In-Service BER Based Estimation of OFDM PAPR and CFO-induced Peak Phase Deviation

High Peak-to-Average Power Ratio (PAPR) of the transmitted OFDM signal is a well-known major drawback of the Orthogonal Frequency-Division Multiplexing (OFDM), so the High-Power Amplifier (HPA) is therefore necessary to operate in its linear region, i.e. with large back-off between the operating input power and its saturation region, so introducing not only in-band distortion, but also the adjacent channel interference. Specifically with the Long-Term Evolution (LTE) systems downlink, some sort of PAPR reduction, such as e.g. clipping, must be utilized. Considering that in many practical situations, determining PAPR demands complex test equipment, such as e.g. Vector Signal Analyzer (VSA), which might not be available, in this paper, we develop a simple Bit-Error-Rate (BER) based model for the (residual) PAPR estimation, by applying link abstraction, i.e. considering the easy measurable BER degradation due to HPA non-linearity, as if it were the consequence of the according level of additive white Gaussian noise (AWGN) abstracting the HPA distortion, while considering high Signal-to-Noise Ratio (SNR) and long enough cyclic prefix (CP), thus neglecting (real) additive noise and time dispersion (i.e. multipath fading). Moreover, the out-of-service BER testing, which requires network operator to interrupt its revenue-generating traffic, can be substituted by in-service BER estimation from in-phase and quadrature-phase eye diagram closures, measured on live traffic, by means of a simple oscilloscope. The analytical model is verified by the appropriate Monte-Carlo simulations

INTEGRATION OF COMPLEMENTARY BIOMARKERS IN PATIENTS WITH FIRST EPISODE PSYCHOSIS: RESEARCH PROTOCOL OF A PROSPECTIVE FOLLOW UP STUDY

In this project, we recruited a sample of 150 patients with first episode of psychosis with schizophrenia features (FEP) and 100 healthy controls. We assessed the differences between these two groups, as well as the changes between the acute phase of illness and subsequent remission among patients over 18-month longitudinal follow-up. The assessments were divided into four work packages (WP): WP1- psychopathological status, neurocognitive functioning and emotional recognition; WP2- stress response measured by saliva cortisol during a stress paradigm; cerebral blood perfusion in the resting state (with single photon emission computed tomography (SPECT) and during activation paradigm (with Transcranial Ultrasonography Doppler (TCD); WP3-post mortem analysis in histologically prepared human cortical tissue of post mortem samples of subjects with schizophrenia in the region that synaptic alteration was suggested by WP1 and WP2; WP4- pharmacogenetic analysis (single gene polymorphisms and genome wide association study (GWAS). We expect that the analysis of these data will identify a set of markers that differentiate healthy controls from patients with FEP, and serve as an additional diagnostic tool in the first episode of psychosis, and prediction tool which can be then used to help tailoring individualized treatment options. In this paper, we describe the project protocol including aims and methods and provide a brief description of planned post mortem studies and pharmacogenetic analysis

Closed-Form Enhanced Detection of Clipped OFDM Symbol

Large peak-to-average power ratio (PAPR) and carrier frequency offset (CFO) are dominant impairments of the orthogonal frequency-division multiplexing (OFDM) symbol transmission that is applied within the state-of-the-art wireless operator networks. In this work, we deal with consequences of the amplitude peak clipping that is commonly used at the transmitter to reduce the PAPR of the OFDM symbol, and thus prevent its non-linear distortion which would otherwise be imposed by the output high-power amplifier (HPA). Accordingly, regardless of the clipping generating mechanism at the transmitter being either inherent (related to the HPA) or deliberate (due to PAPR reduction), the clipped incoming OFDM symbol at the receiver may lead to degraded detection accuracy and transmission performance. However, the methods that have been applied so far at the receiver for compensating non-linear distortion due to clipping, are quite complex and computationally demanding. On the contrary, we propose effective mitigation of the problem to be performed at the receiver, by deriving the closed-form enhanced detection criterion, which requires common measurements of the mean and the rms values, as well as the autocorrelation of the received OFDM symbol comprising both un-clipped and clipped sections. Such improved detection was shown to significantly reduce the side effects of clipping, and restore satisfactory transmission performance – the bit error rate (BER) in particular. The proposed analytical model was preliminarily verified by versatile Monte-Carlo simulations and professional industry-standard vector signal analysis (VSA) test system, as well as by BER testing. The evident convergence of the three methods’ test results leads to the conclusion that the proposed clipped OFDM symbol detection method provides clear improvement with respect to the conventional one

Tumour mutations in long noncoding RNAs enhance cell fitness

Abstract Long noncoding RNAs (lncRNAs) are linked to cancer via pathogenic changes in their expression levels. Yet, it remains unclear whether lncRNAs can also impact tumour cell fitness via function-altering somatic “driver” mutations. To search for such driver-lncRNAs, we here perform a genome-wide analysis of fitness-altering single nucleotide variants (SNVs) across a cohort of 2583 primary and 3527 metastatic tumours. The resulting 54 mutated and positively-selected lncRNAs are significantly enriched for previously-reported cancer genes and a range of clinical and genomic features. A number of these lncRNAs promote tumour cell proliferation when overexpressed in in vitro models. Our results also highlight a dense SNV hotspot in the widely-studied NEAT1 oncogene. To directly evaluate the functional significance of NEAT1 SNVs, we use in cellulo mutagenesis to introduce tumour-like mutations in the gene and observe a significant and reproducible increase in cell fitness, both in vitro and in a mouse model. Mechanistic studies reveal that SNVs remodel the NEAT1 ribonucleoprotein and boost subnuclear paraspeckles. In summary, this work demonstrates the utility of driver analysis for mapping cancer-promoting lncRNAs, and provides experimental evidence that somatic mutations can act through lncRNAs to enhance pathological cancer cell fitness