Recent advances in immunology have opened a new approach to investigating the etiology and pathogenesis of aural cholesteatoma by the immunohistochemical technique. Immunohistochemical and submicroscopic analysis of human cholesteatoma matrices revealed the presence of Langerhans' cells. Several reports have suggested that Langerhans' cells in cholesteatoma are significant, and that the pathogenesis of this disease including bone resorption could be explained as a cell-mediated immune response, but this is still controversial. In this study, Langerhans' cells in cholesteatoma were quantitated and compared with those in postauricular skin and in skin of the open mastoidectomized cavity. The results did not support the hypothesis that Langerhans' cells have a primary role in the development of aural cholesteatoma.
Cholesteatoma, Middle Ear/*immunology/pathology ; Human ; Immunohistochemistry ; Langerhans Cells/pathology/*physiology ; Skin/immunology/pathology

OBJECTIVETo explore the mechanisms of differentiation and development of pancreatic endocrine cells as well as pancreatic regeneration.

METHODSHuman embryonic pancreatic tissue at 7-14 weeks of gestation was collected. Diabetes mellitus rat model was induced with 65 mg/kg of streptozotocin. Insulin, glucagon, somatostatin, nestin, and cytokeratin 19 (CK19) of pancreatic tissues were observed by immunohistochemistry.

RESULTSAt 9 weeks of gestation, pancreatic epithelial cells began to co-express insulin, glucagon, somatostatin, and CK19 before migration. Islet cells gradually congregated along with the increase of aging, and at 14 weeks of gestation histological examination showed islet formation. At 12 weeks of gestation, nestin-positive cells could be seen in the pancreatic mesenchyme. During early embryogenesis, islet cells of pancreatic ducts co-expressed insulin, glucagon, and somatostatin. During pancreatic regeneration after damage, nestin expression of islet cells increased.

CONCLUSIONIn the early stage of embryogenesis, islet cells of primary pancreatic ducts can be differentiated to multipotential endocrine cells before migration. During tissue regeneration, pancreatic stem cells may differentiate and proliferate to form pancreatic islet.

Animals ; Cell Differentiation ; Diabetes Mellitus, Experimental ; chemically induced ; metabolism ; pathology ; Embryonic Development ; physiology ; Epithelial Cells ; cytology ; physiology ; Humans ; Insulin-Secreting Cells ; cytology ; physiology ; Islets of Langerhans ; cytology ; physiology ; Male ; Pancreas ; cytology ; embryology ; physiology ; Pancreatic Ducts ; cytology ; embryology ; physiology ; Rats ; Rats, Sprague-Dawley ; Regeneration ; physiology ; Stem Cells ; cytology ; metabolism ; physiology

AIMTo investigate the chronic effect of palmitic acid (PA) on apoptosis of pancreatic islet beta-cells and the possible mechanism.

METHODSInsulinoma cell line (MIN6 cells) were used in this study. After being incubated in PA (0.1 - 1.6 mml/L) for 24 and 48 hours, MTT method was used to evaluate the livability. After being incubated for 48 h, Hoechst-PI and Annexin-V-FTTC/PI FACS were used to estimate the apoptosis in each group, Western-blotting assay was used to estimate the protein level of p-Akt, Akt, Bax and Bcl-2.

RESULTSChronic PA dose-dependently (1) decreased the availability and increased the apoptosis of MIN6 cells; (2) decreased the phosphorylation of Akt and Bcl-2, but had no significant effects on Akt and Bax.

CONCLUSIONChronic PA dose-dependently induced apoptosis of MIN6 cells, and this effect was possibly regulated by Akt/Bcl-2.

Animals ; Apoptosis ; drug effects ; Cell Line, Tumor ; Cells, Cultured ; Insulinoma ; pathology ; Islets of Langerhans ; pathology ; Mice ; Oxidative Stress ; physiology ; Palmitic Acid ; pharmacology ; Proto-Oncogene Proteins ; metabolism ; Proto-Oncogene Proteins c-akt ; metabolism ; Proto-Oncogene Proteins c-bcl-2 ; Signal Transduction ; drug effects ; physiology ; bcl-2-Associated X Protein ; metabolism