SUMMARYMice pre-treated withCorynebacterium parvumand later challenged withPlasmodium vinckeibecome infected but do not die whereas control mice do. When pre-treated mice were challenged with 1, 10, 1 × 102, 1 × 104, 1 × 105or 1 × 106parasites, the pre-patent periods correlated directly with the number of parasites injected, but the subsequent parasitaemias reached similar levels. This suggests that parasite killing, resulting from pre-treatment withC. parvum, is not triggered until the parasite load has reached a particular threshold. The injection of alloxan monohydrate, which brings about the release of toxic oxygen inter mediates thought to be involved in non-specific immunity, has little effect onP. vinckeiinfections until the parasitaemia is relatively high. This indicates that oxygen-mediated parasite killing also does not occur until the parasitaemia has reached a particular threshold. It is suggested that it is only at relatively high parasitaemias that the factors involved in parasite killing are able to enter the infected red blood cells.
Targeted dual inhibition of c‐Met/VEGFR2 signalling by foretinib improves antitumour effects of nanoparticle paclitaxel in gastric cancer models
