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Biomedical subjects

L H Miller

Publications and source records attributed to L H Miller.

At least 271 records · Page 15Linked to original sources

Erythrocyte receptors for (Plasmodium knowlesi) malaria: Duffy blood group determinants.

Duffy blood group negative human erythrocytes (FyFy) are resistant to infection by Plasmodium knowlesi, a simian malaria that infects Duffy positive human erythrocytes. The P. knowlesi resistance factor, Duffy negative erythrocytes, occurs in high frequency in West Africa, where the people are resistant to vivax malaria. This suggests that Duffy blood group determinants (Fya or Fyb) may be erythrocyte receptors for P. vivax.

Binding Sites↗

Invasion of erythrocytes by malaria merozoites.

An electro-optical system was developed to record microscope images with high resolution at low light intensities. The system was used to study the invasion of erythrocytes by malaria merozoites. Invasion consists of attachment of the anterior end of the parasite to the erythrocyte, deformation of the erythrocyte, and the entry of the parasite by erythrocyte membrane invagination.

Animals↗

Deep vascular schizogony in Plasmodium fragile: organ distribution and ultrastructure of erythrocytes adherent to vascular endothelium.

Erythrocytes infected with Plasmodium fragile, like those infected with P. falciparum and P. coatneyi, adhere to vessels in heart, adipose tissue and, to a lesser ex00 nm knob protrusions on the plasma membrane of infected erythrocytes. The close apposition between knobs and endothelium (1 nm or less) excludes macromolecules such as fibrinogen or antibodies as the adhesive force. The components on the membrane responsible for adhesion at the knobs remain unknown.

Animals↗

Malaria (Plasmodium knowlesi) merozoites: immunity and the surface coat.

Immune serum agglutinated merozoites of Plasmodium knowlesi in culture. Agglutinated merozoites attached to erythorcytes but were usually unable to invade. Marked aggregation of merozoites was associated with reduced invasion of erythrocytes in these cultures. The agglutination and reduced invasion were immunologically specific, for the effect of serum was greatest against homologous strains of P. knowlesi. Merozoite agglutination was caused by the binding of surface coats on adjacent parasites. This coat appeared on the plasma membrane of merozoites after it was exposed to culture medium, both with and without immune serum. The coat consisted of protein or glycoprotein, since it was susceptible to trypsin treatment. It appears that antibodies directed against this surface coat are crucial for reduced invasion of erythrocytes, at least in vitro.

Agglutination↗

Incorporation of nucleic acid precursors by Plasmodium cynomolgi in Anopheles balabacensis.

Autoradiography was used to study the incorporation of tritium-labelled nucleic acid precursors into the sporogonic stages of Plasmodium cynomolgi in Anopheles b. balabacensis. Infected mosquitoes were fed on either 3H-adenine (5, 25 and 50 muCi/ml or 3H-thymidine (50 muCi/ml) for various periods after the blood meal. 3H-adenine was incorporated into DNA and RNA of the developing oocysts and the resulting sporozoites. Midgut epithelial cells incorporated label from 3H-adenine into nuclear and cytoplasmic regions. In both parasite and host tissue RNA-label was removed after RNase treatment. 3H-thymidine was not taken up by the developing oocysts or sporozoites while incorporation into the cell nuclei of the adjacent midgut epithelium and fat-body of the mosquito was shown. The observed incorporation of 3H-adenine, but not 3H-thymidine, into the sporogonic stages of Plasmodium supports the assumption that the malaria parasite needs exogenous sources of purine but relies on the de novo synthesis of pyrimidine during its development in the mosquito.

Adenine↗

Caveola--vesicle complexes in the plasmalemma of erythrocytes infected by Plasmodium vivax and P cynomolgi. Unique structures related to Schüffner's dots.

Erythrocytes infected with Plasmodium vivax and P cynomolgi, characterized by Schüffner's dots on Giemsa-stained thin films, were studied by electron microscopy and immunocytochemistry. A caveola-vesicle complex, which consisted of a caveola surrounded by vesicles, in an alveolar fashion, formed along the erythrocyte plasmalemma. Horseradish-peroxidase-labeled immunoglobulin from a monkey infected with P vivax bound to the vesicle membrane. Cationized ferritin appeared within the vesicles after incubation with viable parasitized erythrocytes, suggesting that these vesicles were pinocytotic in origin. This caveola-vesicle complex probably corresponds to Schüffner's dots because the alteration is unique to vivax- and ovale-type malarias, and its size and distribution are consistent with Schüffner's dots. Clefts observed within the cytoplasm of infected erythrocytes are present in all malarias and are unlikely candidates for Schüffner's data.

Animals↗

Influence of erythrocyte membrane components on malaria merozoite invasion.

Chymotrypsin- and Pronase-treated human erythrocytes were refractory to invasion by P. knowlesi merozoites; invasion was not inhibited by trypsin or neurammidase treatment. These data implicate a surface protein other than sialoglycoprotein as the receptor site for merozoites. Invasion of rhesus erythrocytes was unaffected by pretreatment with these enzymes. Differences in membrane structure of erythrocytes from various species may explain the absence of an enzyme effect on rhesus erythrocytes.

Animals↗