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Detecting occluded objects still remains a challenge for state-of-the-art object detectors. The objective of this work is to improve the detection for such objects, and thereby improve the overall performance of a modern object detector. To this end we make the following four contributions: (1) We propose a simple 'plugin' module for the detection head of two-stage object detectors to improve the recall of partially occluded objects. The module predicts a tri-layer of segmentation masks for the target object, the occluder and the occludee, and by doing so is able to better predict the mask of the target object. (2) We propose a scalable pipeline for generating training data for the module by using amodal completion of existing object detection and instance segmentation training datasets to establish occlusion relationships. (3) We also establish a COCO evaluation dataset to measure the recall performance of partially occluded and separated objects. (4) We show that the plugin module inserted into a two-stage detector can boost the performance significantly, by only fine-tuning the detection head, and with additional improvements if the entire architecture is fine-tuned. COCO results are reported for Mask R-CNN with Swin-T or Swin-S backbones, and Cascade Mask R-CNN with a Swin-B backbone., BMVC 2022

Evasion of autophagy is key for intracellular survival of bacteria in host cells, but its involvement in persistent infection by Helicobacter pylori, a bacterium identified to invade gastric epithelial cells, remains obscure. The aim of this study was to functionally characterize the role of autophagy in H. pylori infection. Autophagy was assayed in H. pylori-infected human gastric epithelium and the functional role of autophagy was determined via genetic or pharmacological ablation of autophagy in mouse and cell line models of H. pylori infection. Here, we showed that H. pylori inhibited lysosomal function and thereby promoted the accumulation of autophagosomes in gastric epithelial cells. Importantly, inhibiting autophagosome formation by pharmacological inhibitors or genetic ablation of BECN1 or ATG5 reduced H. pylori intracellular survival, whereas inhibition of lysosomal functions exerted an opposite effect. Further experiments demonstrated that H. pylori inhibited lysosomal acidification and the retrograde trafficking of mannose-6-phosphate receptors, both of which are known to positively regulate lysosomal function. We conclude that H. pylori subverts autophagy into a pro-survival mechanism through inhibition of lysosomal clearance of autophagosomes. Disruption of autophagosome formation offers a novel strategy to reduce H. pylori colonization in human stomachs. Copyright © 2018 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

Autophagy is a conserved intracellular degradation process enclosing the bulk of cytosolic components for lysosomal degradation to maintain cellular homeostasis. Accumulating evidences showed that a specialized form of autophagy, known as xenophagy, could serve as an innate immune response to defend against pathogens invading inside the host cells. Correspondingly, infectious pathogens have developed a variety of strategies to disarm xenophagy, leading to a prolonged and persistent intracellular colonization. In this review, we first summarize the current knowledge about the general mechanisms of intracellular bacterial infections and xenophagy. We then focus on the ongoing battle between these two processes.

Anesthesia and surgery (A + S) are risk factors for patients to develop postoperative delirium (POD). However, the pathogenesis of POD remains largely to be determined. We employed battery of behavioral tests including open-filed test (OFT), elevated plus maze test (EPMT) and buried food test (BFT) to investigate the role of oxidative stress in the development of POD and to explore the therapeutic target for POD in mice after A + S (simple laparotomy under 1.4% isoflurane anesthesia). We initially found that 6 hours after A + S, mice failed to alter the behavioral changes in OFT and the adenosine triphosphate (ATP) level in hippocampus. After hierarchical cluster analysis, however, there was a significant change in the behavior tests between POD unsusceptible (non-POD) and susceptible (POD-like) mice. Interestingly, cyclosporine A, an inhibitor of mitochondrial permeability transition pore (mPTP) opening, exerted pharmacologically beneficial effects on symptoms, decreased reactive oxygen species (ROS) and ATP, and increased superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) levels in the hippocampus of POD-like mice. These findings suggest that abnormally activated oxidative stress might be involved in the underlying mechanisms of POD. Novel therapeutic agents targeting inhibition of oxidative stress would provide an available strategy for POD treatment.

Evasion of autophagy is key for intracellular survival of bacteria in host cells, but its involvement in persistent infection by Helicobacter pylori, a bacterium identified to invade gastric epithelial cells, remains obscure. The aim of this study was to functionally characterize the role of autophagy in H. pylori infection. Autophagy was assayed in H. pylori-infected human gastric epithelium and the functional role of autophagy was determined via genetic or pharmacological ablation of autophagy in mouse and cell line models of H. pylori infection. Here, we showed that H. pylori inhibited lysosomal function and thereby promoted the accumulation of autophagosomes in gastric epithelial cells. Importantly, inhibiting autophagosome formation by pharmacological inhibitors or genetic ablation of BECN1 or ATG5 reduced H. pylori intracellular survival, whereas inhibition of lysosomal functions exerted an opposite effect. Further experiments demonstrated that H. pylori inhibited lysosomal acidification and the retrograde trafficking of mannose-6-phosphate receptors, both of which are known to positively regulate lysosomal function. We conclude that H. pylori subverts autophagy into a pro-survival mechanism through inhibition of lysosomal clearance of autophagosomes. Disruption of autophagosome formation offers a novel strategy to reduce H. pylori colonization in human stomachs. Copyright © 2018 Pathological Society of Great Britain and Ireland. Published by John WileySons, Ltd.

The use of ammonia as a hydrogen vector has the potential to unlock the hydrogen economy. In this context, this paper presents novel insights into improving the ammonia decomposition activity of ruthenium nanoparticles supported on carbon nanotubes (CNT) by nitrogen doping. Our results can be applied to develop more active systems capable of delivering hydrogen on demand, with a view to move towards the low temperature target of less than 150 °C. Herein we demonstrate that nitrogen doping of the CNT support enhances the activity of ruthenium nanoparticles for the low temperature ammonia decomposition with turnover frequency numbers at 400 °C of 6200 LH2 mol$_{Ru}$$^{-1}$ h$^{-1}$, higher than the corresponding value of unmodified CNT supports under the same conditions (4400 LH$_{2}$ mol$_{Ru}$$^{-1}$ h$^{-1}$), despite presenting similar ruthenium particle sizes. However, when the nitrogen doping process is carried out with cetyltrimethylammonium bromide (CTAB) to enhance the dispersion of CNTs, the catalyst becomes virtually inactive despite the small ruthenium particle size, likely due to interference of CTAB, weakening the metal–support interaction. Our results demonstrate that the low temperature ammonia decomposition activity of ruthenium can be enhanced by nitrogen doping of the CNT support due to simultaneously increasing the support’s conductivity and basicity, electronically modifying the ruthenium active sites and promoting a strong metal–support interaction.

Purpose– This study aims to investigate the role and effect of national culture on social networking web sites (SNWs) use and access across countries while controlling for socio-economic factors, specifically networked readiness, level of education and mobile penetration.Design/methodology/approach– Hofstede's multidimensional framework serves as the conceptual basis for the study. Hierarchical regressions are conducted to test the hypothesized effects of cultural dimensions beyond that of the control variables on the penetration of SNWs using a secondary dataset for 36 countries.Findings– The results provide supporting empirical evidence linking three of Hofstede's cultural dimensions to nations' SNWs use and access.Research limitations/implications– Limitations include the use of secondary data for a limited number of countries. Only three social-economic variables were included as controls on the relationship between culture and SNWs access and usage. Future research will benefit from examining other cultural frameworks (such as Hall's classifications) and potential factors such as a nation's demographic composition and their roles in adoption and diffusion of the SNWs. Further research is needed to validate the results by including more nations and employing time-series data of social media penetration and diffusion.Practical implications– Managerial implications are discussed with respect to formulating more effective online marketing strategies for brand engagement and promotional media choice by accommodating for cultural differences.Originality/value– The paper's original contribution stems from the fact that little can be found in the literature about the influence of national culture on the use of social media. It attempts to establish the importance of understanding cultural impact on consumers' SNWs adoption behavior across countries.