We present new limits on an isotropic stochastic gravitational-wave background (GWB) using a six pulsar dataset spanning 18 yr of observations from the 2015 European Pulsar Timing Array data release. Performing a Bayesian analysis, we fit simultaneously for the intrinsic noise parameters for each pulsar, along with common correlated signals including clock, and Solar System ephemeris errors, obtaining a robust 95% upper limit on the dimensionless strain amplitude A of the background of A < 3.0 × 10 −15 at a reference frequency of 1yr −1 and a spectral index of 13/3, corresponding to a background from inspiralling super-massive black hole binaries, constraining the GW energy density to Ω gw ( f )h 2 < 1.1 × 10 −9 at 2.8 nHz. We also present limits on the correlated power spectrum at a series of discrete frequencies, and show that our sensitivity to a fiducial isotropic GWB is highest at a frequency of ∼ 5×10 −9 Hz. Finally we discuss the implications of our analysis for the astrophysics of supermassive black hole binaries, and present 95% upper limits on the string tension, Gµ/c 2 , characterising a background produced by a cosmic string network for a set of possible scenarios, and for a stochastic relic GWB. For a Nambu-Goto field theory cosmic string network, we set a limit Gµ/c 2 < 1.3 × 10 −7 , identical to that set by the Planck Collaboration, when combining Planck and high-Cosmic Microwave Background data from other experiments. For a stochastic relic background we set a limit of Ω relic gw ( f )h 2 < 1.2 × 10 −9 , a factor of 9 improvement over the most stringent limits previously set by a pulsar timing array. c 0000 RAS arXiv:1504.03692v3 [astro-ph.CO] 9 Sep 2015

Pressure-induced myogenic responses and flow-induced vasodilatory responses have been documented in coronary resistance arterioles, but the interaction of these two mechanisms and the nature of the flow-mediated response are not well understood. Experiments were designed to quantitatively study the interaction of pressure- and flow-induced responses and to characterize the nature of the substance responsible for flow-mediated dilation in isolated coronary arterioles. Subepicardial arterioles (40-80 microns) were isolated from pigs and cannulated with two glass micropipettes and then pressurized via independent reservoir systems. Flow was initiated by simultaneously moving the reservoirs in equal and opposite directions thus generating a pressure gradient (delta P) without changing the mean intraluminal pressure (IP). IP was changed by moving both reservoirs in the same direction to alter myogenic tone in the absence of flow (delta P = 0). Flow-mediated dilation competed with myogenic constriction when flow and pressure were elevated. Also, flow potentiated myogenic dilation when IP was decreased. The magnitude of flow-induced dilation was greatest at an intermediate level of vascular tone (IP = 60 cmH2O) but was attenuated at higher and lower levels of tone. In the presence of flow (delta P = 4 cmH2O), pressure-diameter relationships were shifted upward, and the magnitude of myogenic responsiveness was attenuated. Double-vessel bioassay studies indicated that a transferable substance was released from intact endothelium in response to flow. Flow-induced dilation was not affected by indomethacin but was abolished by NG-monomethyl-L-arginine or by mechanical removal of endothelium.(ABSTRACT TRUNCATED AT 250 WORDS)

Nitric oxide (NO) produced by the vascular endothelium is an important biologic messenger that regulates vessel tone and permeability and inhibits platelet adhesion and aggregation. NO exerts its control of vessel tone by interacting with guanylyl cyclase in the vascular smooth muscle to initiate a series of reactions that lead to vessel dilation. Previous efforts to investigate this interaction by mathematical modeling of NO diffusion and reaction have been hampered by the lack of information on the production and degradation rate of NO. We use a mathematical model and previously published experimental data to estimate the rate of NO production, 6.8 × 10−14μmol ⋅ μm−2 ⋅ s−1; the NO diffusion coefficient, 3,300 μm2s−1; and the NO consumption rate coefficient in the vascular smooth muscle, 0.01 s−1 (1st-order rate expression) or 0.05 μM−1 ⋅ s−1 (2nd-order rate expression). The modeling approach is discussed in detail. It provides a general framework for modeling the NO produced from the endothelium and for estimating relevant physical parameters.

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Preferential oxidation of CO (PROX) is an important reaction for removing small amounts of CO to a parts-per-million level from the hydrogen-rich stream, which will be ultimately supplied as a fuel to polymer−electrolyte membrane fuel cells. The key to the application of PROX is to develop a highly active and selective catalyst that operates well in a wide temperature window (e.g., 80−180°C) and has good resistance to CO 2 and steam. In the past decades, various catalyst formulations have been developed, among which platinum group metal catalysts, including Pt, Ru, and Irin particular, those modified with promoters such as alkali metals and reducible metal oxideshave received a great deal of attention for their significantly improved catalytic activities in the low-temperature range. In this minireview, the recent advances of the platinum group metal catalysts for the PROX reaction are summarized, including performances of unpromoted and promoted catalysts, reaction mechanisms, and kinetics. In addition, the important roles of hydroxyl groups in the PROX reaction are also discussed.

Flow-mediated dilation has been documented in large conduit coronary arteries but not in coronary arterioles. The goal of this study was to determine whether this response occurs in coronary arterioles and whether it competes with myogenic constriction. Subepicardial arterioles (40-80 microns) were isolated and cannulated with two glass micropipettes connected to independent reservoir systems. During zero flow, myogenic responses were studied over the range of intraluminal pressure (IP) between 20 and 140 cmH2O. Myogenic constrictions and dilations was observed when IP was increased (greater than 60 cmH2O) and decreased (less than 60 cmH2O), respectively. Flow was initiated by simultaneously moving the reservoirs in equal and opposite directions, thus generating a pressure gradient (delta P) without changing the mean luminal pressure (range delta P = 4-60 cmH2O). Flow-induced responses were studied at low, intermediate, and high myogenic tones by setting IP at 20, 60, and 100 cmH2O, respectively. The threshold for flow-induced dilation was delta P = 4 cmH2O, and maximum dilation was observed at delta P = 20 cmH2O. Red cell velocities in isolated arterioles at delta P of 4 and 60 cmH2O were 1.2 +/- 0.2 and 15.9 +/- 1.3 mm/s, respectively, which are within the range of those reported for coronary microvessels in vivo. The magnitude of the flow-induced dilation was greatest at the intermediate tone (60 cmH2O IP) but was attenuated at lower and higher IP. After mechanical removal of the endothelium, spontaneous tone and myogenic responses were preserved, but flow-induced dilation and bradykinin-induced dilation were abolished.(ABSTRACT TRUNCATED AT 250 WORDS)

Solid-state refrigeration technology based on caloric effects are promising to replace the currently used vapor compression cycles. However, their application is restricted due to limited performances of caloric materials. Here, we have identified colossal barocaloric effects (CBCEs) in a class of disordered solids called plastic crystals. The obtained entropy changes are about 380 J kg -1 K -1 in the representative neopentylglycol around room temperature. Inelastic neutron scattering reveals that the CBCEs in plastic crystals are attributed to the combination of the vast molecular orientational disorder, giant compressibility and high anharmonic lattice dynamics. Our study establishes the microscopic scenario for CBCEs in plastic crystals and paves a new route to the next-generation solid-state refrigeration technology.

Despite its well-documented importance, the mechanism for nitric oxide (NO) transport in vivo is still unclear. In particular, the effect of hemoglobin-NO interaction and the range of NO action have not been characterized in the microcirculation, where blood flow is optimally regulated. Using a mathematical model and experimental data on NO production and degradation rates, we investigated factors that determine the effective diffusion distance of NO in the microcirculation. This distance is defined as the distance within which NO concentration is greater than the equilibrium dissociation constant (0.25 μM) of soluble guanylyl cyclase, the target enzyme for NO action. We found that the size of the vessel is an important factor in determining the effective diffusion distance of NO. In ∼30- to 100-μm-ID microvessels the luminal NO concentrations and the abluminal effective diffusion distance are maximal. Furthermore, the model suggests that if the NO-erythrocyte reaction rate is as fast as the rate reported for the in vitro NO-hemoglobin reaction, the NO concentration in the vascular smooth muscle will be insufficient to stimulate smooth muscle guanylyl cyclase effectively. In addition, the existence of an erythrocyte-free layer near the vascular wall is important in determining the effective NO diffusion distance. These results suggest that 1) the range of NO action may exhibit significant spatial heterogeneity in vivo, depending on the size of the vessel and the local chemistry of NO degradation, 2) the NO binding/reaction constant with hemoglobin in the red blood cell may be much smaller than that with free hemoglobin, and 3) the microcirculation is the optimal site for NO to exert its regulatory function. Because NO exhibits vasodilatory function and antiatherogenic activity, the high NO concentration and its long effective range in the microcirculation may serve as intrinsic factors to prevent the development of systemic hypertension and atherosclerotic pathology in microvessels.