential data to inform local em

43 tein L2, was significantly different between AMR and non-AMR patients.

44 roteins were significantly decreased in both AMR compartments.

45 l basis for how the identified alleles cause AMR.

46 e glomeruli and the tubulointerstitium cause AMR while inflammatory cytokines such as TNFalpha trigge

47 The Indian isolates have no chromosomal AMR cassette, but carry the IncY plasmid p60006.

48 ent membranes are often remodeled in chronic AMR.

49 patients with complement-independent chronic AMR (n=62, 46%), those in whom missing self was identifi

50 ing self at the time of diagnosis of chronic AMR identifies patients at higher risk for kidney transp

51 plant failure following diagnosis of chronic AMR.

52 pendent NK cell activation to worsen chronic AMR.

53 her incidence of biopsy-proven (sub)clinical AMR (P = 0.032) and a higher extent (g>=1 + ptc>=1) of m

54 iable production of lead compounds to combat AMR.

55 in institutional AMR, even though community AMR increased during the same period.

56 In conclusion, AMR gene prevalence and abundance were not influenced by

57 erial isolates from 9 species that contained AMR phenotypes for 29 antibiotics.

58 iously, we presented MEGARes, a hand-curated AMR database and annotation structure developed to facil

59 Among those <=60 days, AMR to all first-line antimicrobials increased from 7.0%

60 Current methods of determining AMR rely on inefficient phenotypic approaches, and there

61 (8.5 h) and sequenced strains with different AMR profiles.

62 low for identifying genetic features driving AMR based on constructing reference strain-agnostic pan-

63 GS) differed at 3 years postrejection (early AMR 88.3% versus early MAR 77.8% versus late AMR 56.7% v

64 ion at 14 days differed significantly (early AMR 79.6%, early MAR 54.7%, late AMR 23.4%, late MAR 21.

65 for-cause kidney biopsy specimens with early AMR, acute cellular rejection (ACR), or acute tubular ne

66 need for strategies to disrupt environmental AMR transmission in urban informal settlements.

67 nts may be unique hotspots for environmental AMR transmission given: (1) the high density of humans,

68 heir effectiveness in limiting environmental AMR dissemination, lowering the community-level burden o

69 cal setting in the face of rapidly-expanding AMR in childhood BSI.

70 By 9 weeks, 3 of 80 patients had experienced AMR, and 4 of 80 had experienced graft loss.

71 genomic sequencing were used to track faecal AMR gene abundance and diversity and microbiome alpha di

72 srK represents a valuable target in fighting AMR.

73 ating renal transplant recipients with first AMR episodes treated with proteasome inhibitor-based the

74 stematically elucidate the genetic basis for AMR.

75 7, 135 fulfilled the diagnostic criteria for AMR and were enrolled in the study.

76 have made alternative treatment options for AMR pathogens increasingly attractive.

77 body of research demonstrates selection for AMR likely occurs at environmental concentrations of ant

78 ce demonstrating environmental selection for AMR, and of associated human health risks, is a primary

79 prediction models will be valuable tools for AMR research for basic scientists with potential for cli

80 arious approaches to calculating deaths from AMR infections, to compare the tally of deaths by each a

81 Furthermore, AMR plasmids are significantly more prevalent in gonococ

82 Our findings suggest that global AMR gene diversity and abundance vary by region, and tha

83 nuary 1, 2014, and January 31, 2018, and had AMR within the first 30 days posttransplant and treated

84 istributed with multiple occurrences of high AMR.

85 entified 144 AMR genes in total, with higher AMR gene diversity present in young pigs compared to dry

86 d connectivity measurably influence hospital AMR.

87 drug-resistant (XDR) V. cholerae to identify AMR genes and genomic elements that harbor the resistanc

88 iac allograft biopsies with immunopathologic AMR, IR spectroscopy reveals a biochemical signature uni

89 Clonal shifting from CC5 to CC8 has impacted AMR.

90 llance should continue to monitor changes in AMR to inform policies and to monitor drug resistance in

91 unit gamma-1 (LAMC1) expression decreased in AMR, as did glomerular nephrin (NPHS1) and receptor-type

92 proteins were significantly dysregulated in AMR versus ATN (P<0.05).

93 munomodulatory protein linked to the ECM, in AMR glomeruli.

94 as significantly differentially expressed in AMR versus ACR; 112 of 2026 glomerular and 181 of 2399 t

95 mechanisms governing cell-specific injury in AMR remain unclear.

96 The clonal shift was reflected in AMR patterns, with a decrease in erythromycin (86.7% to

97 rmation included in CARD, identify trends in AMR mobility and determine previously undescribed and no

98 ith a significant reduction in institutional AMR, even though community AMR increased during the same

99 cist-led audit and feedback on institutional AMR.

100 apable of integrating RMR and short-interval AMR assessments into a single protocol.

101 approaches, identifying a total of 45 known AMR-conferring genes and alleles across the three organi

102 that feature selection by RSE detects known AMR associations more reliably than common statistical t

103 lic acid, and isoniazid) recapitulates known AMR mechanisms and suggest a biochemical basis for how t

104 ntly (early AMR 79.6%, early MAR 54.7%, late AMR 23.4%, late MAR 21.1%, P < 0.001).

105 been separately analyzed for early and late AMR and mixed acute rejection (MAR).

106 ed with improved DCGS in both early and late AMR.

107 AMR 88.3% versus early MAR 77.8% versus late AMR 56.7% versus late MAR 54.9%, P = 0.02).

108 rs (or connectivity) impact population-level AMR in hospital networks can help optimize antibiotic st

109 Study 2 developed local AMR data with CO(2) insufflation.

110 give rise to anisotropic magnetoresistance (AMR) and the planar Hall effect (PHE) in a FM(16) can ad

111 ably enhanced anisotropic magnetoresistance (AMR) as giant as ~160% in a simple resistor structure ma

112 ent or changes in microbiome diversity, mean AMR gene copy number was consistently high, with some AM

113 esults reveal the extent of plasmid-mediated AMR in the gonococcus, particularly in less wealthy coun

114 2-day repeats and the 10-15 min activity MR (AMR) of 14 subjects at three intensities, using a large

115 ological structure, curation of over 500 new AMR detection models, development of a new classificatio

116 Seventy-two biopsies revealed no AMR (58.5%).

117 from patients with >= pAMR1 (n = 43) and non-AMR (n = 21) were tested for reactivity against a panel

118 significantly different between AMR and non-AMR patients.

119 m 0.80-0.89 with as few as 100 conserved non-AMR genes, with very major error rates ranging from 0.11

120 sufficient variation exists in the core non-AMR genes of a species for predicting AMR phenotypes.

121 ed the classification of cases as AMR or non-AMR, morphometry was performed on biopsies from 48 recip

122 d reactivity to autoantigens compared to non-AMR (P = .002) and healthy controls (n = 94, P < .0001).

123 ture developed to facilitate the analysis of AMR within metagenomic samples (i.e. the resistome).

124 idening in the multidisciplinary approach of AMR.

125 hildren, we identified an extensive array of AMR genes and plasmids, including an identical multidrug

126 e the phenotypic and genotypic assessment of AMR and antibiotic susceptibility.

127 onmental and human health risk assessment of AMR.

128 f CC446 and investigate the genetic basis of AMR.

129 g new resources for community biocuration of AMR molecular reference data.

130 nclude (a) the health and economic burden of AMR in humans,(b) the impact of AMU in animal agricultur

131 could potentially limit the global burden of AMR.

132 We show that the global burdens of AMR estimated in previous studies are not comparable bec

133 ielded important advancements in the care of AMR patients.

134 el route to tackling the global challenge of AMR.

135 he identification of genetic determinants of AMR is a critical component to epidemiological investiga

136 a critical role for MVI in the diagnosis of AMR.

137 n given less attention as a global driver of AMR, especially in urban informal settlements in LMICs-c

138 to play an important role in the ecology of AMR.

139 le the phenotype and true clinical effect of AMR remain to be better defined, the high prevalence of

140 ntions to combat the spread and emergence of AMR.

141 lture on AMR in animals, (c) the fraction of AMR in humans attributable to animal agriculture, and (d

142 dies and their association with histology of AMR (AMRh) and kidney allograft failure.

143 ation and could not explain the histology of AMR in the absence of DSA.

144 as a model for studying the immunobiology of AMR.

145 on after spindle breakdown and initiation of AMR contraction.

146 provides opportunities for investigation of AMR across all microbial genomes in a sample (i.e. the m

147 These results confine the majority of AMR acquisition events in NYS S. Typhimurium to the twen

148 lop tolerable therapeutics for management of AMR, none, to date, have been universally accepted or ob

149 ytotoxicity, which are critical mediators of AMR.

150 pecific ESBL genes, as well as a plethora of AMR genotypes, helping to establish their prevalence and

151 ere collected and related to the presence of AMR, graft histological features, and allograft survival

152 lation as having a high or low prevalence of AMR based on a priori defined criteria.

153 h antimicrobial use and a high prevalence of AMR commensals, cipR S. sonnei may be propelled towards

154 S provided a wealth of data on prevalence of AMR genotypes and plasmid persistence absent from phenot

155 We observed a high prevalence of AMR to first-line treatments recommended by WHO, and mor

156 CC446 isolates demonstrated high rates of AMR, with 51.9% (28/54) being multidrug-resistant (MDR)

157 /B treatment resulted in a rapid reversal of AMR, leading us to treat five additional patients who al

158 The rise of AMR microorganisms can be attributed to a combination of

159 all pose a significant risk for selection of AMR in the environment.

160 hip programs (ASPs) to curb the selection of AMR, but there is a lack of data confirming this benefit

161 features derived from comprehensive sets of AMR genes or whole genome sequences and may not be suita

162 hat SPS phage can both prevent the spread of AMR Salmonella Enteritidis infection in chickens and shi

163 eS suggest its possible role in treatment of AMR.

164 peutics aimed at prevention and treatment of AMR.

165 pangenomics to improve our understanding of AMR gene transfer, adaptation and transmission to discov

166 nd there remains incomplete understanding of AMR mechanisms for many pathogen-antimicrobial combinati

167 vetted through the European Joint Action on AMR and Healthcare-Associated Infections (EU-JAMRAI).

168 ) the impact of AMU in animal agriculture on AMR in animals, (c) the fraction of AMR in humans attrib

169 ternal costs of AMU in animal agriculture on AMR in humans.

170 o reduce the potential longer-term impact on AMR and on access to effective antimicrobials.

171 sed adenoma detection rate but the impact on AMR had not been reported.

172 y their estimated population-level impact on AMR that might help inform antimicrobial stewardship str

173 mens also met Banff criteria for TCMR and/or AMR.

174 in biopsies without evidence of diabetes or AMR=0.919, 95% CI: 0.856 to 0.987).

175 essed COVID-19-associated superinfections or AMR.

176 ections between DNA variation and phenotypic AMR, we developed a new bioinformatics tool, variant map

177 ection positively correlated with phenotypic AMR testing, and resistance to empirical antimicrobials

178 mobility of eight Schizosaccharomyces pombe AMR proteins at different stages of mitosis and cytokine

179 to non-HLA are associated with DSA-positive AMR although their specific role in mediating allograft

180 DSA-positive AMR patients exhibited greater reactivity to autoantigen

181 cted in some cases with probable or possible AMR that lacked the histological lesions conventionally

182 cipients with definite, probable or possible AMR, 31 controls (negative for any posttransplant injury

183 erculosis strains and show that MACs predict AMR phenotypes with accuracy on par with mechanism-agnos

184 xpect this approach to more reliably predict AMR determinants for a wider range of microbial pathogen

185 MR; and (3) build accurate models to predict AMR based on whole genome sequencing data.

186 re non-AMR genes of a species for predicting AMR phenotypes.

187 dy, we explore the possibility of predicting AMR phenotypes using incomplete genome sequence data.

188 hough every effort should be made to prevent AMR to ensure long-term outcomes remain excellent.

189 predictive power in cases where the primary AMR mechanisms result from SNPs or horizontal gene trans

190 Here, we examined priority AMR phenotypes and genotypes of Escherichia coli isolate

191 in the interstate dissemination of priority AMR bacteria.

192 =99.6% shared coding sequence) with priority AMR were found in birds on feedlots separated by distanc

193 As pulmonary AMR is largely refractory to current immunosuppression,

194 mes were sequenced and screened for putative AMR genes and alleles.

195 rfaces with MEGARes to identify and quantify AMR gene accessions contained within a metagenomic seque

196 Ashwell-Morell receptor (AMR) deficiency alone had little effect on platelet upta

197 tion (9.2%) and antibody-mediated rejection (AMR) (13.8%).

198 Antibody-mediated rejection (AMR) accounts for >50% of kidney allograft loss.

199 aft loss due to antibody-mediated rejection (AMR) after kidney transplantation, compared to one desen

200 associated with antibody-mediated rejection (AMR) and allograft loss.

201 a major role in antibody-mediated rejection (AMR) and graft dysfunction.

202 bodies (DSA) on antibody-mediated rejection (AMR) and kidney allograft failure is well established.

203 Antibody-mediated rejection (AMR) driven by the development of donor-specific antibod

204 Active antibody-mediated rejection (AMR) is a potentially devastating complication and consi

205 odies (DSA) and antibody-mediated rejection (AMR) posttransplant.

206 Active antibody-mediated rejection (AMR) that occurs during the amnestic response within the

207 nsitization and antibody-mediated rejection (AMR) treatment by targeting CD20 found on B-lymphocytes.

208 h occurrence of antibody-mediated rejection (AMR) using a recently developed method.

209 t of subsequent antibody-mediated rejection (AMR), even when subclinical.

210 development of antibody-mediated rejection (AMR).

211 tion (TCMR) and antibody-mediated rejection (AMR).

212 survival after antibody-mediated rejection (AMR).

213 shed feature of antibody-mediated rejection (AMR).

214 ding to chronic antibody-mediated rejection (AMR).

215 responsible for antibody-mediated rejection (AMR).

216 ding virulence and antimicrobial resistance (AMR) against ecological and anthropogenic forms of urban

217 ured the burden of antimicrobial resistance (AMR) among confirmed enteric fever cases in Bangladesh,

218 Antimicrobial resistance (AMR) constitutes an international public health threat w

219 re experiencing an antimicrobial resistance (AMR) crisis, brought on by the drying up of the antibiot

220 ut showed sporadic antimicrobial resistance (AMR) gene acquisition, and two that were largely multidr

221 Virulence and antimicrobial resistance (AMR) gene carriage was highly associated with CC.

222 o how this impacts antimicrobial resistance (AMR) gene dynamics.

223 bacter jejuni) and antimicrobial resistance (AMR) genes ( tetW, mecA) in airborne dust.

224 urately identified antimicrobial resistance (AMR) genes in Gram-negative bacteria.

225 esence of multiple antimicrobial resistance (AMR) genes, and two clades exhibited evidence of recent

226 he introduction of antimicrobial resistance (AMR) genes.

227 Antimicrobial resistance (AMR) has been identified by the World Health Organisatio

228 ure contributes to antimicrobial resistance (AMR) in humans, which imposes significant health and eco

229 creasing levels of antimicrobial resistance (AMR) in response to treatment.

230 s in aetiology and antimicrobial resistance (AMR) in the past decade (2008-18).

231 Antimicrobial resistance (AMR) is a global threat.

232 Antimicrobial resistance (AMR) is a growing public health challenge that is expect

233 Antimicrobial resistance (AMR) is a growing threat with severe health and economic

234 Antimicrobial resistance (AMR) is a major challenge in the treatment of infections

235 On the other hand, antimicrobial resistance (AMR) is a major global public health concern and wastewa

236 Antimicrobial resistance (AMR) is a major threat to human health worldwide, and th

237 sing prevalence of antimicrobial resistance (AMR) is a significant threat to global health.

238 Antimicrobial resistance (AMR) is a threat to global public health and the identif

239 Antimicrobial resistance (AMR) is an increasing threat to public health.

240 Antimicrobial resistance (AMR) is now a major global problem largely resulting fro

241 Antimicrobial resistance (AMR) is one of the most significant health threats to so

242 ed surveillance of antimicrobial resistance (AMR) monitor resistance trends and disseminate these dat

243 accurately predict antimicrobial resistance (AMR) phenotypes from bacterial sequence data.

244 The evolution of antimicrobial resistance (AMR) poses a persistent threat to global public health.

245 a and compared the antimicrobial resistance (AMR) profiles of isolates from both host species.

246 The development of antimicrobial resistance (AMR) resulting from widespread antibiotic usage is occur

247 kle the problem of antimicrobial resistance (AMR) surveillance programmes are in place within Europe

248 Antimicrobial resistance (AMR) testing was performed for most common clinical agen

249 ns associated with antimicrobial resistance (AMR) to accurately predict drug susceptibility profiles,

250 ovar distribution, antimicrobial resistance (AMR), and clinical manifestation of NTS gastroenteritis

251 The increase of antimicrobial resistance (AMR), and lack of new classes of licensed antimicrobials

252 ic determinants of antimicrobial resistance (AMR), but they lack causal interpretation.

253 ristics, including antimicrobial resistance (AMR), classic genotyping, and whole-genome sequencing re

254 ong-term impact on antimicrobial resistance (AMR).

255 mediate high-level antimicrobial resistance (AMR).

256 reat concern about antimicrobial resistance (AMR).

257 d proliferation of antimicrobial resistance (AMR).

258 and acquisition of antimicrobial resistance (AMR).

259 ethods to identify antimicrobial-resistance (AMR) genes in bacterial pathogens.

260 Antibiotic Microbial Resistance (AMR) is a major global challenge as it constitutes a sev

261 Antimicrobial resistant (AMR) microorganisms affect nearly 2 million people a yea

262 enomics to study 90 antimicrobial resistant (AMR) S. enterica isolates from bovine and human hosts in

263 evolution of novel antimicrobial resistant (AMR) S. sonnei variants after introduction into Vietnam.

264 mber of deaths from antimicrobial-resistant (AMR) infections are important data for clinicians and pu

265 Allograft biopsies revealed AMR in 63 cases (73%), regardless of kidney function.

266 ciplinary, international task force reviewed AMR cases in the context of four face-to-face meetings.

267 dependent on a contractile actomyosin ring (AMR), composed of F-actin, myosin II, and other actin an

268 nter-population transmission appear to shape AMR S. enterica population structure in different hosts

269 In some AMR bacteria, resistance is encoded by conjugative plasm

270 copy number was consistently high, with some AMR genes present at copy numbers comparable to the bact

271 ages emerged earlier, but showcased sporadic AMR determinant acquisition largely after 1960, includin

272 the interplay of genetic lineages (strains), AMR mechanisms, and AMR vehicles underlying the expansio

273 Both clinical and subclinical AMR groups underwent similar treatment including plasmap

274 Early diagnosis and treatment of subclinical AMR based on the donor-specific antibody (DSA) testing m

275 early diagnosis and treatment of subclinical AMR using DSA monitoring may improve outcomes after kidn

276 The AMR group had a significantly greater percentage of pati

277 a nonuniform tension distribution around the AMR, and that one of the roles of actin turnover is to m

278 in a uniform tension distribution around the AMR.

279 regions predicted to be most burdened by the AMR crisis, there is an urgent need to build effective,

280 e found that the distribution of Myo2 in the AMR anticorrelates with the location of peeling events,

281 been predicted to cleave ECM proteins in the AMR glomeruli.

282 g enzyme, was significantly increased in the AMR tubulointerstitium and in TNFalpha-treated proximal

283 leaching experiments, many components of the AMR have been shown to be mobile and to undergo constant

284 It informs clinicians of the AMR pattern of circulating clone, which would add confid

285 tin and myosin peel off from one side of the AMR, and are pulled across to the opposite side.

286 domly-selected core genes after removing the AMR genes.

287 Metagenomic analysis revealed the AMR genotype, while immunological analysis revealed mass

288 d platelets through a collaboration with the AMR, thereby maintaining a healthy and functional platel

289 entified 94 genes putatively contributing to AMR, including seven class A and C beta-lactamases as we

290 istance trends and disseminate these data to AMR stakeholders.

291 having a much shorter graft survival due to AMR.

292 py reveals a biochemical signature unique to AMR compared with that of nonrejecting cardiac allograft

293 isk of selection for, and human exposure to, AMR in aquatic environments.

294 st with discovery of heretofore unrecognized AMR pathways.

295 han other CCs, and CC398 was associated with AMR gene carriage.

296 tigate the genomic variation associated with AMR in 168 C. jejuni and 92 C. coli strains isolated fro

297 gical lesions conventionally associated with AMR.

298 s for their known or novel associations with AMR; and (3) build accurate models to predict AMR based

299 A without DSA-M (1476), 3 of 6 patients with AMR and low mean fluorescence intensity DSA (<3000) had

300 rophage galactose lectin (MGL) together with AMR mediated clearance of desialylated or cold-stored pl