Background: Urothelial carcinoma (UC) accounts for roughly 90% of bladder cancer, and has a high propensity for diverse differentiation. Recently, certain histologic variants of UC have been recognized to be associated with unfavorable clinical outcomes. Several UC studies have also suggested that tumor budding is a poor prognostic marker. Distant metastasis of UC after radical cystectomy is not uncommon. However, these metastatic lesions are not routinely confirmed with histology. Methods: We investigated the histopathologic features of 13 cases of UC with biopsy-proven distant metastases, with a special emphasis on histologic variants and tumor budding. Results: Lymph nodes (6/13, 46%) were the most common metastatic sites, followed by the lung (4/13, 31%), liver (4/13, 31%), and the adrenal gland (2/13, 15%). The histologic variants including squamous (n=1), micropapillary (n=4), and plasmacytoid (n=1) variants in five cases of UC. Most histologic variants (4/5, 80%) of primary UCs appeared in the metastatic lesions. In contrast, high-grade tumor budding was detected in six cases (46%), including one case of non-muscle invasive UC. Our study demonstrates that histologic variants are not uncommonly detected in distant metastatic UCs. Most histologic variants seen in primary UCs persist in the distant metastatic lesions. In addition, high-grade tumor budding, which occurs frequently in primary tumors, may contribute to the development of distant metastasis. Conclusions Therefore, assessing the presence or absence of histologic variants and tumor budding in UCs of the urinary bladder, even in non-muscle invasive UCs, may be useful to predict distant metastasis.

Colchicine-induced neuromyopathy is an extremely rare complication, and can develop in the setting of acute overdose or chronic administration in therapeutic doses. A 72-year-old man presented with proximal muscle weakness and myalgia. He had angina pectoris and Behçet’s disease, leading to the treatment of colchicine (1.2 mg daily for about 6 years), cyclosporine, methylprednisolone, simvastatin, and aspirin. A biceps brachii muscle biopsy was performed and electron microscopic examination revealed scattered autophagic vacuoles. He was initially treated with steroid pulse therapy. However, muscle weakness did not improve. After the discontinuation of colchicine, muscle power and myalgia improved steadily. There should be heightened awareness of colchicine-induced neuromyopathy because that clinical suspicion is the most important diagnostic clue, and termination of colchicine is the only treatment.

BACKGROUND: Respiratory mucosa defects result in airway obstruction and infection, requiring subsequent functionalrecovery of the respiratory epithelium. Because site-specific extracellular matrix (ECM) facilitates restoration of organfunction by promoting cellular migration and engraftment, previous studies considered decellularized trachea an idealECM; however, incomplete cell removal from cartilage and mucosal-architecture destruction are frequently reported. Here,we developed a decellularization protocol and applied it to the respiratory mucosa of separated porcine tracheas. METHODS: The trachea was divided into groups according to decellularization protocol: native mucosa, freezing–thawing (FT), FT followed by the use of Perasafe-based chemical agents before mucosal separation (wFTP), after mucosalseparation (mFTP), and followed by DNase decellularization (mFTD). Decellularization efficacy was evaluated by DNAquantification and hematoxylin and eosin staining, and ECM content of the scaffold was evaluated by histologic analysisand glycosaminoglycan and collagen assays. Biocompatibility was assessed by cell-viability assay and in vivotransplantation. RESULTS: The mFTP mucosa showed low antigenicity and maintained the ECM to form a proper microstructure.Additionally, tonsil-derived stem cells remained viable when cultured with or seeded onto mFTP mucosa, and the in vivohost response showed a constructive pattern following implantation of the mFTP scaffolds. CONCLUSION These results demonstrated that xenogenic acellular respiratory mucosa matrix displayed suitable biocompatibilityas a scaffold material for respiratory mucosa engineering.

BACKGROUND: Respiratory mucosa defects result in airway obstruction and infection, requiring subsequent functionalrecovery of the respiratory epithelium. Because site-specific extracellular matrix (ECM) facilitates restoration of organfunction by promoting cellular migration and engraftment, previous studies considered decellularized trachea an idealECM; however, incomplete cell removal from cartilage and mucosal-architecture destruction are frequently reported. Here,we developed a decellularization protocol and applied it to the respiratory mucosa of separated porcine tracheas. METHODS: The trachea was divided into groups according to decellularization protocol: native mucosa, freezing–thawing (FT), FT followed by the use of Perasafe-based chemical agents before mucosal separation (wFTP), after mucosalseparation (mFTP), and followed by DNase decellularization (mFTD). Decellularization efficacy was evaluated by DNAquantification and hematoxylin and eosin staining, and ECM content of the scaffold was evaluated by histologic analysisand glycosaminoglycan and collagen assays. Biocompatibility was assessed by cell-viability assay and in vivotransplantation. RESULTS: The mFTP mucosa showed low antigenicity and maintained the ECM to form a proper microstructure.Additionally, tonsil-derived stem cells remained viable when cultured with or seeded onto mFTP mucosa, and the in vivohost response showed a constructive pattern following implantation of the mFTP scaffolds. CONCLUSION These results demonstrated that xenogenic acellular respiratory mucosa matrix displayed suitable biocompatibilityas a scaffold material for respiratory mucosa engineering.