Gotowe bibliografie tematyczne / Antimalaria- Drug

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Gotowa bibliografia na temat „Antimalaria- Drug”

Autor: Grafiati
Data publikacji: 6 września 2023

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Artykuły w czasopismach na temat "Antimalaria- Drug"

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Yousif, M. A., i A. A. Adeel. "Antimalarials prescribing patterns in Gezira state: precepts and practices". Eastern Mediterranean Health Journal 6, nr 5-6 (15.12.2000): 939–47. http://dx.doi.org/10.26719/2000.6.5-6.939.

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A longitudinal pharmacoepidemiological study on prescribing patterns of antimalarials was conducted in Gezira State, Sudan. Different core drug prescribing indicators were identified, measured and correlated. Chloroquine and quinine were the most frequently prescribed antimalaria drugs but in 44.7% of cases, the dosage was inappropriate and did not conform to standard regimens. Due to variable and unmonitored patterns of drug resistance, most medical practitioners in Sudan tend to follow their own protocols to treat severe cases of malaria rather than conforming to standard regimens. We attribute the emergence of a high rate of resistance to malaria chemotherapy to such practices. We recommend interventions to ensure rational prescribing, and call for the formulation of a national antimalarial drugs policy.
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Ujuamala Uloma Ezeani, Penaere Theresa Osahon i Michael Chukwudi Ezeani. "Pattern of anti-malarial drugs and artemether combination therapy adherence in an institution based medical centre, Nigeria". World Journal of Advanced Research and Reviews 8, nr 3 (30.12.2020): 162–70. http://dx.doi.org/10.30574/wjarr.2020.8.3.0437.

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The change in policy guidelines for treating uncomplicated malaria became necessary because the therapeutic efficacy of chloroquine and SP had deteriorated. Hence compliance is a necessity to enable effective check on malaria. This work was carried out to evaluate antimalaria drug prescription and to update its usage in line with WHO guideline on Artemeter Combination therapy in a university based medical center. We utilized descriptive, cross-sectional, retrospective study of antimalaria prescriptions purposely carried out among male and female outpatients with mean age of 22.4±2.8 at a University health facility. This comprised all outpatients prescriptions that contained at least one antimalarial drug filed from October 2018 to September 2019. Systematic sampling was used to select the prescriptions. Based on the total number of 1250 prescriptions containing at least one antimalarial drug, a sampling interval of 5 was calculated and simple balloting was used for the first pick. A total number of two hundred and fifty (250) prescriptions containing at least one antimalarial drug were selected for the study. Out of 250 antimalaria prescriptions, usage of ACT class of Artemeter lumefantrine, Artemeter Amodiaquine and Artemeter Piparaqiune were recorded at 45.6%, 10.4% and 9.6% respectively. Triple combination Artemeter lumefantrine and Sulphadoxine-Pyrimethamine was recorded at 20.4% while Sulphadoxine-Pyrimethamine was recorded at 4%. Combination of antimalarial drugs with antibiotics was recorded at 31.2%. This study showed compliance with National Antimalarial Treatment Guideline for the treatment of malaria infection as it regards the use of artemisinin-based combination therapy. The frequency usage of artemeter lumefantrine was proceeding among other ACTs. The frequency in co-prescription of antibiotics with anti-malaria should be guarded to comply with WHO recommendation.
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Kocisko, David A., i Byron Caughey. "Mefloquine, an Antimalaria Drug with Antiprion Activity In Vitro, Lacks Activity In Vivo". Journal of Virology 80, nr 2 (15.01.2006): 1044–46. http://dx.doi.org/10.1128/jvi.80.2.1044-1046.2006.

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ABSTRACT In view of the effectiveness of antimalaria drugs inhibiting abnormal protease-resistant prion protein (PrP-res) formation in scrapie agent-infected cells, we tested other antimalarial compounds for similar activity. Mefloquine (MF), a quinoline antimalaria drug, was the most active compound tested against RML and 22L mouse scrapie agent-infected cells, with 50% inhibitory concentrations of ∼0.5 and ∼1.2 μM, respectively. However, MF administered to mice did not delay the onset of intraperitoneally inoculated scrapie agent, the result previously observed with quinacrine. While most anti-scrapie agent compounds inhibit PrP-res formation in vitro, many PrP-res inhibitors have no activity in vivo. This underscores the importance of testing promising candidates in vivo.
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Gil, JP, i E. Gil Berglund. "CYP2C8 and antimalaria drug efficacy". Pharmacogenomics 8, nr 2 (luty 2007): 187–98. http://dx.doi.org/10.2217/14622416.8.2.187.

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Hede, K. "Antimalaria Drug Offers Antitumor Strategies". JNCI Journal of the National Cancer Institute 103, nr 20 (4.10.2011): 1490–91. http://dx.doi.org/10.1093/jnci/djr423.

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Bradbury, Jane. "Synthetic antimalaria drug enters clinical trials". Lancet Infectious Diseases 4, nr 10 (październik 2004): 598. http://dx.doi.org/10.1016/s1473-3099(04)01161-2.

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Linda Ekawati, Linda Ekawati, Beta Achromi Nurohmah Beta Achromi Nurohmah, Jufrizal Syahri Jufrizal Syahri i Bambang Purwono Bambang Purwono. "Substituted 3-styryl-2-pyrazoline Derivatives as an Antimalaria: Synthesis, in vitro Assay, Molecular Docking, Druglikeness Analysis and Admet Prediction". Sains Malaysiana 51, nr 10 (31.10.2022): 3215–36. http://dx.doi.org/10.17576/jsm-2022-5110-09.

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The synthesis, in vitro antimalarial assay, molecular docking, drug-likeness analysis, and ADMET prediction of substituted 3-styryl-2-pyrazoline derivatives as antimalaria have been conducted. The synthesis of N-phenyl (1a‒3a) and N-acetyl-substituted (1b‒3b) 3-styryl-2-pyrazolines was carried out using dibenzalacetone derivatives and hydrazine hydrate or phenylhydrazine. An in vitro antimalarial assay was conducted against the chloroquine-sensitive Plasmodium falciparum 3D7 strain, while molecular docking was performed toward the crystal protein of Plasmodium falciparum dihydrofolate reductase-thymidylate synthase (PfDHFR-TS) (PDB ID: 1J3I). Furthermore, the prediction of drug-like properties was determined by assessing Lipinski’s rules, and the pharmacokinetic parameters were also studied in-silico, including absorption, distribution, metabolism, excretion, and toxicity (ADMET). The in vitro assay showed that 3a (IC50 0.101 µM) has excellent antimalarial activity, followed by 2a (0.177 µM), and 1b (0.258 µM). Molecular docking has supported the in vitro assay by showing the lowest CDOCKER energy for 3a (‒56.316 kcal/mol), then 2a (‒51.2603 kcal/mol), and 1b (‒48.8774 kcal/mol). The drug-like properties showed that all of the prepared compounds were acceptable based on Lipinski’s rules and predicted to be potentially orally bioavailable. The ADMET analysis provided information that 3a and 2a could be proposed as the best lead antimalarial drugs with further modification to reduce the lipophilicity and toxicity properties.
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Peter, Sijongesonke, i Blessing Atim Aderibigbe. "Ferrocene-Based Compounds with Antimalaria/Anticancer Activity". Molecules 24, nr 19 (7.10.2019): 3604. http://dx.doi.org/10.3390/molecules24193604.

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Malaria and cancer are chronic diseases. The challenge with drugs available for the treatment of these diseases is drug toxicity and resistance. Ferrocene is a potent organometallic which have been hybridized with other compounds resulting in compounds with enhanced biological activity such as antimalarial and anticancer. Drugs such as ferroquine were developed from ferrocene and chloroquine. It was tested in the 1990s as an antimalarial and is still an effective antimalarial. Many researchers have reported ferrocene compounds as potent compounds useful as anticancer and antimalarial agents when hybridized with other pharmaceutical scaffolds. This review will be focused on compounds with ferrocene moieties that exhibit either an anticancer or antimalarial activity.
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Muhaimin, Muhaimin, Yusnaidar Yusnaidar i Hilda Amanda. "Antimalaria Activity of Macaranga Gigantea Leaves Extracts". Journal of The Indonesian Society of Integrated Chemistry 10, nr 2 (6.04.2019): 23–32. http://dx.doi.org/10.22437/jisic.v10i2.6581.

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The utilization of traditional medicinal plants to medicate malaria caused by Plasmodium is currently more increased along with drug resistance and rising drug prices, and the side effects of using modern medicine. Additionally, Macaranga gigantea plant species have a unique ecological function such as a pioneer plant with good morphological and physiological adaptability to extreme conditions in dealing with natural stress due to pests, temperatures, and UV rays. Therefore, they have a unique biochemical system and a variety of new natural bioactive compounds produced with various activities such as antimicrobial, antioxidant and antiviral in the forest. As the results of previous study, antimalarial activity was shown on the bioactivity of methanol leaves extract of Merkubung (Macaranga gigantea). In short, this study aimed to obtain an active antimalarial fraction of Merkubung leaf (Macaranga gigantea). In this case, fractionation of methanol extract of Merkubung leaf (Macaranga gigantea) was carried out by using different organic solvents followed by an antimalarial bioactivity test using Plasmodium berghei. The results indicated that ethanol fraction of Merkubung left (Macaranga gigantea) had better antimalarial activity than others as a new candidate and supplemental source of antimalarial drugs. Keyword: Macaranga gigantea, malaria, Plasmodium berghei, fraction
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Tahir, Iqmal, Mudasir Mudasir, Irza Yulistia i Mustofa Mustofa. "QUANTITATIVE STRUCTURE-ACTIVITY RELATIONSHIP ANALYSIS (QSAR) OF VINCADIFFORMINE ANALOGUES AS THE ANTIPLASMODIAL COMPOUNDS OF THE CHLOROQUINOSENSIBLE STRAIN". Indonesian Journal of Chemistry 5, nr 3 (15.06.2010): 255–60. http://dx.doi.org/10.22146/ijc.21800.

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Quantitative Structure-Activity Relationship (QSAR) analysis of vincadifformine analogs as an antimalarial drug has been conducted using atomic net charges (q), moment dipole (), LUMO (Lowest Unoccupied Molecular Orbital) and HOMO (Highest Occupied Molecular Orbital) energies, molecular mass (m) as well as surface area (A) as the predictors to their activity. Data of predictors are obtained from computational chemistry method using semi-empirical molecular orbital AM1 calculation. Antimalarial activities were taken as the activity of the drugs against chloroquine-sensitive Plasmodium falciparum (Nigerian Cell) strain and were presented as the value of ln(1/IC50) where IC50 is an effective concentration inhibiting 50% of the parasite growth. The best QSAR model has been determined by multiple linier regression analysis giving QSAR equation: Log (1/IC50) = 9.602.qC1 -17.012.qC2 +6.084.qC3 -19.758.qC5 -6.517.qC6 +2.746.qC7 -6.795.qN +6.59.qC8 -0.190. -0.974.ELUMO +0.515.EHOMO -0.274. +0.029.A -1.673 (n = 16; r = 0.995; SD = 0.099; F = 2.682) Keywords: QSAR analysis, antimalaria, vincadifformine.
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Rozprawy doktorskie na temat "Antimalaria- Drug"

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Kumar, Hirdesh. "Identification of vaccine and drug targets against malaria". Thesis, IIT Delhi, 2016. http://localhost:8080/xmlui/handle/12345678/7008.

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Pongtavornpinyo, Wirichada. "Mathematical modelling of antimalarial drug resistance". Thesis, University of Liverpool, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.428249.

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Matthews, H. "Accelerating antimalarial drug discovery through repositioning". Thesis, University of Salford, 2013. http://usir.salford.ac.uk/36885/.

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Of the plethora of parasitic diseases that afflict mankind, malaria remains the most significant with 100-300 million cases reported annually and 600,000 fatalities. Treatment and control measures have been hampered by the emergence of drug resistance to most antimalarial therapies. Early signs of drug resistance to the current frontline option, the artemisinins, make it imperative that novel drug candidates are discovered. One possible short-term solution is drug repositioning, via screening existing FDA-approved (Food and Drug Administration agency) drug libraries for antimalarial activity. Towards this goal, two, fast, simple, and reliable in vitro SYBR Green-based drug susceptibility assays were optimised. The first, the SYBR Green microplate method offered a medium throughput option that was used to screen two FDA-approved libraries (Z score = 0.68 +0.06), LOPAC and ENZO (~700 compounds). Approximately 60 hits, defined as > 50 % inhibition at 2.5 µM, were identified by the preliminary screen. The SYBR Green flow cytometer method, capable of providing direct parasitaemia estimates and stage-specific information, was used for second-phase characterisation of the hits. From these, antiamoebic compound emetine dihydrochloride hydrate was identified as a potent inhibitor of the multidrug resistant Plasmodium falciparum, strain K1, with an IC50 of 47 nM (95 % confidence interval 44.92-49.17). Further characterisation of the compound involved analysis of the parasite killing profile, to determine the parasite reduction ratio (PRR) and parasite clearance time (PCT) as well drug interaction analysis with existing antimalarials. Emetine was shown to have a similar killing profile to atovaquone inferring a similar mitochondrial mode of action, corroborated by fluorescence staining with the JC-1 mitochondrial probe. Taken together, emetine’s pharmacokinetic matching and synergy with atovaquone provide an exciting drug combination for further investigation. The relatively high hit rate presented in the study, and in vitro workflow outlined for emetine, also showed drug repositioning to be a promising option for antimalarial drug discovery.
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Sumanadasa, Subathdrage Dulangi Madushika. "Investigation of Novel Antimalarial Agents and Novel Target Identification Approaches". Thesis, Griffith University, 2015. http://hdl.handle.net/10072/367036.

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Malaria remains a major global health problem causing >600,000 deaths annually [1]. Efforts to control malaria are hampered by parasite drug resistance, insecticide resistance in mosquitoes, and the lack of an effective vaccine. In the last decade only one new chemotype, the spiroindolones, has progressed to clinical trials for malaria treatment [2, 3]. To address this significant problem the identification and development of new antimalarial agents is a priority. Part of this process includes ensuring that sufficient drug leads are available to prime the drug discovery pipeline, particularly those with novel modes of action in order to limit issues of cross-resistance with existing drugs [4]. While high throughput screening campaigns have identified thousands of potential antimalarial compounds from big Pharma libraries [5, 6], antimalarial target information on most compounds are lacking. Screening different libraries and pharmacophores is also recognised as being crucial to ensure chemical diversity [7]. There is also an increasing interest in repurposing existing drugs or drug classes or using them as starting point for discovery of new antimalarial agents. One of the aims of this thesis was to address the need for new antimalarial drug leads by investigating three compound classes with demonstrated clinical efficacy against cancer, HIV and other human diseases in a so called “piggyback” approach.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Biomolecular and Physical Sciences
Science, Environment, Engineering and Technology
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Uhlemann, Anne-Catrin. "Plasmodium falciparum transporters as antimalarial drug targets". Thesis, St George's, University of London, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.559278.

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Plasmodiumfalciparum malaria poses one of the most important disease problems in the world. Despite decades of effort to improve disease outcome, the emergence and rapid dissemination of multi-drug resistant parasites has led to a disturbing increase in malaria mortality and morbidity. A critical limitation in managing multi-drug resistant falciparum malaria has been the incomplete understanding of both the underlying molecular mechanisms of drug resistance and the mode of action of widely used drugs. This study aimed to characterise the molecular mechanisms underlying multi- drug resistant malaria by studying the role of gene amplification in the P. falciparum multi-drug resistance gene 1 (pfmdrl) in determining parasite response to a variety of antimalarials in vitro and in vivo. In addition, P. falciparum ATPase 6 (PfATP6), a putative drug target of the widely used artemisinins, was also examined for possible drug-modulating mutations. First a real-time peR technique to measure amplification of pfmdri was developed and validated. This technique was used to determine pfmdri copy number in a unique set of field sample set (n = 600) collected in Northern Thailand, an area harbouring the world's most drug-resistant parasites. This allowed a comprehensive analysis of the importance of pfmdri amplification in (1) in vitro resistance to drugs, (2) in vivo response to mefloquine or mefloquine- artesunate therapy, (3) evolution of amplification in pre- and post-treatment samples. Subsequent studies also investigated the prevalence of pfmdrt amplification in Gabon, a Sub-Saharan country with very little mefloquine resistance. In addition, P. falciparum field isolates were studied for possible polymorphisms in PfATP6 and plasmid constructs generated to study the role of single nucleotide point mutations in the putative active site of the enzyme.
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Price, K. E. "Antimalarial drug discovery : exploring the MEP pathway". Thesis, University of Liverpool, 2016. http://livrepository.liverpool.ac.uk/3005814/.

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Silal, Sheetal Prakash. "A simulation model of antimalarial drug resistance". Master's thesis, University of Cape Town, 2009. http://hdl.handle.net/11427/9003.

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Includes bibliographical references (leaves 132-137).
Malaria ranks among the world's most important tropical parasitic diseases with world prevalence figures between 350 and 550 million clinical cases per annum. [WHO, 2008a] 'Treatment and prevention of malaria places a considerable burden on struggling economies where the disease is rampant. Research in malaria does not stop as the change in response to antimalarial drug treatment requires the development of new drugs and innovation in the use of old drugs. This thesis focused on building a model of the spread of resistance to Sulfadoxine/Pyrimethamine (SP) in a setting where both SP and SP in artemisinin-based combination therapy (ACT) are the first line therapies for malaria. The model itself is suitable to any low transmission setting where antimalarial drug resistance exists but the country of choice in this modeling exercise was Mozambique. The model was calibrated using parameters specific to the malaria situation in Mozambique. This model was intended to be used to aid decision making in countries where antimalarial drug resistance exists to help prevent resistance spreading to such an extent that drugs lose their usefulness in curing malaria. The modeling technique of choice was differential equation modeling; a simulation technique that falls under the System Dynamics banner in the Operations Research armamentarium. It is a technique that allowed the modeling of stocks and flows that represent different stages or groupings in the disease process and the rate of movement between these stages respectively. The base model that was built allowed infected individuals to become infectious, to be treated with SP or ACT and to be sensitive to or fail treatment. Individuals were allowed a period of temporary immunity where they would not be reinfected until the residual SP had been eliminated from their bloodstream. The base model was then further developed to include the pharmacokinetic properties of SP where individuals were allowed to be reinfected with certain strains of infection given the level of residual drug in their bloodstream after their current infection had been cleared. The models used in this thesis were built with idea of expanding on previous models and using available data to improve parameter estimates. The model at its core is similar to the resistance model used in Koella and Antia [2003] where differential equation modeling was used to monitor a population as it became infected with a sensitive or resistant infection and then University of Cape Town recovered. The inclusion in the model of the PK component was derived from Prudhomme-O'Meara et al. [2006] where individuals could be reinfected depending on the residual drug in their bloodstream. Rather than modeling simply sensitive and resistant infections, mutations categories were used as was the case in Watkins et al. [2005] population genetics model. The use of mutation categories allowed one to use parameters specific to these categories rather than the sensitive/resistant stratification and this is particularly relevant in Mozambique where all mutation categories still exhibit some degree of sensitivity to treatment i.e. total resistance has not yet developed for any particular mutation category. The last adaptation of the model was to use gametocyte information directly to determine human infectiousness rather than through using a gametocyte switching rate (constant multiplier used to convert parasite density to gametocyte density) as was done in Pongtavompinyo [2006]. The models developed in this thesis found that the existing vector control and drug policy in Mozambique had the major effect of decreasing total prevalence of malaria by approximately 70% in the 11 year period. The distribution of Res3 (presence of DHFR triple) and Res5 (presence of DHFR triple and DHPS double) infections changed over the 11 year period with Res3 infections initially increasing and then decreasing while Res5 infections started low and increased to overtake Res3 infections. The timing of the change in this composition of infection corresponds with the introduction of ACT and thus it appears that the use of ACT prompted the increased prevalence of quintuple parasites over DHFR triple and sensitive parasites. The total number of failures decreased substantially after the introduction of ACT to 17% of its previous level. The results of the base model corresponded with the observed data from the SEACAT study in terms of the magnitude and the trends of the impact of the change to ACT policy, but underestimated the impact of the vector control strategies compared to rapid effect noted in Sharp et al. [2007]. The Scenario testing of the base model showed that vector control is an effective strategy to reduce prevalence and that it is sensitive to the time at which the control is started as it decreased prevalence very gradually. The Scenario testing of the base model also showed that the introduction of ACT in Mozambique had a greater impact on reducing prevalence and that the start time of the ACT strategy did not decrease the effect on prevalence though earlier start times decreased the total number of resistance cases. The ratio of Res5 to Res3 infections increased faster when ACT was the treatment policy than when SP was the policy. Thus higher values of this ratio are associated with ACT being the treatment strategy in place. Thus differential equation modeling is an effective modeling tool to capture the spread of disease and to test the effects of policy interventions as it allows one to assess these effects on populations and averages out individual-level intricacies to better inform policy decisions.
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Kay, Katherine. "Pharmacological modelling to investigate antimalarial drug treatment". Thesis, University of Liverpool, 2013. http://livrepository.liverpool.ac.uk/12413/.

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Malaria remains a major public health concern for billions of people worldwide. Achieving the ambitious goal of malaria eradication requires co-ordination of control strategies dealing with a range of parasite, vector, human, social and environmental factors. Availability of effective antimalarial treatment is a key component in malaria control. However the number of drugs available is limited and drug resistance, particularly in Plasmodium falciparum, has now been reported for all currently available antimalarials. Mathematical models provide the opportunity to explore key features underlying antimalarial drug action, effectiveness and resistance. They further allow investigation into questions that cannot otherwise be easily addressed, either because they are too expensive, unethical or logistically too complex. This thesis aims to develop pharmacological models to investigate antimalarial drug treatment. In Chapter 2 we develop a pharmacokinetic-pharmacodynamic (PK/PD) model of antimalarial drug treatment (calibrated using published data) and use it to investigate the efficacy of artemisinin combination therapies (ACTs). Chapter 3 addresses two assumptions built into the methodology that limit the models future application. The model now allows for (i) time lags and drug concentration profiles for drugs absorbed across the gut wall and, if necessary, converted to another active form (ii) multiple drugs within a treatment regimen (iii) differing modes of drug action in combinations (iv) modelling drugs converted to an active metabolite with similar modes of action. In Chapter 4 we extend the methodology to allow for i) the presence of more than one clone when treatment begins (ii) the acquisition of new clones during treatment follow-up (iii) the tracking of individual clones using molecular markers. We then use these extensions to simulate clinical trial data to determine the best methods of analysis. Chapter 5 details how the drug action components of the extended PK/PD model were incorporated into OpenMalaria; a mathematical model of malaria epidemiology allowing investigation of the effects of various intervention strategies including malaria vaccines, vector control strategies and antimalarial drug treatment. In Chapter 6 we investigate the ability of clinical trials to accurately estimate (WoS) using the extended PK/PD model. Windows of selection (WoS) are often used to quantify the genetic process whereby parasites evolve increasing tolerance to antimalarial drugs. We noted a conspicuous lack of comprehensive, good-quality PK datasets currently available in the literature. Despite this, the models produced results highly consistent with field data. They were applied to investigate the potential implications of drug resistance and to make predications about the future effectiveness of antimalarials. We emphasise the value of mathematical models by simulating ‘field data’ to assess the best methods of analysing clinical trials and to investigate the predictive ability of WoS. While we do not suggest models can replace the information gained in clinical trials, this work does demonstrate the importance of mathematical models capable of generating results consistent with field data.
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Al, Helal Mohammad Abdullah. "Pharmacodynamics of antimalarial endoperoxide drugs". Thesis, University of Liverpool, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.526822.

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Blake, Lynn Dong. "Antimalarial Exoerythrocytic Stage Drug Discovery and Resistance Studies". Scholar Commons, 2016. http://scholarcommons.usf.edu/etd/6182.

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Malaria is a devastating global health issue that affects approximately 200 million people yearly and over half a million deaths are caused by this parasitic protozoan disease. Most commercially available drugs only target the blood stage form of the parasite, but the only way to ensure proper elimination is to treat the exoerythrocytic stages of the parasite development cycle. There is a demand for the discovery of new liver stage antimalarial compounds as there are only two current FDA approved drugs for the treatment of liver stage parasites, one of which fails to eliminate dormant forms and the other inducing hemolytic anemia in patients with G6PD deficiency. In efforts to address the dire need for liver stage drugs, we developed a high-throughput liver stage drug-screening assay to identify liver stage active compounds from a wide variety of chemical libraries with known blood stage activity. The liver stage screen led us to further investigate an old, abandoned compound known as menoctone. Menoctone was developed as a liver stage active antimalarial, however, the development of more potent compounds led to the abandonment of further menoctone research. Our research demonstrated that resistant parasites can transmit mutations through mosquitoes, which was previously believed to not be possible. Furthermore, we studied a novel genetic marker that may indicate potential resistance against malaria parasite infection and the cytotoxic effects associated with the disease. Future experiments aim to identify and advance our methods for the elimination of Plasmodium exoerythrocytic parasites.
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Książki na temat "Antimalaria- Drug"

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Silikas, Nikolaos. Rational drug design of protoberberine antimalarials. Manchester: University of Manchester, 1995.

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Csizmadia, Emanuel. Antimalarial drugs: Costs, safety and efficacy. New York: Nova Biomedical Books, 2009.

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Emanuel, Csizmadia, i Kalnoky Istvan, red. Antimalarial drugs: Costs, safety, and efficacy. Hauppauge, NY: Nova Science, 2009.

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Li, Qigui. Antimalarial drugs: Age of the artemisinins. Hauppauge, N.Y: Nova Science, 2010.

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M, Gomes, Pang L i World Health Organization, red. Interventions to improve antimalarial use. Geneva: World Health Organization, 1998.

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Organization, World Health, red. A Practical handbook on the pharmacovigilance of antimalarial medicines. Geneva, Switzerland: World Health Organization, 2008.

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Kiang, Tony K. L., Kyle John Wilby i Mary H. H. Ensom. Clinical Pharmacokinetic and Pharmacodynamic Drug Interactions Associated with Antimalarials. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-10527-7.

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Staines, Henry M. Treatment and Prevention of Malaria: Antimalarial Drug Chemistry, Action and Use. Basel: Springer Basel, 2012.

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Peters, Wallace. Chemotherapy and drug resistance in malaria. Wyd. 2. London: Academic Press, 1987.

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Central Council for Research in Unani Medicine (India), red. Potential antimalarial herbal drugs from South Eastern India: Bihar and Orissa states. New Delhi: Central Council for Research in Unani Medicine, Ministry of Health & Family Welfare, Govt. of India, 2000.

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Części książek na temat "Antimalaria- Drug"

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Adedeji, Waheed A., Tunde Balogun, Fatai A. Fehintola i Gene D. Morse. "Drug-Drug Interactions of Antimalarial Drugs". W Drug Interactions in Infectious Diseases: Antimicrobial Drug Interactions, 503–14. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-72416-4_12.

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Shah, Naman K., i Neena Valecha. "Antimalarial drug resistance". W Advances in Malaria Research, 383–407. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2016. http://dx.doi.org/10.1002/9781118493816.ch14.

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Kiang, Tony K. L., Kyle John Wilby i Mary H. H. Ensom. "Drug Interaction Potential of Antimalarial Drugs Based on Known Metabolic Properties of Antimalarials". W Clinical Pharmacokinetic and Pharmacodynamic Drug Interactions Associated with Antimalarials, 17–25. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-10527-7_3.

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Pile, Kevin D., Garry G. Graham, Constance H. Katelaris i Richard O. Day. "Antimalarial Drugs". W Compendium of Inflammatory Diseases, 97–101. Basel: Springer Basel, 2016. http://dx.doi.org/10.1007/978-3-7643-8550-7_9.

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Pile, Kevin, Garry G. Graham, Constance H. Katelaris i Richard O. Day. "Antimalarial Drugs". W Encyclopedia of Inflammatory Diseases, 1–6. Basel: Springer Basel, 2013. http://dx.doi.org/10.1007/978-3-0348-0620-6_9-1.

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Parikh, Sunil, Ming-Na Tina Lee i Francesca T. Aweeka. "Antimalarial Agents". W Drug Interactions in Infectious Diseases, 561–79. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-213-7_16.

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Tull, Thomas, i Mark Goodfield. "Antimalarials". W Handbook of Systemic Drug Treatment in Dermatology, 61–66. Wyd. 3. London: CRC Press, 2022. http://dx.doi.org/10.1201/9781003016786-7.

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Meunier, Bernard. "Towards Antimalarial Hybrid Drugs". W Polypharmacology in Drug Discovery, 423–39. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2012. http://dx.doi.org/10.1002/9781118098141.ch21.

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Rosenthal, Philip J. "Antimalarial Drug Resistance: Clinical Perspectives". W Antimicrobial Drug Resistance, 1077–90. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-595-8_27.

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Biagini, Giancarlo A., Patrick G. Bray i Stephen A. Ward. "Mechanisms of Antimalarial Drug Resistance". W Antimicrobial Drug Resistance, 561–74. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-180-2_40.

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Streszczenia konferencji na temat "Antimalaria- Drug"

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Kalogera, Eleftheria, Debarshi Roy, Ashwani Khurana, Susmita Mondal, Xiaoping He, Sean C. Dowdy i Viji Shridhar. "Abstract 261: Quinacrine in endometrial cancer: repurposing an old antimalarial drug". W Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-261.

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Kapelle, Imanuel Berly Delvis, Shielda Natalia Joris, Natelda Rosaldiah Timisela, Esther Kembauw, Marthinus Johanes Saptenno i Fransisca Kissya. "Product diversification of katang-katang leaf (Ipomoea pescaprae) as an antimalarial drug". W THE 7TH INTERNATIONAL CONFERENCE ON BASIC SCIENCES 2021 (ICBS 2021). AIP Publishing, 2023. http://dx.doi.org/10.1063/5.0113993.

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Megantara, Sandra, Jutti Levita i Slamet I. Surantaatmadja. "In Silico Study of Andrographolide as Protease Inhibitors for Antimalarial Drug Discovery". W 3rd International Conference on Computation for Science and Technology (ICCST-3). Paris, France: Atlantis Press, 2015. http://dx.doi.org/10.2991/iccst-15.2015.8.

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Rodriguez Henriquez, P., F. J. Reyes-Muciño i L. M. Amezcua-Guerra. "AB0393 Electrocardiographic disturbances in patients with rheumatoid arthritis using antimalarial drugs". W Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.5668.

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Julianto, Tatang Shabur, Rizki Ariadi Tama i Amri Setyawati. "Synthesis of aryl amino alcohol derivate from turpentine oil as a potential antimalarial drug". W 3RD INTERNATIONAL CONFERENCE ON CHEMISTRY, CHEMICAL PROCESS AND ENGINEERING (IC3PE). AIP Publishing, 2021. http://dx.doi.org/10.1063/5.0062834.

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Abbas, Jamilah, Nina Artanti, Andini Sundowo, Indah Dwiatmi Dewijanti, Muhammad Hanafi, Lisa i Din Syafrudin. "Targetting the hemozoin synthesis pathway for antimalarial drug and detected by TEM (Transmission electron microscope)". W PROCEEDINGS OF THE 3RD INTERNATIONAL SYMPOSIUM ON APPLIED CHEMISTRY 2017. Author(s), 2017. http://dx.doi.org/10.1063/1.5011930.

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Riesco Barcena, C., S. Leal Rodríguez, ME Acosta de la Vega, E. Grau García, C. Pávez Perales, AV Huaylla Quispe, M. De la Rubia i in. "PO.8.175 Antimalarial drugs and electrocardiographic alterations in patients with systemic lupus erythematosus". W 13th European Lupus Meeting, Stockholm (October 5–8, 2022). Lupus Foundation of America, 2022. http://dx.doi.org/10.1136/lupus-2022-elm2022.194.

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Fasinu, Pius. "The metabolism of the 8-aminoquinolines in relation to hemolytic toxicity: exploring current understanding for future antimalarial drug discovery". W ASPET 2023 Annual Meeting Abstracts. American Society for Pharmacology and Experimental Therapeutics, 2023. http://dx.doi.org/10.1124/jpet.122.140510.

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Tisnerat, Camille, Jérémy Schneider, René Pemha, Céline Damiani, Patrice Agnamey, Catherine Mullié, Anne Totet, Alexandra Dassonville-Klimpt i Pascal Sonnet. "Synthesis and biological evaluation of new enantiopure 4-aminoalcohol-quinoline and -fluorene hybrids as antimalarial drugs". W 6th International Electronic Conference on Medicinal Chemistry. Basel, Switzerland: MDPI, 2020. http://dx.doi.org/10.3390/ecmc2020-07397.

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"Virtual Screening the Interaction of Various Compound from Indonesian Plants with the HGXPRT Enzyme to Find a Novel Antimalarial Drug". W The 3rd International Conference on Life Sciences and Biotechnology. Galaxy Science, 2021. http://dx.doi.org/10.11594/nstp.2021.0805.

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Raporty organizacyjne na temat "Antimalaria- Drug"

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Dhawan, B. N. Evaluation of New Antimalarials. Development of New Antimalarial Drugs. Fort Belvoir, VA: Defense Technical Information Center, wrzesień 1991. http://dx.doi.org/10.21236/ada242409.

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Tesfaselassie, Elias. Antimalarial Drug Discovery using Triazoles to Overcome Chloroquine Resistance. Portland State University Library, styczeń 2000. http://dx.doi.org/10.15760/etd.2503.

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Hodson Shirley, Cheryl. The Antimalarial Activity of PL74: A Pyridine-Based Drug Candidate. Portland State University Library, styczeń 2000. http://dx.doi.org/10.15760/etd.1820.

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Basagoitia, Andrea. Do home- or community-based programmes for treating malaria improve health outcomes? SUPPORT, 2017. http://dx.doi.org/10.30846/170313.

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Prompt access to diagnosis and treatment with effective antimalarial drugs is a central component of malaria control. Home- or community-based programmes for managing malaria are one strategy that has been proposed to overcome the geographical barrier to malaria treatment. In these programmes people living in rural settings, such as mothers, volunteers, or community health workers, are trained to recognise fever and provide antimalarial medicines at a low cost or for free.
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Avery, Mitchell A. Directed Synthesis of New Antimalarials Using Computer Aided Drug Design. Fort Belvoir, VA: Defense Technical Information Center, październik 1995. http://dx.doi.org/10.21236/ada303867.

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Avery, Mitchell A. Directed Synthesis of New Antimalarials using Computer Aided Drug Design. Fort Belvoir, VA: Defense Technical Information Center, październik 1995. http://dx.doi.org/10.21236/ada304919.

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Parshikov, I. A., C. E. Hernandes-Luna i E. I. Zaraisky. Microbial transformation of the antimalarial and anticancer drug artemisinin by white-rot basidiomycetes. Global Science Publications, 2018. http://dx.doi.org/10.18411/0972-3005_n4.

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Avery, Mitchell A. Drug Development of the Antimalarial Agent Artemisinin: Total Synthesis, Analog Synthesis, and Structure-Activity Relationship Studies. Fort Belvoir, VA: Defense Technical Information Center, sierpień 1990. http://dx.doi.org/10.21236/adb152141.

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Liebman, Katherine. New 4-Aminoquinoline Compounds to Reverse Drug Resistance in P. falciparum Malaria, and a Survey of Early European Antimalarial Treatments. Portland State University Library, styczeń 2000. http://dx.doi.org/10.15760/etd.2112.

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