X-ray imaging optimization using virtual phantoms and computerized observer modelling.

This study develops and demonstrates a realistic x-ray imaging simulator with computerized observers to maximize lesion detectability and minimize patient exposure. A software package, ViPRIS, incorporating two computational patient phantoms, has been developed for simulating x-ray radiographic images. A tomographic phantom, VIP-Man, constructed from Visible Human anatomical colour images is used to simulate the scattered portion using the ESGnrc Monte Carlo code. The primary portion of an x-ray image is simulated using the projection ray-tracing method through the Visible Human CT data set. To produce a realistic image, the software simulates quantum noise, blurring effects, lesions, detector absorption efficiency and other imaging artefacts. The primary and scattered portions of an x-ray chest image are combined to form a final image for computerized observer studies and image quality analysis. Absorbed doses in organs and tissues of the segmented VIP-Man phantom were also obtained from the Monte Carlo simulations. Approximately 25,000 simulated images and 2,500,000 data files were analysed using computerized observers. Hotelling and Laguerre-Gauss Hotelling observers are used to perform various lesion detection tasks. Several model observer tasks were used including SKE/BKE, MAFC and SKEV. The energy levels and fluence at the minimum dose required to detect a small lesion were determined with respect to lesion size, location and system parameters.

Mutations in the 1A rod domain segment of the keratin 9 gene in epidermolytic palmoplantar keratoderma.

Palmoplantar keratodermas (PPK) constitute a heterogeneous group of diseases marked by the thickening of palms and soles of affected individuals. They are divided into autosomal dominant and autosomal recessive groups by the mode of transmission. The autosomal dominantly transmitted group is further divided into epidermolytic (EPPK, Voerner) and non-epidermolytic (NEPPK, Unna-Thost) types according to the histopathologic findings. Recent development of molecular approaches has confirmed that EPPK and NEPPK are caused by the mutations in keratin 9 and 1 genes, respectively. We have studied three families of EPPK to find the mutation in the keratin 9 gene. DNA sequence analyses revealed single base changes in sequences encoding the highly conserved 1A rod domain segment of the keratin 9 gene in two of the three families. These mutations caused Arg (CGG) to Glu (CAG; R162Q) and Arg (CGG) to Try (TGG; R162W) substitutions. The same arginine position has been mutated in the keratin 10 gene in epidermolytic hyperkeratosis, the keratin 14 gene in epidermolysis bullosa simplex, and the keratin 9 gene in hereditary EPPK in Western patients. In this study we show that unrelated Korean patients have similar mutations.