ライフサイエンスコーパス: DPD

1 DPD activity in PBMCs before each study period was norma

2 DPD activity was markedly suppressed in all patients dur

3 DPD exists in a complex equilibrium between multiple for

4 DPD identifies and highlights discrepancies between any

5 DPD impairment leads to increased exposure to 5-FU and,

6 DPD inactivation persisted for several weeks after compl

7 DPD undergoes spontaneous rearrangements to produce a cl

8 DPD was positive in 48 patients (11.8%; grade 1: 3.9% [n

9 DPD-mediated metabolic inefficiency and improvement of g

10 eads and different forces including PG (0.01 DPD unite) and EOF (zeta potential = - 25 mV, electric f

11 dicate a linear dynamic range of 10(8)-10(3) DPD mRNA copies, with an intra-assay variation of <5%.

12 R) underwent ATTR screening by blinded 99mTc-DPD bone scintigraphy (Perugini Grade-0 negative, 1-3 in

13 The assay also allowed a DPD substrate profile to be conducted, which provided an

14 om monoclonal antibodies b96.11, DP-C, DP-A, DPD, 144, and 221-442.

15 ,3-diphosphono-1,2-propanodicarboxylic acid (DPD) bone scintigraphy (Perugini grade 0: negative; grad

16 ,3-diphosphono-1,2-propanodicarboxylic acid (DPD), and hydroxymethylene diphosphonate (HMDP) for diag

17 ,3-diphosphono-1,2-propanodicarboxylic-acid (DPD) bone scintigraphy.

18 ,3-diphosphono-1,2-propanodicarboxylic-acid (DPD) scintigraphy.

19 comparison between the fimbrolide and alkyl-DPD analogues.

20 ol compound for our recently developed alkyl-DPD panel of AI-2 modulators.

21 We demonstrate that our alkyl-DPD analogues are more potent inhibitors of QS in both V

22 Scriptaid, and the other is a Flavin analog, DPD.

23 to be undertaken with the substrates ATP and DPD.

24 ely correlated with both DPYD expression and DPD enzyme activity in peripheral blood specimens from h

25 ost analysis, as well as pharmacokinetic and DPD enzyme activity analyses.

26 Elevated PYD and DPD (p < 0.05) concentrations were measured in patients

27 PYD and DPD are sensitive and specific bone resorption markers w

28 assay was developed using synthetic PYD and DPD as calibrators to analyze free and total PYD and DPD

29 alibrators to analyze free and total PYD and DPD in urine.

30 ents were also monitored for urinary PYD and DPD production for a 6-mo interval after a palliative in

31 Urinary production of PYD and DPD was measured by high-performance liquid chromatograp

32 tastatic sites were assessed for TP, TS, and DPD gene and protein expression.

33 obtained from the MD (in physical units) and DPD (reduced units) simulations.

34 s(-1)), Km,ATP (150 +/- 30 muM) and Km(app),DPD (1.0 +/- 0.2 mM).

35 ignificant correlation (r(2) = 0.90) between DPD enzyme activity and mRNA levels.

36 Transthyretin-CA (ATTR) was diagnosed by DPD and absence of a clonal immunoglobulin, and light-ch

37 ATTR was diagnosed by DPD and absence of monoclonal protein.

38 ent of the structural diversity displayed by DPD over a broad pH range is even greater than previousl

39 e associated metabolic remodeling induced by DPD also required induction of liver-integrated stress r

40 the QRS-gated DPD yielded higher calculated DPD values (3 [-1 to 6] versus 0 [-4 to 3] mm Hg; P<0.01

41 e examined the method's impact on calculated DPD, PH-LHD subclassification, hemodynamic profiles, and

42 e subsequently used as input to a whole-cell DPD model to predict the RBC shape and corresponding str

43 xpensive MD results using relatively cheaper DPD simulations.

44 ode of depersonalization can lead to chronic DPD.

45 (1) and Co2(DPXM) (3)] and dibenzofuran [Co2(DPD) (2) and Co2(DPDM) (4)] have been synthesized, chara

46 c residues, Asp345 and Asp347 of a conserved DPD sequence and Asp269 of a conserved EGYMD sequence, w

47 omote hydration at the C3 position of cyclic DPD to afford the active tetrahydroxy species.

48 s MME/MEM, PPE/PEP, PPD/PDP, EEP/EPE and DDP/DPD (M=14:0, P=16:0, E=20:5, D=22:6) were analysed by ES

49 (MTHF), and dihydropyrimidine dehydrogenase (DPD) activity in peripheral mononuclear cells.

50 Dihydropyrimidine dehydrogenase (DPD) activity was determined by measuring plasma uracil,

51 Dihydropyrimidine dehydrogenase (DPD) catabolizes endogenous pyrimidines and pyrimidine-b

52 Dihydropyrimidine dehydrogenase (DPD) deficiency constitutes an inborn error in pyrimidin

53 imidines is dihydropyrimidine dehydrogenase (DPD) deficiency, which can result from deleterious polym

54 overexpress dihydropyrimidine dehydrogenase (DPD) in hypoxia, leading to macrophage-induced chemoresi

55 Dihydropyrimidine dehydrogenase (DPD) is a major determinant of 5-FU response and toxicit

56 Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme of the urac

57 Dihydropyrimidine dehydrogenase (DPD) is the initial, rate-limiting enzyme in the catabol

58 intratumor dihydropyrimidine dehydrogenase (DPD) messenger RNA (mRNA) levels and sensitivity to 5-fl

59 ctivated by dihydropyrimidine dehydrogenase (DPD) to therapeutically inactive products, but with toxi

60 lic enzyme, dihydropyrimidine dehydrogenase (DPD), has been shown to be responsible for a pharmacogen

61 of 5-FU by dihydropyrimidine dehydrogenase (DPD), which results in sustained concentrations of 5-FU

62 region for dihydropyrimidine dehydrogenase (DPD, DPYD gene) expression that is relevant to the metab

63 Dihydropyrimidine dehydrogenase (DPD, encoded by DPYD) rapidly degrades 85% of administer

64 zing enzyme dihydropyrimidine dehydrogenase (DPD; ie, DPYD*2A) is strongly associated with fluoropyri

65 inactivates dihydropyrimidine dehydrogenase [DPD]), 5-FU, and leucovorin to simulate this schedule.

66 ks pyridinoline (PYD) and deoxypyridinoline (DPD) are established markers of bone resorption measured

67 s, pyridinoline (PYD) and deoxypyridinoline (DPD), has been correlated to increased bone resorption i

68 of pyridinoline (PYD) and deoxypyridinoline (DPD)] were also measured as well as parameters of calciu

69 ne pyridinoline, PYD, and deoxypyridinoline, DPD) were elevated in the majority of study subjects, we

70 Specifically, we describe DPD as arising from disrupted interoceptive processing a

71 anism of dissolution by particle detachment (DPD) that dominates in mesocrystals formed via crystalli

72 DNA polymorphism detector (DPD) is a new web application developed to help automate

73 d sensitive technique capable of determining DPD mRNA expression levels in nanogram amounts of total

74 The diastolic pressure difference (DPD) is recommended to differentiate between isolated po

75 14) m(-2); hence dislocation-pipe diffusion (DPD) becomes a major contribution at working temperature

76 nd the AI-2 precursor dihydroxypentanedione (DPD) by NTHI 86-028NP.

77 Although dietary protein dilution (DPD) can slow the progression of some aging-related diso

78 minimal desensitization by diphenhydramine (DPD) compared with ~50% desensitization with all other a

79 Depersonalisation disorder (DPD) is a psychopathological condition characterised by

80 Discoipyrroles A-D (DPA-DPD) are recently discovered natural products produced b

81 A dissipative particle dynamics (DPD) approach, combined with a molecular dynamics (MD) s

82 tigated using dissipative particle dynamics (DPD) method.

83 An optimized Dissipative Particle Dynamics (DPD) model with simple scaling rules was developed for s

84 n this study, dissipative particle dynamics (DPD) simulations are employed to investigate the biomech

85 cs (CGMD) and dissipative particle dynamics (DPD) to predict the static and dynamic responses of RBCs

86 ntegration of dissipative particle dynamics (DPD), smoothed particle hydrodynamics (SPH) and computat

87 he RBC, using dissipative particle dynamics (DPD).

88 leterious polymorphisms in the gene encoding DPD (DPYD), including DPYD*2A and c.2846A>T.

89 lation data in physical units and equivalent DPD simulation data for relevant quantities.

90 uced during clone production or evaluation), DPD uses the discrepancies, along with flanking sequence

91 in future pharmacogenetic studies examining DPD deficiency.

92 o humans, macrophages in mice do not express DPD.

93 The molecular basis for DPD deficiency in a British family having a cancer patie

94 suggested as a potential molecular basis for DPD deficiency, even before the complete physical struct

95 wing the recent availability of the cDNA for DPD, there were initial reports of several molecular def

96 Numerous variants within the gene coding for DPD, DPYD, have been described, although only a few have

97 All agonists except for DPD also caused subsequent TAS2R14 internalization and t

98 To understand the mechanism responsible for DPD deficiency, we have determined the genomic structure

99 If matching DNA sequences are found, DPD verifies that they are from the same gene.

100 total DPD and PYD and 8.6 and 7.0% for free DPD and PYD, respectively.

101 PYD and 9.8 and 9.5%, respectively, for free DPD and PYD.

102 al DPD, 100.8% for total PYD, 98.6% for free DPD, and 94.9% for free PYD.

103 e ECG QRS complex to calculate the QRS-gated DPD (diastolic pulmonary artery pressure-QRS-gated PAWP)

104 es reclassified as Cpc-PH based on QRS-gated DPD demonstrated higher pulmonary arterial pressures ver

105 The QRS-gated DPD reclassifies a subset of PH-LHD patients from isolat

106 Within PH-LHD, the QRS-gated DPD yielded higher calculated DPD values (3 [-1 to 6] ve

107 (DPDs) ranging from the case of the Gaussian DPD to the case of the uniform with finite support DPD.

108 A deficiency in human DPD is associated with congenital thymine-uraciluria in

109 omic structure and organization of the human DPD gene.

110 equence variations previously encountered in DPD-deficient patients.

111 increase in PYD and a four-fold increase in DPD above controls during the interval.

112 in UGT1A1 and TPMT, as well as mutations in DPD, in influencing drug disposition and toxicity.

113 mpletely explain the reported variability in DPD function or the resultant differences in treatment r

114 th thymine-uraciluria and completely lacking DPD activity.

115 potent QS agonists than the natural ligand, DPD, in Vibrio harveyi.

116 d in some members of the pedigree having low DPD catalytic activity.

117 Hypoxia-induced macrophage DPD expression was controlled by HIF2a.

118 quency of CASPR2 antibodies in mothers of MD/DPD children (p=0.01).

119 The scaling method was verified for three MD/DPD model liquid pairs under several different nonequili

120 In lean mice, DPD promoted metabolic inefficiency by increasing carboh

121 Moreover, DPD uptake was not competitively inhibited by ribose or

122 r disorders of psychological development (MR/DPD)) compared with 9/176 (5.1%) of the remaining mother

123 were detected in 7/171 (4.1%) mothers of MR/DPD progeny, compared with only 1/171 (0.6%) control mot

124 However, in usual practice, negative DPD values are commonly calculated, potentially related

125 onal and polygenic murine models of obesity, DPD prevented and curtailed the development of impaired

126 Addition of DPD to luxS cells induced flhA transcription in a dose-d

127 icient syntheses of carbocyclic analogues of DPD, which are locked in the cyclic form.

128 e synthesis and evaluation of a new class of DPD analogues, C4-alkoxy-5-hydroxy-2,3-pentanediones, te

129 Furthermore, an optimal concentration of DPD was determined, above and below which biofilm format

130 effect, we show that the physical drivers of DPD are curvature and strain inherently tied to the orig

131 f the linear form and dynamic equilibrium of DPD as crucial requirements for activation of AI-2 based

132 c or chemical (synthetic AI-2 in the form of DPD) complementation re-established the mutualistic grow

133 rsion between the linear and cyclic forms of DPD.

134 Incubation of DPD with viral DNA or the antibiotic gramicidin S result

135 cells did not express significant levels of DPD.

136 We designed and prepared a small library of DPD derivatives, characterized by five different scaffol

137 nal and neurobiologically plausible model of DPD within the active inference framework.

138 electrical methods, no direct observation of DPD at the atomic level has been reported.

139 5-FU to dihydro-fluorouracil, the product of DPD catabolism.

140 apable of rapid and accurate quantitation of DPD mRNA levels in biopsy-sized tissue samples.

141 ication of unrecognized glycation targets of DPD in a prokaryotic system.

142 DPD simulations revealed that the optimized DPD model, expressed in terms of the proposed scaling me

143 ignificant differences in mean TNF-alpha, or DPD levels pre- and post-XRT (P = .1934 and .4922, respe

144 Elevated urinary levels of PYD or DPD were present in 73% of patients and 38% had elevated

145 one marker of bone resorption (i.e., PYD or DPD) and/or serum osteocalcin (group 1).

146 tin machinery as treatment with Scriptaid or DPD reversed mSOD-induced insolubilization of the dynact

147 and peripheral-blood mononuclear cell (PBMC) DPD activity.

148 derived from 4,5-dihydroxy-2,3-pentandione (DPD), has been revealed as a universal signaling molecul

149 is that (4S)-4,5-dihydroxy-2,3-pentanedione (DPD) can undergo a previously undocumented non-enzymatic

150 end product 4,5-dihydroxy-2,3-pentanedione (DPD) during laboratory cultivation.

151 4,5-Dihydroxy-2,3-pentanedione (DPD), a product of the LuxS enzyme in the catabolism of

152 derived from 4,5-dihydroxy-2,3-pentanedione (DPD), and reveal new sophistication in the chemical lexi

153 ed from (4S)-4,5-dihydroxy-2,3-pentanedione (DPD), has been identified in both Gram-negative and Gram

154 e (Hcys) and 4,5-dihydroxy-2,3-pentanedione (DPD), the precursor of the type II bacterial quorum sens

155 near form of 4,5-dihydroxy-2,3-pentanedione (DPD), the precursor of the type II bacterial quorum sens

156 e (Hcys) and 4,5-dihydroxy-2,3-pentanedione (DPD), the precursor of type II bacterial autoinducer (AI

157 cysteine and 4,5-dihydroxy-2,3-pentanedione (DPD), the precursor of type II bacterial quorum sensing

158 e (Hcys) and 4,5-dihydroxy-2,3-pentanedione (DPD), the precursor of type II bacterial quorum-sensing

159 of synthetic 4,5-dihydroxy-2,3-pentanedione (DPD), which cyclizes to form AI-2.

160 derived from 4,5-dihydroxy-2,3-pentanedione (DPD).

161 cid-quenched N,N-diethyl-p-phenylenediamine (DPD) assay was used to measure the accumulation of H2O2

162 xidation of N,N'-dimethyl-p-pheylenediamine (DPD) is used to quantify the biologically more important

163 horylated by LsrK, and the resulting phospho-DPD activates QS.

164 rements of the dissociative photodetachment (DPD) of the F(-)(H2O) anion revealed various dissociatio

165 Postoperative DPD scans demonstrated cardiac localization in all 4 pat

166 versus 8%; P<0.01) versus the usual practice DPD.

167 ession model that included osteocalcin, PYD, DPD, intact PTH, age, years posttransplant, duration of

168 ith a section on quantitation of (99m)Tc-PYP/DPD/HMDP imaging.

169 only a few have been demonstrated to reduce DPD enzyme activity.

170 eviously uncharacterized mechanism regulates DPD expression and may contribute to tumor resistance to

171 oxy-2,3-pentanedione, commonly known as ( S)-DPD, a small signaling molecule that modulates QS in bot

172 simulation results with those of the scaled DPD simulations revealed that the optimized DPD model, e

173 The mean +/- SD DPD activity was 0.21 +/- 0.14 nmol/min/mg and did not c

174 the case of the uniform with finite support DPD.

175 776C85 suppressed DPD activity in peripheral-blood mononuclear cells (PBMC

176 Addition of in vitro-synthesized DPD to cultured B. burgdorferi resulted in differential

177 LuxS for the express purpose of synthesizing DPD and utilizes a form of that molecule as an AI-2 pher

178 ese experiments and corresponding systematic DPD simulations probe the governing constitutive respons

179 ac ATTR corroborated by grade 2 to 3 (99m)Tc-DPD ((99m)Tc-3,3-diphosphono-1,2-propanodicarboxylic aci

180 Prevalence of (99m)Tc-DPD positivity was 3.3% (n = 376/11,527; grade 1: 1.8%,

181 a substantial number of consecutive (99m)Tc-DPD referrals and associated with adverse outcomes.

182 9 male and 114 female participants), (99m)Tc-DPD scintigraphy (Perugini grade 2 or 3) confirmed coexi

183 ardial strain were evaluated against (99m)Tc-DPD scintigraphy as the reference standard to identify A

184 Conclusion When compared against (99m)Tc-DPD scintigraphy as the reference standard, routine 4D c

185 (99m)Tc-DPD scintigraphy may provide useful imaging biomarkers t

186 he aim of this study was to quantify (99m)Tc-DPD uptake by means of SPECT/CT before (223)Ra and compa

187 Results: Total (99m)Tc-DPD uptake of the central skeleton varied between 11% an

188 results in regression of myocardial (99m)Tc-DPD uptake.

189 Conclusion: Positive (99m)Tc-DPD was identified in a substantial number of consecutiv

190 sphono-1,2-propanodicarboxylic-acid ((99m)Tc-DPD) bone scintigraphy between 2010 and 2020 were includ

191 sphono-1,2-propanodicarboxylic acid ((99m)Tc-DPD) scintigraphy before tafamidis initiation and after

192 sphono-1,2-propanodicarboxylic acid ((99m)Tc-DPD) typically show intense uptake in skeletal metastase

193 with suspected cardiac ATTR (grade 1 (99m)Tc-DPD), and 12 asymptomatic individuals with amyloidogenic

194 independently predicted by positive (99m)Tc-DPD.

195 arly disease stage, quantitative [(99m)Tc]Tc-DPD SPECT should be considered to improve early-stage ri

196 enter and underwent quantitative [(99m)Tc]Tc-DPD SPECT/CT allowing SUV(max) and SUV(peak) analysis.

197 predictive value of quantitative [(99m)Tc]Tc-DPD SPECT/CT in suspected and confirmed ATTR-CM accordin

198 no-1,2-propanodicarboxylic acid ([(99m)Tc]Tc-DPD) SPECT may be used for risk-stratifying patients wit

199 Decisions by the heart team (DPD-blinded) resulted in TAVR (333 [81.6%]), surgical AV

200 generality of the model, we anticipate that DPD is widespread for both natural minerals and syntheti

201 Here, we determined that DPD in mice and humans increases serum markers of metabo

202 Taken together, these data indicate that DPD promotes improved glucose homeostasis through an NEA

203 Molecular docking showed that DPD has specific interactions deep within a binding pock

204 The DPD calculated in usual practice is underestimated in PH

205 ike micelles, shown in the AFM image and the DPD snapshot.

206 and mean PAWP were measured to calculate the DPD as per usual practice (diastolic pulmonary artery pr

207 hisms) in the gene (DPYD) that codes for the DPD enzyme.

208 Hence, the DPD simulations and comparisons with available independe

209 ct point mutations or small deletions in the DPD gene associated with 5-fluorouracil toxicity.

210 The physical map of the DPD gene should permit development of rapid assays to de

211 efore the complete physical structure of the DPD gene was known.

212 calculations confirms the sensitivity of the DPD measurements to the subtle dynamics on the low-lying

213 We show that stronger regularity of the DPD results in faster mixing, which is similar to the La

214 information and would ultimately lead to the DPD phenomenology.

215 While LsrK is a critical enzyme within the DPD quorum sensing relay system, kinetic details of this

216 TAMs constituted the main contributors to DPD activity in human colorectal primary or secondary tu

217 ript levels of rbsB increased in response to DPD and as bacteria approached stationary-phase growth.

218 ay variabilities were 9.1 and 8.2% for total DPD and PYD and 8.6 and 7.0% for free DPD and PYD, respe

219 d were 4.1 and 3.8%, respectively, for total DPD and PYD and 9.8 and 9.5%, respectively, for free DPD

220 The mean recoveries were 98.1% for total DPD, 100.8% for total PYD, 98.6% for free DPD, and 94.9%

221 and 2 weeks after chemo-XRT to evaluate TP, DPD, and TNF-alpha mRNA levels.

222 Role of TP and TP:DPD ratio warrants further investigation in a larger cli

223 No association between TP:DPD ratio and efficacy of capecitabine or severity of to

224 Median value of TP:DPD ratios at baseline was 2.65 (range, 0.36 to 11.08).

225 cantly higher enzyme activity than wild-type DPD (120%, P = 0.025; 116%, P = 0.049; 130%, P = 0.0077;

226 ed for mapping dimensionless (reduced units) DPD simulation data to physical units, was based on scal

227 ide preliminary evidence that elevated urine DPD crosslinks may provide a clinical biomarker for PYRO

228 genetic syndrome has been described in which DPD-deficient patients are at risk for toxicity followin

229 pB3, and c.1601G>A-have been associated with DPD deficiency, but no definitive evidence for the clini

230 polymorphisms that have been associated with DPD deficiency.

231 lations, the heterocyclic oxygen atom within DPD appears necessary to promote hydration at the C3 pos