128 research outputs found

    High-energy electron-induced damage production at room temperature in aluminum-doped silicon

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    DLTS and EPR measurements are reported on aluminum-doped silicon that was irradiated at room temperature with high-energy electrons. Comparisons are made to comparable experiments on boron-doped silicon. Many of the same defects observed in boron-doped silicon are also observed in aluminum-doped silicon, but several others were not observed, including the aluminum interstitial and aluminum-associated defects. Damage production modeling, including the dependence on aluminum concentration, is presented

    From conformons to human brains: an informal overview of nonlinear dynamics and its applications in biomedicine

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    Methods of contemporary physics are increasingly important for biomedical research but, for a multitude of diverse reasons, most practitioners of biomedicine lack access to a comprehensive knowledge of these modern methodologies. This paper is an attempt to describe nonlinear dynamics and its methods in a way that could be read and understood by biomedical professionals who usually are not trained in advanced mathematics. After an overview of basic concepts and vocabulary of nonlinear dynamics, deterministic chaos, and fractals, application of nonlinear methods of biosignal analysis is discussed. In particular, five case studies are presented: 1. Monitoring the depth of anaesthesia and of sedation; 2. Bright Light Therapy and Seasonal Affective Disorder; 3. Analysis of posturographic signals; 4. Evoked EEG and photo-stimulation; 5. Influence of electromagnetic fields generated by cellular phones

    On extending actions of groups

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    Problems of dense and closed extension of actions of compact transformation groups are solved. The method developed in the paper is applied to problems of extension of equivariant maps and of construction of equivariant compactifications

    Falsification Of The Atmospheric CO2 Greenhouse Effects Within The Frame Of Physics

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    The atmospheric greenhouse effect, an idea that many authors trace back to the traditional works of Fourier (1824), Tyndall (1861), and Arrhenius (1896), and which is still supported in global climatology, essentially describes a fictitious mechanism, in which a planetary atmosphere acts as a heat pump driven by an environment that is radiatively interacting with but radiatively equilibrated to the atmospheric system. According to the second law of thermodynamics such a planetary machine can never exist. Nevertheless, in almost all texts of global climatology and in a widespread secondary literature it is taken for granted that such mechanism is real and stands on a firm scientific foundation. In this paper the popular conjecture is analyzed and the underlying physical principles are clarified. By showing that (a) there are no common physical laws between the warming phenomenon in glass houses and the fictitious atmospheric greenhouse effects, (b) there are no calculations to determine an average surface temperature of a planet, (c) the frequently mentioned difference of 33 degrees Celsius is a meaningless number calculated wrongly, (d) the formulas of cavity radiation are used inappropriately, (e) the assumption of a radiative balance is unphysical, (f) thermal conductivity and friction must not be set to zero, the atmospheric greenhouse conjecture is falsified.Comment: 115 pages, 32 figures, 13 tables (some typos corrected

    Feasibility studies of the time-like proton electromagnetic form factor measurements with PANDA at FAIR

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    The possibility of measuring the proton electromagnetic form factors in the time-like region at FAIR with the \PANDA detector is discussed. Detailed simulations on signal efficiency for the annihilation of pˉ+p\bar p +p into a lepton pair as well as for the most important background channels have been performed. It is shown that precision measurements of the differential cross section of the reaction pˉ+pe++e\bar p +p \to e^++ e^- can be obtained in a wide angular and kinematical range. The individual determination of the moduli of the electric and magnetic proton form factors will be possible up to a value of momentum transfer squared of q214q^2\simeq 14 (GeV/c)2^2. The total pˉ+pe++e\bar p +p\to e^++e^- cross section will be measured up to q228q^2\simeq 28 (GeV/c)2^2. The results obtained from simulated events are compared to the existing data. Sensitivity to the two photons exchange mechanism is also investigated.Comment: 12 pages, 4 tables, 8 figures Revised, added details on simulations, 4 tables, 9 figure

    Feasibility studies of time-like proton electromagnetic form factors at PANDA at FAIR

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    Simulation results for future measurements of electromagnetic proton form factors at \PANDA (FAIR) within the PandaRoot software framework are reported. The statistical precision with which the proton form factors can be determined is estimated. The signal channel pˉpe+e\bar p p \to e^+ e^- is studied on the basis of two different but consistent procedures. The suppression of the main background channel, i.e.\textit{i.e.} pˉpπ+π\bar p p \to \pi^+ \pi^-, is studied. Furthermore, the background versus signal efficiency, statistical and systematical uncertainties on the extracted proton form factors are evaluated using two different procedures. The results are consistent with those of a previous simulation study using an older, simplified framework. However, a slightly better precision is achieved in the PandaRoot study in a large range of momentum transfer, assuming the nominal beam conditions and detector performance

    Differential Expression of CD163 on Monocyte Subsets in Healthy and HIV-1 Infected Individuals

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    CD163, a haptoglobin-hemoglobin (Hp-Hb) scavenger receptor, expressed by monocytes and macrophages, is important in resolution of inflammation. Age-related non-AIDS co-morbidities in HIV-infected individuals, particularly dementia and cardiovascular disease, result in part from effects of HIV-1 infection on monocyte and macrophage biology. CD163 co-expression on CD14+CD16++ monocytes has been proposed as a useful biomarker for HIV-1 disease progression and the presence of HIV associated dementia. Here we investigated CD163 expression on monocyte subsets ex vivo, on cultured macrophages, and soluble in plasma, in the setting of HIV-1 infection. Whole blood immunophenotyping revealed CD163 expression on CD14++CD16- monocytes but not on CD14+CD16++ monocytes (P = 0.004), supported by CD163 mRNA levels. Incubation with M-CSF induced CD163 protein expression on CD14+CD16++ monocytes to the same extent as CD14++CD16− monocytes. CD163 expression on CD14++CD16+ monocytes from HIV-infected subjects was significantly higher than from uninfected individuals, with a trend towards increased expression on CD14++CD16− monocytes (P = 0.019 and 0.069 respectively), which is accounted for by HIV-1 therapy including protease inhibitors. Shedding of CD163 was shown to predominantly occur from the CD14++CD16− subset after Ficoll isolation and LPS stimulation. Soluble CD163 concentration in plasma from HIV-1 infected donors was similar to HIV-1 uninfected donors. Monocyte CD163 expression in HIV-1 infected patients showed a complicated relationship with classical measures of disease progression. Our findings clarify technical issues regarding CD163 expression on monocyte subsets and further elucidates its role in HIV-associated inflammation by demonstrating that CD163 is readily lost from CD14++CD16− monocytes and induced in pro-inflammatory CD14+CD16++ monocytes by M-CSF. Our data show that all monocyte subsets are potentially capable of differentiating into CD163-expressing anti-inflammatory macrophages given appropriate stimuli. Levels of CD163 expression on monocytes may be a potential biomarker reflecting efforts by the immune system to resolve immune activation and inflammation in HIV-infected individuals

    Differential Expression of CD163 on Monocyte Subsets in Healthy and HIV-1 Infected Individuals

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    CD163, a haptoglobin-hemoglobin (Hp-Hb) scavenger receptor, expressed by monocytes and macrophages, is important in resolution of inflammation. Age-related non-AIDS co-morbidities in HIV-infected individuals, particularly dementia and cardiovascular disease, result in part from effects of HIV-1 infection on monocyte and macrophage biology. CD163 co-expression on CD14+CD16++ monocytes has been proposed as a useful biomarker for HIV-1 disease progression and the presence of HIV associated dementia. Here we investigated CD163 expression on monocyte subsets ex vivo, on cultured macrophages, and soluble in plasma, in the setting of HIV-1 infection. Whole blood immunophenotyping revealed CD163 expression on CD14++CD16- monocytes but not on CD14+CD16++ monocytes (P = 0.004), supported by CD163 mRNA levels. Incubation with M-CSF induced CD163 protein expression on CD14+CD16++ monocytes to the same extent as CD14++CD16− monocytes. CD163 expression on CD14++CD16+ monocytes from HIV-infected subjects was significantly higher than from uninfected individuals, with a trend towards increased expression on CD14++CD16− monocytes (P = 0.019 and 0.069 respectively), which is accounted for by HIV-1 therapy including protease inhibitors. Shedding of CD163 was shown to predominantly occur from the CD14++CD16− subset after Ficoll isolation and LPS stimulation. Soluble CD163 concentration in plasma from HIV-1 infected donors was similar to HIV-1 uninfected donors. Monocyte CD163 expression in HIV-1 infected patients showed a complicated relationship with classical measures of disease progression. Our findings clarify technical issues regarding CD163 expression on monocyte subsets and further elucidates its role in HIV-associated inflammation by demonstrating that CD163 is readily lost from CD14++CD16− monocytes and induced in pro-inflammatory CD14+CD16++ monocytes by M-CSF. Our data show that all monocyte subsets are potentially capable of differentiating into CD163-expressing anti-inflammatory macrophages given appropriate stimuli. Levels of CD163 expression on monocytes may be a potential biomarker reflecting efforts by the immune system to resolve immune activation and inflammation in HIV-infected individuals
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