The automated inflation device was controlled through a custom Labview program with user interface. This program was compiled as an executable, to allow easy access by users and to allow the program to be installed on multiple PCs. However, it should be noted that the executable still requires a deployable version of Labview with associated virtual instrument libraries. Because of this, there is some amount of computational overhead required to run the automated inflation device software. If very high speed inflation/deflation cycles were required, it would be advisable to BMS-199264 hydrochloride develop a stand-alone version of the software, that did not require the overhead of the deployable version of Labview. However, for the time scales of most studies, the Labview-based software we have developed provides more-than-adequate response speed and reproducibility. Prostate cancer is the main cause of cancer-related death in men in most developed countries, and the most common malignancy in American males. In the United States, one over eight men will develop prostate cancer during his life and over 27,360 men are expected to die from the disease this year. Molecular genetics studies of prostate cancer have identified mutations, deletions, or loss of tumor suppressor genes expression in subsets of patients with prostate cancer. However, due to the heterogeneity of prostate cancer itself and the focal nature of oncogene/tumor suppressor gene alterations, the role of these genes in prostate cancer onset and the diagnostic and/or prognostic value of such genes alterations remains uncertain. Loss of heterozygosity points out the presence of suppressor genes at specific chromosomal regions in tumors. Several allelotyping studies reported the telomeric portion of chromosome 12 to be deleted in a variety of solid tumors, including prostate cancer. MITOSTATIN is a novel putative tumor suppressor gene localized at 12q24.1 recently characterized in our laboratory. We have previously demonstrated that this decorin-induced 62-kDa protein is expressed in most human tissues; it affects prostate cancer cell growth and cell death by regulating the level and activation of Hsp27. We have also analyzed by immunohistochemistry the expression of Mitostatin in a series of primary bladder and breast tumors, and observed a FPL-55712 reduction of Mitostatin protein levels in advanced tumor stages.