Prediction of Helicopter Rotor Hover Performance using High Fidelity CFD Methods

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Protein kinase Cδ and c-Abl kinase are required for transforming growth factor β induction of endothelial-mesenchymal transition in vitro.

OBJECTIVE: The origin of the mesenchymal cells responsible for the intimal fibrosis in systemic sclerosis (SSc) has not been fully identified. The present study was undertaken to investigate whether subendothelial mesenchymal cells may emerge through transdifferentiation of endothelial cells (ECs) into myofibroblasts via endothelial-mesenchymal transition (EndoMT) in vitro and to explore the signaling pathways involved in this process. METHODS: Primary mouse pulmonary ECs isolated by immunomagnetic methods with sequential anti-CD34 and anti-CD102 antibody selection were cultured in monolayers. Cell morphology and diacetylated low-density lipoprotein uptake assays confirmed their EC characteristics. The induction of EndoMT was assessed by determination of α-smooth muscle actin (α-SMA), type I collagen, and VE-cadherin expression, and the expression of the transcriptional repressor Snail-1 was analyzed. The signaling pathways involved were examined using small-molecule kinase inhibitors and RNA interference. RESULTS: Transforming growth factor β1 (TGFβ1) induced α-SMA and type I collagen expression and inhibited VE-cadherin. These effects were mediated by a marked increase in Snail-1 expression and were abolished by treatment with either the c-Abl tyrosine kinase inhibitor imatinib mesylate or the protein kinase Cδ (PKCδ) inhibitor rottlerin. The inhibitory effects of imatinib mesylate and rottlerin were mediated by inhibition of phosphorylation of glycogen synthase kinase 3β at residue Ser(9). These observations were confirmed in experiments using small interfering RNA specific for c-Abl and PKCδ. CONCLUSION: These results indicate that c-Abl and PKCδ are crucial for TGFβ-induced EndoMT and that imatinib mesylate and rottlerin or similar kinase inhibitor molecules may be effective therapeutic agents for SSc and other fibroproliferative vasculopathies in which EndoMT plays a pathogenetic role

Numerical Simulations on the PSP Rotor Using HMB3

This work presents CFD analyses of the isolated Pressure Sensitive Paint (PSP) model rotor blade in hover and forward flight using the structured multi-block CFD solver of Glasgow University. In hover, two blade-tip Mach numbers (0.585 and 0.65) were simulated for a range of blade pitch angles using fully-turbulent flow and the k-ω SST model. Results at blade-tip Mach number of 0.585 showed a fair agreement with experimental Figure of Merit and surface pressure coefficients obtained in the Rotor Test Cell (RTC) at NASA Langley Research Center. Comparisons are presented at blade-tip Mach number of 0.65 in terms of integral blade loads, surface pressure coefficients and position of the tip-vortex cores with published numerical data. Finally, the flow around the PSP rotor in forward flight was also computed at medium thrust (CT =0.006) and results were compared with published experimental data

Using the X-ray Emission Lines of Seyfert 2 AGN to Measure Abundance Ratios

We measure the metal abundance ratios in the X-ray photoionized gas located near the narrow line region of a sample of Seyfert 2 AGN. The high-resolution X-ray spectra observed with the Chandra high- and low-energy transmission grating spectrometers are compared with models of the resonant scattering and recombination emission from a plasma in thermal balance, and with multiple temperature zones. The abundance ratios in the sample are close to the Solar values, with slight over-abundances of N in NGC 1068, and of Ne in NGC 4151. Our X-ray spectral models use fewer degrees of freedom than previous works.Comment: 2 pages, 1 figure, to appear in the proceedings of the conference "Multiwavelenth AGN Surveys", held in Cozumel, Mexico, December 200

Endothelial to mesenchymal transition (EndoMT) in the pathogenesis of Systemic Sclerosis-associated pulmonary fibrosis and pulmonary arterial hypertension. Myth or reality?

Systemic Sclerosis (SSc) is a systemic autoimmune disease characterized by progressive fibrosis of skin and multiple internal organs and severe functional and structural microvascular alterations. SSc is considered to be the prototypic systemic fibrotic disorder. Despite currently available therapeutic approaches SSc has a high mortality rate owing to the development of SSc-associated interstitial lung disease (ILD) and pulmonary arterial hypertension (PAH), complications that have emerged as the most frequent causes of disability and mortality in SSc. The pathogenesis of the fibrotic process in SSc is complex and despite extensive investigation the exact mechanisms have remained elusive. Myofibroblasts are the cells ultimately responsible for tissue fibrosis and fibroproliferative vasculopathy in SSc. Tissue myofibroblasts in SSc originate from several sources including expansion of quiescent tissue fibroblasts and tissue accumulation of CD34+ fibrocytes. Besides these sources, myofibroblasts in SSc may result from the phenotypic conversion of endothelial cells into activated myofibroblasts, a process known as endothelial to mesenchymal transition (EndoMT). Recently, it has been postulated that EndoMT may play a role in the development of SSc-associated ILD and PAH. However, although several studies have described the occurrence of EndoMT in experimentally induced cardiac, renal, and pulmonary fibrosis and in several human disorders, the contribution of EndoMT to SSc-associated ILD and PAH has not been generally accepted. Here, the experimental evidence supporting the concept that EndoMT plays a role in the pathogenesis of SSc-associated ILD and PAH will be reviewed