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1                                              DFP 1 mg/mL in drinking water increased retinal Tfrc mRN
2                                              DFP at 60 muM decreased labile iron in ARPE-19 cells, in
3                                              DFP exposure elicited comparable effects on phosphorylat
4                                              DFP formation (Kcat and kcat/Km), DFP decay, and protein
5                                              DFP has also been known to elicit antiproliferative acti
6                                              DFP treated rats, exhibited significantly reduced expres
7                                              DFP treatment significantly altered phosphorylation at r
8                                              DFP was not retina toxic in wild-type (WT) or DKO mice,
9                                          [3H]DFP labeling of chymotrypsin was suppressed by both BAEE
10                                          [3H]DFP reacted with brain microsomes to produce nine distin
11 t with [3H]diisopropylphosphofluoridate ([3H]DFP) to produce radioactive adducts that can be resolved
12 tol deacylase was affinity labelled with [3H]DFP and purified.
13                    Trypsin labeling with [3H]DFP was suppressed by alpha-N-benzoyl-l-arginine ethyl e
14 ould suppress the enzyme's reaction with [3H]DFP.
15 ith the laminin-derived peptide EFPDFP and a DFP peptide from the random screen demonstrated binding
16 ays, and allografting techniques to define a DFP state and the mechanism that governs its differentia
17 s of brain injury in a rodent model of acute DFP exposure.
18  this end, we developed a rat model of acute DFP intoxication and evaluated the efficacy of NV354 as
19 ed phase of learning impairment to sub-acute DFP exposure, which may involve the loss of hippocampal
20           A better tolerance to AN-238 after DFP treatment is due to the selective uptake of AN-238 b
21 amide caused large decreases in firing after DFP, confirming sustained ACh release.
22 ylation was bi-directionally regulated after DFP in striatum versus hippocampus.
23 ent complications but safely protect against DFP-induced seizures and other CNS toxicity, we adopted
24  Da for the active site peptide peak of aged DFP-inhibited NEST, corresponding to a monoisopropyl pho
25 parathion, and dimefox, and the nerve agents DFP, tabun, sarin, cyclosarin, soman, VX, and Russian-VX
26 ins by the brain supernatants of control and DFP-treated hens.
27                         Both neostigmine and DFP applied after AChE inhibition by DFP sometimes elici
28 e DFP) with IMI (2 mg/kg s.c., 30 min before DFP) prevents DFP-induced convulsions and the associated
29 ion of HUP (50 microg/kg s.c., 15 min before DFP) with IMI (2 mg/kg s.c., 30 min before DFP) prevents
30 l change to a final level higher than before DFP.
31 -pretreated mice, the ED(50) of IMI to block DFP-induced mortality is approximately 10 times lower th
32                  The docked poses adopted by DFP at the KDM active sites enabled identification of ne
33 served changes in phosphorylation induced by DFP.
34 veral KDM subfamilies which are inhibited by DFP in cell-free assay.
35 drolysis of polar PC, which was inhibited by DFP.
36 ine and DFP applied after AChE inhibition by DFP sometimes elicited a transient response.
37        The rate of inactivation of rh-PSA by DFP is 30-fold faster in the presence of 0.9 M Na(2)SO(4
38                                    Catalytic DFP degradation by MIP-202(Zr) was evaluated and compare
39                      The efficient catalytic DFP degradation with MIP-202(Zr) at near-neutral pH was
40 axis with pyridostigmine bromide (PB) caused DFP-treated animals to exhibit near normal levels of mem
41 A recent report shows that the iron chelator DFP induces both mitophagy and pexophagy in a BNIP3/NIX-
42                                 In contrast, DFP has no effect on the tolerance of AN-201.
43                                 Deferiprone (DFP) is a hydroxypyridinone-derived iron chelator curren
44 ction by the oral iron chelator deferiprone (DFP).
45 he 3 drugs, deferoxamine (DFO), deferiprone (DFP), and deferasirox (DFX), including their efficacy, p
46 are inhibited by diisopropylfluorophosphate (DFP).
47 xon, dichlorvos, diisopropylfluorophosphate (DFP), and sarin covalently bind to human albumin.
48 other hand, 1 mM diisopropylfluorophosphate (DFP) completely inhibited LCAT but had no effect on PAF-
49 ric detection of diisopropylfluorophosphate (DFP), a F-containing G-type NA simulant.
50 tion with the OP diisopropylfluorophosphate (DFP).
51 os oxon (CPO) or diisopropylfluorophosphate (DFP): human serum albumin (K212, K414, K199, and K351),
52 amidine (pAB) and diisopropylfluorphosphate (DFP) were impaired 1.6-36-fold and 35-478-fold, respecti
53 (AChE) inhibitor, diisopropylflurophosphate (DFP) were administered as single daily injections concom
54 dition, low level diisopropylflurophosphate (DFP) exposure (0.25 mg/kg per day for 2 weeks) in rats r
55              Diisopropylphosphorofluoridate (DFP), the oxygen analogue of MIP, was used for compariso
56                                     In DKOs, DFP over 8 months decreased retinal iron levels to 72% o
57                                         ErSO-DFP and related compounds represent an intriguing new cl
58                               We report ErSO-DFP, a compound that maintains antitumor efficacy, has e
59  benefits of the fermented and non-fermented DFP before in vitro digestion and after (bioaccessible f
60       This study revealed that the fermented DFP exhibited higher health properties than control.
61                 Diisopropyl fluorophosphate (DFP) causes neurotoxicity related to an irreversible inh
62  groups such as diisopropyl fluorophosphate (DFP) or venomous agent X, creating a major challenge for
63  AChE inhibitor diisopropyl fluorophosphate (DFP) usually caused a sustained increase, with an initia
64                 Diisopropyl fluorophosphate (DFP) was used as a nerve gas mimic.
65 a CE inhibitor, diisopropyl fluorophosphate (DFP), to mouse serum in vitro significantly (P < 0.01) p
66 he OP compound, diisopropyl fluorophosphate (DFP).
67 phate substrate diisopropyl fluorophosphate (DFP).
68 d with inactive diisopropyl-fluorophosphate [DFP]-thrombin) and mediated via the protease-activated r
69  complex with diisopropyl fluorophosphonate (DFP, a potent serine hydrolase inhibitor) were determine
70 n, anti-PRCP, diisopropyl-fluorophosphonate (DFP), phenylmethylsulfonyl fluoride (PMSF), and Z-Pro-Pr
71 5 and 1938 for dichlorvos, 1881 and 1994 for DFP, and 1838 and 1938 for sarin; these masses fit a mec
72                      The detection limit for DFP is 2 x 10(-6) M with a potential drop between 40 and
73        Characteristic fragments specific for DFP-labeled lysine appeared at 164.0, 181.2, and 83.8amu
74                           Kinetic values for DFP against NEST were as follows: k(i) = 17 200 +/- 180
75                      Brain supernatants from DFP-treated hens showed enhanced in vitro phosphorylatio
76                                    The [(3)H]DFP-labeled protease was detected as three protein bands
77 PON1 prevent it from being able to hydrolyze DFP with its fluoride leaving group.
78 F subunits in the cytoskeletal inclusions in DFP-treated hen spinal cord cross-sections.
79 r piroxicam or the selective COX-2 inhibitor DFP, but by inhibitors of either secretory or cytosolic
80 that when the acetylcholinesterase inhibitor DFP was co-administered with morphine, both the increase
81            DFP formation (Kcat and kcat/Km), DFP decay, and protein-caged hydrated ferric oxide accum
82                 In breast cancer cell lines, DFP potently inhibits the demethylation of H3K4me3 and H
83  Pefabloc and by 30% in the presence of 1 mM DFP.
84  a nanostructured film of the small molecule DFP-4T, consisting of a fully pai-conjugated diperfluoro
85 M active sites enabled identification of new DFP-based KDM inhibitors which are more cytotoxic to can
86 ocompatibility and water dispersibility, nTG-DFP-COF demonstrates minimal cytotoxicity and exceptiona
87  a nanoscale Covalent Organic Framework, nTG-DFP-COF, specifically designed to enhance fluorescence-g
88 ing tumor targeting accuracy, the use of nTG-DFP-COF will reduce the need for repeat surgeries, facil
89 rent mechanism in the axonal aggregations of DFP-treated hen.
90                               The binding of DFP to Tyr411 of human albumin was confirmed by electros
91 lation state of phosphoproteins in brains of DFP-treated mice; hippocampus and striatum were analyzed
92 filament (NF) subunits in the spinal cord of DFP-treated hens.
93 chiometry of NF-M:NF-L in the spinal cord of DFP-treated hens.
94                             A single dose of DFP (1.7 mg/kg, s.c.) produces mild ataxia in 7-14 days
95                             A single dose of DFP (1.7 mg/kg, sc.) produces mild ataxia in 7-14 days i
96      Hens were treated with a single dose of DFP and sacrificed 1, 5, 10, and 20 days post-treatment.
97                     We studied the effect of DFP administration on Ca2+/calmodulin-dependent phosphor
98       The apparent anti-withdrawal effect of DFP was not reproduced by the selective peripherally act
99   These changes were observed within 24 h of DFP administration and persisted for 10-20 days.
100 with time due to the catalyzed hydrolysis of DFP and the production of fluoride ion.
101                           In the presence of DFP, the electrode potential decreases rapidly with time
102 tion of tau proteins by brain supernatant of DFP-treated hens that includes phosphorylation of a numb
103                           Further testing of DFP for retinal disease involving oxidative stress is wa
104                                   The use of DFP together with these peptide conjugates in nude mice
105                                         Oral DFP was not toxic to the mouse retina.
106 t, and safe therapeutic strategy to overcome DFP toxicity.
107 93 is deleterious for interactions with pAB, DFP and amidolytic substrates, situations where no S2'-P
108 ubstrates are coupled via a diferric peroxo (DFP) intermediate, lambdamax 650 nm, which decays to [Fe
109               Diisopropyl phosphofluoridate (DFP) at high concentration partially inhibited the prote
110             Diisopropyl phosphorofluoridate (DFP) is an organophosphorus ester, which produces organo
111             Diisopropyl phosphorofluoridate (DFP) produces organophosphorus ester-induced delayed neu
112  utilize date by-product (date fruit pomace; DFP).
113                This dynamic fiber precursor (DFP) is directly drawn by pultrusion into HA fibers that
114 I (2 mg/kg s.c., 30 min before DFP) prevents DFP-induced convulsions and the associated neuronal dama
115 motifs containing the signature Asp-Phe-Pro (DFP) tripeptide.
116 ver, the epigenetic mechanisms that regulate DFP differentiation are not known.
117 ith its monocyte chemotactic activity, since DFP- or PMSF-inactivated cathepsin G no longer induced m
118                                Specifically, DFP inhibits the demethylase activities of six KDMs - 2A
119 the rate of endogenous ACh release, and that DFP and reversible AChE inhibitors exert an initial tran
120                        We herein report that DFP chelates the Fe(2+) ion at the active sites of selec
121             These data strongly suggest that DFP derives its anti-proliferative activity largely from
122  to show a temporal relationship between the DFP-induced impairment in performance of a spatial memor
123 02(Zr) using Soxhlet extraction improved the DFP conversion rate and afforded a 2.64-fold improvement
124  domain, and central to the interaction, the DFP phenylalanine side-chain inserts into a major hydrop
125         Dynamic rheology measurements of the DFP and tensile testing of the resulting fibers reveal d
126            This revealed the location of the DFP peptide bound to the FXI apple 2 domain, and central
127 icotine was shown to completely reverse this DFP-induced impairment in memory-related task performanc
128 lude that the level of sustained response to DFP is determined by the rate of endogenous ACh release,
129            The KDM that is most sensitive to DFP, KDM6A, has an IC(50) that is between 7- and 70-fold
130                                      The TTA-DFP-COF membrane opens new avenues for research to addre
131                                         When DFP is used in vivo, 400 nmol/kg cytotoxic somatostatin
132  binding equivalence concentrations at which DFP inhibits ribonucleotide reductase (RNR) activities a
133 as attenuated when Lp(a) was pretreated with DFP suggesting that the serine residue in the pseudo act
134 l (ARPE-19) cells and mice were treated with DFP.
135  all animals die after the same dose without DFP.

 
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