37 resultados para RESIDUAL VARIANCE


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Radio-frequency (RF) impairments, which intimately exist in wireless communication systems, can severely limit the performance of multiple-input-multiple-output (MIMO) systems. Although we can resort to compensation schemes to mitigate some of these impairments, a certain amount of residual impairments always persists. In this paper, we consider a training-based point-to-point MIMO system with residual transmit RF impairments (RTRI) using spatial multiplexing transmission. Specifically, we derive a new linear channel estimator for the proposed model, and show that RTRI create an estimation error floor in the high signal-to-noise ratio (SNR) regime. Moreover, we derive closed-form expressions for the signal-to-noise-plus-interference ratio (SINR) distributions, along with analytical expressions for the ergodic achievable rates of zero-forcing, maximum ratio combining, and minimum mean-squared error receivers, respectively. In addition, we optimize the ergodic achievable rates with respect to the training sequence length and demonstrate that finite dimensional systems with RTRI generally require more training at high SNRs than those with ideal hardware. Finally, we extend our analysis to large-scale MIMO configurations, and derive deterministic equivalents of the ergodic achievable rates. It is shown that, by deploying large receive antenna arrays, the extra training requirements due to RTRI can be eliminated. In fact, with a sufficiently large number of receive antennas, systems with RTRI may even need less training than systems with ideal hardware.

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In this single centre study of childhood acute lymphoblastic leukaemia (ALL) patients treated on the Medical Research Council UKALL 97/99 protocols, it was determined that minimal residual disease (MRD) detected by real time quantitative polymerase chain reaction (RQ-PCR) and 3-colour flow cytometry (FC) displayed high levels of qualitative concordance when evaluated at multiple time-points during treatment (93.38%), and a combined use of both approaches allowed a multi time-point evaluation of MRD kinetics for 90% (53/59) of the initial cohort. At diagnosis, MRD markers with sensitivity of at least 0.01% were identified by RQ-PCR detection of fusion gene transcripts, IGH/TRG rearrangements, and FC. Using a combined RQ-PCR and FC approach, the evaluation of 367 follow-up BM samples revealed that the detection of MRD >1% at Day 15 (P = 0.04), >0.01% at the end of induction (P = 0.02), >0.01% at the end of consolidation (P = 0.01), >0.01% prior to the first delayed intensification (P = 0.01), and >0.1% prior to the second delayed intensification and continued maintenance (P = 0.001) were all associated with relapse and, based on early time-points (end of induction and consolidation) a significant log-rank trend (P = 0.0091) was noted between survival curves for patients stratified into high, intermediate and low-risk MRD groups.

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Wilms' tumor gene 1 (WT1) is overexpressed in the majority (70-90%) of acute leukemias and has been identified as an independent adverse prognostic factor, a convenient minimal residual disease (MRD) marker and potential therapeutic target in acute leukemia. We examined WT1 expression patterns in childhood acute lymphoblastic leukemia (ALL), where its clinical implication remains unclear. Using a real-time quantitative PCR designed according to Europe Against Cancer Program recommendations, we evaluated WT1 expression in 125 consecutively enrolled patients with childhood ALL (106 BCP-ALL, 19 T-ALL) and compared it with physiologic WT1 expression in normal and regenerating bone marrow (BM). In childhood B-cell precursor (BCP)-ALL, we detected a wide range of WT1 levels (5 logs) with a median WT1 expression close to that of normal BM. WT1 expression in childhood T-ALL was significantly higher than in BCP-ALL (P<0.001). Patients with MLL-AF4 translocation showed high WT1 overexpression (P<0.01) compared to patients with other or no chromosomal aberrations. Older children (> or =10 years) expressed higher WT1 levels than children under 10 years of age (P<0.001), while there was no difference in WT1 expression in patients with peripheral blood leukocyte count (WBC) > or =50 x 10(9)/l and lower. Analysis of relapsed cases (14/125) indicated that an abnormal increase or decrease in WT1 expression was associated with a significantly increased risk of relapse (P=0.0006), and this prognostic impact of WT1 was independent of other main risk factors (P=0.0012). In summary, our study suggests that WT1 expression in childhood ALL is very variable and much lower than in AML or adult ALL. WT1, thus, will not be a useful marker for MRD detection in childhood ALL, however, it does represent a potential independent risk factor in childhood ALL. Interestingly, a proportion of childhood ALL patients express WT1 at levels below the normal physiological BM WT1 expression, and this reduced WT1 expression appears to be associated with a higher risk of relapse.

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Chimaerism was assessed in five recipients following sex mismatched allogeneic bone marrow transplantation. Techniques included karyotyping of bone marrow cells, dot blot DNA analysis of blood and bone marrow suspensions, and in vitro amplification of DNA by the polymerase chain reaction (PCR) using blood and bone marrow suspensions and stored bone marrow slides. Results of karyotypic analysis suggested complete chimaerism in four patients, while in one patient mixed chimaerism was detected. Mixed chimaerism was also detected, however, in a second patient using PCR and confirmed by dot blot analysis on all tissues examined. PCR is a sensitive tool for investigation of chimaerism following bone marrow transplantation. Since this technique does not require radioactivity, it is an attractive method for use in a clinical laboratory. This technique represents a further development in the use of DNA methodologies in the assessment of haematological disease.

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The development of the latest generation of wide-body carbon-fibre composite passenger aircraft has heralded a new era in the utilisation of these materials. The premise of superior specific strength and stiffness, corrosion and fatigue resistance, is tempered by high development costs, slow production rates and lengthy and expensive certification programmes. Substantial effort is currently being directed towards the development of new modelling and simulation tools, at all levels of the development cycle, to mitigate these shortcomings. One of the primary challenges is to reduce the extent of physical testing, in the certification process, by adopting a ‘certification by simulation’ approach. In essence, this aspirational objective requires the ability to reliably predict the evolution and progression of damage in composites. The aerospace industry has been at the forefront of developing advanced composites modelling tools. As the automotive industry transitions towards the increased use of composites in mass-produced vehicles, similar challenges in the modelling of composites will need to be addressed, particularly in the reliable prediction of crashworthiness. While thermoset composites have dominated the aerospace industry, thermoplastics composites are likely to emerge as the preferred solution for meeting the high-volume production demands of passenger road vehicles. This keynote presentation will outline recent progress and current challenges in the development of finite-element-based predictive modelling tools for capturing impact damage, residual strength and energy absorption capacity of thermoset and thermoplastic composites for crashworthiness assessments.