Demonstration of sustained and useful converter responses during balanced and unbalanced faults in microgrids

In large power grids where converter penetration is presently low and the network impedance is predominantly reactive, the required response from converters during faults is presently specified by phrases such as “maximum reactive output”. However, in marine and aero power systems most faults are unbalanced, the network impedance is resistive, and converter penetration may be high. Therefore a balanced reactive fault current response to an unbalanced fault may lead to over-voltages or over/under frequency events. Instead, this paper presents a method of controlling the converter as a balanced voltage source behind a reactance, thereby emulating the fault response of a synchronous generator (SG) as closely as possible. In this mode there is a risk of converter destruction due to overcurrent. A new way of preventing destruction but still providing fault performance as close to a SG as possible is presented. Demonstrations are presented of simulations and laboratory testing at the 10kVA 400V scale, with balanced and unbalanced faults. Currents can be limited to about 1.5pu while still providing appropriate unbalanced fault response within a resistive network

Basal rot of narcissus : understanding pathogenicity in fusarium oxysporum f. sp. narcissi

Fusarium oxysporum is a globally distributed soilborne fungal pathogen causing root rots, bulb rots, crown rots and vascular wilts on a range of horticultural plants. Pathogenic F. oxysporum isolates are highly host specific and are classified as formae speciales. Narcissus is an important ornamental crop and both the quality and yield of flowers and bulbs can be severely affected by a basal rot caused by F. oxysporum f. sp. narcissi (FON); 154 Fusarium isolates were obtained from different locations and Narcissus cultivars in the United Kingdom, representing a valuable resource. A subset of 30 F. oxysporum isolates were all found to be pathogenic and were therefore identified as FON. Molecular characterisation of isolates through sequencing of three housekeeping genes, suggested a monophyletic origin with little divergence. PCR detection of 14 Secreted in Xylem (SIX) genes, previously shown to be associated with pathogenicity in other F. oxysporum f. spp., revealed different complements of SIX7, SIX9, SIX10, SIX12 and SIX13 within FON isolates which may suggest a race structure. SIX gene sequences were unique to FON and SIX10 was present in all isolates, allowing for molecular identification of FON for the first time. The genome of a highly pathogenic isolate was sequenced and lineage specific (LS) regions identified which harboured putative effectors including the SIX genes. Real-time RT-PCR, showed that SIX genes and selected putative effectors were expressed in planta with many significantly upregulated during infection. This is the first study to characterise molecular variation in FON and provide an analysis of the FON genome. Identification of expressed genes potentially associated with virulence provides the basis for future functional studies and new targets for molecular diagnostics

Statistics of trajectories in two-state master equations

We derive a simple expression for the probability of trajectories of a master equation. The expression is particularly useful when the number of states is small and permits the calculation of observables that can be defined as functionals of whole trajectories. We illustrate the method with a two-state master equation, for which we calculate the distribution of the time spent in one state and the distribution of the number of transitions, each in a given time interval. These two expressions are obtained analytically in terms of modified Bessel functions.Comment: 4 pages, 3 figure

Bryophytes and their distribution in the Blue Mountains region of New South Wales

The bryophytes (mosses, liverworts and hornworts) that occur in the Blue Mountains region of New South Wales (latitude 33˚–34˚ S, longitude 151˚–151˚40’ E) are listed and information is provided on their distribution in the region. Species lists are based on herbarium specimens and field collections. 348 bryophyte taxa have been recorded from 70 families, including 225 moss taxa (in 108 genera from 45 families), 120 liverwort taxa (in 51 genera from 24 families) and 3 hornwort taxa (in 3 genera from one family). The moss families with most taxa are the Pottiaceae (with 23 taxa in 13 genera), Bryaceae (with 15 taxa in 3 genera) and Fissidentaceae (with 13 taxa). The largest genera are Fissidens (13 taxa), Campylopus (9) and Macromitrium (8). The liverwort family with the most taxa is Lepidoziaceae, with 29 taxa in 10 genera. The largest liverwort genera are Frullania (11 taxa) and Riccardia (8). The species lists include collections from both bushland and urban areas. Natural features of the Blue Mountains, including topography, altitude, climate and vegetation appear to be important factors influencing the number of bryophyte species recorded from each location. The number of collections from particular locations has been considerably influenced by ease of access, particularly proximity to roads, public transport and railway stations. The species lists include many records from areas that were not accessible to the early collectors of the late 19th and early 20th centuries such as Wollemi National Park, Gardens of Stone National Park, Newnes Plateau and Kanangra-Boyd National Park

Muscle Synergies Facilitate Computational Prediction of Subject-Specific Walking Motions.

Researchers have explored a variety of neurorehabilitation approaches to restore normal walking function following a stroke. However, there is currently no objective means for prescribing and implementing treatments that are likely to maximize recovery of walking function for any particular patient. As a first step toward optimizing neurorehabilitation effectiveness, this study develops and evaluates a patient-specific synergy-controlled neuromusculoskeletal simulation framework that can predict walking motions for an individual post-stroke. The main question we addressed was whether driving a subject-specific neuromusculoskeletal model with muscle synergy controls (5 per leg) facilitates generation of accurate walking predictions compared to a model driven by muscle activation controls (35 per leg) or joint torque controls (5 per leg). To explore this question, we developed a subject-specific neuromusculoskeletal model of a single high-functioning hemiparetic subject using instrumented treadmill walking data collected at the subject's self-selected speed of 0.5 m/s. The model included subject-specific representations of lower-body kinematic structure, foot-ground contact behavior, electromyography-driven muscle force generation, and neural control limitations and remaining capabilities. Using direct collocation optimal control and the subject-specific model, we evaluated the ability of the three control approaches to predict the subject's walking kinematics and kinetics at two speeds (0.5 and 0.8 m/s) for which experimental data were available from the subject. We also evaluated whether synergy controls could predict a physically realistic gait period at one speed (1.1 m/s) for which no experimental data were available. All three control approaches predicted the subject's walking kinematics and kinetics (including ground reaction forces) well for the model calibration speed of 0.5 m/s. However, only activation and synergy controls could predict the subject's walking kinematics and kinetics well for the faster non-calibration speed of 0.8 m/s, with synergy controls predicting the new gait period the most accurately. When used to predict how the subject would walk at 1.1 m/s, synergy controls predicted a gait period close to that estimated from the linear relationship between gait speed and stride length. These findings suggest that our neuromusculoskeletal simulation framework may be able to bridge the gap between patient-specific muscle synergy information and resulting functional capabilities and limitations

Do Spinors Frame-Drag?

We investigate the effect of the intrinsic spin of a fundamental spinor field on the surrounding spacetime geometry. We show that despite the lack of a rotating stress-energy source (and despite claims to the contrary) the intrinsic spin of a spin-half fermion gives rise to a frame-dragging effect analogous to that of orbital angular momentum, even in Einstein-Hilbert gravity where torsion is constrained to be zero. This resolves a paradox regarding the counter-force needed to restore Newton's third law in the well known spin-orbit interaction. In addition, the frame-dragging effect gives rise to a {\it long-range} gravitationally mediated spin-spin dipole interaction coupling the {\it internal} spins of two sources. We argue that despite the weakness of the interaction, the spin-spin interaction will dominate over the ordinary inverse square Newtonian interaction in any process of sufficiently high-energy for quantum field theoretical effects to be non-negligible.Comment: V2: published version, mostly minor clarifications from V

Heat shock factor 1 regulates lifespan as distinct from disease onset in prion disease

Prion diseases are fatal, transmissible, neurodegenerative diseases caused by the misfolding of the prion protein (PrP). At present, the molecular pathways underlying prion-mediated neurotoxicity are largely unknown. We hypothesized that the transcriptional regulator of the stress response, heat shock factor 1 (HSF1), would play an important role in prion disease. Uninoculated HSF1 knockout (KO) mice used in our study do not show signs of neurodegeneration as assessed by survival, motor performance, or histopathology. When inoculated with Rocky Mountain Laboratory (RML) prions HSF1 KO mice had a dramatically shortened lifespan, succumbing to disease ≈20% faster than controls. Surprisingly, both the onset of home-cage behavioral symptoms and pathological alterations occurred at a similar time in HSF1 KO and control mice. The accumulation of proteinase K (PK)-resistant PrP also occurred with similar kinetics and prion infectivity accrued at an equal or slower rate. Thus, HSF1 provides an important protective function that is specifically manifest after the onset of behavioral symptoms of prion disease