Abstract. It has been suggested that much of the drop and subsequent recovery of storm time relativistic electron fluxes at geosynchronous orbit can be explained in terms of a fully adiabatic response (all three adiabatic invariants conserved) to magnetic field changes. To calculate this effect, we assume a prestorm electron flux distribution constructed from CRRES satellite data, we use modular magnetospheric magnetic field models to represent the magnetic field configuration before and during the storm, and we use Liouville's theorem to evolve the prestorm electron flux. In this work we focus on the important special case of equatorially mirroring electrons. During the main phase of a storm with a Dst minimum of-100 nT we find that the fully adiabatic effect can cause a flux decrease of up to 2 orders of magnitude, consistent with observed flux decreases. We also find that the magnitude of the fully adiabatic flux decrease is larger for lower energies, again in agreement with observations. The contribution of prestorm electron fluxes to the recovery phase flux increase at synchronous orbit is expected to be small because of losses to the dawnside magnetopause.

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In this review, we summarize the recent progress of activity-based NIR fluorescent probes based on the versatile hemicyanine scaffold for detection, bioimaging, and diagnosis and therapy of diseases.

[1] It has been suggested that drift loss to the magnetopause can be one of the major loss mechanisms contributing to relativistic electron flux dropouts. In this study, we examine details of relativistic electrons' drift physics to determine the extent to which the drift loss through the magnetopause is important to the total loss of the outer radiation belt. We have numerically computed drift paths of relativistic electrons' guiding center for various pitch angles, various measurement positions, and different solar wind conditions using the Tsyganenko T02 model. We specifically demonstrate how the drift loss effect depends on these various parameters. Most importantly, we present various estimates of relative changes of the omnidirectional flux of 1 MeV electrons between two different solar wind conditions based on a simple form of the directional flux function. For a change of the dynamic pressure from 4 nPa to 10 nPa with a fixed IMF B Z = 0 nT, our estimate indicates that after this increase in pressure, the equatorial omnidirectional flux at midnight near geosynchronous altitude decreases by $56 to $97%, depending on the specific pitch angle dependence of the directional flux. The effect rapidly decreases at regions earthward of geosynchronous orbit and shows a general trend of decrease away from midnight. For a change of the IMF B Z from 0 nT to À15 nT with a fixed dynamic pressure of 4 nPa, the relative decrease of the omnidirectional flux at geosynchronous altitude on the nightside is much smaller than that for the pressure increase, but its effect becomes substantial only beyond geosynchronous orbit. Possibilities exist that our results may change to some extent for a different magnetospheric model than the one used here.

The Ctr1 family of integral membrane proteins is necessary for high affinity copper uptake in eukaryotes. Ctr1 is also involved in cellular accumulation of cisplatin, a platinum-based anticancer drug. Although the physiological role of Ctr1 has been revealed, the mechanism of action of Ctr1 remains to be elucidated. To gain a better understanding of Ctr1-mediated copper and cisplatin transport, we have monitored molecular dynamics and transport activities of yeast Saccharomyces cerevisiae Ctr1 and its mutant alleles. Co-expression of functional Ctr1 monomers fused with either cyan or yellow fluorescent protein resulted in fluorescence resonance energy transfer (FRET), which is consistent with multimer assembly of Ctr1. Copper near the K m value of Ctr1 enhanced FRET in a manner that correlated with cellular copper transport. In vitro crosslinking of Ctr1 confirmed that copper-induced FRET reflects conformational changes within pre-existing Ctr1 complexes. FRET assays in membrane-disrupted cells and protein extracts showed that intact cell structure is necessary for Ctr1 activity. Despite Ctr1-dependent cellular accumulation, cisplatin did not change Ctr1 FRET nor did it attenuate copper-induced FRET. A Ctr1 allele defective in copper transport enhanced cellular cisplatin accumulation. N-terminal methionine-rich motifs that are dispensable for copper transport play a critical role for cisplatin uptake. Taken together, our data reveal functional roles for structural remodeling of the Ctr1 multimeric complex in copper transport and suggest distinct mechanisms employed by Ctr1 for copper and cisplatin transport.