110 research outputs found
ReIDTracker Sea: the technical report of BoaTrack and SeaDronesSee-MOT challenge at MaCVi of WACV24
Multi-Object Tracking is one of the most important technologies in maritime
computer vision. Our solution tries to explore Multi-Object Tracking in
maritime Unmanned Aerial vehicles (UAVs) and Unmanned Surface Vehicles (USVs)
usage scenarios. Most of the current Multi-Object Tracking algorithms require
complex association strategies and association information (2D location and
motion, 3D motion, 3D depth, 2D appearance) to achieve better performance,
which makes the entire tracking system extremely complex and heavy. At the same
time, most of the current Multi-Object Tracking algorithms still require video
annotation data which is costly to obtain for training. Our solution tries to
explore Multi-Object Tracking in a completely unsupervised way. The scheme
accomplishes instance representation learning by using self-supervision on
ImageNet. Then, by cooperating with high-quality detectors, the multi-target
tracking task can be completed simply and efficiently. The scheme achieved top
3 performance on both UAV-based Multi-Object Tracking with Reidentification and
USV-based Multi-Object Tracking benchmarks and the solution won the
championship in many multiple Multi-Object Tracking competitions. such as
BDD100K MOT,MOTS, Waymo 2D MO
Technical Report for Argoverse Challenges on Unified Sensor-based Detection, Tracking, and Forecasting
This report presents our Le3DE2E solution for unified sensor-based detection,
tracking, and forecasting in Argoverse Challenges at CVPR 2023 Workshop on
Autonomous Driving (WAD). We propose a unified network that incorporates three
tasks, including detection, tracking, and forecasting. This solution adopts a
strong Bird's Eye View (BEV) encoder with spatial and temporal fusion and
generates unified representations for multi-tasks. The solution was tested in
the Argoverse 2 sensor dataset to evaluate the detection, tracking, and
forecasting of 26 object categories. We achieved 1st place in Detection,
Tracking, and Forecasting on the E2E Forecasting track in Argoverse Challenges
at CVPR 2023 WAD
Generation of CD8+ T cells specific for transporter associated with antigen processing deficient cells
The Wiskott-Aldrich syndrome protein is required for iNKT cell maturation and function
The Wiskott-Aldrich syndrome (WAS) protein (WASp) is a regulator of actin cytoskeleton in hematopoietic cells. Mutations of the WASp gene cause WAS. Although WASp is involved in various immune cell functions, its role in invariant natural killer T (iNKT) cells has never been investigated. Defects of iNKT cells could indeed contribute to several WAS features, such as recurrent infections and high tumor incidence. We found a profound reduction of circulating iNKT cells in WAS patients, directly correlating with the severity of clinical phenotype. To better characterize iNKT cell defect in the absence of WASp, we analyzed wasâ/â mice. iNKT cell numbers were significantly reduced in the thymus and periphery of wasâ/â mice as compared with wild-type controls. Moreover analysis of wasâ/â iNKT cell maturation revealed a complete arrest at the CD44+ NK1.1â intermediate stage. Notably, generation of BM chimeras demonstrated a wasâ/â iNKT cell-autonomous developmental defect. wasâ/â iNKT cells were also functionally impaired, as suggested by the reduced secretion of interleukin 4 and interferon Îł upon in vivo activation. Altogether, these results demonstrate the relevance of WASp in integrating signals critical for development and functional differentiation of iNKT cells and suggest that defects in these cells may play a role in WAS pathology
Mice Lacking NKT Cells but with a Complete Complement of CD8+ T-Cells Are Not Protected against the Metabolic Abnormalities of Diet-Induced Obesity
The contribution of natural killer T (NKT) cells to the pathogenesis of metabolic abnormalities of obesity is controversial. While the combined genetic deletion of NKT and CD8+ T-cells improves glucose tolerance and reduces inflammation, interpretation of these data have been complicated by the recent observation that the deletion of CD8+ T-cells alone reduces obesity-induced inflammation and metabolic dysregulation, leaving the issue of the metabolic effects of NKT cell depletion unresolved. To address this question, CD1d null mice (CD1dâ/â), which lack NKT cells but have a full complement of CD8+ T-cells, and littermate wild type controls (WT) on a pure C57BL/6J background were exposed to a high fat diet, and glucose intolerance, insulin resistance, dyslipidemia, inflammation, and obesity were assessed. Food intake (15.5±4.3 vs 15.3±1.8 kcal/mouse/day), weight gain (21.8±1.8 vs 22.8±1.4 g) and fat mass (18.6±1.9 vs 19.5±2.1 g) were similar in CD1dâ/â and WT, respectively. As would be expected from these data, metabolic rate (3.0±0.1 vs 2.9±0.2 ml O2/g/h) and activity (21.6±4.3 vs 18.5±2.6 beam breaks/min) were unchanged by NKT cell depletion. Furthermore, the degree of insulin resistance, glucose intolerance, liver steatosis, and adipose and liver inflammatory marker expression (TNFα, IL-6, IL-10, IFN-Îł, MCP-1, MIP1α) induced by high fat feeding in CD1dâ/â were not different from WT. We conclude that deletion of NKT cells, in the absence of alterations in the CD8+ T-cell population, is insufficient to protect against the development of the metabolic abnormalities of diet-induced obesity
The 2nd Workshop on Maritime Computer Vision (MaCVi) 2024
The 2nd Workshop on Maritime Computer Vision (MaCVi) 2024 addresses maritime
computer vision for Unmanned Aerial Vehicles (UAV) and Unmanned Surface
Vehicles (USV). Three challenges categories are considered: (i) UAV-based
Maritime Object Tracking with Re-identification, (ii) USV-based Maritime
Obstacle Segmentation and Detection, (iii) USV-based Maritime Boat Tracking.
The USV-based Maritime Obstacle Segmentation and Detection features three
sub-challenges, including a new embedded challenge addressing efficicent
inference on real-world embedded devices. This report offers a comprehensive
overview of the findings from the challenges. We provide both statistical and
qualitative analyses, evaluating trends from over 195 submissions. All
datasets, evaluation code, and the leaderboard are available to the public at
https://macvi.org/workshop/macvi24.Comment: Part of 2nd Workshop on Maritime Computer Vision (MaCVi) 2024 IEEE
Xplore submission as part of WACV 202
Spontaneous focal activation of invariant natural killer T (iNKT) cells in mouse liver and kidney
<p>Abstract</p> <p>Background</p> <p>Invariant natural killer T (iNKT) cells differ from other T cells by their hyperactive effector T-cell status, in addition to the expression of NK lineage receptors and semi-invariant T-cell receptors. It is generally agreed that the immune phenotype of iNKT cells is maintained by repeated activation in peripheral tissues although no explicit evidence for such iNKT cell activity <it>in vivo </it>has so far been reported.</p> <p>Results</p> <p>We used an interferon (IFN)-γ-inducible cytoplasmic protein, Irga6, as a histological marker for local IFN-γ production. Irga6 was intensely expressed in small foci of liver parenchymal cells and kidney tubular epithelium. Focal Irga6 expression was unaffected by germ-free status or loss of TLR signalling and was totally dependent on IFN-γ secreted by T cells in the centres of expression foci. These were shown to be iNKT cells by diagnostic T cell receptor usage and their activity was lost in both CD1 d and Jα-deficient mice.</p> <p>Conclusions</p> <p>This is the first report that supplies direct evidence for explicit activation events of NKT cells <it>in vivo </it>and raises issues about the triggering mechanism and consequences for immune functions in liver and kidney.</p
Central nervous system (CNS)âresident natural killer cells suppress Th17 responses and CNS autoimmune pathology
Natural killer (NK) cells of the innate immune system can profoundly impact the development of adaptive immune responses. Inflammatory and autoimmune responses in anatomical locations such as the central nervous system (CNS) differ substantially from those found in peripheral organs. We show in a mouse model of multiple sclerosis that NK cell enrichment results in disease amelioration, whereas selective blockade of NK cell homing to the CNS results in disease exacerbation. Importantly, the effects of NK cells on CNS pathology were dependent on the activity of CNS-resident, but not peripheral, NK cells. This activity of CNS-resident NK cells involved interactions with microglia and suppression of myelin-reactive Th17 cells. Our studies suggest an organ-specific activity of NK cells on the magnitude of CNS inflammation, providing potential new targets for therapeutic intervention
The impact of transposable element activity on therapeutically relevant human stem cells
Human stem cells harbor significant potential for basic and clinical translational research as well as regenerative
medicine. Currently ~ 3000 adult and ~ 30 pluripotent stem cell-based, interventional clinical trials are ongoing
worldwide, and numbers are increasing continuously. Although stem cells are promising cell sources to treat a
wide range of human diseases, there are also concerns regarding potential risks associated with their clinical use,
including genomic instability and tumorigenesis concerns. Thus, a deeper understanding of the factors and
molecular mechanisms contributing to stem cell genome stability are a prerequisite to harnessing their therapeutic
potential for degenerative diseases. Chemical and physical factors are known to influence the stability of stem cell
genomes, together with random mutations and Copy Number Variants (CNVs) that accumulated in cultured human
stem cells. Here we review the activity of endogenous transposable elements (TEs) in human multipotent and
pluripotent stem cells, and the consequences of their mobility for genomic integrity and host gene expression. We
describe transcriptional and post-transcriptional mechanisms antagonizing the spread of TEs in the human genome,
and highlight those that are more prevalent in multipotent and pluripotent stem cells. Notably, TEs do not only
represent a source of mutations/CNVs in genomes, but are also often harnessed as tools to engineer the stem cell
genome; thus, we also describe and discuss the most widely applied transposon-based tools and highlight the
most relevant areas of their biomedical applications in stem cells. Taken together, this review will contribute to the
assessment of the risk that endogenous TE activity and the application of genetically engineered TEs constitute for
the biosafety of stem cells to be used for substitutive and regenerative cell therapiesS.R.H. and P.T.R. are funded by the Government of Spain (MINECO, RYC-2016-
21395 and SAF2015â71589-P [S.R.H.]; PEJ-2014-A-31985 and SAF2015â71589-
P [P.T.R.]). GGS is supported by a grant from the Ministry of Health of the
Federal Republic of Germany (FKZ2518FSB403)
Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)1.
In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field
- âŠ