[Giant Left Ventricular Aneurysm After Double Patch Closure of Ventricular Septal Perforation Through Right Ventriculotomy].

A 66-year-old man. He had myocardial infarction due to occlusion of the left anterior descending branch, which was subsequently complicated by ventricular septal perforation. Ventricular septal perforation was repaired through right ventricle incision, applying double patches for closure, and injecting glue between the patches. The early postoperative course was good, but the infarcted left ventricular anterior wall remained because of the right ventriculotomy approach. A left ventricular aneurysm was demonstrated on postoperative follow-up echocardiography, which gradually enlarged to become giant. Since symptoms of heart failure such as respiratory distress appeared, left ventriculoplasty was performed 29 months after the perforation of the initial surgery. Since thinned left ventricular wall remains following right ventriculotomy approach, risk of postoperative left ventricular aneurysm should be taken into account.

Venous drainage for minithoracotomy approach in an adult with interrupted inferior vena cava.

For atrial septal defect closure via right minithoracotomy in an adult patient with infra-hepatic interruption of the inferior vena cava with azygos connection, an alternative venous cannulation strategy was applied. In addition to bicaval cannulations to the femoral vein and the internal jugular vein, a 20 Fr straight cannula draining the hepatic vein was added to the proximal IVC through the right atrium wall via a working port. A bloodless operative field in the right atrium was afforded with bicaval encircling. Preoperative imaging test of the continuity of the IVC was important planning cardiac surgery with peripheral cannulations.

K604, a specific acyl­CoA:cholesterol acyltransferase 1 inhibitor, suppresses proliferation of U251­MG glioblastoma cells.

Glioblastoma is the most aggressive type of brain tumor and has a poor prognosis. Increased levels of cholesteryl ester and simultaneous expression of acyl­CoA:cholesterol acyltransferase 1 (ACAT1) in tumor cells indicated that cholesterol esterification is critical to tumor growth. The present study confirmed that human glioblastoma tissues as well as the glioblastoma cell line U251­MG showed significant expression of ACAT1. ACAT1 expression in U251­MG cells increased in a cell proliferation­dependent manner. K604, a selective ACAT1 inhibitor, suppressed the proliferation of U251­MG cells and downregulated the activation of Akt and extracellular signal­regulated kinase in proliferating glioblastoma cells. These results suggested that ACAT1 may be a therapeutic target for the treatment of glioblastoma, with K604 as an effective therapeutic agent.

CD44-expressing undifferentiated carcinoma with rhabdoid features of the pancreas: molecular analysis of aggressive invasion and metastasis.

Carcinoma with rhabdoid features is a rare malignant tumor with a poor prognosis whose molecular mechanism for aggressive behavior is unclear. We describe an undifferentiated pancreatic carcinoma with rhabdoid features that demonstrated extensive invasion and metastasis. Examination of a 63-year-old man with back pain disclosed a retroperitoneal tumor with multiple metastases. Lymph node biopsy revealed an undifferentiated carcinoma of unknown origin. Intensive chemotherapy was ineffective; the patient died 3 months after initial symptoms. Autopsy showed that the tumor displaced the retroperitoneal space: it diffusely invaded and destroyed the pancreas and duodenum. Histology demonstrated tumor cells with eccentric vesicular nuclei, large nucleoli, juxtanuclear eosinophilic inclusions, and poor cell adhesion. Immunohistochemistry showed that tumor cells expressed cytokeratin and vimentin, and electron microscopy confirmed a perinuclear mass of intermediate fibrils and lipid droplets, which indicated an undifferentiated carcinoma with rhabdoid features. Tumor tissue contained hyaluronan; tumor cells strongly expressed CD44, matrix metalloproteinase-9, hypoxia-inducible factor-1α, hyaluronan synthase 2, and acyl-CoA:cholesterol acyltransferase 1 and had a high Ki-67(+) ratio. Since hyaluronan is a ligand for CD44, formation of CD44-hyaluronan complex on the cell surface activates CD44 and this activation may explain why the tumor manifested aggressive invasion and metastasis throughout the clinical course.