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https://www.selleckchem.com/products/4-hydroxynonenal.html 0%) attending nine or more sessions and the community healing ceremony. Exploratory analyses revealed medium effect sizes, ω2 = 0.05-0.08, for reductions in depressive symptoms, improvements in psychological functioning, and self-compassion after the intervention, with small effect sizes, ω2 = 0.03, in anticipated directions for personal growth and spiritual struggles. The results were not impacted by participant engagement in concurrent psychological treatments. Taken together, these findings support the feasibility of the MIG, the potential merit of an interdisciplinary approach to addressing moral injury, and justification for further research into the efficacy of this approach. Psychological stress is a risk factor for irritable bowel syndrome, a functional gastrointestinal pain disorder featuring abnormal brain-gut connectivity. The guanylate cyclase-C (GC-C) agonist linaclotide has been shown to relieve abdominal pain in IBS-C and exhibits antinociceptive effects in rodent models of post-inflammatory visceral hypersensitivity. However, the role GC-C signaling plays in psychological stress-induced visceral hypersensitivity is unknown. Here, we test the hypothesis that GC-C agonism reverses stress-induced colonic hypersensitivity via inhibition of nociceptive afferent signaling resulting in normalization of stress-altered corticotropin-releasing factor (CRF) expression in brain regions involved in pain perception and modulation. Adult female rats were exposed to water avoidance stress or sham stress for 10days, and the effects of linaclotide on stress-induced changes in colonic sensitivity, corticolimbic phospho-extracellular signal-regulated kinase (pERK), and CRF expression wetered corticolimbic activation and CRF expression. GC-C agonism attenuated stress-induced colonic hypersensitivity and ERK phosphorylation, but had no effect on CRF expression, suggesting the analgesic effects of linaclotide occur

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