No abstract available.
Leiomyosarcoma* ; Rectum*

Transesophageal echocardiogram (TEE) was performed in the 86 normal persons using a UM9 of ATL with a 3.5 MHZ transducer in the Heart Center of Dong-A University Hospital during March-September 1990. 1) The transesophageal basal short axis views in the normal were seen in the Fig. 2~6. The Fig. 2 showed 3 aortic valve cusps, Fig. 3 the left coronary artery, Fig. 4 the right pulmonary artery bifurcated from the main pulmonary artery, Fig. 5 3 major vessels of superior vena cava, aorta and pulmonary artery and Fig. 6 the Left atrial appendage. 2) The transesophageal 4-chamber views in the normal were seen in Fig. 7~10. The Fig. 7 showed the left ventricular outflow tract, Fig. 8 right and left atrium and ventricle, Fig. 9 the atrial septum containing the membrane of fossa ovalis and Fig. 10 right atrium and ventricle. 3) The transesophageal transgastric short axis view in the normal was seen in Fig. 11. Fig. 11 showed the transverse image of LV and RV. 4) The transesophageal ascending aorta image was observed in Fig. 3. descending aorta image in Fig. 12 and the transesophageal aortic arch image in Fig. 14. 5) From the transesophageal 4 chamber view the septum-lateral wall dimension of the left ventricle was 5.0cm and the dimension between the apex and the closed mitral valve 6.3cm. The medial-lateral dimension of the left atrial appendage was 3.0cm and the superior-inferior dimension 4.1cm. The dimension of the descending aorta was 2.7cm and the ascending aorta 3.0cm.
Aorta ; Aorta, Thoracic ; Aortic Valve ; Atrial Appendage ; Atrial Septum ; Axis, Cervical Vertebra ; Coronary Vessels ; Echocardiography, Transesophageal ; Heart ; Heart Atria ; Heart Ventricles ; Humans ; Membranes ; Mitral Valve ; Pulmonary Artery ; Transducers ; Vena Cava, Superior

OBJECTIVE: The International Study of Unruptured Intracranial Aneurysms (ISUIA) reported that the 5-year cumulative rupture rate of small unruptured aneurysms less than 7 mm in diameter is very low depending on the aneurysm's location. However, we have seen a large number of ruptured aneurysms less than 7 mm in clinical practice. The purpose of this study was to review our experience and to measure the size and location at which aneurysms ruptured in our patient population. METHODS: We reviewed the characteristics of aneurysms, such as size and location, from the original angiograms of patients who were admitted to our hospital between January 2004 and December 2007. All aneurysms were treated surgically or through endovascular procedures. RESULTS: Interventional or surgical treatment was given to a total of 889 patients, including 568 females and 321 males. At the time of our study, 627 cases were ruptured aneurysms and 262 cases were unruptured aneurysms. Of the ruptured cases, the mean diameter of the aneurysm was 6.28 mm. We found that 71.8% of ruptured aneurysms were smaller than 7 mm in diameter, and 87.9%, were smaller than 10 mm. Based on location, the data show that anterior communicating artery aneurysms most often presented with rupture sizes less than 7 mm (76.8%) and 10 mm (92.1%) in diameter. Most ruptured aneurysms were less than 7 mm in size, although recent studies have noted that small aneurysms are less likely to rupture. CONCLUSION: Although the natural history of unruptured intracranial aneurysms remains controversial, the aneurysm size and location play a signigicant role in determining the risk of rupture. Larger sample sizes and a long term study are needed to reveal the natural history and the rupture risk of unruptured intracranial aneurysms because the size of most ruptured aneurysms was less than 7 mm in diameter in our series.
Aneurysm ; Aneurysm, Ruptured ; Endovascular Procedures ; Female ; Humans ; Intracranial Aneurysm ; Male ; Natural History ; Rupture ; Sample Size

Hyperplastic polyps are common gastric lesions that are characterized by nonneoplastic epithelial hyperplasia. However, to our knowledge, there are no reports of a hyperplastic polyp arising from an endoscopic mucosectomy site of early gastric cancer. We describe the CT findings with a histopathology correlation in a case of a hyperplastic polyp arising from a mucosectomy site that mimicked polypoid gastric cancer.
Endoscopy ; Hyperplasia ; Polyps* ; Stomach Neoplasms*

Mitochondrial NADP+-dependent isocitrate dehydrogenase 2 (IDH2) produces NADPH, which is known to inhibit mitochondrial oxidative stress. Ureteral obstruction induces kidney inflammation and fibrosis via oxidative stress. Here, we investigated the role and underlying mechanism of IDH2 in unilateral ureteral obstruction (UUO)-induced kidney inflammation using IDH2 gene deleted mice (IDH2–/–). Eight- to 10-week-old female IDH2–/– mice and wild type (IDH2+/+) littermates were subjected to UUO and kidneys were harvested 5 days after UUO. IDH2 was not detected in the kidneys of IDH2–/– mice, while UUO decreased IDH2 in IDH2+/+ mice. UUO increased the expressions of markers of oxidative stress in both IDH2+/+ and IDH2–/– mice, and these changes were greater in IDH2–/– mice compared to IDH2+/+ mice. Bone marrow-derived macrophages of IDH2–/– mice showed a more migrating phenotype with greater ruffle formation and Rac1 distribution than that of IDH2+/+ mice. Correspondently, UUO-induced infiltration of monocytes/macrophages was greater in IDH2–/– mice compared to IDH2+/+ mice. Taken together, these data demonstrate that IDH2 plays a protective role against UUO-induced inflammation through inhibition of oxidative stress and macrophage infiltration.

Mitochondrial NADP+-dependent isocitrate dehydrogenase 2 (IDH2) produces NADPH, which is known to inhibit mitochondrial oxidative stress. Ureteral obstruction induces kidney inflammation and fibrosis via oxidative stress. Here, we investigated the role and underlying mechanism of IDH2 in unilateral ureteral obstruction (UUO)-induced kidney inflammation using IDH2 gene deleted mice (IDH2–/–). Eight- to 10-week-old female IDH2–/– mice and wild type (IDH2+/+) littermates were subjected to UUO and kidneys were harvested 5 days after UUO. IDH2 was not detected in the kidneys of IDH2–/– mice, while UUO decreased IDH2 in IDH2+/+ mice. UUO increased the expressions of markers of oxidative stress in both IDH2+/+ and IDH2–/– mice, and these changes were greater in IDH2–/– mice compared to IDH2+/+ mice. Bone marrow-derived macrophages of IDH2–/– mice showed a more migrating phenotype with greater ruffle formation and Rac1 distribution than that of IDH2+/+ mice. Correspondently, UUO-induced infiltration of monocytes/macrophages was greater in IDH2–/– mice compared to IDH2+/+ mice. Taken together, these data demonstrate that IDH2 plays a protective role against UUO-induced inflammation through inhibition of oxidative stress and macrophage infiltration.

Background: Protease-activated protein-2 (PAR2) has been reported to regulate hepatic insulin resistance condition in type 2 diabetes mice. However, the mechanism of lipid metabolism through PAR2 in obesity mice have not yet been examined. In liver, Forkhead box O1 (FoxO1) activity induces peroxisome proliferator-activated receptor γ (PPARγ), leading to accumulation of lipids and hyperlipidemia. Hyperlipidemia significantly influence hepatic steatoses, but the mechanisms underlying PAR2 signaling are complex and have not yet been elucidated. Methods: To examine the modulatory action of FoxO1 and its altered interaction with PPARγ, we utilized db/db mice and PAR2-knockout (KO) mice administered with high-fat diet (HFD). Results: Here, we demonstrated that PAR2 was overexpressed and regulated downstream gene expressions in db/db but not in db+ mice. The interaction between PAR2/β-arrestin and Akt was also greater in db/db mice. The Akt inhibition increased FoxO1 activity and subsequently PPARγ gene in the livers that led to hepatic lipid accumulation. Our data showed that FoxO1 was negatively controlled by Akt signaling and consequently, the activity of a major lipogenesis-associated transcription factors such as PPARγ increased, leading to hepatic lipid accumulation through the PAR2 pathway under hyperglycemic conditions in mice. Furthermore, the association between PPARγ and FoxO1 was increased in hepatic steatosis condition in db/db mice. However, HFD-fed PAR2-KO mice showed suppressed FoxO1-induced hepatic lipid accumulation compared with HFD-fed control groups. Conclusion Collectively, our results provide evidence that the interaction of FoxO1 with PPARγ promotes hepatic steatosis in mice. This might be due to defects in PAR2/β-arrestin-mediated Akt signaling in diabetic and HFD-fed mice.

Long intergenic non-coding RNAs (lincRNAs) have historically been ignored in cancer biology. However, thousands of lincRNAs have been identified in mammals using recently developed genomic tools, including microarray and high-throughput RNA sequencing (RNA-seq). Several of the lincRNAs identified have been well characterized for their functions in carcinogenesis. Here we performed RNA-seq experiments comparing gastric cancer with normal tissues to find differentially expressed transcripts in intergenic regions. By analyzing our own RNA-seq and public microarray data, we identified 31 transcripts, including a known expressed sequence tag, BM742401. BM742401 was downregulated in cancer, and its downregulation was associated with poor survival in gastric cancer patients. Ectopic overexpression of BM742401 inhibited metastasis-related phenotypes and decreased the concentration of extracellular MMP9. These results suggest that BM742401 is a potential lincRNA marker and therapeutic target.
Animals ; DNA, Intergenic/genetics ; Expressed Sequence Tags/*metabolism ; Extracellular Space/metabolism ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Genetic Predisposition to Disease ; Humans ; Male ; Matrix Metalloproteinase 9/metabolism ; Mice ; Mice, Inbred C57BL ; Multivariate Analysis ; Neoplasm Metastasis ; Neoplasm Staging ; Phenotype ; Proportional Hazards Models ; RNA, Long Noncoding/*genetics/metabolism ; RNA, Messenger/genetics/metabolism ; Reproducibility of Results ; Stomach Neoplasms/*genetics/*pathology ; Survival Analysis

BACKGROUND/AIMS: This study reviewes the clinicopathological features, prognosis, and differences in the expression of p53 and Ki-67 immunochemical staining in squamous cell and adenosquamous carcinoma of the stomach. METHODS: From January 1995 to June 2005, 2,282 cases of gastric carcinoma were resected surgically in our hospital and 191 additional cases were resected by endoscopic mucosal resection. Retrospective pathologic review and immunochemical staining of p53 and Ki-67 were performed. RESULTS: The study consists of eight cases (0.032%) of primary squamous cell carcinoma (one case) and adenosquamous carcinoma (seven cases) without early gastric cancer. Six cases (75.0%) were male and two cases were female. The mean age was 66 year-old. The clinical presentation and physical findings did not differ from those of adenocarcinoma. The mean tumor size was 5.2+/-1.7 cm. Macroscopically, five were Borrmann type 3 (62.5%) and three were type 2. At the initial diagnosis, six (75%) were stage IV based on TNM tumor staging. Six cases (75%) progressed despite the therapy while two cases responded to the treatment. The median survival time was 11.0 months (range 4.3+/-17.7). Overexpression of p53 was seen in five cases (62.5%) and their survival was poor when compared to the p53-negative group (p=0.04). The mean Ki-67 labeling index was 70.0+/-20.8%, and was not associated with p53 staining (p>0.05). CONCLUSIONS: Adenosquamous and squamous cell carcinoma of the stomach are very rare. They tend to be at advanced stages on initial diagnosis, and progress rapidly. They show p53 protein overexpression and high Ki-67 labeling index, which might be related to poor prognosis.
Adult ; Aged ; Carcinoma, Adenosquamous/chemistry/mortality/*pathology ; Carcinoma, Squamous Cell/chemistry/mortality/*pathology ; Female ; Humans ; Immunohistochemistry ; Ki-67 Antigen/*analysis ; Male ; Middle Aged ; Stomach Neoplasms/chemistry/mortality/*pathology ; Survival Rate ; Tumor Suppressor Protein p53/*analysis

BACKGROUND/AIMS: Gastritis cystica profunda (GCP) is a rare disease that is characterized by a hyperplastic and cystic dilatation of the pseudopyloric gland with submucosal invasion. GCP is regarded as a benign lesion. However, there is some controversy regarding its malignant potential. This study reviewed the clinical features and association with malignancy. METHODS: From January 2001 to June 2005, 1,010 cases of resected and 1,228 cases of an endoscopic mucosal resection or polypectomy were examined. RESULTS: Thirty-nine cases (1.7%) were confirmed pathologically and were not associated with prior gastric surgery mostly. The mean age was 60.0+/-11.4 years old and there were 29 male patients. The body was most commonly located on the longitudinal axis (57.1%). Eleven cases (28.2%) were not associated any other gastric lesion, the majority of which were the polypoid type (82.0%). However, two cases were found as a hypertrophic mucosal fold, and a submucosal tumor, respectively. Seventeen cases (43.6%) were associated with early gastric cancer. CONCLUSIONS: Despite its rarity, GCP should be considered when an endoscopically polypoid lesion or submucosal tumor (SMT) is found. Because of its association with early gastric cancer or adenoma, more study will be needed to examine the relationship between GCP and gastric carcinogen
Adenoma ; Axis, Cervical Vertebra ; Dilatation ; Gastritis* ; Humans ; Male ; Rare Diseases ; Stomach Neoplasms