High Sensitivity Search for v_e’s from the Sun and Other Sources at KamLAND

Data corresponding to a KamLAND detector exposure of 0.28 kton yr has been used to search for ν̅ _e’s in the energy range 8.3 < E_(ν̅e) < 14.8  MeV. No candidates were found for an expected background of 1.1±0.4 events. This result can be used to obtain a limit on ν̅_e fluxes of any origin. Assuming that all ν̅_e flux has its origin in the Sun and has the characteristic ^8B solar ν_e energy spectrum, we obtain an upper limit of 3.7×10^2  cm^(-2) ^(s-1) (90% C.L.) on the ν̅_e flux. We interpret this limit, corresponding to 2.8×10^(-4) of the standard solar model ^8B ν_e flux, in the framework of spin-flavor precession and neutrino decay models

Response maxima in time-modulated turbulence: Direct Numerical Simulations

The response of turbulent flow to time-modulated forcing is studied by direct numerical simulations of the Navier-Stokes equations. The large-scale forcing is modulated via periodic energy input variations at frequency $\omega$. The response is maximal for frequencies in the range of the inverse of the large eddy turnover time, confirming the mean-field predictions of von der Heydt, Grossmann and Lohse (Phys. Rev. E 67, 046308 (2003)). In accordance with the theory the response maximum shows only a small dependence on the Reynolds number and is also quite insensitive to the particular flow-quantity that is monitored, e.g., kinetic energy, dissipation-rate, or Taylor-Reynolds number. At sufficiently high frequencies the amplitude of the kinetic energy response decreases as $1/\omega$. For frequencies beyond the range of maximal response, a significant change in phase-shift relative to the time-modulated forcing is observed.Comment: submitted to Europhysics Letters (EPL), 8 pages, 8 Postscript figures, uses epl.cl

The Ingestion of 39 or 64 g·h-1 of Carbohydrate is Equally Effective at Improving Endurance Exercise Performance in Cyclists

In an investigator-blind, randomized cross-over design, male cyclists (mean± SD) age 34.0 (± 10.2) years, body mass 74.6 (±7.9) kg, stature 178.3 (±8.0) cm, peak power output (PPO) 393 (±36) W, and VO2max 62 (±9) ml·kg-1·min(-1) training for more than 6 hr/wk for more than 3y (n = 20) completed four experimental trials. Each trial consisted of a 2-hr constant load ride at 95% of lactate threshold (185 ± 25 W) then a work-matched time trial task (~30 min at 70% of PPO). Three commercially available carbohydrate (CHO) beverages, plus a control (water), were administered during the 2-hr ride providing 0, 20, 39, or 64 g·hr-1 of CHO at a fluid intake rate of 1L·hr(-1). Performance was assessed by time to complete the time trial task, mean power output sustained, and pacing strategy used. Mean task completion time (min:sec ± SD) for 39 g·hr(-1) (34:19.5 ± 03:07.1, p = .006) and 64 g·hr(-1) (34:11.3 ± 03:08.5 p = .004) of CHO were significantly faster than control (37:01.9 ± 05:35.0). The mean percentage improvement from control was -6.1% (95% CI: -11.3 to -1.0) and -6.5% (95% CI: -11.7 to -1.4) in the 39 and 64 g·hr(-1) trials respectively. The 20 g·hr(-1) (35:17.6 ± 04:16.3) treatment did not reach statistical significance compared with control (p = .126) despite a mean improvement of -3.7% (95% CI -8.8-1.5%). No further differences between CHO trials were reported. No interaction between CHO dose and pacing strategy occurred. 39 and 64 g·hr-1 of CHO were similarly effective at improving endurance cycling performance compared with a 0 g·hr(-1) control in our trained cyclists

The effects of 10 days of separate heat and hypoxic exposure on heat acclimation and temperate exercise performance

Adaptations to heat and hypoxia are typically studied in isolation but are often encountered in combination. Whether the adaptive response to multiple stressors affords the same response as when examined in isolation is unclear. We examined 1) the influence of overnight moderate normobaric hypoxia on the time course and magnitude of adaptation to daily heat exposure and 2) whether heat acclimation (HA) was ergogenic and whether this was influenced by an additional hypoxic stimulus. Eight males [V̇o2max = 58.5 (8.3) ml·kg-1·min-1] undertook two 11-day HA programs (balanced-crossover design), once with overnight normobaric hypoxia (HAHyp): 8 (1) h per night for 10 nights [[Formula: see text] = 0.156; SpO2 = 91 (2)%] and once without (HACon). Days 1, 6, and 11 were exercise-heat stress tests [HST (40°C, 50% relative humidity, RH)]; days 2-5 and 7-10 were isothermal strain [target rectal temperature (Tre) ~38.5°C], exercise-heat sessions. A graded exercise test and 30-min cycle trial were undertaken pre-, post-, and 14 days after HA in temperate normoxia (22°C, 55% RH; FIO2 = 0.209). HA was evident on day 6 (e.g., reduced Tre, mean skin temperature (T̄sk), heart rate, and sweat [Na+], P < 0.05) with additional adaptations on day 11 (further reduced T̄sk and heart rate). HA increased plasma volume [+5.9 (7.3)%] and erythropoietin concentration [+1.8 (2.4) mIU/ml]; total hemoglobin mass was unchanged. Peak power output [+12 (20) W], lactate threshold [+15 (18) W] and work done [+12 (20) kJ] increased following HA. The additional hypoxic stressor did not affect these adaptations. In conclusion, a separate moderate overnight normobaric hypoxic stimulus does not affect the time course or magnitude of HA. Performance may be improved in temperate normoxia following HA, but this is unaffected by an additional hypoxic stressor

Prolonged anxiety on habituation of the cold shock response

Variation in the cold shock response (CSR) can be explained by physiological factors, habituation; and possibly "psychological" influences. Acute anxiety on cold-water immersion (CWI) increases the magnitude of the CSR in unhabituated volunteers and eliminates the reduction in the response seen after habituation. Recently it was demonstrated that habituation of the CSR includes a significant perceptual component. When the threat of CWI scenario was reduced, anxiety associated with being immersed was also reduced. In contrast, prolonged anxiety during repeat CWIs may prevent habituation. Therefore, it was hypothesized that prolonged anxiety reduces the extent of CSR habituation

Investigation of the Building M6-794 Roofing Fatality, Type A Mishap

The Building M6-794 Roofing Fatality Mishap Investigation Board (Board) was commissioned to gather information; analyze the facts; identify the proximate causes, root causes, and contributing factors relating to the mishap; and recommend appropriate actions to prevent a similar mishap from occurring in the future. During the investigation of this mishap, the Board also examined the fall protection policies of other NASA Centers and operating locations to gain an understanding of how those entities conduct fall protection, as well as the degree to which fall protection is standardized across the Agency

A proposed measurement of the ß asymmetry in neutron decay with the Los Alamos Ultra-Cold Neutron Source

This article reviews the status of an experiment to study the neutron spin-electron angular correlation with the Los Alamos Ultra-Cold Neutron (UCN) source. The experiment will generate UCNs from a novel solid deuterium, spallation source, and polarize them in a solenoid magnetic field. The experiment spectrometer will consist of a neutron decay region in a solenoid magnetic field combined with several different detector possibilities. An electron beam and a magnetic spectrometer will provide a precise, absolute calibration for these detectors. An A-correlation measurement with a relative precision of 0.2% is expected by the end of 2002

Tetraspanin (TSP-17) Protects Dopaminergic Neurons against 6-OHDA-Induced Neurodegeneration in <i>C. elegans</i>

Parkinson's disease (PD), the second most prevalent neurodegenerative disease after Alzheimer's disease, is linked to the gradual loss of dopaminergic neurons in the substantia nigra. Disease loci causing hereditary forms of PD are known, but most cases are attributable to a combination of genetic and environmental risk factors. Increased incidence of PD is associated with rural living and pesticide exposure, and dopaminergic neurodegeneration can be triggered by neurotoxins such as 6-hydroxydopamine (6-OHDA). In C. elegans, this drug is taken up by the presynaptic dopamine reuptake transporter (DAT-1) and causes selective death of the eight dopaminergic neurons of the adult hermaphrodite. Using a forward genetic approach to find genes that protect against 6-OHDA-mediated neurodegeneration, we identified tsp-17, which encodes a member of the tetraspanin family of membrane proteins. We show that TSP-17 is expressed in dopaminergic neurons and provide genetic, pharmacological and biochemical evidence that it inhibits DAT-1, thus leading to increased 6-OHDA uptake in tsp-17 loss-of-function mutants. TSP-17 also protects against toxicity conferred by excessive intracellular dopamine. We provide genetic and biochemical evidence that TSP-17 acts partly via the DOP-2 dopamine receptor to negatively regulate DAT-1. tsp-17 mutants also have subtle behavioral phenotypes, some of which are conferred by aberrant dopamine signaling. Incubating mutant worms in liquid medium leads to swimming-induced paralysis. In the L1 larval stage, this phenotype is linked to lethality and cannot be rescued by a dop-3 null mutant. In contrast, mild paralysis occurring in the L4 larval stage is suppressed by dop-3, suggesting defects in dopaminergic signaling. In summary, we show that TSP-17 protects against neurodegeneration and has a role in modulating behaviors linked to dopamine signaling