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Design for shear strength of concrete beams longitudinally reinforced with GFRP bars
Job Thomas,S. Ramadass 국제구조공학회 2015 Structural Engineering and Mechanics, An Int'l Jou Vol.53 No.1
In this paper, a model for the evaluation of shear strength of fibre reinforced polymer (FRP)-reinforced concrete beams is given. The survey of literature indicates that the FRP reinforced beams testedwith shear span to depth ratio less than or equal to 1.0 is limited. In this study, eight concrete beamsreinforced with GFRP rebars without stirrups are cast and tested over shear span to depth ratio of 0.5 and1.75. The concrete compressive strength is varied from 40.6 to 65.3 MPa. The longitudinal reinforcementratio is varied from 1.16 to 1.75. The experimental shear strength and load-deflection response of the beamsare determined and reported in this paper. A model is proposed for the prediction of shear strength of beamsreinforced with FRP bars. The proposed model accounts for compressive strength of concrete, modulus ofFRP rebar, longitudinal reinforcement ratio, shear span to depth ratio and size effect of beams. The shearstrength of FRP reinforced concrete beams predicted using the proposed model is found to be in betteragreement with the corresponding test data when compared with the shear strength predicted using theeleven models published in the literature. Design example of FRP reinforced concrete beam is also given inthe appendix.
Kurz, Angela R. M.,Pruenster, Monika,Rohwedder, Ina,Ramadass, Mahalakshmi,Schä,fer, Kerstin,Harrison, Ute,Gouveia, Gabriel,Nussbaum, Claudia,Immler, Roland,Wiessner, Johannes R. American Society for Clinical Investigation 2016 The Journal of clinical investigation Vol.126 No.11
<P>Neutrophils need to penetrate the perivascular basement membrane for successful extravasation into inflamed tissue, but this process is incompletely understood. Recent findings have associated mammalian sterile 20-like Kinase 1 (MST1) loss of function with a human primary immunodeficiency disorder, suggesting that MST1 may be involved in immune cell migration. Here, we have shown that MST1 is a critical regulator of neutrophil extravasation during inflammation. Mst1-deficient (Mst1(-/-)) neutrophils were unable to migrate into inflamed murine cremaster muscle venules, instead persisting between the endothelium and the basement membrane. Mst1(-/-) neutrophils also failed to extravasate from gastric submucosal vessels in a murine model of Helicobacter pylori infection. Mechanistically, we observed defective translocation of VLA-3, VLA-6, and neutrophil elastase from intracellular vesicles to the surface of Mst1(-/-) neutrophils, indicating that MST1 is required for this crucial step in neutrophil transmigration. Furthermore, we found that MST1 associates with the Rab27 effector protein synaptotagmin-like protein 1 (JFC1, encoded by Sytl1 in mice), but not Munc13-4, thereby regulating the trafficking of Rab27-positive vesicles to the cellular membrane. Together, these findings highlight a role for MST1 in vesicle trafficking and extravasation in neutrophils, providing an additional mechanistic explanation for the severe immune defect observed in patients with MST1 deficiency.</P>