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1.
Korean Journal of Hepato-Biliary-Pancreatic Surgery ; : 139-141, 2013.
Article in English | WPRIM | ID: wpr-117480

ABSTRACT

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. Conversely, primary splenic cysts have epithelial lining and are subdivided into parasitic and non-parasitic cyst. Non-parasitic primary splenic cyst is considered congenital and comprises about 10% of all splenic cysts. Total or partial splenectomy is the treatment of choice, but parasitic infection must be excluded prior to an operation. In this present report, we described a symptomatic, large primary non-parasitic splenic cyst, which was surgically treated with partial splenectomy.


Subject(s)
Rare Diseases , Spleen , Splenectomy
2.
Korean Diabetes Journal ; : 102-111, 2008.
Article in Korean | WPRIM | ID: wpr-61110

ABSTRACT

BACKGROUND: Insulin receptor substrate 2 (IRS-2) is a key regulator of beta cell proliferation and apoptosis. This study was aimed to investigate effect of the glucolipotoxicity on apoptosis in INS-1 cell, and the effect of Exendin-4, a GLP-1 receptor agonist, on IRS-2 expression in the glucolipotoxicity induced INS-1 cell. The goal was to discover the new action mechanism and function of Exendin-4 in beta cell apoptosis. METHOD: INS-1 cells were cultured in glucolipotoxic condition for 2, 4 or 6 days and were categorized as G groups. Another group in which 50 nM Exendin-4 was added to INS-1 cells, cultured in glucolipotoxic condition, were named as Ex-4 groups. We investigated the expression of IRS-2 by RT-PCR, phosphorylated IRS-2 and phosphorylated Akt protein levels by western blot. We measured the apoptosis ratio of INS-1 cell in glucolipotoxic condition by TUNEL staining in both groups. RESULT: IRS-2 expression of INS-1 cells decreased with correlation to the time of exposure to glucolipotoxic condition. pIRS-2 and pAkt protein levels decreased in the similar pattern in glucolipotoxicity group. However, this effect of glucolipotoxicity on INS-1 cell was inhibited by the Exendin-4 treatment. In the Ex-4 groups, IRS-2 expression, pIRS-2 and pAkt protein levels remained at the similar level to low glucose condition state. Also, apoptosis induced by glucolipotoxicity was suppressed by Exendin-4 treatment significantly. CONCLUSION: We showed that the long-term treatment of Exendin-4 inhibited the apoptosis of beta cells significantly in glucolipotoxic condition and that this effect of Exendin-4 was related with IRS-2 and Akt among the beta cell's intracellular signal transduction pathway.


Subject(s)
Apoptosis , Blotting, Western , Cell Proliferation , Cells, Cultured , Glucagon-Like Peptide 1 , Glucagon-Like Peptide-1 Receptor , Glucose , In Situ Nick-End Labeling , Insulin Receptor Substrate Proteins , Peptides , Phosphorylation , Receptors, Glucagon , Signal Transduction , Venoms
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