Scientific data is continually increasing in complexity, variety and size, making efficient visualization and specifically rendering an ongoing challenge. Traditional rasterization-based visualization approaches encounter performance and quality limitations, particularly in HPC environments without dedicated rendering hardware. In this paper, we present OSPRay, a turn-key CPU ray tracing framework oriented towards production-use scientific visualization which can utilize varying SIMD widths and multiple device backends found across diverse HPC resources. This framework provides a high-quality, efficient CPU-based solution for typical visualization workloads, which has already been integrated into several prevalent visualization packages. We show that this system delivers the performance, high-level API simplicity, and modular device support needed to provide a compelling new rendering framework for implementing efficient scientific visualization workflows.
. Vasoactive effects of methylamine in isolated human blood vessels: role of semicarbazide-sensitive amine oxidase, formaldehyde, and hydrogen peroxide. Am J Physiol Heart Circ Physiol 286: H667-H676, 2004; 10.1152/ajpheart.00690. 2003.-It is hypothesized that methylamine (MA) and semicarbazidesensitive amine oxidase (SSAO) activity are involved in the cardiovascular complications in human diabetics. To test this, we 1) determined the acute vasoactive effects of MA (1-1,000 mol/l) in uncontracted and norepinephrine (NE; 1 mol/l)-precontracted human blood vessels used for coronary artery bypass grafts [left internal mammary artery (LIMA), radial artery (RA), and right saphenous vein (RSV)]; 2) tested whether MA effects in LIMA and RSV were dependent on SSAO activity using the SSAO inhibitor semicarbazide (1 mmol/l, 15 min); 3) determined the effects of MA metabolites formaldehyde and hydrogen peroxide in LIMA and RSV; 4) tested whether the MA response was nitric oxide, prostaglandin, or hyperpolarization dependent; 5) measured the LIMA and RSV cGMP levels after MA exposure; and 6) quantified SSAO activity in LIMA, RA, and RSV. In NE-precontracted vessels, MA stimulated a biphasic response in RA and RSV (rapid contraction followed by prolonged relaxation) and dominant relaxation in LIMA (mean Ϯ SE, %relax-ation: 55.4 Ϯ 3.9, n ϭ 30). The MA-induced relaxation in LIMA was repeatable, nontoxic, and age independent. Semicarbazide significantly blocked MA-induced relaxation (%inhibition: 82.5 Ϯ 4.8, n ϭ 7) and SSAO activity (%inhibition: 98.1 Ϯ 1.3, n ϭ 26) in LIMA. Formaldehyde (%relaxation: 37.3 Ϯ 18.6, n ϭ 3) and H 2O2 (%relax-ation: 55.6 Ϯ 9.0, n ϭ 9) at 1 mmol/l relaxed NE-precontracted LIMA comparable with MA. MA-induced relaxation in LIMA was nitric oxide, prostaglandin, and possibly cGMP independent and blocked by hyperpolarization. We conclude that vascular SSAO activity may convert endogenous amines, like MA, to vasoactive metabolites. amine metabolism; coronary artery bypass grafts; diabetes; H2O2 A CURRENT HYPOTHESIS STATES that chronic methylamine (MA) exposure induces vascular injury and promotes vascular disease, including atherosclerosis, in humans via semicarbazidesensitive amine oxidase-mediated (SSAO) metabolism of MA to injurious metabolites: formaldehyde, H 2 O 2 , and ammonia (NH 3 ) (19, 50-52). Recent clinical and experimental studies support such a relationship. Altered plasma MA levels, MA excretion, and elevated plasma SSAO activity are present in human diseases associated with chronic vascular pathology [e.g., diabetes mellitus and uremia (Refs. 3,5,6,27, and 49; for reviews, see Refs. 19 and 51)]. In the case of Type I diabetes, SSAO plasma levels increase at the onset of disease (6) and plasma SSAO activity positively correlates with the amount of glycosylated hemoglobin, an indicator of the severity of complications in human diabetics (5, 43). Similarly, plasma SSAO activity is elevated within 2 wk after streptozotocin-induced diabetes in rats (22). Thus much circumstantial evidence link...
Increased risk of vasospasm, a spontaneous hyperconstriction, is associated with atherosclerosis, cigarette smoking, and hypertension-all conditions involving oxidative stress, lipid peroxidation, and inflammation. To test the role of the lipid peroxidation-and inflammation-derived aldehyde, acrolein, in human vasospasm, we developed an ex vivo model using human coronary artery bypass graft (CABG) blood vessels and a demonstrated acrolein precursor, allylamine. Allylamine induces hypercontraction in isolated rat coronary artery in a semicarbazide-sensitive amine oxidase activity (SSAO) dependent manner. Isolated human CABG blood vessels (internal mammary artery, radial artery, saphenous vein) were used to determine: (1) vessel responses and sensitivity to acrolein, allylamine, and H 2 O 2 exposure (1 μM-1 mM), (2) SSAO dependence of allylamine-induced effects using SSAO inhibitors (semicarbazide, 1 mM; MDL 72274-E, active isomer; MDL 72274-Z, inactive isomer; 100 μM), (3) the vasoactive effects of two other SSAO amine substrates, benzylamine and methylamine, and (4) the contribution of extracellular Ca 2+ to hypercontraction. Acrolein or allylamine but not H 2 O 2 , benzylamine, or methylamine stimulated spontaneous and pharmacologically intractable hypercontraction in CABG blood vessels that was similar to clinical vasospasm. Allylamine-induced hypercontraction and blood vessel SSAO activity were abolished by pretreatment with semicarbazide or MDL 72274-E but not by MDL 72274-Z. Allylamine-induced hypercontraction also was significantly attenuated in Ca 2+ -free buffer. In isolated aorta of spontaneously hypertensive rat, allylamine-induced an SSAOdependent contraction and enhanced norepinephrine sensitivity but not in Sprague-Dawley rat aorta. We conclude that acrolein generation in the blood vessel wall increases human susceptibility to vasospasm, an event that is enhanced in hypertension.
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