On Path Memory in List Successive Cancellation Decoder of Polar Codes

Polar code is a breakthrough in coding theory. Using list successive cancellation decoding with large list size L, polar codes can achieve excellent error correction performance. The L partial decoded vectors are stored in the path memory and updated according to the results of list management. In the state-of-the-art designs, the memories are implemented with registers and a large crossbar is used for copying the partial decoded vectors from one block of memory to another during the update. The architectures are quite area-costly when the code length and list size are large. To solve this problem, we propose two optimization schemes for the path memory in this work. First, a folded path memory architecture is presented to reduce the area cost. Second, we show a scheme that the path memory can be totally removed from the architecture. Experimental results show that these schemes effectively reduce the area of path memory.Comment: 5 pages, 6 figures, 2 table

Poly[(N,N-dimethyl­formamide-κO)tris­(μ-naphthalene-1-acetato)terbium(III)]

In title compound, [Tb(C12H9O2)3(C3H7NO)]n, the Tb atom is nine-coordinated by nine O atoms from three naphthalene-1-acetate and one N,N-dimethyl­formamide ligands. The Tb atoms are linked by three bridging naphthalene-1-acetate ligands into a chain parallel to the b axis. Further stabilization of the structure is accomplished by non-classical C—H⋯O hydrogen bonds and C—H⋯π interactions

Traumatic Brain Injury Induces Genome-Wide Transcriptomic, Methylomic, and Network Perturbations in Brain and Blood Predicting Neurological Disorders.

The complexity of the traumatic brain injury (TBI) pathology, particularly concussive injury, is a serious obstacle for diagnosis, treatment, and long-term prognosis. Here we utilize modern systems biology in a rodent model of concussive injury to gain a thorough view of the impact of TBI on fundamental aspects of gene regulation, which have the potential to drive or alter the course of the TBI pathology. TBI perturbed epigenomic programming, transcriptional activities (expression level and alternative splicing), and the organization of genes in networks centered around genes such as Anax2, Ogn, and Fmod. Transcriptomic signatures in the hippocampus are involved in neuronal signaling, metabolism, inflammation, and blood function, and they overlap with those in leukocytes from peripheral blood. The homology between genomic signatures from blood and brain elicited by TBI provides proof of concept information for development of biomarkers of TBI based on composite genomic patterns. By intersecting with human genome-wide association studies, many TBI signature genes and network regulators identified in our rodent model were causally associated with brain disorders with relevant link to TBI. The overall results show that concussive brain injury reprograms genes which could lead to predisposition to neurological and psychiatric disorders, and that genomic information from peripheral leukocytes has the potential to predict TBI pathogenesis in the brain