Relevant bibliographies by topics / Malaria – Gene therapy

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Malaria – Gene therapy'

Author: Grafiati
Published: 10 December 2022
Last updated: 31 July 2025

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Journal articles on the topic "Malaria – Gene therapy"

1

Rodrigues, Mauricio M., and Irene S. Soares. "Gene-therapy for malaria prevention." Trends in Parasitology 30, no. 11 (2014): 511–13. http://dx.doi.org/10.1016/j.pt.2014.09.005.

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Shehzad, Raafay. "Gene Therapy: A Promising Therapeutic Strategy for Malaria." University of Ottawa Journal of Medicine 8, no. 2 (2018): 40–44. http://dx.doi.org/10.18192/uojm.v8i2.3651.

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 Malaria is a serious illness caused by the Plasmodium parasite, which places approximately 3.5 billion people at risk. Currently, preventative measures are key in combatting this disease. However, gene therapy is an emerging field that shows promising results for the treatment of malaria, by modifying cells through the delivery of genetic material. Most notable was the discovery of CRISPR-Cas9, which not only allows deleterious mutations to be repaired, but does so with specificity, speed, and simplicity. There are numerous ongoing trials focusing on gene therapy in
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Zhang, De-Liang, Jian Wu, Binal N. Shah, et al. "Erythrocytic ferroportin reduces intracellular iron accumulation, hemolysis, and malaria risk." Science 359, no. 6383 (2018): 1520–23. http://dx.doi.org/10.1126/science.aal2022.

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Malaria parasites invade red blood cells (RBCs), consume copious amounts of hemoglobin, and severely disrupt iron regulation in humans. Anemia often accompanies malaria disease; however, iron supplementation therapy inexplicably exacerbates malarial infections. Here we found that the iron exporter ferroportin (FPN) was highly abundant in RBCs, and iron supplementation suppressed its activity. Conditional deletion of the Fpn gene in erythroid cells resulted in accumulation of excess intracellular iron, cellular damage, hemolysis, and increased fatality in malaria-infected mice. In humans, a pre
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Osman Mirghani, Hyder, Nasser Mansour M Alatawi, Mazan Turki M Alenzi, et al. "Association between Sickle Cell Anemia and Malaria: A Systematic Review of Previous Literature." Saudi Medical Horizons Journal 3, no. 3 (2023): 118–30. http://dx.doi.org/10.54293/smhj.v3i3.82.

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Background: Sickle cell disease (SCD) is a hereditary illness that is prevalent in malaria-prone locations. In these endemic locations, it has historically been linked to high rates of childhood death. This shows that SCD patients with malaria should start effective anti-malarial medication very away. Proguanil was a suitable chemoprophylaxis treatment for these individuals to reduce the prevalence of asymptomatic parasitization and avoid malaria. Sulphadoxine-Pyrimethamine Intermittent Preventive Treatment (IPT) has also demonstrated significant promise in lowering malaria and anemia incidenc
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Ummukulsum Mustapha, Ado Shehu, Attahir Sa’ad Ayuba, et al. "Prevalence of multi drug resistance malaria among patients aged 0 – 14 years attending murtala muhammad specialist hospital Kano State, Nigeria." International Journal of Biological and Pharmaceutical Sciences Archive 6, no. 2 (2023): 037–46. http://dx.doi.org/10.53771/ijbpsa.2023.6.2.0089.

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The Plasmodium falciparum multidrug resistance gene 1 (pfmdr1) is a molecular marker of parasite susceptibility to anti-malarial drugs. This study aimed to evaluate multidrug resistance resistance gene 1 (MDR1) mutation in 0-14years old malaria patients attending Murtala Muhammad Specialist Hospital, Kano, Nigeria. Samples from 100 children with malaria were examined to confirm the malaria parasite density and further genotyped via BigDye (v3.1) terminator cycle sequencing for the presence of two SNPs in pfmdr1on samples with high and moderate parasite densities. All data were analyzed using P
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Oboh, Mary Aigbiremo, Daouda Ndiaye, Hiasindh Ashmi Antony, et al. "Status of Artemisinin Resistance in Malaria Parasite Plasmodium falciparum from Molecular Analyses of the Kelch13 Gene in Southwestern Nigeria." BioMed Research International 2018 (October 3, 2018): 1–5. http://dx.doi.org/10.1155/2018/2305062.

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Evolution and spread of malaria parasite Plasmodium falciparum capable of evading antimalarials are the prime concern to malaria control. The currently effective drug, artemisinin (ART), is under threat due to detection of ART-resistant P. falciparum parasites in the Southeast Asian countries. It has been shown that amino acid (AA) mutations at the P. falciparum Kelch13 (Pfk13) gene provide resistance to ART. Nigeria, a part of the Sub-Saharan Africa, is highly endemic to malaria, contributing quite significantly to malaria, and resistance to chloroquine (CQ) and sulfadoxine-pyrimethamine (SP)
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Sinha, Swati, Supriya Sharma, Kuldeep Singh, et al. "Efficacy and safety of Artemisinin Combination Therapy for the treatment of uncomplicated Plasmodium falciparum malaria across international borders of India." Journal of Vector Borne Diseases 61, no. 1 (2024): 81–89. http://dx.doi.org/10.4103/0972-9062.392254.

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Background & objectives: Malaria due to Plasmodium falciparum (Pf) remains a major public threat in India. Artemisinin-based combination therapy (ACT) has been the country’s first-line drug for uncomplicated Pf malaria. In 2013-2014, Artesunate plus sulfadoxine (AS+SP) was replaced by Artemether Lumefantrine (AL) as the first- line antimalarial in North East (NE) states of the country which are endemic for Pf malaria. Regular monitoring of antimalarial drugs is of utmost importance to achieve the goal of elimination. This study aimed to assess the efficacy and safety of ACT for treating un
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Suwandi, Jhons Fatriyadi, Betta Kurniawan, Hanna Mutiara, and Aila Karyus. "PfCRT GENE POLYMORPHISMS IN PLASMODIUM FALCIPARUM ISOLATES FROM MALARIA PATIENTS IN MALARIA ENDEMIC AREAS USING ACT AS STANDARD THERAPY." Majalah Kedokteran Sriwijaya 54, no. 1 (2022): 15–21. http://dx.doi.org/10.32539/mks.v54i1.15137.

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The pfcrt gene is a biomarker to determine the resistance of Plasmodium falciparum to chloroquine and amodiaquine. When chloroquine was switched to ACT, it is very likely that there will be an increase in wild type strains (pfcrt K76) due to the absence of exposure to chloroquine. Currently chloroquine has not used for malaria treatment. The aims of this study were to identify polymorphisms in the pfcrt gene and phylogenetic analysis of Plasmodium falciparum isolates from malaria patients in Pesawaran Regency, Lampung Province. This research is a laboratory research by analyzing blood samples
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Shittu, Khadijah Abubakar, Ummukulsum Mustapha, Zainab Ummi Mansur, and Abdullahi Abdulkadir Imam. "Detection of Multidrug Resistance Gene 1 (MDR1) Mutation from <i>Plasmodium Falciparum</i> Isolated from some Patients in Kano Metropolis." Dutse Journal of Pure and Applied Sciences 11, no. 1b (2025): 112–25. https://doi.org/10.4314/dujopas.v11i1b.13.

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It has been suspected that the diminishing efficacy of artemisinin-based combination therapies, which are presently the primary therapy for malaria globally, is causing people most especially in northern Nigeria to resort to using alternative antimalarials. To bolster evidence- based strategies for managing resistance, Scientists studied mutations linked to antimalarial resistance in the pfmdr1 gene of Plasmodium falciparum. The study involved the recruitment of one hundred adult malaria patients. Blood samples were examined via microscopy to ascertain the presence of the malaria parasite. The
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Zubair, Abdulhamid Abubakar, Gabriel Adegboyega Ajibade, Ali Ahmed Haroun, et al. "Molecular Surveillance of Artemisinin Combination Therapy Resistance Markers in Kelch13 Gene of Plasmodium falciparum Isolates Collected From Yobe State Nigeria." Avicenna Journal of Clinical Microbiology and Infection 11, no. 2 (2024): 87–96. http://dx.doi.org/10.34172/ajcmi.3524.

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Background: Despite the discovery of artemisinin and artemisinin combination therapies (ACTs), resistance emerged due to single-nucleotide polymorphisms (SNPs) at the Kelch13 propeller domain of Plasmodium falciparum; the predominant parasite causing malaria. This research aimed at surveying the gene responsible for reduced parasite clearance of the first-line antimalarial ACT in Yobe State, Nigeria. Methods: This study analyzed the blood samples of 300 patients (18-50 years) from 3 different hospitals in Yobe State for malaria using a rapid diagnostic test (malarial strip test). The Giemsa mi
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Dissertations / Theses on the topic "Malaria – Gene therapy"

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Bockstael, Olivier. "Evaluation of gene transfer strategies using recombinant adeno-associated viruses for Parkinson's disease cell and gene therapy." Doctoral thesis, Universite Libre de Bruxelles, 2010. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/210010.

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La maladie de Parkinson se caractérise entre autres par une dégénérescence progressive des neurones dopaminergiques de la substance noire pars compacta (SNpc) qui innervent le striatum. Cette dégénération entraîne une baisse de la sécrétion de dopamine dans le striatum qui est responsable de la majorité des symptômes moteurs de la maladie de Parkinson. Plusieurs approches ont été étudiées pour le traitement de la maladie de Parkinson :i) restaurer une synthèse de dopamine dans le striatum par une greffe striatale de neurones dopaminergique ou par un transfert striatal de gènes impliqués dans l
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Maire, Séverine. "Towards Trans-Splicing Gene Therapy for HD : Intronic Targets Identification in the Huntingtin Gene." Thesis, Université Paris-Saclay (ComUE), 2018. http://www.theses.fr/2018SACLS054.

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La maladie de Huntington (MH) est une maladie autosomale dominante causée par une expansion de la répétition CAG codant pour une expansion de la polyglutamine dans le premier exon du gène Huntingtine (HTT). Ce gène code pour une protéine ubiquitaire dont la mutation entraine de graves symptômes moteurs, psychiatriques et cognitifs, dus à la dégénérescence spécifique des neurones GABAergique épineux moyens du striatum. Nous proposons d'utiliser le trans-épissage pour développer un vecteur de thérapie génique qui réduira significativement voir éliminera l'expression de la protéine mutée tout en
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Costa, Verdera Helena. "Towards the development of a gene therapy for Pompe disease : Characterization of the immune phenotype in Pompe disease and comparison of the therapeutic potential of gene therapy with the current standard of care." Electronic Thesis or Diss., Sorbonne université, 2019. http://www.theses.fr/2019SORUS516.

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La maladie de Pompe est une maladie lysosomale causée par des mutations sur l'enzyme α-glucosidase acide (GAA), responsable de la dégradation du glycogène lysosomal. Le déficit en GAA provoque l'accumulation de glycogène dans de multiples tissus, conduisant à une maladie neuromusculaire complexe avec une morbidité et mortalité élevées. En plus des symptômes connus, nos études montrent que le déficit en GAA affecte l’activation et le fonctionnement des cellules immunitaires chez les patients et le modèle murin de la maladie de Pompe. En particulier, nous avons observé une suractivation des cell
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Hajjar, Hélène. "Gene therapy approach on Charcot-Marie-Tooth type 1A rats." Thesis, Montpellier, 2018. http://www.theses.fr/2018MONTT027/document.

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La myéline est une gaine formée par l’enroulement de la membrane plasmique de la cellule de Schwann autour de l’axone dans le nerf périphérique. Lorsque cette gaine est détruite, on parle de démyélinisation, cela provoque de nombreuses maladies, dont les maladies de Charcot Marie Tooth (CMT) de type 1. Les maladies CMT sont héréditaires et atteignent le système nerveux périphérique. Les symptômes communs incluent : une faiblesse musculaire, une démarche maladroite, des troubles de l’équilibre et des pieds très cambrés ou très plats. Le type le plus fréquent est la forme autosomique dominante C
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Sánchez, Moreno Xavier. "Desenvolupament d'una aproximació de teràpia gènica pel tractament de la malaltia de Niemann-Pick tipus C2." Doctoral thesis, Universitat Autònoma de Barcelona, 2020. http://hdl.handle.net/10803/670821.

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La malaltia de Niemann-Pick tipus C2 (NPC2) és una malaltia minoritària d’acumulació lisosòmica (LSD, Lysosomal Storage Disease) d’herència autosòmica recessiva, causada per la deficiència de la NPC2. La proteïna NPC2 intervé en la sortida del colesterol no esterificat del compartiment endo-lisosòmic. La seva deficiència resulta en l’acumulació patològica del colesterol no esterificat als lisosomes, que condueix a la disfunció i mort cel·lular. Com a conseqüència, el pacients desenvolupen una patologia neurològica severa i de caràcter progressiu, que inclou l’atàxia cerebel·losa, la disàrtria
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Rouvière, Laura. "Transfert de gènes dans un modèle murin de la maladie de Sandhoff à l'aide d'un vecteur scAAV9 : intérêt d'une double voie d'administration ?" Thesis, Sorbonne Paris Cité, 2017. http://www.theses.fr/2017USPCB052/document.

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La maladie de Sandhoff est une maladie génétique rare due à des mutations du gène HEXB. Elle se caractérise par un double déficit en hexosaminidase A (αβ) et B (ββ), responsable d’une accumulation de ganglioside GM2 essentiellement dans le système nerveux central (SNC). Cliniquement, la maladie débute dès les premiers mois de vie et le décès survient vers l’âge de 3 ans. A ce jour, aucun traitement n’est disponible pour cette maladie. Le modèle murin obtenu par invalidation du gène Hexb est un bon outil pour le développement d’approches thérapeutiques, car il présente un phénotype proche de la
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COLANTUONI, MARIASILVIA. "Sviluppo preclinico di terapia genica basato sull'espressione di IL-1RA per il trattamento di malattia autoinfiammatorie." Doctoral thesis, Università Vita-Salute San Raffaele, 2022. http://hdl.handle.net/20.500.11768/133061.

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Le malattie autoinfiammatorie sistemiche si manifestano quando il sistema immunitario viene attivato in maniera incontrollata. Un sottogruppo cardinale di queste malattie comprende rare febbri periodiche caratterizzate dalla produzione disregolata della citochina proinfiammatoria interleuchina-1 (IL-1). Non esiste una cura per queste condizioni. Anakinra, il farmaco rappresentante la ricombinante dell'antagonista del recettore IL-1 (IL-1RA), è la terapia principale per questi pazienti. Tuttavia, l’anakinra ha una breve emivita e una scarsa distribuzione dei tessuti. I pazienti gravi rispondono
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Rousselot, Lisa. "Impacts de la modulation du cholestérol cérébral dans la maladie de Parkinson." Electronic Thesis or Diss., université Paris-Saclay, 2023. http://www.theses.fr/2023UPASQ079.

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La maladie de Parkinson (MP) est la maladie neurodégénérative liée à l'âge la plus répandue après la maladie d'Alzheimer. En conséquence, sa prévalence passe de 1% de la population âgée de 50 à 59 ans à 10% de celle âgée de 70 à 79 ans en Europe, en Asie et en Amérique du Nord. Une estimation préoccupante prévoit que le nombre de cas de MP pourrait doubler d'ici 2030 pour atteindre environ 9 millions, alors qu'il n'existe pas de traitement curatif de la MP. Son diagnostic clinique est assez fiable et doit inclure une bradykinésie et au moins une rigidité musculaire, des tremblements au repos o
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Rodríguez, Aguilar Ester. "Caracterització i anàlisi del potencial terapèutic de l’Adenovirus 5/40 quimèric de tropisme específic intestinal com a vector de teràpia gènica per al tractament de la malaltia inflamatòria intestinal." Doctoral thesis, Universitat Autònoma de Barcelona, 2015. http://hdl.handle.net/10803/377475.

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La Malaltia Inflamatòria Intestinal (IBD) engloba un grup de malalties (com la CD i la UC) que es caracteritzen per una inflamació crònica del tub digestiu. La IBD requereix un tractament mèdic i farmacològic a mida, i tot i que actualment existeixen diferents teràpies que permeten millorar la qualitat de vida dels pacients, cap d’aquestes aconsegueix eliminar totalment la malaltia. La teràpia gènica és una de les disciplines de la biomedicina amb més futur pel tractament de malalties d’origen genètic, però també en malalties en que la patologia no està determinada per un sol gen sinó que h
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Vila, Julià Ferran. "Avenços en la teràpia gènica per al MNGIE amb vectors adenoassociats: validació en un model millorat de la malaltia i optimització de seqüència del gen terapèutic." Doctoral thesis, Universitat Autònoma de Barcelona, 2021. http://hdl.handle.net/10803/671813.

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El MNGIE és una malaltia mitocondrial d’herència autosòmica recessiva causada per mutacions en el gen TYMP, que codifica l’enzim timidina fosforilasa (TP). La TP catalitza la degradació de timidina (dThd) i desoxiuridina (dUrd), i la seva absència en pacients causa l’acumulació sistèmica d’aquests metabòlits, tòxica per la funció mitocondrial. A dia d’avui les úniques teràpies efectives són el transplantament de cèl·lules mare hematopoètiques i el transplantament de fetge. No obstant, els transplantaments estan limitats per la necessitat d’un donant compatible i tenen una taxa de mortalitat i
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Books on the topic "Malaria – Gene therapy"

1

V, Rabins Peter, ed. The 36-hour day: A family guide to caring for people with Alzheimer disease, other dementias, and memory loss in later life. 4th ed. Johns Hopkins University Press, 2006.

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V, Rabins Peter, ed. The 36-hour day: A family guide to caring for people who have Alzheimer disease, other dementias, and memory loss in later life. 4th ed. Wellness Central, 1999.

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V, Rabins Peter, ed. The 36-hour day: A family guide to caring for persons with Alzheimer's disease, related dementing illnesses, and memory loss in later life. Johns Hopkins University Press, 1991.

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V, Rabins Peter, ed. The 36-hour day: A family guide to caring for people who have Alzheimer Disease, related dementias, and memory loss. Grand Central Life & Style, 2012.

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V, Rabins Peter, ed. The 36-hour day: A family guide to caring for people who have alzheimer disease, related dementias, and memory loss. 5th ed. Johns Hopkins University Press, 2011.

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36-Hour Day: A Family Guide to Caring for People Who Have Alzheimer Disease, Other Dementias, and Memory Loss. Johns Hopkins University Press, 2017.

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36-Hour Day: The Compassionate Guide to Caring for Someone with Dementia. Johns Hopkins University Press, 2021.

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36-Hour Day: A Family Guide to Caring for People Who Have Alzheimer Disease, Other Dementias, and Memory Loss. Johns Hopkins University Press, 2017.

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The 36-Hour Day, sixth edition : The 36-Hour Day: A Family Guide to Caring for People Who Have Alzheimer Disease, Other Dementias, and Memory Loss. John Hopkins University Press, 2017.

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The 36-Hour Day: A Family Guide to Caring for Persons with Alzheimer Disease, Related Dementing Illnesses, and Memory Loss in Later Life. John Hopkins University Press, 1999.

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Book chapters on the topic "Malaria – Gene therapy"

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Daltry, Jennifer C., Wolfgang Wuster, and Roger S. Thorpe. "The role of ecology in determining venom variation in the Malayan pitviper, Calloselasma rhodostoma." In Venomous Snakes. Oxford University PressOxford, 1996. http://dx.doi.org/10.1093/oso/9780198549864.003.0012.

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Abstract Intraspecific variation in snake venom composition is a widespread phenomenon with important implications for snakebite therapy, yet few attempts have previously been made to identify its cause. The venom from almost 100 Malayan pitvipers (Calloselasma rhodostoma), captured in 36 localities in Vietnam, Thailand, Malaysia and Java, was analysed by using isoelectric focusing (IEF). A clear pattern of geographic variation emerged in the IEF profiles of adult Calloselasma, which was compared to patterns predicted from hypothetical causes by using a partial Mantel test. This test simultane
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Conference papers on the topic "Malaria – Gene therapy"

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Jovanović, Tanja, and Dragana Despot. "The impact of climate changes on microorganisms and their vectors." In 36. Savetovanje dezinfekcija, dezinsekcija i deratizacija jedan svet - jedno zdravlje, Vrnjačka Banja, hotel "Vrnjačke Terme", 28-31.maj 2025.godine. Srpsko veterinarsko društvo, 2024. https://doi.org/10.5937/ddd25149j.

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According to the World Health Organization (WHO), climate changes may represent the greatest global threat to public health in the 21st century, with consequences for every aspect of human life, including health. Climate changes significantly impacts on non-communicable and to a large extent, communicable diseases. A particular risk is associated with vector-borne diseases, due to the direct influence of climate change on both microorganisms and their vectors. The main factors contributing to these changes include rising temperatures, shifts in precipitation patterns, an increased frequency of
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