As modificações da medicina tornaram o conhecimento biomédico soberano, gerando a perda da relação médico-paciente, o que fomentou o movimento pela humanização. Na Universidade Federal do Paraná (UFPR), formou-se o projeto de extensão "ProCura - a arte da vida", a fim de implementar a humanização entre os alunos e em suas relações profissionais. Seus objetivos se baseiam nos pilares: relação estudante-paciente, relação estudante-estudante e formação teórico-reflexiva, e se subdividem nos grupos Cineclube, Clown e Contação de Histórias. De 2010 a 2012, 79 alunos participaram e atenderam 905 pacientes, 505 acompanhantes e 107 funcionários. Apesar de limitações de alcance no que concerne a atingir todos os alunos do Setor de Ciências da Saúde, o projeto pretende fomentar a discussão entre grupos e que seus ideais e atividades se espalhem e permeiem o meio acadêmico.

It has been proposed that neurotrophin-3 acts in a manner that is opposed to nerve growth factor, especially in the modulation of heat hyperalgesia. Injury to the constriction of the infraorbital nerve (CION) is a well-established model of trigeminal neuropathic pain that leads to robust heat, cold, and mechanical hyperalgesia. Here, we assessed the effect of local neurotrophin-3 treatment on CION-induced hyperalgesia, and we examined some mechanisms related to the effect of neurotrophin-3. Neurotrophin-3 (1 µg/50 µl) injected into the upper lip of CION rats caused a significant and long-lasting reduction of CION-induced heat hyperalgesia, but failed to affect cold and mechanical hyperalgesia. Increased levels of neurotrophin-3 were detected in the injured nerve at the time point that represents the peak of heat hyperalgesia. The anti-hyperalgesic effect of neurotrophin-3 was markedly reduced in the presence of an antagonist of TrkA receptors (K-252a, 1 μg/50 μl). Moreover, association of lower doses of neurotrophin-3 with an antibody anti-nerve growth factor resulted in a synergistic anti-hyperalgesic effect in CION rats. Local injection of nerve growth factor (3 µg/50 µl) or the TRPV1 agonist capsaicin (1 μg/50 μl), but not neurotrophin-3 injection (1 µg/50 µl), resulted in long-lasting facial heat hyperalgesia, which was both significantly reduced by previous neurotrophin-3 local treatment. In conclusion, we suggest that neurotrophin-3 is a potent modulator of facial heat hyperalgesia, which may exert an inhibitory influence on the trkA pathway. Neurotrophin-3 treatment may represent a promising approach, especially in pain conditions associated with increased levels of nerve growth factor.