187,979 research outputs found
Twins: mirrors of the immune system
No full textwin studies are a powerful tool to assess genetic and nongenetic factors in multifactorial, immune-mediated diseases. Here, Marco Salvetti and colleagues review important results from such studies and highlight their potential value. Future developments that should help to realize the potential of twin studies are discussed
Numerical Simulations of Transitional Axisymmetric Coaxial Jets
No full textDirect numerical simulations of spatially evolving axisymmetric coaxial jets are carried out using nonreflecting radiative boundary conditions at the outflow. The sensitivity of the numerical solution to the domain size is investigated, pointing out the feedback effect of the boundary conditions on the pressure at the inlet. The effects of the Reynolds number on the characteristics of the flow are studied. In the initial phase following an impulse, the evolution of the startup vortex is found to be independent of the Reynolds number, whereas the circulation per unit length at the vortex center increases with the Reynolds number. The Reynolds number is also found to affect the further development of the shear-layers' instabilities. Finally, the effects of the inlet conditions on the dynamics of vortical structures are investigated. Two simulations are carried out, in which the inlet velocity profile is unperturbed and perturbed randomly, and the results are compared with flow visualizations from experiments. In the unperturbed case the rollup of the external shear layer occurs at a much larger distance from the jets exit than in experiments, whereas in the perturbed case a good agreement with the experiments is obtained
Effects of prostaglandins inhibition on changes in active and inactive renin induced by antihypertensive drugs.
No full textThe behaviour of active (AR) and inactive (IR) renin was studied in 48 hypertensive patients (37 with uncomplicated essential hypertension and 11 with reno-vascular hypertension) treated with indomethacin alone or with AR stimulating (bumetanide, tienilic acid, captopril) and inhibiting (atenolol) drugs before and after indomethacin addition. In 10 pts indomethacin (50mg q.i.d./3 days) reduced (p less than 0.05) AR and to a lesser extent IR. In 6 pts bumetanide (1 mg) increased (p less than 0.05) only AR and this effect was abolished by indomethacin. In 6 pts tienilic acid (250 mg) increased (p less than 0.05) only AR and this action was unchanged by indomethacin. In 11 renovascular pts captopril (100mg) increased AR (p less than 0.01) and lesser IR and both these effects were uninfluenced by indomethacin. In 11 essential hypertensive pts captopril (25mg b.i.d./3 days) increased only AR (p less than 0.02), but after 1 year both AR and IR were increased (p less than 0.05) and these effects were abolished by indomethacin. In all the above reported protocols we did never find any inverse correlation between either AR and IR values or their induced changes. These data suggest that prostaglandins stimulate, even if not to a similar extent, both AR and IR and that drugs, which stimulate renin either through or independently of PGs, did not cause any apparent interconversion of plasma IR into AR. In 6 pts atenolol (100 mg daily/6 days) reduced AR (p less than 0.05) and tended to increase IR. Indomethacin addition further decreased AR and reduced IR (both p less than 0.05 vs atenolol alone): however the proportion (% of total) of IR was still reduced. These findings suggest that beta 1-adrenoreceptors blockade exerts a divergent effect on active and inactive renin and that this action is not influenced by PGs synthesis inhibition
Interaction between oxprenolol and indomethacin on blood pressure in essential hypertensive patients.
No full textA double-blind, cross-over study in 16 patients with essential hypertension was carried out, to evaluate any possible interference by indomethacin, a known prostaglandin-synthetase inhibitor, with the antihypertensive effect of oxprenolol, a non-selective beta-adrenoceptor blocking agent. Both indomethacin and oxprenolol, as well as the two drugs combined, inhibited plasma renin activity; no change was found in urinary sodium excretion or body weight. Oxprenolol alone caused a highly significant decrease in the systolic ( - 10.4 mmHg, p less than 0.001), diastolic ( - 7.4 mmHg, p less than 0.001) and mean ( - 7.7 mmHg, p less than 0.01) blood pressures, whereas indomethacin did not influence blood pressure. When the two drugs were given in combination, blood pressure decreased (systolic: - 5.9 mmHg; diastolic: - 4.0 mmHg; mean: - 4.6 mmHg), but the changes induced in blood pressure were reduced by about 50% when compared with those in the oxprenolol alone period. The data show that indomethacin seems to interfere with the antihypertensive effect of oxprenolol, by an action which may be due to the inhibition of prostaglandin synthesi
Theoretical-study of the potential-energy curves of the diatomic radicals MeIIX .3. application to MgCl, CaF and CaCl radicals and some preliminary remarks
No full textTheoretical-study of the potential-energy curves of the series of diatomic radicals meiix .1. Method and its application to BeF radical
No full textApplication of a direct transmethylation method to the analysis of fatty acid profile in circulating and cultured cells
No full textTheoretical investigation on the crossing states 1-Sigma.g+(2p-2p) and X2-Sigma-g+ of the dimers Li2,Na2,K2 and their positive-ions Li2+,Na2+ and K2+
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Nonadrenergic sympathetic vascular control of the human forearm in hypertension: possible involvement of neuropeptide Y.
No full textAnimal experimental evidence suggests that neuropeptide Y (NPY) is coreleased with norepinephrine (NE) from sympathetic nerve endings and is involved in nonadrenergic neurogenic vascular control of skeletal muscle. We wished to determine whether these findings may be extended to humans. Forearm blood flow (venous occlusion plethysmography) and the regional overflows of NE and NPY-like immunoreactivity (NPY-LI) were studied at rest and during sympathetic nerve activation by lower body negative pressure (LBNP; -10 mm Hg, 10 min) in 10 hypertensive men before and after local alpha-adrenergic blockade by a dose of phenoxybenzamine (60 micrograms x 100 ml-1 x min-1 for 60 min), which most markedly attenuated responses to exogenous NE; propranolol (10 micrograms x 100 ml-1 x min-1) was present throughout. Phenoxybenzamine increased forearm blood flow at rest (11.5 +/- 1.0 vs. 3.9 +/- 0.3 ml x 100 ml-1 x min-1; p less than 0.001). LBNP-evoked reduction of forearm blood flow (37 +/- 2%, p less than 0.001) was attenuated (p less than 0.001) but not abolished (18 +/- 2%, p less than 0.001) by phenoxybenzamine. LBNP increased the overflow of NE from 5.0 +/- 1.7 to 8.2 +/- 3.0 pmol x 100 ml-1 x min-1 (p less than 0.05) and that of NPY-LI from -9.0 +/- 4.4 to 8.0 +/- 4.9 fmol x 100 ml-1 x min-1 (p less than 0.05) after phenoxybenzamine; effects on the evoked overflows of NE and NPY-LI before phenoxybenzamine were slight. Prejunctional inhibitory alpha-adrenoceptors may thus modulate NPY release as well.(ABSTRACT TRUNCATED AT 250 WORD
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