Compensation of undesired effects in MIMO wireless transceivers

This paper presents compensation of all undesired effects (Power Amplifier (PA) nonlinearity, transmitter and receiver antenna crosstalk, before-PA nonlinear crosstalk, Multiple Input Multiple Output (MIMO) channel fading and crosstalk) in MIMO Orthogonal Frequency Division Multiplex (OFDM) wireless systems. It has been demonstrated that reduced-complexity Crossover Digital Predistortion (CO-DPD) algorithm on transmitter side and Matrix Inversion algorithm on receiver side can suppress almost all undesired effects introduced by transmitter, channel and receiver in 4×4 MIMO OFDM System that can be used in modern wireless system applications. A significant complexity reduction is achieved due to the fact that Digital Signal Processing (DSP) during CO-DPD process on transmitter side is done with real instead of complex numbers.

Language impairment in a case of a complex chromosomal rearrangement with a breakpoint downstream of FOXP2

BACKGROUND: We report on a young female, who presents with a severe speech and language disorder and a balanced de novo complex chromosomal rearrangement, likely to have resulted from a chromosome 7 pericentromeric inversion, followed by a chromosome 7 and 11 translocation. RESULTS: Using molecular cytogenetics, we mapped the four breakpoints to 7p21.1-15.3 (chromosome position: 20,954,043-21,001,537, hg19), 7q31 (chromosome position: 114,528,369-114,556,605, hg19), 7q21.3 (chromosome position: 93,884,065-93,933,453, hg19) and 11p12 (chromosome position: 38,601,145-38,621,572, hg19). These regions contain only non-coding transcripts (ENSG00000232790 on 7p21.1 and TCONS_00013886, TCONS_00013887, TCONS_00014353, TCONS_00013888 on 7q21) indicating that no coding sequences are directly disrupted. The breakpoint on 7q31 mapped 200 kb downstream of FOXP2, a well-known language gene. No splice site or non-synonymous coding variants were found in the FOXP2 coding sequence. We were unable to detect any changes in the expression level of FOXP2 in fibroblast cells derived from the proband, although this may be the result of the low expression level of FOXP2 in these cells. CONCLUSIONS: We conclude that the phenotype observed in this patient either arises from a subtle change in FOXP2 regulation due to the disruption of a downstream element controlling its expression, or from the direct disruption of non-coding RNAs.