Relevant bibliographies by topics / Malaria research/mouse model

Contents

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

Academic literature on the topic 'Malaria research/mouse model'

Author: Grafiati
Published: 4 June 2021
Last updated: 12 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Malaria research/mouse model.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Malaria research/mouse model"

1

Semenya, Amma A., JoAnn S. Sullivan, John W. Barnwell, and W. Evan Secor. "Schistosoma mansoni Infection Impairs Antimalaria Treatment and Immune Responses of Rhesus Macaques Infected with Mosquito-Borne Plasmodium coatneyi." Infection and Immunity 80, no. 11 (August 20, 2012): 3821–27. http://dx.doi.org/10.1128/iai.00590-12.

Full text
Abstract:
ABSTRACTMalaria and schistosomiasis are the world's two most important parasitic infections in terms of distribution, morbidity, and mortality. In areas wherePlasmodiumandSchistosomaspecies are both endemic, coinfections are commonplace. Mouse models demonstrate that schistosomiasis worsens a malaria infection; however, just as mice and humans differ greatly, the murine-infectingPlasmodiumspecies differ as much from those that infect humans. Research into human coinfections (Schistosoma haematobium-Plasmodium falciparumversusSchistosoma mansoni-P. falciparum) has produced conflicting results. The rhesus macaque model provides a helpful tool for understanding the role ofS. mansonion malaria parasitemia and antimalarial immune responses usingPlasmodium coatneyi, a malaria species that closely resemblesP. falciparuminfection in humans. Eight rhesus macaques were exposed toS. mansonicercariae. Eight weeks later, these animals plus 8 additional macaques were exposed to malaria either through bites of infected mosquitos or intravenous inoculation. When malaria infection was initiated from mosquito bites, coinfected animals displayed increased malaria parasitemia, decreased hematocrit levels, and suppressed malaria-specific antibody responses compared to those of malaria infection alone. However, macaques infected by intravenous inoculation with erythrocytic-stage parasites did not display these same differences in parasitemia, hematocrit, or antibody responses between the two groups. Use of the macaque model provides information that begins to unravel differences in pathological and immunological outcomes observed between humans withP. falciparumthat are coinfected withS. mansoniorS. haematobium. Our results suggest that migration of malaria parasites through livers harboring schistosome eggs may alter host immune responses and infection outcomes.
APA, Harvard, Vancouver, ISO, and other styles
2

Jiang, Ping, Zhishen Xu, Baiquan Xiao, Zhong Han, Jiehong Huang, Jianbang Xu, Zhaorong Lun, and Wenliang Zhou. "Hydrogen sulfide protects against the development of experimental cerebral malaria in a C57BL/6 mouse model." Molecular Medicine Reports 16, no. 2 (February 2017): 2045–50. http://dx.doi.org/10.3892/mmr.2017.6854.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Sanz, Laura M., M. Belen Jiménez-Díaz, Benigno Crespo, Cristina De-Cozar, M. Jesus Almela, Iñigo Angulo-Barturen, Pablo Castañeda, et al. "Cyclopropyl Carboxamides, a Chemically Novel Class of Antimalarial Agents Identified in a Phenotypic Screen." Antimicrobial Agents and Chemotherapy 55, no. 12 (October 3, 2011): 5740–45. http://dx.doi.org/10.1128/aac.05188-11.

Full text
Abstract:
ABSTRACTMalaria is one of the deadliest infectious diseases in the world, with the eukaryotic parasitePlasmodium falciparumcausing the most severe form of the disease. Discovery of new classes of antimalarial drugs has become an urgent task to counteract the increasing problem of drug resistance. Screening directly for compounds able to inhibit parasite growthinvitrois one of the main approaches the malaria research community is now pursuing for the identification of novel antimalarial drug leads. Very recently, thousands of compounds with potent activity against the parasiteP. falciparumhave been identified and information about their molecular descriptors, antiplasmodial potency, and cytotoxicity is publicly available. Now the challenges are how to identify the most promising chemotypes for further development and how best to progress these compounds through a lead optimization program to generate antimalarial drug candidates. We report here the first chemical series to be characterized from one of those screenings, a completely novel chemical class with the generic name cyclopropyl carboxamides that has never before been described as having antimalarial or other pharmacological activities. Cyclopropyl carboxamides are potent inhibitors of drug-sensitive and -resistant strains ofP. falciparuminvitroand showinvivooral efficacy in malaria mouse models. In the present work, we describe the biological characterization of this chemical family, showing that inhibition of their still unknown target has very favorable pharmacological consequences but the compounds themselves seem to select for resistance at a high frequency.
APA, Harvard, Vancouver, ISO, and other styles
4

Snyder, Edward L., and Roger Y. Dodd. "Reducing the Risk of Blood Transfusion." Hematology 2001, no. 1 (January 1, 2001): 433–42. http://dx.doi.org/10.1182/asheducation-2001.1.433.

Full text
Abstract:
Abstract There are continuing concerns over the safety of the nation's and the world's blood supply. The allogeneic blood supply is tested for antibodies to HIV1/2, HTLVI/II, hepatitis B, hepatitis C (HCV) and syphilis. Testing is also performed for donor ALT (SGOT) levels, for the presence of hepatitis B surface antigen, human immunodeficiency virus (HIV) p24 antigen and, using nucleic acid amplification testing (NAT), for HIV and HCV nucleic acids. Still, there are concerns regarding other pathogenic agents. Dr. Roger Dodd addresses a series of pathogens that are already known to be transmissible by transfusion. These include malaria, Chagas' disease, babesiosis, bacteria and some viral agents. The need for new donor screening assays to protect the integrity and purity of the blood supply must be balanced against the loss of potential donors and the cost of developing and implementing these new screening assays. This issue will be highlighted. Dr. Edward Snyder reviews the status of research into development of systems for pathogen inactivation (PI) of blood and its components. A proactive technology wherein PI reagents such as psoralen, riboflavin, dimethylmethylene blue or inactine are added to blood collection bags could assure multiple log reduction of a variety of pathogens including viruses, bacteria, protozoa and fungi without the need to initially pre-screen the blood for a specific pathogen. Such a program could also cover new pathogens as they enter the blood supply. As a key issue relates to the toxicology of these agents, Dr. Snyder provides data on a novel carcinogenicity assay that uses a heterozygous p53 knock-out mouse model. The criteria likely to be needed for PI technology to be adopted by the transfusion community are summarized.
APA, Harvard, Vancouver, ISO, and other styles
5

Markus, Miles B. "Mouse-Based Research on Quiescent Primate Malaria Parasites." Trends in Parasitology 32, no. 4 (April 2016): 271–73. http://dx.doi.org/10.1016/j.pt.2016.02.006.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Badell, E., V. Pasquetto, P. Druilhe, and N. Van Rooijen. "A mouse model for human malaria erythrocytic stages." Parasitology Today 11, no. 6 (June 1995): 235–37. http://dx.doi.org/10.1016/0169-4758(95)80088-3.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Butcher, Geoff. "A mouse model for human malaria erythrocytic stages: Reply." Parasitology Today 11, no. 6 (June 1995): 224. http://dx.doi.org/10.1016/0169-4758(95)80082-4.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Kautz, Leon, Chloe Latour, Wlodarczyk Myriam, Nicolas Blanchard, Tomas Ganz, Marie Paule Roth, and Helene Coppin. "Erythroferrone Represses Hepcidin Expression in a Mouse Model of Malaria." Blood 124, no. 21 (December 6, 2014): 4022. http://dx.doi.org/10.1182/blood.v124.21.4022.4022.

Full text
Abstract:
Abstract Introduction: Malaria, a mosquito-borne disease caused by a parasite, represents a major global health challenge in developing countries, resulting in over half a million deaths each year. Among the many clinical complications, the multiplication of the parasites in erythrocytes leads to a severe anemia secondary to hemolysis and increased erythrophagocytosis. Malarial anemia is also characterized by insufficient erythropoiesis to compensate for the loss of red blood cells, despite high erythropoietin (EPO) levels. Iron is an essential functional component of erythrocyte hemoglobin, therefore the production of erythrocytes requires the timely delivery of iron to erythroid precursors. The availability of iron for erythropoiesis is controlled by hepcidin-induced endocytosis and degradation of ferroportin, the iron exporter which delivers iron to plasma from absorptive enterocytes and erythrocyte-recycling macrophages. In the late phase of malarial infection, hepcidin is suppressed but the mechanism of suppression is unknown. The erythroid hormone erythroferrone (ERFE) has been recently described as an important regulator of hepcidin expression during increased erythropoietic activity. We assessed hepcidin and erythroferrone expression in mouse malaria and found that ERFE is necessary for hepcidin suppression during malaria infection. Methods: To study the regulation of hepcidin in malaria, we used the rodent malaria parasite Plasmodium berghei K173 (PbK). Mice infected with PbK develop a lethal form of malaria with a high parasitemia and severe anemia and eventually die 18 to 20 days after infection. C57BL/6 mice were challenged intraperitoneally with 106 PbK-parasitized erythrocytes. The parasitemia and the hematologic parameters, were monitored during 18 days (Table 1). Table RBC (106/µL) HGB (g/dL) HCT (%) Parasitemia (%) Controls 8.8 +/- 0.6 15.1 +/- 0.9 39.8 +/- 3.1 0 Day 7 7.7 +/- 0.9 12.6 +/- 1.5 33.8 +/- 4.0 2 +/- 1 Day 9 7.0 +/- 0.3 11.6 +/- 0.6 32.5 +/- 1.6 4 +/- 1 Day 11 5.9 +/- 0.5 9.9 +/- 0.9 27.8 +/- 1.9 4 +/- 1 Day 13 3.8 +/- 0.8 6.6 +/- 1.2 21.5 +/- 2.3 20 +/- 5 Day 16 2.0 +/- 0.7 3.9 +/- 1.2 14.7 +/- 4.5 42 +/- 11 Day 18 1.7 +/- 0.4 3.6 +/- 0.7 14.8 +/- 2.7 68 +/- 10 Results: Thirteen days after infection, mice showed a high parasitemia (20% of infected red blood cells) and significantly decreased RBC (3.8x106/µL), hemoglobin concentration (6.6 g/dL) and hematocrit (21.5%) despite elevated serum EPO levels (not shown). We examined the time course of liver hepcidin expression and serum hepcidin concentration and found that hepcidin production was profoundly reduced 11 to 18 days after infection. As expected given the increase in EPO production after infection, hepcidin suppression was accompanied by an increase in erythroferrone mRNA expression in the bone marrow and the spleen. To determine whether ERFE plays a role in hepcidin suppression during malaria infection, we studied wild-type and Erfe-deficient mice after PbK infection. Erfe-/- mice failed to adequately suppress hepcidin expression after infection with PbK compared with wild-type mice. Figure 1 Figure 1. Conclusion: Erythroferrone may be responsible for hepcidin suppression and compensatory iron acquisition during malaria infection. Funded in part by ANR (project ANR-13-BSV3-0015-01) and FRM (project DEQ2000326528) Disclosures No relevant conflicts of interest to declare.
APA, Harvard, Vancouver, ISO, and other styles
9

Desruisseaux, Mahalia S., FNU Nagajyothi, Shankar Mukherjee, Dumitru A. Iacobas, Herbert B. Tanowitz, and David C. Spray. "Gene expression alterations in a mouse model of cerebral malaria." BMC Proceedings 2, Suppl 1 (2008): P15. http://dx.doi.org/10.1186/1753-6561-2-s1-p15.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Sacci, J. B., M. E. Schriefer, J. H. Resau, R. A. Wirtz, L. J. Detolla, R. B. Markham, and A. F. Azad. "Mouse model for exoerythrocytic stages of Plasmodium falciparum malaria parasite." Proceedings of the National Academy of Sciences 89, no. 9 (May 1, 1992): 3701–5. http://dx.doi.org/10.1073/pnas.89.9.3701.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Malaria research/mouse model"

1

Gilks, C. F. "The surface of Plasmodium chabaudi infected erythrocytes." Thesis, University of Oxford, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.233501.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Watkins, Katherine Ruth. "Investigation of pre-erythrocytic malaria vaccines in a mouse model using transgenic parasites." Thesis, University of Oxford, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.534200.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Achtman, Ariel H. "The B cell response to Plasmodium chabaudi chabaudi : malaria in the mouse model." Thesis, Open University, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.398011.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Min-Oo, Gundula Ellen. "The genetic basis of malaria susceptibility: uncovering novel host factors in a mouse model of blood-stage infection." Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=66739.

Full text
Abstract:
This thesis examines the genetic factors controlling host response to malaria. Recombinant congenic strains AcB55 and AcB61 were identified as uniquely resistant to malaria despite a susceptible genetic background. These mice display splenomegaly, anemia, reticulocytosis and extra-medullary erythropoiesis. Genome wide mapping led to the identification of a mutation in pyruvate kinase (PklrI90N) that is associated with increased survival and decreased peak parasite levels. We found a significant malaria-protective effect with a second Pklr mutation (PklrG338D) on a distinct genetic background (CBA/N), thus validating our initial findings. The mechanism of protection was linked to increased erythrocyte uptake and compensatory erythropoiesis. Subsequently, we showed that PK-deficiency in humans was protective against P.falciparum replication in vitro. A second genetic locus in AcB55, Char9, was identified and localized to a 14Mb C57Bl/6-derived congenic segment. The Vnn1/Vnn3 genes map within the minimal interval and encode a pantetheinase enzyme; they show cis-regulated gene expression A/J-like alleles associated with an absence of mRNA. In addition, no enzymatic activity was detected in A/J tissues. Administration of cysteamine, the product of pantetheinase, to susceptible A/J mice resulted in increased survival and decreased parasite levels. The inhibition of parasite replication by cysteamine suggests a potential for this compound to be used as a novel anti-malarial monotherapy or in combination with current therapeutics. Finally, a third recombinant congenic strain, AcB62, shows rapid parasite replication with an early peak of infection, despite the presence of the PklrI90N mutation. AcB62 mice do display PK-deficiency associated anemia, erythropoiesis, tissue iron overload, and concomitant increases in iron-regulated proteins. We identified a novel locus controlling peak parasite levels in an [AcB6
Cette thèse examine les facteurs génétiques contrôlant la réponse de l'hôte au paludisme. Les souches recombinantes congéniques (RCS) AcB55 et AcB61 ont été identifiées comme présentant une résistance unique au paludisme malgré un fond génétique de susceptibilité. Ces souris développent une splénomégalie, de l'anémie, de la réticulose et une érythropoïèse extra médullaire. Un génome scan a conduit à l'identification d'une mutation de la pyruvate kinase (PklrI90N), laquelle est associée à une survie accrue et à une diminution des niveaux de pic de parasitémie. Un effet protecteur significatif contre le paludisme, du à une seconde mutation de la pyruvate kinase (PklrG338D) sur un fond génétique différent (CBA/N), a également été mis en évidence, validant ainsi nos premiers résultats. Le mécanisme de protection est associé à une augmentation de la phagocytose érythrocytaire et de l'érythropoïèse compensatoire. Nous avons également montré, chez l'humain, qu'un déficit en pyruvate kinase protégeait contre la réplication de P. falciparum in vitro. Un second locus, Char9, a été identifié sur la RCS AcB55 et a été localisé sur un segment congénique de 14Mb dérivé de C57Bl/6. Les gènes Vnn1/Vnn3 sont situés à l'intérieur de l'intervalle minimum et codent pour une enzyme pantéthéinase. Leur expression est régulée en cis et les allèles de type A/J ne codent pour aucun ARNm. Par ailleurs, aucune activité enzymatique n'a été détectée dans les tissus A/J. L'administration de cystéamine (un produit de la pantéthéinase) à des souris susceptibles A/J est responsable d'une survie accrue et d'une diminution des niveaux de parasitémie. L'inhibition de la réplication du parasite par la cystéamine suggère que ce composé pourrait potentiellement être utilisé comme nouvel antipaludéen, en monothérapie ou en combinaison avec des drogues actue
APA, Harvard, Vancouver, ISO, and other styles
5

Wyse, Ana Paula Pintado. "Optimal control for malaria vector for a seasonal mathematical model." Laboratório Nacional de Computação Científica, 2007. http://www.lncc.br/tdmc/tde_busca/arquivo.php?codArquivo=140.

Full text
Abstract:
In the Amazonian region occurs a variation in the malaria incidence, which is related to the pluviometric variation annual. The mathematical model proposed here considers this seasonality and different treatment intensities accessible to the infected people. The numerical evidence the seasonal fluctuation and the relationship between the environment temperature and treatment efficiency, showing that the temperature increase strongly affects the extrinsic latent period,reducing the healthy care efficiency. Because malaria treatment already exists it should be import. For another hand, even the investment in treatment is an efficient form to block the epidemy, it is not always sufficient, because the protozoan has been more resistent to the medicine; then scientists are creating transgenic mosquitoes refractory to malaria to couple with wild one, generating descending transgenic. To avaliate this situation, we consider here a mathematical model that describes the relatioship between these populations. Then, we formulate and solve an optimal control problem indicating how the transgenic mosquitoes should be introduced in the environment. The numerical simulations show the effectiveness of the control.
Na Amazônia ocorre uma variação na incidência de malária que está intimamente relacionada à variação pluviométrica ao longo do ano. O modelo matemático aqui proposto considera esta sazonalidade e diferentes intensidades de tratamento acessíveis às pessoas infectadas. Experimentos numéricos descrevem a flutuação sazonal e evidenciam uma relação inversa entre a temperatura e eficiência do tratamento, mostrando que um aumento na temperatura afeta fortemente o período latente extrínseco, reduzindo a eficiência do investimento em saúde. Como o tratamento para os infectados existe, é importante concentrar esforços nesse sentido para obter sucesso no controle da malária. Por outro lado, embora o investimento em tratamento seja uma forma eficaz de impedir a epidemia, isso nem sempre é suficiente, pois é fato que o protozoário tem se mostrado cada vez mais resistente aos medicamentos; por esse motivo, cientistas estão criando mosquitos transgênicos refratários à malária que devem acasalar com os mosquitos selvagens, gerando descendência transgência. Para avaliar esta situação, consideramos neste trabalho um modelo matemático que descreve de maneira simplificada a relação entre estas duas populações. A partir desse modelo, formulamos e resolvemos um problema de controle ótimo indicando uma forma adequada de introduzir esses mosquitos transgênicos. Experimentos numéricos mostram a eficácia do controle adotado.
APA, Harvard, Vancouver, ISO, and other styles
6

Komuro, Yutaro. "Altered adult neurogenesis in a mouse model of human tauopathy." Case Western Reserve University School of Graduate Studies / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=case1434743393.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Ohashi, Taryn M. "Eradicating Malaria: Improving a Multiple-Timestep Optimization Model of Malarial Intervention Policy." Scholarship @ Claremont, 2013. http://scholarship.claremont.edu/scripps_theses/273.

Full text
Abstract:
Malaria is a preventable and treatable blood-borne disease whose complications can be fatal. Although many interventions exist in order to reduce the impacts of malaria, the optimal method of distributing these interventions in a geographical area with limited resources must be determined. This thesis refines a model that uses an integer linear program and a compartmental model of epidemiology called an SIR model of ordinary differential equations. The objective of the model is to find an intervention strategy over multiple time steps and multiple geographic regions that minimizes the number of days people spend infected with malaria. In this paper, we refine the resolution of the model and conduct sensitivity analysis on its parameter values.
APA, Harvard, Vancouver, ISO, and other styles
8

Huan, Xiang Quan. "Depot cytokines and chemokines for antitumor therapy in a mouse model /." [St. Lucia, Qld.], 2004. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe18435.pdf.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Krishnamurthy, Varun K. "Biomechanical and Molecular Approaches to Aortic Valve Disease in a Mouse Model." University of Cincinnati / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1354297165.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Quiggle, David Douglas. "The effects of R-flurbiprofen in reducing tumors in a multiple intestinal neoplasia mouse model." CSUSB ScholarWorks, 2001. https://scholarworks.lib.csusb.edu/etd-project/2009.

Full text
Abstract:
The design of the proposed study was to administer R-FB to 72-day old Min/+ mice for up to 42 days. In order to capture the process of tumor reduction, animals were necropsied at various time points. At each time point animals were evaluated for tumor loads and presence of apoptotic cells along the small intestine. Studies have shown that when R-flurbiprofen (R-FB) is administered in the Min/+ mouse model it can cause the prevention and regression on intestinal tumors.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "Malaria research/mouse model"

1

Brakebusch, Cord. Mouse as a Model Organism: From Animals to Cells. Dordrecht: Springer Science+Business Media B.V., 2011.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

Pihlajaniemi, Taina, and Cord Brakebusch. Mouse as a Model Organism: From Animals to Cells. Springer, 2014.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

Bentham, James R. The genetics of congenital heart disease. Edited by José Maria Pérez-Pomares, Robert G. Kelly, Maurice van den Hoff, José Luis de la Pompa, David Sedmera, Cristina Basso, and Deborah Henderson. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757269.003.0022.

Full text
Abstract:
Congenital heart disease (CHD) is defined as a structural cardiac malformation resulting from an abnormality of development; 8% of CHD is inherited in a Mendelian fashion and 12% results from chromosomal imbalance. Recurrence risk and new research suggest that even the remaining 80% of patients without an identifiable familial or syndromic basis for disease may have an identifiable genetic cause. The potential to understand these mechanisms is increasing with the advent of new sequencing techniques which have identified multiple or single rare variants and/or copy number variants clustering in cardiac developmental genes as well as common variants that may also contribute to disease, for example by altering metabolic pathways. Work in model organisms such as mouse and zebrafish has been pivotal in identifying CHD candidate genes. Future challenges involve translating the discoveries made in mouse models to human CHD genetics and manipulating potentially protective pathways to prevent disease.
APA, Harvard, Vancouver, ISO, and other styles

Book chapters on the topic "Malaria research/mouse model"

1

Peng, Cong, and Shaoguang Li. "CML Mouse Model in Translational Research." In Methods in Molecular Biology, 253–66. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-058-8_15.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Monach, Paul, Kimie Hattori, Haochu Huang, Elzbieta Hyatt, Jody Morse, Linh Nguyen, Adriana Ortiz-Lopez, Hsin-Jung Wu, Diane Mathis, and Christophe Benoist. "The K/BxN Mouse Model of Inflammatory Arthritis." In Arthritis Research, 269–82. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-402-5_20.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

de Oca, Marcela Montes, Christian Engwerda, and Ashraful Haque. "Plasmodium berghei ANKA (PbA) Infection of C57BL/6J Mice: A Model of Severe Malaria." In Mouse Models of Innate Immunity, 203–13. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-481-4_23.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Kamii, Hideyuki, and Teiji Tominaga. "Filament Perforation Subarachnoid Hemorrhage Mouse Model." In Springer Series in Translational Stroke Research, 231–40. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-16082-1_16.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Belayev, Ludmila. "Blood Injection Intracerebral Hemorrhage Mouse Model." In Springer Series in Translational Stroke Research, 293–302. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-16082-1_21.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Tada, Yoshiteru, Yasuhisa Kanematsu, Miyuki Kanematsu, Yoshitsugu Nuki, Elena I. Liang, Kosuke Wada, Hiroshi Makino, and Tomoki Hashimoto. "A Mouse Model of Intracranial Aneurysm: Technical Considerations." In Intracerebral Hemorrhage Research, 31–35. Vienna: Springer Vienna, 2011. http://dx.doi.org/10.1007/978-3-7091-0693-8_6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Kazuki, Y., T. C. Schulz, T. Shinohara, M. Kadota, R. Nishigaki, T. Inoue, M. Kimura, et al. "A new mouse model for Down syndrome." In Advances in Down Syndrome Research, 1–20. Vienna: Springer Vienna, 2003. http://dx.doi.org/10.1007/978-3-7091-6721-2_1.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Brayton, Cory. "Nature and Nurture: Impacts on Mouse Phenotypes and Translational Research." In Mouse as a Model Organism, 45–76. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-0750-4_3.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Manaenko, Anatol, Nancy Fathali, Shammah Williams, Tim Lekic, John H. Zhang, and Jiping Tang. "Geldanamycin Reduced Brain Injury in Mouse Model of Intracerebral Hemorrhage." In Intracerebral Hemorrhage Research, 161–65. Vienna: Springer Vienna, 2011. http://dx.doi.org/10.1007/978-3-7091-0693-8_27.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Cristina, Carolina, Isabel García-Tornadú, Graciela Díaz-Torga, Marcelo Rubinstein, Malcolm J. Low, and Damasia Becú-Villalobos. "Dopaminergic D2 Receptor Knockout Mouse: An Animal Model of Prolactinoma." In Frontiers of Hormone Research, 50–63. Basel: KARGER, 2006. http://dx.doi.org/10.1159/000094308.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Malaria research/mouse model"

1

Batista, Camila, Helena D’Anunciação De Oliveira, Ana Maria Garcia-Darze, Maiara Lima, Érica Amorim, Adriano Silva, Hugo Caire Castro-Faria-Neto, and Tatiana Maron-Gutierrez. "The effect of combined therapy using rosuvastatin and dihydroarteminin in a pulmonary malaria mouse model." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa4290.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Keller, C. "Imaging Tumor Vasculature By Computed Tomography in vivo For Mouse Tumour Models." In 2nd International University of Malaya Research Imaging Symposium (UMRIS) 2005: Fundamentals of Molecular Imaging. Kuala Lumpur, Malaysia: Department of Biomedical Imaging, University of Malaya, 2005. http://dx.doi.org/10.2349/biij.1.1.e7-52.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Keller, C. "The Next Generation Of Preclinical Mouse Models Of Human Cancer: A Primer For Radiologists." In 2nd International University of Malaya Research Imaging Symposium (UMRIS) 2005: Fundamentals of Molecular Imaging. Kuala Lumpur, Malaysia: Department of Biomedical Imaging, University of Malaya, 2005. http://dx.doi.org/10.2349/biij.1.1.e7-47.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Miermont, Anne, and Priscilla Furth. "Abstract A6: Stat5a and pregnancy protection in the CERM mouse model." In Abstracts: Frontiers in Cancer Prevention Research 2008. American Association for Cancer Research, 2008. http://dx.doi.org/10.1158/1940-6207.prev-08-a6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Melkamu, Tamene, Xuemin Qian, Gerry O'Sullivan, and Fekadu Kassie. "Abstract B41: A mouse model for inflammation-driven lung tumorigenesis." In Abstracts: AACR International Conference on Frontiers in Cancer Prevention Research‐‐ Oct 22-25, 2011; Boston, MA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1940-6207.prev-11-b41.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Kon, Cynthia Mui Lian, and Jane Labadin. "Simulating the spread of malaria using a generic transmission model for mosquito-borne infectious diseases." In INNOVATIONS THROUGH MATHEMATICAL AND STATISTICAL RESEARCH: Proceedings of the 2nd International Conference on Mathematical Sciences and Statistics (ICMSS2016). Author(s), 2016. http://dx.doi.org/10.1063/1.4952532.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Shahabi, Shahram, Ebrahim Mazloomi, Behrooz Ilkhanizadeh, and Ahad Zare. "Subcutaneous Isopathic Immunotherapy of Allergic Asthma in a Mouse Model of Allergic Asthma." In HRI London 2019—Cutting Edge Research in Homeopathy: Presentation Abstracts. The Faculty of Homeopathy, 2020. http://dx.doi.org/10.1055/s-0040-1702082.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Gonzalez-Silva, L., L. Quevedo, T. Moreno, C. Revilla, D. Saur, R. Rad, and I. Varela. "PO-339 Intratumour heterogeneity in a pancreatic cancer mouse model." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.851.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Kulkarni, P. V., C. R. Roney, V. Arora, M. Bennett, P. P. Antich, F. J. Bonte, Floyd D. McDaniel, and Barney L. Doyle. "Radiolabled Polymeric Nanoparticles for Imaging Alzheimer’s Plaques in a Mouse Model of Alzheimer’s Disease (AD)." In APPLICATION OF ACCELERATORS IN RESEARCH AND INDUSTRY: Twentieth International Conference. AIP, 2009. http://dx.doi.org/10.1063/1.3120081.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Gadeau, Alain-pierre, Laura Cetran, Isabelle Belloc, Marie-ange Renault, Larry Fliegel, and Fatima Mraiche. "In Vivo Characterization Of A New Mouse Model Expressing The Na+/h+ Exchanger Isoform 1 Of Dilated Cardiomyopathy." In Qatar Foundation Annual Research Conference Proceedings. Hamad bin Khalifa University Press (HBKU Press), 2014. http://dx.doi.org/10.5339/qfarc.2014.hbpp0193.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "Malaria research/mouse model"

1

Rich, Tyvin A., and Sarah Parsons. The Transgenic TGF-Alpha or EGFR1 Overexpression Mouse Model for Symptom Complex Research. Fort Belvoir, VA: Defense Technical Information Center, September 2009. http://dx.doi.org/10.21236/ada533932.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Malaria research/mouse model' for particular source types:
Journal articles Dissertations / Theses
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography