Variable-size interleaver design for parallel turbo decoder architectures

In this paper, we propose two techniques to design good S-random interleavers, to be used in parallel and serially concatenated codes with interleavers. The interleavers designed according to these algorithms can be shortened, in order to support different block lengths in such a way that all the permutations obtained by pruning, when employed in a parallel turbo decoder, are collision-free. The first technique, suitable for short and medium interleavers, guarantees the same performance of nonparallel interleavers in terms of spreading properties, simulated frame-error probabilities, and obtainable minimum distance of the actual codes. The second algorithm, to be used for large block lengths, permits achieving high degrees of parallelism at the price of a slight degradation of the spread properties, and also to change the degree of parallelism on-the-fly. The operations of a parallel turbo decoder employing these interleavers are described, and an example of the advantages of the proposed techniques is provided in a realistic system framework.     

Design of versatile eIRA codes for parallel decoders

In this paper we propose a semi-random technique for the generation of a class of eIRA codes (a popular class of irregular LDPC codes that can be encoded in linear time) suited to partially parallel decoder implementations. The suggested technique tries to avoid both low-weight codewords and nearcodewords, which limit the performance of the belief propagation decoder. Its effectiveness is verified by comparison with literature results. The obtained codes are versatile, in terms of code-rate and block length, and they are characterized by a low error floor.     

Design of Prunable Interleavers for Parallel Turbo Decoder Architectures

In this paper we propose a technique to implement in a parallel fashion a turbo decoder based on an arbitrary permutation, and to expand its interleaver in order to produce a family of prunable S-random interleavers suitable for parallel implementations. We show that the spread properties of the obtained interleavers are almost optimal and we prove by simulation that they are very competitive in terms of error floor performance. A few details on the decoder architecture are also provided     

Clinical and Functional Study of a De Novo Variant in the PVP Motif of Kv1.1 Channel Associated with Epilepsy,Developmental Delay and Ataxia

Mutations in the KCNA1 gene, encoding the voltage-gated potassium channel Kv1.1, have been associated with a spectrum of neurological phenotypes, including episodic ataxia type 1 and developmental and epileptic encephalopathy. We have recently identified a de novo variant in KCNA1 in the highly conserved Pro-Val-Pro motif within the pore of the Kv1.1 channel in a girl affected by early onset epilepsy, ataxia and developmental delay. Other mutations causing severe epilepsy are located in Kv1.1 pore domain. The patient was initially treated with a combination of antiepileptic drugs with limited benefit. Finally, seizures and ataxia control were achieved with lacosamide and acetazolamide. The aim of this study was to functionally characterize Kv1.1 mutant channel to provide a genotype–phenotype correlation and discuss therapeutic options for KCNA1-related epilepsy. To this aim, we transfected HEK 293 cells with Kv1.1 or P403A cDNAs and recorded potassium currents through whole-cell patch-clamp. P403A channels showed smaller potassium currents, voltage-dependent activation shifted by +30 mV towards positive potentials and slower kinetics of activation compared with Kv1.1 wild-type. Heteromeric Kv1.1+P403A channels, resembling the condition of the heterozygous patient, confirmed a loss-of-function biophysical phenotype. Overall, the functional characterization of P403A channels correlates with the clinical symptoms of the patient and supports the observation that mutations associated with severe epileptic phenotype cluster in a highly conserved stretch of residues in Kv1.1 pore domain. This study also strengthens the beneficial effect of acetazolamide and sodium channel blockers in KCNA1 channelopathies.