Calibration sphere for low-frequency parametric sonars

Author Posting. © Acoustical Society of America, 2007. This article is posted here by permission of Acoustical Society of America for personal use, not for redistribution. The definitive version was published in Journal of the Acoustical Society of America 121 (2007): 1482-1490, doi:10.1121/1.2434244.The problem of calibrating parametric sonar systems at low difference frequencies used in backscattering applications is addressed. A particular parametric sonar is considered: the Simrad TOPAS PS18 Parametric Sub-bottom Profiler. This generates difference-frequency signals in the band 0.5–6 kHz. A standard target is specified according to optimization conditions based on maximizing the target strength consistent with the target strength being independent of orientation and the target being physically manageable. The second condition is expressed as the target having an immersion weight less than 200 N. The result is a 280-mm-diam sphere of aluminum. Its target strength varies from −43.4 dB at 0.5 kHz to −20.2 dB at 6 kHz. Maximum excursions in target strength over the frequency band due to uncertainty in material properties of the sphere are of order ±0.1 dB. Maximum excursions in target strength due to variations in mass density and sound speed of the immersion medium are larger, but can be eliminated by attention to the hydrographic conditions. The results are also applicable to the standard-target calibration of conventional sonars operating at low-kilohertz frequencies

An Osteoblast-Derived Proteinase Controls Tumor Cell Survival via TGF-beta Activation in the Bone Microenvironment

Breast to bone metastases frequently induce a "vicious cycle" in which osteoclast mediated bone resorption and proteolysis results in the release of bone matrix sequestered factors that drive tumor growth. While osteoclasts express numerous proteinases, analysis of human breast to bone metastases unexpectedly revealed that bone forming osteoblasts were consistently positive for the proteinase, MMP-2. Given the role of MMP-2 in extracellular matrix degradation and growth factor/cytokine processing, we tested whether osteoblast derived MMP-2 contributed to the vicious cycle of tumor progression in the bone microenvironment.To test our hypothesis, we utilized murine models of the osteolytic tumor-bone microenvironment in immunocompetent wild type and MMP-2 null mice. In longitudinal studies, we found that host MMP-2 significantly contributed to tumor progression in bone by protecting against apoptosis and promoting cancer cell survival (caspase-3; immunohistochemistry). Our data also indicate that host MMP-2 contributes to tumor induced osteolysis (μCT, histomorphometry). Further ex vivo/in vitro experiments with wild type and MMP-2 null osteoclast and osteoblast cultures identified that 1) the absence of MMP-2 did not have a deleterious effect on osteoclast function (cd11B isolation, osteoclast differentiation, transwell migration and dentin resorption assay); and 2) that osteoblast derived MMP-2 promoted tumor survival by regulating the bioavailability of TGFβ, a factor critical for cell-cell communication in the bone (ELISA, immunoblot assay, clonal and soft agar assays).Collectively, these studies identify a novel "mini-vicious cycle" between the osteoblast and metastatic cancer cells that is key for initial tumor survival in the bone microenvironment. In conclusion, the findings of our study suggest that the targeted inhibition of MMP-2 and/or TGFβ would be beneficial for the treatment of bone metastases