Within these patients, 13 lesions in 12 patients who developed local tumor progression in the follow-up period of at least 8 months were retrospectively reviewed. Imaging obtained before and after RFA was used for creating fused images on a workstation. Ablative margins were assessed using only axial images, and with fused images. The ablative margin was assessed as sufficient in all 13 lesions using side-by-side axial images; however, all lesions

were assessed as insufficient with fused imaging evaluation. The reason for the discrepancy of the assessment results were differences in the respiratory dislocation of the liver in the pre- and CDK and cancer post-RFA images in eight lesions (61.5%), and rotational displacement of the liver and the torso in five (38.5%). The site of local tumor recurrence relative to the HCC lesion was craniocaudal in 12 lesions, dorsoventral in seven and lateral in seven. In all lesions, the site of local tumor recurrence was congruent with the area of the thinnest ablative margin. learn more Assessment of ablative margin with fused imaging revealed insufficiency of ablation previously evaluated as sufficient with conventional axial imaging. Fused imaging evaluation has proved to be an accurate and useful tool for the assessment of RFA margins. “
“Mice deficient in small heterodimer partner (SHP) are protected from diet-induced hepatic steatosis resulting

from increased fatty acid oxidation and decreased lipogenesis. The decreased lipogenesis appears to be a direct consequence of very low expression of peroxisome proliferator-activated receptor gamma 2 (PPAR-γ2), a potent lipogenic transcription factor, in the SHP−/− liver. The current

study focused on the identification of a SHP-dependent regulatory cascade that controls PPAR-γ2 gene expression, thereby regulating hepatic fat accumulation. Illumina BeadChip array (Illumina, Inc., San Diego, CA) and real-time polymerase chain reaction were used to identify genes responsible for the linkage between SHP and PPAR-γ2 using 上海皓元医药股份有限公司 hepatic RNAs isolated from SHP−/− and SHP-overexpressing mice. The initial efforts identify that hairy and enhancer of split 6 (Hes6), a novel transcriptional repressor, is an important mediator of the regulation of PPAR-γ2 transcription by SHP. The Hes6 promoter is specifically activated by the retinoic acid receptor (RAR) in response to its natural agonist ligand, all-trans retinoic acid (atRA), and is repressed by SHP. Hes6 subsequently represses hepatocyte nuclear factor 4 alpha (HNF-4α)-activated PPAR-γ2 gene expression by direct inhibition of HNF-4α transcriptional activity. Furthermore, we provide evidences that atRA treatment or adenovirus-mediated RAR-α overexpression significantly reduced hepatic fat accumulation in obese mouse models, as observed in earlier studies, and the beneficial effect is achieved by the proposed transcriptional cascade.