446 research outputs found
A NASA initiative: Software engineering for reliable complex systems
The objective is the development of methods, technology, and skills that will enable NASA to cost-effectively specify, build, and manage reliable software which can evolve and be maintained over an extended period. The need for such software is rooted in the increasing integration of software and computing components into NASA systems. Current NASA Software Engineering expertise was applied toward some of the largest reliable systems including: shuttle launch; ground support; shuttle simulation; minor control; satellite tracking; and scientific data systems. Unfortunately, no theory exists for reliable complex software systems. NASA is seeking to fill this theoretical gap through a number of approaches. One such approach is to conduct research on theoretical foundations for managing complex software systems. It includes: communication models, new and modified paradigms, and life-cycle models. Another approach is research in the theoretical foundations for reliable software development and validation. It focuses upon formal specifications, programming languages, software engineering systems, software reuse, formal verification, and software safety. Further approaches involve benchmarking a NASA software environment, experimentation within the NASA context, evolution of present NASA methodology, and transfer of technology to the space station software support environment
Information sciences and human factors overview
An overview of program objectives of the Information Sciences and Human Factors Division of NASA's Office of Aeronautics and Space Technology is given in viewgraph form. Information is given on the organizational structure, goals, the research and technology base, telerobotics, systems autonomy in space operations, space sensors, humans in space, space communications, space data systems, transportation vehicle guidance and control, spacecraft control, and major program directions in space
Nanoscale control of exchange bias with BiFeO3 thin films
We demonstrate a direct correlation between the domain structure of
multiferroic BiFeO3 thin films and exchange bias of Co0.9Fe0.1/BiFeO3
heterostructures. Two distinct types of interactions, an enhancement of the
coercive field (exchange enhancement) and an enhancement of the coercive field
combined with large shifts of the hysteresis loop (exchange bias), have been
observed in these heterostructures, which depend directly on the type and
crystallography of the nanoscale (2 nm) domain walls in the BiFeO3 film. We
show that the magnitude of the exchange bias interaction scales with the length
of 109 degree ferroelectric domain walls in the BiFeO3 thin films which have
been probed via piezoresponse force microscopy and x-ray magnetic circular
dichroism.Comment: Accepted to Nano Letters May 200
Ferromagnetism in magnetically doped III-V semiconductors
The origin of ferromagnetism in semimagnetic III-V materials is discussed.
The indirect exchange interaction caused by virtual electron excitations from
magnetic impurity level in the bandgap to the valence band can explain
ferromagnetism in GaAs(Mn) no matter samples are degenerated or not. Formation
of ferromagnetic clusters and percolation picture of phase transition describes
well all available experimental data and allows to predict the Mn-composition
dependence of transition temperature in wurtzite (Ga,In,Al)N epitaxial layers.Comment: 4 pages with 3 figure
Modulation of Syndecan-1 Shedding after Hemorrhagic Shock and Resuscitation
The early use of fresh frozen plasma as a resuscitative agent after hemorrhagic shock has been associated with improved survival, but the mechanism of protection is unknown. Hemorrhagic shock causes endothelial cell dysfunction and we hypothesized that fresh frozen plasma would restore endothelial integrity and reduce syndecan-1 shedding after hemorrhagic shock. A prospective, observational study in severely injured patients in hemorrhagic shock demonstrated significantly elevated levels of syndecan-1 (554Ā±93 ng/ml) after injury, which decreased with resuscitation (187Ā±36 ng/ml) but was elevated compared to normal donors (27Ā±1 ng/ml). Three pro-inflammatory cytokines, interferon-Ī³, fractalkine, and interleukin-1Ī², negatively correlated while one anti-inflammatory cytokine, IL-10, positively correlated with shed syndecan-1. These cytokines all play an important role in maintaining endothelial integrity. An in vitro model of endothelial injury then specifically examined endothelial permeability after treatment with fresh frozen plasma orlactated Ringers. Shock or endothelial injury disrupted junctional integrity and increased permeability, which was improved with fresh frozen plasma, but not lactated Ringers. Changes in endothelial cell permeability correlated with syndecan-1 shedding. These data suggest that plasma based resuscitation preserved endothelial syndecan-1 and maintained endothelial integrity, and may help to explain the protective effects of fresh frozen plasma after hemorrhagic shock
Stabilization of weak ferromagnetism by strong magnetic response to epitaxial strain in multiferroic BiFeO3
Multiferroic BiFeO3 exhibits excellent magnetoelectric coupling critical for magnetic information processing with minimal power consumption. However, the degenerate nature of the easy spin axis in the (111) plane presents roadblocks for real world applications. Here, we explore the stabilization and switchability of the weak ferromagnetic moments under applied epitaxial strain using a combination of first-principles calculations and group-theoretic analyses. We demonstrate that the antiferromagnetic moment vector can be stabilized along unique crystallographic directions ([110] and [-110]) under compressive and tensile strains. A direct coupling between the anisotropic antiferrodistortive rotations and the Dzyaloshinskii-Moria interactions drives the stabilization of the weak ferromagnetism. Furthermore, energetically competing C- and G-type magnetic orderings are observed at high compressive strains, suggesting that it may be possible to switch the weak ferromagnetism "on" and "off" under the application of strain. These findings emphasize the importance of strain and antiferrodistortive rotations as routes to enhancing induced weak ferromagnetism in multiferroic oxides.ope
IRE1Ī±āXBP1 controls T cell function in ovarian cancer by regulating mitochondrial activity
Tumours evade immune control by creating hostile microenvironments that perturb T cell metabolism and effector function 1?4 . However, it remains unclear how intra-tumoral T cells integrate and interpret metabolic stress signals. Here we report that ovarian cancer?an aggressive malignancy that is refractory to standard treatments and current immunotherapies 5?8 ?induces endoplasmic reticulum stress and activates the IRE1Ī±?XBP1 arm of the unfolded protein response 9,10 in T cells to control their mitochondrial respiration and anti-tumour function. In T cells isolated from specimens collected from patients with ovarian cancer, upregulation of XBP1 was associated with decreased infiltration of T cells into tumours and with reduced IFNG mRNA expression. Malignant ascites fluid obtained from patients with ovarian cancer inhibited glucose uptake and caused N-linked protein glycosylation defects in T cells, which triggered IRE1Ī±?XBP1 activation that suppressed mitochondrial activity and IFNĪ³ production. Mechanistically, induction of XBP1 regulated the abundance of glutamine carriers and thus limited the influx of glutamine that is necessary to sustain mitochondrial respiration in T cells under glucose-deprived conditions. Restoring N-linked protein glycosylation, abrogating IRE1Ī±?XBP1 activation or enforcing expression of glutamine transporters enhanced mitochondrial respiration in human T cells exposed to ovarian cancer ascites. XBP1-deficient T cells in the metastatic ovarian cancer milieu exhibited global transcriptional reprogramming and improved effector capacity. Accordingly, mice that bear ovarian cancer and lack XBP1 selectively in T cells demonstrate superior anti-tumour immunity, delayed malignant progression and increased overall survival. Controlling endoplasmic reticulum stress or targeting IRE1Ī±?XBP1 signalling may help to restore the metabolic fitness and anti-tumour capacity of T cells in cancer hosts.Fil: Song, Minkyung. Weill Cornell Medicine; Estados UnidosFil: Sandoval, Tito A.. Weill Cornell Medicine; Estados UnidosFil: Chae, Chang-Suk. Weill Cornell Medicine; Estados UnidosFil: Chopra, Sahil. Weill Cornell Medicine; Estados UnidosFil: Tan, Chen. Weill Cornell Medicine; Estados UnidosFil: Rutkowski, Melanie R.. University of Virginia; Estados UnidosFil: Raundhal, Mahesh. Dana Farber Cancer Institute; Estados Unidos. Harvard Medical School; Estados UnidosFil: Chaurio, Ricardo A.. H. Lee Moffitt Cancer Center & Research Institute; Estados UnidosFil: Payne, Kyle K.. H. Lee Moffitt Cancer Center & Research Institute; Estados UnidosFil: Konrad, Csaba. Weill Cornell Medicine; Estados UnidosFil: Bettigole, Sarah E.. Quentis Therapeutics Inc.; Estados UnidosFil: Shin, Hee Rae. Quentis Therapeutics Inc.; Estados UnidosFil: Crowley, Michael J. P.. Weill Cornell Graduate School of Medical Sciences; Estados UnidosFil: Cerliani, Juan Pablo. Consejo Nacional de Investigaciones CientĆficas y TĆ©cnicas. Instituto de BiologĆa y Medicina Experimental. FundaciĆ³n de Instituto de BiologĆa y Medicina Experimental. Instituto de BiologĆa y Medicina Experimental; ArgentinaFil: Kossenkov, Andrew V.. The Wistar Institute; Estados UnidosFil: Motorykin, Ievgen. Weill Cornell Medicine,; Estados UnidosFil: Zhang, Sheng. Weill Cornell Medicine,; Estados UnidosFil: Manfredi, Giovanni. Weill Cornell Medicine,; Estados UnidosFil: Zamarin, Dmitriy. Memorial Sloan Kettering Cancer Center; Estados UnidosFil: Holcomb, Kevin. Weill Cornell Medicine,; Estados UnidosFil: Rodriguez, Paulo C.. H. Lee Moffitt Cancer Center & Research Institute; Estados UnidosFil: Rabinovich, Gabriel AdriĆ”n. Consejo Nacional de Investigaciones CientĆficas y TĆ©cnicas. Instituto de BiologĆa y Medicina Experimental. FundaciĆ³n de Instituto de BiologĆa y Medicina Experimental. Instituto de BiologĆa y Medicina Experimental; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de QuĆmica BiolĆ³gica; ArgentinaFil: Conejo Garcia, Jose R.. H. Lee Moffitt Cancer Center & Research Institute; Estados UnidosFil: Glimcher, Laurie H.. Dana Farber Cancer Institute; Estados Unidos. Harvard Medical School; Estados UnidosFil: Cubillos-Ruiz, Juan R.. Weill Graduate School Of Medical Sciences; Estados Unidos. Weill Graduate School Of Medical Sciences; Estados Unido
Intraneuronal pyroglutamate-Abeta 3ā42 triggers neurodegeneration and lethal neurological deficits in a transgenic mouse model
It is well established that only a fraction of AĪ² peptides in the brain of Alzheimerās disease (AD) patients start with N-terminal aspartate (AĪ²1D) which is generated by proteolytic processing of amyloid precursor protein (APP) by BACE. N-terminally truncated and pyroglutamate modified AĪ² starting at position 3 and ending with amino acid 42 [AĪ²3(pE)ā42] have been previously shown to represent a major species in the brain of AD patients. When compared with AĪ²1ā42, this peptide has stronger aggregation propensity and increased toxicity in vitro. Although it is unknown which peptidases remove the first two N-terminal amino acids, the cyclization of AĪ² at N-terminal glutamate can be catalyzed in vitro. Here, we show that AĪ²3(pE)ā42 induces neurodegeneration and concomitant neurological deficits in a novel mouse model (TBA2 transgenic mice). Although TBA2 transgenic mice exhibit a strong neuronal expression of AĪ²3ā42 predominantly in hippocampus and cerebellum, few plaques were found in the cortex, cerebellum, brain stem and thalamus. The levels of converted AĪ²3(pE)-42 in TBA2 mice were comparable to the APP/PS1KI mouse model with robust neuron loss and associated behavioral deficits. Eight weeks after birth TBA2 mice developed massive neurological impairments together with abundant loss of Purkinje cells. Although the TBA2 model lacks important AD-typical neuropathological features like tangles and hippocampal degeneration, it clearly demonstrates that intraneuronal AĪ²3(pE)ā42 is neurotoxic in vivo
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