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1 chloroquine-hematin mixture compared to pure hematin.
2 ation of different chromophore parts of beta-hematin.
3 h a high participation of C(m)-parts of beta-hematin.
4 to sites on the fastest growing face of beta-hematin.
5 quine and quinidine on the formation of beta-hematin.
6 bited a novel high-affinity binding site for hematin.
7 assical GST substrates but effectively binds hematin.
8 sis, hypertransfusion, and infusions of i.v. hematin.
9 anism regulates the access of chloroquine to hematin.
10 crystallites are identical to synthetic beta-hematin.
11 e products formed from 15R- and 15S-HPETE by hematin (a nonenzymatic reaction), by liver microsomes i
12 ated whole blood, moderate concentrations of hematin activate the alternative pathway of complement a
13 t chloroquine inhibits the polymerization of hematin, allowing this toxic hemoglobin metabolite to ac
14     Simultaneous recording of the spectra of hematin and chloroquine mixtures with varying compositio
15  may be due to the reduced concentrations of hematin and H-DHA, which deactivate the dual nonclassica
16 sary to wash the pellet, which contains beta-hematin and heme aggregates, sequentially with Tris/SDS
17 ent on the saturable binding of the drugs to hematin and that the inhibition of hematin polymerizatio
18 g resulted in decreased final yields of beta-hematin, and an irreversible drug-induced precipitation
19 ation of sequence-specific DNA by exploiting hematin as biomimetic catalyst toward in situ metallizat
20                Under optimal conditions, the hematin-based electrochemical DNA biosensor presented a
21                               Therefore, the hematin-based signal amplification approach has great po
22                              Compared to CQ, hematin binding affinity of 1 decreased 6.4-fold, and th
23 nding, 13 CQ analogues were chosen and their hematin binding affinity, inhibition of hematin polymeri
24 support the hypothesis that chloroquine (CQ)-hematin binding in the parasite food vacuole leads to in
25  understand the structural specificity of CQ-hematin binding, 13 CQ analogues were chosen and their h
26 nes also form various complexes with soluble hematin, but complexation is insufficient to suppress he
27                  The chemistry relies on the hematin-catalyzed oxidation of nonfluorescent thiamine t
28 embrane diffusion scrubber (DS) is used with hematin-catalyzed oxidation of thiamine to thiochrome fo
29 sonance Raman spectra of the artesunate-beta-hematin complexes were thoroughly analyzed with the help
30                We establish that at elevated hematin concentrations, H-DHA activates two nonclassical
31 ential that are difficult or impossible with hematin-containing digestive vacuoles from P. falciparum
32 ow that quinoline antimalarials inhibit beta-hematin crystal surfaces by three distinct modes of acti
33 -DHA is the generation of macrosteps on beta-hematin crystal surfaces that hinder growth.
34                                  First, beta-hematin crystallites, whose nucleation is promoted by H-
35      We show that these adducts inhibit beta-hematin crystallization and heme detoxification, a pathw
36         We show that these adducts inhibit B-hematin crystallization and heme detoxification, a pathw
37 irst evidence of the molecular mechanisms of hematin crystallization and inhibition by chloroquine, a
38 her studies reveal that chloroquine inhibits hematin crystallization by binding to molecularly flat {
39                                              Hematin crystallization is the primary mechanism of heme
40 y, divergent hypotheses on the inhibition of hematin crystallization posit that drugs act either by t
41  Here we test whether and how H-DHA inhibits hematin crystallization, the main constituent of the hem
42 omoted by H-DHA, incorporate into large beta-hematin crystals and suppress their growth, likely by st
43 nd scanning probe microscopy of growing beta-hematin crystals to elucidate an unexpected mechanism em
44 s and scanning probe microscopy of growing B-hematin crystals to elucidate an unexpected mechanism em
45 rasite, after activation by heme, can form a hematin-dihydroartemisinin adduct (H-DHA).
46 e covalent mono- and di-meso(C(m))-alkylated hematin-dihydroartemisinyl complexes were calculated usi
47 stive vacuole through polymerization of beta-hematin dimers.
48 ows that the external morphology of the beta-hematin DMSO solvate crystals is almost indistinguishabl
49 mmon with chloroquine the inhibition of beta-hematin formation in a cell-free system.
50 ies bound to hematin monomer, inhibited beta-hematin formation in vitro, delayed intraerythrocytic pa
51 s, which are known to initiate/catalyze beta-hematin formation in vitro.
52                   The decreased rate of beta-hematin formation observed at low concentrations of both
53                                      No beta-hematin formation occurred in the absence of a catalytic
54 rate quantification of de novo hemozoin/beta-hematin formation was verified experimentally.
55 how only weak activity as inhibitors of beta-hematin formation, and their activities are only weakly
56  drug chloroquine, a known inhibitor of beta-hematin formation.
57 a spectrophotometric assay for in vitro beta-hematin formation.
58 a widely accepted protocol for in vitro beta-hematin formation.
59 nteractions with Fe(III)PPIX, inhibited beta-hematin formation.
60 e compound inhibits synthetic hemozoin (beta-hematin) formation, with IC(50) values lower than chloro
61 gregates and accurate quantification of beta-hematin formed during the assay.
62 n and characterization of PfCRT-transformed, hematin-free vesicles from D. discoideum cells.
63         This is the first case of the use of hematin given post-OLT to help achieve and maintain remi
64 ophysiology, fundamental questions regarding hematin growth and inhibition remain.
65 athways that transform it into a potent beta-hematin growth inhibitor.
66 tes, lipopolysaccharides, and synthetic beta-hematin had minimal effect.
67 min was used to synthesize the crystal, beta-hematin had no inflammatory activity.
68 ted malarial trophozoites and synthetic beta-hematin have been measured; both materials correspond to
69  for their effects on the inhibition of beta-hematin (hemozoin) formation, and the results were compa
70 ials inhibit crystallization by sequestering hematin in the solution, or by blocking surface sites cr
71      After normalization of liver tests, the hematin infusions have been given intermittently, are we
72 or hematologists because they administer the hematin infusions to treat the acute attacks in patients
73 er lesions, which regressed with glucose and hematin infusions.
74     Well-developed SAR models exist for beta-hematin inhibition, parasite activity, and cellular mech
75                            Evidently, the CQ-hematin interaction is largely a function of its pyridin
76 on quinolines inhibit the crystallization of hematin into hemozoin within the parasite, ultimately le
77          EXP1 efficiently degrades cytotoxic hematin, is potently inhibited by artesunate, and is ass
78 g suggests that the high-affinity binding of hematin may represent a parasite adaptation to blood or
79 )(asym) peak position of the 1:1 chloroquine-hematin mixture compared to pure hematin.
80                           Next, the attached hematin molecules acted as catalyst in accelerating the
81                                  After that, hematin molecules were introduced to the hybridized PNA/
82                         Both series bound to hematin monomer, inhibited beta-hematin formation in vit
83  measure any significant interaction between hematin mu-oxo dimer and 11, the 6-chloro analogue of CQ
84 e out-of-plane pi-electron density in CQ and hematin mu-oxo dimer at the points of intermolecular con
85 merization IC(50) values were normalized for hematin mu-oxo dimer binding affinities, adding further
86 vorable pi-pi interaction observed in the CQ-hematin mu-oxo dimer complex derives from a favorable al
87 ues suggests that other properties of the CQ-hematin mu-oxo dimer complex, rather than its associatio
88 tural determinant in its binding affinity to hematin mu-oxo dimer.
89 like CQ, these analogues bind to two or more hematin mu-oxo dimers in a cofacial pi-pi sandwich-type
90 and, counterproductively, a promoter of beta-hematin nucleation, driven by a boost in the formation o
91 reaction of linoleate 10S-hydroperoxide with hematin or ferrous ions.
92 s act either by the sequestration of soluble hematin or their interaction with crystal surfaces.
93  pheromonal compounds include organic acids, hematin, or ecdysteroids.
94 hematin polymerization and parasite death by hematin poisoning.
95 s a modest correlation between inhibition of hematin polymerization and inhibition of parasite growth
96 correlation between potency of inhibition of hematin polymerization and inhibition of parasite growth
97 parasite food vacuole leads to inhibition of hematin polymerization and parasite death by hematin poi
98  ring are required for activity against both hematin polymerization and parasite growth and that chlo
99 13, the lack of correlation between K(a) and hematin polymerization IC(50) values suggests that other
100 ation and inhibition of parasite growth when hematin polymerization IC(50) values were normalized for
101  drugs to hematin and that the inhibition of hematin polymerization may be secondary to this binding.
102 Bisquinolines 1-10 were potent inhibitors of hematin polymerization with IC50 values falling in the n
103 heir hematin binding affinity, inhibition of hematin polymerization, and inhibition of parasite growt
104 tant alone, play a role in the inhibition of hematin polymerization.
105 Hz; malarial pigment) and synthetic Hz (beta-hematin) promote a similar pattern of beta-chemokine gen
106               Thus, the reaction mediated by hematin promotes opsonization and possible clearance of
107  due solely to the binding of chloroquine to hematin rather than active uptake: using Ro 40-4388, a p
108 cuole to alter the binding of chloroquine to hematin rather than changing the active transport of chl
109                                       In the hematin reaction, the major products are four epoxy alco
110 ggest a key role for pH-dependent changes in hematin receptor concentration in the P. falciparum CQR
111                                 Furthermore, hematin-reconstituted PGHS-1, which was rapidly inhibite
112 of hemoglobin digestion and, by implication, hematin release, we demonstrate a concentration-dependen
113 ent, which is approximately 10(4)x less than hematin's physiological concentration.
114                      All inhibited both beta-hematin (synthetic hemozoin) formation and hemozoin form
115  different assay protocols for in vitro beta-hematin (synthetic identical to hemozoin) formation by t
116 n nucleation in vivo, and nucleation of beta-hematin, the synthetic analogue of hemozoin, was consist
117 chloroquine binding to the monomeric form of hematin, thereby preventing its further crystallization
118  chloroquine flux or reduced drug binding to hematin through an effect on DV pH.
119 neration of enzyme activity, but addition of hematin to the inhibited apoenzyme led to spontaneous re
120                         "Synthetic" HZ (beta-hematin), typically generated from partially purified ex
121 nd its interaction with the target structure hematin was investigated using an advanced, highly paral
122           The high-affinity binding site for hematin was not present in the GST showing the most iden
123 lar interactions between artesunate and beta-hematin were derived with a combination of resonance Ram
124             Single crystals of solvated beta-hematin were grown from a DMSO solution containing the a
125 te breakdown products such as hemoglobin and hematin, which have inflammatory properties.
126 ed the formation of synthetic hemozoin (beta-hematin) with IC(50) values lower than chloroquine and t

 
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