RESUMO
PURPOSE: To implement in software the procedures described in AAPM Task Group 150's draft recommendations for image receptor performance testing, and to evaluate the effectiveness and practicality of these procedures. METHODS: Images of flat fields were acquired using digital x-ray image receptors at 6 cooperating institutions. Four flat field images obtained with each detector spanned a range of input detector air kerma. Software based on AAPM TG150's draft report processed the test images and generated results. Image receptor response and several measures of non-uniformity were evaluated. Images were divided into 10 mm square regions, after eliminating 10 mm borders. For each region, signal (mean), noise (standard deviation) and SNR were calculated. Characteristic signal, noise and SNR were calculated based on average values from all regions. Local non-uniformity for signal (SLN), noise (NLN) and SNR (SNRLN) were expressed as the maximum ratio of the absolute difference between each region's value and its 4 nearest neighbors, to the respective characteristic value. Global non-uniformity (SGN, NGN, SNRGN) were expressed similarly but differences between maximum and minimum values obtained from the regions were used (without comparison to local neighbors). RESULTS: TG150 tests discriminated between good and poorly performing detectors. Improper detector calibration was detectable, with noise non-uniformity proving to be a more sensitive measure than signal or SNR non-uniformity. Detector rotation relative to calibration conditions produced a greater change in signal non-uniformity than the other measures. Image receptor structured noise was characterized by an increase in noise non-uniformity with incident air kerma. CONCLUSIONS: AAPM TG150's proposed approach to image receptor testing was implemented and evaluated. The approach appears to be an effective and practical one for routine quality assurance testing of digital radiographic image receptors.
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PURPOSE: Anomalous pixels may be defined as those pixels whose exposure response relationship is deviant from the typical, expected or calibrated response. A group of anomalous pixels may Result in visible correlated artifacts. Here we demonstrate an approach to identify anomalous pixels and correlated artifacts using flat-field images. METHODS: Using manufacturer specific calibration geometry, sets of four flat-field images per detector were obtained with varying input air kerma values (0.5 to 160 µGy) from 9 digital detectors at 6 institutions. Images obtained before and after calibration, with both proper and improper gain maps and structured artifacts were additionally acquired with some detectors. Image analysis methodology under consideration by AAPM Task Group 150 was used.After eliminating 10mm borders, images were divided into square regions (100mm2 ). Anomalous pixels were identified as pixels within each region with valuesabove or below ±3 standard deviations (SD) relative to the mean value of the region. If these pixels were identified in all four images comprising a set, then they were reported as anomalous. Line artifacts were identified as rows and columns with cumulative profile values that were above or below ±3 SD with respect to the mean value of neighboring profiles in the set of four flat-field mages. Results were verified with visual inspection of the images. RESULTS: For four sets of images, the algorithm did not identify any anomalous pixels, and none were spotted on visible inspection as well, while for five sets of images the identified anomalous pixels matched visual inspection results. Anomalous pixel detection failed in regions with an unusually large number of defects and structured noise, since those regions exhibited relatively large SD. Line artifacts consistent with visual analysis were identified correctly when present. CONCLUSIONS: A practical approach to identify anomalous pixels and correlated artifacts from flat-field images is demonstrated.
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Breast cancer is one of the leading causes of cancer-related deaths amongst women in the USA. The tumor microenvironment has been suggested to be an attractive therapeutic target for treatment of cancers. The glycosaminoglycan chondroitin sulfate, as part of the cellular microenvironment, consists of long linear chains of repeating disaccharide units, which are covalently attached to core proteins to form chondroitin sulfate-proteoglycans. In vitro studies have implicated chondroitin sulfate in various aspects of carcinogenesis, whereas the in vivo roles of chondroitin sulfate are less clear. Drastically elevated levels of chondroitin sulfate have been observed within the stromal compartment of many solid tumors, including human breast carcinomas, the significance of which is unknown. We examined the role of tumor-associated chondroitin sulfate in breast cancer progression. Enzymatic elimination of endogenous chondroitin sulfate by intra-tumor injections of chondroitinase ABC leads to the development of secondary tumors and increased lung metastases, while primary orthotopic tumor growth was not affected. These results establish a metastasis-inhibiting effect of primary breast tumor-associated chondroitin sulfate, which may open novel carbohydrate-based therapeutic strategies to combat breast cancer.
Assuntos
Sulfatos de Condroitina/metabolismo , Neoplasias Pulmonares/secundário , Neoplasias Mamárias Animais/metabolismo , Neoplasias Mamárias Animais/patologia , Animais , Linhagem Celular Tumoral , Proliferação de Células/efeitos dos fármacos , Condroitina ABC Liase/administração & dosagem , Condroitina ABC Liase/farmacologia , Feminino , Injeções , CamundongosRESUMO
Chondroitin-4-sulfotransferase-1(C4ST-1)/carbohydrate sulfotransferase 11 (CHST11) is a Golgi-bound enzyme involved in the biosynthesis of the glycosaminoglycan chondroitin sulfate. The sulfation pattern of chondroitin is tightly regulated during development, injury and disease, with the temporal and spatial expression of chondroitin sulfotransferase genes believed to be a crucial determinant of the fine balance of chondroitin sulfation. We have previously identified mouse C4st-1 as a target gene of ligands of the TGFbeta superfamily of growth factors, which could positively regulate C4st-1 expression in a number of cell types. We have also shown that a gene trap loss-of-function mutation in C4st-1 leads to severe skeletal abnormalities during mouse embryogenesis. In addition, we described a highly specific temporal and spatial expression pattern of C4st-1 during mouse embryogenesis. However, the transcriptional regulatory mechanisms that control C4st-1 gene expression remain unexplored. In order to gain knowledge on the transcriptional regulation of C4ST-1, we used a bioinformatical approach to identify conserved putative long-range cis-regulatory modules in a region of 120 kb spanning the 5' end of the C4ST-1 gene. Luciferase reporter assays in human HEK293T and mouse NmuMG cells identified a functional C4ST-1 promoter, as well as a number of cis-regulatory modules able to positively and negatively regulate C4ST-1 expression. Moreover, we identified TGFbeta- responsive regulatory modules that can function in a cell type-specific fashion. Taken together, our results identify TGFbeta-dependent and -independent cis-regulatory modules of the C4ST-1 gene.