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 −15 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.

This paper presents novel zero-current-transition (ZCT) PWM DC/DC converters without additional current stress and conduction loss on the main switch during the resonance period of the auxiliary cell. The auxiliary cell consists of a resonant inductor, a resonant capacitor, an auxiliary switch and an auxiliary diode in parallel with the main switch and the zero-current-switching (ZCS) ranges of the main and the auxiliary switch of the proposed converters are entirely achieved by operating the auxiliary cell. In addition, the resonant inductor of the proposed ZCT cell helps soft turn-on of the main switch. The theoretical analysis and the operation principle of the new ZCT technique are described in detail using a boost converter as an example. To verify the validity of the proposed ZCT technique, the simulation and the experiment were performed on the nonisolated and the isolated converter, respectively. Here, the nonisolated converter is a boost converter having 100 kHz switching frequency, 1 kW rating power, and the isolated converter is a full-bridge (FB) converter having 50 kHz switching frequency, 1 kW rating power.

Little is known about the underlying mechanisms responsible for the death of activated microglia and the functional consequences of the death of these cells, especially in vivo. We show here that intracortical injection of lipopolysaccharide (LPS) led to upregulation of interleukin‐4 (IL‐4) immunoreactivity, followed by a substantial loss of microglia 3 days later, as visualized by complement receptor type 3 (OX‐42) immunostaining and tomato lectin staining. Cells positive for caspase‐3 and terminal deoxynucleotidyl transferase mediated fluorescein‐dUTP nick‐end labeling (TUNEL) were also localized within LPS‐activated microglia. IL‐4 immunoreactivity was detected as early as 12 hr post‐LPS, disappearing at 72 hr. Surprisingly, IL‐4 immunoreactivity was detected exclusively in microglia, but not in astrocytes or neurons. In addition, IL‐4‐neutralizing antibodies markedly increased the survival of activated microglia at 3 days post‐LPS. The expression of inducible nitric oxide synthase (iNOS) and tumor‐necrosis factor (TNF)‐α was sustained in parallel in activated microglia, consequently increasing neuronal cell death. To our knowledge, this study is the first to show the endogenous expression of IL‐4 in LPS‐activated microglia in vivo. Our findings suggest that IL‐4 may regulate brain inflammation by inducing the death of activated microglia in vivo and increasing neuronal survival.