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 requires genotypes of affected individuals and their

7 TDT was analyzed as a continuous variable using a specif

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

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

10 icantly more frequently than expected (chi 2 TDT ranging from 8.47 [P < .004] to 10.80 [P = .001], de

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

40 f differentially private (DP) mechanisms for TDT.

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

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

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

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

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

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

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

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

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

50 rmined whether this pathway directly impacts TDT development.

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

52 Heterogeneity in TDT results between data sets was, in part, accounted fo

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

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

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

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

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

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

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

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

61 reased power compared with the single marker TDT.

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

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

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

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

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

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

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

69 The effect of TDT was assessed using multivariate analysis.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

85 0S193, marker D10S588 also provided positive TDT results (P = 0.009, Pc = 0.25) but the allele under

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

102 ival time compared with those with a shorter TDT.

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

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

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

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

107 The sib-TDT analysis also showed significant association between

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

109 Significant TDT results indicate both linkage and allelic associatio

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

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

112 0q26.13 displaying a genome-wide significant TDT in combined female and male transmissions and a sign

113 Similar TDT analyses of TGFB2 and HLX1 polymorphisms yielded no

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

138 e used the transmission-disequilibrium test (TDT) method to test for linkage disequilibrium between a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

163 using the transmission/disequilibrium test (TDT).

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

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

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

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

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

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

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

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

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

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

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

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

176 nditioned transmission disequilibrium tests (TDTs).

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

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

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

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

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

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

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

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

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

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

187 The TDT statistics described so far are for autosomal chromo

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

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

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

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

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

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

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

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

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

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

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

199 nalysis of an additional 390 families by the TDT did not extend the evidence further, and reduced sup

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

201 ds the analysis of individual alleles by the TDT.

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

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

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

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

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

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

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

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

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

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

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

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

214 nts and homozygous offspring are used in the TDT.

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

216 roader array of causal scenarios than is the TDT.

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

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

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

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

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

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

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

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

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

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

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

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

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

230 methods, including a conditional form of the TDT.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

257 when a candidate gene is available (1) these TDT-type tests are at least an order of magnitude more e

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

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

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

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

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

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

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

265 Unconditioned TDTs revealed overtransmission of shared epitope alleles

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

267 % compared with 90% (P = .005) in those with TDT less than 2 weeks.

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

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

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