Background/Aims: Spinal cord injury (SCI) frequently impairs defecation, severely affecting the quality of life. This study examines compensatory neural remodeling after SCI, focusing on basal colonic contractility, neural responses to electrical field stimulation, and alterations in excitatory cholinergic and inhibitory nitrergic pathways. Methods: Female Sprague–Dawley rats underwent either sham surgery or T10 spinal cord transection and were categorized into 3 groups: sham, 1-week post-SCI (acute), and 4-week post-SCI (chronic). Colonic contractility was assessed in an organ bath using electrical field stimulation in the presence of a nitric oxide synthase inhibitor. Neural protein expression was analyzed by immunofluorescence and Western blotting. Results: SCI produced region- and time-dependent impairments in colonic contractility, with distinct alterations in the proximal circular and longitudinal muscles across acute and chronic phases. Neural excitability shifted dynamically, showing enhanced excitatory activity in the proximal longitudinal muscle at 1-week and the distal circular muscle at 4-week post-SCI. Protein analysis revealed increased neuronal nitric oxide synthase in the proximal colon, decreasedsoluble guanylyl cyclase in the distal colon, upregulated muscarinic M3 receptor in the proximal colon, and reduced vaso-active intestinal peptide receptor 1 in both proximal and distal regions. Conclusion SCI induces spatiotemporal remodeling of excitatory and inhibitory neural pathways, contributing to colonic dysmotility and revealing potential targets for therapeutic intervention.

Gossypiboma refers to a mass usually made of cotton (e.g., surgical gauze or sponge) that is accidentally left in a patient’s body during surgery. We report the case of a 54-year-old multigravida menopausal woman who previously underwent cesarean section to deliver her second child. She was referred to our medical center after a 7 cm right ovarian mass with malignant potential was discovered. A diagnostic laparotomy was performed then confirmed the presence of a 10 cm gossypiboma attached to a metallic ring. This case is an alarming example highlighting the importance of adequate intraoperative counting of gauze and radiologic evaluation of chronic pelvic pain.

Background/Aims: Histamine-2 receptor antagonists (H2RA) are used to treat acid-related disorders and functional dyspepsia. In contrast to other H2RAs, nizatidine promotes gastric emptying (GE). We investigated the effects of nizatidine and famotidine on intragastric pH and the GE rate in rats exposed to stress. Materials and Methods: We used 8-week-old male Wistar rats. Based on administration of water or drugs after an overnight fast, the animals were categorized into the nonstress-water, stress-water, stress-nizatidine, stress-famotidine, and stress-nizatidine with mosapride groups. The rats had access to pre-weighed food for 10 minutes, and those in the stress groups were exposed to 1 hour of restraint stress. Intragastric pH was measured under isoflurane anesthesia, and the GE rate was measured after the rats were sacrificed. Results: The GE rate was significantly lower in the stress-water and stress-famotidine groups than in the nonstress-water group. However, GE in the stress-nizatidine and stress-nizatidine with mosapride group did not significantly differ from that in the nonstress- water group. The GE rate was significantly higher in the stress-nizatidine with mosapride than in the stress-famotidine group. Intragastric pH was significantly higher in the stress-nizatidine and stress-famotidine groups than in the stress-water group. Nonetheless, there was no significant difference in pH between the stress-nizatidine and stress-famotidine groups. The intragastric pH was slightly but significantly higher in the stress-nizatidine with mosapride group than in the stress-nizatidine and stress-famotidine groups. Conclusions In contrast to famotidine, nizatidine prevents stress-induced GE delay, which suggests that nizatidine is superior to other H2RAs for treatment of functional dyspepsia associated with delayed GE.