Primary non-parasitic splenic cyst: a case report.

Cystic disease of the spleen is a relatively rare disease. It is classified either as a true primary cyst or as a secondary pseudocyst. Most splenic cysts are pseudocysts, which have non-epithelial lining, and are caused by previous abdominal blunt trauma.

Glucocorticoid treatment independently affects expansion and transdifferentiation of porcine neonatal pancreas cell clusters.

The purpose of this study was to determine the effects of duration and timing of glucocorticoid treatment on the expansion and differentiation of porcine neonatal pancreas cell clusters (NPCCs) into β-cells. After transplantation of NPCCs, the ductal cyst area and β-cell mass in the grafts both showed positive and negative correlations with duration of dexamethasone (Dx) treatment. Pdx-1 and HNF-3β gene expression was significantly downregulated following Dx treatment, whereas PGC-1α expression increased.

Transforming growth factor-β induces epithelial to mesenchymal transition and suppresses the proliferation and transdifferentiation of cultured human pancreatic duct cells.

Pancreatic duct cells are considered a potential source of β-cell regeneration, and transforming growth factor-β (TGF-β) has been suggested to perform an important role in these processes, but the underlying mechanism of the signal pathways, especially in humans, remains poorly understood. To evaluate the role of TGF-β1, pancreatic duct cells were isolated from three brain-dead organ donors. Pancreatic cell clusters harvested after islet isolation were dispersed to single cells and cultured in monolayers, then treated with TGF-β1.

Differentially up-regulated genes in proliferating porcine neonatal pancreas cells caused by epidermal growth factor.

Pancreatic duct cells are considered to be a major source for beta-cell regeneration or neogenesis. Although epidermal growth factor (EGF) is a well-known important growth factor for pancreas development, the control of pancreatic duct cell growth and differentiation by EGF is poorly understood. In this study, we focused on identifying the genes that were differentially up-regulated in response to EGF stimulation using monolayer cultured porcine neonatal pancreas cells.