Radiology: Volume 268: Number 2-August 2013 n radiology.rsna.org 563 Purpose:To determine the prevalence of interstitial lung abnormalities (ILAs) at initial computed tomography (CT) examination and the rate of progression of ILAs on 2-year follow-up CT images in a National Lung Screening Trial population studied at a single site. Materials and Methods:The study was approved by the institutional review board and informed consent was obtained from all participants. Image review for this study was HIPAA compliant. We reviewed the CT images of 884 cigarette smokers who underwent low-dose CT at a single site in the National Lung Screening Trial. CT findings were categorized as having no evidence of ILA, equivocal for ILA, or ILA. We categorized the type of ILA as nonfibrotic (ground-glass opacity, consolidation, mosaic attenuation), or fibrotic (ground glass with reticular pattern, reticular pattern, honeycombing). We evaluated the temporal change of the CT findings (no change, improvement, or progression) of ILA at 2-year follow-up. A x 2 with Fisher exact test or unpaired t test was used to determine whether smoking parameters were associated with progression of ILA at 2-year follow-up CT. Results:The prevalence of ILA was 9.7% (86 of 884 participants; 95% confidence interval: 7.9%, 11.9%), with a further 11.5% (102 of 884 participants) who had findings equivocal for ILA. The pattern was fibrotic in 19 (2.1%), nonfibrotic in 52 (5.9%), and mixed fibrotic and nonfibrotic in 15 (1.7%) of the 86 participants with ILA. The percentage of current smokers (P = .001) and mean number of cigarette pack-years (P = .001) were significantly higher in those with ILA than those without. At 2-year follow-up of those with ILA (n = 79), findings of nonfibrotic ILA improved in 49% of cases and progressed in 11%. Fibrotic ILA improved in 0% and progressed in 37% of cases. Conclusion:ILA is common in cigarette smokers. Nonfibrotic ILA improved in about 50% of cases, and fibrotic ILA progressed in about 37%.q RSNA, 2013 interstitial lung abnormalities in a cT lung cancer screening Population: Prevalence and Progression Rate

BACKGROUND: Th e current usual interstitial pneumonitis (UIP)/idiopathic pulmonary fi brosis CT scan classifi cation system excludes probable UIP as a diagnostic category. We sought to determine the predictive eff ect of probable UIP on CT scan on histology and the eff ect of the promoter polymorphism in MUC5B (rs35705950) on histologic and CT scan UIP diagnosis.

Hepatitis C virus (HCV) is a leading cause of chronic hepatitis, cirrhosis, and hepatocellular carcinoma. The absence of culture systems permissive for HCV replication has presented a major bottleneck to antiviral development. We sought to recapitulate the early steps in the life cycle of HCV by means of DNA-based expression of viral genomic sequences. Here we report expression of replicating HCV RNA by using a, to our knowledge, novel binary expression system in which cells were transfected with a T7 polymerase-driven full-length HCV cDNA plasmid containing a cis-acting hepatitis ⌬ ribozyme to control 3 cleavage, and infected with vaccinia-T7 polymerase. HCV genomic and replicative strand synthesis, in addition to protein synthesis, was detectable and depended on full-length HCV sequences. Moreover, the system was capable of generating HCV RNA quasispecies, consistent with the action of the low-fidelity HCV NS5B RNA polymerase. IFN-␣, but not ribavirin, directly inhibited the viral replicative cycle in these cells, identifying the virus itself and not solely the immune system as a direct target of IFN action. The availability of a cell-based test for viral replication will facilitate screening of inhibitory compounds, analysis of IFN-resistance mechanisms, and analysis of virus-host cell interactions.cell-based assay ͉ amantadine ͉ ribavirin I nfection with hepatitis C virus (HCV) is a leading cause of chronic liver disease throughout the world (1). Chronic infection nearly always follows acute exposure to HCV, and chronically infected persons develop cirrhosis and hepatocellular carcinoma at dramatically elevated rates (2). Considering both the failure of humoral immunity to prevent reinfection and the virus' propensity for sequence diversity (3, 4), prospects for the development of an HCV vaccine seem remote. Unfortunately, available antiviral therapies, including IFN-␣ and ribavirin (RBV), have limited effectiveness (5).The lack of tissue-culture systems permissive for HCV replication has limited the development of new treatments. Although self-replicating HCV RNA replicons may permit investigation of RNA replication inhibitors (6), this system is limited to expression of the nonstructural region of the genome and requires mutant viral sequences to replicate (7). The successful introduction of RNA transcripts from an infectious cDNA clone into chimpanzees has made possible the adaptation of clones to animal studies (8). However, the repetitive use of large animals to explore HCV biology is impractical.Although IFN directly inhibits the replication of many viruses and alters immune function (9), current evidence that it directly inhibits HCV replication is inferential. Sequence changes and protein interaction assays implicate several HCV proteins as particular targets of IFN (10, 11). Given the need to screen for antiviral compounds, we developed a system capable of recapitulating the early steps of the HCV life cycle by adapting the infectious cDNA clone with elements that permit HCV RNA replication in vivo....

Radiologists typically spend long hours staring at the computer monitor. This unavoidable nature of our work can lead to detrimental effects on the eyes. Moreover, there is little awareness among radiologists with regards to such potential harm. Ocular hazards, such as computer vision syndrome, are increasingly becoming more relevant to the radiology community. In this article, we discuss the ocular occupational hazards faced by radiologists and suggestions that may help in minimizing such hazards.