No abstract available.
Urinary Tract Infections* ; Urinary Tract*

Nitric oxide (NO) induces apoptotic cell death in murine RAW 264.7 macrophages. To elucidate the roles of SEK1/MKK4, a upstream kinase for both c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK) and p38 kinase, on NO-induced apoptosis, we generated clones of RAW 264.7 cells which stably overexpressd kinase inactive SEK1 (RAW/SEK1-Kl) or wild type SEK1 (RAW/SEK1-WT). Treatment of kinase inactive SEK1 transfected RAW 264.7 cells (RAW/SEK1-Kl) with sodium nitroprusside (SNP), a NO generating agent, significantly decreased the cell viability up to 20% of RAW control cells which were treated with the same amount of SNP. However, RAW/SEK1-WT cells were less susceptible to NO induced apoptosis. For a while, caspase-3 like activity in NO treated RAW/SEK1-Kl cells was significantly increased with parallell to apoptotic death rate. However, caspase1 like activity was not affected by NO in any transfectants. The NO induced apoptosis in RAW/SEK1-Kl cells was significantly prevented by the addition of caspase-3 like inhibitor (N-Ac- DEVD-CHO). In addition, the phosphotransferase activity of JNK1 in NO-treated RAW/SEK1-WT is significantly increased, but not in RAW/SEK1-Kl cells. These results suggest that SEK1 may play anti-apoptotic role in RAW cells from NO-induced apoptosis.
Apoptosis ; Caspase 3 ; Cell Death ; Cell Survival ; Clone Cells ; Macrophages ; Mortality ; Nitric Oxide* ; Nitroprusside ; Phosphotransferases ; Protein Kinases

PURPOSE: Prader-Willi Syndrome(PWS) is caused by absence of paternal contributions of the chromosome region 15q11-q13. To detact this region, high resolutional cytogenetic analysis, FISH with probe at PWS critical region or microsatellite polymorphism can be used. The gene for the small nuclear ribonucleoprotein polypeptide N(SNRPN) is not expressed in patients with PWS. We conducted molecular analysis with RT-PCR with SNRPN primers to find out more useful diagnostic tool in PWS. METHODS: Four patients with obesity and other characteristics of PWS were studied. The exprssion of SNRPN and control gene were studed by RT-PCR from peripheral lymphocytes. RESULTS :The SNRPN expression in reverse transcribed RNA from blood were easily detected in normal control but not in patients with suspected Parder-Willi Syndrome. CONCLUSION: We conclude that SNRPN expression study is a useful diagnostic method for detection of Prader-Willi Syndrome.
Cytogenetic Analysis ; Humans ; Lymphocytes ; Microsatellite Repeats ; Obesity ; Pathology, Molecular* ; Prader-Willi Syndrome* ; Ribonucleoproteins, Small Nuclear ; RNA ; snRNP Core Proteins*

In an attempt to discover the factors contributing to the increased proliferative activity in hepatocytes and subsequent development of HCC, the proliferative activity of hepatocytes was compared with the size of regenerative nodules and HBcAg expression status in the surrounding nontumorous liver of 45 surgically resected hepatocellular carcinomas, including 34 HBV related ones. In the tumor, the difference in proliferative activity and the histological grade was analyzed in terms of p53 gene alteration. The proliferative activity was assessed by immunohistochemical methods using Ki-67 monoclonal antibody. HBcAg expression in the surrounding nontumorous liver correlated with both the inflammatory and proliferative activity of hepatocytes (p<0.05). p53 overexpression was associated with high proliferative activity and aggressive phenotype of tumor. No correlation was observed between the proliferative activity of hepatocytes and the size of regenerative nodules in cirrhosis (p>0.05). p53 overexpression was not evident in surrounding nontumorous liver including cirrhosis. In conclusion, the above results are in line with the view that hepatic carcinogenesis is a mutistep, progressive process. In the initial stage, chronic cellular injury incurred by immumologic reaction against HBcAg seems to play a pivotal role in increased cellular regeneration. However, once transformation of hepatocytes occur the major contributor to tumor growth seems to be alteration in p53 tumor suppresor gene.
Carcinogenesis ; Carcinoma, Hepatocellular* ; Fibrosis ; Genes, p53 ; Hepatitis B Core Antigens* ; Hepatitis B virus ; Hepatocytes ; Liver* ; Phenotype ; Regeneration

Primary sarcomas of the liver are rare. A case of primary malignant fibrous histiocytoma of the liver is reported. A 55-year-old male was admitted with epigastric pain. An abdominal computed tomographic scan disclosed a 10cm, low-density area in the left lobe of the liver. Histological examination of the resected tumor showed bundles of spindle cells arranged in a storiform pattern. In some areas, many bizarre giant cells were scattered. Immunohistochemically, tumor cells were positive for alpha 1-antitrypsin and alpha 1-antichymotrypsin, and weakly positive for vimentin. The tumor cells did not express cytokeratin, desmin or alpha fetoprotein.
alpha 1-Antichymotrypsin ; alpha 1-Antitrypsin ; alpha-Fetoproteins ; Desmin ; Giant Cells ; Histiocytoma, Malignant Fibrous* ; Humans ; Keratins ; Liver* ; Male ; Middle Aged ; Sarcoma ; Vimentin

No abstract available.
Rectal Prolapse* ; Surgical Procedures, Operative*

We report a rare case of adreno-hepatic fusion in a 63-year-old man with a traumatic hepatic rupture. The adrenal tissue was located beneath the Glisson's capsule of the liver, and measured 3.5x2x0.3 cm. On histologic examination, the ectopic tissue was composed of both adrenal cortex and medulla surrounded by a delicate capsule of connective tissue.
Adrenal Cortex ; Choristoma ; Connective Tissue ; Humans ; Liver ; Middle Aged ; Rupture

Edwards syndrome is first introduced by Edwards and characterized by facial anomalies, multiple cardiovascular, gastrointestinal, urogenital, and skeletal malformations. It results from triplication of part or all of chromosome 18 in some or all of the patient's cells. It has an incidence of 1 in 4,500 live births or less and short life expectancy. Recently we experienced a case of 3-day-old female new born infant with this syndrome. Post mortem examination showed progeric face with prominent occiput, large flabby ears, microphthalmia, and micrognathia, bilateral clenched hands with flexion contraction of middle fingers, and bilateral rockerbottom feet. Internal examination revealed horseshoe kidney, esophageal atresia with tracheoesophageal fistula, two accessory spleens, and multiple cardiac anomalies. A trisomy 18 was confirmed by the cytogenetic study.
Infant ; Male ; Female ; Infant, Newborn ; Humans ; Incidence

A few cases of reticulate acropigmentary disorders have been reported in Korea. Most of them were reticulate acropigmentation of Kitamura, but not acropigmentation symmetrica of Dohi. A 21 year-old male patient diagnosed as acropigmentation symmetrica of Dohi had been previously treated with various treatment methods unsuccessfully. Re-treatment with the Q-switched alexandrite laser(755 nm, 100nsec) showed a temporary improvement but a relapse of the lesion was experienced again. We describe a case of acropigmentation symmetrica of hi treated with the Q-switched alexandrite laser.
Humans ; Korea ; Lasers, Solid-State* ; Male ; Recurrence

Pituitary adenoma should be differentiated diagnostically from pituitary hyperplasia, which can be classified by primary, secondary & tertially caused by ectopic tumors. Two cases with marked pituitary enlargement secondary to primary hypothyroidism were reported. The volume of the sellar turcica correlates with circulating TSH level. The subsequent regression with thryoxine therapy indicated hyperplasia rather than adenoma. This observation emphasizes the importance of diagnosing and treating primary hypothyroidism prior to considering surgery for possible pituitary adenoma. A brief review of related literatures was also made.
Adenoma ; Hyperplasia* ; Hypothyroidism* ; Pituitary Neoplasms*