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Sanford Fleeter - One of the best experts on this subject based on the ideXlab platform.

  • Forcing Function Effects on Unsteady Aerodynamic Gust Response: Part 1—Forcing Functions
    Journal of Turbomachinery, 1993
    Co-Authors: Gregory H. Henderson, Sanford Fleeter
    Abstract:

    The fundamental gust modeling assumption is investigated by means of a series of experiments performed in the Purdue Annular Cascade Research Facility. The unsteady periodic flow field is generated by rotating rows of perforated plates and airfoil cascades. In this paper, the measured unsteady flow fields are compared to linear-theory vortical gust requirements, with the resulting unsteady gust response of a downstream stator cascade correlated with linear theory predictions in an accompanying paper. The perforated-plate forcing functions closely resemble linear-theory forcing functions, with the static pressure fluctuations small and the periodic velocity vectors parallel to the downstream mean-relative flow angle over the entire periodic cycle

  • forcing function effects on unsteady aerodynamic gust response part 1 forcing functions
    Volume 5: Manufacturing Materials and Metallurgy; Ceramics; Structures and Dynamics; Controls Diagnostics and Instrumentation; Education, 1992
    Co-Authors: Gregory H. Henderson, Sanford Fleeter
    Abstract:

    The fundamental gust modeling assumption is investigated by means of a series of experiments performed in the Purdue Annular Cascade Research Facility. The unsteady periodic flow field is generated by rotating rows of perforated plates and airfoil cascades. In this paper, the measured unsteady flow fields are compared to linear-theory gust requirements, with the resulting unsteady gust response of a downstream stator cascade correlated with linear theory predictions in an accompanying paper. The perforated-plate forcing functions closely resemble linear-theory forcing functions, with the static pressure fluctuations small and the periodic velocity vectors parallel to the downstream mean-relative flow angle over the entire periodic cycle. In contrast, the airfoil forcing functions exhibit characteristics far from linear-theory gusts, with the alignment of the velocity vectors and the static pressure fluctuation amplitudes dependent on the rotor-loading condition, rotor solidity and the inlet mean-relative flow angle. Thus, these unique data clearly show that airfoil wakes, both compressor and turbine, are not able to be modeled with the boundary conditions of current state-of-the-art linear unsteady aerodynamic theory.Copyright © 1992 by ASME

Gregory H. Henderson - One of the best experts on this subject based on the ideXlab platform.

  • Forcing Function Effects on Unsteady Aerodynamic Gust Response: Part 1—Forcing Functions
    Journal of Turbomachinery, 1993
    Co-Authors: Gregory H. Henderson, Sanford Fleeter
    Abstract:

    The fundamental gust modeling assumption is investigated by means of a series of experiments performed in the Purdue Annular Cascade Research Facility. The unsteady periodic flow field is generated by rotating rows of perforated plates and airfoil cascades. In this paper, the measured unsteady flow fields are compared to linear-theory vortical gust requirements, with the resulting unsteady gust response of a downstream stator cascade correlated with linear theory predictions in an accompanying paper. The perforated-plate forcing functions closely resemble linear-theory forcing functions, with the static pressure fluctuations small and the periodic velocity vectors parallel to the downstream mean-relative flow angle over the entire periodic cycle

  • forcing function effects on unsteady aerodynamic gust response part 1 forcing functions
    Volume 5: Manufacturing Materials and Metallurgy; Ceramics; Structures and Dynamics; Controls Diagnostics and Instrumentation; Education, 1992
    Co-Authors: Gregory H. Henderson, Sanford Fleeter
    Abstract:

    The fundamental gust modeling assumption is investigated by means of a series of experiments performed in the Purdue Annular Cascade Research Facility. The unsteady periodic flow field is generated by rotating rows of perforated plates and airfoil cascades. In this paper, the measured unsteady flow fields are compared to linear-theory gust requirements, with the resulting unsteady gust response of a downstream stator cascade correlated with linear theory predictions in an accompanying paper. The perforated-plate forcing functions closely resemble linear-theory forcing functions, with the static pressure fluctuations small and the periodic velocity vectors parallel to the downstream mean-relative flow angle over the entire periodic cycle. In contrast, the airfoil forcing functions exhibit characteristics far from linear-theory gusts, with the alignment of the velocity vectors and the static pressure fluctuation amplitudes dependent on the rotor-loading condition, rotor solidity and the inlet mean-relative flow angle. Thus, these unique data clearly show that airfoil wakes, both compressor and turbine, are not able to be modeled with the boundary conditions of current state-of-the-art linear unsteady aerodynamic theory.Copyright © 1992 by ASME

Patrice J Morin - One of the best experts on this subject based on the ideXlab platform.

  • phosphorylation of claudin 4 by pkce regulates tight junction barrier function in ovarian cancer cells
    Experimental Cell Research, 2007
    Co-Authors: Theresa Dsouza, Patrice J Morin, Fred E Indig
    Abstract:

    Claudin proteins belong to a large family of transmembrane proteins essential to the formation and maintenance of tight junctions (TJs). In ovarian cancer, TJ protein claudin-4 is frequently overexpressed and may have roles in survival and invasion, but the molecular mechanisms underlying its regulation are poorly understood. In this report, we show that claudin-4 can be phosphorylated by protein kinase C (PKC) at Thr189 and Ser194 in ovarian cancer cells and overexpression of a claudin-4 mutant protein mimicking the phosphorylated state results in the disruption of the barrier function. Furthermore, upon phorbol ester-mediated PKC activation of OVCA433 cells, TJ strength is decreased and claudin-4 localization is altered. Analyses using PKC inhibitors and siRNA suggest that PKCe, an isoform typically expressed in ovarian cancer cells, may be important in the TPA-mediated claudin-4 phosphorylation and weakening of the TJs. Furthermore, immunofluorescence studies showed that claudin-4 and PKCe are co-localized at the TJs in these cells. The modulation of claudin-4 activity by PKCe may not only provide a mechanism for disrupting TJ function in ovarian cancer, but may also be important in the regulation of TJ function in normal epithelial cells.

Michael Koval - One of the best experts on this subject based on the ideXlab platform.

  • junctional adhesion molecule a promotes epithelial tight junction assembly to augment lung barrier function
    American Journal of Pathology, 2015
    Co-Authors: Leslie A Mitchell, Charles A. Parkos, Asma Nusrat, Christina Ward, Mike Kwon, Patrick O Mitchell, David Quintero, Michael Koval
    Abstract:

    Epithelial barrier function is maintained by tight junction proteins that control paracellular fluid flux. Among these proteins is junctional adhesion molecule A (JAM-A), an Ig fold transmembrane protein. To assess JAM-A function in the lung, we depleted JAM-A in primary alveolar epithelial cells using shRNA. In cultured cells, loss of JAM-A caused an approximately 30% decrease in transepithelial resistance, decreased expression of the tight junction scaffold protein zonula occludens 1, and disrupted junctional localization of the structural transmembrane protein claudin-18. Consistent with findings in other organs, loss of JAM-A decreased β1 integrin expression and impaired filamentous actin formation. Using a model of mild systemic endoxotemia induced by i.p. injection of lipopolysaccharide, we report that JAM-A −/− mice showed increased susceptibility to pulmonary edema. On injury, the enhanced susceptibility of JAM-A −/− mice to edema correlated with increased, transient disruption of claudin-18, zonula occludens 1, and zonula occludens 2 localization to lung tight junctions in situ along with a delay in up-regulation of claudin-4. In contrast, wild-type mice showed no change in lung tight junction morphologic features in response to mild systemic endotoxemia. These findings support a key role of JAM-A in promoting tight junction homeostasis and lung barrier function by coordinating interactions among claudins, the tight junction scaffold, and the cytoskeleton.

Yucun Liu - One of the best experts on this subject based on the ideXlab platform.

  • butyrate enhances intestinal epithelial barrier function via up regulation of tight junction protein claudin 1 transcription
    Digestive Diseases and Sciences, 2012
    Co-Authors: Hongbo Wang, Pengyuan Wang, Xin Wang, Yuanlian Wan, Yucun Liu
    Abstract:

    Barrier function is essential for the maintenance of normal intestinal function. Dysregulation of the intestinal barrier underlies a wide range of disorders. Previously, we found that sodium butyrate (NaB) decreased the molecular permeability of intestinal barrier in vivo model, but the mechanism by which NaB facilitated the tightness of tight junctions (TJs) in small intestinal epithelium needed further studies. In vitro culture of the cdx2-IEC monolayer was used to mimic barrier function. The TJs were assessed by transepithelial electrical resistance (TEER) and paracellular flux of fluorescein isothiocyanate-conjugated dextran 40,000 (FD-40), Western blot, Q-RT-PCR, and immunofluorescence. Promoter and chromatin immunoprecipitation (ChIP) assays were also done to analyze the Claudin-1 gene. NaB decreased FD-40 flux, increased TEER and TJ protein Claudin-1 expression, induced ZO-1 and Occludin redistribution in cellular membrane, and reversed the damage effect after calcium (Ca2+) switch assay. Silencing Claudin-1 prevented protective function of NaB from enhancing intestinal barrier integrity. Further studies demonstrated that NaB increased Claudin-1 transcription by facilitating the interaction between transcription factor SP1 and a specific motif within the promoter region of Claudin-1. This SP1 binding motif was located upstream of the coding region (−138 to −76 bp) and indispensable for the transcription of Claudin-1 following NaB treatment. ChIP assay confirmed the association between SP1 and Claudin-1 promoter, and the elimination of the SP1 binding site by point mutation resulted in a significant loss of Claudin-1 transcription after NaB dealing. NaB enhanced intestinal barrier function through increasing Claudin-1 transcription via facilitating the association between SP1 and Claudin-1 promoter.