Lubrication mechanism design for aircraft landing gear bearings

A shock absorber with lubricated bearings for an aircraft landing gear includes a piston that is received in a cylinder, and an upper bearing fixed to the piston that slidably engages an inner surface of the cylinder. A lower bearing extends inwardly from a lower portion of the cylinder and engages an outer surface of the piston. The lower bearing has a center axis and defines an annular bearing surface configured to slidably engage the piston outer surface. The annular bearing surface has a first portion that extends circumferentially more than one hundred eighty degrees about the center axis at a constant radius, defining a circular annular segment. A second portion closes the circular annular segment and defines a shallow channel or pocket in the annular bearing surface. In some embodiments the lower bearing further comprises oppositely disposed frustoconical thrust portions

Aircraft Landing Gear Thermo-Tribomechanical Model and Sensitivity Study

A methodology for characterizing the thermo-tribomechanical response of an aircraft landing gear shock absorber is presented. Structural damage has been reported as a consequence of heat generated by high loads induced by rough runways on the shock absorber bearings and by the high sliding velocities of the shock absorber piston. Therefore, a model that reveals the characteristics of the thermal behavior, and identifies heat sources and sinks in the landing gear shock absorber is developed. The thermo-tribomechanical model framework is presented with representative development of each component. In addition, a sensitivity study of the maximum heat flux to variations of key input parameters is investigated. The numerical results indicate that the runway amplitude dominates the landing gear thermal response

The impact of tau hyperphosphorylation at Ser262 on memory and learning after global brain ischaemia in a rat model of reversible cardiac arrest

An increase in phosphorylated tau (p-tau) is associated with Alzheimer's disease (AD), and brain hypoxia. Investigation of the association of residue-specific tau hyperphosphorylation and changes in cognition, leads to greater understanding of its potential role in the pathology of memory impairment. The aims of this study are to investigate the involvement of the main metabolic kinases, Liver Kinase B1 (LKB1) and Adenosine Monophosphate Kinase Protein Kinase (AMPK), in tau phosphorylation-derived memory impairment, and to study the potential contribution of the other tau kinases and phosphatases including Glycogen Synthase Kinase (GSK-3β), Protein kinase A (PKA) and Protein Phosphatase 2A (PP2A). Spatial memory and learning were tested in a rat global brain ischemic model of reversible cardiac arrest (CA). The phosphorylation levels of LKB1, AMPK, GSK-3β, PP2A, PKA and tau-specific phosphorylation were assessed in rats, subjected to ischaemia/reperfusion and in clinically diagnosed AD and normal human brains. LKB1 and AMPK phosphorylation increased 4 weeks after CA as did AMPK related p-tau (Ser262). The animals showed unchanged levels of GSK-3β specific p-tau (Ser202/Thr205), phospho-PP2A (Tyr307), total GSK-3β, PP2A, phospho-cAMP response element-binding protein (CREB) which is an indicator of PKA activity, and no memory deficits. AD brains had hyperphosphorylated tau in all the residues of Ser262, Ser202 and Thr205, with increased phosphorylation of both AMPK (Thr172) and GSK-3β (Ser9), and reduced PP2A levels. Our data suggests a crucial role for a combined activation of tau kinases and phosphatases in adversely affecting memory and that hyperphosphorylation of tau in more than one specific site may be required to create memory deficits

Resistance to fever induction and impaired acute-phase response in interleukin-1β-deficient mice

AbstractWe used gene targeting in embryonic stem cells to introduce an IL-1β null allele in mice. The IL-1β-deficient mice develop normally and are apparently healthy and fertile. The IL-1β null mice responded normally in models of contact and delayed-type hypersensitivity or following bacterial endotoxin LPS-induced inflammation. The IL-1β-deficlent mice showed equivalent resistance to Listeria monocytogenes compared with wild-type controls. In contrast, when challenged with turpentine, which causes localized inflammation and tissue injury, the IL-1β mutant mice exhibited an impaired acute-phase inflammatory response and were completely resistant to fever development and anorexia. These results highlight a central role for IL-1β as a pyrogen and a mediator of the acute-phase response in a subset of Inflammatory disease models, and support the notion that blocking the action of a single key cytokine can alter the course of specific immune and inflammatory responses