MR images often provide superior anatomic and functional information over CT images, but generally are not used alone without CT images for radiotherapy treatment planning and image guidance. This study aims to investigate the potential of probabilistic classification of voxels from multiple MRI contrasts to generate synthetic CT (“MRCT”) images. The method consists of (1) acquiring multiple MRI volumes: T1-weighted, T2-weighted, two echoes from a ultra-short TE (UTE) sequence, and calculated fat and water image volumes using a Dixon method, (2) classifying tissues using fuzzy c-means clustering with a spatial constraint, (3) assigning attenuation properties with weights based on the probability of individual tissue class being present in each voxel, and (4) generating a MRCT image volume from the sum of attenuation properties in each voxel. The capability of each MRI contrast to differentiate tissues of interest was investigated based on a retrospective analysis of ten patients. For one prospective patient, the correlation of skull intensities between CT and MR was investigated, the discriminatory power of MRI in separating air from bone was evaluated, and the generated MRCT image volume was qualitatively evaluated. Our analyses showed that one MRI volume was not sufficient to separate all tissue types, and T2-weighted images was more sensitive to bone density variation compared to other MRI image types. The short echo UTE image showed significant improvement in contrasting air versus bone, but could not completely separate air from bone without false labeling. Generated MRCT and CT images showed similar contrast between bone and soft/solid tissues. These results demonstrate the potential of the presented method to generate synthetic CT images to support the workflow of Radiation Oncology treatment planning and image guidance.
We report the isolation of TRIP-Br1, a transcriptional regulator that interacts with the PHD-bromodomain of co-repressors of Kru È ppel-associated box (KRAB)-mediated repression, KRIP-1(TIF1b) and TIF1a, as well as the co-activator/adaptor p300/CBP. TRIP-Br1 and the related protein TRIP-Br2 possess transactivation domains. Like MDM2, which has a homologous transactivation domain, TRIP-Br proteins functionally contact DP-1, stimulating E2F-1/DP-1 transcriptional activity. KRIP-1 potentiates TRIP-Br protein co-activation of E2F-1/DP-1. TRIP-Br1 is a component of a multiprotein complex containing E2F-1 and DP-1. Co-expression of the retinoblastoma gene product (RB) abolishes baseline E2F-1/DP-1 transcriptional activity as well as TRIP-Br/KRIP-1 coactivation, both of which are restored by the adenovirus E1A onco-protein. These features suggest that TRIP-Br proteins function at E2F-responsive promoters to integrate signals provided by PHD-and/ or bromodomain-containing transcription factors. TRIP-Br1 is identical to the cyclin-dependent kinase 4 (cdk4)-binding protein p34 SEI-1 , which renders the activity of cyclin D/cdk4 resistant to the inhibitory effect of p16 INK4a during late G 1 . TRIP-Br1(p34 SEI-1 ) is differentially overexpressed during the G 1 and S phases of the cell cycle, consistent with a dual role for TRIP-Br1(p34 SEI-1 ) in the regulation of cell cycle progression through sequential effects on the transcriptional activity of E2F-responsive promoters during G 1 and S phases.
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