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Abstract Specific polar cap auroras, such as 15MLT‐PCA, linked to lobe reconnection due to the influence of the interplanetary magnetic field (IMF) B_ycomponent, were only observed in the summer. Although the variance in ionospheric conductivity between winter and summer has been proposed as a potential explanation for this seasonal dependency, it has also been argued that the differences in lobe reconnection between the winter and summer hemispheres could be the cause. To address this debate, we examined two data periods with similar IMF conditions when the northern hemisphere was in summer and winter, respectively. Using DMSP/SSUSI and AMPERE observations, we detected clear 15MLT‐PCA and associated field‐aligned currents in the summer, but not in the winter. These observations were compared with global MHD simulations from OpenGGCM. Lobe reconnection signatures were identified for both winter and summer in the simulation results. However, a detailed analysis showed that the pattern of lobe reconnection in the winter hemisphere was different from that in the summer. Based on the combined observation and simulation results, we suggest that particular lobe reconnection in summer is critical for generating 15MLT‐PCA, while the winter's reconnection may lead to transient or small‐scale auroral responses that were not easily identified by DMSP/SSUSI observations as a 15MLT‐PCA event. 

Multi-principal element alloys (MPEAs) exhibit outstanding strength attributed to the complex dislocation dynamics as compared to conventional alloys. Here, we develop an atomic-lattice-distortion-dependent discrete dislocation dynamics framework consisted of random field theory and phenomenological dislocation model to investigate the fundamental deformation mechanism underlying massive dislocation motions in body-centered cubic MPEA. Amazingly, the turbulence of dislocation speed is identified in light of strong heterogeneous lattice strain field caused by short-range ordering. Importantly, the vortex from dislocation flow turbulence not only acts as an effective source to initiate dislocation multiplication but also induces the strong local pinning trap to block dislocation movement, thus breaking the strength-ductility trade-off. 

Solid tumors, especially those with aberrant MYCN activation, often harbor an immunosuppressive microenvironment to fuel malignant growth and trigger treatment resistance. Despite this knowledge, there are no effective strategies to tackle this problem. We found that chemokine-like factor (CKLF) is highly expressed by various solid tumor cells and transcriptionally up-regulated by MYCN. Using the MYCN-driven high-risk neuroblastoma as a model system, we demonstrated that as early as the premalignant stage, tumor cells secrete CKLF to attract CCR4-expressing CD4⁺cells, inducing immunosuppression and tumor aggression. Genetic depletion of CD4⁺T regulatory cells abolishes the immunorestrictive and protumorigenic effects of CKLF. Our work supports that disrupting CKLF-mediated cross-talk between tumor and CD4⁺suppressor cells represents a promising immunotherapeutic approach to battling MYCN-driven tumors. 

Screening for drugs that disrupt embryonic development in zebrafish can help identify treatments that suppress metastasis.