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Summary: The energy coupling behavior is propagated through the magnetic field and would seriously affect the operation performance of two‐degree‐of‐freedom motion system based on linear‐rotary motor. This paper proposes a novel double‐stator linear‐rotary switched reluctance motor (DSLR‐SRM) to suppress the energy coupling behavior. First, the structure and operation principles of DSLR‐SRM are presented. The two stators of DSLR‐SRM are radially arranged to perform the independent magnetic circuit and suppress the energy coupling behavior through the magnetic field. Then, an equivalent circuit model is established to shorten the modeling and calculation time. It could be found that the energy coupling behavior directly affects the torque and force performance. Next, the sensitivity of the DSLR‐SRM dimensions is developed. Meanwhile, the dimensions of DSLR‐SRM are optimized to enhance the torque and force output via TOPSIS decision‐making. Finally, the validity of equivalent circuit modeling analysis and optimization results are verified through three‐dimensional finite element model. [ABSTRACT FROM AUTHOR]

Human bronchial epithelial (HBE) cells contribute to asthmatic airway inflammation by secreting cytokines, chemokines, and growth factors, including interleukin (IL)-6, IL-8 and transforming growth factor (TGF) β1, all of which are elevated in asthmatic airways. This study examines the signaling pathways leading to TGFβ1 induced IL-6 and IL-8 in primary HBE cells from asthmatic and non-asthmatic volunteers. HBE cells were stimulated with TGFβ1 in the presence or absence of signaling inhibitors. IL-6 and IL-8 protein and mRNA were measured by ELISA and real-time PCR respectively, and cell signaling kinases by Western blot. TGFβ1 increased IL-6, but inhibited IL-8 production in both asthmatic and non-asthmatic cells; however, TGF induced significantly more IL-6 in asthmatic cells. Inhibition of JNK MAP kinase partially reduced TGFβ1 induced IL-6 in both cell groups. TGFβ1 induced Smad2 phosphorylation, and blockade of Smad2/3 prevented both the TGFβ1 modulated IL-6 increase and the decrease in IL-8 production in asthmatic and non-asthmatic cells. Inhibition of Smad2/3 also increased basal IL-8 release in asthmatic cells but not in non-asthmatic cells. Using CHIP assays we demonstrated that activated Smad2 bound to the IL-6, but not the IL-8 promoter region. We conclude that the Smad2/3 pathway is the predominant TGFβ1 signaling pathway in HBE cells, and this is altered in asthmatic bronchial epithelial cells. Understanding the mechanism of aberrant pro-inflammatory cytokine production in asthmatic airways will allow the development of alternative ways to control airway inflammation. J. Cell. Physiol. 225: 846-854, 2010. © 2010 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]

Hyperplasia of airway smooth muscle (ASM) within the bronchial wall of asthmatic patients has been well documented and is likely due to increased muscle proliferation. We have shown that ASM cells obtained from asthmatic patients proliferate faster than those obtained from non-asthmatic patients. In ASM from non-asthmatics, mitogens act via dual signaling pathways (both ERK- and PI 3-kinase-dependent) to control growth. In this study we are the first to examine whether dual pathways control the enhanced proliferation of ASM from asthmatics. When cells were incubated with 0.1% or 1% FBS, ERK activation was significantly greater in cells from asthmatic subjects (P < 0.05). In contrast, when cells were stimulated with 10% FBS, ERK activity was significantly greater in the non-asthmatic cells. However, cell proliferation in asthmatic cells was still significantly higher in cells stimulated by both 1% and 10% FBS. Pharmacological inhibition revealed that although dual proliferative pathways control ASM growth in cells from non-asthmatics stimulated with 10% FBS to an equal extent ([3H]-thymidine incorporation reduced to 57.2 ± 6.9% by the PI 3-kinase inhibitor LY294002 and 57.8 ± 1.1% by the ERK-pathway inhibitor U0126); in asthmatics, the presence of a strong proliferative stimulus (10% FBS) reduces ERK activation resulting in a shift to the PI 3-kinase pathway. The underlying mechanism appears to be upregulation of an endogenous MAPK inhibitor—MKP-1—that constrains ERK signaling in asthmatic cells under strong mitogenic stimulation. This study suggests that the PI 3-kinase pathway may be an attractive target for reversing hyperplasia in asthma. J. Cell. Physiol. 216: 673–679, 2008, © 2008 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]