Shape sensing of miniature snake-like robots using optical fibers

Snake like continuum robots are increasingly used for minimally invasive surgery. Most robotic devices of this sort that have been reported to date are controlled in an open loop manner. Using shape sensing to provide closed loop feedback would allow for more accurate control of the robot's position and, hence, more precise surgery. Fiber Bragg Gratings, magnetic sensors and optical reflectance sensors have all been reported for this purpose but are often limited by their cost, size, stiffness or complexity of fabrication. To address this issue, we designed, manufactured and tested a prototype two-link robot with a built-in fiber-optic shape sensor that can deliver and control the position of a CO 2 -laser fiber for soft tissue ablation. The shape sensing is based on optical reflectance, and the device (which has a 4 mm outer diameter) is fabricated using 3D printing. Here we present proof-of-concept results demonstrating successful shape sensing - i.e. measurement of the angular displacement of the upper link of the robot relative to the lower link - in real time with a mean measurement error of only 0.7°

Operational benefits from the terminal configured vehicle

The NASA Terminal Configured Vehicle is a flying laboratory used to conduct research and development on improved airborne systems (including avionics) and operational flight procedures, with particular emphasis on utilization in the terminal area environment. The objectives of this technology development activity, focused on conventional transport aircraft, are to develop and demonstrate improvements which can lead to increased airport and runway capacity, increased air traffic controller productivity, energy efficient terminal area operations, reduced weather minima with safety, and reduced community noise by use of appropriate procedures. This paper discusses some early results of this activity in addition to defining present efforts and future research plans

Boundary layer simulator improvement

Boundary Layer Integral Matrix Procedure (BLIMPJ) has been identified by the propulsion community as the rigorous boundary layer program in connection with the existing JANNAF reference programs. The improvements made to BLIMPJ and described herein have potential applications in the design of the future Orbit Transfer Vehicle engines. The turbulence model is validated to include the effects of wall roughness and a way is devised to treat multiple smooth-rough surfaces. A prediction of relaminarization regions is examined as is the combined effects of wall cooling and surface roughness on relaminarization. A turbulence model to represent the effects of constant condensed phase loading is given. A procedure is described for thrust decrement calculation in thick boundary layers by coupling the T-D Kinetics Program and BLIMPJ and a way is provided for thrust loss optimization. Potential experimental studies in rocket nozzles are identified along with the required instrumentation to provide accurate measurements in support of the presented new analytical models

Resistivity of non-crystalline carbon in the 1-100eV range

A resistivity model for non-crystalline, solid-density carbon and hydrocarbons is presented for such materials heated by short-pulse, ultra-intense lasers. Electron-impact excitation of C atoms and ions was included in this model,and calculation of resistivity curves with and without accounting for excitations indicates that excitations contribute >50% of the resistivity in the 3–20 eV range. This implies that electron-impact excitations make a similar contribution to electron-ion scattering, and thus models not accounting for electron-impact excitation may underestimate the resistivity of dense plasmas in this temperature range

Resistivity of non-crystalline carbon in the 1-100eV range

A resistivity model for non-crystalline, solid-density carbon and hydrocarbons is presented for such materials heated by short-pulse, ultra-intense lasers. Electron-impact excitation of C atoms and ions was included in this model,and calculation of resistivity curves with and without accounting for excitations indicates that excitations contribute >50% of the resistivity in the 3–20 eV range. This implies that electron-impact excitations make a similar contribution to electron-ion scattering, and thus models not accounting for electron-impact excitation may underestimate the resistivity of dense plasmas in this temperature range

Aldosterone signaling through transient receptor potential melastatin 7 cation channel (TRPM7) and its α-kinase domain

We demonstrated a role for the Mg2 + transporter TRPM7, a bifunctional protein with channel and α-kinase domains, in aldosterone signaling. Molecular mechanisms underlying this are elusive. Here we investigated the function of TRPM7 and its α-kinase domain on Mg2 + and pro-inflammatory signaling by aldosterone. Kidney cells (HEK-293) expressing wild-type human TRPM7 (WThTRPM7) or constructs in which the α-kinase domain was deleted (ΔKinase) or rendered inactive with a point mutation in the ATP binding site of the α-kinase domain (K1648R) were studied. Aldosterone rapidly increased [Mg2 +]i and stimulated NADPH oxidase-derived generation of reactive oxygen species (ROS) in WT hTRPM7 and TRPM7 kinase dead mutant cells. Translocation of annexin-1 and calpain-II and spectrin cleavage (calpain target) were increased by aldosterone in WT hTRPM7 cells but not in α-kinase-deficient cells. Aldosterone stimulated phosphorylation of MAP kinases and increased expression of pro-inflammatory mediators ICAM-1, Cox-2 and PAI-1 in Δkinase and K1648R cells, effects that were inhibited by eplerenone (mineralocorticoid receptor (MR) blocker). 2-APB, a TRPM7 channel inhibitor, abrogated aldosterone-induced Mg2 + responses in WT hTRPM7 and mutant cells. In 2-APB-treated ΔKinase and K1648R cells, aldosterone-stimulated inflammatory responses were unchanged. These data indicate that aldosterone stimulates Mg2 + influx and ROS production in a TRPM7-sensitive, kinase-insensitive manner, whereas activation of annexin-1 requires the TRPM7 kinase domain. Moreover TRPM7 α-kinase modulates inflammatory signaling by aldosterone in a TRPM7 channel/Mg2 +-independent manner. Our findings identify novel mechanisms for non-genomic actions of aldosterone involving differential signaling through MR-activated TRPM7 channel and α-kinase

A Direct Elliptic Solver Based on Hierarchically Low-rank Schur Complements

A parallel fast direct solver for rank-compressible block tridiagonal linear systems is presented. Algorithmic synergies between Cyclic Reduction and Hierarchical matrix arithmetic operations result in a solver with $O(N \log^2 N)$ arithmetic complexity and $O(N \log N)$ memory footprint. We provide a baseline for performance and applicability by comparing with well known implementations of the $\mathcal{H}$-LU factorization and algebraic multigrid with a parallel implementation that leverages the concurrency features of the method. Numerical experiments reveal that this method is comparable with other fast direct solvers based on Hierarchical Matrices such as $\mathcal{H}$-LU and that it can tackle problems where algebraic multigrid fails to converge

Phosphoinositide 3-kinase-dependent membrane recruitment of p62(dok) is essential for its negative effect on mitogen-activated protein (MAP) kinase activation

A major pathway by which growth factors, such as platelet-derived growth factor (PDGF), regulate cell proliferation is via the receptor tyrosine kinase/Ras/niitogen-activated protein kinase (MAPK) signaling cascade. The output of this pathway is subjected to tight regulation of both positive and negative regulators. One such regulator is p62(dok), the prototype of a newly identified family of adaptor proteins. We recently provided evidence, through the use of p62(dok)-deficient cells, that p62(dok) acts as a negative regulator of growth factor-induced cell proliferation and the Ras/MAPK pathway. We show here that reintroduction of p62(dok) into P62(dok-/-) cells can suppress the increased cell proliferation and prolonged MAPK activity seen in these cells, and that plasma membrane recruitment of p62(dok) is essential for its function. We also show that the PDGF-triggered plasma membrane translocation of p62(dok) requires activation of phosphoinositide 3-kinase (PI3-kinase) and binding of its pleckstrin homology (PH) domain to 3 ' -phosphorylated phosphomositides. Furthermore, we demonstrate that p62(dok) can exert its negative effect on the PDGFR/MAPK pathway independently of its ability to associate with RasGAP and Nck. We conclude that p62(dok) functions as a negative regulator of the PDGFR/Ras/MAPK signaling pathway through a mechanism involving P13-kinase-dependent recruitment of p62(dok) to the plasma membrane