Real-Time Unified Trajectory Planning and Optimal Control for Urban Autonomous Driving Under Static and Dynamic Obstacle Constraints

Trajectory planning and control have historically been separated into two modules in automated driving stacks. Trajectory planning focuses on higher-level tasks like avoiding obstacles and staying on the road surface, whereas the controller tries its best to follow an ever changing reference trajectory. We argue that this separation is (1) flawed due to the mismatch between planned trajectories and what the controller can feasibly execute, and (2) unnecessary due to the flexibility of the model predictive control (MPC) paradigm. Instead, in this paper, we present a unified MPC-based trajectory planning and control scheme that guarantees feasibility with respect to road boundaries, the static and dynamic environment, and enforces passenger comfort constraints. The scheme is evaluated rigorously in a variety of scenarios focused on proving the effectiveness of the optimal control problem (OCP) design and real-time solution methods. The prototype code will be released at https://github.com/WATonomous/control

RALACs: Action Recognition in Autonomous Vehicles using Interaction Encoding and Optical Flow

When applied to autonomous vehicle (AV) settings, action recognition can enhance an environment model's situational awareness. This is especially prevalent in scenarios where traditional geometric descriptions and heuristics in AVs are insufficient. However, action recognition has traditionally been studied for humans, and its limited adaptability to noisy, un-clipped, un-pampered, raw RGB data has limited its application in other fields. To push for the advancement and adoption of action recognition into AVs, this work proposes a novel two-stage action recognition system, termed RALACs. RALACs formulates the problem of action recognition for road scenes, and bridges the gap between it and the established field of human action recognition. This work shows how attention layers can be useful for encoding the relations across agents, and stresses how such a scheme can be class-agnostic. Furthermore, to address the dynamic nature of agents on the road, RALACs constructs a novel approach to adapting Region of Interest (ROI) Alignment to agent tracks for downstream action classification. Finally, our scheme also considers the problem of active agent detection, and utilizes a novel application of fusing optical flow maps to discern relevant agents in a road scene. We show that our proposed scheme can outperform the baseline on the ICCV2021 Road Challenge dataset and by deploying it on a real vehicle platform, we provide preliminary insight to the usefulness of action recognition in decision making

A multicentre randomised controlled trial of day hospital-based falls prevention programme for a screened population of community-dwelling older people at high risk of falls

Objective: to determine the clinical effectiveness of a day hospital-delivered multifactorial falls prevention programme, for community-dwelling older people at high risk of future falls identified through a screening process

Facts about our ecological crisis are incontrovertible: we must take action

Humans cannot continue to violate the fundamental laws of nature or science with impunity, say 94 signatories including Dr Alison Green and Molly Scott Cato MEP. Professor of Sustainability Leadership at the University of Cumbria Jem Bendell joined others in calling for a wider debate about sustainability, featured in The Guardian. We the undersigned represent diverse academic disciplines, and the views expressed here are those of the signatories and not their organisations. While our academic perspectives and expertise may differ, we are united on one point: we will not tolerate the failure of this or any other government to take robust and emergency action in respect of the worsening ecological crisis. The science is clear, the facts are incontrovertible, and it is unconscionable to us that our children and grandchildren should have to bear the terrifying brunt of an unprecedented disaster of our own making

Cytotoxicity of Nubein6.8 peptide isolated from the snake venom of Naja nubiae on melanoma and ovarian carcinoma cell lines

This study was conducted to examine the cytotoxic effects of Nubein6.8 isolated from the venom of the Egyptian Spitting Cobra Naja nubiae on melanoma (A375) and ovarian carcinoma cell lines and to reveal its mode of action. The size of Nubein6.8 (6801.8 Da) and its N-terminal sequence are similar to cytotoxins purified from the venom of other spitting cobras. Nubein6.8 showed a high significant cytotoxic effect on A375 cell line and moderate effect on A2780. A clonogenic assay showed that Nubein6.8 has a significant long-term potency on A375 cell survival when compared to A2780. The molecular intracellular signaling pathways of Nubein6.8 have been investigated using Western blotting analysis, flow cytometry, and microscale protein labeling. This data revealed that Nubein6.8 has DNA damaging effects and the ability to activate apoptosis in both tumor cell lines. Cellular uptake recordings revealed that the labeled-Nubein6.8 was intracellularly present in A375 cells while A2780 displayed resistance against it. SEM examination showed that Nubein6.8 was found to have high accessibility to malignant melanoma cells. The apoptotic effect of Nubein6.8 was confirmed by TEM examination that revealed many evident characteristics for Nubein6.8 apoptotic efficacy on A375 cell sections. Also, TEM reflected many resistant characteristics that faced Nubein6.8 acquisition through ovarian carcinoma cell sections. Accordingly, the snake venom peptide of Nubein6.8 is a promising template for developing potential cytotoxic agents targeting human melanoma and ovarian carcinoma

Shear Stress Markedly Alters the Proteomic Response to Hypoxia in Human Pulmonary Endothelial Cells

Blood flow produces shear stress that homeostatically regulates the phenotype of pulmonary endothelial cells, exerting antiinflammatory and antithrombotic actions and maintaining normal barrier function. Hypoxia due to diseases, such as chronic obstructive pulmonary disease (COPD), causes vasoconstriction, increased vascular resistance, and pulmonary hypertension. Hypoxia-induced changes in endothelial function play a central role in the development of pulmonary hypertension. However, the interactive effects of hypoxia and shear stress on the pulmonary endothelial phenotype have not been studied. Human pulmonary microvascular endothelial cells were cultured in normoxia or hypoxia while subjected to physiological shear stress or in static conditions. Unbiased proteomics was used to identify hypoxia-induced changes in protein expression. Using publicly available single-cell RNA sequencing datasets, differences in gene expression between the alveolar endothelial cells from COPD and healthy lungs were identified. Sixty proteins were identified whose expression changed in response to hypoxia in conditions of physiological shear stress but not in static conditions. These included proteins that are crucial for endothelial homeostasis (e.g., JAM-A [junctional adhesion molecule A], ERG [ETS transcription factor ERG]) or implicated in pulmonary hypertension (e.g., thrombospondin-1). Fifty-five of these 60 have not been previously implicated in the development of hypoxic lung diseases. mRNA for 5 of the 60 (ERG, MCRIP1 [MAPK regulated corepressor interacting protein 1], EIF4A2 [eukaryotic translation initiation factor 4A2], HSP90AA1 [heat shock protein 90 alpha family class A member 1], and DNAJA1 [DnaJ Hsp40 (heat shock protein family) member A1]) showed similar changes in the alveolar endothelial cells of COPD compared with healthy lungs in females but not in males. These data show that the proteomic responses of the pulmonary microvascular endothelium to hypoxia are significantly altered by shear stress and suggest that these shear-hypoxia interactions are important in the development of hypoxic pulmonary vascular disease.Science Foundation IrelandEuropean Commission Horizon 2020Marie Skłodowska-Curie grant2024-02-02 JG check funders list add E