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    ABSTRACT: We demonstrate the simple, noncontact and simultaneous measurement for thickness and water content of black ink films using THz radiation. The experimental setup was shown To generate intense THz radiation, the excitation laser irradiated InAs with 70-degrees-incidence angle. The transmitted THz radiation was collimated by a 10-cm off-axis parabolic mirror, lead to polarizing Michelson interferometers, and detected by a bolometer.
    No preview · Conference Paper · Feb 2002
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    ABSTRACT: It has well been established by comparative genomic hybridizations that melanocytic neoplasms have chromosomal copy number aberrations not seen in benign melanocytic nevi. In a rigorous study involving over 400 melanocytic neoplasms we recently evaluated the potential of a number of chromosomal loci frequently altered in melanoma but not in nevi as potential targets for a fluorescence in situ based assay. After evaluating 14 potential chromosomal loci arranged in various 4 probe panels, 6p25, 6q23, Cep6 and 11q13 were identified as the combination of targets best able to differentiate between malignant melanoma and benign nevi. Melanocytic neoplasms were considered as positive for melanoma if any of the following criteria were met; greater than 29% of enumerated cells showed gains in 6p25; greater than 38% of cells showed gains in 11q13; greater than 55% of cells show more copies of 6p25 than Cep6; or if greater than 42% of cells have less copies of 6q23 than Cep6. In a validation set, this 4 probe assay targeting these loci was able to differentiate between melanoma and nevi with a sensitivity of 86.7% and specificity of 95.4%. In this paper we review the multiple steps involved in development of this assay as well as the subsequent performance of this assay in a number of studies looking at its utility in specific differential diagnoses in melanocytic pathology.
    No preview · Article · Feb 2010 · Giornale Italiano di Dermatologia e Venereologia
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    ABSTRACT: Resistance to transforming growth factor (TGF) β-mediated tumor suppression in melanoma appears to be a crucial step in tumor aggressiveness since it is usually coupled with the ability of TGFβ to drive the oncogenic process via autocrine and paracrine effects. In this review, we will focus mainly on the mechanisms of escape from TGFβ-induced cell cycle arrest because the mechanisms of resistance to TGFβ-mediated apoptosis are still essentially speculative. As expected, some of these mechanisms can directly affect the function of the main downstream effectors of TGFβ, Smad2 and Smad3, resulting in compromised Smad-mediated antiproliferative activity. Other mechanisms can counteract or overcome TGFβ-mediated cell cycle arrest independently of the Smads. In melanoma, some models of resistance to TGFβ have been suggested and will be described. In addition, we propose additional models of resistance taking into consideration the information available on the dysregulation of fundamental cellular effectors and signaling pathways in melanoma.
    Full-text · Article · Oct 2010 · Carcinogenesis
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