FAS expression inversely correlates with PTEN level in prostate cancer and a PI 3-kinase inhibitor synergizes with FAS siRNA to induce apoptosis

Fatty acid synthase (FAS), a key enzyme of the fatty acid biosynthetic pathway, has been shown to be overexpressed in various types of human cancer and is, therefore, considered to be an attractive target for anticancer therapy. However, the exact mechanism of overexpression of the FAS gene in tumor cells is not well understood. In this report, we demonstrate that the expression of the tumor suppressor gene PTEN has a significant inverse correlation with FAS expression in the case of prostate cancer in the clinical setting, and inhibition of the PTEN gene leads to the overexpression of FAS in vitro. We also found that the combination of the expression status of these two genes is a better prognostic marker than either gene alone. Furthermore, our results indicate that the specific inhibition of FAS gene by siRNA leads to apoptosis of prostate tumor cells, and inhibition of PI 3-kinase pathway synergizes with FAS siRNA to enhance tumor cell death. These results provide a strong rationale for exploring the therapeutic use of an inhibitor of the PTEN signaling pathway in conjunction with the FAS siRNA to inhibit prostate tumor growth.     

Treatment with TAE of subcapsular hematoma as a complication of extracorporeal shock wave lithotripsy (ESWL): a case report

A 58-year-old man with a left renal stone and with poor controlled hypertension was attacked by sudden onset of left renal colic pain, gross hematuria and nausea at 3 hours after ESWL. Ultrasonography and enhanced computed tomography revealed severe subcapsular hematoma, which compressed the left kidney. Since serum hemoglobin level continued to decrease in spite of 7 days of conservative therapy, we performed transfusion of red blood cells and selective transarterial embolization (TAE). Renal angiography showed multiple pseudo-aneurysms of arteriole at the lower pole of the left kidney. Embolization of left renal artery was effective to relieve patient's symptom and to stabilize the serum hemoglobin level.     

Use of a modified Dumon stent for postoperative bronchopleural fistula

This report describes a case of a postoperative bronchopleural fistula successfully managed with a modified Dumon stent. Surgical interventions for the bronchopleural fistula with empyema were subsequently avoided. Dumon stent is an acceptable option for the treatment of postoperative bronchopleural fistulas.     

Biochemical and immunohistochemical studies on dysmyelination of quaking mutant mice in vivo and in vitro

Dysmyelination in the central nervous system of the quaking mutant mouse was studied biochemically and immunohistochemically. We found, by measuring CNPase activity, that myelination in the central nervous system of quaking mice was affected to a different degree in different areas. The pallium cerebri was the most severely affected and the medulla and spinal cord were least affected. The density of astroglia observed by GFA staining wash higher in the white matter of quaking mice than in controls, but the total area of the white matter in the cerebellum was smaller in the quaking mice than in the controls. The DNA content in the pallium cerebri and brain stem showed no increase and that of the cerebellum was even lower in quaking mice than in the controls. Hypertrophy of the astroglia was observed in the white matter of the cerebellum of quaking mice, though Bergmann astroglial fibers in the molecular layer did not show any hypertrophy. The cerebella of quaking mice in primary culture showed very poor myelination under the phase-contrast microscope. However, Purkinje cells from the quaking mutants appeared normal with regard to Bodian silver impregnation, hematoxylineosin staining, and Purkinje cell specific P 400 protein. Addition of the conditioned culture medium of qk/qk to the culture of the control cerebellum did not interfere with the myelination. We concluded that the cause of dysmyelination in the quaking mouse could be a genetic defect of the oligodendroglia rather than hypertrophy of the astroglial cells.