413 research outputs found

    Paper Session II-B - Automated Software Systems for the CELSS Project

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    The National Aeronautics and Space Administration (NASA) Biomedical Operations and Research Office (MD), Life Sciences Group (MD-RES), at Kennedy Space Center (KSC), Florida, is conducting research in the design and development of Controlled Ecological Life Support Systems (CELSS) for use in long-term human-tended space colonization efforts. The project seeks to perfect the engineering systems required for maintaining food and oxygen recycling, replenishment, and generation for astronauts engaged in missions wherein regular Earth-based resupply would be difficult and economically infeasible, as in a lunar base or a Mars exploration mission. Major components of CELSS are crop production, resource recovery (waste management), and monitor and control. These components must be integrated to produce a reliable system with minimal mass and volume which requires that we minimize buffers (e.g. support equipment size and capacity) and optimize control. One element of the computerized control and monitoring component of the CELSS project at KSC is the Universal Networked Data Acquistition and Control Engine (UNDACE), the software designed to automatically monitor and control the operations and environments of the crop production and resource recovery components

    Differential role for trehalose metabolism in salt-stressed maize

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    Little is known about how salt impacts primary metabolic pathways of C4 plants, particularly related to kernel development and seed set. Osmotic stress was applied to maize (Zea mays) B73 by irrigation with increasing concentrations of NaCl from the initiation of floral organs until 3 d after pollination. At silking, photosynthesis was reduced to only 2% of control plants. Salt treatment was found to reduce spikelet growth, silk growth, and kernel set. Osmotic stress resulted in higher concentrations of sucrose (Suc) and hexose sugars in leaf, cob, and kernels at silking, pollination, and 3 d after pollination. Citric acid cycle intermediates were lower in salt-treated tissues, indicating that these sugars were unavailable for use in respiration. The sugar-signaling metabolite trehalose-6-phosphate was elevated in leaf, cob, and kernels at silking as a consequence of salt treatment but decreased thereafter even as Suc levels continued to rise. Interestingly, the transcripts of trehalose pathway genes were most affected by salt treatment in leaf tissue. On the other hand, transcripts of the SUCROSE NONFERMENTING-RELATED KINASE1 (SnRK1) marker genes were most affected in reproductive tissue. Overall, both source and sink strength are reduced by salt, and the data indicate that trehalose-6-phosphate and SnRK1 may have different roles in source and sink tissues. Kernel abortion resulting from osmotic stress is not from a lack of carbohydrate reserves but from the inability to utilize these energy reserves

    Fermilab Main Injector Beam Position Monitor Upgrade

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    An upgrade of the Beam Position Monitor (BPM) signal processing and data acquisition system for the Fermilab Main Injector is described. The Main Injector is a fast cycling synchrotron that accelerates protons or antiprotons from 8 to 150 GeV. Each Main Injector cycle can have a totally different magnet ramp, RF frequency configuration, beam bunch structure, and injection/extraction pattern from the previous cycle. The new BPM system provides the capabilities and flexibility required by the dynamic and complex machine operations. The system offers measurement capability in the 2.5 MHz and 53 MHz channels to detect the range of bunch structures for protons and antiprotons in both wideband (turn-by-turn) and narrowband (closed-orbit) modes. The new BPM read-out system is based on the digital receiver concept and is highly configurable, allowing the signal processing of nearly all Main Injector beam conditions, including the detection of individual batches. An overview of the BPM system in the Main Injector operating environment, some technology details and first beam measurements are presented

    New Mechanics of Traumatic Brain Injury

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    The prediction and prevention of traumatic brain injury is a very important aspect of preventive medical science. This paper proposes a new coupled loading-rate hypothesis for the traumatic brain injury (TBI), which states that the main cause of the TBI is an external Euclidean jolt, or SE(3)-jolt, an impulsive loading that strikes the head in several coupled degrees-of-freedom simultaneously. To show this, based on the previously defined covariant force law, we formulate the coupled Newton-Euler dynamics of brain's micro-motions within the cerebrospinal fluid and derive from it the coupled SE(3)-jolt dynamics. The SE(3)-jolt is a cause of the TBI in two forms of brain's rapid discontinuous deformations: translational dislocations and rotational disclinations. Brain's dislocations and disclinations, caused by the SE(3)-jolt, are described using the Cosserat multipolar viscoelastic continuum brain model. Keywords: Traumatic brain injuries, coupled loading-rate hypothesis, Euclidean jolt, coupled Newton-Euler dynamics, brain's dislocations and disclinationsComment: 18 pages, 1 figure, Late

    Micro-finance, women’s empowerment and fertility decline in Bangladesh: How important was women’s agency?

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    As Nobel Prize winner Amartya Sen has argued “[Bangladesh’s development achievements have] important lessons for other countries across the globe, [in particular a focus on] reducing gender inequality”. A major avenue through which this emphasis has been manifest lies, according to this narrative, in enhancements to women’s agency for instrumental and intrinsic reasons particularly through innovations in family planning and microfinance. The “Bangladesh paradox” of improved wellbeing despite low economic growth over the last four decades is claimed as a paradigmatic case of the spread of both modern family planning programmes and microfinance leading to women’s empowerment and fertility reduction. In this paper we show that the links between microfinance, empowerment and fertility reduction, are fraught with problems, and far from robust; hence the claimed causal links between microfinance and family planning via women’s empowerment needs to be further reconsidered

    Mechanisms for the Evolution of a Derived Function in the Ancestral Glucocorticoid Receptor

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    Understanding the genetic, structural, and biophysical mechanisms that caused protein functions to evolve is a central goal of molecular evolutionary studies. Ancestral sequence reconstruction (ASR) offers an experimental approach to these questions. Here we use ASR to shed light on the earliest functions and evolution of the glucocorticoid receptor (GR), a steroid-activated transcription factor that plays a key role in the regulation of vertebrate physiology. Prior work showed that GR and its paralog, the mineralocorticoid receptor (MR), duplicated from a common ancestor roughly 450 million years ago; the ancestral functions were largely conserved in the MR lineage, but the functions of GRs—reduced sensitivity to all hormones and increased selectivity for glucocorticoids—are derived. Although the mechanisms for the evolution of glucocorticoid specificity have been identified, how reduced sensitivity evolved has not yet been studied. Here we report on the reconstruction of the deepest ancestor in the GR lineage (AncGR1) and demonstrate that GR's reduced sensitivity evolved before the acquisition of restricted hormone specificity, shortly after the GR–MR split. Using site-directed mutagenesis, X-ray crystallography, and computational analyses of protein stability to recapitulate and determine the effects of historical mutations, we show that AncGR1's reduced ligand sensitivity evolved primarily due to three key substitutions. Two large-effect mutations weakened hydrogen bonds and van der Waals interactions within the ancestral protein, reducing its stability. The degenerative effect of these two mutations is extremely strong, but a third permissive substitution, which has no apparent effect on function in the ancestral background and is likely to have occurred first, buffered the effects of the destabilizing mutations. Taken together, our results highlight the potentially creative role of substitutions that partially degrade protein structure and function and reinforce the importance of permissive mutations in protein evolution

    Dibutyltin Disrupts Glucocorticoid Receptor Function and Impairs Glucocorticoid-Induced Suppression of Cytokine Production

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    BACKGROUND: Organotins are highly toxic and widely distributed environmental chemicals. Dibutyltin (DBT) is used as stabilizer in the production of polyvinyl chloride plastics, and it is also the major metabolite formed from tributyltin (TBT) in vivo. DBT is immunotoxic, however, the responsible targets remain to be defined. Due to the importance of glucocorticoids in immune-modulation, we investigated whether DBT could interfere with glucocorticoid receptor (GR) function. METHODOLOGY: We used HEK-293 cells transiently transfected with human GR as well as rat H4IIE hepatoma cells and native human macrophages and human THP-1 macrophages expressing endogenous receptor to study organotin effects on GR function. Docking of organotins was used to investigate the binding mechanism. PRINCIPAL FINDINGS: We found that nanomolar concentrations of DBT, but not other organotins tested, inhibit ligand binding to GR and its transcriptional activity. Docking analysis indicated that DBT inhibits GR activation allosterically by inserting into a site close to the steroid-binding pocket, which disrupts a key interaction between the A-ring of the glucocorticoid and the GR. DBT inhibited glucocorticoid-induced expression of phosphoenolpyruvate carboxykinase (PEPCK) and tyrosine-aminotransferase (TAT) and abolished the glucocorticoid-mediated transrepression of TNF-alpha-induced NF-kappaB activity. Moreover, DBT abrogated the glucocorticoid-mediated suppression of interleukin-6 (IL-6) and TNF-alpha production in lipopolysaccharide (LPS)-stimulated native human macrophages and human THP-1 macrophages. CONCLUSIONS: DBT inhibits ligand binding to GR and subsequent activation of the receptor. By blocking GR activation, DBT may disturb metabolic functions and modulation of the immune system, providing an explanation for some of the toxic effects of this organotin
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