A reflection on the essence of gratitude in palliative care: healing in severe disease and professional affirmation through accompanying patients until the end.

Background: Gratitude has sparked interest in the world of health. It is considered as a personality characteristic or as an emotion. However, little has been explored in the context of the interpersonal relationship of caring. An exploration in the context of end of life is ground-breaking. Objectives: This study analyses and reflects on the object of gratitude from the perspective of both the persons being cared for and the professionals providing health care. What are patients and their family members grateful for in palliative care? What is the reason for gratitude? What do these health professionals perceive when there is gratitude? These questions were answered considering the gratitude generated in health care encounters, not gratitude as personality trait. Methods: The phenomenological approach was used starting from lived clinical experiences. In the light of the dialogue between clinical experiences and philosophy, this study proposes an explanation of the 'real' or essential object of gratitude in palliative care. It was conducted within the context of palliative care. The study materials were manifestations of gratitude expressed or felt in clinical encounters and published in newspapers or shared in daily encounters. These were the basis for analysis and reflection and interdisciplinary dialogue. Findings: The analyses performed indicated healing or deep relief in serious diseases as objects of gratitude according to patients' perspective, and professional self-affirmation until the end according to the professionals' perspective. Conclusion: The two perspectives shared an important common fact, namely, the need to consider the persons in their entirety, and the importance of not losing sight of the value they have. This concept would characterize the nature of gratitude, its object being the 'objective good' for patients, family members, and palliative care professionals.

Diapause induces functional axonal regeneration after necrotic insult in C. elegans.

Many neurons are unable to regenerate after damage. The ability to regenerate after an insult depends on life stage, neuronal subtype, intrinsic and extrinsic factors. C. elegans is a powerful model to test the genetic and environmental factors that affect axonal regeneration after damage, since its axons can regenerate after neuronal insult. Here we demonstrate that diapause promotes the complete morphological regeneration of truncated touch receptor neuron (TRN) axons expressing a neurotoxic MEC-4(d) DEG/ENaC channel. Truncated axons of different lengths were repaired during diapause and we observed potent axonal regrowth from somas alone. Complete morphological regeneration depends on DLK-1 but neuronal sprouting and outgrowth is DLK-1 independent. We show that TRN regeneration is fully functional since animals regain their ability to respond to mechanical stimulation. Thus, diapause induced regeneration provides a simple model of complete axonal regeneration which will greatly facilitate the study of environmental and genetic factors affecting the rate at which neurons die.

The Molecular Interplay between Axon Degeneration and Regeneration.

Neurons face a series of morphological and molecular changes following trauma and in the progression of neurodegenerative disease. In neurons capable of mounting a spontaneous regenerative response, including invertebrate neurons and mammalian neurons of the peripheral nervous system (PNS), axons regenerate from the proximal side of the injury and degenerate on the distal side. Studies of Wallerian degeneration slow (WldS /Ola) mice have revealed that a level of coordination between the processes of axon regeneration and degeneration occurs during successful repair. Here, we explore how shared cellular and molecular pathways that regulate both axon regeneration and degeneration coordinate the two distinct outcomes in the proximal and distal axon segments. © 2018 Wiley Periodicals, Inc. Develop Neurobiol 00: 000-000, 2018.