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 that AA cancers harbor significant

3 TMA and cadaverine inhibited LPS-stimulated TNF-alpha an

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

5 TMA is then converted in the liver to trimethylamine oxi

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

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

8 known composition of volatile gases (NH(3), TMA, DMA and H(2)S) in the ppb-ppm regime.

9 ion (ppb to ppm regime) of volatiles (NH(3), TMA, ethanol, and H(2)S) generated from chicken meat spo

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

11 ost of the variance in ascorbic acid (>90%), TMA (>42%) and TP (>69%).

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

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

14 phoblastic leukemia, the patient developed a TMA due to CD and reached end-stage renal disease.

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

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

17 tween 4 and 24 Raman spectra, 4 acquisitions/TMA core).

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

19 The thiol-Michael addition (TMA) is a powerful methodology to click several fragment

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

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

22 ays for the tpp47 gene were performed on all TMA-positive specimens, as well as specimens from 20 ran

23 standard consisting of the 3 alternate (Alt) TMA tests was used to evaluate the clinical performance

24 ologic transcription-mediated amplification (TMA) analyte-specific reagent (ASR) assay adds a second

25 l-time transcription-mediated amplification (TMA) assay performed on rectal and pharyngeal mucosal sw

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

27 tional transcription-mediated amplification (TMA) NAAT for the detection of M. genitalium 16S rRNA.

28 using transcription-mediated amplification (TMA) technology.

29 three transcription-mediated amplification (TMA) tests for M. genitalium, each targeting unique rRNA

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

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

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

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

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

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

36 eased CO(2) linearly prevented melanosis and TMA formation, whereas decreased O(2) concentration gave

37 dicated synergistic effects on melanosis and TMA inhibition.

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

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

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

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

42 ascorbic acid, total monomeric anthocyanins (TMA) and total phenolics (TP) in strawberries (p<0.05),

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

44 using the coherent Transfer Matrix Approach (TMA) to describe the behavior of the three main class of

45 g a multi-cancer tissue microarray approach (TMA).

46 These tumor microenvironment-activated ARBs (TMA-ARBs) remain intact and inactive in circulation whil

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

48 We investigated tissue micro arrays (TMAs) with tumor samples of two independent cohorts of R

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

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

51 ever, the management of pregnancy-associated TMA remains ill defined.

52 nd manage an episode of pregnancy-associated TMA.

53 t of possible causes of pregnancy-associated TMA.

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

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

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

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

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

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

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

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

62 Staining of p53 and PARP1 in breast cancer TMAs and comparison with the TCGA database indicated a h

63 yde targets the gut microbial enzyme choline TMA-lyase (CutC).

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

65 -Catenin-1) was performed on the constructed TMAs.

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

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

68 each patient, 2 consecutive sections of each TMA block were cut.

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

70 ated extended-release oxymorphone can elicit TMA.

71 rular filtration rate at 5 years, especially TMA.

72 male subjects independently across all five TMAs, regardless of disease state (p = 8.66e-15).

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

74 heric nitrogen-containing compounds, and for TMA, we experimentally confirm this.

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

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

77 erium Eubacterium limosum Instead of forming TMA, carnitine is demethylated by the newly discovered m

78 cificity, and strain inclusivity of all four TMA tests were determined using nine laboratory strains

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

80 no single commensal capable of l-carnitine->TMA transformation, multiple community members that conv

81 imonensis promoted the complete l-carnitine->TMA transformation.

82 rming each step of the l-carnitine->gammaBB->TMA transformation were identified.

83 econd gut microbial transformation, gammaBB->TMA, was diet inducible (l-carnitine, omnivorous).

84 ps in a metaorganismal l-carnitine->gammaBB->TMA->TMAO pathway in subjects.

85 Gut microbiota gammaBB->TMA/TMAO transformation is induced by omnivorous dietary

86 patients undergoing genetic testing, 34 had TMA.

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

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

89 by the Affirm and Candida vaginitis Hologic TMA ASR assays was assessed using microscopy for yeast a

90 s an effective therapeutic strategy for hrTA-TMA, but some patients with severe disease lacked a comp

91 sly reported untreated cohort with same hrTA-TMA features that had 1-year post-HSCT survival of 16.7%

92 CT recipients who had high-risk TA-TMA (hrTA-TMA) and multiorgan injury treated with the complement b

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

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

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

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

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

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

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

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

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

102 e different pathways and enzymes involved in TMA metabolism in marine bacteria.

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

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

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

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

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

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

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

110 bolism and a potential target for inhibiting TMA production.

111 the discovery that betaine aldehyde inhibits TMA production from choline by human gut bacterial isola

112 gammaBB, followed by (b) transformation into TMA via low-abundance microbiota in omnivores, and to a

113 um (AMG) assay, an in vitro diagnostic (IVD) TMA test that targets 16 s rRNA of M. genitalium Analyti

114 red about the microbial metabolism of marine TMA.

115 might be more similar to complement-mediated TMA syndromes, which are well known to rheumatologists w

116 ents suspected of having complement-mediated TMA.

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

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

119 life-threatening thrombotic microangiopathy (TMA) caused by acquired or congenital severe deficiency

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

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

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

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

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

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

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

131 , and glomerular thrombotic microangiopathy (TMA).

132 characterized by thrombotic microangiopathy (TMA).

133 nt with an acute thrombotic microangiopathy (TMA).

134 with widespread thrombotic microangiopathy (TMA).

135 ts in regions of thrombotic microangiopathy (TMA).

136 he prototypes of thrombotic microangiopathy (TMA).

137 fferent forms of thrombotic microangiopathy (TMA).

138 h renal-specific thrombotic microangiopathy (TMA).

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

140 analyzed by IHC on tumor tissue microarray (TMA) cores and by gene expression profiling with EdgeSeq

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

142 Tissue microarray (TMA) samples from 415 tissues collected from three cance

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

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

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

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

147 The use of tissue microarrays (TMA) in studies that profile TIL burden is attractive bu

148 Tissue Microarrays (TMA) were constructed from these samples.

149 erived xenografts (PDX), tissue microarrays (TMA), and The Cancer Genome Atlas (TCGA) database.

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

151 Profiler method on five tissue microarrays (TMAs) of cardiac tissues across a diverse set of disease

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

153 from single sections and tissue microarrays (TMAs).

154 y specimens (embedded in tissue microarrays [TMAs]) from 483 patients treated in 3 Canadian instituti

155 lso raises several questions about microbial TMA metabolism in the marine environments and proposes p

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

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

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

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

160 Combining mucosal TMA testing and serological testing may increase the sen

161 e diagnosed based on positive rectal mucosal TMA assay results alone, and both also tested positive b

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 Notably, TMA-ARBs alleviate immunosuppression and improve T lymph

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

166 ventional and practical number (e.g. <=3) of TMA cores is adequate for correct ordinal categorisation

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

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

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

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

171 also developed, by sequential combination of TMA and CuAAC click reaction, as an easy and quick way t

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

173 ity rate, consistent with the development of TMA.

174 urrently known about the sources and fate of TMA in marine environments and the different pathways an

175 sider alternative disorders with features of TMA (preeclampsia/eclampsia; hemolysis elevated liver en

176 modest hypertension but no other features of TMA.

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

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

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

180 Mediators of TMA syndromes overlap with those released in cytokine st

181 oach, we also analysed the optimal number of TMA cores required to provide an accurate representation

182 and complement activation in pathogenesis of TMA in mice.

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

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

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

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

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

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

189 is approach takes into account the timing of TMA in pregnancy or postpartum, coexisting symptoms, fir

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

195 that helps to differentiate aHUS from other TMAs.

196 Differential diagnosis with other TMAs is particularly difficult when the first TTP event

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

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

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

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

201 be mediated by increased acetate and reduced TMA production by gut microbiota, thus, improving gut in

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

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

204 to the development of VEGF inhibitor-related TMA.

205 ed both the systemic thrombophilia and renal TMA phenotypes.

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

207 well as specimens from 20 randomly selected TMA-negative men.

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

209 h or without Adamts13 (-/-) developed severe TMA.

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

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

212 er by effectively forming intermediate SnY2 -TMA complexes.

213 , but has also been linked to renal-specific TMA.

214 linicians evaluating patients with suspected TMA.

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

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

217 Treatment was discontinued because TA-TMA resolved at a median of 66 days (IQR 41-110).

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

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

220 nt-associated thrombotic microangiopathy (TA-TMA), and untreated patients have dismal outcomes.

221 diatric HSCT recipients who had high-risk TA-TMA (hrTA-TMA) and multiorgan injury treated with the co

222 ngraftment was associated with subsequent TA-TMA development.

223 with complement activation and subsequent TA-TMA.

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

225 a addressing individual susceptibility to TA-TMA.

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

227 the presence of an ion, tetramethylammonium (TMA(+)), common to each phase.

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

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

230 The TMA was immunostained for PCSK9.

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

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

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

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

235 olecular capsules by taking advantage of the TMA click reaction.

236 but are gravely insufficient for any of the TMA disorders that involve disorders of complement.

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

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

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

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

241 atherosclerosis and heart disease, and these TMA-producing enzymes are therefore important drug targe

242 for future discovery of drugs targeting this TMA-producing enzyme in human gut.

243 nd CD34 immunohistochemistry were applied to TMA sections.

244 he oxygen-dependent cleavage of carnitine to TMA and malic semialdehyde.

245 olates that are unable to convert choline to TMA, suggesting that additional members of the gut micro

246 and further convert the released choline to TMA.

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

248 gencia timonensis, that converted gammaBB to TMA.

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

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

251 antation was associated with post-transplant TMA.

252 ously presented with a post-renal transplant TMA.

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

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

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

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

257 Trimethylamine (TMA) is common in marine environments.

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

259 intestinal bacteria-derived trimethylamine (TMA) following metabolism of certain dietary nutrients,

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

261 he atmospherically important trimethylamine (TMA) and dimethylamine and generalized by the study of t

262 y that converts choline into trimethylamine (TMA) is broadly linked to human disease.

263 isease-associated metabolite trimethylamine (TMA).

264 biota-dependent formation of trimethylamine (TMA) and trimethylamine N-oxide (TMAO) via a multistep p

265 or 12 days) and formation of trimethylamine (TMA) concurrent with limited total viable count (TVC), E

266 Bacterial formation of trimethylamine (TMA) from carnitine in the gut microbiome has been linke

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 rmalized endotoxemia, plasma trimethylamine (TMA) levels, and restored the Th17 and Treg content in m

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

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

273 red meat, is metabolized to trimethylamine (TMA) by the gut microbiota.

274 l metabolism of carnitine to trimethylamine (TMA) in the gut can accelerate atherosclerosis and heart

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

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

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

278 identification of currently uncharacterized TMA-producing bacteria.

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

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

281 pecimens and 410 rectal specimens with valid TMA results.

282 Using a virtual TMA approach, we also analysed the optimal number of TMA

283 At least 1 specimen was TMA positive for 12 of 24 men with syphilis (sensitivity

284 the mammalian gastrointestinal tract, where TMA metabolism by microorganisms has been studied intens

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

286 upporting a definite causal association with TMA.

287 dence supporting a probable association with TMA.

288 5% CI, 4.4-13.9 days) of RNA detectable with TMA.

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

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

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

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

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

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

295 ement factor C4d in kidneys of patients with TMA.

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

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

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

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

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