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1 elevant bioactive metal chelators related to clioquinol.
2 c metal chelating agents desferrioxamine and clioquinol.
3 howed decreased cell death when treated with clioquinol.
4 ch was inhibited by Cu2+ chelators including clioquinol.
5 brain rose by about 15% in mice treated with clioquinol.
6 n, cholesterol, and the proposed efficacy of clioquinol.
7 led trial in 36 patients with AD showed that clioquinol (250-750 mg daily) reduced plasma concentrati
8 xin rotenone and opposed by those induced by clioquinol, a compound with demonstrated therapeutic eff
9 tion (iAbeta5, a beta-sheet breaker peptide; clioquinol, a copper-zinc chelator) on the ability of is
10 mproved potencies up to 86-fold greater than clioquinol, a known cytotoxic compound.
11                       The MFAO-2s outperform clioquinol, a metal attenuator that has been investigate
12 ly, in a tissue culture model, we found that clioquinol, a metal chelator in clinical trials for AD t
13                                              Clioquinol, a metal chelator, has been used for many yea
14 ington's disease, we examined the effects of clioquinol, a metal-binding compound currently in clinic
15 evels of intracellular zinc, indicating that clioquinol acts as a zinc ionophore.
16                                 In addition, clioquinol alone exhibits similar effects in prostate ca
17 view examines the recent studies relating to Clioquinol and AD, and anticipates the imminent results
18                                Thioflavin T, clioquinol and emodin are promising leads in AD and PD r
19     Finally, the Abeta aggregation inhibitor clioquinol and gamma-secretase inhibitor L-685,458 atten
20 the last two decades, the potent activity of clioquinol and nitroxoline against several targets and t
21 ell death, and contrary to previous reports, clioquinol and other hydroxyquinoline compounds do not a
22  4 and 3.2 microM, respectively) compared to clioquinol and pyrrolidine dithiocarbamate (IC50 of 10 a
23 hydroxyquinoline derivatives nitroxoline and clioquinol are used to treat microbial infections; howev
24 ation for the current clinical assessment of clioquinol as an antineoplastic agent.
25 We report here that after binding to copper, clioquinol can inhibit the proteasomal chymotrypsin-like
26                             The finding that clioquinol could modulate plasma concentrations of amylo
27               The 8-hydroxyquinolines (8-HQ) clioquinol (CQ) and PBT2 were developed for their abilit
28                                              Clioquinol (CQ) is shown to sequester Cu(2+) more effect
29 istration of the bioavailable metal chelator clioquinol (CQ) on susceptibility to the Parkinson's-ind
30                            The antiparasitic clioquinol (CQ) represents a class of novel anticancer d
31          The antifungal and amoebicidal drug clioquinol (CQ) was withdrawn from the market when it wa
32                                              Clioquinol (CQ), an 8-OHQ previously reported to reduce
33 istration of the bioavailable iron chelator, clioquinol (CQ), to older mice was found to protect agai
34  on the cytotoxic activity of 5-Cl-7-I-8-HQ (clioquinol, CQ) copper complex (Cu(CQ)).
35 ed 9 week study of a mouse model of AD, oral clioquinol decreased brain Abeta by 49% without systemic
36                                              Clioquinol exerts its anti-parasitic actions by acting a
37 s, such as desferrioxamine (Fe chelator) and clioquinol (Fe, Cu, and Zn chelator), which reduce Abeta
38 ises the issue of specific iron chelators or clioquinol for control of oxidative damage in Parkinson'
39                        Our results show that clioquinol has anticancer effects both in vitro and in v
40 mplexes were also >100-fold more potent than clioquinol in a tumor spheroid model, with values simila
41  the imminent results of a Phase II trial of Clioquinol in AD, due in March 2002.
42           Biochemical analysis revealed that clioquinol induced cancer cell death through apoptotic p
43                                     Although clioquinol induced modest inhibition of SOD1 activity in
44 ver, dihydrotestosterone partially inhibited clioquinol-induced AR suppression and apoptosis only in
45        In an in vivo xenografts mouse model, clioquinol inhibited tumor growth of xenografts over a 6
46 ain deposits in vitro and one such compound, clioquinol, inhibits Abeta deposition in the Tg2576 mous
47                     Our results suggest that clioquinol is a candidate therapy for Huntington's disea
48                                              Clioquinol is a drug that acts on amyloid by perturbing
49      Our study provides strong evidence that clioquinol is able to target tumor proteasome in vivo in
50                                              Clioquinol is capable of forming stable complexes with c
51                          The metal chelator, clioquinol, is reported by Cherny et al. to reduce Abeta
52              The zinc-binding 8-OH-quinoline clioquinol markedly reduced AbetaO synaptic targeting, w
53 dition of dihydrotestosterone did not affect clioquinol-mediated proteasome inhibition in both prosta
54                                   To test if clioquinol might act as an ionophore, a fluorescent prob
55 effect was rescued with the Zn(2+) chelators clioquinol or TPEN.
56     Most recently, it has been reported that clioquinol possesses antitumor effects.
57  by ferritin transgene or the metal chelator clioquinol prevent oxidative damage and MPTP toxicity in
58                               Treatment with clioquinol reduced the viability of eight different huma
59 he reduced heme site, and (3) chelators like clioquinol remove Cu from these aggregates, while drugs
60 heet breaker peptide iAbeta5 or the chelator clioquinol, respectively.
61                              The addition of clioquinol resulted in elevated levels of intracellular
62 he Abeta aggregation inhibitors, iAbeta5 and clioquinol, selectively attenuated caspase-3 activation
63  perturbing amyloid's metallo-chemistry, and Clioquinol treatment has been shown to be beneficial in
64                                              Clioquinol treatment of transgenic Huntington's mice (R6
65                     Animal studies show that clioquinol treatment significantly inhibits the growth o
66                                              Clioquinol was identified as a prototype metal-protein-a
67                                              Clioquinol was withdrawn because of concerns of its asso
68   Moreover, the Abeta aggregation inhibitor, clioquinol, was able to attenuate isoflurane-induced cas
69 ease was inhibited by in vivo treatment with clioquinol, which suggests that brain Abeta accumulation