683 research outputs found

    Turbulent channel flow over an anisotropic porous wall - drag increase and reduction

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    The effect of the variations of the permeability tensor on the close-to-the-wall behaviour of a turbulent channel flow bounded by porous walls is explored using a set of direct numerical simulations. It is found that the total drag can be either reduced or increased by more than 20 % by adjusting the permeability directional properties. Drag reduction is achieved for the case of materials with permeability in the vertical direction lower than the one in the wall-parallel planes. This configuration limits the wall-normal velocity at the interface while promoting an increase of the tangential slip velocity leading to an almost ‘one-component’ turbulence where the low- and high-speed streak coherence is strongly enhanced. On the other hand, strong drag increase is found when high wall-normal and low wall-parallel permeabilities are prescribed. In this condition, the enhancement of the wall-normal fluctuations due to the reduced wall-blocking effect triggers the onset of structures which are strongly correlated in the spanwise direction, a phenomenon observed by other authors in flows over isotropic porous layers or over ribletted walls with large protrusion heights. The use of anisotropic porous walls for drag reduction is particularly attractive since equal gains can be achieved at different Reynolds numbers by rescaling the magnitude of the permeability only

    Spatial fluctuations in transient creep deformation

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    We study the spatial fluctuations of transient creep deformation of materials as a function of time, both by Digital Image Correlation (DIC) measurements of paper samples and by numerical simulations of a crystal plasticity or discrete dislocation dynamics model. This model has a jamming or yielding phase transition, around which power-law or Andrade creep is found. During primary creep, the relative strength of the strain rate fluctuations increases with time in both cases - the spatially averaged creep rate obeys the Andrade law ϵt∼t−0.7\epsilon_t \sim t^{-0.7}, while the time dependence of the spatial fluctuations of the local creep rates is given by Δϵt∼t−0.5\Delta \epsilon_t \sim t^{-0.5}. A similar scaling for the fluctuations is found in the logarithmic creep regime that is typically observed for lower applied stresses. We review briefly some classical theories of Andrade creep from the point of view of such spatial fluctuations. We consider these phenomenological, time-dependent creep laws in terms of a description based on a non-equilibrium phase transition separating evolving and frozen states of the system when the externally applied load is varied. Such an interpretation is discussed further by the data collapse of the local deformations in the spirit of absorbing state/depinning phase transitions, as well as deformation-deformation correlations and the width of the cumulative strain distributions. The results are also compared with the order parameter fluctuations observed close to the depinning transition of the 2dd Linear Interface Model or the quenched Edwards-Wilkinson equation.Comment: 27 pages, 18 figure

    Defective iron supply for erythropoiesis and adequate endogenous erythropoietin production in the anemia associated with systemic-onset juvenile chronic arthritis.

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    peer reviewedSystemic-onset juvenile chronic arthritis (SoJCA) is associated with high levels of circulating interleukin-6 (IL-6) and is frequently complicated by severe microcytic anemia whose pathogenesis is unclear. Therefore, we studied 20 consecutive SoJCA patients with hemoglobin (Hb) levels <12 g/dL, evaluating erythroid progenitor proliferation, endogenous erythropoietin production, body iron status, and iron supply for erythropoiesis. Hb concentrations ranged from 6.5 to 11.9 g/dL. Hb level was directly related to mean corpuscular volume (r = .82, P < .001) and inversely related to circulating transferrin receptor (r = -.81, P < .001) suggesting that the severity of anemia was directly proportional to the degree of iron-deficient erythropoiesis. Serum ferritin ranged from 18 to 1,660 microgram/L and was unrelated to Hb level. Bone marrow iron stores wore markedly reduced in the three children investigated, and they also showed increased serum transferrin receptor and normal-to-high serum ferritin. All 20 patients had elevated IL-6 levels and normal in vitro growth of erythroid progenitors. Endogenous erythropoietin (epo) production was appropriate for the degree of anemia as judged by both the observed to predicted log (serum epo) ratio 10.95 +/- 0.12) and a comparison of the serum epo-Hb regression found in these subjects with that of thalassemia patients. Multiple regression analysis showed that serum transferrin receptor was the parameter most closely related to hemoglobin concentration: variation in circulating transferrin receptor explained 61% of the variation in Hb level (P < .001). In 10 severely anemic patients, amelioration of anemia following intravenous iron administration resulted in normalization of serum transferrin receptor. Defective iron supply to the erythron rather than blunted epo production is the major cause of the microcytic anemia associated with SoJCA. A true body-iron deficiency caused by decreased iron absorption likely complicates long-lasting inflammation in the most anemic children, and this can be recognized by high serum transferrin receptor levels. Although oral iron is of no benefit, intravenous iron saccharate is a safe and effective means for improving iron availability for erythropoiesis and correcting this anemia. Thus, while chronically high endogenous IL-6 levels do not appear to blunt epo production, they are probably responsible for the observed abnormalities in iron metabolism. Anemia of chronic disease encompasses a variety of anemic conditions whose peculiar features may specifically correlate with the type of cytokine(s) predominantly released

    Secondary malignancies after high-dose chemotherapy in germ cell tumor patients: A 34-year retrospective study of the European Society for Blood and Marrow Transplantation (EBMT)

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    We aimed to assess the incidence and risk factors of secondary malignancy (SM) in the young adult patients who received high-dose chemotherapy (HDCT) for germ cell tumors (GCT). The EBMT database was interrogated. Criteria for patient selection included adult male GCT and HDCT administered in any line of therapy. Cumulative incidence methods were used to estimate the time-to-SM diagnosis. Univariable Fine and Gray proportional hazard regression evaluated risk factors of SM occurrence. From 1981 to 2015, 9153 autografts were identified. Among 5295 patients, 59 cases of SM, developed after a median follow-up of 3.8 years, were registered. Of these patients, 23 (39%) developed hematologic SM, 34 (57.6%) solid SM (two patients had uncoded SM). Twenty-year cumulative incidence of solid versus hematologic SM was 4.17% (95% CI: 1.78-6.57) versus 1.37% (95% CI: 0.47-2.27). Median overall survival after SM was significantly shorter for patients who developed hematologic SM versus solid SM (8.6 versus 34.4 months, p = 0.003). Age older than 40 years at the time of HDCT was significantly associated with hematologic, but not solid, SM development (p = 0.004 versus p = 0.234). SM occurrence post-HDCT showed different patterns of incidence and mortality in GCT. These data may be important to optimize patient selection, counseling and follow-up after HDCT

    Impact of the rs1024611 polymorphism of ccl2 on the pathophysiology and outcome of primary myelofibrosis

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    Single nucleotide polymorphisms (SNPs) can modify the individual pro-inflammatory background and may therefore have relevant implications in the MPN setting, typified by aberrant cytokine production. In a cohort of 773 primary myelofibrosis (PMF), we determined the contribution of the rs1024611 SNP of CCL2—one of the most potent immunomodulatory chemokines—to the clinical and biological characteristics of the disease, demonstrating that male subjects carrying the homozygous genotype G/G had an increased risk of PMF and that, among PMF patients, the G/G genotype is an independent prognostic factor for reduced overall survival. Functional characterization of the SNP and the CCL2-CCR2 axis in PMF showed that i) homozygous PMF cells are the highest chemokine producers as compared to the other genotypes; ii) PMF CD34+ cells are a selective target of CCL2, since they uniquely express CCR2 (CCL2 receptor); iii) activation of the CCL2-CCR2 axis boosts pro-survival signals induced by driver mutations via Akt phosphorylation; iv) ruxolitinib effectively counteracts CCL2 production and down-regulates CCR2 expression in PMF cells. In conclusion, the identification of the role of the CCL2/CCR2 chemokine system in PMF adds a novel element to the pathophysiological picture of the disease, with clinical and therapeutic implications
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