Applications of Machine Learning to Flight Dynamics Operations

No abstract availabl

Embodied cognitive ecosophy: the relationship of mind, body, meaning and ecology

The concept of embodied cognition has had a major impact in a number of disciplines. The extent of its consequences on general knowledge and epistemology are still being explored. Embodied cognition in human geography has its own traditions and discourses but these have become somewhat isolated in the discipline itself. This paper argues that findings in other disciplines are of value in reconceptualising embodied cognition in human geography and this is explored by reconsidering the concept of ecosophy. Criticisms of ecosophy as a theory are considered and recent work in embodied cognition is applied to consider how such criticisms might be addressed. An updated conceptualisation is proposed, the embodied cognitive ecosophy, and three characteristics arising from this criticism and synthesis are presented with a view to inform future discussions of ecosophy and emotional geography

Search for three-nucleon short-range correlations in light nuclei

We present new data probing short-range correlations (SRCs) in nuclei through the measurement of electron scattering off high-momentum nucleons in nuclei. The inclusive ^{4}He/^{3}He cross section ratio is observed to be both x and Q^{2} independent for 1.52, our data support the hypothesis that a previous claim of three-nucleon correlation dominance was an artifact caused by the limited resolution of the measurement. While 3N-SRCs appear to have an important contribution, our data show that isolating 3N-SRCs is significantly more complicated than for 2N-SRCs.United States. Department of Energy (Contract DE-AC05-06OR23177)United States. Department of Energy (Contract DE-AC02-06CH11357)United States. Department of Energy (Contract DE-FG02-96ER40950

Regulation of the Ysh1 endonuclease of the mRNA cleavage/polyadenylation complex by ubiquitinmediated degradation.

Mutation of the essential yeast protein Ipa1 has previously been demonstrated to cause defects in premRNA 3ʹ end processing and growth, but the mechanism underlying these defects was not clear. In this study, we show that the ipa1-1 mutation causes a striking depletion of Ysh1, the evolutionarily conserved endonuclease subunit of the 19-subunit mRNA Cleavage/Polyadenylation (C/P) complex, but does not decrease other C/P subunits. YSH1 overexpression rescues both the growth and 3ʹ end processing defects of the ipa1-1 mutant. YSH1 mRNA level is unchanged in ipa1-1 cells, and proteasome inactivation prevents Ysh1 loss and causes accumulation of ubiquitinated Ysh1. Ysh1 ubiquitination is mediated by the Ubc4 ubiquitin-conjugating enzyme and Mpe1, which in addition to its function in C/P, is also a RING ubiquitin ligase. In summary, Ipa1 affects mRNA processing by controlling the availability of the C/P endonuclease and may represent a regulatory mechanism that could be rapidly deployed to facilitate reprogramming of cellular responses.post-print4,60 M

Autoimmunity in Arabidopsis acd11 Is Mediated by Epigenetic Regulation of an Immune Receptor

Certain pathogens deliver effectors into plant cells to modify host protein targets and thereby suppress immunity. These target modifications can be detected by intracellular immune receptors, or Resistance (R) proteins, that trigger strong immune responses including localized host cell death. The accelerated cell death 11 (acd11) “lesion mimic” mutant of Arabidopsis thaliana exhibits autoimmune phenotypes such as constitutive defense responses and cell death without pathogen perception. ACD11 encodes a putative sphingosine transfer protein, but its precise role during these processes is unknown. In a screen for lazarus (laz) mutants that suppress acd11 death we identified two genes, LAZ2 and LAZ5. LAZ2 encodes the histone lysine methyltransferase SDG8, previously shown to epigenetically regulate flowering time via modification of histone 3 (H3). LAZ5 encodes an RPS4-like R-protein, defined by several dominant negative alleles. Microarray and chromatin immunoprecipitation analyses showed that LAZ2/SDG8 is required for LAZ5 expression and H3 lysine 36 trimethylation at LAZ5 chromatin to maintain a transcriptionally active state. We hypothesize that LAZ5 triggers cell death in the absence of ACD11, and that cell death in other lesion mimic mutants may also be caused by inappropriate activation of R genes. Moreover, SDG8 is required for basal and R protein-mediated pathogen resistance in Arabidopsis, revealing the importance of chromatin remodeling as a key process in plant innate immunity

The CUAVA-1 CubeSat—A Pathfinder Satellite for Remote Sensing and Earth Observation

In this paper we report a 3U CubeSat named CUAVA-1 designed by the ARC Training Centre for CubeSats, UAVs, and Their Applications (CUAVA). CUAVA, funded by the Australian Research Council, aims to train students, develop new instruments and technology to solve crucial problems, and help develop a world-class Australian industry in CubeSats, UAVs, and related products. The CUAVA-1 project is the Centre’s first CubeSat mission, following on from the 2 Australian satellites INSPIRE-2 and UNSW-EC0 CubeSats that launched in 2017. The mission is designed to serve as a precursor for a series of Earth observations missions and to demonstrate new technologies developed by our partners. We also intend to use the satellite to provide students hands-on experiences and to gain experience for our engineering, science and industry teams for future, more complex, missions

Quantifying Co-Oligomer Formation by α-Synuclein.

Small oligomers of the protein α-synuclein (αS) are highly cytotoxic species associated with Parkinson's disease (PD). In addition, αS can form co-aggregates with its mutational variants and with other proteins such as amyloid-β (Aβ) and tau, which are implicated in Alzheimer's disease. The processes of self-oligomerization and co-oligomerization of αS are, however, challenging to study quantitatively. Here, we have utilized single-molecule techniques to measure the equilibrium populations of oligomers formed in vitro by mixtures of wild-type αS with its mutational variants and with Aβ40, Aβ42, and a fragment of tau. Using a statistical mechanical model, we find that co-oligomer formation is generally more favorable than self-oligomer formation at equilibrium. Furthermore, self-oligomers more potently disrupt lipid membranes than do co-oligomers. However, this difference is sometimes outweighed by the greater formation propensity of co-oligomers when multiple proteins coexist. Our results suggest that co-oligomer formation may be important in PD and related neurodegenerative diseases.The authors are grateful for financial support provided by Dr Tayyeb Hussain Scholarship and the ERC (669237) (M. Iljina), the Schiff Foundation (A. Dear), Alzheimer’s Research UK and Marie-Curie Individual Fellowship (S. De), a fellowship from Fondazione Caritro, Trento (BANDO 2017 PER PROGETTI DI RICERCA SVOLTI DA GIOVANI RICERCATORI POST-DOC) (L. Tosatto), the Boehringer Ingelheim Fonds and the Studienstiftung des deutschen Volkes (P. Flagmeier), the Centre for Misfolding Diseases (A. Dear, P. Flagmeier, C. Dobson, T. Knowles), the ERC (669237) and the Royal Society (D. Klenerman). We are grateful to S. Preet for the expression and purification of A90C ɑS. We thank Y. Ye for providing tau k18

Scaling analysis reveals the mechanism and rates of prion replication in vivo

Prions consist of pathological aggregates of cellular prion protein and have the ability to replicate, causing neurodegenerative diseases, a phenomenon mirrored in many other diseases connected to protein aggregation, including Alzheimer's and Parkinson's diseases. However, despite their key importance in disease, the individual processes governing this formation of pathogenic aggregates, as well as their rates, have remained challenging to elucidate in vivo. Here we bring together a mathematical framework with kinetics of the accumulation of prions in mice and microfluidic measurements of aggregate size to dissect the overall aggregation reaction into its constituent processes and quantify the reaction rates in mice. Taken together, the data show that multiplication of prions in vivo is slower than in in vitro experiments, but efficient when compared with other amyloid systems, and displays scaling behavior characteristic of aggregate fragmentation. These results provide a framework for the determination of the mechanisms of disease-associated aggregation processes within living organisms