Calibration of PCB-132 Sensors in a Shock Tube

While PCB-132 sensors have proven useful for measuring second-mode instability waves in many hypersonic wind tunnels, they are currently limited by their calibration. Until now, the factory calibration has been all that was available, which is a single-point calibration at an amplitude three orders of magnitude higher than a second-mode wave. In addition, little information has been available about the frequency response or spatial resolution of the sensors, which is important for measuring high-frequency instability waves. These shortcomings make it difficult to compare measurements at different conditions and between different sensors. If accurate quantitative measurements could be performed, comparisons of the growth and breakdown of instability waves could be made in different facilities, possibly leading to a method of predicting the amplitude at which the waves break down into turbulence, improving transition prediction. A method for calibrating the sensors is proposed using a newly-built shock tube at Purdue University. This shock tube, essentially a half-scale version of the 6-Inch shock tube at the Graduate Aerospace Laboratories at Caltech, has been designed to attain a moderate vacuum in the driven section. Low driven pressures should allow the creation of very weak, yet still relatively thin shock waves. It is expected that static pressure rises within the range of second-mode amplitudes should be possible. The shock tube has been designed to create clean, planar shock waves with a laminar boundary layer to allow for accurate calibrations. Stronger shock waves can be used to identify the frequency response of the sensors out to hundreds of kilohertz

Constraints Imposed by the Shape of Marine Magnetic Anomalies on the Magnetic Source

A two-layer source model for marine magnetic anomalies can accommodate several observations made on the shapes of anomalies in the Pacific and southeast Indian oceans. The layers are defined on the basis of cooling history and magnetic properties. The upper layer consists of rapidly cooled basalts, which acquire a strong magnetization near the ridge axis. This layer, with narrow transition zones, can account for the observed short polarity events. The lower layer consists of moderately magnetized, slowly cooled intrusive rocks in the lower oceanic crust. The transition zones in this layer are broad, sloping boundaries reflecting the delayed acquisition of magnetization with depth as, for example, along a sloping Curie point isotherm. The lower layer can account for a skewness discrepancy of 10°-15° in the observed skewness of some anomalies. It is shown that the upper layer has to contribute about three quarters of the total amplitude of magnetic anomalies in order for this model to simulate the observed shape of the anomalies. The model predicts that a deep drill hole located just to the older side of a reversal boundary in the upper part of the oceanic crust should encounter a magnetization polarity reversal within the lower oceanic crust

Ultrahigh Resolution Marine Magnetic Anomaly Profiles: A Record of Continuous Paleointensity Variations?

A distinctive pattern of small-scale marine magnetic anomalies (25-100 nT amplitude, 8-25 km wavelength: tiny wiggles) is superimposed on the more generally recognized seafloor spreading pattern between anomalies 24 and 27 in the Indian Ocean. By normalizing and stacking multiple profiles, it is demonstrated that this pattern of tiny wiggles is a high-resolution recording of paleodipole field behavior between chrons C24 and C27. The pattern of tiny wiggles between anomalies 26 and 27 is compared to an ultrafast spreading (82 mm/yr half rate) profile from the southeast Pacific where a similar signal is observed, confirming the paleodipole field origin of the anomalies. Two basic models are considered in which the tiny wiggles are attributed either to short polarity intervals or to paleointensity fluctuations. We conclude that tiny wiggles are most likely caused by paleointensity fluctuations of the dipole field and are a ubiquitous background signal to most fast spreading magnetic profiles. The implications of this study are that (1) tiny wiggles may provide information on the temporal evolution of the geomagnetic dynamo; (2) the small-scale anomalies observed in the Jurassic quiet zones may be due to paleointensity fluctuations; (3) tiny wiggles are potential time markers in large regions of uniform crustal polarity such as the Cretaceous quiet zones; and (4) much of the variance in anomaly profiles normally attributed to crustal emplacement processes, particularly at fast and ultrafast spreading rates, is actually due to intensity variations in the paleomagnetic field

A New Geomagnetic Polarity Time Scale for the Late Cretaceous and Cenozoic

We have constructed a magnetic polarity time scale for the Late Cretaceous and Cenozoic based on an analysis of marine magnetic profiles from the world's ocean basins. This is the first time, since Heirtzler et al. (1968) published their time scale, that the relative widths of the magnetic polarity intervals for the entire Late Cretaceous and Cenozoic have been systematically determined from magnetic profiles. A composite geomagnetic polarity sequence was derived based primarily on data from the South Atlantic. Anomaly spacings in the South Atlantic were constrained by a combination of finite rotation poles and averages of stacked profiles. Fine-scale information was derived from magnetic profiles on faster spreading ridges in the Pacific and Indian Oceans and inserted into the South Atlantic sequence. Based on the assumption that spreading rates in the South Atlantic were smoothly varying but not necessarily constant, a time scale was generated by using a spline function to fit a set of nine age calibration points plus the zero-age ridge axis to the composite polarity sequence. The derived spreading history of the South Atlantic shows a regular variation in spreading rate, decreasing in the Late Cretaceous from a high of almost 70 mm/yr (full rate) at around anomaly 33-34 time to a low of about 30 mm/yr by anomaly 27 time in the early Paleocene, increasing to about 55 mm/yr by about anomaly 15 time in the late Eocene, and then gradually decreasing over the Oligocene and the Neogene to the recent rate of about 32 mm/yr. The new time scale has several significant differences from previous time scales. For example, chron C5n is ~0.5 m.y. older and chrons C9 through C24 are 2-3 m.y. younger than in the chronologies of Berggren et al. (1985b) and Harland et al. (1990). Additional small-scale anomalies (tiny wiggles) that represent either very short polarity intervals or intensity fluctuations of the dipole field have been identified from several intervals in the Cenozoic including a large number of tiny wiggles between anomalies 24 and 27. Spreading rates on several other ridges, including the Southeast Indian Ridge, the East Pacific Rise, the Pacific-Antarctic Ridge, the Chile Ridge, the North Pacific, and the Central Atlantic, were analyzed in order to evaluate the accuracy of the new time scale. Globally synchronous variations in spreading rate that were previously observed around anomalies 20, 6C, and in the late Neogene have been eliminated. The new time scale helps to resolve events at the times of major plate reorganizations. For example, anomaly 3A (5.6 Ma) is now seen to be a time of sudden spreading rate changes in the Southeast Indian, Pacific-Antarctic, and Chile ridges and may correspond to the time of the change in Pacific absolute plate motion proposed by others. Spreading rates in the North Pacific became increasingly irregular in the Oligocene, culminating in a precipitous drop at anomaly 6C time

Peak rates of diuresis in healthy humans during oral fluid overload

Objective. To determine whether rates of intestinal fluid absorption and renal diuresis can match high rates of fluid ingestion in healthy humans exposed to oral fluid overload, thereby preventing the development of hyponatraemia either by reverse sodium movement across the intestine (the Priestley-Haldane effect) or by expansion of the extracellular fluid volume.Methods. Changes in renal function and in plasma chemical measurements in response to an oral fluid overload (0.9 - 1.8 1/ h x 3 h) were investigated in 6 healthy control subjects at rest, and in a subject with a history of exercise induced symptomatic hyponatraemia, during both prolonged (160-minute) exercise and at rest.Findings. All control subjects gained weight (2.7 ± 0.2 kg, mean ± standard error of mean (SEM)) because the rate of oral fluid intake exceeded the peak rate of urine production (778 ± 39 rnl / h). Blood volume rose by 7.1 (± 0.5)% and plasma sodium concentrations fell progressively from 144 ± 2.6 to 136 ± 1.1 mmol/ 1 (P < 0.05) in the control subjects. Plasma potassium and angiotensin II concentrations were unchanged and creatinine clearance was normal ( -125 rnl/min). Free water clearance reached a maximum of 11.2 ± 0.9 rnl/min after 2 hours. The increase in body mass could be accounted for by calculated or measured changes in extra- and intracellular fluid volumes. Similar changes were measured in the subject with a previous history of symptomatic hyponatraernia.Conclusion. The rate of intestinal fluid absorption appeared to match the rate of oral fluid ingestion and there was no  evidence of fluid accumulation in the intestine with reverse sodium movement from the extracellular space into intestinal fluid. The results of this study are therefore at variance with the Priestley-Haldane hypothesis and suggest that reverse sodium movement did not contribute to the hyponatraernia induced by oral fluid overload in these subjects. Rather it appears that humans may have a limited capacity to excrete fluid at rates in excess of -900 rnl/ h in response to higher rates of oral fluid intake. When the rate of intestinal fluid absorption matches the rate of fluid ingestion and exceeds the kidneys' maximum capacity for fluid excretion, the excess fluid accumulates in the extra- and intracellular fluid compartments, inducing the dilutional hyponatraemia of water intoxication. These findings may have relevance to other clinical conditions in which hyponatraemia develops in response to high rates of oral or intravenous fluid provision

Effects of pressure on spin fluctuations and the exchange interaction in La2CuO4 as determined by two‐magnon Raman scattering (abstract)

We have measured the two‐magnon Raman scattering spectrum of magnetic La2CuO4 at pressures of up to 100 kbar. Analysis of the moments of the two‐magnon line shape indicates that the renormalization parameters resulting from spin fluctuations are essentially pressure independent in this pressure range. Our results provide the first direct determination of the pressure dependence of the in‐plane exchange coupling constant J. The pressure dependence of J is compared with that of the Néel temperature and discussed in the context of recent theories for quasi‐two‐dimensional magnetic systems.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/71024/2/JAPIAU-69-8-5392-1.pd

Control and Non-Payload Communications (CNPC) Prototype Radio Validation Flight Test Report

This report provides an overview and results from the unmanned aircraft (UA) Control and Non-Payload Communications (CNPC) Generation 5 prototype radio validation flight test campaign. The radios used in the test campaign were developed under cooperative agreement NNC11AA01A between the NASA Glenn Research Center and Rockwell Collins, Inc., of Cedar Rapids, Iowa. Measurement results are presented for flight tests over hilly terrain, open water, and urban landscape, utilizing radio sets installed into a NASA aircraft and ground stations. Signal strength and frame loss measurement data are analyzed relative to time and aircraft position, specifically addressing the impact of line-of-sight terrain obstructions on CNPC data flow. Both the radio and flight test system are described

Cell-Autonomous Death of Cerebellar Purkinje Neurons with Autophagy in Niemann-Pick Type C Disease

Niemann-Pick type C is a neurodegenerative lysosomal storage disorder caused by mutations in either of two genes, npc1 and npc2. Cells lacking Npc1, which is a transmembrane protein related to the Hedgehog receptor Patched, or Npc2, which is a secreted cholesterol-binding protein, have aberrant organelle trafficking and accumulate large quantities of cholesterol and other lipids. Though the Npc proteins are produced by all cells, cerebellar Purkinje neurons are especially sensitive to loss of Npc function. Since Niemann-Pick type C disease involves circulating molecules such as sterols and steroids and a robust inflammatory response within the brain parenchyma, it is crucial to determine whether external factors affect the survival of Purkinje cells (PCs). We investigated the basis of neurodegeneration in chimeric mice that have functional npc1 in only some cells. Death of mutant npc1 cells was not prevented by neighboring wild-type cells, and wild-type PCs were not poisoned by surrounding mutant npc1 cells. PCs undergoing cell-autonomous degeneration have features consistent with autophagic cell death. Chimeric mice exhibited a remarkable delay and reduction of wasting and ataxia despite their substantial amount of mutant tissue and dying cells, revealing a robust mechanism that partially compensates for massive PC death