Relevant bibliographies by topics / Resistance to anti-malaria drugs

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Academic literature on the topic 'Resistance to anti-malaria drugs'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Resistance to anti-malaria drugs"

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Yusuf, Yenni. "ANTI-MALARIAL DRUG RESISTANCE." Majalah Kedokteran Andalas 37, no. 1 (May 3, 2015): 64. http://dx.doi.org/10.22338/mka.v37.i1.p64-69.2014.

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AbstrakTujuan studi ini adalah untuk menjelaskan mekanisme resistensi parasit malaria danusaha-usaha yang dapat dilakukan untuk menghadapi munculnya strain parasit yangresisten terhadap artemisinin. Metode yang digunakan adalah studi kepustakaan. ResistensiP.falciparum terhadap obat-obat anti malaria disebabkan oleh perubahan spontan yangterjadi pada beberapa gen seperti P.falciparum multi drug resistance1 (Pfmdr1), P.falciparumchloroquine transporter (Pfcrt), P.falciparum dihydropteroate synthase (Pfdhps), P.falciparumdihydrofolate reductase (Pfdhfr), and P.falciparum multidrug resistance-associated proteins(Pfmrp). Penyebaran resistensi tersebut dipengaruhi oleh tingkat transmisi di sebuah wilayah.WHO telah menjalankan usaha untuk menanggulangi penyebaran resistensi tersebut misalnyadengan merekomendasikan penghentian monoterapi artemisinin, dan pemberian anti malariasetelah konfirmasi laboratorium. Selain itu, perlu adanya penggunaan obat kombinasi, produksirejimen dosis tetap, dan pengembangan obat anti malaria baru. Kesimpulan dari hasil studiini ialah munculnya malaria resisten terhadap artemisinin akan menghambat usaha eradikasimalaria karena itu diperlukan usaha-usaha untuk menanggulanginya.AbstractThe objective of this study was to describe the development of anti-malarial drug resistanceof the parasites and the efforts taken to contain the emergence of artemisinin resistant malaria.This was a literature study. The development of resistance to anti-malarial drugs are due tospontaneous changes in certain genes such as of P.falciparum multi drug resistance1 (Pfmdr1),P.falciparum chloroquine resistance transporter (Pfcrt), P.falciparum dihydropteroate synthase(Pfdhps), P.falciparum dihydrofolate reductase (Pfdhfr), and P.falciparum multidrug resistanceassociatedproteins (Pfmrp). The spread of the resistance depends on the transmission ratewithin each area. WHO has established a global plan to contain the spread of this resistance,such as recommendation to withdraw artemisinin-based monotherapies and administrationof treatment after laboratory confirmation. In addition, administration of anti-malarial drugcombination, production of fixed dose regimen and development of new drugs are necessary.The Conclusion is emergence of artemisinin resistant malaria will threaten malaria eradicationthus some efforts are necessarily needed to contain it.Afiliasi penulis: Bagian Parasitologi Fakultas Kedokteran Universitas Hasanudin
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Friedrich, M. J. "Resistance to Malaria Drugs." JAMA 305, no. 7 (February 16, 2011): 663. http://dx.doi.org/10.1001/jama.2011.134.

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Vale, Valdicley Vieira, Dayse Lúcia do Nascimento Brandão, Milena Cristina Martins Da Silva, Denise Bueno, Michael Dean Green, Sandro Percário, and Maria Fani Dolabela. "Malaria parasite resistance vicious cycle." Revista Eletrônica Acervo Saúde 11, no. 18 (December 18, 2019): e1708. http://dx.doi.org/10.25248/reas.e1708.2019.

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Objective: This paper analyzes the "vicious" cycle of malaria treatment as a consequence of restricted access to anti-malarial drugs. Literature review: Lack of public health policies in affected countries limits access to medicines. This leads patients to acquire drugs in "parallel" markets under the risk of quality deviations or falsified products. The use of these products can aggravate the disease, lead to death, and contribute to parasite resistance to drugs. There are reports of Plasmodium strains resistant to different antimalarial drugs, this creates the need to look for new therapeutic alternatives. These new drugs begin to be counterfeit or people use low quality drugs, selectung resistant strains again, making necessary further research to identify other therapeutic possibilities, restarting this vicious cycle. Final considerations: Therefore, it is important to create conditions for using good quality medicines supervised by health professionals, and ensure research of new alternatives, evaluating their activity on the parasite or the disease.
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Bell, Angus, and Daniela Boehm. "Anti-disease Therapy for Malaria - ‘Resistance Proof’?" Current Pharmaceutical Design 19, no. 2 (November 1, 2012): 300–306. http://dx.doi.org/10.2174/1381612811306020300.

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Salomone, Salvatore, and Théophile Godfraind. "Drugs that reverse chloroquine resistance in malaria." Trends in Pharmacological Sciences 11, no. 11 (November 1990): 475–76. http://dx.doi.org/10.1016/0165-6147(90)90135-u.

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Rout, Usha K., A. S. Sanket, Brijesh S. Sisodia, Pradyumna K. Mohapatra, Sanghamitra Pati, Rajni Kant, and Gaurav R. Dwivedi. "A Comparative Review on Current and Future Drug Targets Against Bacteria & Malaria." Current Drug Targets 21, no. 8 (June 20, 2020): 736–75. http://dx.doi.org/10.2174/1389450121666200129103618.

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Long before the discovery of drugs like ‘antibiotic and anti-parasitic drugs’, the infectious diseases caused by pathogenic bacteria and parasites remain as one of the major causes of morbidity and mortality in developing and underdeveloped countries. The phenomenon by which the organism exerts resistance against two or more structurally unrelated drugs is called multidrug resistance (MDR) and its emergence has further complicated the treatment scenario of infectious diseases. Resistance towards the available set of treatment options and poor pipeline of novel drug development puts an alarming situation. A universal goal in the post-genomic era is to identify novel targets/drugs for various life-threatening diseases caused by such pathogens. This review is conceptualized in the backdrop of drug resistance in two major pathogens i.e. “Pseudomonas aeruginosa” and “Plasmodium falciparum”. In this review, the available targets and key mechanisms of resistance of these pathogens have been discussed in detail. An attempt has also been made to analyze the common drug targets of bacteria and malaria parasite to overcome the current drug resistance scenario. The solution is also hypothesized in terms of a present pipeline of drugs and efforts made by scientific community.
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Chahar, Madhvi, Anup Anvikar, and Neena Valecha. "Development and Evaluation of a Novel HNB Based Isothermal Amplification Assay for Fast Detection of Pyrimethamine Resistance (S108N) in Plasmodium falciparum." International Journal of Environmental Research and Public Health 16, no. 9 (May 10, 2019): 1635. http://dx.doi.org/10.3390/ijerph16091635.

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Sulphadoxine and pyrimethamine (SP) have been used as long-acting partner antimalarial drugs in artemisinin combination therapy (ACT) for falciparum malaria. The emergence and increasing spread of SP resistance in malaria-endemic areas have become a challenge for the control of malaria. Therefore, regular monitoring of the mutation status of partner drugs is important for the better management of drug policy. There are limitations with traditional molecular methods and there is an urgent need for an easy method for diagnosis of drug resistance. In this study we have introduced and developed a novel single nucleotide polymorphism loop-mediated isothermal amplification (SNP–LAMP) approach based on a hydroxynaphthol blue (HNB) indicator for the easier and quicker detection of pyrimethamine resistance in Plasmodium falciparum malaria. To implement this novel approach, many sets of LAMP primers were designed and tested. Finally, one set of forward inner primer M1 (FIPM1) of LAMP primer was selected that specifically distinguishes pyrimethamine-resistant P. falciparum malaria. The LAMP reactions were optimized at 60–66 °C for 45 min. High sensitivity (7 parasites/µL) was observed with 10−4 fold dilutions (<2 ng DNA) of genomic DNA. Moreover, this approach has the potential to be applied even in laboratories unfamiliar with PCR or other molecular methods, and in future, this can be helpful for the better management of anti-malarial policy.
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Sharma, Vijay. "Therapeutic Drugs for Targeting Chloroquine Resistance in Malaria." Mini-Reviews in Medicinal Chemistry 5, no. 4 (April 1, 2005): 337–51. http://dx.doi.org/10.2174/1389557053544029.

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Singh, Gajinder Pal. "Dimension reduction of Malaria Box data allows efficient compound prioritization." F1000Research 5 (November 18, 2016): 2701. http://dx.doi.org/10.12688/f1000research.10121.1.

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Background: New anti-malarial drugs are needed to meet the challenge of artemisinin resistance and to achieve malaria elimination and eradication. The new anti-malarial compounds are expected to have many desirable properties, such as activity against multiple stages of Plasmodium, low host cytotoxicity, and low propensity for resistance development, but whether and how these properties might be linked to each other is not clear. A better understanding of the relationship between activities of compounds against different stages of Plasmodium could help in the development of strategies to prioritize compounds with maximum potential for further development. Methods: We utilized the large amount of data that has recently been generated on 400 anti-malarial Malaria Box compounds and performed statistical analyses, such as rank correlation, hierarchical clustering, and principal-component analyses, to test associations between activities against different stages of Plasmodium, other pathogens, and human cells. Results: We found significant positive correlations between the activities of compounds against different stages of Plasmodium. Our results also show toxicity associated with assays conducted at higher compound concentrations. Principal-component analyses (PCA) of the data allowed differentiation of Plasmodium-specific activity from general toxicity and predicted success in in vitro evolution of resistance. We found that a single principal-component can capture most of the desirable properties of Malaria Box compounds and can be used to rank compounds from most desirable to least desirable activity-profile. Conclusions: Here, we provide a systematic strategy to prioritize Malaria Box compounds for further development. This approach may be applied for prioritization of anti-malarial compounds in general.
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Peters, W. "The problem of drug resistance in malaria." Parasitology 90, no. 4 (April 1985): 705–15. http://dx.doi.org/10.1017/s003118200005232x.

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The resistance in human malaria is mainly of practical importance in relation to Plasmodium falciparum. Strains resistant not only to chloroquine but also to dihydrofolate reductase inhibitors, and even to potentiating combinations of these with sulphonamides or sulphones, are appearing in an ever increasing geographical area which now includes tropical Africa and India. Few new drugs are available or foreseen for the near future, mefloquine and artemisinine being the leading contenders. It is vital that all measures possible should be taken to protect such new compounds, their deployment in the form of judiciously selected combinations with other antimalarials being an essential procedure that should be followed. Drugs in new chemical classes and with different modes of action are still urgently needed. Reliance should not be placed on drugs alone to control malaria on a community basis.
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Dissertations / Theses on the topic "Resistance to anti-malaria drugs"

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Bray, Patrick Gerrard. "Plasmodium falciparum : studies on the mechanism of chloroquine resistance and its reversal." Thesis, University of Liverpool, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.316597.

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Gunsaru, Bornface. "Simplified Reversed Chloroquines to Overcome Malaria Resistance to Quinoline-based Drugs." PDXScholar, 2010. https://pdxscholar.library.pdx.edu/open_access_etds/400.

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Malaria is a major health problem, mainly in developing countries, and causes an estimated 1 million deaths per year. Plasmodium falciparum is the major type of human malaria parasite, and causes the most infections and deaths. Malaria drugs, like any other drugs, suffer from possible side effects and the potential for emergence of resistance. Chloroquine, which was a very effective drug, has been used since about 1945, but its use is severely limited by resistance, even though it has mild side effects, and is otherwise very efficacious. Research has shown that there are chloroquine reversal agents, molecules that can reinstate antimalarial activity of chloroquine and chloroquine-like drugs; many such reversal agents are composed of two aromatic groups linked to a hydrogen bond acceptor several bonds away. By linking a chloroquine-like molecule to a reversal agent-like molecule, it was hoped that a hybrid molecule could be made with both antimalarial and reversal agent properties. In the Peyton Lab, such hybrid "Reversed Chloroquine" molecules have been synthesized and shown to have better antimalarial activity than chloroquine against the P. falciparum chloroquine-sensitive strain D6, as well as the P. falciparum chloroquine-resistant strains Dd2 and 7G8. The work reported in this manuscript involves simplifying the reversal agent head group of the Reversed Chloroquine molecules, to a single aromatic ring instead of the two rings groups described by others; this modification retained, or even enhanced, the antimalarial activity of the parent Reversed Chloroquine molecules. Of note was compound PL154, which had IC50 values of 0.3 nM and 0.5 nM against chloroquine-sensitive D6 and chloroquine-resistant Dd2. Compound PL106 was made to increase water solubility (a requirement for bioavailability) of the simplified Reversed Chloroquine molecules. Molecular modifications inherent to PL106 were not very detrimental to the antimalarial activity, and PL106 was found to be orally available in mice infected with P. yoelli, with an ED50 value of about 5.5 mg/kg/d. Varying the linker length between the quinoline ring and the protonatable nitrogen, or between the head group and the protonatable nitrogen, did not have adverse effects on the antimalarial activities of the simplified Reversed Chloroquine molecules, in accord with the trends observed for the original design of Reversed Chloroquine molecules as found from previous studies in the Peyton Lab. The simplified Reversed Chloroquine molecules even tolerated aliphatic head groups (rather than the original design which specified aromatic rings), showing that major modifications could be made on the Reversed Chloroquine molecules without major loss in activity. A bisquinoline compound, PL192, was made that contained secondary nitrogens at position 4 of the quinoline ring (PL192 is a modification of piperaquine, a known antimalarial drug that contains tertiary nitrogens at position 4 of the quinoline ring); this compound was more potent than piperaquine which had an IC50 value of 0.7 nM against CQS D6 and an IC50 of 1.5 nM against CQR Dd2, PL192 had IC50 values of 0.63 nM against chloroquine sensitive D6 and 0.02 nM against chloroquine resistant Dd2. Finally, the mechanism of action of these simplified "Reversed Chloroquines" was evaluated; it was found that the simplified "Reversed Chloroquines" behaved like chloroquine in inhibiting β-hematin formation and in heme binding. However, the simplified "Reversed Chloroquines" were found to inhibit chloroquine transport for chloroquine resistant P. falciparum chloroquine resistance transporter expressed in Xenopus oocytes to a lesser extant than the classical reversal agent verapamil. From these studies it was noted that the simplified "Reversed Chloroquines" may not behave as well as classical reversal agents would in restoring chloroquine efficacy, but they are very potent, and so could be a major step in developing drug candidates against malaria.
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Ochekpe, N. A. "Some applications of HPLC in the biguanide antimalarial drugs." Thesis, Open University, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.383660.

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Hayton, Karen. "The genetics of resistance to antifolate and sulfa drugs in malaria parasites." Thesis, University of Edinburgh, 2000. http://hdl.handle.net/1842/14032.

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Drug resistance is one of the major obstacles facing malaria control. Resistance to the combination sulfadoxine/pyrimethamine (S/P) (Fansidar) is now widespread, although the mechanism by which this arises is still not fully understood. Therefore, the molecular basis of S/P resistance was studied in the rodent malaria parasite, Plasmodium chadaubi. S/P resistant mutants were selected from a clone already resistant to the pyrimethamine, AS (PYR), caused by the presence of an asparagine at position 106 in its dihydrofolate reductase (DHFR). Two S/P resistant clones, AS (50S/P) and AS (75S/P), were selected and chosen for further analysis. AS (PYR) parasites were eliminated by S/P treatment, whereas AS (50S/P) and AS (75S/P) recrudesced following S/P pressure. However, each mutant possessed a different drug resistant phenotype. The AS (75S/P) clone always recrudesced before the AS (50S/P) clone following treatment with S/P, while AS (50S/P) always appeared before AS (75S/P) when treated with either sulfadoxine or pyrimethamine alone. Mutations in the genes encoding the targets of sulfadoxine and pyrimethamine, dihydropteroate synthase (DHPS) and DHFR, have been implicated in the mechanism of S/P resistance in P. falciparum. The P. chabaudi dhps gene was cloned by homology and sequenced. The sequence analysis of the both dhfr and dhps genes of AS (75S/P) and AS(50S/P) did not reveal any polymorphisms when compared to the sequences of the AS (PYR) genes. The mechanism of resistance of S/P in these drug-selected lines is not therefore conferred by additional mutations in these genes. To determine the genetic basis of the S/P resistance, AS (50S/P) was crossed with a drug sensitive clone, AJ. Sixteen independent recombinant progeny clones were phenotyped for their susceptibility to S/P and pyrimethamine and genotyped for the influence of 30 chromosome-specific markers. Linkage analysis shows that mutant dhfr is a major determinant of S/P resistance in P. chabaudi. Quantitative trait analysis suggested that other loci, which may be involved in S/P resistance, are present on chromosomes 4, 5, and 9.
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Visser, Hanri. "Mechanisms of resistance to new generation anti-TB drugs." Thesis, Stellenbosch : Stellenbosch University, 2015. http://hdl.handle.net/10019.1/96863.

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Thesis (MScMedSc)--Stellenbosch University, 2015.
ENGLISH ABSTRACT: Drug resistance in Mycobacterium tuberculosis is an increasing global problem. Drug resistance is mostly caused by single nucleotide polymorphisms (SNPs) within the bacterial genome. This observed increase in global incidence of drug resistant tuberculosis (TB) has sparked the search for new anti-TB drugs and the repurposing of drugs that are currently used against other organisms or species of mycobacteria. One such repurposed drug, clofazimine (CFZ), is currently used for the treatment of leprosy, caused by Mycobacterium leprae. The mechanism of action of CFZ is not clear, but it is hypothesized that CFZ is reduced by a mycobacterial type II NADH oxidoreductase (NDH-2). The reduction of CFZ drives the production of reactive oxygen species (ROS) which is toxic to the pathogen. The aim of this study was to elucidate the mechanism of CFZ resistance. Towards this aim, spontaneous in vitro CFZ resistant mutants were selected, characterized and whole genome was used identify SNPs which may cause CFZ resistance. Mutations were identified in a transcriptional regulator encoded by Rv0678, fatty-acid-AMP ligase, or FadD28 (Rv2941) and glycerol kinase or GlpK (Rv3696c). Mutations in Rv0678 have previously been shown to play a role in both CFZ resistance and bedaquiline (BDQ) cross-resistance, while no link has been found between CFZ resistance and mutations in fadD28 and glpK. The novel, non-synonymous SNP identified in Rv0678 resulted in the replacement of an alanine residue with threonine at codon 84, which is located in the DNA binding domain. Virtual modelling of the mutated Rv0678 protein showed that the A84T mutation may influence DNA binding, possibly due to its proximity to the DNA binding domain. This mutation caused a change in hydrophobicity, which may influence binding to DNA. Previous studies showed that mutations in Rv0678 resulted in the upregulation of mmpL5, a putative efflux pump. However, the mechanism whereby CFZ resistance occurs via increased abundance of this efflux pump in the cell wall is not clear and needs further investigation. The cross-resistance between CFZ and BDQ, caused by mutations in Rv0678, is of concern and may influence the planning of anti-TB drug regimens for the future. The roles of the other two mutations identified in this study in CFZ resistance is also not clear and requires further investigation. Finally, the findings of this study support the role of Rv0678 in CFZ resistance thereby suggesting that this gene could be useful as a diagnostic marker to test for CFZ resistance in clinical isolates.
AFRIKAANSE OPSOMMING: Middelweerstandigheid in Mycobacterium tuberculosis is 'n wêreldwye toenemende probleem. Middelweerstandigheid word meestal veroorsaak deur enkel nukleotied polimorfismes (SNPs) in die bakteriële genoom. Hierdie toename in middelweerstandige tuberkulose (TB) het gelei tot die soektog na nuwe anti-TB-middels en die alternatiewe aanwending van middels wat tans teen ander organismes of spesies van mikobakterieë gebruik word. Een so 'n alternatiewe middel, clofazimine (CFZ), word tans gebruik vir die behandeling van melaatsheid wat veroorsaak word deur Mycobacterium leprae. CFZ se meganisme van werking is nie duidelik nie, maar dit word vermoed dat CFZ gereduseer word deur 'n mikobakteriële tipe II NADH oksidoreduktase (NDH-2). Die reduksie van CFZ dryf die produksie van reaktiewe suurstof spesies wat giftig is vir die patogeen. Die doel van hierdie studie was om die meganisme van CFZ weerstandigheid te ondersoek. Om hierdie doel te bereik was spontane in vitro CFZ weerstandige mutante gekies, gekarakteriseer en heel genoom volgorde bepaling is gebruik om SNPs te identifiseer wat CFZ weerstandigheid veroorsaak. Mutasies in Rv0678, 'n transkripsie reguleerder, vetsuur-AMP ligase, of FadD28 (Rv2941) en gliserol kinase of GlpK (Rv3696c) geïdentifiseer. Dit is al voorheen gevind dat mutasies in Rv0678 ‘n rol speel in beide CFZ weerstandigheid en bedaquiline (BDQ) kruis-weerstandigheid, terwyl geen verband gevind is tussen CFZ weerstandigheid en mutasies in fadD28 en glpK nie. Die nuwe, nie-sinonieme SNP, geïdentifiseer in Rv0678 het gelei to die vervanging van 'n alanien aminosuur met treonien by kodon 84, wat geleë is in die DNS bindings domein. Virtuele modellering van die gemuteerde Rv0678 proteïen het getoon dat die A84T mutasie DNS binding moontlik kan beïnvloed, as gevolg van sy nabyheid aan die DNS bindings domein. Hierdie mutasie veroorsaak 'n verandering in die hidrofobiese natuur, wat DNS binding kan beïnvloed. Vorige studies het getoon dat mutasies in Rv0678 lei tot die opregulering van mmpL5, 'n waarskynlike uitvloei pomp. Die meganisme waardeur CFZ weerstandigheid veroorsaak, deur ‘n groot aantal van hierdie uitvloei pompe in die selwand, is nie duidelik nie en moet verder ondersoek word. Die kruis-weerstandigheid tussen CFZ en BDQ, wat veroorsaak word deur mutasies in Rv0678, is van belang en kan die beplanning van anti-TB middel behandeling vir die toekoms beïnvloed. Die rolle van die ander twee mutasies, wat in hierdie studie geïdentifiseer is, in CFZ weerstandigheid is ook nie duidelik nie en vereis verdere ondersoek. Ten slotte, die bevindinge van hierdie studie steun die rol van Rv0678 in CFZ weerstandigheid en dit dui daarop dat hierdie geen gebruik kan word as 'n diagnostiese merker om vir CFZ weerstandigheid te toets in kliniese isolate.
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Matthews, Amanda. "A Mathematical Model for Anti-Malarial Drug Resistance." VCU Scholars Compass, 2009. http://scholarscompass.vcu.edu/etd/1721.

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Despite the array of medical advances of our modern day society, infectious diseases still plague millions of people worldwide. Malaria, in particular, causes substantial suffering and death throughout both developed and developing countries. Aside from the socioeconomic challenges presented by the disease's prevalence in impoverished nations, one of the major difficulties scientists have encountered while attempting to eradicate the disease is the parasite's ability to become resistant to new drugs and methods of treatment. In an effort to better understand the dynamics of malaria, we analyze a mathematical model that accounts for both the treatment aspect as well as the drug resistance that accompanies it. Simulations demonstrating the effects of treatment rates and the level of resistance are studied and discussed in hopes of shedding additional light on the characteristics of this devastating epidemic.
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Adagu, Ipemida Sullayman. "Pharmacological and molecular characterisation of Plasmodium falciparum isolates from Zaria, Nigeria." Thesis, London School of Hygiene and Tropical Medicine (University of London), 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.336559.

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White, Alex William. "The design of novel inhibitors of poly (ADP-ribose) polymerase to potentiate cytotoxic drugs." Thesis, University of Newcastle Upon Tyne, 1996. http://hdl.handle.net/10443/1025.

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The abundant nuclear enzyme poly (ADP-ribose)polymerase (P ARP) catalyses the formation of long homopolymeric chains of ADP-ribose, utilising NAD+ as a substrate, as the immediate cellular response to DNA damage. PARP recognises a damaged section of DNA and initiates polymer synthesis, which is believed to act as a signal to effect the repair of the lesion. A selective, potent PARP inhibitor could block the recognition, and hence repair, of DNA damage induced by cancer chemotherapy. Since increased DNA repair is regarded as a mechanism whereby tumour cells can become resistant to treatment, PARP inhibitors have therapeutic potential as resistance modifying agents. From a study of PARP inhibitors such as 3-hydroxybenzarnide (A), benzimidazole derivatives (B) were proposed as inhibitors of the enzyme, and the synthesis and biological evaluation of a series of such molecules has been achieved. Substituted 2-aryl benzirnidazoles have proved to be highly potent PARP inhibitors (B;R= 4'NO2Ph, IC5o= 59 nM), under a permeabilised cell assay the nitro phenyl derivative (B; R= 4'N02Ph) is the most potent compound reported to date (IC50= 19 nM). 2-Methyl benzirnidazole-4-carboxamide (B; R= Me) has been shown to potentiate the in vitro cytotoxicity of the antitumour agent temozolomide in L1210 cells, and the synthesis of benzimidazole inhibitors suitable for pre-clinical in vivo eluation has also been investigated, This thesis demonstrates that benzimidazole PARP inhibitors have promising potential for clinical development as resistance modifying agents.
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Smith, Victoria. "Mechanisms of resistance to novel cell signalling inhibitor based anti-cancer drugs." Thesis, Institute of Cancer Research (University Of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.271024.

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Lindström, Anna. "Resistance to antiviral drugs in HIV and HBV /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-239-X/.

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Books on the topic "Resistance to anti-malaria drugs"

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Hiscox, Stephen, Julia Gee, and Robert I. Nicholson, eds. Therapeutic Resistance to Anti-Hormonal Drugs in Breast Cancer. Dordrecht: Springer Netherlands, 2009. http://dx.doi.org/10.1007/978-1-4020-8526-0.

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Arrow, Kenneth Joseph, Hellen Gelband, and Claire Panosian. Saving lives, buying time: Economics of malaria drugs in an age of resistance. Edited by Institute of Medicine (U.S.). Committee on the Economics of Antimalarial Drugs and NetLibrary Inc. Washington, D.C: National Academies Press, 2004.

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Julia, Gee, Nicholson Robert I, and SpringerLink (Online service), eds. Therapeutic Resistance to Anti-Hormonal Drugs in Breast Cancer: New Molecular Aspects and their Potential as Targets. Dordrecht: Springer Netherlands, 2009.

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Enzybiotics: Antibiotic enzymes as drugs and therapeutics. Hoboken, N.J: John Wiley & Sons, 2010.

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Chŏng, Yun-hŭi. Chʻuksan hwanʼgyŏng ŭi naesŏng chosa mit yŏnghyang pʻyŏngka =: A study on antibiotic resistance and effect assessment in domestic livestock environment. [Seoul]: Sikpʻum Ŭiyakpʻum Anjŏnchʻŏng, 2007.

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

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Policies and incentives for promoting innovation in antibiotic research. [S.l.]: European Observatory on Health Systems and Policies, 2010.

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Arora, Gunjan, Andaleeb Sajid, and Vipin Chandra Kalia, eds. Drug Resistance in Bacteria, Fungi, Malaria, and Cancer. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-48683-3.

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Antimicrobial drug resistance. [Totowa, N.J.]: Humana Press, 2009.

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Global Project on Anti-tuberculosis Drug Resistance Surveillance 1994-1997. Anti-tuberculosis drug resistance in the world. Geneva: Global Tuberculosis Programme, WHO, 1997.

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Book chapters on the topic "Resistance to anti-malaria drugs"

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Bhetariya, Preetida J., Neha Sharma, Pragati Singh, Priyanka Tripathi, Santosh K. Upadhyay, and Poonam Gautam. "Human Fungal Pathogens and Drug Resistance Against Azole Drugs." In Drug Resistance in Bacteria, Fungi, Malaria, and Cancer, 387–428. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-48683-3_18.

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Mehlotra, Rajeev K., and Peter A. Zimmerman. "Resistance to Antimalarial Drugs: Parasite and Host Genetic Factors." In Malaria: Genetic and Evolutionary Aspects, 81–124. Boston, MA: Springer US, 2006. http://dx.doi.org/10.1007/0-387-28295-5_5.

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Satake, Kazuhiro, Yu Toyoda, and Hiroshi Nakagawa. "Drugs Affecting Epigenetic Modifications of ABC Transporters for Drug Resistance." In Resistance to Targeted Anti-Cancer Therapeutics, 273–97. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-09801-2_11.

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Lange, Joep M. A., and Julio S. G. Montaner. "Anti-Retroviral Therapy and Resistance to Anti-Retroviral Drugs." In AIDS Pathogenesis, 221–42. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-017-0685-8_13.

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Audino, Anthony N., and Mitchell S. Cairo. "Resistance to Checkpoint Blockade Inhibitors and Immunomodulatory Drugs." In Resistance to Targeted Anti-Cancer Therapeutics, 155–79. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-24424-8_7.

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Patel, Atish, De-Shen Wang, Hong-May Sim, Suresh V. Ambudkar, and Zhe-Sheng Chen. "ABC Transporter Modulatory Drugs from Marine Sources: A New Approach to Overcome Drug Resistance in Cancer." In Resistance to Targeted Anti-Cancer Therapeutics, 183–208. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-09801-2_8.

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Patel, Atish, De-Shen Wang, Hong-May Sim, Suresh V. Ambudkar, and Zhe-Sheng Chen. "Erratum to: ABC Transporter Modulatory Drugs from Marine Sources: A New Approach to Overcome Drug Resistance in Cancer." In Resistance to Targeted Anti-Cancer Therapeutics, E1. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-09801-2_12.

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Wang, Man-Tzu, Hongmei Jiang, Debasish Boral, and Daotai Nie. "Cancer Stem Cells in Resistance to Cytotoxic Drugs: Implications in Chemotherapy." In Resistance to Targeted Anti-Cancer Therapeutics, 151–61. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7070-0_8.

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Wollheim, Frank A. "Mechanisms of Gold Resistance." In Basis for Variability of Response to Anti-Rheumatic Drugs, 178–83. Basel: Birkhäuser Basel, 1988. http://dx.doi.org/10.1007/978-3-0348-9160-8_16.

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Cappuzzo, Federico. "Resistance to anti-angiogenic drugs and therapeutic options." In Guide to Targeted Therapies: Treatment Resistance in Lung Cancer, 61–66. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-20741-4_6.

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Conference papers on the topic "Resistance to anti-malaria drugs"

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Settleman, Jeff. "Abstract IA09: Non-mutational resistance to anti-cancer drugs." In Abstracts: AACR Precision Medicine Series: Targeting the Vulnerabilities of Cancer; May 16-19, 2016; Miami, FL. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1557-3265.pmccavuln16-ia09.

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Corso, Simona, Maria Apicella, and Silvia Giordano. "Abstract B12: Understanding the role of the tumor microenvironment in mediating resistance to anti-MET drugs." In Abstracts: AACR Precision Medicine Series: Drug Sensitivity and Resistance: Improving Cancer Therapy; June 18-21, 2014; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1557-3265.pms14-b12.

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Dereli-Korkut, Zeynep, and Sihong Wang. "Microfluidic Cell Arrays to Mimic 3D Tissue Microenvironment." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80411.

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Abstract:
We developed a functional high throughput 3D microfluidic living cell array (MLC) for anti-cancer drug screening and mechanism discovery. Contemporary drug screening methods suffer from low sample throughput and lack of abilities of mimicking the 3D microenvironment of mammalian tissues. The poor performance of anti-cancer drugs limits the efficacy at controlling the complex disease system like cancer. Systematic studies of apoptotic signaling pathways can be prominent approaches for searching active and effective treatments with less drug resistance. Hence, innovative bio-devices are needed to represent tumor microenvironment to understand the molecular signatures of apoptosis for testing new anticancer therapies targeting apoptosis. Our novel 3D MLC design is the prototype of a high-throughput drug screening platform targeting apoptotic signaling pathways.
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Shimoda, M., Y. Chihara, N. Kagara, Y. Naoi, A. Shimomura, K. Shimazu, SJ Kim, and S. Noguchi. "Abstract P3-06-05: Importance of TGFβ-SMAD3 axis in resistance to anti-HER2 drugs." In Abstracts: Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium; December 8-12, 2015; San Antonio, TX. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.sabcs15-p3-06-05.

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Balasaniantc, Goar, Zhanna Rakisheva, Anna Zepke, Akmaral Akisheva, and Nataliya Solovjeva. "Spreading of resistance to group A anti-tuberculosis drugs among TB patients in Astana city." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa4744.

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Berger, C. A., C. Allender, M. N. Hunat, A. G. Sedusta, C. A. Sacopon, J. Sabalboro, J. E. Bascuña, et al. "Frequency of Herero-Resistance to First- and Second-Line Anti-Tuberculosis (TB) Drugs in a Population-Based Sample of Drug-Resistant TB Patients." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a5165.

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Panova, Anna, Anatoliy Vinokurov, Denis Lagutkin, Alexandra Gracheva, Aleksander Nikolaev, Anastasia Samoilova, and Irina Vasilyeva. "Application of next-generation sequencing to detect MTB resistance to first- and second-line anti-TB drugs." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.1605.

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Chhajed, Prashant N., Arvind Kate, H. S. Sandeepa, Parag Chaudhari, Santhakumar Subramanian, David Miedinger, Joerg Leuppi, and Michael Tamm. "Resistance Pattern To WHO CATEGORY IV Anti-Tuberculous Drugs In Patients Suspected Of Multidrug Resistance Tuberculosis Presenting To A Specialist Clinic In Mumbai, India." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a3310.

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Wallin, Jeffrey J., Jane Guan, Yang Xiao, Tom O'Brien, Marcia Belvin, and Lori S. Friedman. "Abstract 298: Mutant PIK3CA increases the expression of individual tubulin isoforms and promotes resistance to anti-mitotic chemotherapy drugs." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-298.

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Wu, Xiaojuan, Hui Xiao, Chenglong Li, and Jiayuh Lin. "Abstract 2050: Persistent STAT3 signaling contributes to the resistance of anti cancer drugs doxorubicin and cisplatin, and MEK inhibitor AZD6244 in human sarcoma cells." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-2050.

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Reports on the topic "Resistance to anti-malaria drugs"

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Gunsaru, Bornface. Simplified Reversed Chloroquines to Overcome Malaria Resistance to Quinoline-based Drugs. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.400.

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Collins, Tammy R., and Tao-shih Hsieh. Mechanistic Basis of Sensitivity/Resistance Towards Anti-Cancer Drugs Targeting Topoisomerase II. Fort Belvoir, VA: Defense Technical Information Center, April 2005. http://dx.doi.org/10.21236/ada437191.

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Collins, Tammy R., and Tao-shih Hsieh. Mechanistic Basis of Sensitivity/Resistance Towards Anti-cancer Drugs Targeting Topoisomerase II. Fort Belvoir, VA: Defense Technical Information Center, April 2006. http://dx.doi.org/10.21236/ada455978.

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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, January 2000. http://dx.doi.org/10.15760/etd.2112.

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