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The complex life cycle of the protozoan parasite is characterized by distinct invasive forms of the sporozoite and merozoite that invade hepatocytes and erythrocytes in the vertebrate host, respectively, and the ookinetes inside the insect vector that penetrates the mosquito midgut epithelium [1] [6].
In contrast, for invasive forms of the parasite (sporozoite, merozoite, etc).
In humans, P. falciparum merozoites (invasive forms of the parasite) employ a host of parasite proteins to rapidly invade erythrocytes.
Highly specific cell-cell interactions between the invasive forms of the parasite and the corresponding host cells are pivotal steps in the complex life cycle of P. falciparum, which depend on specific molecular interactions of cell surface molecules.
The merozoite surface protein 1 (MSP1) gene encodes the major surface antigen of invasive forms of the Plasmodium erythrocytic stages and is considered a candidate vaccine antigen against malaria.
The merozoite surface protein 1 (MSP1) is the major surface antigen of invasive forms of the erythrocytic stages of Plasmodium and has been proposed as a vaccine antigen against malaria [ 12].
Similar(53)
Human malaria is caused by the cyclical invasion of the host's red blood cells (RBCs) by the invasive form of the parasite, the merozoite.
Primary MNAs are classified histologically as either low-grade appendiceal mucinous neoplasm (LAMN) showing no classic infiltrative invasion or mucinous adenocarcinoma [ 2] which reflects a high-grade, invasive form of the disease associated with a worse prognosis.
In contrast, seven of nine animals that received the placebo did develop an invasive form of the disease.
In contrast, seven of nine mice receiving a placebo did develop the invasive form of the disease within the same time period.
Invasion involves extracellular protein interactions between host erythrocyte receptors and ligands on the merozoite, the invasive form of the parasite.
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