parasitemia/tyrosine

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Inhibition of an Erythrocyte Tyrosine Kinase with Imatinib Prevents Plasmodium falciparum Egress and Terminates Parasitemia.

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With half of the world's population at risk for malaria infection and with drug resistance on the rise, the search for mutation-resistant therapies has intensified. We report here a therapy for Plasmodium falciparum malaria that acts by inhibiting the phosphorylation of erythrocyte membrane band 3

Diagnosis of trypanosomiasis in experimental mice and field-infected camels by detection of antibody to trypanosome tyrosine aminotransferase.

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Sera from animals with acute and chronic Trypansoma evansi infections were examined directly for trypanosome tyrosine aminotransferase activity and indirectly for their ability to inhibit tyrosine aminotransferase activity. It was shown that sera from acutely infected mice and camels with high

New chemical scaffolds for human african trypanosomiasis lead discovery from a screen of tyrosine kinase inhibitor drugs.

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Human African trypanosomiasis (HAT) is caused by the protozoan Trypanosoma brucei. New drugs are needed to treat HAT because of undesirable side effects and difficulties in the administration of the antiquated drugs that are currently used. In human proliferative diseases, protein tyrosine kinase

Protein 3-nitrotyrosine formation during Trypanosoma cruzi infection in mice.

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Nitric oxide (.NO) is a diffusible messenger implicated in Trypanosoma cruzi resistance. Excess production of .NO and oxidants leads to the generation of nitrogen dioxide (.NO2), a strong nitrating agent. Tyrosine nitration is a post-translational modification resulting from the addition of a nitro

Human autoantibodies specific for neurotrophin receptors TrkA, TrkB, and TrkC protect against lethal Trypanosoma cruzi infection in mice.

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Patients with Chagas' disease remain asymptomatic for many years, presumably by keeping the etiological agent Trypanosoma cruzi in check through protective immunity against. Recently, we found that T. cruzi uses TrkA, a receptor tyrosine kinase responsive to neurotrophin nerve growth factor in

Infection by Trypanosoma cruzi metacyclic forms deficient in gp82 but expressing a related surface molecule, gp30.

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Trypanosoma cruzi metacyclic trypomastigotes invade and replicate in the gastric mucosal epithelium after oral infection. In this study we analyzed the process of infection by T. cruzi isolates deficient in the expression of gp82, the metacyclic stage-specific surface glycoprotein implicated in

Molecular basis of non-virulence of Trypanosoma cruzi clone CL-14.

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We investigated the properties of metacyclic trypomastigotes of non-virulent Trypanosoma cruzi clone CL-14, as compared to the parental isolate CL. In contrast to the CL isolate, which produces high parasitemias in mice, metacyclic forms of clone CL-14 failed to produce patent infection. In vitro,

Testosterone-induced persistent susceptibility to Plasmodium chabaudi malaria: long-term changes of lincRNA and mRNA expression in the spleen.

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Testosterone (T) is known to induce persistent susceptibility to blood-stage malaria of Plasmodium chabaudi in otherwise resistant female C57BL/6 mice, which is associated with permanent changes in mRNA expression of the liver. Here, we investigate the spleen as the major effector against

Increased excretion of aromatic amino acid catabolites in animals infected with Trypanosoma brucei evansi.

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Aromatic amino acid catabolism by Trypanosoma brucei evansi was investigated in vivo using C3HeB/FeJ mice. The major catabolites detected by gas chromatography in the urines of infected animals were phenylpyruvic acid, 4-hydroxyphenylpyruvic acid, and indole-3-pyruvic acid. Identity of each compound

Pulmonary vascular disease associated with schistosomiasis.

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In this article we focus on the pathogenesis and clinical characteristics of schistosomiasis infection on the lung vasculature. Overall, the basic biology and understanding of Schistosoma immune responses and their effect on the cardiopulmonary system is limited in both animal and human models,

Syk inhibitors interfere with erythrocyte membrane modification during P falciparum growth and suppress parasite egress.

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Band 3 (also known as the anion exchanger, SLCA1, AE1) constitutes the major attachment site of the spectrin-based cytoskeleton to the erythrocyte's lipid bilayer and thereby contributes critically to the stability of the red cell membrane. During the intraerythrocytic stage of Plasmodium

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