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1.
Med Phys ; 39(6Part24): 3914, 2012 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-28518664

RESUMO

PURPOSE: The role of breast density in cancer detection has been well characterized, and newer modalities such as breast tomosynthesis and breast CT (bCT) were developed to improve cancer detection in the dense breast by reducing anatomical complexity. Anatomical noise was characterized on a small cohort of patient images and compared across digital mammography, tomosynthesis, and bCT images. METHODS AND MATERIALS: An IRB-approved and HIPPA-compliant clinical study was performed on women undergoing breast biopsy, and mammography, tomosynthesis, and bCT were performed on both breasts immediately prior to biopsy. A total of 23 women participated in this study, and the unaffected breast (no lesion) was evaluated. A total of 1000 regions of interest were sampled on each image data set, and the 2D noise power spectrum (NPS) was evaluated. This was radially averaged to produce a 1D NPS, and the NPS was fit to a power law: ln{NPS(f)} = alpha+betaxln(f), over an anatomically-relevant range of spatial frequencies. The slope, beta, was averaged across patients and compared between modalities and projections. RESULTS: The value of beta was determined for bCT data sets, and they were 1.75 (0.424), 1.83 (0.352), and 1.79 (0.397), for the coronal, sagittal and axial views, respectively. For tomosynthesis, beta was 3.06 (0.361) and 3.10 (0.315) for the CC and MLO views, respectively. For mammography, these values were 3.17 (0.226) and 3.30 (0.236), for the CC and MLO views, respectively. The values of beta for breast CT were significantly different than those for tomosynthesis and mammography (p<0.001, all 12 comparisons). CONCLUSIONS: The results of this investigation demonstrate that the anatomical complexity of the breast, as characterized by the parameter beta, is statistically similar between mammography and tomosynthesis, a somewhat surprising finding. The breast CT image data, however, demonstrate a statistically-significant reduction in beta across all projections. Funded in part by Hologic Corporation and by a grant from the National Institute of Biomedical Imaging and Bioengineering, EB002138.

2.
J Mol Cell Cardiol ; 32(7): 1341-52, 2000 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-10860774

RESUMO

Current research from both clinical and basic science perspectives indicates that cytokines play an important role in the genesis of cardiovascular pathology. Specifically, levels of cytokines such as interleukin-1 (IL-1), tumor necrosis factor- alpha (TNF- alpha), and interleukin-6 (IL-6) have been found to be elevated in both acute myocardial injury as well as situations of chronic dysfunction. Further, therapies directed primarily at interfering with cytokine action have suggested that such an immunomodulatory approach may be beneficial in some of these circumstances of myocardial injury. We recently reported that IL-1 beta induces a hypertrophic state in cultured neonatal rat cardiac myocytes that differs from other well described hypertrophic phenotypes in terms of myocardial gene expression (such as skeletal alpha -actin, sACT), an effect that appeared to co-localize with that of the negative regulator yin yang-1 (YY1).(1)In the present study, we further localize the area in the sACT promoter responsible for the IL-1 effect. These investigations indicate that sequences in and around the third upstream serum response element (SRE3) bind YY1 and are required for IL-1 beta mediated repression. This element is also capable of transferring both IL-1 beta and YY1-mediated transcriptional repression to a heterologous promoter. In support of an IL-1 beta induced post-translational modification of YY1 that results in an increase in DNA-binding activity,(32)P-labeling experiments reveal an increase in phosphorylated YY1 in IL-1 beta treated cells and phosphatase-treated myocyte nuclear proteins lose their ability to bind to the YY1 site. In summary, these results provide evidence that sequences within the SRE3 of the skeletal actin promoter represent an IL-1 beta response element and suggest that IL-1 beta activates the negative transcription factor YY1 by both transcriptional and post-transcriptional mechanisms.


Assuntos
Proteínas de Ligação a DNA/metabolismo , Interleucina-1/farmacologia , Interleucina-1/fisiologia , Miocárdio/metabolismo , Fatores de Transcrição/metabolismo , Actinas/genética , Animais , Animais Recém-Nascidos , Sítios de Ligação , Western Blotting , Células Cultivadas , DNA/metabolismo , Proteínas de Ligação a DNA/genética , Eletroforese em Gel de Poliacrilamida , Fatores de Ligação de DNA Eritroide Específicos , Camundongos , Músculo Esquelético/metabolismo , Fosforilação , Plasmídeos , Regiões Promotoras Genéticas , RNA Mensageiro/metabolismo , Ratos , Proteínas Repressoras/metabolismo , Fatores de Transcrição/genética , Transcrição Gênica , Transfecção , Fator de Transcrição YY1 , Dedos de Zinco
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