Two way coupled hypersonic fluid structure interaction simulations with Eilmer

Fluid Structure Interactions (FSI), if not managed appropriately are known to have contributed to the loss of several aerospace vehicles. As done for the X-43, FSI can be designed-out by making structures sufficiently rigid and by providing appropriate damping. In hypersonic cruise vehicles, this strategy is not applicable as stringent weight limits and large thermal loads result in structures with reduced stiffness [12]. Thus, the accurate simulation and prediction of FSI are essential to allow for the most effective design. In hypersonics, aeroelastic effects can result in rapid variations in pressure and thermal evolutions. The level of coupling between fluid and structure is typically is strong or two-way, which means that CFD and FEM solvers have to continuously exchange information in terms of nodal forces and displacement in order to produce an accurate solution. In this paper we present details of a fast implementation and first results of a FEM solver in the Eilmer CFD solver. Details are provided on the formulation of the structural solver, the fluid solver to appropriately account for the deforming boundaries, and the coupling approach. The results show that the simulations are in broad agreement with experimental data, but that an off-set exists in response frequency and amplitude. The resulting capability, with its ability to conduct time–accurate FSI simulations is a good tool to further investigate the underlying effects driving hypersonic FSI

High Frequency of Endothelial Colony Forming Cells Marks a Non-Active Myeloproliferative Neoplasm with High Risk of Splanchnic Vein Thrombosis

Increased mobilization of circulating endothelial progenitor cells may represent a new biological hallmark of myeloproliferative neoplasms. We measured circulating endothelial colony forming cells (ECFCs) in 106 patients with primary myelofibrosis, fibrotic stage, 49 with prefibrotic myelofibrosis, 59 with essential thrombocythemia or polycythemia vera, and 43 normal controls. Levels of ECFC frequency for patient's characteristics were estimated by using logistic regression in univariate and multivariate setting. The sensitivity, specificity, likelihood ratios, and positive predictive value of increased ECFC frequency were calculated for the significantly associated characteristics. Increased frequency of ECFCs resulted independently associated with history of splanchnic vein thrombosis (adjusted odds ratio = 6.61, 95% CI = 2.54–17.16), and a summary measure of non-active disease, i.e. hemoglobin of 13.8 g/dL or lower, white blood cells count of 7.8×109/L or lower, and platelet count of 400×109/L or lower (adjusted odds ratio = 4.43, 95% CI = 1.45–13.49) Thirteen patients with splanchnic vein thrombosis non associated with myeloproliferative neoplasms were recruited as controls. We excluded a causal role of splanchnic vein thrombosis in ECFCs increase, since no control had elevated ECFCs. We concluded that increased frequency of ECFCs represents the biological hallmark of a non-active myeloproliferative neoplasm with high risk of splanchnic vein thrombosis. The recognition of this disease category copes with the phenotypic mimicry of myeloproliferative neoplasms. Due to inherent performance limitations of ECFCs assay, there is an urgent need to arrive to an acceptable standardization of ECFC assessment

Proceedings of the 21st Australasian Fluid Mechanics Conference

This work discusses the design of a panel flutter experiment in aMach 5.8 free-piston compression-heated Ludwieg tube. Smalltest duration, low freestream pressure and limited space availablewithin the coreflow have driven the choice of boundaryconditions, material and panel geometry. The test piece is a 100mm long and 40 mm wide aluminium panel. The panel boundarycondition is clamped-free-clamped-free, with the free edgesparallel to the flow direction. The aerodynamic load can be variedby changing the inclination of the panel with respect to thefreestream. The pressure in the cavity underneath the panel isreproduced passively by channelling the external flow and creatinga recirculation region. Several strategies are employed toreduce the pressure differential between windward and cavityside of the panel. On the basis of steady-state simulations, analyticalresults and empirical laws, it is possible to state thatpanel can experience flutter during the test. Further investigationshould focus on start-up transients and temperature effects

Hypersonic transitional shock-wave-boundary-layer interaction on a flat plate

This work presents an experimental and numerical study of hypersonic transitional shock-wave-boundary-layer interaction, wherein transition occurs between separation and reattachment in the detached shear layer. Experiments were conducted in a free-piston compression-heated Ludwieg tube that provided a Mach 5.8 flow at a freestream Reynolds number of 7x106 m-1. A shock generator deflected the flow by 10 degrees, resulting in an oblique shock impinging on a flat plate. The shock triggered transition in the boundary layer and the formation of Gortler-like vortices downstream of reattachment. Heat flux and pressure distributions on the plate were measured globally using infrared thermography and pressure-sensitive paint. Oil film visualization was employed to evaluate the boundary-layer reattachment. Numerical results consist of Reynolds-averaged Navier-Stokes and fully laminar steady-state three-dimensional simulations. Shock-induced transition is considered to be the cause of the overshoot in peak pressure and peak heating of approximately 15%, in agreement with previous studies. Gortler instability, triggered by the concave nature of the bubble at separation, is identified as the main mechanism leading to boundary-layer transition, resulting in heat-flux variations of less than 30%. By comparing numerical results against thermographic values it is possible to delineate the extent of transition. Within this region, the disturbance amplification factor was estimated to be approximately between 6 and 10, in reasonable agreement with other relevant numerical and experimental data

Constitutively released adenosine diphosphate regulates proplatelet formation by human megakaryocytes

Background The interaction of adenosine diphosphate with its P2Y(1) and P2Y(12) receptors on platelets is important for platelet function. However, nothing is known about adenosine diphosphate and its function in human megakaryocytes. DESIGN AND METHODS: We studied the role of adenosine diphosphate and P2Y receptors on proplatelet formation by human megakaryocytes in culture. RESULTS: Megakaryocytes expressed all the known eight subtypes of P2Y receptors, and constitutively released adenosine diphosphate. Proplatelet formation was inhibited by the adenosine diphosphate scavengers apyrase and CP/CPK by 60-70% and by the P2Y(12) inhibitors cangrelor and 2-MeSAMP by 50-60%, but was not inhibited by the P2Y(1) inhibitor MRS 2179. However, the active metabolites of the anti-P2Y(12) drugs, clopidogrel and prasugrel, did not inhibit proplatelet formation. Since cangrelor and 2-MeSAMP also interact with P2Y(13), we hypothesized that P2Y(13), rather than P2Y(12) is involved in adenosine diphosphate-regulated proplatelet formation. The specific P2Y(13) inhibitor MRS 2211 inhibited proplatelet formation in a concentration-dependent manner. Megakaryocytes from a patient with severe congenital P2Y(12) deficiency showed normal proplatelet formation, which was inhibited by apyrase, cangrelor or MRS 2211 by 50-60%. The platelet count of patients with congenital delta-storage pool deficiency, who lack secretable adenosine diphosphate, was significantly lower than that of patients with other platelet function disorders, confirming the important role of secretable adenosine diphosphate in platelet formation. Conclusions This is the first demonstration that adenosine diphosphate released by megakaryocytes regulates their function by interacting with P2Y(13). The clinical relevance of this not previously described physiological role of adenosine diphosphate and P2Y(13) requires further exploration

Megakaryocytes Contribute to the Bone Marrow-MatrixEnvironment by Expressing Fibronectin, Type Iv Collagen and Laminin

Megakaryocytes associate with the bone marrow vasculature where they convert their cytoplasm into proplatelets that protrude through the vascular endothelium into the lumen and release platelets. The extracellular matrix (ECM) microenvironment plays a critical role in regulating these processes. In this work we demonstrate that, among bone marrow ECM components, fibronectin, type IV collagen, and laminin are the most abundant around bone marrow sinusoids and constitute a pericellular matrix surrounding megakaryocytes. Most importantly, we report, for the first time, that megakaryocytes express components of the basement membrane and that these molecules contribute to the regulation of megakaryocyte development and bone marrow ECM homeostasis both in vitro and in vivo. In vitro, fibronectin induced a threefold increase in the proliferation rate of mouse hematopoietic stem cells leading to higher megakaryocyte output with respect to cells treated only with thrombopoietin or other matrices. However, megakaryocyte ploidy level in fibronectin‐treated cultures was significantly reduced. Stimulation with type IV collagen resulted in a 1.4‐fold increase in megakaryocyte output, while all tested matrices supported proplatelet formation to a similar extent in megakaryocytes derived from fetal liver progenitor cells. In vivo, megakaryocyte expression of fibronectin and basement membrane components was upregulated during bone marrow reconstitution upon 5‐fluorouracil induced myelosuppression, while only type IV collagen resulted upregulated upon induced thrombocytopenia. In conclusion, this work demonstrates that ECM components impact megakaryocyte behavior differently during their differentiation and highlights a new role for megakaryocyte as ECM‐producing cells for the establishment of cell niches during bone marrow regeneration

Oscillating shock impinging on a flat plate at Mach 6

This work discusses the design, measurement and simulation of an experiment in a Mach 6 wind tunnel involving an oscillating shock impinging on a flat plate. The design of the oscillating shock-generator is performed using piston theory. The oscillation frequency is designed to be larger than 30 Hz, to match typical fuselage natural frequencies of hypersonic vehicles and technology demonstrators, such as the X-33 and the X-43. The shock generator is free to pitch, resulting in a shock that varies in intensity and impingement point, with a maximum flow deflection angle of 10 degrees. Transition appears to take place just downstream the separated region for both static (with a fixed flow deflection angle) and dynamic experiments. Transition decreases the peak pressure levels while determining a rise in the heat-flux distribution. The motion of the reattachment point appears to lag behind the numerical predictions by a fifth of the oscillation period. Görtler-like vortices are observed in the reattachment region; while their magnitude is a function of the shock strength, their spanwise distribution appears to be unaffected by the motion of the shock generator

Megakaryocytes contribute to the bone marrow-matrix environment by expressing fibronectin, type IV collagen, and laminin

Megakaryocytes associate with the bone marrow vasculature where they convert their cytoplasm into proplatelets that protrude through the vascular endothelium into the lumen and release platelets. The extracellular matrix (ECM) microenvironment plays a critical role in regulating these processes. In this work we demonstrate that, among bone marrow ECM components, fibronectin, type IV collagen, and laminin are the most abundant around bone marrow sinusoids and constitute a pericellular matrix surrounding megakaryocytes. Most importantly, we report, for the first time, that megakaryocytes express components of the basement membrane and that these molecules contribute to the regulation of megakaryocyte development and bone marrow ECM homeostasis both in vitro and in vivo. In vitro, fibronectin induced a threefold increase in the proliferation rate of mouse hematopoietic stem cells leading to higher megakaryocyte output with respect to cells treated only with thrombopoietin or other matrices. However, megakaryocyte ploidy level in fibronectin‐treated cultures was significantly reduced. Stimulation with type IV collagen resulted in a 1.4‐fold increase in megakaryocyte output, while all tested matrices supported proplatelet formation to a similar extent in megakaryocytes derived from fetal liver progenitor cells. In vivo, megakaryocyte expression of fibronectin and basement membrane components was upregulated during bone marrow reconstitution upon 5‐fluorouracil induced myelosuppression, while only type IV collagen resulted upregulated upon induced thrombocytopenia. In conclusion, this work demonstrates that ECM components impact megakaryocyte behavior differently during their differentiation and highlights a new role for megakaryocyte as ECM‐producing cells for the establishment of cell niches during bone marrow regeneration