ライフサイエンスコーパス: DDD

1 DDD data indicated higher total use of antimicrobials in

2 DDD-CLS pacing significantly reduced syncope burden and

3 DDD-E2 complexes interact with multiple ubiquitin E3 lig

4 total DDD of non-opioid analgesics was 0.029 DDD/day/person, and that of opioid-based analgesics was

5 nd that of opioid-based analgesics was 0.037 DDD/day/person across Australia.

6 age: 31 years [Q1-Q3: 24-41 years]), and >=1 DDD per day (47% female, median age: 33 years [Q1-Q3: 25

7 rs, <1 defined daily dose (DDD) per day, >=1 DDD per day determined at start of follow-up, and 1 year

8 Comparing >=1 DDD per day with prior users, elevated standardized 10-y

9 dian age: 30 years [Q1-Q3: 23-41 years]), <1 DDD per day (47% female, median age: 31 years [Q1-Q3: 24

10 th reduced AAA growth rate; an increase of 1 DDD statin per day was associated with an adjusted chang

11 than the lower-middle income countries (6.11 DDD/TID).

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

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

14 A median difference in PPI use of -257 DDD was found for the year after surgery compared to the

15 habitants per day (DDD/TID) in 2008 to 18.26 DDD/TID in 2018.

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

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

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

19 pooled gabapentinoid consumption rate (39.92 DDD/TID) in 2018, which was more than six times higher t

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

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

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

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

24 um release yielded no difference between AAA/DDD and controls in calcium content of the sarcoplasmic

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

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

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

28 o protein-truncating variants in MECP2 among DDD study participants.

29 g proteins CFHR5, CFHR1, and CFH in C3GN and DDD compared to controls.

30 3G cases confirmed the diagnosis of C3GN and DDD in 80.6 % based on ApoE staining.

31 nd CFHR proteins were comparable in C3GN and DDD.

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

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

34 The majority of DDT and DDD is buried within a thin sediment layer consistent wi

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

36 t to a high risk of disease recurrence (both DDD and C3GN) in allograft recipients.

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

38 dle branch block-like dyssynchrony caused by DDD pacing could be acutely reverted by right atrial pac

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

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

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

42 otentially pathogenic variants identified by DDD in this size range by 42.9%.

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

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

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

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

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

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

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

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

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

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

53 is of single-cell snapshot time series data, DDD approximates the continuous time Perron-Frobenius op

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

55 y dose per ten thousand inhabitants per day (DDD/TID) in 2008 to 18.26 DDD/TID in 2018.

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

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

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

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

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

61 a total modern burden of ~30-36 tonnes (DDT, DDD and DDE) in this area.

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

63 propose Dynamic Distribution Decomposition (DDD), an operator approximation approach to infer a cont

64 at could have therapeutic potential to delay DDD.

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

66 and difference-in-difference-in-differences (DDD) models were estimated using multivariable linear pr

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

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

69 f C3 glomerulopathy - dense deposit disease (DDD) and C3 glomerulonephritis (C3GN) - have overlapping

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

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

72 the dense deposits of dense deposit disease (DDD), apart from components of the complement pathway.

73 onephritis (C3GN) and dense deposit disease (DDD), both of which are characterized by bright glomerul

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

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

76 recipient developed a donor-derived disease (DDD).

77 blished Deciphering Developmental Disorders (DDD) and GeneDx cohorts with developmental disorders.

78 ailable deciphering developmental disorders (DDD) dataset.

79 rom the Deciphering Developmental Disorders (DDD) study and 9720 controls, and found one gene, RAB2A,

80 of the Deciphering Developmental Disorders (DDD) study and discovered 63 rare, damaging variants in

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

82 rom the Deciphering Developmental Disorders (DDD) study for de novo mutations in the 5' untranslated

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

84 to the Deciphering Developmental Disorders (DDD) study.

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

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

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

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

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

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

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

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

93 dihydrofolate reductase degradation domain (DDD) with a hemagglutinin (HA) tag, GFP-DDDHA, which was

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

95 A defined daily dose (DDD) approach was used to evaluate whether the associati

96 Defined daily dose (DDD) data from the European Centre for Disease Preventio

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

98 ups were prior users, <1 defined daily dose (DDD) per day, >=1 DDD per day determined at start of fol

99 Drug classes and Defined Daily Dose (DDD) were obtained from the Pharmacy register using the

100 orld Health Organization defined daily dose [DDD] per day), medium (0.6 to <1.1 DDDs per day), or hig

101 otics was calculated as defined daily doses (DDD) of antibiotics per 1000 inhabitants per day (DID).

102 , calculated monthly as defined daily doses (DDD) per 1000 resident days (DRD).

103 e was defined as >= 180 Defined Daily Doses (DDD) per year.

104 osure was quantified by defined daily doses (DDD).

105 ) 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

106 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

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

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

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

110 n (AAI pacing), whereas during dyssynchrony (DDD pacing), the lateral wall was more loaded, and the s

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

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

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

114 However, on electron microscopy (EM), DDD is characterized by dense osmiophilic mesangial and

115 1,1-dichloro-2,2-bis(4-chlorophenyl)ethane (DDD) and 1,1-dichloro-2,2-bis(4-chlorophenyl)ethylene (D

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

117 0-0.99, 0.82 for DDD 1.00-1.49, and 0.58 for DDD >=1.50; P = .002 for trend) compared with no statin

118 istribution HR: 0.79 for DDD <0.50, 0.78 for DDD 0.50-0.99, 0.82 for DDD 1.00-1.49, and 0.58 for DDD

119 0-0.99, 0.85 for DDD 1.00-1.49, and 0.79 for DDD >=1.50; P = .002 for trend) and the composite outcom

120 and amputation (subdistribution HR: 0.79 for DDD <0.50, 0.78 for DDD 0.50-0.99, 0.82 for DDD 1.00-1.4

121 DDD <0.50, 0.78 for DDD 0.50-0.99, 0.82 for DDD 1.00-1.49, and 0.58 for DDD >=1.50; P = .002 for tre

122 DDD <0.50, 0.92 for DDD 0.50-0.99, 0.85 for DDD 1.00-1.49, and 0.79 for DDD >=1.50; P = .002 for tre

123 ause death (HR: 0.95 for DDD <0.50, 0.92 for DDD 0.50-0.99, 0.85 for DDD 1.00-1.49, and 0.79 for DDD

124 anner for both all-cause death (HR: 0.95 for DDD <0.50, 0.92 for DDD 0.50-0.99, 0.85 for DDD 1.00-1.4

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

126 -1 complex was 1:1.69, whereas the ratio for DDD-2 was 1:2.85, almost the mixing ratio in the crystal

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

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

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

130 non-MDR and MDR sequence types under higher DDD regimes.

131 h scattered pigmentation that mimicked human DDD.

132 e was a six-to-nine-fold increase of C5-9 in DDD compared to C3GN.

133 -fold increase in apolipoprotein E (ApoE) in DDD compared to C3GN.

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

135 Why the deposits appear dense in DDD and not in C3GN is not known.

136 Thus, our study shows that dense deposits in DDD are enriched with ApoE compared to C3GN and control

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

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

139 red the dense deposit staining in the GBM in DDD but not in C3GN or control cases.

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

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

142 The SLPs programmed in DDD-(ZZ)(x) -FFPC self-assemble into higher-order struct

143 n of terminal complement pathway proteins in DDD compared to C3GN.

144 readth of phenotypic information recorded in DDD to augment diagnosis and disease variant discovery i

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

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

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

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

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

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

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

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

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

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

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

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

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

158 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)

159 for all 4 outcomes, indicated by a negative DDD coefficient for preterm birth (-0.43 percentage poin

160 89.3 +/- 1.8% of DDT, 63.2 +/- 1.9% of DDD, and 50.9 +/- 1.6% of DDE were degraded by sulfide (

161 We demonstrate the ability of DDD to reconstruct dynamically important cell states and

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

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

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

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

166 lipoprotein E are present in the deposits of DDD, as revealed by mass spectroscopy and confirmed by b

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

168 ings suggest a new modality for diagnosis of DDD and introduce potential new mechanisms for understan

169 sed as an adjunct to EM for the diagnosis of DDD and might be valuable when EM is not available.

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

171 y mass spectrometry (MS) in 12 cases each of DDD, C3GN, and pretransplant kidney control biopsies.

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

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

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

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

176 percent of recipients developed symptoms of DDD within 30 days of transplantation, and all bacterial

177 The latter value is typical of DDD-AAA H-bond dimers, consistent with proton transfer a

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

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

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

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

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

183 ommon mechanism involving a catalytic DED or DDD motif.

184 ion of EDDX (sum of o,p'-DDT, p,p'-DDT, o,p'-DDD, p,p'-DDD, o,p'-DDE, and p,p'-DDE) was 82 pg/m(3) fo

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

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

187 9 +/- 26 pg/L in Lake Erie, followed by p,p'-DDD with an average concentration of 37 +/- 8 pg/L in La

188 ), p,p'-dichlorodiphenyldichloroethane (p,p'-DDD), p,p'-dichlorodiphenyldichloroethylene (p,p'-DDE),

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

190 X (sum of o,p'-DDT, p,p'-DDT, o,p'-DDD, p,p'-DDD, o,p'-DDE, and p,p'-DDE) was 82 pg/m(3) for Istanbul

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

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

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

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

195 ng phospho-ablated (AAA) and phosphomimetic (DDD) cMyBP-C as well as controls, we found that cMyBP-C

196 on propensity of the FFPC tail without polar DDD head.

197 ocus future efforts to recognize and prevent DDD.

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

199 y of DDT and its immediate daughter products DDD (dichloro-diphenyl-dichloroethane) and DDE (dichloro

200 that DDT and its first degradation products, DDD (dichlorodiphenyldichloroethane) and DDE (dichlorodi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

222 5% had deterioration of symptoms during the DDD pacing arm.

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

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

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

226 e sequence data from 4,293 probands from the DDD Study with severe developmental disorders for pathog

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

228 in therapy; however, not all findings in the DDD analysis were statistically significant.

229 likely diagnoses identified in MEF2C in the DDD cohort, but these would all be missed in standard cl

230 clinical cohort and for 85% of cases in the DDD dataset, outperforming other established HPO-based m

231 R bases across all genes well covered in the DDD dataset.

232 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

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

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

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

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

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

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

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

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

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

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

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

244 ous variants in SPTBN2 as causative in three DDD probands.

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

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

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

248 The mean per capita weighted total DDD of non-opioid analgesics was 0.029 DDD/day/person, a

249 This solid tumor DDD database should facilitate target identification for

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

251 After 8 weeks of remodeling under DDD pacing, however, an almost homogeneous work distribu

252 e potential new mechanisms for understanding DDD pathophysiology.

253 Unexpected DDD was rare, occurring in 0.18% of all transplant recip

254 he quaterthiophene (4T)-based peptide units (DDD-4T) and sulfur atom ordering along the NbS(3) (100)

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

256 We use DDD to find previously identified subpopulations of cell

257 will have improved survival with DDDR versus DDD alone.

258 ight atrial and right ventricular free wall (DDD) pacing lead to LV dilatation, a thinned septum, and

259 periods with i2i communication failure when DDD pacing was not possible, 97.3+/-1.8% were resolved w

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

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

262 % confidence interval [CI]: 47% to 90%) with DDD-CLS compared with 28% (95% CI: 9.7% to 53.5%) with s

263 in the presence of variants associated with DDD.

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

265 2, in 6 unrelated patients and families with DDD in whom mutations in KRT5, POFUT1, and POGLUT1 have

266 homogeneous work distribution was found with DDD pacing, whereas with AAI pacing, the thin septum sho

267 nts from previously studied individuals with DDD.

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

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

270 iants and haplotypes common to patients with DDD.

271 ic and treatment algorithm for patients with DDD.

272 curred in about one third of recipients with DDD, with higher rates associated with malignancy transm