4,257 research outputs found
The 2D/3D dynamics of wall-bounded low-Rm magnetohydrodynamic (MHD) turbulence
No full textWith this experimental study, we give evidence that the dynamics of low-Rm MHD turbulence depends on the diffusion length l_z, which corresponds to the distance over which the Lorentz force is able to diffuse momentum before it is balanced by inertia
Spinoloricus cinziae (Phylum Loricifera), a new species from a hypersaline anoxic deep basin in the Mediterranean Sea
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Triangular Constellations in Flows
No full textParticles advected on the surface of a fluid can exhibit fractal clustering. The local structure of a fractal set is described by its dimension , which is the exponent of a power-law relating the mass in a ball to its radius : . It is desirable to characterise the {\em shapes} of constellations of points sampling a fractal measure, as well as their masses. The simplest example is the distribution of shapes of triangles formed by triplets of points, which we investigate for fractals generated by chaotic dynamical systems. The most significant parameter describing the triangle shape is the ratio of its area to the radius of gyration squared. We show that the probability density of has a phase transition: is independent of and approximately uniform below a critical flow compressibility , which we estimate. For the distribution appears to be described by two power laws: when , and when
Exact two-dimensionalization of low-magnetic-Reynolds-number flows subject to a strong magnetic field
No full textWe investigate the behavior of flows, including turbulent flows, driven by a horizontal body-force and subject to a vertical magnetic field, with the following question in mind: for very strong applied magnetic field, is the flow mostly two-dimensional, with remaining weak three-dimensional fluctuations, or does it become exactly 2D, with no dependence along the vertical? We restrict attention to low-magnetic-Reynolds number (Rm) flow. Because liquid metals have low magnetic Prandtl number, such low- flows can have a kinetic Reynolds number as large as one million and therefore be strongly turbulent. We first focus on the quasi-static approximation, i.e. the asymptotic limit of vanishing magnetic Reynolds number Rm << 1: we prove that the flow becomes exactly 2D asymptotically in time, regardless of the initial condition and provided the interaction parameter N is larger than a threshold value. We call this property absolute two-dimensionalization: the attractor of the system is necessarily a (possibly turbulent) 2D flow. We then consider the full-magnetohydrodynamic equations and we prove that, for low enough Rm and large enough N, the flow becomes exactly two-dimensional in the long-time limit provided the initial vertically-dependent perturbations are infinitesimal. We call this phenomenon linear two-dimensionalization: the (possibly turbulent) 2D flow is an attractor of the dynamics, but it is not necessarily the only attractor of the system. Some 3D attractors may also exist and be attained for strong enough initial 3D perturbations. These results shed some light on the existence of a dissipative anomaly for magnetohydrodynamic flows subject to a strong external magnetic field
Attenuated responses to angiotensin II in follitropin receptor knockout mice, a model of menopause-associated hypertension
No full textActivation of the renin-angiotensin system has been implicated in the development of hypertension in menopausal women. We investigated whether blood pressure is elevated and whether angiotensin II (Ang II)-induced vascular reactivity is increased in follitropin receptor knockout (FORKO) female mice. These mice are estrogen-deficient and have characteristics similar to postmenopausal women. Serum estradiol levels were significantly reduced in FORKO versus wild-type mice (1.4±0.2 versus 15±3 pg/mL, P<0.01). Blood pressure, measured by telemetry, was significantly increased in FORKO (120±2/92±2 mm Hg) compared with wild-type counterparts (110±1/85±2 mm Hg, P<0.05). Vascular dose responses to acetylcholine (endothelium-dependent dilation) and sodium nitroprusside (endothelium-independent dilation) were not different. Ang II–induced vasoconstriction was blunted in FORKO compared with wild-type mice (P<0.05). Media-to-lumen ratio was significantly increased in FORKO (6.2±0.5%) versus control mice (5.2±0.3%), indicating vascular remodeling. Aortic ·O2− levels, NADH-inducible ·O2− generation, and plasma levels of thiobarbituric acid reactive substances (TBARS), indexes of oxidative stress, were not significantly different between wild-type and FORKO mice. Vascular AT1 receptor content, assessed by immunoblotting, was reduced by 40% in FORKO compared with wild-type mice (P<0.01). This was associated with decreased circulating Ang II levels in FORKO versus control mice. These data indicate that FORKO mice have increased blood pressure, vascular remodeling, and attenuated vascular responses to Ang II. Our findings suggest that vascular Ang II signaling is downregulated in female FORKO mice and that Ang II may not play an important role in blood pressure elevation in this model of menopause-associated hypertension
Endothelin antagonism on aldosterone-induced oxidative stress and vascular remodeling
No full textEndothelin A (ETA) receptor blockade has prevented vascular remodeling in aldosterone and salt-induced hypertension. To evaluate effects of the ETA receptor antagonist, BMS 182874, compared with the aldosterone antagonist, spironolactone, on vascular remodeling in aldosterone-infused rats not exposed to a high salt diet, Sprague-Dawley rats were infused subcutaneously with aldosterone (0.75 μg/h) and treated with BMS 182874 (40 mg · kg−1 · d−1), spironolactone, or hydralazine (both 25 mg · kg−1 · d−1) while receiving a normal salt diet for 6 weeks. Aldosterone increased systolic BP (P<0.01), plasma endothelin (3.33±0.32 versus 1.85±0.40 pmol/L in control, P<0.05), systemic oxidative stress as shown by plasma thiobarbituric acid–reacting substances and vascular nicotinamide adenine dinucleotide phosphate (NADPH) activity. Aldosterone increased small artery media thickness (17.7±0.9 versus 13.6±0.8 μm in control, P<0.05) and media/lumen ratio (7.6±0.4 versus 5.5±0.4% in control, P<0.05), with growth index of 21% indicating hypertrophic remodeling. Laser confocal microscopy showed increased collagen and fibronectin deposition and intercellular adhesion molecule-1 (ICAM-1) content in the vessel wall of aldosterone-infused rats. The 3 treatments lowered BP, although hydralazine was slightly less effective. BMS 182874 and spironolactone decreased oxidative stress, normalized the hypertrophic remodeling, decreased collagen and fibronectin deposition, and reduced ICAM-1 abundance in the vascular wall of aldosterone-infused rats, whereas hydralazine only reduced NADPH activity in aorta but did not affect the remaining parameters. Vascular remodeling of small arteries occurs in aldosterone-infused rats exposed to a normal salt diet and may be mediated in part by ET-1 via stimulation of ETA receptors. Endothelin blockade may exert beneficial effects on vascular remodeling, fibrosis, oxidative stress, and adhesion molecule expression in aldosterone-induced hypertension
The Decay of Wall Bounded MHD Turbulence at Low RM
No full textWe have developed a new spectral method to simulate flows with very fine boundary layers present. We apply it to calculate the evolution of freely decaying MHD turbulence between isolating walls. By comparison them with results obtained in fully periodic domain we quantify the influence of the channel walls on the character of freely decaying MHD turbulence
Endothelium-restricted overexpression of human endothelin-1 causes vascular remodeling and endothelial dysfunction
No full textSpironolactone improves Angiotensin-induced vascular changes and oxidative stress
No full textAngiotensin II plays an important role in vascular remodeling. We investigated the role of aldosterone, which is stimulated by angiotensin II, as a mediator of angiotensin II–induced vascular structural and functional alterations. Sprague-Dawley rats (n=8 to 12/group) received angiotensin II (120 ng/kg per minute, subcutaneously) for 14 days ± spironolactone or hydralazine (25 mg/kg per day). An additional group received aldosterone (750 ng/h, subcutaneously) ± spironolactone. Systolic blood pressure was increased by angiotensin II (P<0.001) and reduced by spironolactone and hydralazine (P<0.001). Aldosterone-induced increase of blood pressure was reduced by spironolactone (P<0.05). In mesenteric small arteries studied on a pressurized myograph, media/lumen ratio was increased (P<0.001) and acetylcholine-mediated relaxation was impaired in angiotensin II–infused rats (P<0.001); both were partially improved by spironolactone (P<0.05) but not by hydralazine. Aldosterone-induced increase of media/lumen ratio (P<0.001) and impaired response to acetylcholine (P<0.001) were normalized by spironolactone. Response to sodium nitroprusside was similar in all groups. Aortic NADPH oxidase activity was increased (P<0.01) by angiotensin II and reduced by spironolactone and hydralazine. Aldosterone also increased (P<0.05) activation of NADPH oxidase, an effect abolished by spironolactone. Plasma thiobarbituric acid–reactive substances (a marker of oxidative stress), higher in angiotensin II and aldosterone rats (P<0.001), were normalized by spironolactone. In conclusion, spironolactone, which inhibited aldosterone actions, partially corrected structural and functional angiotensin II–induced abnormalities. These effects were associated with reduced vascular NADPH oxidase activity and decreased plasma markers of oxidative stress. Our findings suggest that aldosterone may mediate some of angiotensin II–induced vascular effects in hypertension, in part via increased oxidative stress
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