Person re-identification (Re-ID) is an important task in video surveillance which automatically searches and identifies people across different cameras. Despite the extensive Re-ID progress in RGB cameras, few works have studied the Re-ID between infrared and RGB images, which is essentially a cross-modality problem and widely encountered in real-world scenarios. The key challenge lies in two folds, i.e., the lack of discriminative information to re-identify the same person between RGB and infrared modalities, and the difficulty to learn a robust metric towards such a large-scale cross-modality retrieval. In this paper, we tackle the above two challenges by proposing a novel cross-modality generative adversarial network (termed cmGAN). To handle the issue of insufficient discriminative information, we leverage the cutting-edge generative adversarial training to design our own discriminator to learn discriminative feature representation from different modalities. To handle the issue of large-scale cross-modality metric learning, we integrates both identification loss and cross-modality triplet loss, which minimize inter-class ambiguity while maximizing cross-modality similarity among instances. The entire cmGAN can be trained in an end-to-end manner by using standard deep neural network framework. We have quantized the performance of our work in the newly-released SYSU RGB-IR Re-ID benchmark, and have reported superior performance, i.e., Cumulative Match Characteristic curve (CMC) and Mean Average Precision (MAP), over the state-of-the-art works [Wu et al., 2017], respectively.

Prostaglandin E 2 (PGE 2 ) is both an inflammatory mediator released at the site of tissue inflammation and a neuromodulator that alters neuronal excitability and synaptic processing. The effects of PGE 2 are mediated by four G-protein-coupled EP receptors (EP1-EP4). Here we show that the EP4 receptor subtype is expressed by a subset of primary sensory dorsal root ganglion (DRG) neurons, and that its levels, but not that of the other EP1-3 subtypes, increase in the DRG after complete Freund' adjuvant-induced peripheral inflammation. Administration of both an EP4 antagonist [AH23848, (4Z)-7-[(rel-1S,2S,5R)-5-((1,1Ј-biphenyl-4-yl)methoxy)-2-(4-morpholinyl)-3-oxocyclopentyl]-4-heptenoic acid] and EP4 knockdown with intrathecally delivered short hairpin RNA attenuates inflammation-induced thermal and mechanical behavioral hypersensitivity, without changing basal pain sensitivity. AH23848 also reduces the PGE 2 -mediated sensitization of capsaicin-evoked currents in DRG neurons in vitro. These data suggest that EP4 is a potential target for the pharmacological treatment of inflammatory pain.