An Object-Centric Hierarchical Pose Estimation Method Using Semantic High-Definition Maps for General Autonomous Driving.

To achieve Level 4 and above autonomous driving, a robust and stable autonomous driving system is essential to adapt to various environmental changes. This paper aims to perform vehicle pose estimation, a crucial element in forming autonomous driving systems, more universally and robustly. The prevalent method for vehicle pose estimation in autonomous driving systems relies on Real-Time Kinematic (RTK) sensor data, ensuring accurate location acquisition. However, due to the characteristics of RTK sensors, precise positioning is challenging or impossible in indoor spaces or areas with signal interference, leading to inaccurate pose estimation and hindering autonomous driving in such scenarios. This paper proposes a method to overcome these challenges by leveraging objects registered in a high-precision map. The proposed approach involves creating a semantic high-definition (HD) map with added objects, forming object-centric features, recognizing locations using these features, and accurately estimating the vehicle's pose from the recognized location. This proposed method enhances the precision of vehicle pose estimation in environments where acquiring RTK sensor data is challenging, enabling more robust and stable autonomous driving. The paper demonstrates the proposed method's effectiveness through simulation and real-world experiments, showcasing its capability for more precise pose estimation.

Caffeic Acid Cyclohexylamide Rescues Lethal Inflammation in Septic Mice through Inhibition of IκB Kinase in Innate Immune Process.

Targeting myeloid differentiation protein 2 (MD-2) or Toll-like receptor 4 (TLR4) with small molecule inhibitor rescues the systemic inflammatory response syndrome (SIRS) in sepsis due to infection with Gram-negative bacteria but not other microbes. Herein, we provided IκB kinase ß (IKKß) in innate immune process as a molecular target of caffeic acid cyclohexylamide (CGA-JK3) in the treatment of polymicrobial TLR agonists-induced lethal inflammation. CGA-JK3 ameliorated E. coli lipopolysaccharide (LPS, MD-2/TLR4 agonist)-induced endotoxic shock, cecal ligation and puncture (CLP)-challenged septic shock or LPS plus D-galactosamine (GalN)-induced acute liver failure (ALF) in C57BL/6J mice. As a molecular basis, CGA-JK3 inhibited IKKß-catalyzed kinase activity in a competitive mechanism with respect to ATP, displaced fluorescent ATP probe from the complex with IKKß, and docked at the ATP-binding active site on the crystal structure of human IKKß. Furthermore, CGA-JK3 inhibited IKKß-catalyzed IκB phosphorylation, which is an axis leading to IκB degradation in the activating pathway of nuclear factor-κB (NF-κB), in macrophages stimulated with TLR (1/2, 2/6, 4, 5, 7, 9) agonists from Gram-positive/negative bacteria and viruses. CGA-JK3 consequently interrupted IKKß-inducible NF-κB activation and NF-κB-regulated expression of TNF-α, IL-1α or HMGB-1 gene, thereby improving TLRs-associated redundant inflammatory responses in endotoxemia, polymicrobial sepsis and ALF.