Two-person Graph Convolutional Network for Skeleton-based Human Interaction Recognition

Graph convolutional networks (GCNs) have been the predominant methods in skeleton-based human action recognition, including human-human interaction recognition. However, when dealing with interaction sequences, current GCN-based methods simply split the two-person skeleton into two discrete graphs and perform graph convolution separately as done for single-person action classification. Such operations ignore rich interactive information and hinder effective spatial inter-body relationship modeling. To overcome the above shortcoming, we introduce a novel unified two-person graph to represent inter-body and intra-body correlations between joints. Experiments show accuracy improvements in recognizing both interactions and individual actions when utilizing the proposed two-person graph topology. In addition, We design several graph labeling strategies to supervise the model to learn discriminant spatial-temporal interactive features. Finally, we propose a two-person graph convolutional network (2P-GCN). Our model achieves state-of-the-art results on four benchmarks of three interaction datasets: SBU, interaction subsets of NTU-RGB+D and NTU-RGB+D 120

Regulation of welding residual stress in laser-welded AISI 304 steel-niobium joints using a Cu interlayer

Residual stress and deformation in a welded joint will significantly reduce its service life, and thus the analysis and regulation of residual stresses are very important. In this paper, a SYSWELD software was used to numerically simulate the temperature field, residual stress field, and the welding deformation during welding with and without a Cu interlayer. Thermocouples were used to measure the thermal cycle curves, and X-ray diffraction (XRD) was used to measure the residual stresses of the joints. The results show that the addition of a Cu interlayer does not significantly change the temperature field, and that the high temperature region on the niobium side is wider. In addition, the peak temperature in the centre of the welds and the temperature gradient perpendicular to the weld are greatly reduced by a Cu interlayer. Furthermore, a Cu interlayer contributes to a certain increase in both transverse and longitudinal residual stresses. Because the weld involves three different materials, steel, niobium, and Cu, the residual stresses in the welds are more complex. The simulation of the welding deformation shows that the transverse shrinkage in the thickness direction can be homogenized by the Cu interlayer, which leads to a significant reduction in deformation.acceptedVersio

USP25 inhibits neuroinflammatory responses after cerebral ischemic stroke by deubiquitinating TAB2

Cerebral ischemic stroke is a leading cause of morbidity and mortality globally. However, the mechanisms underlying ischemic stroke injury remain poorly understood. Here, it is found that deficiency of the ubiquitin-specific protease USP25 significantly aggravate ischemic stroke injury in mice. USP25 has no impact on neuronal death under hypoxic conditions, but reduced ischemic stroke-induced neuronal loss and neurological deficits by inhibiting microglia-mediated neuroinflammation. Mechanistically, USP25 restricts the activation of NF-κB and MAPK signaling by regulating TAB2. As a deubiquitinating enzyme, USP25 removeds K63-specific polyubiquitin chains from TAB2. AAV9-mediated TAB2 knockdown ameliorates ischemic stroke injury and abolishes the effect of USP25 deletion. In both mouse and human brains, USP25 is markedly upregulated in microglia in the ischemic penumbra, implying a clinical relevance of USP25 in ischemic stroke. Collectively, USP25 is identified as a critical inhibitor of ischemic stroke injury and this data suggest USP25 may serve as a therapeutic target for ischemic stroke.</p

IL-21 promotes myocardial ischaemia/reperfusion injury through the modulation of neutrophil infiltration.

BACKGROUND AND PURPOSE: The immune system plays an important role in driving the acute inflammatory response following myocardial ischaemia/reperfusion injury (MIRI). IL-21 is a pleiotropic cytokine with multiple immunomodulatory effects, but its role in MIRI is not known. EXPERIMENTAL APPROACH: Myocardial injury, neutrophil infiltration and the expression of neutrophil chemokines KC (CXCL1) and MIP-2 (CXCL2) were studied in a mouse model of MIRI. Effects of IL-21 on the expression of KC and MIP-2 in neonatal mouse cardiomyocytes (CMs) and cardiac fibroblasts (CFs) were determined by real-time PCR and ELISA. The signalling mechanisms underlying these effects were explored by western blot analysis. KEY RESULTS: IL-21 was elevated within the acute phase of murine MIRI. Neutralization of IL-21 attenuated myocardial injury, as illustrated by reduced infarct size, decreased cardiac troponin T levels and improved cardiac function, whereas exogenous IL-21 administration exerted opposite effects. IL-21 increased the infiltration of neutrophils and increased the expression of KC and MIP-2 in myocardial tissue following MIRI. Moreover, neutrophil depletion attenuated the IL-21-induced myocardial injury. Mechanistically, IL-21 increased the production of KC and MIP-2 in neonatal CMs and CFs, and enhanced neutrophil migration, as revealed by the migration assay. Furthermore, we demonstrated that this IL-21-mediated increase in chemokine expression involved the activation of Akt/NF-κB signalling in CMs and p38 MAPK/NF-κB signalling in CFs. CONCLUSIONS AND IMPLICATIONS: Our data provide novel evidence that IL-21 plays a pathogenic role in MIRI, most likely by promoting cardiac neutrophil infiltration. Therefore, targeting IL-21 may have therapeutic potential as a treatment for MIRI. LINKED ARTICLES: This article is part of a themed section on Spotlight on Small Molecules in Cardiovascular Diseases. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v175.8/issuetoc

Network capacity of wireless ad hoc networks with delay constraint

The capacity of wireless ad hoc networks has been widely studied since the pioneer works by Gupta and Kumar [3], and Gross-glauser and Tse [4]. Various asymptotic results on capacity and capacity-delay tradeoffs have been obtained, whereas most of those investigated the asymptotic performance in large networks and addressed the delay caused by node mobility, In this paper the tradeoff between throughput capacity and average transmission delay of arbitrary scale wireless ad hoc networks is investigated. We consider a network with N nodes randomly distributed in a disk area of radius R. A new criterion of transmission concurrency is introduced to describe the concurrent transmitting capability of the network. And by using a constructive scheme, where a balanced scheduling strategy and a minimal length route selection mechanism are proposed, an analytical expression of the relationship between the throughput capacity T and the average transmission delay D is derived. A case study is also provided to give numerical results