Test and Evaluation of GRISSOM-1 CubeSat Communication Subsystem

The Grissom-1 mission (GM1), slated to launch in September 2022, is the first in a series of 6-Unit CubeSat satellites built and operated by the Air Force Institute of Technology’s (AFIT’s) Center for Space Research and Assurance (CSRA). Mission success for GM1 depends on a comprehensive campaign of testing and assessment to confirm the components, design, and assembly of all systems and subsystems within the satellite. This paper specifically focuses on the testing and analysis of all communication links between the spacecraft, the ground system, and the Satellite Operations Center (SOC) being hosted at the Air Force Instituteof Technology at Wright Patterson Air Force Base. Additionally, the paper will cover the potential for future missions for the GM1 based off the analysis of the current link. Specific to the GM1, analysis is performed on the spacecraft’s Cadet Plus software-defined radio (SDR), as developed by the Space Dynamics Laboratory, and its communication capabilities with the Mobile CubeSat Command and Control (MC3) network, the National Instruments USRP-2292 ground station SDR, and COSMOS Command and Control (C2) software. Testing and assessment occurred in both lab settings and simulated operational scenarios. This paper includes characterization of individual components, anechoic chamber downlink and uplink signal measurements and results, link margin calculations, plus direct point-to-point testing results. Experimental data describing the results of each test using the local instance of an MC3 ground station software. The research culminates in a full characterization of the Cadet Plus SDR, an analysis of the GM1 to MC3 communication interaction, and any limitations revealed as attributable to the 6U spacecraft

Tuning electronic structures via epitaxial strain in Sr2IrO4 thin films

We have synthesized epitaxial Sr2IrO4 thin-films on various substrates and studied their electronic structures as a function of lattice-strains. Under tensile (compressive) strains, increased (decreased) Ir-O-Ir bond-angles are expected to result in increased (decreased) electronic bandwidths. However, we have observed that the two optical absorption peaks near 0.5 eV and 1.0 eV are shifted to higher (lower) energies under tensile (compressive) strains, indicating that the electronic-correlation energy is also affected by in-plane lattice-strains. The effective tuning of electronic structures under lattice-modification provides an important insight into the physics driven by the coexisting strong spin-orbit coupling and electronic correlation.Comment: 9 pages, 5 figures, 1 tabl

Tuning Electronic Structure via Exipatial Strain in Sr\u3csub\u3e2\u3c/sub\u3eIrO\u3csub\u3e4\u3c/sub\u3e Thin Films

We have synthesized epitaxial Sr2IrO4 thin-films on various substrates and studied their electronic structure as a function of lattice-strain. Under tensile (compressive) strain, increased (decreased) Ir-O-Ir bond-angle is expected to result in increased (decreased) electronic bandwidth. However, we have observed that the two optical absorption peaks near 0.5 eV and 1.0 eV are shifted to higher (lower) energies under tensile (compressive) strain, indicating that the electronic-correlation energy is also affected by in-plane lattice-strain. The effective tuning of electronic structure under lattice-modification provides an important insight into the physics driven by the coexisting strong spin-orbit coupling and electronic correlation

Questioning Glutamate Excitotoxicity in Acute Brain Damage: The Importance of Spreading Depolarization

Background: Within 2 min of severe ischemia, spreading depolarization (SD) propagates like a wave through compromised gray matter of the higher brain. More SDs arise over hours in adjacent tissue, expanding the neuronal damage. This period represents a therapeutic window to inhibit SD and so reduce impending tissue injury. Yet most neuroscientists assume that the course of early brain injury can be explained by glutamate excitotoxicity, the concept that immediate glutamate release promotes early and downstream brain injury. There are many problems with glutamate release being the unseen culprit, the most practical being that the concept has yielded zero therapeutics over the past 30 years. But the basic science is also flawed, arising from dubious foundational observations beginning in the 1950s Methods: Literature pertaining to excitotoxicity and to SD over the past 60 years is critiqued. Results: Excitotoxicity theory centers on the immediate and excessive release of glutamate with resulting neuronal hyperexcitation. This instigates poststroke cascades with subsequent secondary neuronal injury. By contrast, SD theory argues that although SD evokes some brief glutamate release, acute neuronal damage and the subsequent cascade of injury to neurons are elicited by the metabolic stress of SD, not by excessive glutamate release. The challenge we present here is to find new clinical targets based on more informed basic science. This is motivated by the continuing failure by neuroscientists and by industry to develop drugs that can reduce brain injury following ischemic stroke, traumatic brain injury, or sudden cardiac arrest. One important step is to recognize that SD plays a central role in promoting early neuronal damage. We argue that uncovering the molecular biology of SD initiation and propagation is essential because ischemic neurons are usually not acutely injured unless SD propagates through them. The role of glutamate excitotoxicity theory and how it has shaped SD research is then addressed, followed by a critique of its fading relevance to the study of brain injury. Conclusions: Spreading depolarizations better account for the acute neuronal injury arising from brain ischemia than does the early and excessive release of glutamate.Grants to RDA from the Canadian Heart & Stroke Foundation, National Science Engineering and Research Council and the New Frontiers in Research Fund, to E.F from the National Research, Development and Innovation Office of Hungary, grant no. K134377; and the EU’s Horizon 2020 research and innovation program under grant agreement No. 739593, and to JPD from the DFG (German research Council) (DFG DR323/5-1,DFG DR 323/10-1) BMBF Bundesministerium fuer Bildung und Forschung (Era-Net Neuron EBio2, with funds from BMBF 01EW2004)

The Critical Role of Spreading Depolarizations in Early Brain Injury: Consensus and Contention

Background: When a patient arrives in the emergency department following a stroke, a traumatic brain injury, or sudden cardiac arrest, there is no therapeutic drug available to help protect their jeopardized neurons. One crucial reason is that we have not identified the molecular mechanisms leading to electrical failure, neuronal swelling, and blood vessel constriction in newly injured gray matter. All three result from a process termed spreading depolarization (SD). Because we only partially understand SD, we lack molecular targets and biomarkers to help neurons survive after losing their blood flow and then undergoing recurrent SD. Methods: In this review, we introduce SD as a single or recurring event, generated in gray matter following lost blood flow, which compromises the Na/K pump. Electrical recovery from each SD event requires so much energy that neurons often die over minutes and hours following initial injury, independent of extracellular glutamate. Results: We discuss how SD has been investigated with various pitfalls in numerous experimental preparations, how overtaxing the Na/K ATPase elicits SD. Elevated K or glutamate are unlikely natural activators of SD. We then turn to the properties of SD itself, focusing on its initiation and propagation as well as on computer modeling. Conclusions: Finally, we summarize points of consensus and contention among the authors as well as where SD research may be heading. In an accompanying review, we critique the role of the glutamate excitotoxicity theory, how it has shaped SD research, and its questionable importance to the study of early brain injury as compared with SD theory.This work was supported by grants from the Heart and Stroke Foundation of Canada and the National Science and Engineering Research Council of Canada to RDA, an NIH grant (NS106901) to CWS, a National Research, Development and Innovation Office of Hungary grant (K1343777) and EU Horizon 2020 research and innovation program (739953) to EF and from DFG Deutsche Forschungsgemeinschaft (German Research Council) (DFG DR 323/5-1), DFG DR 323/10-1, and BMBF Bundesministerium fuer Bildung und Forschung (EraNet Neuron EBio2, with funds from BMBF 01EW2004) to JPD

Affordances, constraints and information flows as ‘leverage points’ in design for sustainable behaviour

Copyright @ 2012 Social Science Electronic PublishingTwo of Donella Meadows' 'leverage points' for intervening in systems (1999) seem particularly pertinent to design for sustainable behaviour, in the sense that designers may have the scope to implement them in (re-)designing everyday products and services. The 'rules of the system' -- interpreted here to refer to affordances and constraints -- and the structure of information flows both offer a range of opportunities for design interventions to in fluence behaviour change, and in this paper, some of the implications and possibilities are discussed with reference to parallel concepts from within design, HCI and relevant areas of psychology

The Shifting Imaginaries of Corporate Crime

This article begins by setting out an analysis of the process of conventionalizing corporate crime that arises from the symbiotic relationship between states and corporations. Noting briefly the empirical characteristics of four broad categories of corporate crime and harm, the article then turns to explore the role of the state in its production and reproduction. We then problematize the role of the state in the reproduction of corporate crime at the level of the global economy, through the “crimes of globalization” and “ecocide,” warning of the tendency in the research literature to oversimplify the role of states and of international organizations. The article finishes by arguing that, as critical academics, it is our role to ensure that corporate crime is never normalized and fully conventionalized in advanced capitalist societies

Integrated Personal Health Records: Transformative Tools for Consumer-Centric Care

<p>Abstract</p> <p>Background</p> <p>Integrated personal health records (PHRs) offer significant potential to stimulate transformational changes in health care delivery and self-care by patients. In 2006, an invitational roundtable sponsored by Kaiser Permanente Institute, the American Medical Informatics Association, and the Agency for Healthcare Research and Quality was held to identify the transformative potential of PHRs, as well as barriers to realizing this potential and a framework for action to move them closer to the health care mainstream. This paper highlights and builds on the insights shared during the roundtable.</p> <p>Discussion</p> <p>While there is a spectrum of dominant PHR models, (standalone, tethered, integrated), the authors state that only the integrated model has true transformative potential to strengthen consumers' ability to manage their own health care. Integrated PHRs improve the quality, completeness, depth, and accessibility of health information provided by patients; enable facile communication between patients and providers; provide access to health knowledge for patients; ensure portability of medical records and other personal health information; and incorporate auto-population of content. Numerous factors impede widespread adoption of integrated PHRs: obstacles in the health care system/culture; issues of consumer confidence and trust; lack of technical standards for interoperability; lack of HIT infrastructure; the digital divide; uncertain value realization/ROI; and uncertain market demand. Recent efforts have led to progress on standards for integrated PHRs, and government agencies and private companies are offering different models to consumers, but substantial obstacles remain to be addressed. Immediate steps to advance integrated PHRs should include sharing existing knowledge and expanding knowledge about them, building on existing efforts, and continuing dialogue among public and private sector stakeholders.</p> <p>Summary</p> <p>Integrated PHRs promote active, ongoing patient collaboration in care delivery and decision making. With some exceptions, however, the integrated PHR model is still a theoretical framework for consumer-centric health care. The authors pose questions that need to be answered so that the field can move forward to realize the potential of integrated PHRs. How can integrated PHRs be moved from concept to practical application? Would a coordinating body expedite this progress? How can existing initiatives and policy levers serve as catalysts to advance integrated PHRs?</p