Gliding Velocity Research Articles

Flight Trajectory Optimization of Sailplane After Rope Break

A study was performed to characterize an optimum return trajectory for a sailplane after a rope-break failure during an aerotow launch procedure. The performance of an SGS 1-26E sailplane was simulated using the equations of motion for quasi-steady flight in a time-stepping routine and published aerodynamic polar data. A gradient-based optimization algorithm was implemented using the simulated trajectory considering the glide velocity, bank angles, and runway offset angle to determine the minimum rope-break altitude from which a successful return could be theoretically produced. The SGS 1-26E sailplane was used in a flight-test campaign for empirical turn modeling and validation of the performance simulation. The minimum altitude where a return trajectory and downwind runway landing could be successfully completed after a rope-break event was observed to be 76.4 ft above ground level. A headwind and crosswind presence was observed to decrease the minimum rope-break altitude with increasing wind velocity up to a critical value, after which rope-break altitudes began to increase. These minimum rope-break altitudes serve as a theoretical indication that safe trajectories can be performed at lower failure altitudes than the commonly practiced decision altitude of 200 ft for certain wind conditions.

Differences between elite and sub-elite swimmers in a 100 m breaststroke: a new race analysis approach with time-series velocity data

ABSTRACT The purpose of the present study was to investigate differences in a 100 m breaststroke time-trial between elite and sub-elite swimmers. Elite and sub-elite male swimmers (seven each; 772.1 ± 35.2 and 610.6 ± 24.7 FINA point, respectively) performed 100 m breaststroke, which was recorded by a multi-camera system that provided the mean and time-series velocity data in the glide, pull-out, and clean-swimming segments. The mean velocity in each segment was compared between the groups using an independent-samples t-test (for the 1st lap) and two-way mixed-design ANOVA (for the 2nd—4th laps), which suggested a larger mean clean-swimming (in all laps; 7–11% difference) and glide (in the 2nd and 3rd lap; about 13% difference) velocity for the elite swimmers. The time-series data displayed faster velocity in elite swimmers than in the sub-elite group during the first part (up to 40% time) of the glide segment (p < 0.05). Differences in the clean-swimming segment between the groups were observed (p < 0.001) apart from the first 5–15% time of the segment. No differences in the pull-out and at the beginning of the clean-swimming imply that coaches and swimmers should not assume that a good clean-swimming technique also guarantees fast velocity in these segments.

Correlation of early-stage growth process conditions with dislocation evolution in MOCVD-based GaP/Si heteroepitaxy

To identify the complex relationships between early-stage growth processes and the resultant defect microstructure in GaP/Si heteroepitaxy, a holistic study of several key metal–organic chemical vapor deposition (MOCVD) parameters was conducted, focusing on Si surface preparation and GaP atomic layer epitaxy (ALE) based nucleation processes. Crystalline defects related to the lattice mismatch and/or interfacial heterovalency, namely misfit dislocations (MD), threading dislocations (TD), and stacking fault pyramids (SFP), were quantitatively characterized via electron channeling contrast imaging (ECCI) and correlated against the different process variations. Choice of Si surface preparation method between the two examined (dilute SiH4 annealing versus Si2H6 based homoepitaxy) had little impact on resultant GaP film morphology and defect content, whereas differing GaP ALE nucleation conditions produced much more substantial changes. In particular, the initial precursor species (tert-butylphosphine versus triethygallium) and ALE cycle purge times both yielded significant influence over threading dislocation densities (TDD) in thin (100 nm), post-critical thickness GaP/Si films, with TDD spanning two orders of magnitude, from 6.7 × 107 cm−2 to 7.1 × 105 cm−2, depending on the specific process conditions employed. SFP densities were also found to follow a similar trend, ranging from 2.0 × 107 cm−2 to 1.8 × 105 cm−2, but with no apparent causal relationship between SFP density and TDD. To help explain the dramatic differences observed, detailed, large-area MD network characterization was used to provide statistically-relevant quantitative analyses of the critical dislocation dynamics (introduction rates and glide velocities) associated with the different process variants. These extracted values are then correlated against the ALE process variants to provide insight into the potential mechanistic roles of the different growth processes.

Effects of stress on the evolution of Σ-shaped dislocation arrays in a 4H-SiC epitaxial layer

Five Σ-shaped dislocation arrays in 100-mm-diameter, 12-μm-thick 4H-SiC epitaxial wafers were observed using photoluminescence mapping. The structure of the Σ-shaped dislocation arrays was characterized using nondestructive analytical techniques of photoluminescence mapping, microphotoluminescence spectroscopy, and x-ray topography. Each Σ-shaped dislocation array consists of two basal plane dislocations (BPDs) at the interfacial dislocation terminal points and two half-loop arrays. The interfacial dislocation pairs nucleate from BPDs in the substrate. Three independent stresses lead to interfacial dislocations: thermal stress (τT), stress induced by misfit strain (τM), and interaction force (τI). The main cause of interfacial dislocation formation is attributed to the development of τT within the wafer due to temperature nonuniformity. τM and τI also contribute to the formation of interfacial dislocations. Larger stresses increase the BPD glide velocity in the interfacial dislocations, thereby producing longer Σ-shaped dislocation arrays.

The ALS-Associated FUS (P525L) Variant Does Not Directly Interfere with Microtubule-Dependent Kinesin-1 Motility.

Deficient intracellular transport is a common pathological hallmark of many neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS). Mutations in the fused-in-sarcoma (FUS) gene are one of the most common genetic causes for familial ALS. Motor neurons carrying a mutation in the nuclear localization sequence of FUS (P525L) show impaired axonal transport of several organelles, suggesting that mislocalized cytoplasmic FUS might directly interfere with the transport machinery. To test this hypothesis, we studied the effect of FUS on kinesin-1 motility in vitro. Using a modified microtubule gliding motility assay on surfaces coated with kinesin-1 motor proteins, we showed that neither recombinant wildtype and P525L FUS variants nor lysates from isogenic ALS-patient-specific iPSC-derived spinal motor neurons expressing those FUS variants significantly affected gliding velocities. We hence conclude that during ALS pathogenesis the initial negative effect of FUS (P525L) on axonal transport is an indirect nature and requires additional factors or mechanisms.

Mechanical Force Rather Than Strong Binding Intermediates Extends Activation of Regulated Actin

Recent evidence demonstrates that the gliding time of thin filaments in a motility assay is extended by force but questions arise about the mechanism. To address whether the force is mechanical, we varied the density of myosin immobilized on the surface in contact with actin filaments regulated by native complex of tropomyosin and troponin. Compared with low myosin density, we expected the average run times to be longer at high myosin density because previous results showed that the measured gliding velocity was greater. However, persistence of strong binding crossbridge intermediates could extend average run time by delaying deactivation. Competing chemical binding and mechanical force mechanisms can be distinguished in the probability density distributions of run time frequencies. Because chemical potential is constant in the motility assay, chemical states turn over at constant rate and, hence, have probability given by a Poisson distribution. in this scenario, Poisson rate is given by the odds of a pause, and hence, run times between pauses fit an exponential distribution that slopes negatively for all observable run times. However, we determined that relative density of observed run times fits an exponential only at low myosin density. At the higher myosin density, the relative frequency of short run times fit the positive slope of a gamma distribution, which derives from waiting times between Poisson events. Reaction intermediates including strong binding myosin respond to a thermodynamic potential and, hence, cannot explain the gamma distributed response observed. Cumulative densities of run-time frequencies at both myosin densities fit a model in which mechanical force contributes to the activation of thin filaments. We propose that the integral force of myosin delays the transition state during activation. Work supported by NIH R01-HL128683 (JRP) and leave supported by UWG (HGZ).

Statistical mechanics of kinks on a gliding screw dislocation

The ability of a body-centered cubic metal to deform plastically is limited by the thermally activated glide motion of screw dislocations, which are line defects with a mobility exhibiting complex dependence on temperature, stress, and dislocation segment length. We derive an analytical expression for the velocity of dislocation glide, based on a statistical mechanics argument, and identify an apparent phase transition marked by a critical temperature above which the activation energy for glide effectively halves, changing from the formation energy of a double kink to that of a single kink. The analysis is in quantitative agreement with direct kinetic Monte Carlo simulations.

A dislocation-based model for the microstructure evolution and the flow stress of a Ti5553 alloy

The plastic deformation at high temperatures of two-phase titanium alloys is modelled using a mesoscale approach to describe the complex interactions between different populations of dislocation densities. The static and dynamic recovery, as well as of continuous dynamic recrystallization, is modelled. The flow stresses of both α and β phases are calculated using constitutive equations combined with a load partitioning model between the α and β phases. The dislocation populations are separated into three categories, named mobile, immobile and walls, and separated rate equations are developed for each reaction between them. Several microstructure features are calculated, such as mean subgrain size, grain size, dislocation densities and boundary misorientation. Additionally, glide velocity is also estimated. Hot compression experiments of a Ti-5553 alloy at temperatures between 1073 K and 1193 K and strain rates between 0.001 s−1 and 10 s−1 are used for validation. The flow softening observed in the α+β domain is attributed to the change in load partitioning. Moreover, the decrease in grain and subgrain size with the increase in strain rate and decrease in temperature is well predicted by the proposed model as well as the evolution of a fully static recrystallized microstructure into a continuous dynamic recrystallized one.

N-terminal β-strand of single-headed kinesin-1 can modulate the off-axis force-generation and resultant rotation pitch.

In in vitro microtubule gliding assays, most kinesins drive the rotation of gliding microtubules around their longitudinal axes in a corkscrew motion. The corkscrewing pitch is smaller than the supertwisted protofilament pitch of microtubules, indicating that the corkscrewing pitch is an inherent property of kinesins. To elucidate the molecular mechanisms through which kinesins corkscrew the microtubule, we performed three-dimensional tracking of a quantum dot bound to a microtubule translocating over a surface coated with single-headed kinesin-1 s under various assay conditions to alter the interactions between the kinesin and microtubule. Although alternations in kinesin concentration, ionic strength, and ATP concentration changed both gliding and rotational velocities, the corkscrewing pitch remained left-handed and constant at ~0.3 μm under all tested conditions apart from a slight increase in pitch at a low ATP concentration. We then used our system to analyze the effect of point mutations in the N-terminal β-strand protruding from the kinesin motor core and found mutations that decreased the corkscrewing pitch. Our findings confirmed that the corkscrewing motion of microtubules is caused by the intrinsic properties of the kinesin and demonstrates that changes in the active or retarding force originating from the N-terminal β-strand in the head modulate the pitch.

Effect of Light Element Impurities on the Edge Dislocation Glide in Nickel and Silver: Molecular Dynamics Simulation

The influence of light element (C, N, O) impurities on the edge dislocation glide in fcc metals (Ni, Ag) is studied by molecular dynamics simulation. The introduction of impurity atoms is found to increase the dislocation glide threshold stress significantly, from 10 MPa in the pure metals at a temperature of 300 K to 1000–2000 MPa after the introduction of 10 at % impurity atoms. The increase in the threshold stress with the concentration of impurity atoms is shown to be caused by the Suzuki mechanism, i.e., the pinning of impurity atoms by the stacking fault between partial dislocations. The energies of binding of impurity atoms to stacking faults were determined for the metals under study. When temperature increases, the dislocation glide velocity in the pure metals decreases. After the introduction of impurity atoms, this dependence is reversed: the dislocation velocity increases gradually with temperature.

Molecular Dynamics Simulation of the Edge Dislocation Glide in Nickel and Silver in the Presence of Interstitial Light Element Atoms

The edge dislocation glide velocity in fcc metals (nickel, silver) is studied at various temperatures, tangential stresses, and contents of interstitial atoms of light elements (carbon, nitrogen, oxygen) by molecular dynamics simulation. The glide velocity of partial dislocations in pure metals decreases with increasing temperature at low tangential stresses (~10 MPa) and increases at relatively high tangential stresses (~102 MPa or higher). The introduction of interstitial atoms retards dislocation glide. This effect is more pronounced in nickel than in silver, which is mainly due to the difference in the lattice parameters: the lattice parameter of nickel is smaller than that of silver.

Impact of Regulatory Light Chain Mutation (K104E) on the Atpase and Motor Properties of Human Cardiac Myosin

Mutations in the cardiac myosin heavy chain (MYH7) as well as the essential (MYL3) and regulatory (MYL2) light chains are known to lead to cardiomyopathies with variable phenotypes, including hypertrophic (HCM) and dilated (DCM) cardiomyopathy. We investigated the impact of the HCM-associated regulatory light chain (RLC) mutation (K104E) on myosin ATPase kinetics and in vitro motility. We expressed and purified human cardiac myosin subfragment 1 (M2B-S1) and exchanged on the human ventricular RLC, with the mutant or WT RLC. A mouse model of K104E was found to cause cardiac hypertrophy, fibrosis, and diastolic dysfunction in older animals suggesting a slow development of HCM, while variable penetrance of the mutation in human populations suggest the impact of K104E may be subtle. We found that maximum actin-activated ATPase activity and the actin-dependence of ATPase were similar in K104E and WT. Actin gliding velocities in the in vitro motility assay were slightly increased in K104E. We found that the ADP release rate constant in the presence of actin also was slightly increased in K104E compared to WT. Our results suggest that HCM-associated RLC mutations may only have a minor impact on unloaded ATPase kinetics and in vitro actin gliding, which may suggest other factors could be altered by the mutation such as mechanical load and myosin regulation. Future experiments will address the impact of the mutation in mouse cardiac vs. human cardiac myosin as well as the impact of the mutation on load-dependent motility and the off state (super-relaxed state) of cardiac myosin.

Glide of C-core partial dislocations along edges of expanding double-Shockley stacking faults in heavily nitrogen-doped 4H-SiC

The glide of C-core partial dislocations (PDs) that enclose double-Shockley stacking faults (DSFs) expanding in heavily nitrogen-doped 4H-SiC crystals was studied experimentally. We successively annealed a heavily doped SiC crystal with a nitrogen concentration of 4.9 × 1019 cm−3, and the DSF expansion during high-temperature annealing was investigated with photoluminescence (PL) imaging and synchrotron X-ray topography techniques. The glide velocities of 90° and 30° C-core PDs for DSF expansion in the temperature ranges of 600 °C–725 °C and 975 °C–1150 °C, respectively, were evaluated by collating the PL and synchrotron X-ray topography images. Finally, the activation energies and pre-exponential factors for the gliding of the C-core PDs were obtained from the temperature dependences of the dislocation velocities.

Max-Range Glides in Engine Cutoff Emergencies Under Severe Wind

Engine cutoff is a recurring emergency in general aviation. It may be caused by an engine malfunction, fuel leak, or improper aircraft maintenance. Such an event, coupled with adverse weather, may endanger passengers and crew. This work obtains max-range optimal trajectories that exploit to the utmost the airframe dynamic capability, accounting for intense in-plane and crosswinds. This study proves that the optimal trajectory in terms of minimal altitude loss must maintain constant heading and velocity. A novel equation for the optimal glide velocity is then derived, whose unique solution depends only on the aircraft’s optimal velocity in still air and the wind vector. An explicit analytical expression is obtained for the optimal velocity in strict crosswinds. The results are demonstrated by applying them to the Cessna 172 airframe, in realistic engine cutoff scenarios, and it is shown that using these results can significantly increase the maximal glide range in scenarios combining strong crosswinds and in-plane winds. This paper formulates a range-maximization algorithm that yields the reachability envelope, the optimal landing site, and flight instructions that enable the pilot to follow the optimal path. These results can also enhance the common charts in glider manuals to account for non-negligible crosswinds.

A Brownian Ratchet Model Explains the Biased Sidestepping of Single-Headed Kinesin-3 KIF1A

The kinesin-3 motor KIF1A is involved in long-ranged axonal transport in neurons. To ensure vesicular delivery, motors need to navigate the microtubule lattice and overcome possible roadblocks along the way. The single-headed form of KIF1A is a highly diffusive motor that has been shown to be a prototype of a Brownian motor by virtue of a weakly bound diffusive state to the microtubule. Recently, groups of single-headed KIF1A motors were found to be able to sidestep along the microtubule lattice, creating left-handed helical membrane tubes when pulling on giant unilamellar vesicles in vitro. A possible hypothesis is that the diffusive state enables the motor to explore the microtubule lattice and switch protofilaments, leading to a left-handed helical motion. Here, we study the longitudinal rotation of microtubules driven by single-headed KIF1A motors using fluorescence-interference contrast microscopy. We find an average rotational pitch of ≃1.5μm, which is remarkably robust to changes in the gliding velocity, ATP concentration, microtubule length, and motor density. Our experimental results are compared to stochastic simulations of Brownian motors moving on a two-dimensional continuum ratchet potential, which quantitatively agree with the fluorescence-interference contrast experiments. We find that single-headed KIF1A sidestepping can be explained as a consequence of the intrinsic handedness and polarity of the microtubule lattice in combination with the diffusive mechanochemical cycle of the motor.

High-rate dislocation motion in stable nanocrystalline metals

Abstract

The Transition from Static to Dynamic Boundary Friction of a Lubricated Spreading and a Non-Spreading Adhesive Contact by Macroscopic Oscillatory Tribometry

Lubricated poly(ether ether ketone) (PEEK) and polyamide (PA46)–steel tribosystems were investigated. They show a complex but systematic transition behavior from static to boundary friction, to dynamic friction or to mixed-lubrication. Nonstandard macroscopic oscillatory tribometry as well as gliding experiments were carried out. A previous study showed that the surface and interfacial energies of PEEK, lubricant and steel can indicate trends in the tribological behavior. In the current study, these findings are confirmed for PA46 and a wider range of lubricants. It was shown that a reversal of the order of the work of spreading of two lubricants by switching from PEEK to PA46 as polymer component in the tribological system also resulted in a reversal of the coefficient of friction (COF) at low gliding velocities for these systems. The adhesion threshold of PA46 with the non-spreading lubricants water, glycerine, a water–glycerine mixture, ethylene glycol and poly-1-decene decreased with increasing solving tendency of the lubricants in contrast to the previous results for spreading lubricants for PEEK. Furthermore, the onset of forced wetting was studied for lubricants with different surface and interfacial energies and viscosities η. In general, a 1/η dependency was observed for the velocity which marks the onset of forced wetting. This agrees with theoretical models.

Activation of mammalian cytoplasmic dynein in multimotor motility assays

Long-range intracellular transport is facilitated by motor proteins, such as kinesin-1 and cytoplasmic dynein, moving along microtubules (MTs). These motors often work in teams for the transport of various intracellular cargos. Although transport by multiple kinesin-1 motors has been studied extensively in the past, collective effects of cytoplasmic dynein are less well understood. On the level of single molecules, mammalian cytoplasmic dynein is not active in the absence of dynactin and adaptor proteins. However, when assembled into a team bound to the same cargo, processive motility has been observed. The underlying mechanism of this activation is not known. Here, we found that in MT gliding motility assays the gliding velocity increased with dynein surface density and MT length. Developing a mathematical model based on single-molecule parameters, we were able to simulate the observed behavior. Integral to our model is the usage of an activation term, which describes a mechanical activation of individual dynein motors when being stretched by other motors. We hypothesize that this activation is similar to the activation of single dynein motors by dynactin and adaptor proteins.This article has an associated First Person interview with the first author of the paper.

Uncured PDMS inhibits myosin in vitro motility in a microfluidic flow cell

The myosin motor powers cardiac contraction and is frequently implicated in hereditary heart disease by its mutation. Principal motor function characteristics include myosin unitary step size, duty cycle, and force-velocity relationship for translating actin under load. These characteristics are sometimes measured in vitro with a motility assay detecting fluorescent labeled actin filament gliding velocity over a planar array of surface immobilized myosin. Assay miniaturization in a polydimethylsiloxane/glass (PDMS/glass) hybrid microfluidic flow channel is an essential component to a small sample volume assay applicable to costly protein samples however the PDMS substrate dramatically inhibits myosin motility. Myosin in vitro motility in a PDMS/glass hybrid microfluidic flow cell was tested under a variety of conditions to identify and mitigate the effect of PDMS on myosin. Substantial contamination by unpolymerized species in the PDMS flow cells is shown to be the cause of myosin motility inhibition. Normal myosin motility recovers by either extended cell aging (~20 days) to allow more complete polymerization or by direct chemical extraction of the unpolymerized species from the polymer substrate. PDMS flow cell aging is the low cost alternative compatible with the other PDMS and glass modifications needed for in vitro myosin motility assaying.

Physical Modeling for the Gradual Change of Pitch Angle of Underwater Glider in Sea Trial

A gradual change of the pitch angle was observed for a glider in a sea trial in August 2014. It took place when the glider moved in both upward and downward glides between the sea surface and a depth of 1200 m and there was neither any internal mass movement nor buoyancy engine regulation in the steady glide. In this paper, this phenomenon is validated via a nonlinear dynamic model, which is restricted to the vertical plane. The model is based on Kirchhoff's equations of motion for a submerged rigid body and takes the seawater pressure, temperature, and density, and the deformation of the pressure hull of the glider into consideration. While the variations of aforementioned four parameters influence many physical parameters, including added mass, buoyancy, center of buoyancy (CB), hydrodynamic forces, and torques, their effects on glide velocity appear to be the primary cause for the gradual change of pitch angle observed. To minimize the gradual change of pitch angle, two effective approaches are proposed and validated, namely increasing the lift/drag ratio and decreasing the hydrodynamic torque coefficients.