Resilience following spinal cord injury: a phenomenological view.

STUDY DESIGN: Qualitative research design involving semi-structured focus groups. OBJECTIVES: To increase current understanding of how persons with spinal cord injuries (SCI) define resilience and what factors contribute to their resilience or the resilience of others. SETTING: Inpatient rehabilitation program in a large urban city in the Southwestern United States. METHODS: A convenience sample of 28 participants (14 current patients; 14 former patients) participated in semi-structured focus groups led by the research investigators. RESULTS: Through a constant comparative analysis of the data, six themes emerged in participants' responses regarding what they believed contributed to their own resilience in adapting to SCI. The six themes included psychological strength, social support, perspective, adaptive coping, spirituality or faith, and serving as a role model or inspiring others. CONCLUSION: Consistent with previous research findings, individuals with SCI identified positive thinking (for example, optimism, hope and positive attitude), perseverance and determination, and social support from friends and family as important contributors to their ability to adapt in spite of experiencing traumatic events that resulted in SCI. Findings provide richness and depth to current empirical conceptualizations of resilience.

p38 mitogen-activated protein kinase activates peroxisome proliferator-activated receptor alpha: a potential role in the cardiac metabolic stress response.

The expression of enzymes involved in fatty acid beta-oxidation (FAO), the principal source of energy production in the adult mammalian heart, is controlled at the transcriptional level via the nuclear receptor peroxisome proliferator-activated receptor alpha (PPARalpha). Evidence has emerged that PPARalpha activity is activated as a component of an energy metabolic stress response. The p38 mitogen-activated protein kinase (MAPK) pathway is activated by cellular stressors in the heart, including ischemia, hypoxia, and hypertrophic growth stimuli. We show here that PPARalpha is phosphorylated in response to stress stimuli in rat neonatal cardiac myocytes; in vitro kinase assays demonstrated that p38 MAPK phosphorylates serine residues located within the NH(2)-terminal A/B domain of the protein. Transient transfection studies in cardiac myocytes and in CV-1 cells utilizing homologous and heterologous PPARalpha target element reporters and mammalian one-hybrid transcription assays revealed that p38 MAPK phosphorylation of PPARalpha significantly enhanced ligand-dependent transactivation. Cotransfection studies performed with several known coactivators of PPARalpha demonstrated that p38 MAPK markedly increased coactivation specifically by PGC-1, a transcriptional coactivator implicated in myocyte energy metabolic gene regulation and mitochondrial biogenesis. These results identify PPARalpha as a downstream effector of p38 kinase-dependent stress-activated signaling in the heart, linking extracellular stressors to alterations in energy metabolic gene expression.