ライフサイエンスコーパス: PTC

1 PTC included five weekly sessions and a 1-month booster.

2 PTC RBC administration was associated with a lower risk

3 PTC RBC transfusion was associated with a 95% reduction

4 PTC RBC transfusion was associated with a 98% reduction

5 PTC suppression is mediated by the base pairing of a nea

6 PTC suppression therapy utilizes small molecules that su

7 PTC Therapeutics, Cystic Fibrosis Foundation, US Food an

8 PTC-to-ATC transformation was also observed in primary B

9 PTCs are a frequent cause of human genetic diseases, and

10 1030 PTC providers were trained between Dec 5, 2012, and Dec

11 ed rep1 protein by 23.1% (PTC124) and 17.2% (PTC-414) and restored biochemical function as confirmed

12 r than 2.5 layers assessed in a sample of 25 PTCs around 1 year after transplantation is indicative o

13 he matched cohort included 113 subjects (31% PTC RBC group).

14 re, we describe the genomic landscape of 496 PTCs.

15 on assays (98 +/- 2% [PTC124] and 68 +/- 5% [PTC-414]).

16 In all 1,704 PTCs, microPTC (mPTC) with maximum diameter less than or

17 Among 61,775 PTC patients, 54,926 underwent total thyroidectomy and 6

18 identity of the amino acid(s) inserted at a PTC during this process in mammalian cells, or how the s

19 s that suppress translation termination at a PTC to restore synthesis of a full-length protein.

20 rmits pairing of a near-cognate complex at a PTC.

21 PTC in exon 14, whereas D1037Rfs 82 causes a PTC in the last exon (exon 15).

22 R1032Gfs 25 introduces a PTC in exon 14, whereas D1037Rfs 82 causes a PTC in the

23 Readthrough of a PTC allows ribosomal A-site insertion of a near-cognate

24 n of a model epitope encoded downstream of a PTC at levels sufficient to activate CD8(+) T cells.

25 processing lead to selective retention of a PTC-containing intron in EIF2B5.

26 The level of sensitivity of a PTC-containing mRNA to NMD is multifactorial.

27 ansition from NMD complexes that recognize a PTC to those that promote mRNA decay.

28 d identified the amino acids inserted when a PTC occupies the ribosomal A site in control, ataluren-t

29 pharmacologic NMD inhibition combined with a PTC "read-through" drug led to restoration of full-lengt

30 ring of a near-cognate aminoacyl-tRNA with a PTC and subsequently, the amino acid becomes incorporate

31 d that betaAR activity during, but not after PTC training initiates the activation of two plasticity-

32 ome the dominant form taking up 56.5% of all PTCs in 2013 while only 43.1% in 2008.

33 ty of ataluren (PTC124) and its novel analog PTC-414: (1) the chm(ru848) zebrafish, the only nonsense

34 medullary thyroid carcinoma (9/12, 75%) and PTC (14/30, 47%).

35 ionship between patient age at diagnosis and PTC-specific mortality with respect to BRAF status in 2,

36 s in the region, forkhead box E1 (FOXE1) and PTC susceptibility candidate 2 (PTCSC2), is regulated by

37 liferation and increases apoptosis of MM and PTC cells.

38 We show that BRAF mutations in both MM and PTC drive increased expression of oncomiR-3151, which is

39 s a previously unidentified player in MM and PTC pathogenesis, which is driven by BRAF-dependent and

40 therapeutic approach in BRAF-mutated MM and PTC patients.

41 for targeted treatment strategies in MM and PTC.

42 ntiation characteristics of Thyroid MSCs and PTC MSCs were comparable with bone marrow MSCs.

43 comprehensive study on the use of PTC124 and PTC-414 as successful nonsense suppression agents for th

44 chr5:1,295,228C>T and chr5:1,295,250C>T) and PTC-specific mortality in 1051 patients (764 women and 2

45 chr5:1,295,228C>T and chr5:1,295,250C>T) and PTC-specific mortality in 1051 patients (764 women and 2

46 soluble cystine accumulation induces apical PTC dedifferentiation, which causes transfer of the harm

47 ation, for a mean number of BM layers around PTC and in serial biopsies.

48 he function of CLIP2 in radiation-associated PTC, the CLIP2 gene regulatory network was reconstructed

49 ctome in the context of radiation-associated PTC.

50 Greater improvement at PTC also occurred for grass allergen peptide 8x6Q2W vers

51 eated at ATCs and MTCs than those treated at PTCs (3.2% and 3.5% vs 0.4%; P < .001).

52 Adolescents treated at PTCs were more likely to be injured by a blunt than pene

53 adolescents was lower among those treated at PTCs, compared with those treated at ATCs and MTCs.

54 tal mortality compared with those treated at PTCs.

55 I, 1.05-2.01) compared with those treated at PTCs.

56 of death when compared with those treated at PTCs.

57 ed at MTCs, and 0.6% for children treated at PTCs.

58 diate the insertion of near-cognate tRNAs at PTCs.

59 We report here that besides PTC events, translation kinetics depend on steric constr

60 t miRNAs is differentially expressed between PTC tissue and normal tissue from the same patient.

61 still unclear how NMD discriminates between PTCs and normal stop codons.

62 n diverse subtypes of thyroid nodules beyond PTC, including a variety of samples with benign histopat

63 PTC-containing mRNAs, increased eIF4E-bound PTC-containing mRNA levels, and subsequent eIF4E-depende

64 In conclusion, BVE-PTC progression could be contained via p53-dependent OIS

65 In contrast, BVE-PTC transplants continued to grow when transplanted into

66 nsformation was also observed in primary BVE-PTC tumors.

67 progression of Braf(V600E)-induced PTC (BVE-PTC) under normal TSH, we transplanted BVE-PTC tumors su

68 E-PTC) under normal TSH, we transplanted BVE-PTC tumors subcutaneously into nude and TPO-Braf(WT) mic

69 erns and associated patient deaths caused by PTC.

70 erns and associated patient deaths caused by PTC.

71 Subjects were dichotomized by PTC RBC transfusion.

72 that some variant CFTR proteins generated by PTC suppression exhibit reduced maturation and activity,

73 melanoma (MM) and papillary thyroid cancer (PTC) and is causally involved in malignant cell transfor

74 ted with increased papillary thyroid cancer (PTC) risk with an odds ratio of approximately 1.8 as det

75 Papillary thyroid cancer (PTC) was diagnosed in 97% of patients and poorly differe

76 S-like family with papillary thyroid cancer (PTC), applying a combined linkage-based and whole-genome

77 stratification of papillary thyroid cancer (PTC), but whether this is generally applicable, particul

78 prognostic role in papillary thyroid cancer (PTC), with a distinct staging dichotomization at 45 year

79 af(V600E) -induced papillary thyroid cancer (PTC).

80 ons can coexist in papillary thyroid cancer (PTC).

81 genic thyroids and papillary thyroid cancer (PTC).

82 ons can coexist in papillary thyroid cancer (PTC).

83 ears or older with papillary thyroid cancer (PTC); patients younger than age 45 years are perceived t

84 TPO-Cre) leads to papillary thyroid cancers (PTC) that rapidly progress to poorly differentiated thyr

85 roximately 40% of papillary thyroid cancers (PTC).

86 y (TCGA study) of papillary thyroid cancers (PTC).

87 embrane (BM) around peritubular capillaries (PTC) can be used in a cohort of patients with de novo do

88 ial increase in papillary thyroid carcinoma (PTC) among children exposed to the radioiodine fallout h

89 ass confirmed a papillary thyroid carcinoma (PTC) and enlarged metastatic lymph nodes.

90 Papillary thyroid carcinoma (PTC) displays strong but so far largely uncharacterized

91 Papillary thyroid carcinoma (PTC) remained to be the most common type counting 86.4%

92 Papillary thyroid carcinoma (PTC), the most frequent thyroid cancer, is characterized

93 ith a precursor papillary thyroid carcinoma (PTC).

94 ed with risk of papillary thyroid carcinoma (PTC).

95 lysis of eight papillary thyroid carcinomas (PTC) to comprehensively characterize miRNAs involved in

96 ns detected in papillary thyroid carcinomas (PTC).

97 We have delivered a primary trauma care (PTC) programme that encompasses both a "provider" and "t

98 programme has delivered primary trauma care (PTC) training in nine sub-Saharan African countries acro

99 shown that human beta-globin mRNAs carrying PTCs in close proximity to the translation initiation AU

100 ter reagents under phase-transfer catalysis (PTC).

101 e.g. K2CO3) and/or phase transfer catalysts (PTC) (e.g. kryptofix 2.2.2) associated with fluorine-18

102 angements at the peptidyltransferase center (PTC) of the ribosome.

103 A away from the peptidyl transferase center (PTC) is functionally significant.

104 that target the peptidyl transferase center (PTC) on the large subunit of the ribosome.

105 of the nascent peptidyl transferase center (PTC) through Nsa2.

106 ite side of the peptidyl-transferase center (PTC).

107 ormation at the peptidyl transferase center (PTC).

108 hildren treated at pediatric trauma centers (PTCs) compared with those treated at adult trauma center

109 Whether pediatric trauma centers (PTCs), mixed trauma centers (MTCs), or adult trauma cent

110 al tunnel to the peptidyltransferase centre (PTC).

111 s 2 to 4 of a 4-day posttreatment challenge (PTC) in the EEU after the grass pollen season.

112 e the association of center characteristics (PTC, ATC, or MTC) on mortality among patients aged 15 to

113 hey introduce a premature termination codon (PTC) and prevent the formation of full-length protein.

114 f a premature translation termination codon (PTC) in an atypical sequence context.

115 A premature termination codon (PTC) in the ORF of an mRNA generally leads to production

116 or at least one premature termination codon (PTC) mutation in COL7A1, and previous studies have shown

117 ipts containing premature termination codon (PTC) mutations by nonsense-mediated mRNA decay (NMD) is

118 at introduces a premature termination codon (PTC) that prevents synthesis of the full-length peptide

119 erting a U A: G premature termination codon (PTC) to tryptophan (U G: G) was improved from approximat

120 usion creates a premature termination codon (PTC), that leads to a 65kDa truncated protein isoform th

121 s and exogenous Premature Termination Codon (PTC)-containing mRNA isoforms and its effects are dose-,

122 d generation of premature termination codon (PTC)-containing mRNAs.

123 ets, unlike for premature termination codon (PTC)-containing reporter mRNAs when compared with their

124 As containing a premature termination codon (PTC).

125 cer, result in premature termination codons (PTC) and the rapid degradation of their mRNAs by nonsens

126 uced readthrough over premature stop codons (PTCs) is a potentially attractive therapy for genetic di

127 nscripts that contain premature stop codons (PTCs) to mitigate their potentially harmful consequences

128 In-frame premature termination codons (PTCs) account for approximately 11% of all disease-assoc

129 pts containing premature termination codons (PTCs) are not always degraded efficiently and can genera

130 NAs containing premature termination codons (PTCs) are rapidly degraded through nonsense-mediated mRN

131 cripts bearing premature termination codons (PTCs) are selectively degraded to maintain transcriptomi

132 RNAs harboring premature termination codons (PTCs) but also regulates the abundance of a large number

133 Premature termination codons (PTCs) in an mRNA ORF inactivate gene function by causing

134 ts often carry premature termination codons (PTCs), which trigger nonsense-mediated decay (NMD), a cy

135 ive exons with premature termination codons (PTCs).

136 mRNAs carrying premature termination codons (PTCs).

137 des mRNAs with premature termination codons (PTCs).

138 ssociated with premature termination codons (PTCs).

139 months from diagnosis (n = 204), to compare PTC to usual care (UC).

140 mounts of mutant proteins from NMD-competent PTC-containing constructs was not affected by inhibition

141 ontaining mRNAs expressed from NMD-competent PTC-containing constructs were as stable as their PTC-fr

142 During Pavlovian threat (fear) conditioning (PTC), sensory and neuromodulatory inputs converge on pos

143 dy investigates the effect of 28 consecutive PTCs and the training challenges that exist between diff

144 nfection, may induce post-treatment control (PTC) of HIV infection with HIV RNA maintained at <50 cop

145 induce a state of 'post-treatment control' (PTC) in some patients, in whom viraemia remains undetect

146 fect of a psychosocial telephone counseling (PTC) intervention on QOL domains and associations with b

147 form a novel genetic background that defines PTC with the worst clinicopathologic outcomes, providing

148 ion of Braf(V600E) (TPO-Braf(V600E)) develop PTC rapidly with high levels of serum thyroid-stimulatin

149 ild-type Cyp24a1 (BVE(Cyp24a1-wt)) developed PTC at 5 weeks of age.

150 Eight of 12 different PTC alleles responded to treatment and produced full len

151 ration of a unique translocon complex dubbed PTC (Pchlide-dependent translocon complex) in the plasti

152 near-cognate aminoacyl-tRNA selection during PTC suppression.

153 Explaining PTC could help our understanding of the processes that m

154 Kaplan-Meier analyses revealed a flat PTC-specific patient survival curve with neither mutatio

155 odulates aversive memory formation following PTC through two molecularly and temporally distinct sign

156 at betaAR activity during, but not following PTC sets in motion cascading molecular events for the ac

157 arboring neither mutation, HRs (95% CIs) for PTC-specific mortality were 3.08 (0.87-10.84) for BRAF V

158 erican Joint Committee on Cancer staging for PTC in patients younger than age 45 years does not inclu

159 age cut point in current staging systems for PTC and argue for considering a revision in how we antic

160 Guidelines recommend total thyroidectomy for PTC tumors >1 cm, based on older data demonstrating an o

161 t guidelines suggest total thyroidectomy for PTC tumors >1 cm.

162 ucted using global mRNA expression data from PTC patient samples.

163 is significantly associated with death from PTC in a linear fashion, without an apparent age cut poi

164 nstrate that p53 constrains progression from PTC to ATC.

165 clear p27, a CDK2 inhibitor, in samples from PTC.

166 he treatment of patients with RDEB harboring PTC mutation in COL7A1.

167 age 45 years undergoing surgery for stage I PTC (no distant metastases) were identified from the Nat

168 In PTC samples from patients, upregulation of TGF-beta, p27

169 value of assessing the mean number of BM in PTC for early prediction of progression to chronic antib

170 the prognostic power of this genetic duet in PTC-specific mortality.

171 the prognostic power of this genetic duet in PTC-specific mortality.

172 1 TYPE A1, TENASCIN, and SOD3 expression in PTC MSCs compared to Thyroid MSCs, suggesting the presen

173 use of patient age as a high-risk factor in PTC and call for differentiation between patients with B

174 nce that Cyp24a1 functions as an oncogene in PTC, where its overexpression activates multiple signali

175 Here, we fine-mapped the 9q22 region in PTC and controls and detected an approximately 33-kb lin

176 ng-observed age-associated mortality risk in PTC is dependent on BRAF status; age is a strong, contin

177 portance of rigorous control of serum TSH in PTC patients.

178 we found COL1A1 and LOX to be upregulated in PTC and expressed at highest levels in PDTC and anaplast

179 siveness of PTC, but its prognostic value in PTC-related mortality remains to be specifically establi

180 romoter mutations were rare and subclonal in PTCs, they were clonal and highly prevalent in advanced

181 Increased PTC apoptosis allowed luminal shedding of cystine crysta

182 ly used antibiotic in humans that can induce PTC readthrough and suppress nonsense mutations at high

183 l modelling of the risk of radiation-induced PTC.

184 igate the progression of Braf(V600E)-induced PTC (BVE-PTC) under normal TSH, we transplanted BVE-PTC

185 s of interaction with the ribosome influence PTC read-through efficiency.

186 er carcinomas) and extended the set of known PTC driver alterations to include EIF1AX, PPM1D, and CHE

187 components of pharmaceutical gentamicin lack PTC readthrough activity but the minor component gentami

188 me-wide association studies of lipid levels (PTC=0.004, PHDL-C=0.008 and Ptriglycerides=0.00003) and

189 lly functional progenitor toxin complexes (M-PTC), which protects BoNT in the gastrointestinal tract

190 Our results suggest that assembly of the M-PTC depends on the environmental pH and that the complex

191 t observed in the crystal structure of the M-PTC.

192 For most PTCs, impaired secretion/function produced by readthroug

193 n rapamycin-treatment as compared to the non-PTC isoform.

194 onstructs, we show that a fraction ( 30%) of PTC-containing mRNAs expressed from NMD-competent PTC-co

195 testes, characterized by an accumulation of PTC-containing transcripts and the transcriptome-wide dy

196 ated to be involved in the aggressiveness of PTC, but its prognostic value in PTC-related mortality r

197 tic regression determined the association of PTC RBC transfusion with outcomes.

198 etion, which induced polysome association of PTC-containing mRNAs, increased eIF4E-bound PTC-containi

199 lack of apoptosis and metastatic behavior of PTC.

200 gh-risk clinicopathologic characteristics of PTC than they were individually.

201 strate a simple 4-genotype classification of PTC, particularly CPTC, with a disease-specific mortalit

202 strate a simple 4-genotype classification of PTC, particularly CPTC, with a disease-specific mortalit

203 Rapamycin-treatment also causes depletion of PTC-containing mRNA isoforms from polyribosomes, undersc

204 The recognition and elimination of PTC-containing transcripts by NMD required that the muta

205 These discoveries reduced the fraction of PTC cases with unknown oncogenic driver from 25% to 3.5%

206 age to risk stratification and management of PTC.

207 that governs the differentiated phenotype of PTC.

208 an restore mRNA integrity in the presence of PTC and can be used as part of a strategy to restore ful

209 d of SMG9 do not appear to have reduction of PTC-containing transcripts but do display global transcr

210 rovides a consistent and effective source of PTC readthrough activity to study the potential of nonse

211 ently validated a workflow for the typing of PTC clinical samples into CLIP2-positive and CLIP2-negat

212 ly patients with the conventional variant of PTC were analyzed.

213 be used for the individual classification of PTCs into CLIP2-positive and -negative cases-a prerequis

214 n=33), two independent validation cohorts of PTCs (n=115) were investigated.

215 Recently, the investigation of PTCs from a cohort of young patients exposed to the post

216 treatment with either PTC124 (42 +/- 5%) or PTC-414 (36 +/- 11%), although an increase in REP1 prote

217 PTC124 or PTC-414 treatment of chm(ru848) embryos led to a approxi

218 engths where a patient may show either VR or PTC, depending on the size of the latent reservoir at tr

219 with the remainder at MTCs (7572 [25.6%]) or PTCs (1639 [5.5%]).

220 It was not found in 138 other PTC families.

221 Other PTCs were edited, but less efficiently.

222 iated early during primary infection permits PTC by limiting the size of the latent reservoir, which,

223 caregivers, investigational site personnel, PTC Therapeutics employees, and all other study personne

224 urea compounds, such as phenylthiocarbamide (PTC) and 6-n-propylthiouracil (PROP), is inherited.

225 The ability to taste phenylthiocarbamide (PTC) and 6-n-propylthiouracil (PROP) is a polymorphic tr

226 BRAFV600E-positive PTC was often conventional or tall cell variant (58%), w

227 Conversely, RAS-positive PTC was commonly follicular variant (87%), with infreque

228 Analogously, RAS and PAX8/PPARG-positive PTCs were histologically similar.

229 BRAFV600E and RET/PTC-positive PTCs were histologically similar.

230 at aminoglycosides are able to overcome RDEB PTC mutations by inducing "read-through" and incorporati

231 Of 1415 subjects, 50 received PTC RBC transfusion.

232 and baseline scores, participants receiving PTC had significantly improved depression and improved g

233 C2 specifically and synergistically regulate PTC endocytosis and transport processes.

234 sy MT for BRAF, RAS, PAX8-PPARgamma, and RET-PTC expedites optimal initial surgery for differentiated

235 BRAFV600E and RET/PTC-positive PTCs were histologically similar.

236 or PAX8/PPARG-positive TCs, BRAFV600E or RET/PTC-positive TCs were more often associated with stage I

237 r TC with routine testing for BRAF, RAS, RET/PTC, and PAX8/PPARG alterations.

238 metastasis was highest in patients with RET/PTC-positive TC (10.8%, P = 0.02).

239 ns revealed that defective endocytosis in S1 PTCs led to partial compensatory uptake by S3 PTCs, sugg

240 TCs led to partial compensatory uptake by S3 PTCs, suggesting displacement of endocytic load and inju

241 However, some PTC-containing mRNAs evade NMD, and might generate mutan

242 It was found in 7/1,170 sporadic PTC cases and in 0/1,404 controls (p = 0.004).

243 Little evidence exists supporting PTC interventions to mitigate this.

244 Several agents are known to suppress PTCs but are poorly efficacious or toxic.

245 on a continuous influx of newly synthesized PTC-containing mRNAs, indicating that truncated mutant p

246 Of 497 TCGA PTC individuals, 138 (27%) were found to carry this germ

247 This trial confirms that PTC benefits mood and QOL cancer-specific and gynecologi

248 Our study shows that PTC courses led to improvement in trauma management know

249 These results suggest that PTC suppression in combination with CFTR modulators may

250 Our findings suggest that PTC-containing mRNAs are potent and regulatable sources

251 The PTC of the ErmBL-SRC appears to adopt an uninduced state

252 The PTC RBC group received 1.3 units of RBCs (median), and 5

253 The PTC-containing SRSF6 transcript exhibits a shorter half-

254 crosstalk between the NMD machinery and the PTC-bound ribosome, a central mechanistic step of RNA su

255 h" and incorporation of an amino acid at the PTC site.

256 ss depends on the rate of translation at the PTC.

257 rrect positioning of their CCA-ends into the PTC thus making peptide bond formation impossible.

258 , we have revealed the mode of action of the PTC inhibitor madumycin II, an alanine-containing strept

259 presented epitopes encoded downstream of the PTC or other stop codons.

260 ErmCL-induced perturbations of the PTC prevent stable binding and accommodation of the amin

261 catalytically efficient organization of the PTC, highlighting the importance of proteins in the RNA-

262 WT-like" configuration to this region of the PTC, providing insight into the resistance mechanism of

263 eral tolerance to epitopes downstream of the PTC.

264 o the nascent polypeptide at the site of the PTC.

265 ted to a catalytically inactive state of the PTC.

266 variable and major gentamicins suppress the PTC readthrough activity of B1.

267 d mRNA decay (NMD) pathway and show that the PTC-containing mRNAs are recognized by the UPF1 ATPase,

268 ibosome to re-initiate translation 3' to the PTC and the specific sequence and secondary structure of

269 elix 89 before relocation of helix 89 to the PTC.

270 ontaining constructs were as stable as their PTC-free counterparts in a steady state.

271 ning reporter mRNAs when compared with their PTC-free counterparts.

272 These PTC-containing mRNAs were monosome-enriched and rarely c

273 x was tested for its ability to read-through PTC mutations in cells derived from patients with RDEB.

274 tic measure of the contrast between tissues: PTC.

275 onjunctivitis symptom score from baseline to PTC) occurred across days 2 to 4 with grass allergen pep

276 prevalent AS event in plants, often leads to PTC-carrying splice variants that are insensitive to NMD

277 t the S346F mutation in SRRM2 predisposes to PTC by affecting alternative splicing of unidentified do

278 g gene FOXE1 underlies the predisposition to PTC triggered by rs965513.

279 rough, namely Gln, Lys, or Tyr at UAA or UAG PTCs and Trp, Arg, or Cys at UGA PTCs.

280 UAA or UAG PTCs and Trp, Arg, or Cys at UGA PTCs.

281 osphine borane compounds was performed under PTC to obtain C60-amino acid or dipeptide derivatives in

282 for understanding the mechanisms underlying PTC, and eventually HIV-1 eradication.

283 Using PTC-containing human genomic beta-globin constructs, we

284 Knowledge was assessed with a validated PTC multiple choice questionnaire and clinical confidenc

285 uet were seen when only conventional-variant PTC (CPTC) was analyzed (HR, 54.46; 95% CI, 12.26-241.82

286 ine transcarbamylase gene containing various PTC-inducing non-sense mutations is able to generate and

287 higher odds of death when treated at ATCs vs PTCs (OR, 1.78; 95% CI, 1.05-3.40), but there was no ass

288 membrane conductance regulator (CFTR) W1282X PTC (a UGA codon) in the context of its three upstream a

289 rs965513) that significantly associates with PTC risk.

290 When used in cells with PTC-mutated p53, pharmacologic NMD inhibition combined w

291 Phe or S346F; rs149019598) cosegregated with PTC in the family.

292 Adult patients with PTC tumors 1.0-4.0 cm undergoing thyroidectomy in the Na

293 Results A total of 31,802 patients with PTC were included.

294 Patients and Methods Patients with PTC who had surgery were identified from the SEER databa

295 ull-length endogenous protein, patients with PTC-inducing non-sense mutations may still present T cel

296 ow we anticipate prognosis for patients with PTC.

297 ) in patients younger than age 45 years with PTC.

298 tio, 6.68; 95% CI, 2.03-21.99) compared with PTCs but was not different between level I and II center

299 (324/469) of hemophilia B (HB) patients with PTCs.

300 ficial for the treatment of CF patients with PTCs.