1,993 research outputs found

    Flow-field surveys on the windward side of the NASA 040A space shuttle orbiter at 31 deg angle of attack and Mach 20 in helium

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    Pitot pressure and flow angle distributions in the windward flow field of the NASA 040A space shuttle orbiter configuration and surface pressures were measured, at a Mach number of 20 and an angle of attack of 31 deg. The free stream Reynolds number, based on model length, was 5.39 x 10 to the 6th power. Results show that cores of high pitot pressure, which are related to the body-shock-wing-shock intersections, occur on the windward plane of symmetry in the vicinity of the wing-body junction and near midspan on the wing. Theoretical estimates of the flow field pitot pressures show that conical flow values for the windward plane of symmetry surface are representative of the average level over the entire lower surface

    Erythrocytes and Vascular Function: Oxygen and Nitric Oxide

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    Erythrocytes regulate vascular function through the modulation of oxygen delivery and the scavenging and generation of nitric oxide (NO). First, hemoglobin inside the red blood cell binds oxygen in the lungs and delivers it to tissues throughout the body in an allosterically regulated process, modulated by oxygen, carbon dioxide and proton concentrations. The vasculature responds to low oxygen tensions through vasodilation, further recruiting blood flow and oxygen carrying erythrocytes. Research has shown multiple mechanisms are at play in this classical hypoxic vasodilatory response, with a potential role of red cell derived vasodilatory molecules, such as nitrite derived nitric oxide and red blood cell ATP, considered in the last 20 years. According to these hypotheses, red blood cells release vasodilatory molecules under low oxygen pressures. Candidate molecules released by erythrocytes and responsible for hypoxic vasodilation are nitric oxide, adenosine triphosphate and S-nitrosothiols. Our research group has characterized the biochemistry and physiological effects of the electron and proton transfer reactions from hemoglobin and other ferrous heme globins with nitrite to form NO. In addition to NO generation from nitrite during deoxygenation, hemoglobin has a high affinity for NO. Scavenging of NO by hemoglobin can cause vasoconstriction, which is greatly enhanced by cell free hemoglobin outside of the red cell. Therefore, compartmentalization of hemoglobin inside red blood cells and localization of red blood cells in the blood stream are important for healthy vascular function. Conditions where erythrocyte lysis leads to cell free hemoglobin or where erythrocytes adhere to the endothelium can result in hypertension and vaso constriction. These studies support a model where hemoglobin serves as an oxido-reductase, inhibiting NO and promoting higher vessel tone when oxygenated and reducing nitrite to form NO and vasodilate when deoxygenated. How erythrocytes modulate vascular tone has been widely studied over the last two decades. The vasodilation of the vasculature under hypoxic conditions has inspired much research ranging from the effect of oxygen partial pressure on smooth muscle cell contractility and endothelial nitric oxide synthase (eNOS) activity to nitrite reduction by hemoglobin (Hb) inside erythrocytes and subsequent production of nitric oxide. Here we review how red blood cells (RBCs) and hemoglobin regulate vascular function and blood flow

    Response of selected microorganisms to experimental planetary environments

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    The anaerobic utilization of phosphite or phosphine and the significance of this conversion to potential contamination of Jupiter were investigated. A sporeforming organism was isolated from Cape Canaveral soil which anaerobically converts hypophosphite to phosphate. This conversion coincides with an increase in turbidity of the culture and with phosphate accumulation in the medium. Investigations of omnitherms (organisms which grow over a broad temperature range, i.e. 3 -55 C were also conducted. The cellular morphology of 28 of these isolates was investigated, and all were demonstrated to be sporeformers. Biochemical characterizations are also presented. Procedures for replicate plating were evaluated, and those results are also presented. The procedures for different replicate-plating techniques are presented, and these are evaluated on the basis of reproducibility, percentage of viable transfer, and ease of use. Standardized procedures for the enumeration of microbial populations from ocean-dredge samples from Cape Canaveral are also presented

    Operational Comparison of Three Electrofishing Systems

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    Three different electrofishing systems were compared to determine their relative efficiency with respect to species and numbers of fish collected. These results indicated that modifications or changes in electrofishing gear during a monitoring program should not be made unless it can be demonstrated that collecting efficiency is not altered

    Redox signals at the ER-mitochondria interface control melanoma progression.

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    Reactive oxygen species (ROS) are emerging as important regulators of cancer growth and metastatic spread. However, how cells integrate redox signals to affect cancer progression is not fully understood. Mitochondria are cellular redox hubs, which are highly regulated by interactions with neighboring organelles. Here, we investigated how ROS at the endoplasmic reticulum (ER)-mitochondria interface are generated and translated to affect melanoma outcome. We show that TMX1 and TMX3 oxidoreductases, which promote ER-mitochondria communication, are upregulated in melanoma cells and patient samples. TMX knockdown altered mitochondrial organization, enhanced bioenergetics, and elevated mitochondrial- and NOX4-derived ROS. The TMX-knockdown-induced oxidative stress suppressed melanoma proliferation, migration, and xenograft tumor growth by inhibiting NFAT1. Furthermore, we identified NFAT1-positive and NFAT1-negative melanoma subgroups, wherein NFAT1 expression correlates with melanoma stage and metastatic potential. Integrative bioinformatics revealed that genes coding for mitochondrial- and redox-related proteins are under NFAT1 control and indicated that TMX1, TMX3, and NFAT1 are associated with poor disease outcome. Our study unravels a novel redox-controlled ER-mitochondria-NFAT1 signaling loop that regulates melanoma pathobiology and provides biomarkers indicative of aggressive disease

    Operational Comparison of Three Electrofishing Systems

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    Student perceptions of teaching quality in five countries: A partial credit model approach to assess measurement invariance

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    This study examines measurement invariance of student perceptions of teaching quality collected in five countries: Indonesia (n students = 6,331), the Netherlands (n students = 6,738), South Africa (n students = 3,422), South Korea (n students = 6,997) and Spain (n students = 4,676). The administered questionnaire was the My Teacher Questionnaire (MTQ). Student perceived teachers’ teaching quality was estimated using the partial credit model (PCM). Tests for differential item functioning (DIF) were used to assess measurement invariance. Furthermore, if DIF was found, it was explored whether an application of a quasi-international calibration, which estimates country-unique parameters for DIF items, can provide more valid estimates for between-country comparisons. Results indicate the absence of non-uniform DIF, but presence of uniform DIF among most items. This suggests that direct comparisons of raw mean or sum scores between countries is not advisable. Details of the set of invariant items are provided. Furthermore, results suggest that the quasi-international calibration is promising, but also that this approach needs further exploration in the context of student perceptions of teaching quality

    Structure and oxidation kinetics of the Si(100)-SiO2 interface

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    We present first-principles calculations of the structural and electronic properties of Si(001)-SiO2 interfaces. We first arrive at reasonable structures for the c-Si/a-SiO2 interface via a Monte-Carlo simulated annealing applied to an empirical interatomic potential, and then relax these structures using first-principles calculations within the framework of density-functional theory. We find a transition region at the interface, having a thickness on the order of 20\AA, in which there is some oxygen deficiency and a corresponding presence of sub-oxide Si species (mostly Si^+2 and Si^+3). Distributions of bond lengths and bond angles, and the nature of the electronic states at the interface, are investigated and discussed. The behavior of atomic oxygen in a-SiO2 is also investigated. The peroxyl linkage configuration is found to be lower in energy than interstitial or threefold configurations. Based on these results, we suggest a possible mechanism for oxygen diffusion in a-SiO2 that may be relevant to the oxidation process.Comment: 7 pages, two-column style with 6 postscript figures embedded. Uses REVTEX and epsf macros. Also available at http://www.physics.rutgers.edu/~dhv/preprints/index.html#ng_sio

    Mechanisms of Hemolysis-Associated Platelet Activation

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    Background Intravascular hemolysis occurs after blood transfusion, in hemolytic anemias, and in other conditions, and is associated with hypercoagulable states. Hemolysis has been shown to potently activate platelets in vitro and in vivo, and several mechanisms have been suggested to account for this, including: (i) direct activation by hemoglobin (Hb); (ii) increase in reactive oxygen species (ROS); (iii) scavenging of nitric oxide (NO) by released Hb; and (iv) release of intraerythrocytic ADP. Objective To elucidate the mechanism of hemolysis-mediated platelet activation. Methods We used flow cytometry to detect PAC-1 binding to activated platelets for in vitro experiments, and a Siemens\u27 Advia 120 hematology system to assess platelet aggregation by using platelet counts from in vivo experiments in a rodent model. Results We found that Hb did not directly activate platelets. However, ADP bound to Hb could cause platelet activation. Furthermore, platelet activation caused by shearing of red blood cells (RBCs) was reduced in the presence of apyrase, which metabolizes ADP to AMP. The use of ROS scavengers did not affect platelet activation. We also found that cell-free Hb enhanced platelet activation by abrogating the inhibitory effect of NO on platelet activation. In vivo infusions of ADP and purified (ADP-free) Hb, as well as hemolysate, resulted in platelet aggregation, as shown by decreased platelet counts. Conclusion Two primary mechanisms account for RBC hemolysis-associated platelet activation: ADP release, which activates platelets; and cell-free Hb release, which enhances platelet activation by lowering NO bioavailability
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