Despite all the significant advances in pedestrian detection brought by computer vision for driving assistance, it is still a challenging problem. One reason is the extremely varying lighting conditions under which such a detector should operate, namely day and nighttime. Recent research has shown that the combination of visible and non-visible imaging modalities may increase detection accuracy, where the infrared spectrum plays a critical role. The goal of this paper is to assess the accuracy gain of different pedestrian models (holistic, part-based, patch-based) when training with images in the far infrared spectrum. Specifically, we want to compare detection accuracy on test images recorded at day and nighttime if trained (and tested) using (a) plain color images; (b) just infrared images; and (c) both of them. In order to obtain results for the last item, we propose an early fusion approach to combine features from both modalities. We base the evaluation on a new dataset that we have built for this purpose as well as on the publicly available KAIST multispectral dataset.

Cold allodynia is a common symptom of neuropathic and inflammatory pain following peripheral nerve injury. The mechanisms underlying this disabling sensory alteration are not entirely understood. In primary somatosensory neurons, cold sensitivity is mainly determined by a functional counterbalance between cold-activated TRPM8 channels and Shaker-like Kv1.1-1.2 channels underlying the excitability brake current I Here we studied the role of I in damage-triggered painful hypersensitivity to innocuous cold. We found that cold allodynia induced by chronic constriction injury (CCI) of the sciatic nerve in mice, was related to both an increase in the proportion of cold-sensitive neurons (CSNs) in DRGs contributing to the sciatic nerve, and a decrease in their cold temperature threshold. I density was reduced in high-threshold CSNs from CCI mice compared with sham animals, with no differences in cold-induced TRPM8-dependent current density. The electrophysiological properties and neurochemical profile of CSNs revealed an increase of nociceptive-like phenotype among neurons from CCI animals compared with sham mice. These results were validated using a mathematical model of CSNs, including I and TRPM8, showing that a reduction in I current density shifts the thermal threshold to higher temperatures and that the reduction of this current induces cold sensitivity in former cold-insensitive neurons expressing low levels of TRPM8-like current. Together, our results suggest that cold allodynia is largely due to a functional downregulation of I in both high-threshold CSNs and in a subpopulation of polymodal nociceptors expressing TRPM8, providing a general molecular and neural mechanism for this sensory alteration. This paper unveils the critical role of the brake potassium current I in damage-triggered cold allodynia. Using a well-known form of nerve injury and combining behavioral analysis, calcium imaging, patch clamping, and pharmacological tools, validated by mathematical modeling, we determined that the functional expression of I is reduced in sensory neurons in response to peripheral nerve damage. This downregulation not only enhances cold sensitivity of high-threshold cold thermoreceptors signaling cold discomfort, but it also transforms a subpopulation of polymodal nociceptors signaling pain into neurons activated by mild temperature drops. Our results suggest that cold allodynia is linked to a reduction of I in both high-threshold cold thermoreceptors and nociceptors expressing TRPM8, providing a general model for this form of cold-induced pain.

We thank Ardem Patapoutian and Paul Heppenstall for providing the Piezo2 fl/fl and Advillin-Cre mice respectively, and Salvador Sala for helping with current kinetic analysis. Mireille Tora and Eva Quintero are acknowledged for excellent technical assistance and Carlos Ramos and Sergio Javaloy for illustrations. We also thanks all members of the Sensory Transduction and Nociception Group for useful comments and suggestions. The authors gratefully acknowledge the financial support received by the Spanish Government projects: SAF2016-77233R (A.Gomis and F.V.

Background:The functional role of the TRPM8 N terminus remains poorly understood. Results: Truncation of the first 40 residues increases TRPM8 responses to cold and menthol, whereas deletions within the 40 -60-residue region yield nonfunctional channels retained in the ER. Conclusion: Initial N terminus of TRPM8 is important for proper biogenesis and function. Significance: Variations within the N terminus can modulate thermal and chemical sensitivity of TRPM8.