453 research outputs found

    NIVEAUX DE L'EUROPIUM-155

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    Le spectre d'électrons et le spectre [γ de 155Sm [MATH] 155Eu (22 min) ont été observés à haute résolution. Un schéma de niveaux est proposé

    A first approach to the distortion analysis of nonlinear analog circuits utilizing X-parameters

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    In this contribution a first approach to the distortion analysis of nonlinear 2-port-networks with X-parameters is presented. The X-parameters introduced by Verspecht and Root (2006) offer the possibility to describe nonlinear microwave 2-port-networks under large signal conditions. On the basis of X-parameter measurements with a nonlinear network analyzer (NVNA) behavioral models can be extracted for the networks. These models can be used to consider the nonlinear behavior during the design process of microwave circuits. The idea of the present work is to extract the behavioral models in order to describe the influence of interfering signals on the output behavior of the nonlinear circuits. Hereby, a simulator is used instead of a NVNA to extract the X-parameters. Assuming that the interfering signals are relatively small compared to the nominal input signal, the output signal can be described as a superposition of the effects of each input signal. In order to determine the functional correlation between the scattering variables, a polynomial dependency is assumed. The required datasets for the approximation of the describing functions are simulated by a directional coupler model in Cadence Design Framework. The polynomial coefficients are obtained by a least-square method. The resulting describing functions can be used to predict the system's behavior under certain conditions as well as the effects of the interfering signal on the output signal

    STF Optimierung von single-bit CT ΣΔ Modulatoren basierend auf skalierten Filterkoeffizienten

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    Die vorliegende Arbeit beschäftigt sich mit dem Signalübertragungsverhalten von single-bit continuous-time (CT) ΣΔ Modulatoren. Dabei liegt der Fokus der Untersuchung auf dem Peaking der Signaltransferfunktion (STF). Dieser Effekt kann die Performance und die Stabilität des Gesamtsystems negativ beeinflussen, da bei auftretendem STF-Peaking Signale außerhalb des Signalbands verstärkt werden. In dieser Arbeit wird ein neuer Ansatz zur Reduktion des Peakings vorgestellt, der auf der Optimierung der Systemdynamik basiert. Dabei werden die Filterkoeffizienten des Modulators systematisch angepasst. Anhand eines Beispielsystems wird gezeigt, dass der Ansatz genutzt werden kann, um das Übertragungsverhalten des Modulators abhängig vom Ausgangssystem zu verändern. So kann entweder die Systemsperformance verbessert werden, ohne Peaking in der STF zu erzeugen, oder das STF-Peaking reduziert werden, ohne die Systemperformance stark zu beeinflussen.DF

    Malignant Peripheral Nerve Sheath Tumors State of the Science: Leveraging Clinical and Biological Insights into Effective Therapies.

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    Malignant peripheral nerve sheath tumor (MPNST) is the leading cause of mortality in patients with neurofibromatosis type 1. In 2002, an MPNST consensus statement reviewed the current knowledge and provided guidance for the diagnosis and management of MPNST. Although the improvement in clinical outcome has not changed, substantial progress has been made in understanding the natural history and biology of MPNST through imaging and genomic advances since 2002. Genetically engineered mouse models that develop MPNST spontaneously have greatly facilitated preclinical evaluation of novel drugs for translation into clinical trials led by consortia efforts. Continued work in identifying alterations that contribute to the transformation, progression, and metastasis of MPNST coupled with longitudinal follow-up, biobanking, and data sharing is needed to develop prognostic biomarkers and effective prevention and therapeutic strategies for MPNST

    Malignant Peripheral Nerve Sheath Tumors State of the Science: Leveraging Clinical and Biological Insights into Effective Therapies.

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    Malignant peripheral nerve sheath tumor (MPNST) is the leading cause of mortality in patients with neurofibromatosis type 1. In 2002, an MPNST consensus statement reviewed the current knowledge and provided guidance for the diagnosis and management of MPNST. Although the improvement in clinical outcome has not changed, substantial progress has been made in understanding the natural history and biology of MPNST through imaging and genomic advances since 2002. Genetically engineered mouse models that develop MPNST spontaneously have greatly facilitated preclinical evaluation of novel drugs for translation into clinical trials led by consortia efforts. Continued work in identifying alterations that contribute to the transformation, progression, and metastasis of MPNST coupled with longitudinal follow-up, biobanking, and data sharing is needed to develop prognostic biomarkers and effective prevention and therapeutic strategies for MPNST

    Phase 2 randomized, flexible crossover, double-blinded, placebo-controlled trial of the farnesyltransferase inhibitor tipifarnib in children and young adults with neurofibromatosis type 1 and progressive plexiform neurofibromas

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    Background RAS is dysregulated in neurofibromatosis type 1 (NF1) related plexiform neurofibromas (PNs). The activity of tipifarnib, which blocks RAS signaling by inhibiting its farnesylation, was tested in children and young adults with NF1 and progressive PNs. Methods Patients aged 3–25 years with NF1-related PNs and imaging evidence of tumor progression were randomized in a double-blinded fashion to receive tipifarnib (200 mg/m2 orally every 12 h) or placebo (phase A) and crossed over to the opposite treatment arm at the time of tumor progression (phase B). PN volumes were measured with MRI, and progression was defined as ≥20% volume increase. Time to progression (TTP) in phase A was the primary endpoint, and the trial was powered to detect whether tipifarnib doubled TTP compared with placebo. Toxicity, response, and quality of life were also monitored. Results Sixty-two patients were enrolled. Tipifarnib and placebo were well tolerated. On phase A, the median TTP was 10.6 months on the placebo arm and 19.2 months on the tipifarnib arm (P = .12; 1-sided). Quality of life improved significantly compared with baseline on the tipifarnib arm but not on the placebo arm. Volumetric tumor measurement detected tumor progression earlier than conventional 2-dimensional (WHO) and 1-dimensional (RECIST) methods. Conclusions Tipifarnib was well tolerated but did not significantly prolong TTP of PNs compared with placebo. The randomized, flexible crossover design and volumetric PN assessment provided a feasible and efficient means of assessing the efficacy of tipifarnib. The placebo arm serves as an historical control group for phase 2 single-arm trials directed at progressive PNs

    Growth dynamics of plexiform neurofibromas: a retrospective cohort study of 201 patients with neurofibromatosis 1

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    BACKGROUND: To examine the natural growth dynamics of internal plexiform neurofibromas (PNs) in patients with neurofibromatosis 1 (NF1). METHODS: Two hundred and one NF1 patients underwent whole body MRI (WBMRI). Tumour burden was estimated volumetrically. Non-parametric Spearman’s rho correlation coefficients were used to analyse the relationship of growth rate to tumour volume and age. Chi-squared and Mann–Whitney U tests were used for analysing the association of tumour occurrence with sex or age. Chi-squared tests were used to analyse the association of tumour growth with age group. RESULTS: Seventy-one of 171 patients with serial WBMRI exams had internal PNs (median follow up 2.2 years [1.1 to 4.9 years]). Median whole body tumour volume was 86.4 mL [5.2 to 5878.5 mL]) with a median growth rate of 3.7%/year (−13.4 to 111%/year) that correlated with larger whole body tumour volume (P<0.001) and lower age (P=0.004). No new PNs developed in 273.0 patient-years among patients without tumours. Rate of new tumour development among patients with PNs was 0.6%/year (95% confidence interval 0.02 to 3.4%). Twenty-seven (13.5%) tumours increased significantly and were more frequent among children (P<0.001). Growth rate of tumours was inversely correlated with age (Spearman’s rho=−0.330, P<0.001). Seventy-one (35.5%) tumours had smaller volumes on follow up (median −3.4%/year [−0.07% to −35.9%/year]). CONCLUSION: Children with NF1 and internal PNs are at risk for tumour growth. Most PNs grow slowly or not at all, and some decrease in size. New tumours are infrequent in NF1 patients with PNs and unlikely in patients without PNs
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