Error Prediction for Adaptive Modulation and Coding In Multiple-Antenna . . .

In this paper, the problem of Packet Error Rate prediction is addressed in the multiple-antenna broadband OFDM context, and its impact on Adaptive Modulation and Coding (AMC) is quantified. The analysis is based on a physical layer comprising various modulation and coding schemes, ranging from robust space-time block coding (STBC) modes to high bit rate spatial division multiplexing (SDM) modes, and also hybrid SDM-STBC schemes. For each mode the expression of several Link Quality Metrics enabling PER prediction in the broadband OFDM channel, such as instantaneous SNR, capacity, or exponential e#ective SNR metrics are provided. Their advantages and limitations are investigated. Finally

An Alternative Approach to ChIP-Seq Normalization Enables Detection of Genome-Wide Changes in Histone H3 Lysine 27 Trimethylation upon EZH2 Inhibition

<div><p>Chromatin immunoprecipitation and DNA sequencing (ChIP-seq) has been instrumental in inferring the roles of histone post-translational modifications in the regulation of transcription, chromatin compaction and other cellular processes that require modulation of chromatin structure. However, analysis of ChIP-seq data is challenging when the manipulation of a chromatin-modifying enzyme significantly affects global levels of histone post-translational modifications. For example, small molecule inhibition of the methyltransferase EZH2 reduces global levels of histone H3 lysine 27 trimethylation (H3K27me3). However, standard ChIP-seq normalization and analysis methods fail to detect a decrease upon EZH2 inhibitor treatment. We overcome this challenge by employing an alternative normalization approach that is based on the addition of <i>Drosophila melanogaster</i> chromatin and a <i>D</i>. <i>melanogaster-</i>specific antibody into standard ChIP reactions. Specifically, the use of an antibody that exclusively recognizes the <i>D</i>. <i>melanogaster</i> histone variant H2Av enables precipitation of <i>D</i>. <i>melanogaster</i> chromatin as a minor fraction of the total ChIP DNA. The <i>D</i>. <i>melanogaster</i> ChIP-seq tags are used to normalize the human ChIP-seq data from DMSO and EZH2 inhibitor-treated samples. Employing this strategy, a substantial reduction in H3K27me3 signal is now observed in ChIP-seq data from EZH2 inhibitor treated samples.</p></div

<i>D</i>. <i>melanogaster</i> tag counts from H3K27me3 ChIP-seq reactions are elevated in EZH2 inhibitor treated samples.

<p>H2Av bound regions of the <i>D</i>. <i>melanogaster</i> genome were determined using the H2Av antibody in ChIP-seq reactions containing <i>D</i>. <i>melanogaster</i> S2 or OSS chromatin. <i>D</i>. <i>melanogaster</i> tags from ChIP-seq spike-in reactions were mapped only to these pre-defined H2Av regions. <b>(A)</b> H3K27me3 ChIP-seq reactions with <i>D</i>. <i>melanogaster</i> spike-in in KARPAS-422 cells have a substantial increase in <i>D</i>. <i>melanogaster</i> tags in spike-in libraries prepared from CPI-360 treated cells both at 4 days and 8 days after treatment. <b>(B)</b> The increase was not observed in the control H3K9me3 reactions. <b>(C)</b> H3K27me3 ChIP-seq reactions with <i>D</i>. <i>melanogaster</i> spike-in in PC9 cells have a substantial increase in <i>D</i>. <i>melanogaster</i> tags in spike-in libraries prepared from GSK126 treated cells. <b>(D)</b> The substantial increase in tags was not observed in the control H3K4me3 ChIP-seq spike-in reactions.</p

Reduced H3K27me3 binding is detected by ChIP-qPCR.

<p><b>(A)</b> ChIP was performed using chromatin from KARPAS-422 cells treated with the EZH2 inhibitor CPI-360. qPCR using the positive control primer <i>MYT1</i> showed reduced H3K27me3 occupancy in the presence of the inhibitor. <b>(B)</b> ChIP was performed using chromatin from PC9 cells treated with the EZH2 inhibitor GSK126. qPCR using the positive control primer <i>MYT1</i> showed reduced H3K27me3 occupancy in cells treated with the inhibitor. (<b>C</b>) Libraries were generated from KARPAS-422 cells using 15 cycles of PCR amplification. Library DNA was diluted and qPCR was performed using positive control primers for <i>MYT1</i> and <i>CCND2</i>. (<b>D</b>) Libraries were generated from PC9 cells as described in (C) and library DNA was used for qPCR using positive control primers for <i>MYT1</i> and <i>CCND2</i>. All experiments are represented as the mean of two independent experiments with qPCRs performed in triplicate ±SD. The <i>ACTB</i> promoter served as a negative control for all experiments.</p