Effect of region-of-interest placement in bolus tracking cerebral computed tomography angiography.

INTRODUCTION: Premature or delayed triggering of semiautomatic contrast tracking during intracranial computed tomographic angiography can occur due to artifact from dense contrast in the superior vena cava or brachiocephalic veins near the anterior aortic arch. We determine if placement of bolus tracking region-of-interest in the posterior thoracic aorta can prevent suboptimal intracranial arterial opacification. METHODS: Intracranial computed tomography angiographies from 80 patients performed on the same scanner were retrospectively evaluated. Thirty-seven consecutive patients with bolus tracking region-of-interest (ROI) placed in the anterior thoracic aorta (group A) and 43 consecutive patients with ROI placed in the posterior thoracic arch (group B) were identified. Two neuroradiologists scored the quality of intracranial computed tomography angiography on a four-point scale. Quantitative measurement of intracranial arterial opacification was also performed. The proportions of patients with poorest quality score as well as the proportions of the patients with the worst degree of intracranial arterial opacification (<10th percentile) were compared between groups A and B using two-sample proportion test. RESULTS: Qualitative evaluation of the intracranial computed tomography angiography showed 4 (11%) patients in group A with poor quality (score of 1), while all patients in group B scored 2 or higher (p = 0.028). Seven (19%) patients in group A had the lowest quantitative score (mean arterial opacification < 10th percentile) while 1 (2.5%) patient in group B had the lowest score (p = 0.018). CONCLUSION: Bolus tracking in the posterior thoracic aorta reduces the chance of suboptimal intracranial computed tomography angiography.

Distinct roles for the RSC and Swi/Snf ATP-dependent chromatin remodelers in DNA double-strand break repair.

The failure of cells to repair damaged DNA can result in genomic instability and cancer. To efficiently repair chromosomal DNA lesions, the repair machinery must gain access to the damaged DNA in the context of chromatin. Here we report that both the RSC and Swi/Snf ATP-dependent chromatin-remodeling complexes play key roles in double-strand break (DSB) repair, specifically by homologous recombination (HR). RSC and Swi/Snf are each recruited to an in vivo DSB site but with distinct kinetics. We show that Swi/Snf is required earlier, at or preceding the strand invasion step of HR, while RSC is required following synapsis for completion of the recombinational repair event.

Yeast RSC function is required for organization of the cellular cytoskeleton via an alternative PKC1 pathway.

RSC is a 15-protein ATP-dependent chromatin-remodeling complex related to Snf-Swi, the prototypical ATP-dependent nucleosome remodeler in budding yeast. Despite insight into the mechanism by which purified RSC remodels nucleosomes, little is known about the chromosomal targets or cellular pathways in which RSC acts. To better understand the cellular function of RSC, a screen was undertaken for gene dosage suppressors of sth1-3ts, a temperature-sensitive mutation in STH1, which encodes the essential ATPase subunit. Slg1p and Mid2p, two type I transmembrane stress sensors of cell wall integrity that function upstream of protein kinase C (Pkc1p), were identified as multicopy suppressors of sth1-3ts cells. Although the sth1-3ts mutant exhibits defects characteristic of PKC1 pathway mutants (caffeine and staurosporine sensitivities and an osmoremedial phenotype), only upstream components and not downstream effectors of the PKC1-MAP kinase pathway can suppress defects conferred by sth1-3ts, suggesting that RSC functions in an alternative PKC1-dependent pathway. Moreover, sth1-3ts cells display defects in actin cytoskeletal rearrangements and are hypersensitive to the microtubule depolymerizing drug, TBZ; both of these defects can be corrected by the high-copy suppressors. Together, these data reveal an important functional connection between the RSC remodeler and PKC1-dependent signaling in regulating the cellular architecture.