Human Motion Trajectory Prediction: A Survey

With growing numbers of intelligent autonomous systems in human environments, the ability of such systems to perceive, understand and anticipate human behavior becomes increasingly important. Specifically, predicting future positions of dynamic agents and planning considering such predictions are key tasks for self-driving vehicles, service robots and advanced surveillance systems. This paper provides a survey of human motion trajectory prediction. We review, analyze and structure a large selection of work from different communities and propose a taxonomy that categorizes existing methods based on the motion modeling approach and level of contextual information used. We provide an overview of the existing datasets and performance metrics. We discuss limitations of the state of the art and outline directions for further research.Comment: Submitted to the International Journal of Robotics Research (IJRR), 37 page

Telomeric expression sites are highly conserved in trypanosoma brucei

Subtelomeric regions are often under-represented in genome sequences of eukaryotes. One of the best known examples of the use of telomere proximity for adaptive purposes are the bloodstream expression sites (BESs) of the African trypanosome Trypanosoma brucei. To enhance our understanding of BES structure and function in host adaptation and immune evasion, the BES repertoire from the Lister 427 strain of T. brucei were independently tagged and sequenced. BESs are polymorphic in size and structure but reveal a surprisingly conserved architecture in the context of extensive recombination. Very small BESs do exist and many functioning BESs do not contain the full complement of expression site associated genes (ESAGs). The consequences of duplicated or missing ESAGs, including ESAG9, a newly named ESAG12, and additional variant surface glycoprotein genes (VSGs) were evaluated by functional assays after BESs were tagged with a drug-resistance gene. Phylogenetic analysis of constituent ESAG families suggests that BESs are sequence mosaics and that extensive recombination has shaped the evolution of the BES repertoire. This work opens important perspectives in understanding the molecular mechanisms of antigenic variation, a widely used strategy for immune evasion in pathogens, and telomere biology

How Infection and Vaccination Are Linked to Acute and Chronic Urticaria: A Special Focus on COVID-19

Since more than a century ago, there has been awareness of the connection between viral infections and the onset and exacerbation of urticaria. Our knowledge about the role of viral infection and vaccination in acute and chronic urticaria improved as a result of the COVID-19 pandemic but it has also highlighted knowledge gaps. Viral infections, especially respiratory tract infections like COVID-19, can trigger the onset of acute urticaria (AU) and the exacerbation of chronic urticaria (CU). Less frequently, vaccination against viruses including SARS-CoV-2 can also lead to new onset urticaria as well as worsening of CU in minority. Here, with a particular focus on COVID-19, we review what is known about the role of viral infections and vaccinations as triggers and causes of acute and chronic urticaria. We also discuss possible mechanistic pathways and outline the unmet needs in our knowledge. Although the underlying mechanisms are not clearly understood, it is believed that viral signals, medications, and stress can activate skin mast cells (MCs). Further studies are needed to fully understand the relevance of viral infections and vaccinations in acute and chronic urticaria and to better clarify causal pathways

How Infection and Vaccination Are Linked to Acute and Chronic Urticaria: A Special Focus on COVID-19

Since more than a century ago, there has been awareness of the connection between viral infections and the onset and exacerbation of urticaria. Our knowledge about the role of viral infection and vaccination in acute and chronic urticaria improved as a result of the COVID-19 pandemic but it has also highlighted knowledge gaps. Viral infections, especially respiratory tract infections like COVID-19, can trigger the onset of acute urticaria (AU) and the exacerbation of chronic urticaria (CU). Less frequently, vaccination against viruses including SARS-CoV-2 can also lead to new onset urticaria as well as worsening of CU in minority. Here, with a particular focus on COVID-19, we review what is known about the role of viral infections and vaccinations as triggers and causes of acute and chronic urticaria. We also discuss possible mechanistic pathways and outline the unmet needs in our knowledge. Although the underlying mechanisms are not clearly understood, it is believed that viral signals, medications, and stress can activate skin mast cells (MCs). Further studies are needed to fully understand the relevance of viral infections and vaccinations in acute and chronic urticaria and to better clarify causal pathways

Structure of the LDL receptor extracellular domain at endosomal pH

The low-density lipoprotein receptor mediates cholesterol homeostasis through endocytosis of lipoproteins. It discharges its ligand in the endosome at pH Ͻ 6. In the crystal structure at pH ϭ 5.3, the ligand-binding domain (modules R2 to R7) folds back as an arc over the epidermal growth factor precursor homology domain (the modules A, B, ␤ propeller, and C). The modules R4 and R5, which are critical for lipoprotein binding, associate with the ␤ propeller via their calcium-binding loop. We propose a mechanism for lipoprotein release in the endosome whereby the ␤ propeller functions as an alternate substrate for the ligand-binding domain, binding in a calcium-dependent way and promoting lipoprotein release. The low-density lipoprotein receptor (LDL-R) regulates cholesterol homeostasis in mammalian cells. LDL-R removes cholesterolcarrying lipoproteins from plasma circulation in a process known as receptor-mediated endocytosis (1). Ligands bound extracellularly by LDL-R at neutral pH are internalized and then released in the endosomes ( pH Ͻ 6), leading to their subsequent lysosomal degradation. The receptor then recycles to the cell surface. Mutations in the LDL-R gene cause familial hypercholesterolemia (FH), one of the most common simply inherited genetic diseases (2). FH heterozygotes exhibit a reduced rate of receptor-mediated removal of plasma LDL by the liver, ultimately leading to early onset coronary heart disease and atherosclerosis. More than 920 mutations in LDL-R are known, some of which have been functionally characterized (2, 3). The extracellular domain of LDL-R is composed of a "ligand-binding domain" (with cysteine-rich repeats R1 to R7) and an "epidermal growth factor (EGF) precursor homology domain" (with the EGF-like repeats A, B, and C, as well as a ␤ propeller between B and C) (4, 5). LDL-R binds LDL via the single protein in LDL, the 550-kD apolipoprotein B (apoB) (6); deleting R3, R4, R5, R6, or R7 reduces LDL binding to Ͻ20% of that of the wild-type LDL-R (7). LDL-R also binds to very low density lipoprotein (VLDL), ␤-VLDL, intermediate density lipoprotein (IDL), and chylomicron remnants via the 33-kD apolipoprotein E (apoE) (8, 9); disrupting R5 decreases ␤-VLDL binding to 30 to 50% of that of the wild-type receptor, whereas disrupting R4 or R6 reduces binding only slightly (7). At neutral pH, negative charges on repeats R1 to R7 are thought to interact with positive charges on apoB and apoE. Indeed, LDL binding to LDL-R can be disrupted competitively with polycations or permanently by selective chemical modification of positively charged residues on apoE or apoB Dissociation of ligands is crucial for receptor recycling and hence proper receptor function; mutations in LDL-R that impair ligand release produce FH (2). Deletion mutagenesis studies in LDL-R and the related VLDL-R have indicated that, although the ligand-binding domain is sufficient for binding lipoprotein particles, the receptor requires the EGF precursor homology domain for ligand release (16-18). The structural basis for LDL-R's ability to recognize a diverse group of lipoprotein particles, all varying in size, and release them at acidic pH is unknown. High-resolution crystal structures of modules R5 (12) and ␤ propeller-C (5) are known, and solution NMR structures are known for single and tandem repeats, including R1, R2, R5, R6, A, and B Structure determination. The extracellular domain of human LDL-R (residues 1 to 699) was crystallized at pH ϭ 5.3, with the symmetry of space group P3 1 21 (28). Soaking crystals in sodium 12-tungstophosphate (Na 3 PW 12 O 40 ) improved their diffractive quality and incorporated large anomalous scatterers. The asymmetric unit contains a single protein molecule and two tungsten clusters as well as half of a tungsten cluster on a crystallographic twofold axis. Data collection, structure determination, and model statistics are given in Monomer description. There is clear electron density in the crystal structure for the modules R2, R3, R4, R5, R6, R7, A, B, ␤ propeller, and C In the crystal, each monomer forms major contacts with five neighboring symmetry-related molecules. Although the relative orien

Large-Scale Slat Noise Studies within the Project OPENAIR

The present contribution summarizes the slat noise research activity within work package WP4.2 (Wing Systems) of the EC co-financed project OPENAIR (Optimisation for low environmental noise impact aircraft) conducted by the partners Airbus and DLR. It involves both experimental and numerical studies at the large-scale (1:3.3) swept high-lift wing model F15-LS. Experiments were performed in the Large Low-speed Facility DNW-LLF • to extend current slat noise validation data bases towards more realistic test conditions than in precursor projects to support the further development of DLR’s numerical slat noise prediction capability and • to verify the documented noise reduction benefit of established slat noise reduction concepts from precursor projects for these extended test conditions. Slat noise reduction concepts that have been revisited and further developed were • optimized slat gap and overlap settings as well as • an adaptive slat concept that actively reduces the gap width to reduce noise under typical approach conditions but restores the original gap width / maximum lift if necessary. OPENAIR slat noise studies build upon the outcome of the forerunner project TIMPAN, where the noise differences attributed to slat setting variations were numerically predicted and experimentally validated at a fourfold smaller 1:13.2-scaled 2D high-lift system (F16 model). FEM analysis served to specify technically feasible adaptive slat profile bending, accounting for conventional actuator specifications, feasible skin materials and critical aerodynamic loads determined by the flight envelope. Two selected adaptive slat shapes were finally realized as solid model parts that were tested in the DNW-LLF (fully closed gap, intermediate gap width). Main results were: The adaptive slat with closed gap provides a noise reduction of order 5 dB at wing level, equivalent to a full elimination of the slat noise source. Modified slat settings or an adaptive slat with intermediate gap width are suited to reduce slat noise by about 2─3 dB at wing level while producing negligible aerodynamic impact at the operative test angles of attack. Comparisons of CAA (Computational Aeroacoustics) prediction results with the DNW-LLF measurement data revealed a generally good reproduction of the observed trends with the restriction that measured differences to be resolved were relatively small for most of the tested slat setting variants. Overall, major results from the TIMPAN project were reproduced within OPENAIR. Particularly, the expectation of a relatively broad optimum for aeroacoustically optimized slat settings, as deduced from the former TIMPAN results, is supported by both the measurement and CAA results

Nonlinear effects in resonant layers in solar and space plasmas

The present paper reviews recent advances in the theory of nonlinear driven magnetohydrodynamic (MHD) waves in slow and Alfven resonant layers. Simple estimations show that in the vicinity of resonant positions the amplitude of variables can grow over the threshold where linear descriptions are valid. Using the method of matched asymptotic expansions, governing equations of dynamics inside the dissipative layer and jump conditions across the dissipative layers are derived. These relations are essential when studying the efficiency of resonant absorption. Nonlinearity in dissipative layers can generate new effects, such as mean flows, which can have serious implications on the stability and efficiency of the resonance