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Low-density parity-check (LDPC) codes have shown superior error-correcting performance in a variety of data storage system studies, including traditional longitudinal magnetic recording systems. However, perpendicular magnetic recording systems (of increasing interest) exhibit impairments different from longitudinal magnetic recording systems, and thus present new challenges for error-correcting codes. In this effort, we evaluate a structured LDPC code using a perpendicular magnetic recording channel model that includes impairments such as transition noise, nonlinear transition shift, transition percolation, and baseline wander (BLW). The channel model, as well as the LDPC encoder and the decoder are implemented in field-programmable gate array (FPGA) hardware. The LDPC coded system is evaluated down to bit error rate (BER) of [10.sup.-12] and frame error rate (FER) of [10.sup.-8]. The impact of individual impairments on coding performance is studied separately. The soft output Viterbi algorithm (SOVA) + LDPC system maintains its superior error-correcting performance under the perpendicular recording channel. Index Terms--Baseline wander (BLW), EPR4, field-programmable gate array (FPGA), low-density parity-check (LDPC) code, magnetic recording, nonlinear transition shift, partial erasure, perpendicular magnetic recording, transition percolation.

We present the results of performance evaluation of partial response (PR) targets for perpendicular recording by simulation using a field programmable gate array (FPGA). Previous research proposed several PR targets for perpendicular recording channels. We evaluated the bit error rate (BER) performance of those PR targets. Different PR targets led to not only different BERs for given signal-to-noise ratios (SNRs), but also different slopes of BER versus SNR curves. The result can be explained in terms of error event distributions of the corresponding PR targets. In the FPGA simulation, additive white Gaussian noise was used, but no jitter noise was introduced. The soft output Viterbi algorithm is used as the channel detector. A rate-8/9 low-density parity check code with code length 4923 and column weight 3 is used as the error correcting code. Two channel iterations are applied. We attain BERs as low as 10-12. Our results also show that the BER behavior of the PR4 target is significantly different from that of the [1 2 2 1] target. Index Terms--Field programmable gate array (FPGA), partial response (PR) target, perpendicular recording, soft-output Viterbi algorithm (SOVA).

Baseline wander (BLW) is one of major sources of bit errors in perpendicular recording. In this paper, we present a method to compensate for BLW by per-survivor processing (PSP), i.e., along each surviving path in the Viterbi algorithm (VA). We apply the PSP method in VA in timing recovery loop and SOVA for iterative decoding. Simulation results show that the cycle slip rate and bit error rate are lowered and approach ideal case where there is no BLW. Index Terms--Baseline wander (BLW), per-survivor processing (PSP).

Low-density parity check (LDPC) codes have shown near-capacity performance in additive white Gaussian noise (AWGN) channels. However, in magnetic recording systems, the readback signals suffer from various impairments (namely, transition noise, nonlinear transition shift, and partial erasure) in addition to AWGN. In this paper, we describe an FPGA-based advanced magnetic recording channel simulator (that includes these impairments) and an LDPC coding system. The error correcting performances of LDPC codes in the presence of such realistic impairments are investigated down to bit error rate (BER) of [10.sup.-11] and frame error rate (FER) of [10.sup.-8]. Index Terms--EPR4, FPGA, LDPC code, magnetic recording, nonlinear transition shift, partial erasure.

We here report a genome-editing strategy to correct spinal muscular atrophy (SMA). Rather than directly targeting the pathogenic exonic mutations, our strategy employed Cas9 and guide-sgRNA for the targeted disruption of intronic splicing-regulatory elements. We disrupted intronic splicing silencers (ISSs, including ISS-N1 and ISS + 100) of survival motor neuron (SMN) 2, a key modifier gene of SMA, to enhance exon 7 inclusion and full-length SMN expression in SMA iPSCs. Survival of splicing-corrected iPSC-derived motor neurons was rescued with SMN restoration. Furthermore, co-injection of Cas9 mRNA from Streptococcus pyogenes (SpCas9) or Cas9 from Staphylococcus aureus (SaCas9) alongside their corresponding sgRNAs targeting ISS-N1 into zygotes rescued 56% and 100% of severe SMA transgenic mice (Smn −/−, SMN2 tg/−). The median survival of the resulting mice was extended to >400 days. Collectively, our study provides proof-of-principle for a new strategy to therapeutically intervene in SMA and other RNA-splicing-related diseases. [ABSTRACT FROM AUTHOR]

The process of neuronal migration is precisely regulated by different molecules during corticogenesis. The FAK (focal adhesion kinase) plays a critical role in embryogenesis and is involved in cell motility through focal adhesions, but the underlying mechanisms on inordinate expression are unclear. To investigate the effect of FAK overexpression on neuronal migration spatiotemporally, mice FAK was transfected into the neurons in vivo by electroporation. Results showed that exogenous FAK distributed in the cytoplasm (in vivo) and co-localized with vinculin (in vitro) and induced aberrant neuronal migration via phosphorylation of FAK at Tyr925 during cerebral cortex development. Meanwhile, FAK Y925F mutant also induced aberrant neuronal migration like inordinate FAK/GFP phenotype. All these results implied that FAK-induced abnormal phenotype depended on phosphorylation of FAK at Tyr925, and this demonstrated that the overexpression of FAK impaired neuronal migration through its phosphorylation and activity of FAK during corticogenesis. [ABSTRACT FROM AUTHOR]