Antimalarial Properties of Sida cordifolia L. Leaf Extract in Mice: Survivability Depends Less on Parasitaemia Suppression.

Sida cordifolia has been used to treat malaria in Ghana albeit without scientific evidence of antimalarial activity and safety. This work aimed to assess the antimalarial properties and acute toxicity of the aqueous leaf extract of S. cordifolia in murine models. Aqueous extract of the plant was analysed for both suppressive and curative antimalarial properties in chloroquine-sensitive ANKA strains of rodent Plasmodium berghei-infected mice. Acute toxicity evaluation was performed in rats according to the OECD 425 guidelines. The extract displayed antiplasmodial activity in vivo with ED50 of 117.49 ± 15.22 mg/kg and 144.84 ± 18.17 mg/kg in suppressive and curative studies, respectively. The highest % parasitaemia suppression exerted was 76.90 ± 0.64% and 61.50 ± 0.97%, respectively, in the suppressive and curative studies. Survival of infected mice treated with the extract was significantly prolonged. This was dependent on the dose of the extract but imperfectly related to the % parasitaemia suppression. Related antimalarial parameters including percentage hematocrit, changes in body weight, and temperature of experimental mice indicated alleviation of malarial symptoms of treated animals. The extract did not show toxicity in rats. Sida cordifolia L. has antimalarial properties, and was safe. It suppressed parasitaemia in both suppressive and curative studies, was not toxic to animals and prolonged the life of infected animals under treatment. This, therefore, justifies the traditional use of S. cordifolia for the treatment of malaria in Ghana.

Genetic analysis of Caenorhabditis elegans Haspin-like genes shows that hasp-1 plays multiple roles in the germline.

Haspin is a histone kinase that promotes error-free chromosome segregation by recruiting the chromosomal passenger complex (CPC) to mitotic and meiotic chromosomes. Haspin remains less well studied than other M-phase kinases, and the models explaining Haspin function have been developed primarily in mitotic cells. Here, we generate strains containing new conditional or nonsense mutations in the Caenorhabditis elegans Haspin homologs hasp-1 and hasp-2 and characterize their phenotypes. We show that hasp-1 is responsible for all predicted functions of Haspin and that loss of function of hasp-1 using classical and conditional alleles produces defects in germline stem cell proliferation and spermatogenesis, and confirms its role in oocyte meiosis. Genetic analysis suggests that hasp-1 acts downstream of the Polo-like kinase plk-2 and shows synthetic interactions between hasp-1 and two genes expected to promote recruitment of the CPC by a parallel pathway that depends on the kinase Bub1. This work adds to the growing understanding of Haspin function by characterizing a variety of roles in an intact animal.