Dark Tourism in the land of Sunshine: An intercultural business model for the routes of death and disaster in Portugal

The main goal of this dissertation is the creation and subsequent implementation of dark tourism routes in Portugal, following a business model that already exists in other cultures. This typology of tourism is an extension of cultural tourism and is classified by the search for places where once disasters, suffering and death occurred. Thus, concentration camps, inactive prisons, serial killers' homes, cemeteries, and all other places that fit into the patterns of death, tragedy and suffering can be considered dark tourism sites. In Portugal, there are some places associated with the practice of dark tourism, although this type of business is not yet sufficiently explored. Therefore, this dissertation intends to use the country’s heritage, which is one of the levers for promoting tourism and an important factor of development, thus justifying the elaboration of a conceptual map associated with tourism. With the delineation of routes in this dissertation, we intend not only to introduce this market niche in the country, but also to contribute innovatively to the tourist dynamics, in order to blur the existing seasonality, which arises from the demand for sun and sea tourism. With the conception and design of these routes, we intend to make a pioneering contribution to the creation of a platform to promote dark tourism in the country. The creation of a business model and a marketing plan results from the need to assess the viability of the implementation of this project, and to discuss the best strategies for implementing it

Reduced nerve injury-induced neuropathic pain in kinin B1 receptor knock-out mice

Injury to peripheral nerves often results in a persistent neuropathic pain condition that is characterized by spontaneous pain, allodynia, and hyperalgesia. Nerve injury is accompanied by a local inflammatory reaction in which nerve-associated and immune cells release several pronociceptive mediators. Kinin B1 receptors are rarely expressed in nontraumatized tissues, but they can be expressed after tissue injury. Because B1 receptors mediate chronic inflammatory painful processes, we studied their participation in neuropathic pain using receptor gene-deleted mice. In the absence of neuropathy, we found no difference in the paw-withdrawal responses to thermal or mechanical stimulation between B1 receptor knock-out mice and 129/J wild-type mice. Partial ligation of the sciatic nerve in the wild-type mouse produced a profound and long-lasting decrease in thermal and mechanical thresholds in the paw ipsilateral to nerve lesion. Threshold changed neither in the sham-operated animals nor in the paw contralateral to lesion. Ablation of the gene for the B1 receptor resulted in a significant reduction in early stages of mechanical allodynia and thermal hyperalgesia. Furthermore, systemic treatment with the B1 selective receptor antagonist des-Arg9-[Leu8]-bradykinin reduced the established mechanical allodynia observed 7-28 d after nerve lesion in wild-type mice. Partial sciatic nerve ligation induced an upregulation in B1 receptor mRNA in ipsilateral paw, sciatic nerve, and spinal cord of wild-type mice. Together, kinin B1 receptor activation seems to be essential to neuropathic pain development, suggesting that an oral-selective B1 receptor antagonist might have therapeutic potential in the management of chronic pain