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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 is currently hosted by the Harvard Institute of Prot
8                                              DPD undergoes spontaneous rearrangements to produce a cl
9                                              DPD-mediated metabolic inefficiency and improvement of g
10 dicate a linear dynamic range of 10(8)-10(3) DPD mRNA copies, with an intra-assay variation of <5%.
11                     The assay also allowed a DPD substrate profile to be conducted, which provided an
12 om monoclonal antibodies b96.11, DP-C, DP-A, DPD, 144, and 221-442.
13 ,3-diphosphono-1,2-propanodicarboxylic-acid (DPD) bone scintigraphy.
14  comparison between the fimbrolide and alkyl-DPD analogues.
15 ol compound for our recently developed alkyl-DPD panel of AI-2 modulators.
16                We demonstrate that our alkyl-DPD analogues are more potent inhibitors of QS in both V
17 Scriptaid, and the other is a Flavin analog, DPD.
18 to be undertaken with the substrates ATP and DPD.
19 ely correlated with both DPYD expression and DPD enzyme activity in peripheral blood specimens from h
20 ost analysis, as well as pharmacokinetic and DPD enzyme activity analyses.
21                             Elevated PYD and DPD (p < 0.05) concentrations were measured in patients
22                                      PYD and DPD are sensitive and specific bone resorption markers w
23  assay was developed using synthetic PYD and DPD as calibrators to analyze free and total PYD and DPD
24 alibrators to analyze free and total PYD and DPD in urine.
25 ents were also monitored for urinary PYD and DPD production for a 6-mo interval after a palliative in
26                Urinary production of PYD and DPD was measured by high-performance liquid chromatograp
27 tastatic sites were assessed for TP, TS, and DPD gene and protein expression.
28  s(-1)), Km,ATP (150 +/- 30 muM) and Km(app),DPD (1.0 +/- 0.2 mM).
29 ignificant correlation (r(2) = 0.90) between DPD enzyme activity and mRNA levels.
30 ent of the structural diversity displayed by DPD over a broad pH range is even greater than previousl
31 e associated metabolic remodeling induced by DPD also required induction of liver-integrated stress r
32  the QRS-gated DPD yielded higher calculated DPD values (3 [-1 to 6] versus 0 [-4 to 3] mm Hg; P<0.01
33 e examined the method's impact on calculated DPD, PH-LHD subclassification, hemodynamic profiles, and
34 e subsequently used as input to a whole-cell DPD model to predict the RBC shape and corresponding str
35 (1) and Co2(DPXM) (3)] and dibenzofuran [Co2(DPD) (2) and Co2(DPDM) (4)] have been synthesized, chara
36 c residues, Asp345 and Asp347 of a conserved DPD sequence and Asp269 of a conserved EGYMD sequence, w
37 omote hydration at the C3 position of cyclic DPD to afford the active tetrahydroxy species.
38 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
39 (MTHF), and dihydropyrimidine dehydrogenase (DPD) activity in peripheral mononuclear cells.
40             Dihydropyrimidine dehydrogenase (DPD) activity was determined by measuring plasma uracil,
41             Dihydropyrimidine dehydrogenase (DPD) catabolizes endogenous pyrimidines and pyrimidine-b
42             Dihydropyrimidine dehydrogenase (DPD) deficiency constitutes an inborn error in pyrimidin
43 imidines is dihydropyrimidine dehydrogenase (DPD) deficiency, which can result from deleterious polym
44             Dihydropyrimidine dehydrogenase (DPD) is a major determinant of 5-FU response and toxicit
45             Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme of the urac
46             Dihydropyrimidine dehydrogenase (DPD) is the initial, rate-limiting enzyme in the catabol
47  intratumor dihydropyrimidine dehydrogenase (DPD) messenger RNA (mRNA) levels and sensitivity to 5-fl
48 ctivated by dihydropyrimidine dehydrogenase (DPD) to therapeutically inactive products, but with toxi
49 lic enzyme, dihydropyrimidine dehydrogenase (DPD), has been shown to be responsible for a pharmacogen
50  of 5-FU by dihydropyrimidine dehydrogenase (DPD), which results in sustained concentrations of 5-FU
51             Dihydropyrimidine dehydrogenase (DPD, encoded by DPYD) rapidly degrades 85% of administer
52 zing enzyme dihydropyrimidine dehydrogenase (DPD; ie, DPYD*2A) is strongly associated with fluoropyri
53 inactivates dihydropyrimidine dehydrogenase [DPD]), 5-FU, and leucovorin to simulate this schedule.
54 ks pyridinoline (PYD) and deoxypyridinoline (DPD) are established markers of bone resorption measured
55 s, pyridinoline (PYD) and deoxypyridinoline (DPD), has been correlated to increased bone resorption i
56 of pyridinoline (PYD) and deoxypyridinoline (DPD)] were also measured as well as parameters of calciu
57 ne pyridinoline, PYD, and deoxypyridinoline, DPD) were elevated in the majority of study subjects, we
58                   DNA polymorphism detector (DPD) is a new web application developed to help automate
59 d sensitive technique capable of determining DPD mRNA expression levels in nanogram amounts of total
60           The diastolic pressure difference (DPD) is recommended to differentiate between isolated po
61 14) m(-2); hence dislocation-pipe diffusion (DPD) becomes a major contribution at working temperature
62 nd the AI-2 precursor dihydroxypentanedione (DPD) by NTHI 86-028NP.
63           Although dietary protein dilution (DPD) can slow the progression of some aging-related diso
64                      Discoipyrroles A-D (DPA-DPD) are recently discovered natural products produced b
65 cs (CGMD) and dissipative particle dynamics (DPD) to predict the static and dynamic responses of RBCs
66 he RBC, using dissipative particle dynamics (DPD).
67 leterious polymorphisms in the gene encoding DPD (DPYD), including DPYD*2A and c.2846A>T.
68 uced during clone production or evaluation), DPD uses the discrepancies, along with flanking sequence
69  in future pharmacogenetic studies examining DPD deficiency.
70                      The molecular basis for DPD deficiency in a British family having a cancer patie
71 suggested as a potential molecular basis for DPD deficiency, even before the complete physical struct
72 wing the recent availability of the cDNA for DPD, there were initial reports of several molecular def
73 Numerous variants within the gene coding for DPD, DPYD, have been described, although only a few have
74  To understand the mechanism responsible for DPD deficiency, we have determined the genomic structure
75         If matching DNA sequences are found, DPD verifies that they are from the same gene.
76  total DPD and PYD and 8.6 and 7.0% for free DPD and PYD, respectively.
77 PYD and 9.8 and 9.5%, respectively, for free DPD and PYD.
78 al DPD, 100.8% for total PYD, 98.6% for free DPD, and 94.9% for free PYD.
79 e ECG QRS complex to calculate the QRS-gated DPD (diastolic pulmonary artery pressure-QRS-gated PAWP)
80 es reclassified as Cpc-PH based on QRS-gated DPD demonstrated higher pulmonary arterial pressures ver
81                                The QRS-gated DPD reclassifies a subset of PH-LHD patients from isolat
82                 Within PH-LHD, the QRS-gated DPD yielded higher calculated DPD values (3 [-1 to 6] ve
83                        A deficiency in human DPD is associated with congenital thymine-uraciluria in
84 omic structure and organization of the human DPD gene.
85 equence variations previously encountered in DPD-deficient patients.
86  increase in PYD and a four-fold increase in DPD above controls during the interval.
87  in UGT1A1 and TPMT, as well as mutations in DPD, in influencing drug disposition and toxicity.
88 mpletely explain the reported variability in DPD function or the resultant differences in treatment r
89 th thymine-uraciluria and completely lacking DPD activity.
90  potent QS agonists than the natural ligand, DPD, in Vibrio harveyi.
91 d in some members of the pedigree having low DPD catalytic activity.
92 quency of CASPR2 antibodies in mothers of MD/DPD children (p=0.01).
93                                In lean mice, DPD promoted metabolic inefficiency by increasing carboh
94                                    Moreover, DPD uptake was not competitively inhibited by ribose or
95 r disorders of psychological development (MR/DPD)) compared with 9/176 (5.1%) of the remaining mother
96  were detected in 7/171 (4.1%) mothers of MR/DPD progeny, compared with only 1/171 (0.6%) control mot
97         However, in usual practice, negative DPD values are commonly calculated, potentially related
98 onal and polygenic murine models of obesity, DPD prevented and curtailed the development of impaired
99                                  Addition of DPD to luxS cells induced flhA transcription in a dose-d
100 icient syntheses of carbocyclic analogues of DPD, which are locked in the cyclic form.
101 e synthesis and evaluation of a new class of DPD analogues, C4-alkoxy-5-hydroxy-2,3-pentanediones, te
102     Furthermore, an optimal concentration of DPD was determined, above and below which biofilm format
103 f the linear form and dynamic equilibrium of DPD as crucial requirements for activation of AI-2 based
104 c or chemical (synthetic AI-2 in the form of DPD) complementation re-established the mutualistic grow
105 rsion between the linear and cyclic forms of DPD.
106                                Incubation of DPD with viral DNA or the antibiotic gramicidin S result
107 electrical methods, no direct observation of DPD at the atomic level has been reported.
108 5-FU to dihydro-fluorouracil, the product of DPD catabolism.
109 apable of rapid and accurate quantitation of DPD mRNA levels in biopsy-sized tissue samples.
110 ication of unrecognized glycation targets of DPD in a prokaryotic system.
111 ignificant differences in mean TNF-alpha, or DPD levels pre- and post-XRT (P = .1934 and .4922, respe
112            Elevated urinary levels of PYD or DPD were present in 73% of patients and 38% had elevated
113  one marker of bone resorption (i.e., PYD or DPD) and/or serum osteocalcin (group 1).
114 tin machinery as treatment with Scriptaid or DPD reversed mSOD-induced insolubilization of the dynact
115 and peripheral-blood mononuclear cell (PBMC) DPD activity.
116  derived from 4,5-dihydroxy-2,3-pentandione (DPD), has been revealed as a universal signaling molecul
117 is that (4S)-4,5-dihydroxy-2,3-pentanedione (DPD) can undergo a previously undocumented non-enzymatic
118  end product 4,5-dihydroxy-2,3-pentanedione (DPD) during laboratory cultivation.
119              4,5-Dihydroxy-2,3-pentanedione (DPD), a product of the LuxS enzyme in the catabolism of
120 derived from 4,5-dihydroxy-2,3-pentanedione (DPD), and reveal new sophistication in the chemical lexi
121 ed from (4S)-4,5-dihydroxy-2,3-pentanedione (DPD), has been identified in both Gram-negative and Gram
122 near form of 4,5-dihydroxy-2,3-pentanedione (DPD), the precursor of the type II bacterial quorum sens
123 e (Hcys) and 4,5-dihydroxy-2,3-pentanedione (DPD), the precursor of the type II bacterial quorum sens
124 e (Hcys) and 4,5-dihydroxy-2,3-pentanedione (DPD), the precursor of type II bacterial autoinducer (AI
125 cysteine and 4,5-dihydroxy-2,3-pentanedione (DPD), the precursor of type II bacterial quorum sensing
126 e (Hcys) and 4,5-dihydroxy-2,3-pentanedione (DPD), the precursor of type II bacterial quorum-sensing
127 of synthetic 4,5-dihydroxy-2,3-pentanedione (DPD), which cyclizes to form AI-2.
128 derived from 4,5-dihydroxy-2,3-pentanedione (DPD).
129 cid-quenched N,N-diethyl-p-phenylenediamine (DPD) assay was used to measure the accumulation of H2O2
130 xidation of N,N'-dimethyl-p-pheylenediamine (DPD) is used to quantify the biologically more important
131 rements of the dissociative photodetachment (DPD) of the F(-)(H2O) anion revealed various dissociatio
132                                Postoperative DPD scans demonstrated cardiac localization in all 4 pat
133 versus 8%; P<0.01) versus the usual practice DPD.
134 ession model that included osteocalcin, PYD, DPD, intact PTH, age, years posttransplant, duration of
135  only a few have been demonstrated to reduce DPD enzyme activity.
136 eviously uncharacterized mechanism regulates DPD expression and may contribute to tumor resistance to
137                              The mean +/- SD DPD activity was 0.21 +/- 0.14 nmol/min/mg and did not c
138                            776C85 suppressed DPD activity in peripheral-blood mononuclear cells (PBMC
139             Addition of in vitro-synthesized DPD to cultured B. burgdorferi resulted in differential
140 LuxS for the express purpose of synthesizing DPD and utilizes a form of that molecule as an AI-2 pher
141 ese experiments and corresponding systematic DPD simulations probe the governing constitutive respons
142 ac ATTR corroborated by grade 2 to 3 (99m)Tc-DPD ((99m)Tc-3,3-diphosphono-1,2-propanodicarboxylic aci
143 with suspected cardiac ATTR (grade 1 (99m)Tc-DPD), and 12 asymptomatic individuals with amyloidogenic
144                     Here, we determined that DPD in mice and humans increases serum markers of metabo
145     Taken together, these data indicate that DPD promotes improved glucose homeostasis through an NEA
146                                          The DPD calculated in usual practice is underestimated in PH
147 ike micelles, shown in the AFM image and the DPD snapshot.
148 and mean PAWP were measured to calculate the DPD as per usual practice (diastolic pulmonary artery pr
149 hisms) in the gene (DPYD) that codes for the DPD enzyme.
150                                   Hence, the DPD simulations and comparisons with available independe
151 ct point mutations or small deletions in the DPD gene associated with 5-fluorouracil toxicity.
152                      The physical map of the DPD gene should permit development of rapid assays to de
153 efore the complete physical structure of the DPD gene was known.
154 calculations confirms the sensitivity of the DPD measurements to the subtle dynamics on the low-lying
155   While LsrK is a critical enzyme within the DPD quorum sensing relay system, kinetic details of this
156 ript levels of rbsB increased in response to DPD and as bacteria approached stationary-phase growth.
157 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
158 d were 4.1 and 3.8%, respectively, for total DPD and PYD and 9.8 and 9.5%, respectively, for free DPD
159     The mean recoveries were 98.1% for total DPD, 100.8% for total PYD, 98.6% for free DPD, and 94.9%
160  and 2 weeks after chemo-XRT to evaluate TP, DPD, and TNF-alpha mRNA levels.
161                            Role of TP and TP:DPD ratio warrants further investigation in a larger cli
162                    No association between TP:DPD ratio and efficacy of capecitabine or severity of to
163                           Median value of TP:DPD ratios at baseline was 2.65 (range, 0.36 to 11.08).
164 cantly higher enzyme activity than wild-type DPD (120%, P = 0.025; 116%, P = 0.049; 130%, P = 0.0077;
165 genetic syndrome has been described in which DPD-deficient patients are at risk for toxicity followin
166 pB3, and c.1601G>A-have been associated with DPD deficiency, but no definitive evidence for the clini
167 polymorphisms that have been associated with DPD deficiency.
168 lations, the heterocyclic oxygen atom within DPD appears necessary to promote hydration at the C3 pos

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