An Evaluation of Antimalarial Combinations against Plasmodium berghei in the Mouse

Jacobs, Richard L.; Alling, David W.; Cantrell, William

doi:10.2307/3275719

Cited by 21 publications

(7 citation statements)

References 3 publications

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“…By 1966, in vivo data were accumulating to contradict the WHO's claim. Furthermore, there was no evidence of potentiation between chloroquinepyrimethamine or chloroquine-primaquine (Jacobs et al, 1963;Young et al, 1963).…”

Section: A the "Old" Combinationsmentioning

confidence: 99%

“…Yet even as early as 1967, Harinasuta et al (1967) suggested combination regimens containing three drugs, each with a different mode of action. He cautioned against using DHFR/DHPS inhibitor combinations because of their flat dose-activity lines (Jacobs et al, 1963;Peters, 1968;quoted in Peters, 1975), which he warned might facilitate the development of resistance.…”

Section: A the "Old" Combinationsmentioning

confidence: 99%

“…An early paper on the efficacy of sulfadoxine-pyrimethamine wisely cautioned that the combination of pyrimethamine and sulfadoxine, whose dose activity regression lines are nearly flat, might lead to rapid development of parasite drug resistance (see Jacobs et al, 1963;Harinasuta et al, 1967).…”

Section: Mechanisms Of Resistance Of Malaria Parasites To Antifolatesmentioning

confidence: 99%

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Mechanisms of Resistance of Malaria Parasites to Antifolates

2005

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Section: A the "Old" Combinationsmentioning

confidence: 99%

Section: A the "Old" Combinationsmentioning

confidence: 99%

Section: Mechanisms Of Resistance Of Malaria Parasites To Antifolatesmentioning

confidence: 99%

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Mechanisms of Resistance of Malaria Parasites to Antifolates

2005

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“…At this time, however, antimalarial drug screening depended entirely on in vivo experiments using animal models of malaria [188][189][190]. Given that the antimalarial activity of a compound can vary between different Plasmodium species, and that the PfCRT-based resistance mechanism appears to be unique to P. falciparum, it is possible that these early experiments have overlooked compounds that are in fact active against drug-resistant P. falciparum.…”

Section: To the Rescuementioning

confidence: 99%

Know your enemy: understanding the role of PfCRT in drug resistance could lead to new antimalarial tactics

Summers

Nash

Martin

2012

Cell. Mol. Life Sci.

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The prevention and treatment of malaria is heavily dependent on antimalarial drugs. However, beginning with the emergence of chloroquine (CQ)-resistant Plasmodium falciparum parasites 50 years ago, efforts to control the disease have been thwarted by failed or failing drugs. Mutations in the parasite's 'chloroquine resistance transporter' (PfCRT) are the primary cause of CQ resistance. Furthermore, changes in PfCRT (and in several other transport proteins) are associated with decreases or increases in the parasite's susceptibility to a number of other antimalarial drugs. Here, we review recent advances in our understanding of CQ resistance and discuss these in the broader context of the parasite's susceptibilities to other quinolines and related drugs. We suggest that PfCRT can be viewed both as a 'multidrug-resistance carrier' and as a drug target, and that the quinoline-resistance mechanism is a potential 'Achilles' heel' of the parasite. We examine a number of the antimalarial strategies currently undergoing development that are designed to exploit the resistance mechanism, including relatively simple measures, such as alternative CQ dosages, as well as new drugs that either circumvent the resistance mechanism or target it directly.

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“…The mixture ratio was estimated based on the membrane volume of RBCs and the total membrane volume required to fully coat 1 mg of PLGA nanoparticles. Parameters used for the estimation include mean surface area of mouse RBCs (75 μm 2 ) (34), membrane thickness of RBC (7 nm), density of 50∶50 PLGA nanoparticles (1.34 g∕cm 3 ) (35), red blood cell concentration in mouse blood (7 billion per mL) (36), and the mean particle size as measured by DLS before and after the RBC-membrane coating (Fig. S4).…”

Section: Methodsmentioning

confidence: 99%

Erythrocyte membrane-camouflaged polymeric nanoparticles as a biomimetic delivery platform

Zhang

Aryal

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

1,952

1,742

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Efforts to extend nanoparticle residence time in vivo have inspired many strategies in particle surface modifications to bypass macrophage uptake and systemic clearance. Here we report a top-down biomimetic approach in particle functionalization by coating biodegradable polymeric nanoparticles with natural erythrocyte membranes, including both membrane lipids and associated membrane proteins for long-circulating cargo delivery. The structure, size and surface zeta potential, and protein contents of the erythrocyte membrane-coated nanoparticles were verified using transmission electron microscopy, dynamic light scattering, and gel electrophoresis, respectively. Mice injections with fluorophore-loaded nanoparticles revealed superior circulation half-life by the erythrocytemimicking nanoparticles as compared to control particles coated with the state-of-the-art synthetic stealth materials. Biodistribution study revealed significant particle retention in the blood 72 h following the particle injection. The translocation of natural cellular membranes, their associated proteins, and the corresponding functionalities to the surface of synthetic particles represents a unique approach in nanoparticle functionalization.biomimetic nanoparticle | drug delivery | long circulation | red blood cell membrane

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An Evaluation of Antimalarial Combinations against Plasmodium berghei in the Mouse

Cited by 21 publications

References 3 publications

Mechanisms of Resistance of Malaria Parasites to Antifolates

Mechanisms of Resistance of Malaria Parasites to Antifolates

Know your enemy: understanding the role of PfCRT in drug resistance could lead to new antimalarial tactics

Erythrocyte membrane-camouflaged polymeric nanoparticles as a biomimetic delivery platform

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