2,124 research outputs found

    BOW SHOCK FRAGMENTATION DRIVEN BY A THERMAL INSTABILITY IN LABORATORY ASTROPHYSICS EXPERIMENTS

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    The role of radiative cooling during the evolution of a bow shock was studied in laboratory-astrophysics experiments that are scalable to bow shocks present in jets from young stellar objects. The laboratory bow shock is formed during the collision of two counter-streaming, supersonic plasma jets produced by an opposing pair of radial foil Z-pinches driven by the current pulse from the MAGPIE pulsed-power generator. The jets have different flow velocities in the laboratory frame and the experiments are driven over many times the characteristic cooling time-scale. The initially smooth bow shock rapidly develops small-scale non-uniformities over temporal and spatial scales that are consistent with a thermal instability triggered by strong radiative cooling in the shock. The growth of these perturbations eventually results in a global fragmentation of the bow shock front. The formation of a thermal instability is supported by analysis of the plasma cooling function calculated for the experimental conditions with the radiative packages ABAKO/RAPCAL.Comment: 9 pages, 5 figures, Accepted for publication in The Astrophysical Journal on 5th November 201

    The structure of bow shocks formed by the interaction of pulsed-power driven magnetised plasma flows with conducting obstacles

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    We present an experimental study of the development and structure of bow shocks produced by the interaction of a magnetised, collisional, super-Alfvénic plasma flow with conducting cylindrical obstacles. The plasma flow with an embedded, frozen-in magnetic field (ReM ∼ 20) is produced by the current-driven ablation of fine aluminium wires in an inverse, exploding wire array z-pinch. We show that the orientation of the embedded field with respect to the obstacles has a dramatic effect on the bow shock structure. When the field is aligned with the obstacle, a sharp bow shock is formed with a global structure that is determined simply by the fast magneto-sonic Mach number. When the field is orthogonal to the obstacle, magnetic draping occurs. This leads to the growth of a magnetic precursor and the subsequent development of a magnetised bow shock that is mediated by two-fluid effects, with an opening angle and a stand-off distance, that are both many times larger than in the parallel geometry. By changing the field orientation, we change the fluid regime and physical mechanisms that are responsible for the development of the bow shocks. MHD simulations show good agreement with the structure of well-developed bow shocks. However, collisionless, two-fluid effects will need to be included within models to accurately reproduce the development of the shock with an orthogonal B-field

    Ubiquitous [Na+]i/[K+]i-Sensitive Transcriptome in Mammalian Cells: Evidence for Ca2+i-Independent Excitation-Transcription Coupling

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    Stimulus-dependent elevation of intracellular Ca2+ ([Ca2+]i) affects the expression of numerous genes – a phenomenon known as excitation-transcription coupling. Recently, we found that increases in [Na+]i trigger c-Fos expression via a novel Ca2+i-independent pathway. In the present study, we identified ubiquitous and tissue-specific [Na+]i/[K+]i-sensitive transcriptomes by comparative analysis of differentially expressed genes in vascular smooth muscle cells from rat aorta (RVSMC), the human adenocarcinoma cell line HeLa, and human umbilical vein endothelial cells (HUVEC). To augment [Na+]i and reduce [K+]i, cells were treated for 3 hrs with the Na+,K+-ATPase inhibitor ouabain or placed for the same time in the K+-free medium. Employing Affymetrix-based technology, we detected changes in expression levels of 684, 737 and 1839 transcripts in HeLa, HUVEC and RVSMC, respectively, that were highly correlated between two treatments (p<0.0001; R2>0.62). Among these Na+i/K+i-sensitive genes, 80 transcripts were common for all three types of cells. To establish if changes in gene expression are dependent on increases in [Ca2+]i, we performed identical experiments in Ca2+-free media supplemented with extracellular and intracellular Ca2+ chelators. Surprisingly, this procedure elevated rather than decreased the number of ubiquitous and cell-type specific Na+i/K+i-sensitive genes. Among the ubiquitous Na+i/K+i-sensitive genes whose expression was regulated independently of the presence of Ca2+ chelators by more than 3-fold, we discovered several transcription factors (Fos, Jun, Hes1, Nfkbia), interleukin-6, protein phosphatase 1 regulatory subunit, dual specificity phosphatase (Dusp8), prostaglandin-endoperoxide synthase 2, cyclin L1, whereas expression of metallopeptidase Adamts1, adrenomedulin, Dups1, Dusp10 and Dusp16 was detected exclusively in Ca2+-depleted cells. Overall, our findings indicate that Ca2+i-independent mechanisms of excitation-transcription coupling are involved in transcriptomic alterations triggered by elevation of the [Na+]i/[K+]i ratio. There results likely have profound implications for normal and pathological regulation of mammalian cells, including sustained excitation of neuronal cells, intensive exercise and ischemia-triggered disorders

    Blockage of longitudinal flow in Meniere's disease: A human temporal bone study

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    Conclusion: Blockage of the endolymphatic duct is a significant finding in Meniere's disease. The position of the utriculo-endolymphatic valve (UEV) and blockage of the ductus reuniens in the temporal bones were not found to be directly indicative of Meniere's disease. Objective: Comparison of blockage of the longitudinal flow of endolymph between ears affected by Meniere's disease and normal ears. Methods: We examined 21 temporal bones from 13 subjects who had Meniere's disease and 21 normal temporal bones from 12 controls. Results: The endolymphatic duct was blocked in five (23%) ears affected by Meniere's disease (p = 0.016). The utricular duct was blocked in 16 (76%) ears affected by Meniere's disease and 11 (52%) normal ears (p = 0.112). The saccular duct was blocked in 6 (28%) of ears affected by Meniere's disease and 16 (76%) normal ears (p = 0.001). The ductus reuniens was blocked in 10 (47%) ears affected by Meniere's disease and 10 (47%) normal ears (p = 1.000)

    Agent based modelling helps in understanding the rules by which fibroblasts support keratinocyte colony formation

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    Background: Autologous keratincoytes are routinely expanded using irradiated mouse fibroblasts and bovine serum for clinical use. With growing concerns about the safety of these xenobiotic materials, it is desirable to culture keratinocytes in media without animal derived products. An improved understanding of epithelial/mesenchymal interactions could assist in this. Methodology/Principal Findings: A keratincyte/fibroblast o-culture model was developed by extending an agent-based keratinocyte colony formation model to include the response of keratinocytes to both fibroblasts and serum. The model was validated by comparison of the in virtuo and in vitro multicellular behaviour of keratinocytes and fibroblasts in single and co-culture in Greens medium. To test the robustness of the model, several properties of the fibroblasts were changed to investigate their influence on the multicellular morphogenesis of keratinocyes and fibroblasts. The model was then used to generate hypotheses to explore the interactions of both proliferative and growth arrested fibroblasts with keratinocytes. The key predictions arising from the model which were confirmed by in vitro experiments were that 1) the ratio of fibroblasts to keratinocytes would critically influence keratinocyte colony expansion, 2) this ratio needed to be optimum at the beginning of the co-culture, 3) proliferative fibroblasts would be more effective than irradiated cells in expanding keratinocytes and 4) in the presence of an adequate number of fibroblasts, keratinocyte expansion would be independent of serum. Conclusions: A closely associated computational and biological approach is a powerful tool for understanding complex biological systems such as the interactions between keratinocytes and fibroblasts. The key outcome of this study is the finding that the early addition of a critical ratio of proliferative fibroblasts can give rapid keratinocyte expansion without the use of irradiated mouse fibroblasts and bovine serum

    Karyotype, Sex Determination, and Meiotic Chromosome Behavior in Two Pholcid (Araneomorphae, Pholcidae) Spiders: Implications for Karyotype Evolution

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    There are 1,111 species of pholcid spiders, of which less than 2% have published karyotypes. Our aim in this study was to determine the karyotypes and sex determination mechanisms of two species of pholcids: Physocyclus mexicanus (Banks, 1898) and Holocnemus pluchei (Scopoli, 1763), and to observe sex chromosome behavior during meiosis. We constructed karyotypes for P. mexicanus and H. pluchei using information from both living and fixed cells. We found that P. mexicanus has a chromosome number of 2n = 15 in males and 2n = 16 in females with X0-XX sex determination, like other members of the genus Physocyclus. H. pluchei has a chromosome number of 2n = 28 in males and 2n = 28 in females with XY-XX sex determination, which is substantially different from its closest relatives. These data contribute to our knowledge of the evolution of this large and geographically ubiquitous family, and are the first evidence of XY-XX sex determination in pholcids

    Studies of the Decay B+- -> D_CP K+-

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    We report studies of the decay B+- -> D_CP K+-, where D_CP denotes neutral D mesons that decay to CP eigenstates. The analysis is based on a 29.1/fb data sample of collected at the \Upsilon(4S) resonance with the Belle detector at the KEKB asymmetric e+ e- storage ring. Ratios of branching fractions of Cabibbo-suppressed to Cabibbo-favored processes involving D_CP are determined to be B(B- -> D_1 K-)/B(B- -> D_1 pi-)=0.125 +- 0.036 +- 0.010 and B(B- -> D_2 K-)/B(B- -> D_2 pi-)=0.119 +- 0.028 +- 0.006, where indices 1 and 2 represent the CP=+1 and CP=-1 eigenstates of the D0 - anti D0 system, respectively. We also extract the partial rate asymmetries for B+- -> D_CP K+-, finding A_1 = 0.29 +- 0.26 +- 0.05 and A_2 = -0.22 +- 0.24 +- 0.04.Comment: 10 pages, 2 figures, submitted to Physical Review Letter
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