Objective. This study was to evaluate the utility of the compound graft for tubularized urethroplasty by seeding mesothelial cells onto autogenous granulation tissue. Methods. Silastic tubes were implanted subcutaneously in 18 male rabbits, of which nine underwent omentum biopsies simultaneously for in vitro expansion of mesothelial cells. The granulation tissue covering the tubes was harvested 2 weeks after operation. Mesothelial cells were seeded onto and cocultured with the tissue for 7 days. A pendulous urethral segment of 1.5 cm was totally excised. Urethroplasty was performed with mesothelial cell-seeded tissue tubes in an end-to-end fashion in nine rabbits and with unseeded grafts in others as controls. Serial urethrograms were performed at 1, 2, and 6 months postoperatively. Meanwhile, the neourethra was harvested and analyzed grossly and histologically. Results. Urethrograms showed cell-seeded grafts maintained wide at each time point, while strictures formation was found in unseeded grafts. Histologically, layers of urothelium surrounded by increasingly organized smooth muscles were observed in seeded grafts. In contrast, myofibroblasts accumulation and extensive scarring occurred in unseeded grafts. Conclusions. Mesothelial cell-seeded granulation tissue tube can be successfully used for tubularized urethroplasty in male rabbits.

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Background: Neuropathic pain is a troublesome pathological condition without suitable treatments. Anterior Cingulate Cortex (ACC) is a core brain region to process pain emotion. In this study, we performed RNA sequencing analysis to reveal transcriptomic profiles of the ACC in a rat chronic constriction injury (CCI) model.Results: A total of 1628 differentially expressed genes (DEGs) were identified by comparing the sham-operated rats and rats of 12 hours, 1, 3, 7 and 14 days after surgery, respectively. Most of the DEGs were involved in inflammatory and immune process. Although these inflammatory-related DEGs were generally increased after CCI, they demonstrated different kinetics in time-series expression with the development of neuropathic pain affection. Specifically, the expression of Ccl5 , Cxcl9 and Cxcl13 were kept going up after CCI, indicating a potentially effect of these genes on initiation and maintenance of neuropathic pain affection. The expression of Ccl2 , Ccl3 , Ccl4 , Ccl6 and Ccl7 were initially upregulated at 12 hours after CCI and then they fell back after that. Similarly, the expression of Rac2 , Cd68 , Icam-1 , Ptprc , Itgb2 , Fcgr2b were rised at 12 hours and 1 day, but fell back at 3 days after CCI. However, the expression of all of the above two clusters of genes were increased again at 7 days after CCI, when the neuropathic pain affection was developed. The initial increase of these genes may indicate an early response of ACC to nerve injury, whereas the later increase of these genes may indicate their involvement in the developing of neuropathic pain affection. Gene Ontology analysis, KEGG pathway enrichment and interaction network analysis further showed a high connectivity degree among these chemokine targeting genes. Similar expressional changes of these genes were also found in the rat spinal dorsal taking charge of the processing of nociception.Conclusions: Our results indicate chemokines and their targeting genes in ACC may be differentially involved in the initiation and maintenance of neuropathic pain affection. These genes could be the target not only the nociception but also the pain affection subsequent to nerve injury.