Vortex Shedding from a Ground Tracking Radar Antenna and its 3D Tip Flow Characteristics

Abstract: High-speed ground tracking radar systems rotating at about 60 rpm are currently being implemented as modern air traffic control systems in airports. The flow induced vibration and noise generation of the newly developed radar antennas are the two serious problems that jeopardize the successful deployment of the new ground aircraft tracking systems. This paper deals with the viscous flow details of the highly three-dimensional antenna tip section and the vortex shedding characteristics at Re=426,000. The current analysis uses a 3D computational approach for the computation of viscous flow details with the highly 3 D tip geometry. A 2D unsteady computation of the vortex shedding phenomena is also presented. This paper is a continuation of the computational study dealing with the determination of aerodynamic drag coefficients on ASDE-X (Advanced Surface Detection Equipment) antenna cross sections previously presented in Gumusel et al. [1]

Decreased plasma nociceptin/orphanin FQ levels after acute coronary syndromes

Foregoing researches made on the N/OFQ system brought up a possible role for this system in cardiovascular regulation. In this study we examined how N/OFQ levels of the blood plasma changed in acute cardiovascular diseases. Three cardiac patient groups were created: enzyme positive acute coronary syndrome (EPACS, n = 10), enzyme negative ACS (ENACS, n = 7) and ischemic heart disease (IHD, n = 11). We compared the patients to healthy control subjects (n = 31). We found significantly lower N/OFQ levels in the EPACS [6.86 (6.21–7.38) pg/ml], ENACS [6.97 (6.87–7.01) pg/ml and IHD groups [7.58 (7.23–8.20) pg/ml] compared to the control group [8.86 (7.27–9.83) pg/ml]. A significant correlation was detected between N/OFQ and white blood cell count (WBC), platelet count (PLT), creatine kinase (CK), glutamate oxaloacetate transaminase (GOT) and cholesterol levels in the EPACS group.Decreased plasma N/OFQ is closely associated with the presence of acute cardiovascular disease, and the severity of symptoms has a significant negative correlation with the N/OFQ levels. We believe that the rate of N/OFQ depression is in association with the level of ischemic stress and the following inflammatory response. Further investigations are needed to clarify the relevance and elucidate the exact effects of the ischemic stress on the N/OFQ system

Effect of ischemic preconditioning on reactive oxygen species-mediated ischemia-reperfusion injury in the isolated perfused rat lung

Objective: To investigate the protective effect of ischemic preconditioning (IP) in the early phase of reperfusion injury

Elevated semicarbazide-sensitive amine oxidase (SSAO) activity in lung with ischemia-reperfusion injury: Protective effect of ischemic preconditioning plus SSAO inhibition

Ischemic preconditioning (IP) has been shown to protect the lung against ischemia-reperfusion (I/R) injury. Although the production of reactive oxygen species (ROS) has been postulated to play a crucial role in LIR injury, the sources of these radicals in I/R and the mechanisms of protection in IP remain unknown. Since it was postulated that deamination of endogenous and exogenous amines by semicarbazide-sensitive amine oxidase (SSAO) in tissue damage leads to the overproduction of hydrogen peroxide (H2O2), we investigated the possible contribution of tissue SSAO to excess ROS generation and lipid peroxidation during I/R and IP of the lung. Male Wistar rats were randomized into 6 groups: control lungs were subjected to 30 min of perfusion in absence and presence of SSAO inhibitor, whereas the lungs of the I/R group were subjected to 2 h of cold ischemia following the 30 min of perfusion in absence and presence of SSAO inhibitor. IP was performed by two cycles of 5 min ischemia followed by 5 min of reperfusion prior to 2 h of hypothermic ischemia in absence and presence of SSAO inhibitor. Lipid peroxidation, reduced (GSH) and oxidized (GSSG) glutathione levels, antioxidant enzyme activities, SSAO activity, and H2O2 release were determined in tissue samples of the study groups. Lipid peroxidation, glutathione disulfide (GSSG) content, SSAO activity and H2O, release were increased in the I/R group, whereas GSH content, GSH/GSSG ratio and antioxidant enzyme activities were decreased. SSAO activity, H2O2 release, GSSG content and lipid peroxidation were markedly decreased in the IP group, whereas GSH content, GSH/GSSG ratio and antioxidant enzyme activities were significantly increased. SSAO activity was found to be positively correlated with H2O2 production in all study groups. Increased lipid peroxidation, SSAO activity, GSSG and H2O2 contents as well as decreased GSH and antioxidant enzyme levels in I/R returned to their basal levels when IP and SSAO inhibition were applied together. The present study suggests that application of I P and SSAO inhibition together may be more effective than IP alone against I/R injury in the lung. (c) 2005 Elsevier Inc. All rights reserved

THE PULMONARY VASCULAR-RESPONSE TO PROPOFOL IN THE ISOLATED-PERFUSED RAT LUNG

This study investigated the effect of propofol on the pulmonary vascular bed of the rat. Propofol (5 x 10(-6) to 5 x 10(-4) M) did not alter the basal perfusion pressure in isolated rat lungs perfused at a constant flow (0.03 mL g body wt(-1) min(-1)) with Krebs-Henseleit solution. When perfusion pressure was elevated by raising the K+ concentration to 30 mM (depolarizing Krebs-Henseleit solution), propofol decreased it in a concentration-dependent manner. Indomethacin (3 x 10(-6) M) and N-G-nitro-L-arginine methyl ester (10(-4) M) did not affect the response to propofol, which excluded the role of cyclo-oxygenase metabolites and nitric oxide, respectively. The ATP-sensitive K+ (K-ATP(+)) channel blocker glibenclamide (3 x 10(-6) and 10(-5) M) inhibited the vasodilator effect of propofol. When lungs were perfused with Ca2+-free depolarizing Krebs-Henseieit solution, 0.1-2.5 mM Ca+2 produced a concentration-dependent presser response. Propofol (5 x 10(-5) M) attenuated the vasopressor response to Ca2+ significantly. In conclusion, the activation of K-ATP(+) channels is probably the major mechanism of the vasodilator effect of propofol, at clinically relevant concentrations, in the rat lung. The Ca2+ antagonistic property of propofol is evident only at higher concentrations