ライフサイエンスコーパス: TDT

1 TDT 067 demonstrated lower MFC values for T. rubrum and

2 TDT 067 demonstrated potent activity against the dermato

3 TDT 067 has more potent antifungal activity against derm

4 TDT 067 is a novel carrier-based dosage form (liquid spr

5 TDT analysis showed significant association at the CRH l

6 TDT patients with diabetes mellitus had significantly hi

7 TDT requires genotypes of affected individuals and their

8 TDT was analyzed as a continuous variable using a specif

9 TDT(ae) always maintains correct type I error rates for

10 paper, the authors propose a new test, the 1-TDT, to detect linkage between a candidate locus and a d

11 ed TDT analysis gave similar results, with a TDT statistic (TDT chi2=5.45) corresponding to a P value

12 In multivariate analysis, TDT had no impact on overall survival (P = .4095) compar

13 Both chi(2) analysis and TDT suggested an association between IFN-gamma allele 2

14 fluenced by host factors, tumor factors, and TDT.

15 We have implemented the combined sib-TDT and TDT, in addition to parametric and non-parametric linkag

16 VCS and TDT function together in small cytoplasmic foci that app

17 The family-based TDT analysis gave similar results, with a TDT statistic

18 Family-based TDT showed a significant association of SLE with a N673S

19 sting single-marker TDTs and haplotype-based TDTs.

20 ll count, no significant differences between TDT groups were observed.

21 Retinal neuron loss was determined by TDT-mediated dUTP nick-end labeling assay, inner retinal

22 S2785 (but not D1S229) were linked to SLE by TDT.

23 Unadjusted 2-year OS rates, stratified by TDT of 0 to 5, 6 to 10, 11 to 15, and >15 days, were 51%

24 types are often unavailable, the X-linkage C-TDT may allow for more power than is provided by the X-l

25 an overall test (i.e., a combined-TDT, or C-TDT).

26 ured tumors in three dimensions to calculate TDT and specific growth rate (SGR).

27 to rare variants in families usually combine TDT statistics at individual variants and therefore lack

28 est (XS-TDT) and the reconstruction-combined TDT for X-chromosome markers (XRC-TDT) are the first ass

29 gestive evidence for linkage in the combined TDT in those families in which affected siblings did not

30 ombined in an overall test (i.e., a combined-TDT, or C-TDT).

31 sent, however, the results are more complex: TDT is more powerful when population substructure is sub

32 Using a DRB1-conditioned TDT to assess whether an independent effect existed, we

33 ation with the HLA-DR2 allele was confirmed (TDT; P < 0.001).

34 nterface and can be applied to case-control, TDT trio and quantitative trait data.

35 While the median difference (TDT-HET empirical power - TDT empirical power) is approx

36 op privacy-preserving approaches to disclose TDT statistics with a guarantee that the risk of family

37 e probabilities, which we name as the dosage-TDT (dTDT).

38 We provide a guideline on applying our DP TDT in a real dataset in analyzing Kawasaki disease with

39 pproach, called the "evolutionary tree" (ET)-TDT, is developed for two cases: when haplotype transmis

40 Simulations show the ET-TDT can be more powerful than other proposed methods und

41 ymorphisms are found within the gene, the ET-TDT can be useful for determining which polymorphisms af

42 intensive first-line AML treatment evolves, TDT data suggest that it may be a feasible approach to w

43 This paper develops five TDT-type tests for use with quantitative traits.

44 39; P = 0.04) were prognostic biomarkers for TDT irrespective of treatment, and baseline TBR predicte

45 f differentially private (DP) mechanisms for TDT.

46 Furthermore, TDT was not associated with response rate and early deat

47 In this study we generalize TDT using mixed linear models to allow greater statistic

48 mpared with the conventional and generalized TDT methods, our procedure is more flexible and powerful

49 NG and NIMH data sets, the results of global TDT of the entire haplotype set were significant and con

50 in women who were treated by surgery and had TDT more than 6 weeks was 80% compared with 90% (P = .00

51 cioeconomic status (7.7%) were shown to have TDT more than 6 weeks.

52 However TDT analyses for these PLG variants did not demonstrate

53 ons and that, in most cases, the power of HS-TDT is higher than the power of the existing single-mark

54 icle, we propose a haplotype-sharing TDT (HS-TDT) for linkage or association between a disease-suscep

55 Our simulation results show that the HS-TDT has the correct type I error rate in structured popu

56 rmined whether this pathway directly impacts TDT development.

57 In TDT analysis, comparison of the overall haplotypes, tran

58 Moreover, overnight improvement in TDT performance correlated with EEG power density during

59 at 0.75-1.0 Hz) over brain areas involved in TDT learning.

60 relationship with hematologic parameters in TDT patients.

61 ic increases and decreases, respectively, in TDT fiber number.

62 Although ectopic TpnC4 in TDT muscles was able to maintain jumping ability, TpnC41

63 o identify factors associated with indolent (TDT > 365 days) and rapid (TDT < 90 days) tumor growth.

64 more power than is provided by the X-linkage TDT alone.

65 Young women with breast cancer with a longer TDT have significantly decreased survival time compared

66 univariate and multivariate analyses, longer TDT was associated with worse CR and OS in younger (univ

67 In multivariate analysis, longer TDT, estrogen receptor negative status, having public or

68 reased power compared with the single marker TDT.

69 than the power of the existing single-marker TDTs and haplotype-based TDTs.

70 Median TDT (169 days; IQR 74-408 days) and SGR (0.4% per day) w

71 Median TDT was 3 days (interquartile range, 2-7).

72 (n = 242 patients from four centers), median TDT was 229 days (interquartile range [IQR], 89-627) and

73 Similarly, the median TDT was 19, 34, and 52 d in controls, the radiotherapy g

74 The median TDT was 8 days (interquartile range, 4-16) and was signi

75 To obtain an unbiased multihaplotype TDT, we must either count transmissions from one randoml

76 e tergal depressor of the trochanter muscle (TDT, or jump muscle), which functions in the escape resp

77 e tergal depressor of the trochanter muscle (TDT; jump muscle).

78 study, we report the in vitro activities of TDT 067 against dermatophytes, compared with those of th

79 l was performed to assess the association of TDT with survival while accounting for covariates (age,

80 f 0 to 5, 6 to 10, 11 to 15, and >15 days of TDT, adjusted for influence of established prognostic va

81 The effect of TDT was assessed using multivariate analysis.

82 We analyzed influence of TDT on remission, early death, and overall survival (OS)

83 Clinical investigation of TDT 067 for the topical treatment of onychomycosis is wa

84 The MICs of TDT 067 and comparators against 25 clinical strains each

85 Finally, the power of TDT(std) is at least that of TDT(ae) for simulations wit

86 y, the power of TDT(std) is at least that of TDT(ae) for simulations with errorless data.

87 such an approach by combining the theory of TDT with that of measured haplotype analysis (MHA).

88 rTDT returns minimum and maximum values of TDT that are consistent with all the possible completion

89 ow" strategy that reduced the variability of TDT P values relative to the single-locus results.

90 to be associated with schizophrenia based on TDT analysis of 80 British trios.

91 The original TDT requires families in which the genotypes are known f

92 the data may be used jointly in one overall TDT-type procedure that tests for linkage in the presenc

93 Overall, TDT 067 MIC(50) values (defined as the lowest concentrat

94 rom UK (P(TDT) = 1.4 x 10(-5)) and Mexico (P(TDT) = 0.015).

95 as two independent sets of trios from UK (P(TDT) = 1.4 x 10(-5)) and Mexico (P(TDT) = 0.015).

96 er and greater significance than the popular TDT analysis of incomplete data.

97 A positive TDT at D12S83 suggests that we have greatly narrowed the

98 0S193, marker D10S588 also provided positive TDT results (P = 0.009, Pc = 0.25) but the allele under

99 median difference (TDT-HET empirical power - TDT empirical power) is approximately 0 for all MOI, the

100 the test, various researchers have proposed TDT-based methods for haplotype transmission.

101 n disequilibrium test (TDT) and quantitative TDT (and quantitative pedigree disequilibrium test) anal

102 ed with indolent (TDT > 365 days) and rapid (TDT < 90 days) tumor growth.

103 inflated false-positive rate among reported TDT-derived associations and that genotyping fidelity mu

104 here an extension to the TDT, called robust TDT (rTDT), able to handle incomplete genotypes on both

105 We demonstrate that for all RV-TDT methods, using proper analysis strategies, type I er

106 umber of sequence-based trio studies, the RV-TDT is extremely beneficial to elucidate the involvement

107 The power of the RV-TDT methods was evaluated and compared to the analysis o

108 The RV-TDT was also used to analyze exome data from 199 Simons

109 od, by Spielman and Ewens, and the TDT and S-TDT can be combined in an overall test (i.e., a combined

110 scribe a method, called the "sib TDT" (or "S-TDT"), that overcomes this problem by use of marker data

111 The sib-TDT, or S-TDT, which utilizes families with affected and unaffecte

112 the sib transmission/disequilibrium test (S-TDT).

113 The S-TDT can be applied to diseases with late age at onset su

114 hers that are suitable for analysis by the S-TDT.

115 sent article, we propose a haplotype-sharing TDT (HS-TDT) for linkage or association between a diseas

116 ival time compared with those with a shorter TDT.

117 ticle, we describe a method, called the "sib TDT" (or "S-TDT"), that overcomes this problem by use of

118 Sib-TDT analysis showed that some gene variants were signifi

119 We have implemented the combined sib-TDT and TDT, in addition to parametric and non-parametri

120 he sib transmission/disequilibrium test (Sib-TDT, p = 0.81).

121 The sib-TDT analysis also showed significant association between

122 The sib-TDT, or S-TDT, which utilizes families with affected and

123 Significant TDT results indicate both linkage and allelic associatio

124 literature search and located 79 significant TDT-derived associations between a microsatellite marker

125 However, significant TDT results are often interpreted as implying tight link

126 0q26.13 displaying a genome-wide significant TDT in combined female and male transmissions and a sign

127 Similar TDT analyses of TGFB2 and HLX1 polymorphisms yielded no

128 However, some TDTs are formulated in a rigid form, with reduced potent

129 ween time from diagnosis to treatment start (TDT) and prognosis in a large real-world data set from t

130 gave similar results, with a TDT statistic (TDT chi2=5.45) corresponding to a P value of.02.

131 developed an extension of the TDT statistic (TDT-HET) that allows for locus heterogeneity among coded

132 re trained on a texture discrimination task (TDT) after baseline sleep, and were tested 24 h later, a

133 receive the trap-door harvesting technique (TDT) or the epithelialized free gingival graft harvestin

134 ays (Drexel), and Tucker-Davis Technologies (TDT) microwire arrays are evaluated over a 31-day period

135 uces a new transmission/disequilibrium test (TDT(ae)) that allows for random genotyping errors.

136 particular transmission/disequilibrium test (TDT(std)), which assumes that data are errorless, and in

137 The transmission disequilibrium test (TDT) analyses of our data revealed significant associati

138 nalyzed by transmission disequilibrium test (TDT) analysis (FBAT software) for three dentition groups

139 Transmission disequilibrium test (TDT) and quantitative TDT (and quantitative pedigree dis

140 The transmission disequilibrium test (TDT) and the pedigree disequilibrium test (PDT) were con

141 he popular transmission/disequilibrium test (TDT) approach for fine mapping, in the following ways: F

142 The transmission/disequilibrium test (TDT) developed by Spielman et al. can be a powerful fami

143 DT and the transmission/disequilibrium test (TDT) for special family structures.

144 plying the transmission disequilibrium test (TDT) genome-wide to three large sets of human pedigrees

145 e that the transmission/disequilibrium test (TDT) has higher power than the affected-sib-pair (ASP) m

146 uch as the transmission/disequilibrium test (TDT) have become very popular during the past few years,

147 sis by the transmission disequilibrium test (TDT) in 1159 families with at least one diabetic child,

148 ase by the transmission disequilibrium test (TDT) in a UK data set of type 1 diabetic families (n = 1

149 The transmission disequilibrium test (TDT) is a powerful family-based association test employe

150 The transmission-disequilibrium test (TDT) is a robust test for detecting QTL.

151 The transmission disequilibrium test (TDT) is a useful method to locate mutations linked to di

152 When the transmission/disequilibrium test (TDT) is applied to multilocus haplotypes, a bias may be

153 udies, the Transmission/Disequilibrium Test (TDT) measures the over-transmission of an allele in a tr

154 The transmission-disequilibrium test (TDT) of Spielman et al. is a family-based linkage-disequ

155 The transmission/disequilibrium test (TDT) originally was introduced to test for linkage betwe

156 The transmission/disequilibrium test (TDT) proposed by Spielman et al. can be a powerful test

157 rean), the transmission/disequilibrium test (TDT) revealed a highly significant deviation for transmi

158 nts, and a transmission disequilibrium test (TDT) showed strong over-transmission of this variant.

159 extend the transmission disequilibrium test (TDT) to include cases with missing parental genotype.

160 e used the transmission disequilibrium test (TDT) to investigate familial association in the ALSPAC s

161 he classic transmission disequilibrium test (TDT) to one that accounts for locus heterogeneity.

162 The transmission/disequilibrium test (TDT) was also performed in a subset of this cohort (46 p

163 The transmission disequilibrium test (TDT) was computed to test for nonrandom transmission fro

164 sed by the transmission/disequilibrium test (TDT) was of borderline significance (p-value 0.048).

165 The transmission disequilibrium test (TDT) was used to determine if affected offspring receive

166 uch as the transmission disequilibrium test (TDT) were motivated by concern that sample-based methods

167 The transmission/disequilibrium test (TDT), a family-based test of linkage and association, is

168 erform the transmission/disequilibrium test (TDT), although the TDT can perform better under an addit

169 uch as the transmission/disequilibrium test (TDT), but this comes at a considerable cost in the need

170 using the transmission disequilibrium test (TDT), confirmed the 480-bp allele as the high-risk allel

171 use of the transmission/disequilibrium test (TDT), individual markers yielded significant linkage dis

172 Like the transmission disequilibrium test (TDT), the likelihood-ratio test (LRT) based on this mode

173 gle-marker transmission/disequilibrium test (TDT), then the rapid increase in the degrees of freedom

174 tiallelic, transmission-disequilibrium test (TDT), we found overall skewing of transmission of PARP a

175 The transmission/disequilibrium test (TDT), which detects linkage between a marker and disease

176 using the transmission disequilibrium test (TDT), which is robust to population substructure and adm

177 d with the transmission/disequilibrium test (TDT), which simultaneously evaluates linkage and associa

178 using the transmission/disequilibrium test (TDT).

179 own as the transmission/disequilibrium test (TDT).

180 ted by the transmission/disequilibrium test (TDT).

181 sed on the transmission-disequilibrium test (TDT).

182 The transmission/disequilibrium (TD) test (TDT), proposed, by Spielman et al., for binary traits is

183 otype, and transmission/disequilibrium test [TDT]) will have no power if the loci are examined indivi

184 rformed transmission/disequilibrium testing (TDT) and haplotype analysis, since a linkage-disequilibr

185 d using transmission disequilibrium testing (TDT) and multitest corrections.

186 s using transmission disequilibrium testing (TDT) were also used.

187 ion and transmission disequilibrium testing (TDT) were performed in lupus families.

188 ing, by transmission/disequilibrium testing (TDT), that the same haplotype is associated with CD (chi

189 Transmission/disequilibrium tests (TDT) based on family designs are robust to population st

190 including transmission disequilibrium tests (TDT) were performed in a multi-ethnic cohort of 718 fami

191 Transmission/disequilibrium tests (TDTs) were also performed.

192 nditioned transmission disequilibrium tests (TDTs).

193 propionic acid (MPA) and 1-tetradecanethiol (TDT) was formed on the surface of the electrode to immob

194 Transfusion-dependent beta-thalassemia (TDT) and sickle cell disease (SCD) are severe monogenic

195 with transfusion-dependent beta-thalassemia (TDT) mainly chronic anemia, iron overload and iron chela

196 usions in transfusion-dependent thalassemia (TDT) and iron chelation impairs quality of life(1).

197 ent, we find GC is always more powerful than TDT; furthermore, contrary to previous results, we show

198 The results indicate that TDT(std) shows a significant increase in type I error wh

199 Here, we report that TDT encodes the mRNA-decapping enzyme.

200 It was reported that TDT 067 (a topical formulation of 15 mg/ml terbinafine i

201 Our study suggests that TDT is not related to survival.

202 The TDT exploits within-family associations that are not aff

203 The TDT has an efficiency of 1/2 for parent-offspring pairs

204 The TDT is equivalent to a randomized experiment and, theref

205 The TDT is positive at the D12S83 locus (global chi2 = 16.41

206 The TDT requires data (marker genotypes) for affected indivi

207 The TDT statistics described so far are for autosomal chromo

208 The TDT(std) statistic is computed on all trios that show Me

209 sion/disequilibrium test (TDT), although the TDT can perform better under an additive model of inheri

210 ative method, by Spielman and Ewens, and the TDT and S-TDT can be combined in an overall test (i.e.,

211 Both the TDT(std) and the TDT(ae) statistics are computed as two times a log-likel

212 ower comparison between the TDT(std) and the TDT(ae), for errorless data.

213 ted child from each sibship and to apply the TDT to those data.

214 the disease locus itself, tests such as the TDT can be far more powerful than conventional linkage t

215 nd that researchers use methods, such as the TDT(ae), that allow for errors in genotype data.

216 s and perform a power comparison between the TDT(std) and the TDT(ae), for errorless data.

217 Both the TDT(std) and the TDT(ae) statistics are computed as two

218 ght be some that can be analyzed only by the TDT and others that are suitable for analysis by the S-T

219 ountries by isolating, and evaluating by the TDT, two novel microsatellites within 70 kb of D18S487.

220 erful than the mean test; in such cases, the TDT has essentially no power to detect linkage.

221 To date, the TDT and most other family-based association tests have b

222 require individual genotyping to derive the TDT statistic, whereas all the offspring can be pooled.

223 As a test for linkage disequilibrium, the TDT makes the assumption that any allelic association pr

224 oposed test has higher power than either the TDT or the mean test when the extent of LD ranges from m

225 Recently, Ewens and Spielman extended the TDT for use in sibships with at least one affected and o

226 We extended the TDT to test for RV associations using four commonly used

227 s the correct type I error rate.Finally, the TDT-HET statistic shows highly significant p-values for

228 rvested sites, and 69.21 +/- 7.08 uL for the TDT group, a ratio of 4.18 (P < 0.01).

229 tatistically significant correlation for the TDT-harvest sites (P = 0.02).

230 Given the TDT results in the present cohort with UC, IBD5 may also

231 However, the TDT analysis showed significant excess transmission of t

232 ren can be included in the TDT; however, the TDT is a valid chi2 test of association only if transmis

233 In the TDT analysis, alleles of three of these SNPs showed sign

234 nts and homozygous offspring are used in the TDT.

235 eir affected children can be included in the TDT; however, the TDT is a valid chi2 test of associatio

236 roader array of causal scenarios than is the TDT.

237 e is a collapsing for which the power of the TDT is greater than that for the original microsatellite

238 Efficiency of the TDT is increased in multiplex families and by inclusion

239 e strategy that may improve the power of the TDT is to group marker alleles within a locus, on the ba

240 tes shows that the validity and power of the TDT may vary by an order of magnitude, depending on the

241 By identifying the origins of the TDT muscle, from founder cells specified in the mesothor

242 We have developed an extension of the TDT statistic (TDT-HET) that allows for locus heterogene

243 d an error model into the calculation of the TDT statistic.

244 situations considered, but extension of the TDT to allow inclusion of information from unaffected si

245 allowing application of the principle of the TDT to sibships without parental data.

246 These extensions of the TDT will be valuable for the study of diseases of late o

247 Factors affecting the power of the TDT(ae) are discussed.

248 luate the type I error rate and power of the TDT(ae) under a variety of simulations and perform a pow

249 must be discarded to ensure validity of the TDT, thereby sacrificing information.

250 ses a stringent test for the validity of the TDT.

251 methods, including a conditional form of the TDT.

252 t can be regarded as a generalization of the TDT.

253 lues and exponential mechanisms based on the TDT test statistic and the shortest Hamming distance (SH

254 They include Laplace mechanisms based on the TDT test statistic, P-values, projected P-values and exp

255 Second, rather than performing the TDT at each marker separately, we propose a single test

256 Recently, the TDT has been used to test for association in the presenc

257 the limitations of the present research, the TDT resulted in a significantly higher leakage than the

258 w that the SDT can be more powerful than the TDT for testing linkage disequilibrium, especially for d

259 age and generally are more powerful than the TDT with a single, randomly chosen, affected child from

260 The fact that the TDT passes this test means that a wide range of problems

261 Thus, for ASP data, it seems clear that the TDT should be used when LD is strong but that the mean t

262 that we obtain PPBs, we conjecture that the TDT-HET may be a useful method for correctly identifying

263 be a risk factor when identified through the TDT, and it appears to be protective when identified thr

264 thout parents, this test is analogous to the TDT and is completely robust to nonrandom mating pattern

265 number of founder cells contributing to the TDT at the early pupal stage.

266 Family-based samples lend themselves to the TDT despite its inefficiency compared with cases and unr

267 ive-marker) haplotypes were subjected to the TDT using a "moving-window" strategy that reduced the va

268 m relative both to Curtis's tests and to the TDT using trios comprising an affected sib and its paren

269 We propose here an extension to the TDT, called robust TDT (rTDT), able to handle incomplete

270 the LRT is asymptotically equivalent to the TDT, the proposed test can be regarded as a generalizati

271 LRT can be regarded as an alternative to the TDT.

272 For analysis of trios, we use the TDT test.

273 affected individuals was examined using the TDT and the pedigree disequilibrium test (PDT), and case

274 ial benefits and the challenges of using the TDT to study transmission distortion and provide candida

275 nalyses of linkage disequilibrium, using the TDT, suggested association and linkage of ADHD with DAT1

276 ng for established prognostic variables, the TDT hazard ratio as a continuous variable was 1.00 (P =

277 that show Mendelian consistency, whereas the TDT(ae) statistic is computed on all trios.

278 following ways: First, in contrast with the TDT approach, all markers contribute information, regard

279 It provides power comparable with the TDT in many settings and may substantially outperform it

280 Consistent with the TDT result, the PDT analysis revealed no significant ass

281 The thermodynamic dislocation theory (TDT) is based on two highly unconventional assumptions:

282 We have extended these TDT methods to test for linkage between X-linked markers

283 y's aim was to quantify tumor doubling time (TDT) and identify correlates associated with indolent an

284 The tumor doubling time (TDT), that is, the time to reach twice the preirradiatio

285 lso, we have extended multi-locus methods to TDT-HET and have demonstrated that the empirical power m

286 We generalized the traditional TDT to process these inferred dosage probabilities, whic

287 lurite-resistance/dicarboxylate transporter (TDT) family or the Na(+) coupled divalent anion-sodium s

288 ect of time from AML diagnosis to treatment (TDT) on complete remission (CR) and overall survival (OS

289 impact of time from diagnosis to treatment (TDT) on overall survival, early death, and response rate

290 The wild-type TDT comprises over 20 large muscle fibers and four small

291 We obtain an unbiased TDT for individual haplotypes by calculating the correct

292 Unconditioned TDTs revealed overtransmission of shared epitope alleles

293 e a haplotype-based framework for group-wise TDT (gTDT) that is flexible to encompass a variety of ge

294 analyses revealed that grafts harvested with TDT exhibited a significantly higher mean number of medi

295 going myeloablation, two patients - one with TDT and the other with SCD - received autologous CD34+ c

296 to January 2019, a total of 79 patients with TDT over the age of 18 who were on iron-chelation therap

297 % compared with 90% (P = .005) in those with TDT less than 2 weeks.

298 n-combined TDT for X-chromosome markers (XRC-TDT) are the first association-based methods for testing

299 sibling transmission/disequilibrium test (XS-TDT) and the reconstruction-combined TDT for X-chromosom

300 tient age was 60 years (range, 17-87 years), TDT 4 days (range, 1-78 days), and 45% had sAML.