ライフサイエンスコーパス: TMA

1 TMA allows multiplexing of subsamples, permitting standa

2 TMA analysis revealed a marked increase in nuclear, but

3 TMA has also uncovered double-mutant combinations that p

4 TMA is also a complication of preeclampsia, a disease ch

5 TMA leads gave excellent sensing and pacing characterist

6 TMA leads performed similarly in Fontan patients.

7 TMA monooxygenase (Tmm), a bacterial flavin-containing m

8 TMA Navigator also supports network inference approaches

9 TMA pacing leads had excellent longevity, initial, and c

10 TMA presentations in the critically ill, drug-induced TM

11 limus arm (9% vs 21% VOD, P = .05; 1% vs 10% TMA, P = .06).

12 blot analysis in B6J TMA-resistant and 129Sv TMA-prone mice, demonstrated major differences in vascul

13 nous VEGFA supply failed to rescue any 129Sv TMA lesions.

14 endothelial Vegfr2 expression level in 129Sv TMA-prone mice compared with B6J TMA-resistant mice.

15 DMAs(V), 25 +/- 1.4% MAs(V) and 10 +/- 1.2% TMAs(V)O.

16 ieved by the automated method (81%) on 5,338 TMA images from 1,853 breast cancer patients.

17 Forty-two of 48 TMA leads remain active at last follow-up.

18 Among 92 TMA-exposed workers continuously monitored for sIgG and

19 A TMA-like state also developed in guinea pigs IV administ

20 lysis of 161 prostate biopsies arranged in a TMA and marked with biotin-labeled CG3-aptamer showed mo

21 y IHC in 8179 prostate cancer specimens in a TMA format.

22 the significance of CHKA overexpression on a TMA, including a large series of endometrial hyperplasia

23 iduals with INF2 mutations presenting with a TMA also had aHUS risk haplotypes, potentially accountin

24 sidered in patients presenting with an acute TMA, especially in patients with nondeficient ADAMTS13 (

25 y TTP/aHUS Registry presenting with an acute TMA.

26 In addition, TMA has been proved to be a good spoilage indicator also

27 After TMA binding, NADP(+) bends and interacts with D317, shut

28 es mice to lethal acute kidney failure after TMA injury.

29 poor survival (<20% at 1 year), whereas all TMA subjects without proteinuria and a normal sC5b-9 ser

30 ammonium ions, such as tetramethyl ammonium (TMA), alter the usual correlation between DNA GC-content

31 A by a transcription-mediated amplification (TMA) assay, with DENV types and viral loads determined b

32 Transcription-mediated amplification (TMA) enhances detection of Neisseria gonorrhoeae and Chl

33 using transcription-mediated amplification (TMA) technology.

34 ercial transcription-mediated amplification (TMA), residual material was subjected to Mycoplasma geni

35 ion of transcription-mediated amplification (TMA)-based urethral swab and first-void urine screening

36 y, the systemic blocking of Vegfr2 amplified TMA lesions only in B6J mice.

37 d an approach termed triple-mutant analysis (TMA).

38 r H (CFH) are also features of both ARMD and TMA, we hypothesized that VEGF and CFH interact.

39 s carrying the clinical diagnosis of C3G and TMA, respectively.

40 In particular, because choline and TMA bind to DNA in a manner that is found to be distinct

41 The sequence-specific nature of choline and TMA binding provides a rationale for the enhanced stabil

42 ration data, microarray expression data, and TMA analysis indicate that TP53 haploinsufficiency and i

43 There was no platelet deposition, and TMA severity, as well as microvascular injury scores (gl

44 ence of a causal link between type I IFN and TMA.

45 f such an association between type I IFN and TMA.

46 f anchovy marinades, the chemical (TVB-N and TMA), oxidative (peroxides value, K230, thiobarbituric a

47 uickly developed large-vessel thrombosis and TMA, leading to graft failure with shortened survival.

48 (2-hydroxy-N,N,N-trimethylethanaminium) and TMA are preferentially localized in the minor groove of

49 Volatilization of Me2AsH and TMAs(III) from contaminated soil is thus possible with t

50 ounced demethylation of MAs(V), DMAs(V), and TMAs(V)O was found during the reaction of THB with HCl,

51 Workplace exposure to trimellitic anhydride (TMA) can elicit TMA-specific IgE (sIgE), which may lead

52 oxicants, identifying trimellitic anhydride (TMA) for further study on the basis of inducing a robust

53 phenols (TSP), total monomeric anthocyanins (TMA), radical scavenging activity (RSA), ferric reducing

54 r the formation of detectable particles are: TMA, -(168 +/- 19) kcal mol(-1); DMA, -(134 +/- 30) kcal

55 lly ill, drug-induced TMA, cancer-associated TMA, and hematopoietic transplant-associated TMA (TA-TMA

56 in genetic susceptibility to HSCT-associated TMA based on recipient genotype.

57 TMA, and hematopoietic transplant-associated TMA (TA-TMA) and their specific treatment, where applica

58 Active acute graft-versus-host disease at TMA diagnosis was the only factor associated with worse

59 For transmural atrial (TMA) lead access, a bipolar, steroid-eluting transvenous

60 ve half-reaction, this intermediate attracts TMA through electronic interactions.

61 microarrays and Western blot analysis in B6J TMA-resistant and 129Sv TMA-prone mice, demonstrated maj

62 el in 129Sv TMA-prone mice compared with B6J TMA-resistant mice.

63 hydroxo hafnium cluster isolated from base, [TMA]6 [Hf6 (mu-O2 )6 (mu-OH)6 (OH)12 ]38 H2 O.

64 gG (sIgG) responses can discriminate between TMA-exposed workers with and without sIgE responses.

65 Given that both TMA tissue cores and clinical tumor biopsies analyze onl

66 munohistochemical analysis of a human breast TMA showed that LASP-1 is absent in normal human breast

67 alis pharyngeal detections were confirmed by TMA-based alternative target testing.

68 t on a large study utilizing a breast cancer TMA comprised of 207 different patients.

69 A more common TMA is thrombotic thrombocytopenic purpura, which is cau

70 renal sections with histologically confirmed TMA obtained from a heterogeneous patient group.

71 ce for total monomeric anthocyanin contents (TMA), while it had only 12% and 13% of the variance for

72 e bacteria and is responsible for converting TMA to TMAO.

73 emonstrated that glomerular Vegfr2-dependent TMA lesions are an underevaluated common hallmark of ant

74 children undergoing HSCT who did not develop TMA.

75 higher magnitude are more likely to develop TMA sIgE sensitization.

76 re to trimellitic anhydride (TMA) can elicit TMA-specific IgE (sIgE), which may lead to occupational

77 ated extended-release oxymorphone can elicit TMA.

78 rular filtration rate at 5 years, especially TMA.

79 Eosinophil-mediated events following TMA contact toxicant reactions increase skin sensory ner

80 (39%) met previously published criteria for TMA.

81 and acute and long-term lead performance for TMA leads placed 1998 to 2004.

82 Although our microbiota are responsible for TMA formation from carnitine, the underpinning molecular

83 LEX + Eculizumab improved graft survival for TMA patients (P = 0.036).

84 orts network inference approaches useful for TMA datasets, which often constitute comparatively few m

85 preserved for MAs(V) and DMAs(V) but not for TMAs(V)O.

86 and cell-type specific networks derived from TMA expression data offer insights into the molecular lo

87 SH scores were available in 1,212 cases from TMAs, and the overall rate of false-negative cases was 1

88 Incorporation of M. genitalium TMA into comprehensive testing programs would detect M.

89 patients undergoing genetic testing, 34 had TMA.

90 ng multi-institutional registry (the Harvard TMA Research Collaborative).

91 ion requirements were decreased, and hepatic TMA was noticeably absent in recipients of continuous co

92 Only in HR-TMA were glomerular ADAMTS13 and CD55 down-regulated.

93 way toward microthrombosis exclusively in HR-TMA.

94 ther thrombotic microangiopathies, post-HSCT TMA remains poorly understood.

95 e between 2010 and 2013 for severe post-HSCT TMA.

96 utoantibodies in six children with post-HSCT TMA.

97 be involved in the pathogenesis of post-HSCT TMA.

98 In humans, TMA is produced exclusively by the intestinal microbiota

99 (n = 11) exceeded the MTCD because of 2 HUS/TMA/HUS-like events.

100 mated longitudinally (years 2006 to 2014) in TMA-exposed workers recruited in low, medium, and high e

101 favorably with previously published data in TMA after allogeneic HSCT.

102 ity of choline diet-dependent differences in TMA/TMAO levels was not maintained to the end of the stu

103 In conclusion, C4d is a common finding in TMA, regardless of the underlying clinical condition.

104 screens all exons of all genes implicated in TMA and C3G.

105 biomarkers of cellular processes involved in TMA in patients with aHUS longitudinally, during up to 1

106 y elucidated microbial pathways resulting in TMA production into genomic orthologs, we demonstrate ho

107 onfirming that these genes are sufficient in TMA formation.

108 An increased awareness of drug-induced TMA is also essential because the key to their diagnosis

109 ntations in the critically ill, drug-induced TMA, cancer-associated TMA, and hematopoietic transplant

110 nt with a direct dose-dependent drug-induced TMA.

111 ed for all published reports of drug-induced TMA.

112 ct microbial TMA lyases, and to both inhibit TMA production from physiologic polymicrobial cultures (

113 anol (DMB), is shown to non-lethally inhibit TMA formation from cultured microbes, to inhibit distinc

114 ents suspected of having complement-mediated TMA.

115 The thrombotic microangiopathies (TMAs) and C3 glomerulopathies (C3Gs) include a spectrum

116 e development of thrombotic microangiopathy (TMA) after hematopoietic stem cell transplantation (HSCT

117 egulation in the thrombotic microangiopathy (TMA) atypical hemolytic uremic syndrome (aHUS) resulted

118 rome (aHUS) is a thrombotic microangiopathy (TMA) characterized by excessive activation of the altern

119 Thrombotic microangiopathy (TMA) commonly involves injury of kidney glomerular endot

120 he occurrence of thrombotic microangiopathy (TMA) following IV abuse of extended-release oxymorphone

121 Thrombotic microangiopathy (TMA) is a life-threatening condition that affects some,

122 plant-associated thrombotic microangiopathy (TMA) leads to generalized endothelial dysfunction that c

123 Thrombotic microangiopathy (TMA) occurring after allogeneic hematopoietic stem cell

124 Thrombotic microangiopathy (TMA) significantly predicted graft failure (P = 0.045).

125 drome, a type of thrombotic microangiopathy (TMA) that causes renal failure.

126 (aHUS) develop a thrombotic microangiopathy (TMA) that in most cases is attributable to mutations tha

127 ions, glomerular thrombotic microangiopathy (TMA) was found as a common genetic background-dependent

128 isease (VOD) and thrombotic microangiopathy (TMA) were lower in the nonsirolimus arm (9% vs 21% VOD,

129 a major role in thrombotic microangiopathy (TMA), a disorder that can occur in a variety of clinical

130 vation, systemic thrombotic microangiopathy (TMA), and vital organ damage.

131 development of a thrombotic microangiopathy (TMA), and widespread end organ injury.

132 ith syndromes of thrombotic microangiopathy (TMA), including thrombotic thrombocytopenic purpura and

133 h a rare form of thrombotic microangiopathy (TMA), known as atypical hemolytic uremic syndrome (aHUS)

134 syndrome (HUS), thrombotic microangiopathy (TMA), or HUS-like events, exceeding the MTCD.

135 eported to cause thrombotic microangiopathy (TMA), yet evidence supporting a direct association is of

136 with widespread thrombotic microangiopathy (TMA).

137 characterized by thrombotic microangiopathy (TMA).

138 nt with an acute thrombotic microangiopathy (TMA).

139 , and glomerular thrombotic microangiopathy (TMA).

140 study, the application of tissue microarray (TMA) analysis to a sample of femoral bone specimens from

141 g 71 patients on a breast tissue microarray (TMA) as a model for investigation.

142 primary breast tumours a tissue microarray (TMA) containing biopsies from 483 patients with primary

143 onal images from Stanford Tissue Microarray (TMA) Database.

144 NSCLC from digitized H&E tissue microarray (TMA) slides.

145 HCC tissue to construct a tissue microarray (TMA).

146 as using AQUA analysis of tissue microarray (TMA).

147 ease using an osteosarcoma tumor microarray (TMA) (n = 62).

148 The use of tissue microarrays (TMA) and advances in digital scanning microscopy has ena

149 demonstrated that large tissue microarrays (TMA) can be imaged in a matter of minutes.

150 strate scanning of large tissue microarrays (TMA) in 3-orders of magnitude smaller time per essential

151 T-PCR, Western blotting, tissue microarrays (TMA), and uptake assays of [(3)H]-labeled choline.

152 nt clinical cohorts from tissue microarrays (TMA: n = 208 patients) and whole sections (WS: n = 99 pa

153 Tissue microarrays (TMAs) allow multiplexed analysis of tissue samples and a

154 istochemical staining of tissue microarrays (TMAs) from 223 biliary tract cancers (BTCs) was used to

155 f surgical resections or tissue microarrays (TMAs) from invasive breast carcinoma tissue were tested

156 (AA) and 144 White TNBC tissue microarrays (TMAs) pooled from four hospitals.

157 We used four different tissue microarrays (TMAs) with a total of 859 Ta/T1 urothelial carcinomas fr

158 step in TMAO generation, commensal microbial TMA production, on diet-induced atherosclerosis.

159 ured microbes, to inhibit distinct microbial TMA lyases, and to both inhibit TMA production from phys

160 ogram (OISP) has been implemented to monitor TMA exposure and immunologic outcomes.

161 tes the utility of longitudinally monitoring TMA-specific antibodies in an OISP as exposed workers wi

162 sible with a limit of detection of 0.08 mg N-TMA kg(-1) in freshwater fish and 1 mg N-TMA kg(-1) in m

163 g N-TMA kg(-1) in freshwater fish and 1 mg N-TMA kg(-1) in marine fish.

164 tably, C4d deposits were present in 88.1% of TMA cases, and the various clinical conditions had disti

165 pathway activation was observed in 90.5% of TMA cases.

166 C5b-9 deposits were present in 78.6% of TMA cases and in 39.6% of controls (n=53), but the stain

167 f IV drug abuse when presented with cases of TMA.

168 rent drugs have been suspected as a cause of TMA.

169 critical determinant for the development of TMA secondary to VEGF inhibition.

170 A central feature of TMA is to interrogate mutants that are synthetically sic

171 modest hypertension but no other features of TMA.

172 olving gut microbiota-dependent formation of TMA and host hepatic flavin monooxygenase 3-dependent (F

173 se 3-dependent (FMO3-dependent) formation of TMA-N-oxide (TMAO), a metabolite shown to be both mechan

174 expressing sFlt-1 presented all hallmarks of TMA, including thrombocytopenia, schistocytosis, anemia,

175 nd hypertension were the earliest markers of TMA.

176 m) and elucidated the catalytic mechanism of TMA oxidation by RnTmm.

177 However, the molecular mechanism of TMA oxygenation by Tmm has not been explained.

178 Microbial metabolism of TMA containing nutrients can lead to formation of the pr

179 20 nm shows a response of 12% for 0.5 ppm of TMA vapour in 54% relative humidity, with response and r

180 ese findings reveal the catalytic process of TMA oxidation by marine bacterial Tmm and first show tha

181 t that targeting gut microbial production of TMA specifically and non-lethal microbial inhibitors in

182 web-based application for remote scoring of TMA images, which exploits the value of Microsoft Silver

183 on has been used for multi-centre scoring of TMA slides composed of tissues from several Phase III br

184 on about the three-dimensional structures of TMA-producing enzymes is important for microbiota-target

185 activation as part of a prospective study of TMA in HSCT recipients.

186 ADAMTS13 therapy ameliorated all symptoms of TMA in ADAMTS13(-/-) mice overexpressing sFlt-1 and norm

187 composition, markedly enhanced synthesis of TMA and TMAO, and increased atherosclerosis, but this di

188 elevated sC5b-9) in the blood at the time of TMA diagnosis were associated with very poor survival (<

189 At the time of TMA diagnosis, infections were present in 50% of the pat

190 d to Mycoplasma genitalium research-use-only TMA.

191 id before it reacts with MAs(V), DMAs(V), or TMAs(V)O.

192 m from healthy controls (P < .001) and other TMAs (P < .001).

193 a novel assay to distinguish aHUS from other TMAs based on the hypothesis that paroxysmal nocturnal h

194 Differentiating aHUS from other TMAs, especially thrombotic thrombocytopenic purpura (TT

195 en difficult, to distinguish aHUS from other TMAs, such as thrombotic thrombocytopenic purpura; howev

196 that helps to differentiate aHUS from other TMAs.

197 c acid (DMAs(V)), and trimethylarsine oxide (TMAs(V)O) by the reaction of sodium tetrahydridoborate(1

198 rsenate (DMAs(V)) and trimethylarsine oxide (TMAs(V)O).

199 nt monooxygenases (FMOs) efficiently oxidize TMA to TMAO.

200 In particular, TMA has been reported in association with recombinant ty

201 risk assessment and intervention to prevent TMA in highly susceptible transplant recipients.

202 of cntAB enables Escherichia coli to produce TMA, confirming that these genes are sufficient in TMA f

203 her mutant (E205D, E205A) is able to produce TMA.

204 Similar to VEGF inhibitor-related TMA in humans, these mice exhibited severely impaired ki

205 Risk factors for VEGF inhibitor-related TMA remain unknown.

206 to the development of VEGF inhibitor-related TMA.

207 ed both the systemic thrombophilia and renal TMA phenotypes.

208 mice carrying this mutation developed renal TMA as well as systemic thrombophilia involving large bl

209 vival analysis in an independent replication TMA of 330 melanomas confirmed the association of HMGA2

210 as lower and that of PAI-1 was higher in rTx-TMA than in the controls.

211 tPA and inversely with that of PAI-1 in rTx-TMA.

212 oform the otherwise insoluble sulfate salt, (TMA)2SO4 (tetramethylammonium sulfate).

213 Serum TMA-specific antibody (IgG, IgG4, and IgE) levels were e

214 termine the incidence of moderate and severe TMA and factors associated with poor overall outcomes.

215 All 12 patients had severe TMA with neurological and/or renal involvement.

216 ective observations, we conclude that severe TMA occurred in 18% of HSCT recipients in our cohort and

217 ase in the tin halide solution to form SnY2 -TMA complexes (Y = I(-) , F(-) ) in the first-step depos

218 er by effectively forming intermediate SnY2 -TMA complexes.

219 linicians evaluating patients with suspected TMA.

220 ury and underscore ongoing risk for systemic TMA and progression to organ damage.

221 to the clinical overlap between GVHD and TA-TMA.

222 s more common in subjects with histologic TA-TMA (75%) compared with controls (8%).

223 d with HSCT recipients without histologic TA-TMA.

224 laining the dramatic hypertension seen in TA-TMA.

225 riteria alone, subjects were divided into TA-TMA (n = 8) and non-TA-TMA (control) groups (n = 12).

226 nt-associated thrombotic microangiopathy (TA-TMA) is a common and poorly recognized complication of h

227 T)-associated thrombotic microangiopathy (TA-TMA) is not completely understood.

228 nt-associated thrombotic microangiopathy (TA-TMA) occurs frequently after hematopoietic stem cell tra

229 were divided into TA-TMA (n = 8) and non-TA-TMA (control) groups (n = 12).

230 ngraftment was associated with subsequent TA-TMA development.

231 with complement activation and subsequent TA-TMA.

232 hematopoietic transplant-associated TMA (TA-TMA) and their specific treatment, where applicable, wil

233 a addressing individual susceptibility to TA-TMA.

234 zed that kidney tissue from children with TA-TMA would more frequently show C4d deposition compared w

235 uently observed and only in subjects with TA-TMA.

236 eliminary reports of HSCT recipients with TA-TMA.

237 rmed by repeat testing or alternative-target TMA at a rate of 98.7%.

238 ree energy reported for tetramethylammonium (TMA(+)), a frequently utilized surrogate of methonium.

239 It is shown that TMA can facilitate homogeneous film formation of a SnI2

240 way abundance in public data sets shows that TMA production potential is associated with symptomatic

241 The TMA was immunostained for PCSK9.

242 ment of all the potential etiologies for the TMA findings including acquired TTP will allow for a mor

243 Finally, we classify each core in the TMA and achieve high diagnostic accuracy on a patient ba

244 ch in histidine and cysteine residues in the TMA-L1 region of eukaryotic chloroplast copper ATPases.

245 limitations and caveats, and results of the TMA analysis of post mortem diagenesis in bone are discu

246 Most of the TMA produced is passively absorbed into portal circulati

247 Moreover, C5b-9 was present in >75% of the TMA samples, suggesting that terminal complement inhibit

248 amage are central in the pathogenesis of the TMA, with the treatment directed at the underlying disea

249 e the survival prediction framework with the TMA cohort (P<0.036 for both tumour types).

250 th enhancements for automated application to TMA data.

251 nd CD34 immunohistochemistry were applied to TMA sections.

252 tAB is essential in carnitine degradation to TMA.

253 Exposure to TMA, but not dinitrofluorobenzene, resulted in a robust

254 alysis and exposing C4a-hydroperoxyflavin to TMA for oxidation.

255 hanisms underpinning carnitine metabolism to TMA in human microbiota and assign the role of this nove

256 o a 6-month audit of clinical C. trachomatis TMA (12,999 specimens) on the basis of the C. trachomati

257 antation was associated with post-transplant TMA.

258 ously presented with a post-renal transplant TMA.

259 mono- (MAs(III)), di- (DMAs(III)) and tri- (TMAs(III)) methylarsenicals.

260 bridging moieties of both trimethylaluminum (TMA) and dimethylaluminum chloride (DMACl) surface speci

261 Trimethylamine (TMA) and TMAO levels were initially higher in recipients

262 Trimethylamine (TMA) and trimethylamine N-oxide (TMAO) are widespread in

263 Trimethylamine (TMA) N-oxide (TMAO), a gut-microbiota-dependent metaboli

264 etary nutrients possessing a trimethylamine (TMA) moiety, namely choline/phosphatidylcholine and L-ca

265 Herein, trimethylamine (TMA) is employed as the additional Lewis base in the tin

266 ough microbial production of trimethylamine (TMA) and its subsequent oxidation to trimethylamine N-ox

267 termine the concentration of trimethylamine (TMA), dimethylamine (DMA) and methylamine (MA) in fish.

268 ty index included the use of trimethylamine (TMA-N), total volatile basis nitrogen (TVB-N), histamine

269 low, we review literature on trimethylamine (TMA), a microbiota-generated metabolite linked to athero

270 cteria produce its precursor trimethylamine (TMA) from carnitine, choline, or choline-containing comp

271 t cleaves choline to produce trimethylamine (TMA) and acetaldehyde.

272 phosphatidylcholine produces trimethylamine (TMA), which is further metabolized to a proatherogenic s

273 New evidence suggests that trimethylamine (TMA)-containing nutrients within these foods, including

274 okinetics (PK) and toxicity; trimethylamine (TMA) as a potentially toxic microbiome metabolite; and v

275 of the reaction of MSA with trimethylamine (TMA) on a silicon powder at atmospheric pressure in synt

276 om the reactions of MSA with trimethylamine (TMA), dimethylamine (DMA), methylamine (MA), and ammonia

277 (Me2AsH) (21 +/- 1.0%) and trimethylarsine (TMAs(III)) (10 +/- 1.2%).

278 V. myrtillus berries showed much higher TSP, TMA, RSA and FRAP values than V. uliginosum subsp. gault

279 identification of currently uncharacterized TMA-producing bacteria.

280 Subsequent studies using TMA were performed with wild type versus eosinophil-defi

281 Follow-up studies using TMA with wild type versus eosinophil-deficient PHIL mice

282 rachomatis, N. gonorrhoeae, and T. vaginalis TMA screening.

283 rpose of this study was to determine whether TMA-specific IgG (sIgG) responses can discriminate betwe

284 upporting a definite causal association with TMA.

285 dence supporting a probable association with TMA.

286 5% CI, 4.4-13.9 days) of RNA detectable with TMA.

287 ence for a causal association of a drug with TMA and systematically searched for all published report

288 genes were identified only in nonwhites with TMA and were associated with high mortality (71%).

289 olvement and retinal ischemia occurred, with TMA evident on kidney biopsy.

290 In contrast, patients with TMA had an increase in rare and novel variants only in c

291 Sixty-five percent of patients with TMA had genetic variants in at least one gene compared w

292 ultiple complement pathways in patients with TMA who had gene variants, including variants predicted

293 ement factor C4d in kidneys of patients with TMA.

294 were increased in patients of all races with TMA, but nonwhites had more variants than whites (2.5 [r

295 Subjects with TMA had a significantly higher nonrelapse mortality (43.

296 Identifying individuals with TMAs who may not respond to eculizumab will avoid prolon

297 ext studied 31 samples from 25 patients with TMAs, including 9 with aHUS and 12 with TTP.

298 ne gene compared with 9% of patients without TMA (P < .0001).

299 puter algorithm, compared with those without TMA and without gene variants.

300 1 year post-HSCT compared with those without TMA.