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

Author: Grafiati

Published: 4 June 2021

Last updated: 12 February 2022

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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11

Vercellotti, Gregory M., and John D. Belcher. "Heme and the Vasculature: How the Endothelium Protects Itself Against Toxic Iron." Blood 116, no. 21 (November 19, 2010): SCI—25—SCI—25. http://dx.doi.org/10.1182/blood.v116.21.sci-25.sci-25.

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Abstract Abstract SCI-25 Iron-derived reactive oxygen species (ROS) are involved in the pathogenesis of numerous vascular disorders. Heme-derived iron plays an instrumental role in the pathology of intravascular hemolytic diseases including malaria, sickle cell anemia, transfusion reactions, DIC and PNH. Heme catalyzed oxidative stress promotes a pro-inflammatory/prothrombogenic endothelium, diminution of bio-available nitric oxide (NO) and attraction of leukocytes and platelets. The vasculature is protected against heme-catalyzed injury by plasma proteins including haptoglobin, hemopexin, albumin, alpha-1-microglobulin and by scavenger receptors for heme complexes including CD163 and CD91. Heme and its concomitant oxidative stress induces the cytoprotective and rate-limiting enzyme in heme catabolism, heme oxygenase-1 (HO-1). In the process, HO-1 releases three enzymatic byproducts: carbon monoxide (CO), biliverdin/bilirubin, and iron, which stimulates ferritin synthesis. These HO-1 by-products have established anti-oxidant and anti-inflammatory properties. Human patients and mouse models elevate HO-1 in response to chronic hemolysis. Of all sites in the body, the endothelium may be at greatest risk of exposure to heme. Heme greatly potentiates endothelial cell killing mediated by leukocytes and other sources of ROS. As a defense against heme, endothelial cells upregulate HO-1 and ferritin. If cultured endothelial cells are briefly pulsed with heme and are then incubated for a prolonged period (16 h), the cells become highly resistant to oxidant-mediated injury and to the accumulation of endothelial lipid peroxidation products. This protection is associated with induction of both HO-1 and ferritin. H-ferritin with its ferroxidase activity is especially cytoprotective. In animal models, increased expression of HO-1 has been shown to protect tissues against ischemia-reperfusion injury, oxidative stress, inflammation, transplant rejection, apoptosis, and cell proliferation. Conversely, HO-1 null mice (hmox-1−/−) and human patients deficient in HO-1 are especially prone to oxidative stress and inflammation. Sickle cell anemia is an archetypal example of heme-induced oxidative stress and cytoprotective adaptation. The sickle patient and sickle mouse models defend and adapt to hemolysis by increasing their defenses against heme. HO-1 plays an essential role in the inhibition and resolution of vaso-occlusion in sickle cell anemia. HO-1 and its products, carbon monoxide and biliverdin, modulate vaso-occlusion through multiple mechanisms including reducing oxidative stress, inhibiting NF-kB, down-regulating endothelial cell adhesion molecules, decreasing red blood cell hemolysis and altering vascular tone. However, sickle cell patients often have adaptive increases in HO-1 activity which are insufficient to completely handle the excessive heme burden, particularly during acute bouts of hemolysis. HO-1 gene therapy in sickle mice using Sleeping Beauty-mediated transposition of an HO-1 transgene provides a promising non-viral approach to significantly enhance HO-1 expression in sickle cell anemia. Strategies to minimize heme-iron activation of the vasculature including increasing HO-1 and its products, anti-oxidants, iron chelators, increasing haptoglobin, hemopexin and/or their receptors CD163/CD91 should be explored in hemolytic disease states. Disclosures: Vercellotti: Sangart: Consultancy, Research Funding. Belcher:Sangart: Research Funding.

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Touitou, Elka, Judith H. Waknine, Biana Godin, and Jacob Golenser. "Treatment of malaria in a mouse model by intranasal drug administration." International Journal for Parasitology 36, no. 14 (December 2006): 1493–98. http://dx.doi.org/10.1016/j.ijpara.2006.07.006.

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13

Couto, Joana, Miray Tonk, Joana Ferrolho, Sandra Antunes, Andreas Vilcinskas, José de la Fuente, Ana Domingos, and Alejandro Cabezas-Cruz. "Antiplasmodial activity of tick defensins in a mouse model of malaria." Ticks and Tick-borne Diseases 9, no. 4 (May 2018): 844–49. http://dx.doi.org/10.1016/j.ttbdis.2018.03.011.

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14

Mohmmed, Asif, Palakodeti V. N. Dasaradhi, Raj K. Bhatnagar, Virander S. Chauhan, and Pawan Malhotra. "In vivo gene silencing in Plasmodium berghei—a mouse malaria model." Biochemical and Biophysical Research Communications 309, no. 3 (September 2003): 506–11. http://dx.doi.org/10.1016/j.bbrc.2003.08.027.

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15

Anderson, John W., Dimitri Sarantakis, Jacek Terpinski, T. R. Santha Kumar, Han-Chun Tsai, Mack Kuo, Arba L. Ager, et al. "Novel diaryl ureas with efficacy in a mouse model of malaria." Bioorganic & Medicinal Chemistry Letters 23, no. 4 (February 2013): 1022–25. http://dx.doi.org/10.1016/j.bmcl.2012.12.022.

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16

Le Bras, Alexandra. "A mouse model for IPF research." Lab Animal 49, no. 6 (May 27, 2020): 171. http://dx.doi.org/10.1038/s41684-020-0568-3.

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17

Yamamoto, Kouichi, Misuzu Matsui, Tomoko Morimoto, Yumiko Yamamoto, Noriaki Takeda, and Atsushi Yamatodani. "A mouse model for emesis research." Japanese Journal of Pharmacology 79 (1999): 75. http://dx.doi.org/10.1016/s0021-5198(19)34323-9.

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18

Won, Jungyeon, Lan Ying Shi, Wanda Hicks, Jieping Wang, Ronald Hurd, Jürgen K. Naggert, Bo Chang, and Patsy M. Nishina. "Mouse Model Resources for Vision Research." Journal of Ophthalmology 2011 (2011): 1–12. http://dx.doi.org/10.1155/2011/391384.

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The need for mouse models, with their well-developed genetics and similarity to human physiology and anatomy, is clear and their central role in furthering our understanding of human disease is readily apparent in the literature. Mice carrying mutations that alter developmental pathways or cellular function provide model systems for analyzing defects in comparable human disorders and for testing therapeutic strategies. Mutant mice also provide reproducible, experimental systems for elucidating pathways of normal development and function. Two programs, the Eye Mutant Resource and the Translational Vision Research Models, focused on providing such models to the vision research community are described herein. Over 100 mutant lines from the Eye Mutant Resource and 60 mutant lines from the Translational Vision Research Models have been developed. The ocular diseases of the mutant lines include a wide range of phenotypes, including cataracts, retinal dysplasia and degeneration, and abnormal blood vessel formation. The mutations in disease genes have been mapped and in some cases identified by direct sequencing. Here, we report 3 novel alleles ofCrxtvrm65,Rp1tvrm64, andRpe65tvrm148as successful examples of the TVRM program, that closely resemble previously reported knockout models.

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Barker, P. M. "Mouse model for cystic fibrosis research." BMJ 305, no. 6863 (November 14, 1992): 1229. http://dx.doi.org/10.1136/bmj.305.6863.1229-c.

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Willimann, K., H. Matile, N. A. Weiss, and B. A. Imhof. "In vivo sequestration of Plasmodium falciparum-infected human erythrocytes: a severe combined immunodeficiency mouse model for cerebral malaria." Journal of Experimental Medicine 182, no. 3 (September 1, 1995): 643–53. http://dx.doi.org/10.1084/jem.182.3.643.

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Cerebral malaria is a fatal complication of infection by Plasmodium falciparum in man. The neurological symptoms that characterize this form of malarial disease are accompanied by the adhesion of infected erythrocytes to the vasculature of the brain. To study this phenomenon in vivo, an acute phase severe combined immunodeficiency (SCID) mouse model was developed in which sequestration of P. falciparum-infected human erythrocytes took place. During acute cerebral malaria in humans, the expression of intercellular adhesion molecule-1 (ICAM-1) is induced in vascular endothelium by inflammatory reactions. Acute phase ICAM-1 expression can also be obtained in SCID mice. The endothelium of the midbrain region was the most responsive to such inflammatory stimulus. It is noteworthy that the reticular formation in the midbrain controls the level of consciousness, and loss of consciousness is a symptom of cerebral malaria. We found that infected human erythrocytes were retained 24 times more than normal erythrocytes in ICAM-1-positive mouse brain. Sequestration to the brain was reduced by anti-ICAM-1 antibodies. These in vivo results were confirmed by the binding of P. falciparum-infected erythrocytes to the ICAM-1-positive endothelium in tissue sections of mouse brain. We conclude that the SCID mouse serves as a versatile in vivo model that allows the study of P. falciparum-infected erythrocyte adhesion as it occurs in human cerebral malaria. Upregulation of ICAM-1 expression in the region of the midbrain correlates with increased retention of malaria-infected erythrocytes and with the symptoms of cerebral malaria.

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Min, Byung Soh. "Mouse Model for Colorectal Cancer Metastasis Research." Korean Journal of Clinical Oncology 8, no. 1 (June 30, 2012): 4–8. http://dx.doi.org/10.14216/kjco.12001.

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Comfort, Nathaniel. "The prisoner as model organism: malaria research at Stateville Penitentiary." Studies in History and Philosophy of Science Part C: Studies in History and Philosophy of Biological and Biomedical Sciences 40, no. 3 (September 2009): 190–203. http://dx.doi.org/10.1016/j.shpsc.2009.06.007.

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23

Torre, Sabrina, David Langlais, and Philippe Gros. "Genetic analysis of cerebral malaria in the mouse model infected with Plasmodium berghei." Mammalian Genome 29, no. 7-8 (June 19, 2018): 488–506. http://dx.doi.org/10.1007/s00335-018-9752-9.

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Badell, Edgar, Claude Oeuvray, Alicia Moreno, Soe Soe, Nico van Rooijen, Ahmed Bouzidi, and Pierre Druilhe. "Human Malaria in Immunocompromised Mice." Journal of Experimental Medicine 192, no. 11 (December 4, 2000): 1653–60. http://dx.doi.org/10.1084/jem.192.11.1653.

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We have recently described that sustained Plasmodium falciparum growth could be obtained in immunodeficient mice. We now report the potential of this new mouse model by assaying the effect of the passive transfer of antibodies (Abs) which in humans have had a well-established effect. Our results show that the total African adult hyperimmune immunoglobulin Gs (HI-IgGs) strongly reduce P. falciparum parasitemia similarly to that reported in humans, but only when mice are concomitantly reconstituted with human monocytes (HuMNs). In contrast, neither HI-IgGs nor HuMNs alone had any direct effect upon parasitemia. We assessed the in vivo effect of epitope-specific human Abs affinity-purified on peptides derived either from the ring erythrocyte surface antigen (RESA) or the merozoite surface protein 3 (MSP3). The inoculation of low concentrations of anti-synthetic peptide from MSP3, but not of anti-RESA Abs, consistently suppressed P. falciparum in the presence of HuMNs. Parasitemia decrease was stronger and faster than that observed using HI-IgGs and as fast as that induced by chloroquine. Our observations demonstrate that this mouse model is of great value to evaluate the protective effect of different Abs with distinct specificity in the same animal, a step hardly accessible and therefore never performed before in humans.

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Butala, Parag, Caroline Szpalski, Marc Soares, Edward H. Davidson, Denis Knobel, and Stephen M. Warren. "Zmpste24−/− Mouse Model for Senescent Wound Healing Research." Plastic and Reconstructive Surgery 130, no. 6 (December 2012): 788e—798e. http://dx.doi.org/10.1097/prs.0b013e31826d102b.

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Ramezani, A., J. Noronha, V. W. K. Tsoi, C. Zhang, S. Asad, S. E. Read, B. Ngan, and S. Joshi. "A simple SCID mouse model for HIV research." Transfusion Science 17, no. 1 (March 1996): 99–108. http://dx.doi.org/10.1016/0955-3886(95)00063-1.

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Jumani, R. S., K. Bessoff, M. S. Love, P. Miller, E. E. Stebbins, J. E. Teixeira, M. A. Campbell, et al. "A Novel Piperazine-Based Drug Lead for Cryptosporidiosis from the Medicines for Malaria Venture Open-Access Malaria Box." Antimicrobial Agents and Chemotherapy 62, no. 4 (January 16, 2018): e01505-17. http://dx.doi.org/10.1128/aac.01505-17.

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ABSTRACTCryptosporidiosis causes life-threatening diarrhea in children under the age of 5 years and prolonged diarrhea in immunodeficient people, especially AIDS patients. The standard of care, nitazoxanide, is modestly effective in children and ineffective in immunocompromised individuals. In addition to the need for new drugs, better knowledge of drug properties that drivein vivoefficacy is needed to facilitate drug development. We report the identification of a piperazine-based lead compound forCryptosporidiumdrug development, MMV665917, and a new pharmacodynamic method used for its characterization. The identification of MMV665917 from the Medicines for Malaria Venture Malaria Box was followed by dose-response studies,in vitrotoxicity studies, and structure-activity relationship studies using commercial analogues. The potency of this compound againstCryptosporidium parvumIowa and field isolates was comparable to that againstCryptosporidium hominis. Furthermore, unlike nitazoxanide, clofazimine, and paromomycin, MMV665917 appeared to be curative in a NOD SCID gamma mouse model of chronic cryptosporidiosis. MMV665917 was also efficacious in a gamma interferon knockout mouse model of acute cryptosporidiosis. To determine if efficacy in this mouse model of chronic infection might relate to whether compounds are parasiticidal or parasitistatic forC. parvum, we developed a novelin vitroparasite persistence assay. This assay suggested that MMV665917 was parasiticidal, unlike nitazoxanide, clofazimine, and paromomycin. The assay also enabled determination of the concentration of the compound required to maximize the rate of parasite elimination. This time-kill assay can be used to prioritize early-stageCryptosporidiumdrug leads and may aid in planningin vivoefficacy experiments. Collectively, these results identify MMV665917 as a promising lead and establish a new method for characterizing potential anticryptosporidial agents.

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Ohno, Tamio, Yuki Miyasaka, Masako Kuga, Kaori Ushida, Miyoko Matsushima, Tsutomu Kawabe, Yoshiaki Kikkawa, Masashi Mizuno, and Masahide Takahashi. "Mouse NC/Jic strain provides novel insights into host genetic factors for malaria research." Experimental Animals 68, no. 3 (2019): 243–55. http://dx.doi.org/10.1538/expanim.18-0185.

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Ntim, Stephanie B., and Katherine J. Johnson. "The art of malaria education: an arts-based malaria education model, Pepease-Kwahu, Ghana." International Journal Of Community Medicine And Public Health 6, no. 12 (November 27, 2019): 5042. http://dx.doi.org/10.18203/2394-6040.ijcmph20195443.

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Background: Malaria is a major health concern in Ghana as well as other countries in West Africa, where it is estimated that more than 300 million people are at risk of malaria infection. While prior research has highlighted promising school-based interventions often facilitated through textbook information or teacher-based lectures to promote awareness about the disease, less is known as to how well such interventions are able to actively involve and engage students in learning about malaria in their schools.Methods: This research examines the role of the performing arts as a heuristic for student-centered teaching and learning about malaria. Using a convergent parallel mixed-methods study design, an arts-based malaria education model was deployed in a junior high school in Pepease-Kwahu, Ghana.Results: The proposed product included a peer-peer education model through which students (n=77) demonstrated their learning of malaria through their own creation and participation in poetry, song, dance, and drama performances. Pre- and post- paper-based surveys, coupled with focus groups with student participants (n=10) were used to examine the impact of this program.Conclusions: Research findings currently show that the arts-based malaria education program can be beneficial to students, by requiring them to use the performing arts to engage with information about malaria transmission, prevention, and treatment. Students correctly identified that the malarial parasite is transmitted by a mosquito bite, and they correctly identified symptoms of malaria, although students were reluctant to say that they will regularly use insecticide-treated bed nets as a preventive measure for malaria.

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Montosi, E., S. Manzoni, A. Porporato, and A. Montanari. "An ecohydrological model of malaria outbreaks." Hydrology and Earth System Sciences 16, no. 8 (August 16, 2012): 2759–69. http://dx.doi.org/10.5194/hess-16-2759-2012.

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Abstract. Malaria is a geographically widespread infectious disease that is well known to be affected by climate variability at both seasonal and interannual timescales. In an effort to identify climatic factors that impact malaria dynamics, there has been considerable research focused on the development of appropriate disease models for malaria transmission driven by climatic time series. These analyses have focused largely on variation in temperature and rainfall as direct climatic drivers of malaria dynamics. Here, we further these efforts by considering additionally the role that soil water content may play in driving malaria incidence. Specifically, we hypothesize that hydro-climatic variability should be an important factor in controlling the availability of mosquito habitats, thereby governing mosquito growth rates. To test this hypothesis, we reduce a nonlinear ecohydrological model to a simple linear model through a series of consecutive assumptions and apply this model to malaria incidence data from three South African provinces. Despite the assumptions made in the reduction of the model, we show that soil water content can account for a significant portion of malaria's case variability beyond its seasonal patterns, whereas neither temperature nor rainfall alone can do so. Future work should therefore consider soil water content as a simple and computable variable for incorporation into climate-driven disease models of malaria and other vector-borne infectious diseases.

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Lauterwasser, Erica M. W., Shaun D. Fontaine, Hao Li, Jiri Gut, Kasiram Katneni, Susan A. Charman, Philip J. Rosenthal, Matthew Bogyo, and Adam R. Renslo. "Trioxolane-Mediated Delivery of Mefloquine Limits Brain Exposure in a Mouse Model of Malaria." ACS Medicinal Chemistry Letters 6, no. 11 (October 7, 2015): 1145–49. http://dx.doi.org/10.1021/acsmedchemlett.5b00296.

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Min-Oo, G., A. Fortin, M.-F. Tam, P. Gros, and MM Stevenson. "Phenotypic expression of pyruvate kinase deficiency and protection against malaria in a mouse model." Genes & Immunity 5, no. 3 (March 18, 2004): 168–75. http://dx.doi.org/10.1038/sj.gene.6364069.

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Ngo-Thanh, Ha, Trang Dam Thuy, Kazutomo Suzue, Wataru Kamitani, Hideaki Yokoo, Koji Isoda, Chikako Shimokawa, Hajime Hisaeda, and Takashi Imai. "Long-term acrylamide exposure exacerbates brain and lung pathology in a mouse malaria model." Food and Chemical Toxicology 151 (May 2021): 112132. http://dx.doi.org/10.1016/j.fct.2021.112132.

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Kuhen, Kelli L., Arnab K. Chatterjee, Matthias Rottmann, Kerstin Gagaring, Rachel Borboa, Jennifer Buenviaje, Zhong Chen, et al. "KAF156 Is an Antimalarial Clinical Candidate with Potential for Use in Prophylaxis, Treatment, and Prevention of Disease Transmission." Antimicrobial Agents and Chemotherapy 58, no. 9 (June 9, 2014): 5060–67. http://dx.doi.org/10.1128/aac.02727-13.

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ABSTRACTRenewed global efforts toward malaria eradication have highlighted the need for novel antimalarial agents with activity against multiple stages of the parasite life cycle. We have previously reported the discovery of a novel class of antimalarial compounds in the imidazolopiperazine series that have activity in the prevention and treatment of blood stage infection in a mouse model of malaria. Consistent with the previously reported activity profile of this series, the clinical candidate KAF156 shows blood schizonticidal activity with 50% inhibitory concentrations of 6 to 17.4 nM againstP. falciparumdrug-sensitive and drug-resistant strains, as well as potent therapeutic activity in a mouse models of malaria with 50, 90, and 99% effective doses of 0.6, 0.9, and 1.4 mg/kg, respectively. When administered prophylactically in a sporozoite challenge mouse model, KAF156 is completely protective as a single oral dose of 10 mg/kg. Finally, KAF156 displays potentPlasmodiumtransmission blocking activities bothin vitroandin vivo. Collectively, our data suggest that KAF156, currently under evaluation in clinical trials, has the potential to treat, prevent, and block the transmission of malaria.

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Hausmann Muela, Susanna, Joan Muela Ribera, Elizabeth Toomer, and Koen Peeters Grietens. "The PASS-model: a model for guiding health-seeking behavior and access to care research." Malaria Reports 2, no. 1 (December 13, 2012): 3. http://dx.doi.org/10.4081/malaria.2012.e3.

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The mobilization of affordable measures and treatments has brought health services and health care tools closer to the poor. This is particularly the case in the context of malaria control and elimination efforts. Still, the other side of delivery is use: the targeted populations have to access and accept these resources. Although the need to better align the delivery and user sides is increasingly recognised, there still is a gap between this awareness and researchers’ response to adequately address the community side in a way that actionable results can be achieved. In order to avoid actions based on preconceptions, practical applications should draw from theoretical knowledge. Furthermore, in order to get a total view, such applications should consider the full array of potential factors relevant for access to care or health-seeking behavior (HSB). We believe that one of the reasons why theoretically-based, holistic approaches to HSB and access to care still are scarce is the lack of a hands-on and easy-to-use model that allows the researcher to ask the right questions and to interpret the results. In this article, we present such a model, the PASSmodel for HSB and access to care. Founded on theory, the model facilitates the formulation of questions to cover the broad array of elements that guide HSB and access to care. It is adaptable to different contexts and research questions. The goal is that any researcher interested in situating health behavior in a given social, political, and economic landscape can use this tool for any health condition, in low income as well as high income countries.

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Darling, Thayer K., Michael P. Schenk, Chengjing C. Zhou, Franklin M. Maloba, Patrice N. Mimche, Jonathan M. Gibbins, Shawn M. Jobe, and Tracey J. Lamb. "Platelet α-granules contribute to organ-specific pathologies in a mouse model of severe malaria." Blood Advances 4, no. 1 (December 31, 2019): 1–8. http://dx.doi.org/10.1182/bloodadvances.2019000773.

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Key Points Nbeal2 deficiency leads to significantly reduced lung and brain pathology and enhanced survival in a mouse model of malaria. Both antibody-dependent and antibody-independent platelet depletion in mice recapitulate the findings observed in Nbeal2−/− mice.

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Buskbjerg Jager, Sara, Giulia Ronchi, Christian Bjerggaard Vaegter, and Stefano Geuna. "The Mouse Median Nerve Experimental Model in Regenerative Research." BioMed Research International 2014 (2014): 1–6. http://dx.doi.org/10.1155/2014/701682.

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Sciatic nerve crush injury in rat animal model is one of the most common experimental models used in regenerative research. However, the availability of transgenic mouse for nerve regeneration studies is constantly increasing and, therefore, the shift from rat model to mouse model is, in some cases, necessary. Moreover, since most of the human nerve lesions occur in the upper limb, it is also advantageous to shift from sciatic nerve to median nerve. In this study we described an experimental model which involves lesions of the median nerve in the mouse. Data showed that the finger flexor muscle contraction strength, assessed to evaluate the motor function recovery, and reached values not different from the control already 20 days after injury. The degree of nerve regeneration evaluated with stereological methods in light microscopy showed that, 25 days after injury, the number of regenerated myelinated fibers was comparable to the control, but they were smaller with a thinner myelin thickness. Stereological analysis made in electron microscopy confirmed these results, although the total number of fibers quantified was significantly higher compared to light microscopy analysis, due to the very small size of some fibers that can be detected only in electron microscopy.

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Wada, Kosuke, Hiroshi Makino, Kenji Shimada, Fumiaki Shikata, Atsushi Kuwabara, and Tomoki Hashimoto. "Translational Research Using a Mouse Model of Intracranial Aneurysm." Translational Stroke Research 5, no. 2 (November 6, 2013): 248–51. http://dx.doi.org/10.1007/s12975-013-0296-8.

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Wang, Bailing, Hongri Liu, Kaixin Wang, Guodong Xin, and Jia Song. "Research Notes: User Identification Model Based on Mouse Behaviors." International Journal of Software Engineering and Knowledge Engineering 28, no. 02 (February 2018): 175–92. http://dx.doi.org/10.1142/s0218194018400028.

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This study investigates the user identification method based on the computer mouse dynamic behaviors. One of the purposes is to refine seven types of mouse actions, and about 110 dimensional features have been employed from user session statistics and operating characteristics. And then, two basic techniques, principal component analysis (PCA) and weighted multiclassifier, are used to lay out the mouse behavior. Combing PCA and the new proposed classifier, two experiments on identification and authentication have been carried out. By validating the selected mouse data, the accuracy rate is as high as 85% in the identification experiment, and the false rejection rate (FRR) reaches 5.5% and false acceptance rate (FAR) reaches 8.8% in the authentication experiment. The results show that the proposed methods and the selected features can be well applied in practice.

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Klotz, F. W., J. D. Chulay, W. Daniel, and L. H. Miller. "Invasion of mouse erythrocytes by the human malaria parasite, Plasmodium falciparum." Journal of Experimental Medicine 165, no. 6 (June 1, 1987): 1713–18. http://dx.doi.org/10.1084/jem.165.6.1713.

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Plasmodium falciparum malaria merozoites require erythrocyte sialic acid for optimal invasion of human erythrocytes. Since mouse erythrocytes have the form of sialic acid found on human erythrocytes (N-acetyl neuraminic acid), mouse erythrocytes were tested for invasion in vitro. The Camp and 7G8 strains of P. falciparum invaded mouse erythrocytes at 17-45% of the invasion rate of human erythrocytes. Newly invaded mouse erythrocytes morphologically resembled parasitized human erythrocytes as shown on Giemsa-stained blood films and by electron microscopy. The rim of parasitized mouse erythrocytes contained the P. falciparum 155-kD protein, which is on the rim of ring-infected human erythrocytes. Camp but not 7G8 invaded rat erythrocytes, indicating receptor heterogeneity. These data suggest that it may be possible to adapt the asexual erythrocytic stage of P. falciparum to rodents. The development of a rodent model of P. falciparum malaria could facilitate vaccine development.

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Stelzer, Marie K., Henry C. Pitot, Amy Liem, Johannes Schweizer, Charles Mahoney, and Paul F. Lambert. "A Mouse Model for Human Anal Cancer." Cancer Prevention Research 3, no. 12 (October 6, 2010): 1534–41. http://dx.doi.org/10.1158/1940-6207.capr-10-0086.

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Stephens, Robin, and Jean Langhorne. "Effector Memory Th1 CD4 T Cells Are Maintained in a Mouse Model of Chronic Malaria." PLoS Pathogens 6, no. 11 (November 24, 2010): e1001208. http://dx.doi.org/10.1371/journal.ppat.1001208.

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Falanga, Pierre B., and Eugene C. Butcher. "Late treatment with anti-LFA-1 (CD11a) antibody prevents cerebral malaria in a mouse model." European Journal of Immunology 21, no. 9 (September 1991): 2259–63. http://dx.doi.org/10.1002/eji.1830210938.

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Montosi, E., S. Manzoni, A. Porporato, and A. Montanari. "An eco-hydrologic model of malaria outbreaks." Hydrology and Earth System Sciences Discussions 9, no. 3 (March 5, 2012): 2831–54. http://dx.doi.org/10.5194/hessd-9-2831-2012.

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Abstract. Malaria is a geographically widespread infectious disease that is well known to be affected by climate variability at both seasonal and interannual timescales. In an effort to identify climatic factors that impact malaria dynamics, there has been considerable research focused on the development of appropriate disease models for malaria transmission and their consideration alongside climatic datasets. These analyses have focused largely on variation in temperature and rainfall as direct climatic drivers of malaria dynamics. Here, we further these efforts by considering additionally the role that soil water content may play in driving malaria incidence. Specifically, we hypothesize that hydro-climatic variability should be an important factor in controlling the availability of mosquito habitats, thereby governing mosquito growth rates. To test this hypothesis, we reduce a nonlinear eco-hydrologic model to a simple linear model through a series of consecutive assumptions and apply this model to malaria incidence data from three South African provinces. Despite the assumptions made in the reduction of the model, we show that soil water content can account for a significant portion of malaria's case variability beyond its seasonal patterns, whereas neither temperature nor rainfall alone can do so. Future work should therefore consider soil water content as a simple and computable variable for incorporation into climate-driven disease models of malaria and other vector-borne infectious diseases.

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Swanson, Phillip A., Aron E. Lukacher, and Eva Szomolanyi-Tsuda. "Immunity to polyomavirus infection: The polyomavirus–mouse model." Seminars in Cancer Biology 19, no. 4 (August 2009): 244–51. http://dx.doi.org/10.1016/j.semcancer.2009.02.003.

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46

Mandt, Rebecca E. K., Maria Jose Lafuente-Monasterio, Tomoyo Sakata-Kato, Madeline R. Luth, Delfina Segura, Alba Pablos-Tanarro, Sara Viera, et al. "In vitro selection predicts malaria parasite resistance to dihydroorotate dehydrogenase inhibitors in a mouse infection model." Science Translational Medicine 11, no. 521 (December 4, 2019): eaav1636. http://dx.doi.org/10.1126/scitranslmed.aav1636.

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Resistance has developed in Plasmodium malaria parasites to every antimalarial drug in clinical use, prompting the need to characterize the pathways mediating resistance. Here, we report a framework for assessing development of resistance of Plasmodium falciparum to new antimalarial therapeutics. We investigated development of resistance by P. falciparum to the dihydroorotate dehydrogenase (DHODH) inhibitors DSM265 and DSM267 in tissue culture and in a mouse model of P. falciparum infection. We found that resistance to these drugs arose rapidly both in vitro and in vivo. We identified 13 point mutations mediating resistance in the parasite DHODH in vitro that overlapped with the DHODH mutations that arose in the mouse infection model. Mutations in DHODH conferred increased resistance (ranging from 2- to ~400-fold) to DHODH inhibitors in P. falciparum in vitro and in vivo. We further demonstrated that the drug-resistant parasites carrying the C276Y mutation had mitochondrial energetics comparable to the wild-type parasite and also retained their fitness in competitive growth experiments. Our data suggest that in vitro selection of drug-resistant P. falciparum can predict development of resistance in a mouse model of malaria infection.

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Et. al., Yusuf Aliyu Adamu,. "Malaria Prediction Model Using Machine Learning Algorithms." Turkish Journal of Computer and Mathematics Education (TURCOMAT) 12, no. 10 (June 7, 2021): 7488–96. http://dx.doi.org/10.17762/turcomat.v12i10.5655.

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Measures have been taking to ensure the safety of individuals from the burden of vector-borne disease but it remains the causative agent of death than any other diseases in Africa. Many human lives are lost particularly of children below five years regardless of the efforts made. The effect of malaria is much more challenging mostly in developing countries. In 2019, 51% of malaria fatality happen in Africa which it increased by 20% in 2020 due to the covid-19 pandemic. The majority of African countries lack a proper or a sound health care system, proper environmental settlement, economic hardship, limited funding in the health sector, and absence of good policies to ensure the safety of individuals. Information has to become available to the peoples on the effect of malaria by making public awareness program to make sure people become acquainted with the disease so that certain measure can be maintained. The prediction model can help the policymakers to know more about the expected time of the malaria occurrence based on the existing features so that people will get to know the information regarding the disease on time, health equipment and medication to be made available by government through it policy. In this research weather condition, non-climatic features, and malaria cases are considered in designing the model for prediction purposes and also the performance of six different machine learning classifiers for instance Support Vector Machine, K-Nearest Neighbour, Random Forest, Decision Tree, Logistic Regression, and Naïve Bayes is identified and found that Random Forest is the best with accuracy (97.72%), AUC (98%) AUC, and (100%) precision based on the data set used in the analysis.

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Groffen, John, Jan-Willem Voncken, Vesa Kaartinen, Christine Morris, and Nora Heisterkamp. "Ph-positive Leukemia: A Transgenic Mouse Model." Leukemia & Lymphoma 11, sup1 (January 1993): 19–24. http://dx.doi.org/10.3109/10428199309047857.

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Opitz, Oliver G., Michael Quante, Alexander von Werder, Steffen Heeg, and Hubert E. Blum. "A Mouse Model of Oral-Esophageal Carcinogenesis." Oncology Research and Treatment 28, no. 1 (December 23, 2004): 44–48. http://dx.doi.org/10.1159/000082039.

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Nair, D., G. Gallos, W. L. Yang, and T. S. Ravikumar. "A nude mouse model for studying radiofrequency ablation." European Journal of Cancer 37 (April 2001): S298. http://dx.doi.org/10.1016/s0959-8049(01)81592-6.

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