Finding the complete path and weight enumerators of convolutional codes

A method for obtaining the complete path enumerator T(D, L, I) of a convolutional code is described. A system of algebraic equations is solved, using a new algorithm for computing determinants, to obtain T(D, L, I) for the (7,1/2) NASA standard code. Generating functions, derived from T(D, L, I) are used to upper bound Viterbi decoder error rates. This technique is currently feasible for constraint length K less than 10 codes. A practical, fast algorithm is presented for computing the leading nonzero coefficients of the generating functions used to bound the performance of constraint length K less than 20 codes. Code profiles with about 50 nonzero coefficients are obtained with this algorithm for the experimental K = 15, rate 1/4, code in the Galileo mission and for the proposed K = 15, rate 1/6, 2-dB code

Quantization effects in Viterbi decoding rate 1/n convolutional codes

A Viterbi decoder's performance loss due to quantizing data from the additive white Gaussian noise (AWGN) channel is studied. An optimal quantization scheme and branch metric calculation method are presented. The uniformly quantized channel capacity C(sub u)(q) is used to determine the smallest number of quantization bits q that does not cause a significant loss. The quantizer stepsize which maximizes C(sub u)(q) almost minimizes the decoder bit error rate (BER). However, a slightly larger stepsize is better, like the value that minimizes the Bhattacharyya bound. The range and renormalization of state metrics is analyzed, in particular for K = 15 decoders such as the Big Viterbi Decoder (BVD) for the Galileo mission. These results are required to design reduced hardware complexity Viterbi decoders with a negligible quantization loss

Compressed/reconstructed test images for CRAF/Cassini

A set of compressed, then reconstructed, test images submitted to the Comet Rendezvous Asteroid Flyby (CRAF)/Cassini project is presented as part of its evaluation of near lossless high compression algorithms for representing image data. A total of seven test image files were provided by the project. The seven test images were compressed, then reconstructed with high quality (root mean square error of approximately one or two gray levels on an 8 bit gray scale), using discrete cosine transforms or Hadamard transforms and efficient entropy coders. The resulting compression ratios varied from about 2:1 to about 10:1, depending on the activity or randomness in the source image. This was accomplished without any special effort to optimize the quantizer or to introduce special postprocessing to filter the reconstruction errors. A more complete set of measurements, showing the relative performance of the compression algorithms over a wide range of compression ratios and reconstruction errors, shows that additional compression is possible at a small sacrifice in fidelity

Induction of Blood Brain Barrier Tight Junction Protein Alterations by CD8 T Cells

Disruption of the blood brain barrier (BBB) is a hallmark feature of immune-mediated neurological disorders as diverse as viral hemorrhagic fevers, cerebral malaria and acute hemorrhagic leukoencephalitis. Although current models hypothesize that immune cells promote vascular permeability in human disease, the role CD8 T cells play in BBB breakdown remains poorly defined. Our laboratory has developed a novel murine model of CD8 T cell mediated central nervous system (CNS) vascular permeability using a variation of the Theiler's virus model of multiple sclerosis. In previous studies, we observed that MHC class II−/− (CD4 T cell deficient), IFN-γR−/−, TNF-α−/−, TNFR1−/−, TNFR2−/−, and TNFR1/TNFR2 double knockout mice as well as those with inhibition of IL-1 and LTβ activity were susceptible to CNS vascular permeability. Therefore, the objective of this study was to determine the extent immune effector proteins utilized by CD8 T cells, perforin and FasL, contributed to CNS vascular permeability. Using techniques such as fluorescent activated cell sorting (FACS), T1 gadolinium-enhanced magnetic resonance imaging (MRI), FITC-albumin leakage assays, microvessel isolation, western blotting and immunofluorescent microscopy, we show that in vivo stimulation of CNS infiltrating antigen-specific CD8 T cells initiates astrocyte activation, alteration of BBB tight junction proteins and increased CNS vascular permeability in a non-apoptotic manner. Using the aforementioned techniques, we found that despite having similar expansion of CD8 T cells in the brain as wildtype and Fas Ligand deficient animals, perforin deficient mice were resistant to tight junction alterations and CNS vascular permeability. To our knowledge, this study is the first to demonstrate that CNS infiltrating antigen-specific CD8 T cells have the capacity to initiate BBB tight junction disruption through a non-apoptotic perforin dependent mechanism and our model is one of few that are useful for studies in this field. These novel findings are highly relevant to the development of therapies designed to control immune mediated CNS vascular permeability