A sodium saccharin (NaSac) diet was used to induce cell damage and regeneration in the urothelium of the male rat urinary bladder. Foci of terminally differentiated superficial cell exfoliation were detected after 5 weeks and their number increased after 10 and 15 weeks of the diet. At the sites of superficial cell loss, regenerative simple hyperplasia developed. Within 5 weeks of NaSac removal, regeneration re-established normal differentiated urothelium. In order to follow urothelial differentiation during regeneration we studied the expression of uroplakins and cytokeratins by means of immunocytochemistry and immunohistochemistry, respectively. Normal urothelium was characterised by terminally differentiated superficial cells which expressed uroplakins in their luminal plasma membrane and cytokeratin 20 (CK20) in the cytoplasm. Basal and intermediate cells were CK20 negative and cytokeratin 17 (CK17) positive. In hyperplastic urothelium all cells synthesised CK17, but not CK20. Differentiation of the superficial layer was reflected in three successive cell types: cells with microvilli, cells with rounded microridges and those with a rigid-looking plasma membrane on the luminal surface. The cells with microvilli did not stain with anti-uroplakin antibody. When the synthesis of uroplakins was detected rounded microridges were formed. With the elevated expression of uroplakins the luminal plasma membrane becomes rigid-looking which is characteristic of asymmetric unit membrane of terminally differentiated cells. During differentiation, synthesis of CK17 ceased in superficial cells while the synthesis of CK20 started. These results indicate that during urothelial regeneration after NaSac treatment, specific superficial cell types develop in which the switch to uroplakin synthesis and transition from CK17 to CK20 synthesis are crucial events for terminal differentiation.

Abnormal nitric oxide (NO) synthesis has been implicated in the pathogenesis of both periodontal disease and diabetes mellitus. In diabetic patients, increased inducible NO synthase in inflamed gingiva correlated with NO in gingival crevicular fluid. Although increased NO reflected more-severe inflammation, it was associated with reductions in CFU of Prevotella intermedia, a major periodontopathogen, highlighting dual roles for NO.

Localized juvenile periodontitis (LJP) is associated with a destruction of periodontal tissues and the presence of Actinobacillus actinomycetemcomitans (AA). Lipopolysaccharide (LPS) from AA was found to induce a significant macrophage production of nitric oxide (NO). Increased nitric oxide synthase (NOS) activity was found to be negatively correlated with the neutrophil chemotactic response. The aim of this study was to determine the occurrence and distribution of inducible NOS (iNOS) in human gingival tissue from LJP patients. The distribution of iNOS was assessed by monoclonal antibody against iNOS. Cellular markers (CD 3, CD 20, and CD 68) were used to determine the cellular origin of iNOS. The immunostaining revealed the appearance of iNOS in inflamed compared to noninflamed gingival tissues. Macrophages expressed high levels of iNOS that may cause some damage to the periodontal tissues. This study suggests that iNOS activity in macrophages may modify abnormalities of neutrophil function.

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A primary angiosarcoma of the testis in a 74-year-old patient was a highly anaplastic epthelioid angiosarcoma, which was positive for endothelial markers immunohistochemically. The tumour was unrelated to testicular germ cell neoplasm; the patient had received no previous radiation or chemotherapy.