The radial density gradient (Gr) of Galactic cosmic rays in the ecliptic plane points outward from the Sun. This indicates an increasing density of cosmic ray particles beyond the Earth’s orbit. Due to this gradient and the direction of the Sun’s interplanetary magnetic field (IMF) above and below the IMF wavy neutral sheet, there exists an anisotropic flow of cosmic ray particles approximately perpendicular to the ecliptic plane (i.e. in the direction parallel to BIMF × Gr). This effect is called the north–south anisotropy (ξNS) and manifests as a diurnal variation in sidereal time in the particle intensity recorded by a cosmic ray detector. By analysing the yearly averaged sidereal diurnal variation recorded by five neutron monitors and six muon telescopes from 1957 to 1990, we have deduced probable values of the average rigidity spectrum and magnitude of ξNS. Furthermore, we have used determined yearly amplitudes of ξNS to infer the magnitude of Gr for particles with rigidities in excess of 10 GV.

The transport processes of D-glucose in Plasmodium yoelii-infected mouse erythrocytes were investigated using 2-deoxy-D-glucose (2DOG), a non-metabolizable analogue of D-glucose. Infected cells showed an increase in the uptake of 2DOG compared to uninfected controls, and an effect which was more prominent in cells with mature-stage parasites. Kinetic studies measuring the initial rates of 2DOG uptake revealed two components in infected cells with late trophozoite and schizont-stage parasites: a simple diffusion system and a carrier (transporter)-mediated system. The transporter was common for D-glucose and 2DOG and had a kinetic constant indicating a high affinity for 2DOG (the Km = 0·18 mM and the Vmax = 0·61 mmol/1010 cells/min), as compared to the constant of the mouse erythrocyte carrier (the Km = 10 mM and the Vmax = 1·8 mmol/1010 cells/min). Determination of the distribution of [3H]2DOG in infected cells and experiments with metabolic inhibitors indicated that the simple diffusion system localizes in the membrane of host cells and the transporter in the parasite plasma membrane. The parasite glucose transporter was much less sensitive to cytochalasin B than that of the host cells and the uptake of 2DOG via the transporter was dependent on energy. Based on these findings, the following features emerge: D-glucose first gains access to the cytosol of infected erythrocytes via the simple diffusion system, which appears after infection by the parasite, and an active uptake against the concentration gradient takes place at the parasite plasma membrane via the parasite glucose transporter in an energy dependent manner. Finally, an energy transduction mechanism for the transport of glucose across the parasite plasma membrane is discussed.