Manual actuator

An actuator for an exercising machine employable by a crewman aboard a manned spacecraft is presented. The actuator is characterized by a force delivery arm projected from a rotary imput shaft of an exercising machine and having a force input handle extended orthogonally from its distal end. The handle includes a hand-grip configured to be received within the palm of the crewman's hand and a grid pivotally supported for angular displacement between a first position, wherein the grid is disposed in an overlying juxtaposition with the hand-grip, and a second position, angularly displaced from the first position, for affording access to the hand-grip, and a latching mechanism fixed to the sole of a shoe worn by the crewman for latching the shoe to the grid when the grid is in the first position

Conductive elastomeric extensometer

Bridge circuit, in which conductive elastomeric material is the variable leg, precisely measures surface area changes in the human body. Circuits are used singularly, or in quantity by adding elements and amplifier circuits. Elastomeric strips can be located in a form-fitting garment

Impact of external sources of infection on the dynamics of bovine tuberculosis in modelled badger populations

Background The persistence of bovine TB (bTB) in various countries throughout the world is enhanced by the existence of wildlife hosts for the infection. In Britain and Ireland, the principal wildlife host for bTB is the badger (Meles meles). The objective of our study was to examine the dynamics of bTB in badgers in relation to both badger-derived infection from within the population and externally-derived, trickle-type, infection, such as could occur from other species or environmental sources, using a spatial stochastic simulation model. Results The presence of external sources of infection can increase mean prevalence and reduce the threshold group size for disease persistence. Above the threshold equilibrium group size of 6–8 individuals predicted by the model for bTB persistence in badgers based on internal infection alone, external sources of infection have relatively little impact on the persistence or level of disease. However, within a critical range of group sizes just below this threshold level, external infection becomes much more important in determining disease dynamics. Within this critical range, external infection increases the ratio of intra- to inter-group infections due to the greater probability of external infections entering fully-susceptible groups. The effect is to enable bTB persistence and increase bTB prevalence in badger populations which would not be able to maintain bTB based on internal infection alone. Conclusions External sources of bTB infection can contribute to the persistence of bTB in badger populations. In high-density badger populations, internal badger-derived infections occur at a sufficient rate that the additional effect of external sources in exacerbating disease is minimal. However, in lower-density populations, external sources of infection are much more important in enhancing bTB prevalence and persistence. In such circumstances, it is particularly important that control strategies to reduce bTB in badgers include efforts to minimise such external sources of infection

Surface charge algebra in gauge theories and thermodynamic integrability

Surface charges and their algebra in interacting Lagrangian gauge field theories are investigated by using techniques from the variational calculus. In the case of exact solutions and symmetries, the surface charges are interpreted as a Pfaff system. Integrability is governed by Frobenius' theorem and the charges associated with the derived symmetry algebra are shown to vanish. In the asymptotic context, we provide a generalized covariant derivation of the result that the representation of the asymptotic symmetry algebra through charges may be centrally extended. Finally, we make contact with Hamiltonian and with covariant phase space methods.Comment: 40 pages Latex file, published versio

Formation of central massive objects via tidal compression

For a density that is not too sharply peaked towards the center, the local tidal field becomes compressive in all three directions. Available gas can then collapse and form a cluster of stars in the center, including or even being dominated by a central black hole. We show that for a wide range of (deprojected) Sersic profiles in a spherical potential, the tidal forces are compressive within a region which encloses most of the corresponding light of observed nuclear clusters in both late-type and early-type galaxies. In such models, tidal forces become disruptive nearly everywhere for relatively large Sersic indices n >= 3.5. We also show that the mass of a central massive object (CMO) required to remove all radial compressive tidal forces scales linearly with the mass of the host galaxy. If CMOs formed in (progenitor) galaxies with n ~ 1, we predict a mass fraction of ~ 0.1-0.5%, consistent with observations of nuclear clusters and super-massive black holes. While we find that tidal compression possibly drives the formation of CMOs in galaxies, beyond the central regions and on larger scales in clusters disruptive tidal forces might contribute to prevent gas from cooling.Comment: 19 pages, 4 figures. Accepted for publication in ApJ. High resolution version available at http://www-obs.univ-lyon1.fr/labo/perso/eric.emsellem/preprint

Space Station Gas-Grain Simulation Facility: Microgravity Particle Research

A wide variety of experiments significant to Exobiology, Planetary Science, Astrophysics, Atmospheric Science, and basic Chemistry and Physics involves the physical interactions of small particles (micrometer to centimeter in size). In many astro-geophysical systems (atmospheric clouds, interstellar clouds, planetary rings, Titan\u27s organic aerosols, Martian dust storms, lightning, etc.), processes involving small particles determine the overall behavior of the system. Condensation of particles from a gas, aggregation of small particles into larger ones, low velocity collisions, and charge accumulation are a few of the processes that influence particles in these systems. Examples of particles undergoing these processes include interstellar grains, protoplanetary particles, atmospheric aerosols, combustion products, and abiotic organic polymers. Although processes of the type described above span a wide range of disciplines, the study of these processes places common fundamental constraints on particle handling. Two common constraints are the need for long time periods during which the particles must be suspended and low relative velocities between particles. Experiments involving small particles generally require material be suspended for periods substantially longer than are practical in Earth\u27s 1 g gravitational field. However, one can investigate these processes with a general-purpose particle research facility (in particular, with the proposed Gas-Grain Simulation Facility) on the Space Station 1 \u273 . Because of the very low gravitational acceleration (microgravity) in the Earth orbital environment, many experiments deemed impractical or impossible to perform on Earth will become feasible. Such experiments are those in which gravity either interferes directly with the phenomenon under study (e.g., gravitational convection masks diffusional processes) or in which gravity precludes the establishment of the proper experimental conditions (e.g., in 1 g, gravity accelerates test objects to unacceptable velocities)

Endogenous Nutritive Support after Traumatic Brain Injury: Peripheral Lactate Production for Glucose Supply via Gluconeogenesis.

We evaluated the hypothesis that nutritive needs of injured brains are supported by large and coordinated increases in lactate shuttling throughout the body. To that end, we used dual isotope tracer ([6,6-(2)H2]glucose, i.e., D2-glucose, and [3-(13)C]lactate) techniques involving central venous tracer infusion along with cerebral (arterial [art] and jugular bulb [JB]) blood sampling. Patients with traumatic brain injury (TBI) who had nonpenetrating head injuries (n=12, all male) were entered into the study after consent of patients' legal representatives. Written and informed consent was obtained from healthy controls (n=6, including one female). As in previous investigations, the cerebral metabolic rate (CMR) for glucose was suppressed after TBI. Near normal arterial glucose and lactate levels in patients studied 5.7±2.2 days (range of days 2-10) post-injury, however, belied a 71% increase in systemic lactate production, compared with control, that was largely cleared by greater (hepatic+renal) glucose production. After TBI, gluconeogenesis from lactate clearance accounted for 67.1% of glucose rate of appearance (Ra), which was compared with 15.2% in healthy controls. We conclude that elevations in blood glucose concentration after TBI result from a massive mobilization of lactate from corporeal glycogen reserves. This previously unrecognized mobilization of lactate subserves hepatic and renal gluconeogenesis. As such, a lactate shuttle mechanism indirectly makes substrate available for the body and its essential organs, including the brain, after trauma. In addition, when elevations in arterial lactate concentration occur after TBI, lactate shuttling may provide substrate directly to vital organs of the body, including the injured brain

Which lab tests are best when you suspect hypothyroidism?

Thyroid-stimulating hormone (TSH) level is the preferred test for initial evaluation of suspected primary hypothyroidism (strength of recommendation [SOR]: C, expert opinion). If TSH is abnormal, a free thyroxine (T4) level will further narrow the diagnosis. Obtain a triiodothyronine (T3) level if TSH is undetectable and free T4 is normal. When assessing the adequacy of replacement therapy in primary hypothyroidism, the TSH is the most important parameter to monitor (SOR: C, expert opinion). Because TSH levels can't be used to monitor central hypothyroidism, use free T4 and T3 concentrations (SOR: C, case series)

Lactate: brain fuel in human traumatic brain injury: a comparison with normal healthy control subjects.

We evaluated the hypothesis that lactate shuttling helps support the nutritive needs of injured brains. To that end, we utilized dual isotope tracer [6,6-(2)H2]glucose, that is, D2-glucose, and [3-(13)C]lactate techniques involving arm vein tracer infusion along with simultaneous cerebral (arterial [art] and jugular bulb [JB]) blood sampling. Traumatic brain injury (TBI) patients with nonpenetrating brain injuries (n=12) were entered into the study following consent of patients' legal representatives. Written and informed consent was obtained from control volunteers (n=6). Patients were studied 5.7±2.2 (mean±SD) days post-injury; during periods when arterial glucose concentration tended to be higher in TBI patients. As in previous investigations, the cerebral metabolic rate for glucose (CMRgluc, i.e., net glucose uptake) was significantly suppressed following TBI (p<0.001). However, lactate fractional extraction, an index of cerebral lactate uptake related to systemic lactate supply, approximated 11% in both healthy control subjects and TBI patients. Further, neither the CMR for lactate (CMRlac, i.e., net lactate release), nor the tracer-measured cerebral lactate uptake differed between healthy controls and TBI patients. The percentages of lactate tracer taken up and released as (13)CO2 into the JB accounted for 92% and 91% for control and TBI conditions, respectively, suggesting that most cerebral lactate uptake was oxidized following TBI. Comparisons of isotopic enrichments of lactate oxidation from infused [3-(13)C]lactate tracer and (13)C-glucose produced during hepatic and renal gluconeogenesis (GNG) showed that 75-80% of (13)CO2 released into the JB was from lactate and that the remainder was from the oxidation of glucose secondarily labeled from lactate. Hence, either directly as lactate uptake, or indirectly via GNG, peripheral lactate production accounted for ∼70% of carbohydrate (direct lactate uptake+uptake of glucose from lactate) consumed by the injured brain. Undiminished cerebral lactate fractional extraction and uptake suggest that arterial lactate supplementation may be used to compensate for decreased CMRgluc following TBI