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Sensor calibration is the fundamental block for a multi-sensor fusion system. This paper presents an accurate and repeatable LiDAR-IMU calibration method (termed LI-Calib), to calibrate the 6-DOF extrinsic transformation between the 3D LiDAR and the Inertial Measurement Unit (IMU).Regarding the high data capture rate for LiDAR and IMU sensors, LI-Calib adopts a continuous-time trajectory formulation based on B-Spline, which is more suitable for fusing highrate or asynchronous measurements than discrete-time based approaches. Additionally, LI-Calib decomposes the space into cells and identifies the planar segments for data association, which renders the calibration problem well-constrained in usual scenarios without any artificial targets. We validate the proposed calibration approach on both simulated and real-world experiments. The results demonstrate the high accuracy and good repeatability of the proposed method in common humanmade scenarios. To benefit the research community, we opensource our code at https://github.com/APRIL-ZJU/ lidar_IMU_calib

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There are numerous types of pathological changes in human immunodeficiency virus (HIV)-associated neurocognitive disorder (HAND), including apoptosis of neurons. HIV-1 transactivator of transcription (Tat) protein, which is encoded by HIV-1, may promote apoptosis in HAND. Forkhead box O3 (FOXO3) is a multispecific transcription factor that has roles in many biological processes, including cellular apoptosis. The aim of this study was to determine whether FOXO3 is activated by HIV-1 Tat and to investigate its role in neuronal apoptosis in HAND. We employed tissue staining and related molecular biological experimental methods to confirm our hypothesis. The in vivo experimental results demonstrated that the expression of nuclear FOXO3 increased in the apoptotic neurons of the cerebral cortexes of rhesus macaques infected with simian human immunodeficiency virus (SHIV). The in vitro investigation showed that HIV-1 Tat activated FOXO3, causing it to move from the cytoplasm to the nucleus via the c-Jun N-terminal kinase (JNK) signaling pathway in SH-SY5Y cells. Moreover, FOXO3 down-regulated expression of the anti-apoptosis gene B-cell lymphoma 2 (Bcl-2) and up-regulated the expression of the pro-apoptosis gene Bcl-2-like 11 (Bim) after entering the nucleus, eventually causing cellular apoptosis. Finally, reduction of nuclear FOXO3 reversed cellular apoptosis. Our results suggest that HIV-1 Tat induces FOXO3 to translocate from the cytoplasm to the nucleus via the JNK signaling pathway, leading to neuronal apoptosis. Agents targeting FOXO3 may provide approaches for restoring neuronal function in HAND.

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