2,366 research outputs found

    Numerical simulation of flow over a rough bed

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    This paper presents results of a direct numerical simulation (DNS) of turbulent flow over the rough bed of an open channel. We consider a hexagonal arrangement of spheres on the channel bed. The depth of flow has been taken as four times the diameter of the spheres and the Reynolds number has been chosen so that the roughness Reynolds number is greater than 70, thus ensuring a fully rough flow. A parallel code based on finite difference, domain decomposition, and multigrid methods has been used for the DNS. Computed results are compared with available experimental data. We report the first- and second-order statistics, variation of lift/drag and exchange coefficients. Good agreement with experimental results is seen for the mean velocity, turbulence intensities, and Reynolds stress. Further, the DNS results provide accurate quantitative statistics for rough bed flow. Detailed analysis of the DNS data confirms the streaky nature of the flow near the effective bed and the existence of a hierarchy of vortices aligned with the streamwise direction, and supports the wall similarity hypothesis. The computed exchange coefficients indicate a large degree of mixing between the fluid trapped below the midplane of the roughness elements and that above it

    A Wake-Up Call: Quality of Care After Resident Duty Hour Reform

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    On first glance, it seems self-evident: sleep-deprived physicians-intraining (residents) are more likely to make mistakes that could harm patients. Like pilots and truck drivers, these new physicians might need restrictions on how much they work. Such restrictions were created in 2003, but the impact of these new rules is unclear. Are patients any safer? Is hospital care more fragmented? Who’s doing the work that residents performed prior to duty hour reform? This Issue Brief summarizes several studies that offer evidence about the impact of these regulations on patient mortality, as well as on residents’ perceptions of the effects on quality of care, medical education, and residents’ quality of life

    Application of magnetically induced hyperthermia on the model protozoan Crithidia fasciculata as a potential therapy against parasitic infections

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    Magnetic hyperthermia is currently an EU-approved clinical therapy against tumor cells that uses magnetic nanoparticles under a time varying magnetic field (TVMF). The same basic principle seems promising against trypanosomatids causing Chagas disease and sleeping sickness, since therapeutic drugs available display severe side effects and drug-resistant strains. However, no applications of this strategy against protozoan-induced diseases have been reported so far. In the present study, Crithidia fasciculata, a widely used model for therapeutic strategies against pathogenic trypanosomatids, was targeted with Fe_{3}O_{4} magnetic nanoparticles (MNPs) in order to remotely provoke cell death using TVMFs. The MNPs with average sizes of d approx. 30 nm were synthesized using a precipitation of FeSO_{4}4 in basic medium. The MNPs were added to Crithidia fasciculata choanomastigotes in exponential phase and incubated overnight. The amount of uploaded MNPs per cell was determined by magnetic measurements. Cell viability using the MTT colorimetric assay and flow cytometry showed that the MNPs were incorporated by the cells with no noticeable cell-toxicity effects. When a TVMF (f = 249 kHz, H = 13 kA/m) was applied to MNP-bearing cells, massive cell death was induced via a non-apoptotic mechanism. No effects were observed by applying a TVMF on control (without loaded MNPs) cells. No macroscopic rise in temperature was observed in the extracellular medium during the experiments. Scanning Electron Microscopy showed morphological changes after TVMF experiments. These data indicate (as a proof of principle) that intracellular hyperthermia is a suitable technology to induce the specific death of protozoan parasites bearing MNPs. These findings expand the possibilities for new therapeutic strategies that combat parasitic infections.Comment: 9 pages, four supplementary video file

    The pancreatic-function test - method and normal values

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    No Abstrac

    Infrasonic Detection of a Large Bolide over South Sulawesi, Indonesia on October 8, 2009: Preliminary Results

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    In the morning hours of October 8, 2009, a bright object entered Earth's atmosphere over South Sulawesi, Indonesia. This bolide disintegrated above the ground, generating stratospheric infrasound returns that were detected by infrasonic stations of the global International Monitoring System (IMS) Network of the Comprehensive Nuclear-Test-Ban Treaty Organization (CTBTO) at distances up to 17 500 km. Here we present instrumental recordings and preliminary results of this extraordinary event. Using the infrasonic period-yield relations, originally derived for atmospheric nuclear detonations, we find the most probable source energy for this bolide to be 70+/-20 kt TNT equivalent explosive yield. A unique aspect of this event is the fact that it was apparently detected by infrasound only. Global events of such magnitude are expected only once per decade and can be utilized to calibrate infrasonic location and propagation tools on a global scale, and to evaluate energy yield formula, and event timing

    НАУКОВІ ДОСЛІДЖЕННЯ ВЧЕНИХ КВГУ-КГІ-ДГІ В ГАЛУЗІ МЕТАЛУРГІЇ (1900-1930 рр.)

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    Перші зародки промислового вуглевидобутку на Півдні Російської імперії (Лисячий Байрак під Лисичанськом) і виробництва металу (м. Луганськ) виник-ли у 90-х роках ХVІІІ с. У наступні десятиліття ці взаємопов’язані галузі розвивалися дуже повільно. А трохи раніше спроба почати видобуток залізної руди і виплавку з неї гарматних ядер на Криворіжжі була невдалою, тому майже на сто років про ці поклади руд забули

    Self-renewal of single mouse hematopoietic stem cells is reduced by JAK2V617F without compromising progenitor cell expansion

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    Recent descriptions of significant heterogeneity in normal stem cells and cancers have altered our understanding of tumorigenesis, emphasizing the need to understand how single stem cells are subverted to cause tumors. Human myeloproliferative neoplasms (MPNs) are thought to reflect transformation of a hematopoietic stem cell (HSC) and the majority harbor an acquired V617F mutation in the JAK2 tyrosine kinase, making them a paradigm for studying the early stages of tumor establishment and progression. The consequences of activating tyrosine kinase mutations for stem and progenitor cell behavior are unclear. In this article, we identify a distinct cellular mechanism operative in stem cells. By using conditional knock-in mice, we show that the HSC defect resulting from expression of heterozygous human JAK2V617F is both quantitative (reduced HSC numbers) and qualitative (lineage biases and reduced self-renewal per HSC). The defect is intrinsic to individual HSCs and their progeny are skewed toward proliferation and differentiation as evidenced by single cell and transplantation assays. Aged JAK2V617F show a more pronounced defect as assessed by transplantation, but mice that transform reacquire competitive self-renewal ability. Quantitative analysis of HSC-derived clones was used to model the fate choices of normal and JAK2-mutant HSCs and indicates that JAK2V617F reduces self-renewal of individual HSCs but leaves progenitor expansion intact. This conclusion is supported by paired daughter cell analyses, which indicate that JAK2-mutant HSCs more often give rise to two differentiated daughter cells. Together these data suggest that acquisition of JAK2V617F alone is insufficient for clonal expansion and disease progression and causes eventual HSC exhaustion. Moreover, our results show that clonal expansion of progenitor cells provides a window in which collaborating mutations can accumulate to drive disease progression. Characterizing the mechanism(s) of JAK2V617F subclinical clonal expansions and the transition to overt MPNs will illuminate the earliest stages of tumor establishment and subclone competition, fundamentally shifting the way we treat and manage cancers
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