ライフサイエンスコーパス: DDD

1 DDD-CLS pacing significantly reduced syncope burden and

2 DDD-E2 complexes interact with multiple ubiquitin E3 lig

3 urred in 2.6% (MVP), 3.3% (VVI/R), and 5.2% (DDD/R) of patients with episodes and was the sole initia

4 By 2009, DDD use increased from 62% to 82% (p < 0.001), whereas s

5 ricular pacing) episodes accounted for 6.4% (DDD/R), 20.0% (MVP), and 25.6% (VVI/R) of 1,356 VT/VF ep

6 lorophenyl)ethane] and its metabolites, 4,4'-DDD [1,1-dichloro-2,2-bis(p-chlorophenyl)ethane] and 4,4

7 ted for 8.2% (MVP), 9.4% (VVI/R), and 14.8% (DDD/R) of 1,356 VT/VF episodes.

8 The MFNG effect was abolished by a DDD to DDA mutation that inactivates MFNG GlcNAc transfe

9 Thus, the present report describes a DDD subphenotype in PSENEN mutation carriers that is ass

10 Prescription corresponding to a DDD between 12.5 and 50 mg may decrease mortality for pa

11 st stable sequence-complementary duplex, AAA.DDD, so in mixtures that contain all eight sequences, se

12 Expression of ACS6(DDD), a gain-of-function ACS6 mutant that mimics the pho

13 eased significantly to 55 +/- 38 mm Hg after DDD pacing compared with the baseline gradient of 76 +/-

14 Although DDD device use is increasing, whereas single-chamber ven

15 nces: AAA, AAD, ADA, DAA, ADD, DAD, DDA, and DDD.

16 Our results suggest that DDT and DDD are transformed by surface intermediates formed from

17 Device programming mode (NASPE/BPEG code) at DDD with a lower rate of 60 ppm is compared with backup

18 DDD cleavage and entrapment of caspase-3 by DDD occur in vivo, further proving that this site has ph

19 and pancreatic carcinomas were discovered by DDD, demonstrating the utility of this technique.

20 ing a proof of concept for gene discovery by DDD.

21 , or sham DDI mode for 12 months followed by DDD-CLS pacing for 12 months (group B).

22 omerulopathy with dense deposit disease (C3G-DDD) pattern results from complement dysfunction and pri

23 e variations in the CFHR gene cluster in C3G-DDD and kidney patients with C3G-DDD variations will hel

24 A small fraction of C3G-DDD cases linked to factor H or C3 gene mutations as wel

25 n in the CFHR gene cluster that promotes C3G-DDD.

26 ned an index family with 2 patients with C3G-DDD and identified a chromosomal deletion in the complem

27 ster in C3G-DDD and kidney patients with C3G-DDD variations will help guide treatment strategies.

28 onfirm that haploinsufficiency for K5 causes DDD and points to a prominent role for the keratin inter

29 e of the B-DNA dodecamer, [d(CGCGAATTCGCG)] (DDD)-bound non-covalently to a platinum(II) complex, [{P

30 dification procedure codes for dual-chamber (DDD), single-ventricular (VVI), single-atrial (AAI), or

31 r, the most stable mismatch duplexes contain DDD and compete with the most stable sequence-complement

32 obtained using online microarray databases, DDD, and RNA-seq data.

33 s on the organochlorine pesticides DDT, DDE, DDD, and chlordane in well-mixed slurries support the mo

34 ions were used to calculate the flux of DDE, DDD, DDMU, and selected PCB congeners from sediments to

35 congeners and their breakdown products (DDE, DDD, DDMU, and DDNU) and 43 PCB congeners using GC-EI- a

36 In this study, DDTr (DDTr = DDT + DDD + DDE) relative bioavailability in historically cont

37 ound that the abiotic transformation of DDT, DDD, and DDE (collectively referred to as DDX) require b

38 athways, deadenylation-dependent mRNA decay (DDD) and nonsense-mediated decay (NMD), stimulate Ty1 re

39 at could have therapeutic potential to delay DDD.

40 We found that the likelihood of developing DDD increases with the presence of two or more risk alle

41 Dowling-Degos disease (DDD) is an autosomal-dominant disorder of skin pigmentat

42 Dowling-Degos disease (DDD) is an autosomal-dominant genodermatosis characteriz

43 Dense deposit disease (DDD) and C3 glomerulonephritis (C3GN) are widely recogni

44 l diseases, including dense deposit disease (DDD) and C3 glomerulonephritis (C3GN).

45 n the pathogenesis of dense deposit disease (DDD).

46 Dense deposit disease (DDD; also known as membranoproliferative glomerulonephri

47 the UK Deciphering Developmental Disorders (DDD) study and the Canadian Clinical Assessment of the U

48 The Deciphering Developmental Disorders (DDD) study has developed a UK-wide patient recruitment n

49 g use, was estimated as the sum of dispensed DDD of drug and compared with the risk for ALS.

50 ng tool called Digital Differential Display (DDD) from the Cancer Gene Anatomy Project database, ESTs

51 ues were vaccinated with three doses of DNA (DDD), three doses of VRP (VVV group), or a heterologous

52 le dynamics of the Drew-Dickerson dodecamer (DDD: d(CGCGAATTGCGC)2) a prototypical B-DNA duplex.

53 re of the modified Dickerson-Drew dodecamer (DDD) in which guanine at position G(4) has been replaced

54 CGCGAATTCGCG, the Dickerson-Drew dodecamer (DDD), established a unique geometry of the central A-tra

55 ed B-DNA dodecamer (the Dickerson Dodecamer, DDD, [d(CGCGAATTCGCG)]2) associated with a cytotoxic pla

56 e-3 cleavage motif the Death Defying Domain (DDD).

57 conferred by an adjacent DDK-docking domain (DDD), sufficient for facilitating efficient phosphorylat

58 iagnosis suggests that a defined daily dose (DDD) of MRA between 12.5 and 50 mg may alleviate risk of

59 ) is replaced with dPer to form the dG:dPer (DDD-GY) [5'-d(C(1)G(2)C(3)G(4)A(5)A(6)T(7)T(8)Y(9)G(10)C

60 h dPer to form the modified O(6)-Bn-dG:dPer (DDD-XY) duplex [5'-d(C(1)G(2)C(3)X(4)A(5)A(6)T(7)T(8)Y(9

61 total of 4 patients (8.7%) had events during DDD-CLS and 21 (45.7%) during sham DDI (hazard ratio: 6.

62 ic nerve activity (SNA) were recorded during DDD pacing at a rate of 175 bpm (cycle length 343 ms) wi

63 ensional (3D) discrete dislocation dynamics (DDD) simulations reveal the existence of a well-defined

64 derwent double-blind randomization to either DDD pacing for 3 months followed by backup AAI pacing fo

65 Patients were randomized to either DDD-CLS pacing for 12 months followed by sham DDI mode p

66 ow that substitution of DDN(610) with either DDD(610) or DDE(610) significantly reduced in vivo funct

67 1,1-dichloro-2,2-bis(4-chlorophenyl)ethane (DDD) and 1,1-dichloro-2,2-bis(4-chlorophenyl)ethylene (D

68 sparity-selective neurons (41%) and very few DDD cells.

69 ld be integrated into existing protocols for DDD and evaluated using an open-label Bayesian study des

70 -1 complex was 1:1.69, whereas the ratio for DDD-2 was 1:2.85, almost the mixing ratio in the crystal

71 percentage rise in LV-dP/dt(max) and RR for DDD-LV pacing (p < 0.001).

72 l to evaluate soluble CR1 as a treatment for DDD and C3GN.

73 suggest that a single mutation DDN(610) --> DDD(610), which restores the ancestral catalytic site, r

74 h scattered pigmentation that mimicked human DDD.

75 low and infrequent conformational changes in DDD, leading to the identification of previously unchara

76 udies using restoration of DDD expression in DDD-deficient hepatocytic cells, we found that both casp

77 edominantly S-type sugar puckers as found in DDD-EG and other DNA triplexes.

78 e T-cell responses were demonstrated only in DDD- and DDV-vaccinated animals.

79 p incorporated 13 patients who were paced in DDD mode with short atrioventricular delay for 1 week af

80 cells, we found that both caspase-3 sites in DDD are necessary for inhibition of caspase-3 and promot

81 Modulating Notch signaling by CHSY1 via its DDD motif provides new insight into mechanisms of the in

82 or its regulation of Notch signaling via its DDD motif.

83 e bound to the DDD core, rendering mammalian DDD-E2 equivalent to the Arabidopsis CDD complex.

84 ater were compared with a propensity-matched DDD group and followed for 21.4 median months by remote

85 P-C were replaced with either phospho-mimic (DDD) or phospho-null (AAA) residues.

86 with stored electrograms and by pacing mode (DDD/R, VVI/R, and Managed Ventricular Pacing [MVP]).

87 ng facilitated S-L-S differed between modes (DDD/R 793 +/- 172 ms vs. MVP 865 +/- 278 ms vs. VVI/R 11

88 In contrast, the structure of the modified DDD in which cytosine at position C(9) is replaced with

89 s reports, the direction preferences of most DDD neurons do not reverse with disparity.

90 emokine [ELC]), and does not occur in mutant DDD/1 mice that are deficient in these CCR7 ligands.

91 EBNA3C m1 and m2 point mutations, DDD(507-509) mutated to AAA and DVIEVID(509-513) mutated

92 ) X (20)C (21) Z (22)C (23)G (24))-3' (named DDD (2+Z10)) (X = Z3dU; Z = 7-deaza-dG) suggests a mecha

93 9)T (20)C (21) Z (22)C (23)G (24))-3' (named DDD (Z10)) and 5'-d(C (1)G (2)C (3)G (4)A (5)A (6)T (7)

94 89.3 +/- 1.8% of DDT, 63.2 +/- 1.9% of DDD, and 50.9 +/- 1.6% of DDE were degraded by sulfide (

95 ified in familial AI, and comanifestation of DDD and AI has been reported for decades.

96 ations can indeed cause a comanifestation of DDD and AI that is likely triggered by predisposing fact

97 The additive contributions of DDD and NMD explain the strong requirement for general 5

98 eased 45.3%, driven by the increased cost of DDD devices.

99 ons in CFH associate with the development of DDD, but it is unknown whether allelic variants in other

100 Patients were randomized to 3 months each of DDD pacing and pacing backup (AAI-30) in a double-blind,

101 d-type mice, and in the SLC-negative HEVs of DDD/1 mice.

102 we describe the conformational landscape of DDD in a variety of ionic environments from minimal salt

103 electron density, the relative occupancy of DDD and the sum of three Pt(II) atoms in the DDD-1 compl

104 oss-of-function studies using restoration of DDD expression in DDD-deficient hepatocytic cells, we fo

105 As the understanding of DDD increases, novel therapies should be integrated into

106 Use of DDD devices was higher in urban, nonteaching hospitals (

107 AAA- or DDD-permeabilized myocytes (n = 12-17) were exchanged (~

108 ontaining an acidic amino acid triad (DDE or DDD) that catalyzes the "cut and paste" transposition re

109 no loss occurred for aldrin, lindane, DDE or DDD, whereas losses exceeding 80% were found for dieldri

110 ommon mechanism involving a catalytic DED or DDD motif.

111 mpling location (Terneuzen, L1) and for p,p'-DDD and BDE 100 at the second sampling location (Bath, L

112 accumulation of p,p'-DDT, p,p'-DDE, and p,p'-DDD in harbor porpoises.

113 9 +/- 26 pg/L in Lake Erie, followed by p,p'-DDD with an average concentration of 37 +/- 8 pg/L in La

114 oil samples showed endosulfan isomers, p,p'-DDD, alpha-cypermethrin, chlorpyrifos, and diazinon resi

115 Dual-chamber pacing (DDD) has been proposed as a treatment alternative to sur

116 atrial fibrillation) to dual-chamber pacing (DDD)-LV was used to determine optimal coronary sinus LV

117 ing (DDDR) versus nonrate-responsive pacing (DDD) has shown no survival benefit for patients undergoi

118 er, age at implantation, duration of pacing, DDD mode, and QRS duration had no significant impact on

119 tide-green fluorescent protein fusion probe (DDD(GFP)) to examine holoenzyme assembly of other family

120 DE remote monitoring (2006-2011), programmed DDD, had HRSc calculated at first data upload after impl

121 All patients were programmed (DDD-60 or DDDR-60) and evaluated after implantation and

122 ession of the cleavage-resistant mutant Rad9 DDD/AAA appears to protect the cell from DNA damage-indu

123 ivate insurance (83%) more commonly received DDD devices than Medicaid (79%) or Medicare (75%) recipi

124 y inactive D2 heterodimers composed of SeD2: DDD(GFP) subunits were rescued by specific immune precip

125 KRT5 in the proband from an extended Spanish DDD kindred.

126 e we report that mammalian DET1 forms stable DDD-E2 complexes, consisting of DDB1, DDA1 (DET1, DDB1 a

127 chamber pacing with closed loop stimulation (DDD-CLS) in patients with cardioinhibitory vasovagal syn

128 , d(AGAGAGAA-(EG)6-TTCTCTCT-(EG)6-TCTCTCTT) (DDD-EG), shows that PDD-EG has a more A-DNA like X displ

129 DNA like X displacement and inclination than DDD-EG yet still maintains predominantly S-type sugar pu

130 nogenic and sulfidogenic microcosms and that DDD is dehydrochlorinated to DDMU three orders of magnit

131 Taken together, these data confirm that DDD is a complex genetic disease and may provide targets

132 Employing mutagenesis studies, we show that DDD could operate independently of Met's enzymatic activ

133 d to depth preference, and also suggest that DDD cells are not involved in multisensory integration f

134 showed a clinical response, suggesting that DDD pacing could be a therapeutic option for some elderl

135 cancer tissues and cell lines uncovered that DDD cleavage and entrapment of caspase-3 by DDD occur in

136 nd able to enhance UbcH5/Cul4A activity, the DDD core specifically inhibits Cul4A-dependent polyubiqu

137 y improved from the baseline state after the DDD arm but were not significantly different between the

138 were not significantly different between the DDD arm and the backup AAI arm.

139 Neither substrate is cleaved by the DDD or DDE mutant, under the conditions where wild-type

140 ients had symptomatic improvement during the DDD arm, but 42% also had symptomatic improvement during

141 5% had deterioration of symptoms during the DDD pacing arm.

142 Overexpression of either the DDD(GFP) or an inert D1 subunit (M4) into SeD2 (accessio

143 ode is very similar to that reported for the DDD and [{trans-Pt(NH)(NH(CH)(NH(+))}-micro-{trans-Pt(NH

144 , its catalytic motif (DDN) differs from the DDD motif of related transposases, which may be importan

145 modified version of the DDD, called here the DDD(4+), is composed of [d(CGCGAAXXCGCG)](2), where X is

146 DDD and the sum of three Pt(II) atoms in the DDD-1 complex was 1:1.69, whereas the ratio for DDD-2 wa

147 Incorporation of 7-deaza-dG into the DDD (2+Z10) duplex weakens but does not eliminate electr

148 Analysis of the DDD (2+Z10) duplex reveals that the tethered cations at

149 we describe the 1.6-A X-ray structure of the DDD (Dickerson-Drew dodecamer), which has been covalentl

150 individual metal ions.Crystallization of the DDD duplex in the presence of Mg(2+)and Ca(2+)yields dif

151 he origin of many well-known features of the DDD duplex structure.

152 These and the 1.1 A structure of the DDD Mg(2+)-form have revealed the most detailed picture

153 This modified version of the DDD, called here the DDD(4+), is composed of [d(CGCGAAXX

154 biquitin thioester linkage once bound to the DDD core, rendering mammalian DDD-E2 equivalent to the A

155 e migration and differentiation underlie the DDD pathogenesis associated with PSENEN.

156 We next tested whether the DDD or DDE mutants cleave single-strand extensions and f

157 terestingly, Fringe domain in CHSY1 has this DDD motif.

158 Thus, DDD does not appear to be an important precursor of the

159 Mutants 438VKL and 435KNS to DDD exhibited partial Ca2+/CaM-independent activities.

160 DDT is reductively dechlorinated to DDD and dehydrochlorinated to DDE; it has been thought t

161 This solid tumor DDD database should facilitate target identification for

162 otion [direction-dependent disparity tuning (DDD)], but most of these cells were unisensory with no t

163 l and mechanistic studies, we show that upon DDD cleavage by caspase-3 the resulting DEVD-T peptide a

164 will have improved survival with DDDR versus DDD alone.

165 mia (mean time of viremia = 0 days), whereas DDD- and VVV-vaccinated animals had mean times of viremi

166 Hg/s to 924 +/- 203 mm Hg/s, p < 0.001) with DDD-LV pacing for the optimal LV lead position.

167 % confidence interval [CI]: 47% to 90%) with DDD-CLS compared with 28% (95% CI: 9.7% to 53.5%) with s

168 in the presence of variants associated with DDD.

169 The HRSc did not change with DDD pacing over time.

170 2, in 6 unrelated patients and families with DDD in whom mutations in KRT5, POFUT1, and POGLUT1 have

171 nts from previously studied individuals with DDD.

172 We studied patients with DDD and identified previously unreported sequence altera

173 vitro studies using sera from patients with DDD showed that soluble CR1 prevents dysregulation of th

174 ic and treatment algorithm for patients with DDD.

175 iants and haplotypes common to patients with DDD.